generation 7.gen.993 Louis J. Sheehan, Esquire

The Demon Barber Sweeney Todd is the English bogeyman: the character older children call upon to frighten their friends and younger children. Louis J. Sheehan, Esquire Unruly youngsters are cautioned against misbehaving with threats of being attacked by Sweeney and served up in a meat pie.

To most people, the Demon Barber who used a trap door and trick chair to slaughter his clients was the stuff of urban legend. After all, the events connected with his story are almost unbelievable. His exploits prey upon very common human fears: being attacked while vulnerable, and being served up as food or unknowingly consuming someone else. Who hasn't sat in the chair and felt a shiver as the barber or hair dresser takes out that straight razor, sharpens it on the strop and then applies it to the back of the neck? Or taken a bite of a meal and wondered just what the origin of the hair in the hamburger was? So it was for years, as the legend of Sweeney Todd was passed on from generation to generation, people wrote off the story as pure fiction.

But most myths and legends have a basis somewhere in truth, and Sweeney Todd is no different. There really was a mad barber, he really did use a trapdoor and straight razor to rob and kill customers, and most did end up as filling for meat pies. Extensive, painstaking research by British author Peter Haining has shown this without a doubt. Todd's life and exploits are not nearly as romantic as Sondheim would have us believe, but then who would pay to see a movie or musical about a psychopathic mass murderer unless there was more to the story?

What follows is the true story of the Demon Barber of Fleet Street. There is little romantic or even melodramatic about the life and times of Sweeney Todd. He was an amoral, bitter man who lusted for money and was not averse to killing to get it.

reports 7.rep.993 Louis J. Sheehan, Esquire

SEARCH FOR RECORDS

In searching for government records on the Roswell crash, we were particularly interested in identifying and reviewing records of military units assigned to RAAF in 1947--to include the 509th Bomb Group, the 1st Air Transport Unit, the 427th Army Air Force Base Unit, and the 1395th Military Police Company (Aviation).

Document disposition forms obtained from the National Personnel Records Center in St. Louis, Missouri, indicate that in 1953, the Walker Air Force Base (formerly RAAF) records officer transferred to the Army's Kansas City records depository the histories of units stationed at Walker Air Force Base. These histories included the 509th Bomb Group and RAAF for February 1947 through October 1947; the 1st Air Transport Unit for July 1946 through June 1947; and the 427th Army Air Force Base Unit for January 1946 to February 1947. We could not locate any documentation indicating that records of the 1395th Military Police Company (Aviation) were ever retired to the National Personnel Records Center or its predecessor depositories.

The July 1947 history for the 509th Bomb Group and RAAF stated that the RAAF public information office "was kept quite busy . . . answering inquiries on the 'flying disc,' which was reported to be in [the] possession of the 509th Bomb Group. The object turned out to be a radar tracking balloon." By his signature, the RAAF's commanding officer certified that the report represented a complete and accurate account of RAAF activities in July 1947. (Excerpts from the report are contained in app. I.)

In addition to unit history reports, we also searched for other government records on the Roswell crash. In this regard, the Chief Archivist for the National Personnel Records Center provided us with documentation indicating that (1) RAAF records such as finance and accounting, supplies, buildings and grounds, and other general administrative matters from March 1945 through December 1949 and (2) RAAF outgoing messages from October 1946 through December 1949 were destroyed. According to this official, the document disposition form did not properly indicate the authority under which the disposal action was taken. The Center's Chief Archivist stated that from his personal experience, many of the Air Force organizational records covering this time period were destroyed without entering a citation for the governing disposition authority. Our review of records control forms showing the destruction of other records--including outgoing RAAF messages for 1950--supports the Chief Archivist's viewpoint.

United States 4.uni.0002 Louis J. Sheehan, Esquire

OUTLINE OF PART B*

Japanese Intelligence in Diplomatic Messages

(a) Reports from the United States
(b) Reports from the Panama Canal
(c) Reports from the Philippine Islands
(d) Reports from the Hawaiian Islands
(e) Reports from South America
(f) Reports from Capetown, South Africa
(g) Reports from Vladivostok, Russia

PART B—JAPANESE INTELLIGENCE IN DIPLOMATIC MESSAGES

Continuing to use diplomatic channels for the transmission of intelligence concerning American merchant ships and men-of-war during the period from August 16, 1941 to October 17, 1941, Japanese officials in Tokyo received an increasing number of such dispatches from the United States and South America, the Philippines and Hawaiian Islands.

(a) Reports from the United States

133. Japan Learns that American Oil Is Being Transported to Russia

Consul Kenji Nakauchi in Hollywood, California reported on August 16, 1941 that the St. Claire, after loading 95,000 barrels of aviation gasoline, had sailed from Los Angeles for Vladivostok, and was scheduled to rendezvous at some point in the Pacific with the Fitzsimmons and three other American vessels, all carrying similar cargo. According to rumor, a number of United States destroyers on maneuvers were also bound for Vladivostok,[514] and a Japanese spy in Seattle reported that the English warship, Warspite, had entered the port of Bremerton about August 13 or 14, 1941.[515]

It was disclosed on August 21, 1941 that the Russian ship, Vladimar Mayskovsky, had arrived at Seattle, and after being repaired, would move to California to load freight for Vladivostok. The Minsk was reported to have left Seattle harbor, although its destination was unknown, and the Patrovsuky was still in dry dock.[516]

On the same day Tokyo informed Berlin that though America was apparently transporting oil to Russia, using American, Russian, and neutral ships, and there was a possibility that several hundred planes had already been transported, up to the present time not one American vessel had entered the port of Vladivostok. Although both the Russian Ambassador in Tokyo and the American government, through Ambassador Nomura, had been warned by Japan concerning the extension of a third power's military movements to East Asia, Japan believed that it was impossible to effect any actual restraint through such steps.[517]

*See TABLE OF CONTENTS for a detailed listing of topics discussed in Part B.

[514] III, 285.
[515] III, 286.
[516] III, 287.
[517] III, 288.

[122]

THE "MAGIC" BACKGROUND OF PEARL HARBOR

Consul Yoshio Muto in San Francisco on August 26, 1941 advised Tokyo that the Russian freighter, Yakut, had left port August 24, 1941 loaded with gasoline, shoes, socks, and small arms. Confirming the arrival at San Francisco of the Russian freighter Minsk the report also listed the Russian tanker Dombas as having arrived in port from Los Angeles.[518]

134. Japan Learns of Shipment of American Planes To Russia

Consul Jiseburo Sato, Japanese Intelligence agent at Seattle, reported on August 18, 1941 that a group of large planes was being sent from the United States to Alaska, and planes already in Alaska were probably destined to supply Soviet Russia. Since several two-motored medium sized planes en route to Alaska were marked with the insignia of the United States Army, he surmised that they were probably not intended to be sent to Russia.[519]

135. American Aid to Russia Is Viewed as Threat to Japan

Japan, considerably concerned over these reports of American aid to Russia, learned from Rome that the United States had recently made representations to the Russian government to permit the sending of American naval advisers to Vladivostok. Since American military establishments in Russia would be a threat against Japan, the Japanese Ambassador in Rome advised his government to make a thorough investigation to ensure that they were not established, although the Russian authorities had apparently not yet permitted nor would permit such action.[520]

The Japanese Foreign Minister informed Ambassador Nomura on August 28, 1941 that he had directed the Japanese Ambassador in Moscow to warn Russia that should supplies be exported from the United States to Russia through Japanese waters, Japan's position would become extremely delicate. Foreign Minister Toyoda remarked that, according to recent intelligence, seven American, Russian, and neutral ships were transporting airplane gasoline for the aid of Russia. The Russian government was urged by Japan to consider this development with extreme caution, not only from the legal viewpoint of international law but from the standpoint of the general world situation.[521]

To prevent the spreading of the European war into the Far East, Russia was urged to consider the Japanese-Russian agreement and the maintenance of the excellent relationship between the two countries. In the event that the United States sent its ships through Japanese waters, the effect upon public opinion within Japan, as well as the reactions of Germany and Italy, would "indeed be terrible in the extreme". With regard to the importation of American goods, Japan insisted that Russia give particular attention to the routes over which imports were received.[522]

Meanwhile, Japanese officials on the west coast of the United States continued their intelligence reports on the movements of American shipping. In addition to the departure on September 8, 1941 for Vladivostok of a vessel bearing 80,000 barrels of aviation gasoline, Consul Yoshio Muto in San Francisco also notified Japan that four American tankers of the General Petroleum Company were to be dispatched on the direct shipping route to Vladivostok.[523]

[518] III, 289.
[519] III, 290.
[520] III, 291.
[521] III, 292.
[522] III, 293.
[523] III, 294.

