Metcalf DD- 595 - History

Metcalf DD- 595 - History


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Metcalf
(DD-595; dp. 2,050; 1. 376'4"; b. 39'8", dr. 17'9", s. 35 k.; cpl. 273; a. 5 5", 10 40mm., 7 20mm., 8 21" tt.;cl. Fletcher)

Metcalf (DD-595) was laid down by Puget Sound Navy Yard, Bremerton, Wash., 10 August 1943, Launched 25 September 1944; sponsored by Mrs. Harold C. Pound, and commissioned 18 November 1944, Comdr. David L. Martineau in command.

Following shakedown off San Diego, Calif., Metcalf was assigned to the Pacific Fleet for duty. The destroyer departed Bremerton, Wash., 19 February 1945 for the Carolines via Pearl Harbor, Hawaii, arriving Ulithi 16 March.

Just in time to join the armada of warships staging there for the Okinawa campaign, Metcalf operated with Escort Carrier Group 3. From 27 March her group furnished close air support for the landings at Kerama Ketto (26 March) and Okinawa ([April), and made raids on the neighboring Japanese-held islands until 20 April. During this period the ship rescued half a dozen pilots and crewmembers of downed carrier planes. She also performed radar picket and screen operations.

Metcalf departed on the 20th for the Philippines via Guam, reporting to commander, 7th Fleet, at Leyte 30 April. The destroyer spent May and June convoying the fast cruisers and transports being assembled for the Borneo invasion.

On 9 June Metcalf arrived off Brunei Bay, Borneo, for 2 days patrol of the South China Sea before beginning shore bombardment in support of the Australian landing at Brunei Bay the 10th. After action on Miri-Lutong, south of Brunei Bay, from 19 to 21 June, she reached Balikpapan on the 27th for operations with TF 74 prior to the main landing by Australian troops 1 July.

Metcalf reported to commander, Philippine sea frontier 4 August for duty escorting convoys between the Philippines and Okinawa. She was 1 day out of Okinawa in antisubmarine formation for Convoy 10R-204 when the Japanese capitulated

Assigned to the newly formed North China Force, the destroyer departed Okinawa 4 September to participate in the landing of Army occupation forces at Korea. Metcalf joined Shields (DD-596), Tart (DD-594), and Conner (DD-582) in leading TU 78.1.15 into Jinsen 8 September through the mine-infested Yellow Sea. She stood ready to provide fire support for the landing troops the next day if needed.

On the 12th Metcalf got underway through the Yellow Sea for operations supporting the occupation of China. Her ports of call included Darien, Chingwangtao, Taku, Chefoo, Shanghai, and Hong Rong.

In early 1946 Metcalf steamed for the west coast, via Pearl Harbor, arriving San Diego to report in March to the 16th (Inactive Reserve) Fleet. She decommissioned March 1946, and entered the Pacific Reserve Fleet there. After berthing at Long Beach, Calif., from 1 July 1951 into 1960, Metcalf moved to Stockton, Calif., where she remains in reserve through 1969.

Metcalf received three battle stars for World War II service.


USS Metcalf (DD 595)

Decommissioned in March 1946.
Stricken 2 January 1971.
Sold 6 June 1972 and broken up for scrap.

Commands listed for USS Metcalf (DD 595)

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CommanderFromTo
1T/Cdr. David Louis Martineau, USN18 Nov 19445 Feb 1946

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Notable events involving Metcalf include:

27 Jun 1945
In the morning HrMs Tromp (A/Capt. F. Stam, RNN) bombarded Japanese shore guns off Balikpapan.

Later that day Tromp joined Task Force 74.1 which was made up of the Australian heavy cruiser HMAS Shropshire (Capt. C.A.G. Nichols, MVO, DSO, RN), the Australian light cruiser HMAS Hobart (Capt. R.S. Dowling, RAN), the Australian destroyer HMAS Arunta (Cdr. A.E. Buchanan, DSO, RAN) and the US destroyers USS Hart (Cdr. W.D. Coleman, USN) and USS Metcalf (Cdr. D.L. Martineau, USN). ( 1 )

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DD-595 Metcalf

Metcalf (DD-595) was laid down by Puget Sound Navy Yard, Bremerton, Wash., 10 August 1943, Iaunched 25 September 1944 sponsored by Mrs. Harold C. Pound, and commissioned 18 November 1944, Comdr. David L. Martineau in command.