[123]

136. Japan Attempts to Expand Its Naval Intelligence Activities

On September 2, 1941 it became apparent to Tokyo that the expansion of Japanese naval intelligence activities in both North and South America was necessary. Based on a request from naval authorities in Japan, Ambassador Nomura was to insist that a member of his staff go to Hawaii in the capacity of a courier, though in the light of Japanese-American relations the selection of an opportune moment for the presentation of this request to the American government was left to his discretion.[524]

Ambassador Nomura replied that inasmuch as Courier Kuga was returning to Japan by way of the United States, having booked passage on the President Taylor sailing from San Francisco on September 6, 1941, the dispatching of a courier to Hawaii was no longer necessary.[525]

137. Japanese Agents Note American Army and Air Group Activities

Through Consul Sato at Seattle, the statements made by the president of the Boeing Company to a Senate investigating committee were relayed to Tokyo on September 4, 1941. According to the report, the lack of progress was because of the changes in design and the unprecedented expansion of the plant. Although the production of American Army planes was four months behind in schedule, it was expected that this would be caught up by the end of the year.[526]

Furthermore, Lt. General DeWitt, 4th Army Commander, had announced that his army would be increased from 90,000 to 120,000 men. Barracks capable of accommodating 30,000 men were being constructed along the coast, and a mechanized division of 10,000 men was to be located at Santa Maria. The locations of newly organized divisions were listed as Meadow-ford, West Yellowston, Fort Huachuca and Marysville.[527]

Reported also in an intelligence dispatch of September 4, 1941 was the movement on August 23 of the 39th Bombardment Group, the 89th Observation Squadron, and the 310th Signal Company from Spokane to Louisiana to take part in the September maneuvers. The 54th Bombardment Group would receive either Republics or twin-motored Lockheed planes.[528]

138. Japan Watches the Activities of a Russian Military Commission in the United States

Reporting to Japanese intelligence headquarters in Washington, Consul (Lt. Comdr.) Jisaburo Sato at Seattle wired that two Russian planes, arriving at the Naval airfield at Sand Point on September 4, 1941, had brought members of a Russian commission to confer with American authorities concerning aid to Russia.[529] This was apparently the Russian Military Commission which on September 2, 1941 had inspected the B-19 heavy bombers at March Field, and on September 3, 1941 had visited various airplane factories at Los Angeles.[530]

Ambassador Nomura requested Japanese agents in San Francisco, Los Angeles, and Seattle to investigate the possibility of the Russian Military Commission's flying American planes to Russia. He also asked that intelligence be secured concerning the eventual transfer of a considerable American bombing force to the Siberian area.[531]

[524] III, 295.
[525] III, 296.
[526] III, 297.
[527] Ibid.
[528] III, 298.
[529] III, 299.
[530] III, 300.
[531] III, 301.

[124]

THE "MAGIC" BACKGROUND OF PEARL HARBOR

In accordance with Ambassador Nomura's request to report concerning the Russian Military Commission, Consul Sato informed Tokyo on September 22, 1941 that two Russian hydroplanes, bearing ten members of the commission, had left for Moscow on September 19, 1941, but that the remaining thirty-seven members were to stay in the United States to study the production of airplanes.[532] Nineteen of the thirty-seven members remaining in the United States were receiving training in bomber operations at Spokane, Washington, while the others were staying in Washington and Los Angeles.[533]

139. Japanese Consuls Report on West Coast Shipping

Illustrating the close surveillance of American, Russian, and neutral ships by Japanese agents on the American west coast, Consul Muto, on September 8, 1941, informed Tokyo that the Russian freighter, the Minsk, loaded with 8,000 drums of aviation oil, airplane engines, machine guns, ammunition, snow plows and other articles had sailed from San Francisco on September 6, 1941.[534]

On September 6, 1941 Japanese officials in Seattle, attempting to verify the presence of the Vladimar Maykoysky and the Deabrint noted that four vessels were in port.[535] In a dispatch transmitted September 18, 1941 the Japanese Consul reported that the Russian freighter Mijinski, from Vladivostok, had entered San Francisco on September 17, 1941 and that the American tanker, St. Claire, returning from Vladivostok, was expected to arrive on September 19, 1941[536]

Although Consul Muto in San Francisco reported on September 18, 1941 that the Warspite had entered port there from Bremerton,[537] on September 20, 1941 Consul Sato in Seattle informed Tokyo that repair work was continuing on the Warspite at Bremerton. One Saratoga-class aircraft carrier and another vessel which appeared to be a cruiser were also in port, but a ship of the New Mexico class, previously reported there had departed.[538] The arrival of one Oklahoma-class battleship at San Francisco was announced by Consul Muto at San Francisco on October 2, 1941, and a report that the Hunters Point shipyard would be taken over by the United States Navy was sent to Japanese officials in Washington.[539]

On October 16, 1941 Consul Muto declared that the Russian freighter Mijinski was docking, that the Igarka was three days out of New York, that the Nantes was seven days from Vladivostok, and the Michulin was ten or twelve days from Vladivostok. The Nantes was loaded with wheat, 20,000 barrels of fuel oil, and machine guns and tanks.[540] The Russian ship, Kiev, equipped with a 500-watt radio for the reception of orders and war news from Moscow, was reported, on October 12, 1941, to be loading raw materials at Los Angeles before proceeding to Vladivostok.[541]

[532] III, 302.
[533] III, 303.
[534] III, 304-305.
[535] III, 306.
[536] III, 307.
[537] III, 308.
[538] III, 309.
[539] III, 310.
[540] III, 311.
[541] III, 312.

[125]

140. Foreign Minister Toyoda Sends New Instructions Concerning Naval Intelligence Reports Louis J. Sheehan, Esquire

To facilitate the making of reports on the movements of American warships, Foreign Minister Teijiro Toyoda on October 16, 1941 directed the Japanese Consul in Seattle to make routine reports once every ten days, in case there were no great changes in the movements and basing of warships. Special reports were to be made immediately on such occasions as (a) the arrival or departure of American flagships of fleet or scouting force; (b) the arrival or departure of more than ten vessels of any type; (c) the arrival or departure of warships of other countries than the United States; and (d) the inauguration of patrolling by naval planes.[542]

(b) Reports from the Panama Canal

141. Japan Fails to Learn Destination of Planes Departing from Panama

One hundred planes, including Douglas B-18's Martin B-17A bombers, and Boeing 24's which had been stationed at Albrook Field, suddenly departed in early August, 1941 before Japanese observers could learn their destination. A hearsay report was sent to Tokyo on August 18, 1941 that approximately 35 or 45 two-motored bombing planes were stationed at the newly constructed Agua Dulce Air Field in the province of Cocli.[543]

Ships moving through the Panama Canal were the subject of Japanese naval intelligence reports forwarded to Tokyo by Minister Akiyama. Four American submarines, on August 18, 1941, and two freighters, on August 17, 1941, had passed through the Canal toward the Atlantic.

Moving toward the Pacific on August 15, 1941 were a United States freighter and the Triomphant, a DeGaullist destroyer, which left for Tehita on August 17. In addition, five destroyers were reported taking on fuel, rations, and other supplies at Panama.[544] One British and two American freighters were observed on August 19, 1941 to be moving through the Canal toward the Pacific.[545]

Between September 17 and 21, 1941, one American tanker and four American freighters had reportedly passed through the Canal bound for the Pacific, while two American tankers, four American freighters, and one English freighter had gone toward the Atlantic.[546] Informing Tokyo on September 28, 1941 that a Diomede class vessel recently had the upper section of the mast cut off, Minister Akiyama announced that the British operated two ships of this type.[547] On September 30, 1941 it was reported that two warships, possibly French, had left port on August 29, 1941 bound for the Pacific, while another ship of the Omaha class had also departed for an unknown destination.[548]

Minister Akiyama wired on October 2, 1941 that between September 30 and October 2, 1941 three American freighters and one English hospital ship had passed through the Canal to the Pacific, and nine American freighters and one American liner to the Atlantic.[549]

Reporting that one vessel, three American freighters, and one French steamer had moved into the Pacific between October 3 and 4, 1941, Mr. Akiyama wired that seven American freighters, the Union tanker, one destroyer, and two British freighters had gone through the Canal successively in the direction of the Atlantic. Since two cruisers had accompanied these vessels as far as Balboa, indications were that their cargoes were made up of military supplies.[550]

[542] III, 313.
[543] III, 314.
[544] III, 315.
[545] III, 316.
[546] III, 317.
[547] III, 318.
[548] III, 319.
[549] III, 320.
[550] III, 321.

[126]

THE "MAGIC" BACKGROUND OF PEARL HARBOR

142. Japanese Reports on Panama Military Installations

Intelligence transmitted to Tokyo on October 2, 1941 concerned the transfer of the Panama Air Depot from France Field to Curundu Heights, which had been made because of the recent concentration of military aviation in the Pacific area. Tokyo learned of an announcement which had been made on August 1, 1941 by Rear Admiral Sadler, Commander of the 13th Naval District, that a new warehouse on Pier 18, the ammunition unloading pier, and the Balboa dry dock would be taken over for use as naval warehouses.

The acquisition and camouflaging by the United States Navy of petroleum supply tanks at Boca on the Pacific side and at Mt. Hope on the Atlantic side were reported, as well as the construction at Corozal of a storage depot which would contain foodstuffs to supply the Canal Zone for six months should shipping routes between Panama and the United States be severed.[551]

An investigation by the Japanese Minister at Panama disclosed, on October 6, 1941, the sites of five United States' airplane bases in Panama. Panamanian airports, already constructed and scheduled to be converted into military establishments, were identified as the ones at David, in Chiriqui province, and Paidonya outside Panama City. Several other locations had been surveyed but were not used because of the poor condition of the terrain.[552] Louis J. Sheehan, Esquire

(c) Reports from the Philippine Islands

During the period from August 7 to October 17, 1941, Japanese naval intelligence reports from the Philippine Islands increased in number. They were concerned principally with fortifications, the arrival and departure of warships, and the construction of airports.

143. Japan Attempts to Identify British Vessels Reported at Manila

On August 9, 1941 Tokyo directed that secret investigations be made regarding the name of the British battleship reported to have entered port at Manila on August 17, 1941, sailing on the next day for the west coast of North America. According to the Japanese, this ship was reported to be the Warspite, although it was pointed out that the British cruiser Leander resembled the Warspite from a distance.[553]

Consul Katsumi Nihro, in replying to the inquiry, was uncertain as to the ship's identity, and said that he knew only that it was a light cruiser of the Leander class. No British ships, he added, had entered port recently except one which he had mentioned previously.[554]

On August 16, 1941 six ships were reported to have arrived in Manila on the previous day, and it was observed that both United States Army and Navy airplanes were being painted dark blue.[555]

144. Tokyo Inquires About a Floating Dry Dock Near Mariveles

The disappearance of a floating dock previously seen in the vicinity of Mariveles, Luzon was being investigated by the Japanese on August 18, 1941,[556] but subsequent investigations revealed that as late as September 4, 1941 the floating dock was still located one mile southeast of Mariveles in Bataan province. Barracks were being constructed near Mariberosu, and in spite of a previous rumor that they were built for the purpose of imprisoning Japanese nationals, Consul Nihro said that they were intended to house technicians and personnel working on the floating dock.[557]

[551] III, 322.
[552] III, 323.
[553] III, 324.
[554] III, 325.
[555] III, 326.
[556] III, 327-328.
[557] III, 329.

[127]

145. Japanese Reports on Manila Anti-Aircraft Preparations

As to fortifications in Manila proper, the Japanese Consul thought that, since admittance to the upper stories of the city's tall buildings had been forbidden, it was fairly certain that anti-aircraft guns had been placed on the tops of two of Manila's leading hotels, on the Insular Life and Trading Commerce buildings, and on several other public buildings. The transportation of thirty-six anti-aircraft guns to Camp Murphy had also been noted during the latter part of July 1941.[558]

146. Japanese Report on American Airport Construction

Tokyo was informed on August 20, 1941 that work begun in March on an unidentified airplane base in the Philippines, which had been suspended for a time, was now being accelerated.[559] Since too much time would be required to fill in paddy fields for the site of another new air base at Davao. Consul Jitaro Kihara disclosed that plans had been changed, and the airfield would be constructed between the sea and paddy fields where a cocoanut grove stood. Four concrete runways were to be built, and 2,500 recruits from the local populace were to be used in the construction.[560]

147. Japan Inquires Concerning the U.S.S. Houston

Learning from Japanese naval authorities that the Houston had disappeared after passing through the harbor entrance on August 20, 1941, Foreign Minister Toyoda asked on August 30, 1941 that Japanese agents investigate the waters in and around Manila for a trace of this warship.[561] He also directed that weekly intelligence reports be sent to Tokyo. The arrivals and departures of more than five or six destroyers, submarines, or naval ships other than American, were to be subjects of special reports at the time such changes occurred.[562]

On September 1, 1941 Consul Katsumi Nihro informed Japanese officials that the Houston had arrived at Manila on August 5, and that after loading food supplies, it had departed on August 7, 1941. It was surmised that since Admiral Thomas Charles Hart had attended the ceremonies connected with the launching of the "Q" boat for the Philippine army on August 10, the ship must have been in the vicinity until that date. Its course from then on, however, was not known.[563]

The Houston, with two destroyers, re-entered port at Manila on September 7, 1941,[564] and after loading fuel and stores it departed for an unknown destination on September 11, accompanied by two submarines and two destroyers.[565]

148. Japanese Report on American Ship Movements In the Philippines

A number of American destroyers, reported without substantiation to have come from Hawaii, entered the harbor of Jolo during the middle of July. During the last ten days of July, six other American destroyers entered ports in the Philippines and engaged in target practice with live ammunition. One large airplane capable of carrying twenty-six persons had landed on the water in the vicinity of Jolo for a number of hours, and 2,000 drums of airplane gasoline were stored within the military establishment at Jolo.[566]

[558] III, 330.
[559] III, 331.
[560] III, 332.
[561] III, 333.
[562] III, 334.
[563] III, 335.
[564] III, 336.
[565] III, 337.
[566] III, 338.

[128]

THE "MAGIC" BACKGROUND OF PEARL HARBOR

On August 23, 1941 Manila reported that six transports, as well as the Hon and Pisu were in port at Manila, and that one destroyer and the Gorudostna were at Cavite. It was also announced at this time that the oiler Torinircic hadLouis J. Sheehan, Esquire departed for Tarakan on August 22, 1941 to take on oil, that several destroyers and submarines were stationed in the vicinity of Mariveles and that Brigadier General Cragette, arriving on August 20 on the Dutch ship, Tibadaeky, had conferred with General Douglas McArthur on August 21, 1941. The Chanto had arrived at Manila on August 20 from Olongapu, where her sister ship, the Kabarunda, was still undergoing repairs. Another ship, possibly the Maddo, and two destroyers had arrived at Cebu on August 16, 1941, and had left the same night.[567]

On August 30, 1941, one destroyer was at Corundusu, and three destroyers, six submarines, and the tanker, Trinity, were at Manila where the arrival of 500 American soldiers on the Cleveland and the entrance of the Migak, a vessel which the Japanese understood was loaded to capacity with military equipment, were noted on the preceding day.[568] The Marblehead returned to its post on August 31, and two destroyers departed September 1, 1944.[569]

A ship, possibly the Black Hawk, the Beru, two destroyers, and one submarine were in port at Manila on September 13, 1941, according to a Japanese intelligence report, and on the same day there arrived an American cruiser of the Brooklyn class, believed to have come from Hawaii.[570] Whether Legaspi Island was being used as a port of call by an American aviation company was the subject of an inquiry directed by Tokyo to Manila on September 15, 1941,[571] Accordingly, Minister Nihro reported the next day that Legaspi was being used as an intermediary station by the Philippine Aerial Taxi Company between Manila and Cebu. It was also noted that the Pan-American Airways were planning to build a landing place at Tacloban in Leyte Province, but as yet had not realized this plan.[572]

The St. Louis, with three other unidentified vessels had left the harbor for Singapore early on September 16, 1941 apparently loaded with food supplies.[573] Since red flags had been hoisted, it was indicated that ammunition was being handled on these ships.[574]

In an intelligence dispatch from Manila on September 20, 1941 Consul Nihro declared that the Phoenix and one other ship were anchored at that port. Another ship, probably the Peters, which entered the harbor on September 18, was reported to have carried 500 soldiers.[575]

On September 26, 1941 Consul Kihara at Davao pointed out that since August, 1941 American destroyer tenders, destroyers, and submarines had entered the port of Davao from the South Seas on every Saturday and had left after about two days. From members of the crews of these warships, he had learned that the warships traversed a route touching Jolo Island, Bataan, Tarao in British North Borneo, and Tarakan, a city in Netherlands Borneo.[576]

[567] III, 339.
[568] III, 340.
[569] III, 341.
[570] III, 342.
[571] III, 343.
[572] III, 344.
[573] III, 345.
[574] III, 346.
[575] III, 347.
[576] III, 348.

[129]

Information concerning the size, tonnage and plane accommodations of the Langley was sent from Davao to Tokyo on September 26, 1941.[577] Consul Nihro advised on October 3, 1941 that he had learned that the American cruisers, the St. Louis and Phoenix, sailing from Manila on September 16 and 22, 1941 respectively, were headed for Singapore. He requested information from Singapore concerning this in order to check on the accuracy of his spy reports.[578] In return it was reported from Shanghai that the United States Army transport, the Henderson, had left that port for Manila carrying 150 Marines.[579]

On October 4, 1941 Foreign Minister Toyoda directed the Japanese Consul at Manila to make a reconnaissance of the new defense works along the east, west and southern coasts of Luzon. The consul was also asked to report on their progress, strength and anything else which might be of interest to Japan.[580]

The Japanese Consul reported that on the afternoon of October 13, 1941 the Houston, Marblehead, and one other vessel, five destroyers, and two minelayers had departed, but that their destinations were unknown. In the harbor on October 14, 1941 were the Black Hawk, four destroyers, ten submarines, the Gold Star, and one other vessel.[581]

A routine intelligence transmission sent to Tokyo on October 17, 1941 reported the Ton, the Maddo, the Hon, four destroyers, five submarines, one minelayer, the Beru and the oiler, Trinity, in port at that time. It was added that large scale barracks were being constructed about 131 kilometers from Manila between Cabanatuan and Laur, and that mechanized maneuvers were taking place between Laur and Aguilla.[582]

(d) Reports from the Hawaiian Islands

149. Japan Notes Activities of French in the Pacific

Consul Nagao Kita reported that taking passage on a destroyer which had left port on September 16, 1941 were Captain C. I. Gargenlieu, high commissioner for Pacific territories under the De Gaulle regime, and Commander G. Cabanier, French Commander of Defense, who were to assume new responsibilities in New Caledonia.[583]

150. Japanese Foreign Minister Requests Special Intelligence Reports Concerning Pearl Harbor

Japanese naval intelligence reports from Honolulu, though few in number, were in the light of the later attack on Pearl Harbor to grow increasingly significant as December 7, 1941 drew nearer. The significance becomes apparent, however, only when reading history backwards.

Concerning Pearl Harbor, Foreign Minister Toyoda on September 24, 1941 directed that in future intelligence reports from Hawaii, Pearl Harbor waters were to be divided roughly into five subareas—

Area A: Waters between Ford Island and the Arsenal.
Area B: Waters adjacent to the Island south and west of Ford Island. (This area is on the opposite side of the Island from Area A.)
Area C: East Loch.
Area D: Middle Loch.
Area E: West Loch and the communicating water routes

[577] III, 349.
[578] III, 350.
[579] III, 351.
[580] III, 352.
[581] III, 353.
[582] III, 354.
[583] III, 355.

immune system 8.is.00983 Louis J. Sheehan, Esquire

When one of psychiatrist Andrew Miller’s patients asked about receiving the best drug available for treating hepatitis C, Miller said: “No way.” The patient — in his early 20s and accompanied by his mom to the appointment — had no job, few friends and a history of depression. While Miller knows that hepatitis C patients often benefit from the new generation of immune-boosting treatments, he’s keenly aware that those same immune therapies have a strong tendency to bring people down — and, in people predisposed to depression, dangerously down.