Following shakedown off San Diego, Calif., Metcalf was assigned to the Pacific Fleet for duty. The destroyer departed Bremerton, Wash., 19 February 1945 for the Carolines via Pearl Harbor, Hawaii, arriving Ulithi 16 March.

Just in time to join the armada of warships staging there for the Okinawa campaign, Metcalf operated with Escort Carrier Group 3. From 27 March her group furnished close air support for the landings at Kerama Retto (26 March) and Okinawa (April), and made raids on the neighboring Japanese-held islands until 20 April. During this period the ship rescued half a dozen pilots and crew members of downed carrier planes. She also performed radar picket and screen operations.

Metcalf departed on the 20th for the Philippines via Guam, reporting to commander, 7th Fleet, at Leyte 30 April. The destroyer spent May and June convoying the fast cruisers and transports being assembled for the Borneo invasion.

On 9 June Metcalf arrived off Brunei Bay, Borneo, for 2 days patrol of the South China Sea before beginning shore bombardment in support of the Australian landing at Brunei Bay the 10th. After action on Miri-Lutong, south of Brunei Bay, from 19 to 21 June, she reached Balikpapan on the 27th for operations with TF 74 prior to the main landing by Australian troops 1 July.

Metcalf reported to commander, Philippine sea frontier 4 August for duty escorting convoys between the Philippines and Okinawa. She was 1 day out of Okinawa in antisubmarine formation for Convoy 10R-204 when the Japanese capitulated

Assigned to the newly formed North China Force, the destroyer departed Okinawa 4 September to participate in the landing of Army occupation forces at Korea. Metcalf joined Shields (DD-596), Hart (DD-594), and Conner (DD-582) in leading TU 78.1.15 into Jinsen 8 September through the mine-infested Yellow Sea. She stood ready to provide fire support for the landing troops the next day if needed.

On the 12th Metcalf got underway through the Yellow Sea for operations supporting the occupation of China. Her ports of call included Darien, Chinwangto, Taku, Chefoo, Shanghai, and Hong Kong.

In early 1946 Metcalf steamed for the west coast, via Pearl Harbor, arriving San Diego to report in March to the 16th (Inactive Reserve) Fleet. She decommissioned March 1946, and entered the Pacific Reserve Fleet there. After berthing at Long Beach, Calif., from 1 July 1951 into 1960, Metcalf moved to Stockton, Calif., where she remained in reserve until stricken 2 January 1971 and sold for scrap 6 June 1972.


Metcalf DD- 595 - History

Papers (1930-1990) of U.S. Navy admiral, U.S. Naval Academy Class of 1933, including correspondence, diaries, photographs, reports, orders, speeches, programs, and miscellany.

Biographical/historical information

David L. Martineau was born in Oshkosh, WI (December 4, 1910), and attended high school in Chicago, where he commanded the ROTC unit. Concurrently, Martineau served in the Illinois National Guard and won a senatorial appointment to the United States Naval Academy (USNA), entering as a midshipman (1929) and graduating as a commissioned ensign (1933). Prior to World War II, Martineau served on battleships, cruisers, and destroyers, and during the first years of the war, worked as the USNA midshipman duty officer and aide to the superintendent in Annapolis, MD (1941-1943). Martineau then commanded the destroyers USS PHELPS (DD-360) and USS METCALF (DD-595) in the Pacific Theatre (1943-1945). After the war, Martineau served in Naval shore administrative and personnel positions (1946-1949, 1952-1957), commanded the destroyer USS CHARLES H. ROAN (DD-853, 1949-1951), the destroyer tender USS EVERGLADES (AD-24, 1957-1958), and the heavy cruiser USS LOS ANGELES (CA-135, 1958-1959) before his retirement as a rear admiral (November, 1959). Awards received include a Silver Star, two Bronze Stars, and a commendation ribbon. Martineau then worked in the private sector and served as military consultant to the House Armed Services Committee on Vietnam.