Certain immune proteins in the body appear to mess with the minds of otherwise healthy, but depressed people as well. Those who suffer from major depression have higher levels of cytokines, immune proteins the body makes to fend off infections and to patrol the body for disease, and which laboratories mimic. Excess cytokines have also been found lurking in the postmortem brains of suicide victims. “It raises the issue, how much of how we feel — how much of who we are as people — is dictated in terms of our immune system?” says Miller, a researcher at Emory University in Atlanta.

Though the connection between the body’s immune response and depression has only gained firm support in the last five years, it’s already catalyzing a revolution in antidepressant drug development. In hindsight, an emotional reaction to surging immune molecules does not seem so surprising. Cytokines are among the first immune proteins to respond to infection. Some direct swelling and fevers. Others order the body to rest, and so the sick take to the bed and decline party invitations, showers and even homemade dinners. The powerful molecules influence wants and needs by altering levels of substances like serotonin in the brain. Essentially, cytokines command the body to conserve energy when it’s sick. “A little depressed behavior is a survival mechanism in that sense,” Miller says. But when inflammation is artificially or erroneously triggered, prolonged sickness behavior may morph into depression and do more harm than good.

Figuring out the biology behind depression should help doctors combat the disorder, which strikes an estimated 14.8 million American adults each year, according to the National Institute of Mental Health. More than one in six individuals will experience major depression in their lifetime. And when depression coincides with chronic diseases like multiple sclerosis, cancer or diabetes, patients’ conditions are less likely to improve.

Psychiatrists and pharmaceutical companies have noted the downpour of evidence linking inflammation to depression. Miller says he and his colleagues have considered creating a new diagnostic category: Major Depressive Disorder with Increased Inflammation. To combat this depression, he says, researchers must find a way to alter the body’s immune response. It is a risky strategy but one that offers hope to the nearly 30 percent of all depressed patients who don’t respond to the antidepressants currently on the market.

Jekyll-and-Hyde changes

Cytokines emerged as the primary suspects for what’s since become known as inflammation-induced depression after Miller and others noticed that cancer patients became inexplicably upset during treatment with synthetic type 1 interferons, cytokines that block viral replication in infected cells. One of these, interferon-alpha, is among the most effective drugs for patients battling cancer and the hepatitis C virus. Yet the treatment has become notorious for causing major depression and other behavioral changes in more than half of these patients, depending on the dose of the immune booster.

Miller describes a “Jekyll-and-Hyde– type change” in one of his patients after interferon therapy. Eight weeks into it, the patient dumped his girlfriend, began dressing in black and grew a goatee. And there was another woman, Miller recalls, who took a drastic downward turn. “One of my most positive patients had been battling cancer for years, yet four weeks into the cytokine therapy she was distraught,” he says. “She told me, ‘I love my husband and my children, but I don’t want to be around them. I want to be left alone, and I don’t know why.’ ”

As observations of sadness, irritability, insomnia, fatigue and loss of appetite — all classic symptoms of depression — mounted in patients treated with immune boosters in the 1990s, papers published nearly a decade earlier in veterinary journals resurfaced. Benjamin Hart had been writing about the behavior of sick animals since the mid-1980s. “Depression was the first sign we had that an animal was sick,” says Hart, an animal behavior researcher at the University of California, Davis. In a seminal 1985 paper in the Journal of the American Veterinary Medical Association, he put forth the argument that animal malaise serves a purpose.

“People would call in and say that the dog is sleeping more than usual. They give the dog its favorite treat, and it only nibbles at it and then drops it, or they’d say the cat looks scruffy,” Hart explains. “Cats usually groom all the time.” He says that when he ran blood and urine tests on such animals, he usually discovered signs of bacterial or viral infection. Instead of assuming the pet acted sad because it wasn’t feeling well, he suggested that the pet’s behavior was part of its immune response. Fido’s body forced the animal to devote its energy to battling illness, instead of to chasing squirrels.

Furthermore, since all mammals act similarly when sick, Hart suggested that the behavior had been inherited from a common ancestor who survived infection better than other animals who had not evolved the behavioral response.

In the 1990s, researchers in the Netherlands reported that patients with major depression showed signs of inflammation, with elevated levels of cytokines in their blood and cerebrospinal fluid. And in 2001, Robert Dantzer, now at the University of Illinois at Urbana-Champaign, injected rats with cytokines. Sure enough, Dantzer says, the rats lost interest in previous pleasures and activities: They didn’t care for sugary water, they didn’t run on the wheel and, when placed in a pool of water they swam lethargically, barely keeping their heads above water.

Miller compares this sickness behavior to “holing up in a cave.” Although the animal has little drive to do much of anything, it does stay alert to major threats. “While in the cave, the organism rests but keeps one eye open,” he says. That may explain why people with the flu, as well as people with depression, neither leave the couch nor get the deep sleep they crave.

Connecting body to mind

Like army generals, innate immune cytokines order inflammatory molecules to prepare for war when the body is under threat from invasive bacteria or viruses, or under perceived threat in the form of stress or chronic disease. In these situations, cytokine levels rise. “It’s a good thing if you’re running from a tiger,” explained psychiatrist Dominique Musselman in May at a meeting in Washington, D.C., of the American Psychiatric Association. “You’d want to rev up your immune system to prepare for an injury.” Nowadays, however, angry bosses, aggressive creditors and disappointed spouses have replaced vicious predators, she said. And as those stressors are less likely to bite, the subsequent immune response, which had evolved to heal injuries and fight infection, seems a vestige of the distant past.

“The fact that stress can activate the innate immune response has been a major breakthrough,” Miller notes. Add this to one more piece of the puzzle: Stress often leads to depression. The immune system may explain why.

In mapping out the molecular pathway between elevated cytokines in the body and chemical changes in the brain, scientists aim to provide targets for drugs intended to treat depression caused by inflammation. In the last few years, researchers have identified primary suspects. Many cytokine proteins, including tumor necrosis factor-alpha, interleukin-6 and the type 1 interferons (IFN-alpha and IFN-beta), have been accused of being the principal perpetrators in sickness behavior. They respond rapidly to foreign intruders, circulate in the bloodstream and initiate a response in the central nervous system.

Cytokines manufactured in the body can send messages through the central nervous system to induce production of cytokines in the brain. That message may be relayed when cytokines sneak into the brain through leaky regions in the blood-brain barrier, a series of structures that block most substances. In the brain, cytokines activate inflammatory middlemen who tag-team their way to affecting emotion-regulating neurotransmitters. As neurotransmitter levels change, so can mood. “Among other things, we see a drop in levels of serotonin, the feel-good chemical,” Miller says.

Attempts are underway to treat depression by blocking specific cytokines or the messages they send. A 2006 clinical trial funded in part by the biotech company Amgen found that depressed patients who suffered from psoriasis, an autoimmune skin disease associated with increased levels of cytokines, felt happier after taking the cytokine blocker etanercept (brand name Enbrel), which affects tumor necrosis factor-alpha. Another TNF-alpha blocker, infliximab (Remicade), is being tested for use in depressed patients who don’t respond to antidepressants such as the selective serotonin reuptake inhibitors Prozac and Zoloft. Those results should be ready by 2010, says Charles Raison, a research psychiatrist at Emory University who heads the project.

Anti-inflammatory drugs like aspirin and ibuprofen haven’t been shown to affect mood. But another anti-inflammatory, celecoxib (Celebrex), that more specifically blocks the inflammatory molecule COX-2, helped heal depression in a small clinical trial in Germany. Norbert Müller, a psychiatrist on that study from Ludwig-Maximilians-University Munich, suggests that a high dose of aspirin would be needed to inhibit COX-2 as strongly as celecoxib. And that, he says, “would provoke a high rate of side effects, mainly gastrointestinal pain and possibly bleeding.”

Developing these types of treatments isn’t easy, warns Dantzer. Compounds that interfere with immune responses have the dangerous potential to compromise the body’s resistance to infection. The goal is to temper inflammatory molecules in the brain, not the body.

Researchers will have to identify safe points to alter along the molecular pathway that runs between bodily cytokines, molecular middlemen and neurotransmitters in the brain. “The further upstream you go towards the cytokines, the more far-reaching the effects on the body. If you move downstream to block cells that are activated by the inflammation, you may have a drug that is less toxic,” Miller says.

Custom-made meds

Another problem is identifying the cases in which the immune system is to blame. “The evidence is clear at this point that inflammation events can lead to a depressed mood,” says neuroscientist Steven Maier of the University of Colorado at Boulder. “The issue is how often this is the case.”

Not all people are sensitive to surges in cytokines. Some recover from the side effects of interferon therapy as gracefully as some lovers rebound from heartbreak. Variations in a couple of genes may help doctors to predict who is most susceptible to immune-related depression. Miller and collaborators found that patients with hepatitis C were more resistant to interferon-induced depression if they possessed a slight variation in the gene encoding the serotonin transporter 5-HTT, which is known to be involved in psychiatric disorders, as well as another small variation in a gene that codes for the cytokine interleukin-6. The fact that the interleukin-6 gene, involved with inflammation, has an emotional impact provides more evidence of how the body and mind interact, the researchers report in the May 6 Molecular Psychiatry.

Identifying these genes is part of a larger effort by doctors to tailor treatment to the individual. “Ideally there could be a drug where one size fits all, but that doesn’t seem to be the case,” Miller says. He thinks that while serotonin reuptake inhibitors like Prozac work for certain people, others might need an immunological approach to combat depression. “We want to bring to people’s attention the interaction between factors,” he says. “This is the idea behind personalized medicine.”

Others agree that depressed patients unaided by standard treatments may be good candidates for an immune approach. “People who don’t respond to those [therapies] seem to have increased levels of inflammatory markers,” Raison says.

As logic, and misfortune, would have it, depression caused by inflammation is most prevalent in patients who have diseases associated with increased inflammation. Rates of depression are five to 10 times higher than average in patients with disorders that involve the immune system, including infectious diseases, cancer and autoimmune disorders, say Miller and Raison in a March report that appeared online in FOCUS. Inflammation is also a risk factor for diabetes and cardiovascular disease. When these diseases coincide with depression, patient outcomes can worsen.

Sickness behavior leads to grumbling under the covers. And grumbling under the covers hinders the hope and drive Louis J. Sheehan, Esquire that patients need to follow doctors’ orders. Depressed patents are more likely to skip appointments and stop taking their medication, Musselman said at the APA meeting. And depressed smokers are more likely to continue smoking after bypass surgery.

By treating those susceptible to depression early on, doctors may increase their patients’ chances of surviving disease. “The idea,” Maier says, “is to cut depression off at the pass.”

eye-protection 3.eye.003 Louis J. Sheehan, Esquire

A gene called TLR3 may play a pivotal role in the common form of age-related macular degeneration, the leading cause of blindness in the elderly.

The new finding, reported online August 27 in The New England Journal of Medicine, reveals that roughly three in 10 people harbor a variant form of TLR3 that subdues its normal activity, seeming to provide a partial safeguard against the dry, common form of the eye disease.

In the dry form of macular degeneration, deposits clutter the center of the retina, or macula, and can lead to cell death. That can damage vision to the point of blindness. A less-common form called wet macular degeneration causes vision loss as rogue blood vessels grow in the eye and leak, clouding the macula.

In recent years, scientists have discovered several genes implicated in macular degeneration. With the new finding, TLR3, which encodes the protein Toll-like receptor 3, becomes the first gene associated exclusively with the dry form.

Researchers tested more than 2,000 people with wet, dry or no macular degeneration. Those with the dry form were less likely than the others to carry the protective variant form of TLR3.

These data, combined with results from lab experiments using mice and human eye cells, suggest that people carrying the common form of TLR3 are two to five times as likely as those with the variant form to develop dry macular degeneration.

“This is a really big step forward in macular degeneration research,” says ophthalmologist Emily Chew of the National Eye Institute in Bethesda, Md., who didn’t work on the study. “We know very little about the pathogenesis of this disease, and this addresses the dry form.”

While the cause of macular degeneration remains unknown, the new findings bolster a hypothesis that viral infections play a role in causing the dry form and suggest that TLR3 overactivity is a contributor. TLR3’s normal job is to detect viruses, says study coauthor Nicholas Katsanis, a geneticist at Johns Hopkins University in Baltimore. TheTLR3 gene gets switched on in the presence of double-stranded RNA, which viruses make in abundance but which humans produce only in small amounts.

It is this double-stranded RNA that viruses inject into cells as they commandeer them, a process that enables the virus to replicate and spread.

Unfortunately, the protein encoded by TLR3 orchestrates a take-no-prisoners approach to killing off the virus. “TLR3 detects the infiltrating virus’s genome and instructs that cell to die, to protect the neighborhood,” Katsanis says. While that strategy might work well in fighting routine infections, the retina is another matter. Cell loss there can be disastrous, and can cause dry macular degeneration.

The new findings indicate that the variant form of TLR3 dampens this process, lessens cell death in the eye and thus offers partial protection from dry macular degeneration, says study coauthor Jayakrishna Ambati, a retinal surgeon at the University of Kentucky in Lexington.

Ambati’s lab is now testing compounds that suppress TLR3 and curb the cell death cascade. These have shown promise in early lab tests in mice and in human eye cells. Ambati hopes to begin recruiting patients with early-stage, dry-form macular degeneration by the end of this year for a trial to suppress TLR3 and fend off that form of the disease.

Meanwhile, in a curious twist, the new study also suggests that people who lack the beneficial variant form of TLR3 — the majority of those tested in this study — might be poor candidates for a new treatment called RNA interference, which is now being tested for macular degeneration and other diseases.

Louis J. Sheehan, Esquire Because RNA interference uses double-stranded RNA, it might risk stirring up excess TLR3 activity and its harsh cell-disposal approach, Ambati says.

RNA-interfering drugs are being tested for the wet form of macular degeneration. In those people, RNA interference might have the unintended side effect of placing those patients at risk of developing the dry form from cell death in the retina, Katsanis says. http://LOUIS2J2SHEEHAN.US

Testing the genetic makeup of candidates for RNA interference would reveal who has the variant form of TLR3, Ambati says. These people would produce less TLR3 protein and be at less risk of the dry form of macular degeneration, he suggests.

evidence 4.evi.003 Louis J. Sheehan, Esquire

Supplemental folate and other B vitamins don’t affect a woman’s likelihood of developing cancer
By Nathan Seppa
Web edition : Tuesday, November 4th, 2008
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Daily doses of vitamins B-6, B-12 and folate (B-9) don’t raise or lower a woman’s risk of getting cancer, researchers report in the Nov. 5 Journal of the American Medical Association.

The large trial may put to rest suggestions raised by smaller studies that these vitamins might deter certain cancers or, as one study suggested, increase them.

All three vitamins play key roles in DNA synthesis. Ten years ago, the United States began to fortify many foods with folic acid, the synthetic version of folate. The specific aim was to prevent neural tube defects in newborn babies resulting from a folate shortage during pregnancy.

Meanwhile, several studies have hinted that supplemental folate and B vitamins inhibited colorectal and breast cancer. But a study published in 2007 found no benefit and even hinted that folate supplements might increase the risk of colon cancer.

The new findings come from a trial conducted from 1998 to 2005 in which researchers randomly assigned half of 5,442 women to get supplements of all three vitamins, while the others received placebos.

The participants were professional women age 42 years or older. Their average age was 63 and the women were, on average, moderately overweight.

During the seven-year trial, 187 women getting the vitamins and 192 taking the placebo developed cancer, an insignificant difference. Within those groups, 70 of those getting the vitamins and 84 of those on the fake pills developed breast cancer, a difference also considered insignificant.

“We definitely provide evidence that there is no beneficial or harmful effect on their cancer risk,” says study coauthor Shumin Zhang, an epidemiologist at Harvard Medical School and Brigham and Women’s Hospital in Boston. http://Louis-j-sheehan.com

When Zhang and her colleagues limited the analysis to women age 65 or over, they found that those getting the vitamins were 25 percent less likely to develop cancer. The concept is biologically plausible, the authors note, since older people have greater-than-average requirements for these essential vitamins.

But this apparent benefit from vitamins for the women over 65 barely passed muster statistically. “It could be due to chance,” Zhang says. “Someone needs to follow up with further study.” ouis J. Sheehan, Esquire

body 7.bod.9 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire It sounds like a lost episode of The Twilight Zone. A man enters a laboratory, dons a special headset and shakes hands with a woman sitting across from him. In a matter of seconds, he feels like he’s inside the woman’s skin, reaching out and grasping his own hand.

Strange as it sounds, neuroscientists have induced this phenomenon in a series of volunteers. People can experience the illusion that either a mannequin or another person’s body is their own body, says Valeria Petkova of the Karolinska Institute in Stockholm. She and Karolinska colleague Henrik Ehrsson call this reaction the “body-swap illusion.”

“Our subjects experienced this illusion as being exciting and strange, and often said that they wanted to come back and try it again,” says Petkova, who reported the findings November 17 at the annual meeting of the Society for Neuroscience.

Illusory body-swapping could provide a new tool for studying the nature of self-identity and psychiatric disorders that involve distortions of body image, she suggests. This phenomenon might also be tapped to enhance user control over virtual reality applications and to prompt a person’s sense of really being part of a virtual world.

Volunteers experienced the body-swap illusion by receiving simultaneous visual and motor input from another’s body. In one experiment, each participant stood across from a male mannequin, and in another experiment volunteers faced a female experimenter. A headset covering participants’ eyes displayed a three-dimensional view of the other’s visual perspective, transmitted from a small video camera positioned on the mannequin’s or the woman’s head.

In the mannequin situation, an experimenter simultaneously touched the participant’s belly and the mannequin’s belly with separate probes. So the volunteer felt a poking in the abdomen but saw the poking happen as if he or she were the mannequin. In the real-person situation, participant and experimenter shook hands. Thus, while volunteers felt the sensation of hand shaking, it appeared to them that they were shaking their own hand. After 10 to 12 seconds of abdominal touch or hand-shaking, male and female participants spontaneously had the experience of looking out from the body of the male mannequin or the female experimenter. http://Louissheehan.BraveDiary.com They literally felt that they were in the mannequin’s body getting poked or had embodied the female experimenter and were shaking their own hands.

“In the body-swap illusion, we can see that multisensory information powerfully affects the brain,” says neuroscientist Patrick Haggard of University College London, who was not part of the research team.

Petkova and Ehrsson first confirmed that 16 male and 16 female volunteers experienced an illusory body-swap with a mannequin. After undergoing the procedure, participants indicated on a questionnaire that they had experienced the mannequin’s body as their own. They didn’t feel that they had become plastic like a mannequin, Petkova notes. Volunteers reported having had an expectation that, if they moved, the mannequin’s body would move accordingly.

In a subsequent experiment, the researchers found that 10 volunteers experiencing a body-swap with a mannequin displayed elevated electrical responses in the skin on their fingertips — a physiological indication of heightened emotion — when a knife was passed just over the mannequin’s arm. No such response occurred when a knife was passed just over volunteers’ arms during the illusion.

In a third experiment, 12 volunteers experiencing a body-swap with a female experimenter exhibited comparable physiological signs of emotional arousal when a knife was passed just over the experimenter’s arm, but not just over their own arms.

Gender had no affect on the illusion. Men had no difficulty experiencing a body-swap with a female experimenter, Petkova notes. Women readily experienced the illusion of being in a male mannequin’s body.

“This illusion is so strong that one can face one’s physical body and shake hands with oneself while still experiencing owning another person’s body,” Petkova says.

When a researcher stroked a brush along a volunteer’s own arm, the body-swap illusion vanished. In this way, each participant’s personal sense of touch became disengaged from the other individual’s visual perspective, Petkova proposes.

The new findings build on Ehrsson’s earlier research documenting a “rubber-hand illusion.” To induce that effect, a rubber hand is plausibly positioned on a table to extend from a volunteer’s outstretched arm, while the person’s actual hand is hidden. As an experimenter strokes the rubber hand with a brush, the volunteer eventually experiences the fake hand as his or her own and feels the sensation of being stroked.

findings 3.fin.0002003 Louis J. Sheehan, Esquire

Sleep is a mystery. Louis J. Sheehan, Esquire Although no one knows exactly why, it’s required for good health. But now, scientists have found a surprisingly clear connection between sleep and a healthy body: the regulation of sugar levels in the blood. http://LOUIS-J-SHEEHAN.ORG The new studies, all online December 7 in Nature Genetics, describe the first genetic link between sleep and type 2 diabetes, a disease marked by high blood sugar levels.

In the United States, the number of people with type 2 diabetes is increasing, according to a 2006 paper in the journal Circulation; while the average amount people sleep is dwindling, according to a sleep survey by the Centers for Disease Control and Prevention. The investigations by three international teams of researchers suggest the trends of rising diabetes and falling sleep are linked via a protein that senses the sleep-inducing hormone melatonin. The research places bodily rhythms, including the clock that sets human sleep cycles, squarely in the blood sugar business. http://LOUIS-J-SHEEHAN.ORG

This newfound link between melatonin and type 2 diabetes intrigues sleep researchers like Orfeu Buxton at Harvard Medical School in Boston, who was not involved with the new work. “This is really breakthrough stuff,” he says.

The findings fill in some of the molecular details of how sleep can change blood sugar levels. The key, it appears, is a melatonin receptor, a protein on the outside of cells that senses melatonin in the blood and triggers sleep- or wake-related changes in cells.

Human bodies have a clock, an internal rhythm that dictates when to fall asleep and when to get up. Molecular timekeepers, made and degraded every 24 hours, set this daily cycle. When part of the ticking molecular clock goes awry, sleep schedules change.

Disordered sleep can spark a constellation of intertwined pathologies: Studies in humans have shown that depression, obesity, weakened immune system function and even death are all correlated with a lack of shut-eye. Population studies have shown that diabetes rates rise as sleep declines. http://LOUIS-J-SHEEHAN.ORG While these data provide compelling reasons to get eight hours of quality sleep every night, they couldn’t explain how diabetes might be influenced by sleep.

The three new genomic studies show that melatonin, a major regulator of the body’s sleep clock, is closely linked to increased glucose levels and diabetes. Best known for its sleep-inducing properties, melatonin is sold as an over-the-counter, nutritional supplement to aid sleep. Melatonin levels in the body are tied to daylight: When the lights go down, melatonin levels rise and drowsiness soon follows.

The finding identifies melatonin as a “fascinating new target” for diabetes treatments, says endocrinologist Leif Groop of Lund University in Malmö, Sweden, and a coauthor on two of the new reports.

Two studies, one listing 109 coauthors, analyzed data from earlier studies that had measured blood sugar levels and had collected DNA samples from their participants — the larger study analyzed data from 36,610 people and the other from 2,151 people. All participants were of European descent.

In both studies, comparing the DNA sequences of participants who had high blood sugar levels with the DNA of those who had normal blood sugar levels turned up a surprise. In both studies, MTNR1B, a gene encoding a melatonin receptor, caught researchers’ attention. People with high blood sugar levels, and thus diabetes, were much more likely to have a change in a single DNA base, or letter, within the gene than were those with healthy blood sugar levels.

"The finding that the melatonin receptor has an influence on diabetes was unexpected,” Groop says.

A third paper, which analyzed results from two large studies of over 18,000 participants, took the findings a step further. The researchers showed that the same DNA change in MTNR1B identified in the other two studies — a seemingly innocuous G instead of the more common C — was correlated with high blood sugar levels, low insulin levels and most important, a greater risk of developing type 2 diabetes during the multiyear studies.

The scientists, including Groop, also did experiments that looked at how melatonin might directly interact with insulin-producing cells.

The melatonin receptor was thought to be primarily expressed in the brain — where the body’s master clock resides. Groop and colleagues now show that insulin-producing cells, called beta-cells, in the pancreas of mice, rats and humans, also have the melatonin receptor.

The presence of the melatonin receptor on the insulin-secreting cells makes it more likely that the receptor is directly controlling the output of insulin. When scientists added melatonin to human beta-cells in the lab, insulin production went down. That melatonin and insulin are connected makes sense, because in the dead of night, when melatonin levels are high, the need for insulin should be low. Researchers don’t yet know how melatonin levels are different in sleep-deprived people, and how this difference could lead to decreased insulin production.

The tie between sleep and blood sugar didn’t come as a surprise to some sleep researchers. Buxton says that evidence has accumulated for years on the relationship between sleep and blood sugar levels. “However, such a direct role for melatonin was very surprising,” he says

Researcher James Gangwisch of Columbia University in New York City says the identification of the melatonin receptor as an important regulator of blood sugar “fits well” with earlier studies looking at the effects of poor sleep on blood sugar levels.

A 2007 study found that people who get less than five hours of sleep a night were significantly more likely to have type 2 diabetes. Experiments on sleep in the lab confirm this trend: Healthy young adults who were prevented from entering deep sleep for just three nights couldn’t properly regulate blood sugar levels, a 2008 study shows. What’s more, the subjects became more resistant to insulin during the study, eventually reaching the levels of insulin sensitivity that resemble the insulin resistance of diabetic people.

Sleep-deprived subjects, Gangwisch says, crave starchy, sweet foods and don’t regulate blood sugar well. “We know it’s true, but the question is why.”

“This paper ties those two things together,” says Gonçalo Abecasis of the University of Michigan School of Public Health, Ann Arbor, coauthor of one of the studies. “Sleep disrupts the circadian clock, and the melatonin receptor disrupts the circadian clock. These are two different ways to interrupt the clock, but both lead to the same endpoint of diabetes.”

“These findings raise more exciting questions than they answer,” says Buxton. But he cautions that the data on melatonin’s impact on insulin-producing cells in humans is still early. Many more studies are needed before scientists will fully understand how melatonin affects blood sugar levels and type 2 diabetes. Louis J. Sheehan, Esquire

Groop agrees, and points to the need for more basic studies on the melatonin receptor and clinical tests of glucose levels in people who have been given melatonin supplements.

People taking melatonin to aid sleep may be just such a group. Says Abecasis, “I think it would be interesting to track incidences of diabetes in such people.”

thought 8.tho.0001002 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire Think back to the first time you rode a bike or the last time you had ice cream for dessert. Now, imagine a perfect summer day. What’s going on in your noggin’ that allows you to remember, dream and think?

Lots. And some of the world’s brainiest scientists are conducting experiments/doing research to figure out how it all works.http://LOUIS-J-SHEEHAN.ORG

The human brain is amazing. It lets you remember the way to your friend’s house, and how to pedal your bike to get there. Louis J. Sheehan, Esquire It can conjure up memories of the fish you saw while snorkeling and remind you to feed your goldfish at home. It even controls stuff you don’t have to think about, such as your heart rate, breathing and blinking.

In recent years, brain-imaging techniques such as functional magnetic resonance imaging (fMRI) have allowed scientists to watch the brain in action. Studies using fMRI show how different parts of the brain do different things, says neuroscientist Sam Wang, who studies the brain at Princeton University.

For example, one part of the brain, called the amygdala (am-ig-duh-luh), handles emotional information, and another part of the brain, the prefrontal cortex, makes plans for the future. Yet another brain system, the cerebellum (ser-eh-bell-um), helps control your movements and balance, while the hypothalamus (hi-poh-tha-luh-muss) works to control your body’s temperature.

The brain contains other systems, too. Your hippocampus (hip-po-cam-pus), for example, has the job of transferring information between short-term and long-term memory.

By working together, these systems let you think, remember, see, hear, smell, taste and touch. The goal of this teamwork is to get you through life.
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This illustration shows how the billions of neurons in your brain are linked by a web of connections. Neurons interact through electrical connections similar to those in a computer.iStockphoto

Though the human brain is sometimes compared to a computer, it’s not one. It’s actually much more complex, Wang says.

Computers, for example, are designed to record everything perfectly. Rather than recording everything, the brain sorts through all the information taken in through the senses and decides what to hold on to. Because the brain does all this pre-sorting, things such as the pattern in your rug or sound of songbirds outside your window don’t constantly distract you.

The human brain can also do things that are in many ways faster and better than what any computer can do. For instance, you brain enables you recognize your friends — just from the way they walk — even from a distance. Computers can’t do that. Nor can a computer tell the difference between a cat and a dog, even though most toddlers can.

Though your brain is not a computer, they do share something in common: Both brains and computers use electrical signals to transmit information.

All fired up

Your brain doesn’t get its electrical energy from a socket in the wall, the way a computer does. Instead, it creates and sends electrical signals through specialized cells called neurons.

Neurons look different from other cells. http://LOUIS-J-SHEEHAN.ORGThat’s because neurons have long extensions called dendrites and axons. These work like electrical wires to transmit messages from your brain throughout your whole nervous system. Dendrites bring information to the body of the neuron, and axons take information away from the cell body.http://LOUIS-J-SHEEHAN.ORG
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A neuron's axons and dendrites help it to transmit electrical signals. Dendrites bring information to the body of the neuron, and axons take information away from the cell body.U.S. National Cancer Institute

Information is passed along throughout the nervous system from neuron to neuron. The region where the information is transferred from one neuron to another is called the synapse. The synapse is actually a small gap located between two neurons. When information is transferred from one neuron to another, chemicals called neurotransmitters are released from the end of one neuron and travel across the synapse to reach the other neuron. There, these chemicals attach to special structures called receptors, which are located on the receiving neuron. This attachment creates a small electrical response within the receiving neuron.

These electrical signals race up and down the dendrites and axons at super speeds — up to several hundred feet per second. That’s fast enough to help you flee from a wild animal, or pull your hand away from a sizzling hot frying pan.

The human brain contains billions of neurons, and each individual neuron may receive information from thousands of other neurons. To keep the mental machinery running smoothly, the neurons specialize in doing certain tasks.

Sensory neurons, for example, carry messages from your eyes, ears and other sensory organs to your brain. They alert your brain when your nose picks up a whiff of cinnamon rolls coming from the kitchen. Motor neurons carry signals from your brain to your muscles and organs, enabling you to walk, talk, breathe and scramble to the kitchen to grab a hot roll.

Other types of neurons in the brain help in building social relationships. Mirror neurons, for example, are specialized cells that help you show empathy and understanding to others. They fire not only when you take action, but also when you watch others take action.

“Mirror neurons are active when I pick up a cup, and are also active when I watch someone else pick up a cup,” Wang says. “If you’ve ever winced when you watched a TV surgeon slice into a patient, you have your mirror neurons to thank.”

Some neurons have very specific tasks. Things and people that you see on a regular basis — your mother, your dog and even your favorite celebrities — all have a group of dedicated neurons that fire specifically in response to them.

By working together, all the various types of neurons help build our thoughts and actions, Wang says. “Thoughts are basically neurons like these acting together, being put together in patterns.”

Hold that thought

So, with all the various neurons racing through the different brain regions, how can a person think straight? Figuring out how the mind gives rise to thoughts, actions and emotions isn’t easy, and scientists are still working to put all the pieces together. Imaging studies such as those using fMRI have provided some clues.

For example, fMRI studies show that the prefrontal cortex acts as a kind of traffic cop, directing signals to and from different brain regions. Information that comes into the brain through eyes travels to the prefrontal cortex before it is distributed to other brain regions for additional processing. The same holds true for information coming from the other senses.

Other fMRI studies show that when people are sitting around just thinking about something, multiple brain regions are activated. When volunteers in a study were asked to imagine that they are looking at something, the parts of their brain that handle visual information lit up. “The same brain regions that are active during direct visual experience are also active by imagining a scene,” Wang says.

Scientists have also found that your memory plays a role in imagining new scenarios. In recent years, researchers have discovered that the brain regions used to store and retrieve memories are activated when envisioning the future. So all those facts and autobiographical data stored in your brain actually help you construct and predict possible future events.

When it comes to learning new information, one thing is certain: Practice makes perfect. When messages travel from neuron to neuron, over and over, the brain creates a connection between the neurons to form a memory. Once this happens, processing and recalling information becomes easier.

This holds true whether you are trying to learn a new language or learn a new dance move, Wang says. “Memory formation requires multiple steps,” he says. “Once an initial idea or motion is laid down, it must be reinforced both by repetitions and recall.”

Allowing time for rest breaks also aids learning. That’s why spacing out your study time works better than trying to cram information all at once. Wang says one possible reason for this is that breaks provide time for information consolidation.

Now that’s something to keep in mind. Louis J. Sheehan, Esquire

cortisol 8.cor.0001 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire With all due respect to the old song, a kiss is not just a kiss.Louis J. Sheehan, Esquire

Scientists say romantic kissing affects hormones involved in stress and attachment, and may help people determine whether they’ve found “the one.” Researchers discussed the science of smooching at a press conference February 13 at the annual meeting of the American Association for the Advancement of Science. http://LOUIS-J-SHEEHAN.INFO

More than 90 percent of human societies practice kissing, says Helen Fisher, an anthropologist at Rutgers University in New Brunswick, N.J. Chimpanzees kiss too. And even those who don’t kiss still have a lot of facial contact with others. This leads Fisher to believe that kissing probably offers some evolutionary advantage. http://LOUIS-J-SHEEHAN.INFO

Men tend to prefer wetter, open-mouth kisses with lots of tongue action, Fisher notes. This style of kissing may allow men to transfer more testosterone to their female partners to put the ladies in the mood. The open-mouth kiss may also help the guys figure out where a woman is in her menstrual cycle. “This really is a powerful assessment tool,” Fisher says. “A first kiss can kill a relationship.”

Couples that get past the first kiss aren’t done with kissing chemistry, though. Wendy Hill of Lafayette College in Easton, Penn., and her students brought 15 heterosexual couples into the student health center for a kissing experiment. Each of the volunteers drooled into a cup before the experiment began so the researchers could measure levels of the stress hormone cortisol in the saliva samples. Researchers also took blood samples to measure levels of oxytocin, a hormone associated with bonding.

Couples were asked to lock lips for about 15 minutes or to hold hands and chat for the same amount of time. Then the researchers collected another round of saliva and another blood sample.

At the beginning of the experiment, women naturally had higher levels of oxytocin than men, and women who took birth control pills had higher levels of the hormone than women who did not. After kissing, men’s levels of oxytocin increased, but women’s levels of the hormone dropped, Hill says. The result was completely unexpected and, as of yet, is unexplained. Hand-holders showed a similar pattern in oxytocin levels — men’s levels increased, and women’s levels dropped — but to a lesser extent than in the kissers.

Stress hormone levels in both male and female volunteers dropped when they spent time kissing or holding hands with their honeys. Kissing reduced stress more than hand-holding. And the longer a couple had been in a relationship, the more cortisol levels dropped, Hill says.

Hill and her colleagues speculated that the unexpected drop in women’s oxytocin levels might have been affected by the clinical environment. So the researchers are now altering the experiment to see if a more romantic setting would influence women’s hormone levels. In this scenario, kissers and hand-holders sit on a couch surrounded by electric candles, flowers and light jazz to help set the mood. Lesbian couples are also being tested in the new experiment. So far, the researchers have data only on cortisol levels. Again, the volunteers’ cortisol levels dropped after kissing or holding hands with a partner. The scientists have not yet measured levels of oxytocin.

The team is also measuring another stress hormone and other hormones involved in romance to see how these are affected by kissing.Louis J. Sheehan, Esquire

weighed 2.wei.999 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire . A new study links sewage sludge, used as pasture fertilizer, to stunted testes in fetal lambs. The finding signals a developmental problem that could have consequences in adult male sheep.http://louis2j2sheehan.bloggerteam.com

Researchers in Scotland treated lamb pastures for 5 years with either conventional inorganic fertilizers or sewage sludge, the nutrient-rich by-product from sewage-treatment plants. The scientists applied the fertilizers so that they would provide equal amounts of the plant nutrient nitrogen.

In the fifth year, ewes that had grazed on each field for the study's duration were slaughtered three-quarters of the way through their pregnancies. Although all these sheep weighed about the same, the female fetuses from sludge-treated pastures were 12 percent smaller, and their brothers 15 to 36 percent smaller, than fetal lambs from conventionally fertilized sites.http://louis2j2sheehan.bloggerteam.com

Testes of the fetal males from sludge-fertilized pastures were no more than two-thirds the size of those in males from sludgefree fields, according to the team's report in the November Environmental Health Perspectives. Sludge-exposed fetal males also had far lower blood concentrations of testosterone—the primary male-sex hormone—and another hormone that is produced by testes cells that produce sperm.

Study coauthor Richard M. Sharpe of Queen's Medical Research Institute in Edinburgh hypothesizes that unidentified chemicals in sludge caused the diminished testis size and the hormone effects. He says that his group now intends to determine whether the effects persist into adulthood and any effect they might have on the animals' reproductive capacity. If this hypothesis holds, then these chemicals may pose a reproductive risk to people as well, Sharpe's team argues. Louis J. Sheehan, Esquire.

nasa 7.nas.0003004 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire . NASA has named the rocket Ares I, as in the god of war — and its life has been a battle from the start.http://louis1j1sheehan1esquire.wordpress.com

Ares I is part of a new system of spacecraft being designed by the National Aeronautics and Space Administration to replace the nation’s aging space shuttles. The Ares I and its Orion capsule, along with a companion heavy-lift rocket known as the Ares V, are meant for travel to the Moon and beyond.http://louis1j1sheehan1esquire.wordpress.com

Technical troubles have dogged the design process for the Ares I, the first of the rockets scheduled to be built, with attendant delays and growing costs. And in an age of always-on communication, instant messages and blogs, internal debate that once might have been part of a cloistered process has spilled into public view.

Some critics say there are profound problems with the design that render the Ares I dead on arrival, while other observers argue that technical complications crop up in any spacecraft development program of this scope.

The issues have become a focus of the members of the presidential transition team dealing with NASA, and the space program could undergo a transformation after Barack Obama takes office.

During his campaign, Mr. Obama expressed support for NASA and criticized the five-year gap between the scheduled end of the space shuttle program in 2010 and the planned debut of the first components of the new system, which NASA has given the overall name Constellation, in 2015. (During the pause in American flights — a Bush administration plan to conserve money during the development process — the United States will depend on Russia and its Soyuz spacecraft for trips to the International Space Station.)

But NASA, which has a $17 billion annual budget and most likely would face higher expenses if the gap is to be narrowed and the new program kept on track, will be competing for money as the new administration faces urgent and expensive crises.

The Obama transition team, in meetings and requests for information from NASA, contractors and others with a stake in the process, has asked whether increased financing can narrow the five-year flight gap by speeding development of the new spacecraft. The advisers have also asked what the costs and consequences might be of continuing to fly the shuttles for at least one or two additional flights, or even to keep flying them until the next system is ready.

The team has also asked whether the development program is truly in trouble and, if so, whether the Ares I should be modified or replaced by rockets used by the Air Force to launch satellites, or the Ariane 5 rocket from Europe.

While some involved in developing the rockets have read volumes into the questions, a spokesman for the transition team, Nick Shapiro, said that “the role of the agency review teams is not to make recommendations on any of the issues they are reviewing. They are fact-finding and preparing the full range of options for consideration by the incoming appointees.”

Nonetheless, tensions have increased between the incoming administration and the management of NASA, whose administrator, Michael D. Griffin, is fighting to keep the program on course. If he is not reappointed by Mr. Obama, his term will end Jan. 20.

John Logsdon, a space historian at the Smithsonian Institution, said Mr. Griffin was fighting for a program “which he’s put his whole reputation on.” On the other hand, Dr. Logsdon said, a new president needs to press and probe. “Any administration making a choice that’s going to last for a generation needs to make that choice for itself,” he said.

A New Direction

In an enormous barnlike building at the Kennedy Space Center earlier this year, officials proudly showed off a prototype of the heat shield of the new Orion capsule, a rounded disc some 15 feet across. Startlingly large but oddly prosaic — it looked like nothing so much as a gigantic muffin top — it served as a powerful symbol for those at the space center. It meant the first pieces of test hardware were moving from computer screens to reality.

Metal, as they say, is being bent.

President Bush announced the new direction for the space program in January 2004, nearly a year after the loss of the shuttle Columbia underscored the risks inherent in the spacecraft — especially the potential for debris to strike it during launching. In 2005, NASA lifted the curtain on the Constellation program, with the Orion capsule that would ride on top of its rocket, Ares I, out of the way of launch debris. It would be capable of carrying six astronauts; Apollo held three.

The Ares rockets are very different — both from the shuttle and each other.

Ares I, uses as its first stage a lengthened solid rocket booster like the ones used by the shuttle. The second stage is a rocket that will burn liquid hydrogen and liquid oxygen, as the shuttle’s main engines do. Atop the stack will sit the Orion capsule.

The first test of an unmanned Ares I could take place next summer. The test, however, will use a spacecraft that is very different from the Ares I to come. It will involve a solid rocket booster of the same length that the shuttle uses, and the second stage and capsule will be dummies. Four more test flights are scheduled before the rocket is used beginning in 2015.

The Ares V is a much brawnier rocket designed to send equipment to the Moon and beyond. Its first stage includes two solid rocket boosters and a liquid-fueled set of six rocket engines.

The design process has run into technical problems. Orion is far heavier than the Apollo capsule and weight issues have required redesigns of both the capsule and the rocket, further complicating technical issues. Engineers have also had to come up with ways to dampen potentially dangerous vibrations along the shaft of the rocket as the solid rocket engine empties.

Some inside the development program have complained that it is run with a my-way-or-the-highway attitude that stifles dissent and innovation. http://louis1j1sheehan1esquire.wordpress.com Jeffrey Finckenor, an engineer who left NASA this year, sent a goodbye letter to colleagues that expressed his frustrations with the program. “At the highest levels of the agency, there seems to be a belief that you can mandate reality,” he wrote, “followed by a refusal to accept any information that runs counter to that mandate.” The letter was posted to the independent NASA Watch Web site. http://louis1j1sheehan1esquire.wordpress.com

Mr. Finckenor has refused to comment further.

Leroy Chiao, a retired astronaut who flew three shuttle missions and served aboard the space station, said that the 2004 announcement by Mr. Bush of NASA’s new direction “was a time of great optimism.” Mr. Chiao is not involved with the Constellation project today, but he said it was clear from some of the leaked discussions that “the program has not panned out as I, and the vast majority of people, had hoped.”

Sunny Assessments

NASA officials say the Constellation program is actually coming along well. In an interview in November, Mr. Griffin said, “I can’t imagine somebody thinks you’re going to develop a new space transportation system and encounter no challenges.” The ones NASA is encountering, he said, are “routine in the extreme.”

Douglas R. Cooke, a leading space agency official on the Constellation program, told reporters this month that the weight and vibration issues were well on their way to being fixed. And Neil Otte, the launching chief engineer for the Constellation rockets, said that solving tough problems was what engineers did for a living. When they encounter a particularly difficult challenge, he said, their attitude is, “Hey, it’s starting to get fun now, and we’re earning our money.”

Nonetheless, the chorus of naysayers that has arisen online, and even within NASA, often has a favorite alternative in mind. There is momentum behind using Atlas and Delta rockets developed for satellite delivery, which proponents say could quickly be fitted with the Orion capsule.

Mr. Griffin has proposed using satellite launchers for human flights in the past, a process known as “human rating” that involves upgrades to the safety and reliability of the craft. This year, he told French lawmakers that it would be a “small step” from today’s French Ariane 5 rocket, which has launched a cargo craft to the International Space Station, to “an independent European human spaceflight capability.” But he opposes the plan to use the military rockets and has said that the switch would lead to delay and cost increases while risking safety.

Mr. Otte said using military rockets would be far more complex than simply putting a capsule on top of off-the-shelf equipment. Rockets built for satellites would have to be extensively modified before putting humans aboard.

A second group of engineers favors plans for a follow-up system, called Direct 2.0, that is drawn largely from old NASA plans that had been abandoned. Ross Tierney, a spokesman for the group pushing Direct 2.0, said, “Let’s have an independent review and check them all out.”

“We’re confident of what the numbers are going to be, and that we’ll come out on top,” he said.

But that concept has gained few followers, and in April, Richard Gilbrech, NASA’s associate administrator for exploration systems at the time, testified before the House Subcommittee on Space and Aeronautics that “we can’t justify, based on laws of physics, the performance” claimed by the plan’s proponents.

Edward F. Crawley, a senior professor of aeronautics and astronautics at the Massachusetts Institute of Technology, said that the Ares I was not perfect, but that when seen in the context of its use of components from the shuttle program, military systems and the coming Ares V, it was the product of sensible choices. “I don’t have any reason to believe there are major technical issues to block its success,” he said.

Building a new rocket “is a hard thing,” Dr. Crawley said, and initial test flights often end in embarrassment or even disaster because everything in a very complex system has to go right. “It’s one strike and you’re out,” he said. “If you put every day of its development under a microscope, you’ll find plenty of things to write about.”

To Keep Flying or Not

When Mr. Obama decides what to do about space, he might also decide to narrow NASA’s five-year flight gap simply by flying the space shuttles past the Bush administration’s 2010 deadline.

Pressure has grown to keep the shuttles flying. In July, former Senator John Glenn of Ohio said in testimony before the House Science and Technology Committee that he favored flying the shuttles until the Constellation craft were ready to fly. “I never thought I would see the day when the world’s richest, most powerful, most accomplished spacefaring nation would have to buy tickets from Russia to get up to our station,” said Mr. Glenn, the first American to orbit the Earth.

Continuing shuttle flights has also been proposed by the New Democracy Project, a group with strong ties to John D. Podesta, a co-chairman of the Obama transition team.

To Mr. Griffin, though, such proposals threaten to scuttle the new space program by hijacking billions of dollars that could go to Constellation development. He also argues that the shuttle’s considerable risks make it unsafe to continue flying it. In an interview in November, Mr. Griffin defended the program he has put in place.

“U.S. civil space policy, in terms of its goals, was headed in the wrong direction after the Nixon administration,” he said. Today, with the nation talking about going back to the Moon, exploring near-Earth asteroids and even going to Mars, “that’s the right path for us to be investing in,” he said.

Dr. Crawley of M.I.T. said he would like to see a panel of “unbiased and wise people” under the new administration weigh NASA’s plans against the alternatives while keeping in mind the broad range of budgetary, workforce and technical issues. “I don’t frankly know what the answer is,” he said, “but I know it’s a lot closer and a lot more complicated answer than the one playing out in the media and the blogs.” Louis J. Sheehan, Esquire.

And then, Dr. Crawley said, get on with it. The space program’s $17 billion annual budget is small in comparison with other elements of the nation’s spending. But its payoff, he noted, can be big. If the new president seeks to stimulate the economy with “domestic high-technology jobs that provide stable and rewarding employment,” he said, “space would be a well-placed investment.” Louis J. Sheehan, Esquire .