Scope and arrangement

The collection's early correspondence (1930) consists of one letter that describes Martineau's Midshipmen's Cruise to Europe on board the battleship USS UTAH (BB-31). This trip to France, Germany, Norway, and Scotland is extensively described in Martineau's handwritten diary (June-August, 1930). Specific entries pertain to a shipmate's suicide in Paris (July) and his burial at sea (August) a visit to the German Naval Academy (July) observing surgery in Edinburgh (July) gunnery practice (August 26) and specifications of the heavy cruiser USS PENSACOLA (CA-24, August 28). Throughout the journal,Martineau details shipboard duties and training, tourist sites, social activities, and impressions of local people.

Pre-World War II correspondence is mainly comprised of Martineau's Navy orders and notices of promotion for his service on the battleship USS MISSISSIPPI (BB-41, 1933-1935) the minelayer USS OGLALA (CM-4) during the Aleutian Islands Survey Expedition in Kiska Harbor (1935) the battleship USS CALIFORNIA (BB-44, 1935-1936) the heavy cruiser USS VINCENNES (CA-44, 1937-1938) the destroyer USS BROOME (DD-210, 1938-1940) and the battleship USS ARKANSAS (BB-33, 1940-1941).

World War II correspondence (1944-1945) is sparse and concerns Martineau's command of the destroyers USS PHELPS (DD-350) and USS METCALF (DD-595). Postwar communications relate to assignments in several naval administrative positions (1946-1949, 1951-1957), including many associated with Martineau's efforts before the House Committee on Armed Services concerning Career Incentive legislation (1955). Correspondents during this period include Assistant Secretary of Defense Carter L. Burgess, Chief of Naval Operations Arleigh A. Burke, Rear Admiral Elton W. Grenfell, Surgeon General B. W. Hogan, Secretary of the Navy Charlie Thomas, Governor LeRoy Collins of Florida, publisher Malcolm Forbes, and numerous congressional legislators. Another group of orders pertains to Martineau's command of the destroyer USS CHARLES H. ROAN (DD-853, 1949-1951), the destroyer tender USS EVERGLADES (AD-24, 1957-1959), and the heavy cruiser USS LOS ANGELES (CA-135, 1958-1959).

After retirement, correspondence reflects Martineau's interest in a strong Navy and national defense, and many letters to the editors of various publications are included, as well as letters referring to Martineau's many speaking engagements (1967-1991, undated). Personal correspondence (1977-1987) includes letters from Rear Admiral Warren C. Hamm, Jr., Commander U.S. Naval Forces in Korea (1977-1979), Commander of Amphibious Group Two of the U.S. Atlantic Fleet (1979-1981), Deputy Commander in Chief of the Iberian Atlantic Area (1985-1987), and formerly under Rear Admiral Martineau's command. Other personal letters from Martineau's former classmate Edwards "Pete" Brown (1984-1989, undated) concern Brown's unlawful dismissal from the USNA (1933).

Other files detail the histories, actions, and reunions pertaining to the PHELPS, METCALF, EVERGLADES, and LOS ANGELES. Included are Martineau's handwritten war diaries for the PHELPS (March-June, 1944) and METCALF (December, 1944-September, 1945), as well as typescript journals of crewmen aboard these vessels. The diaries mention many battles and campaigns throughout the Pacific Theatre including Pearl Harbor (December 7, 1941) Bouganville Island (February, 1942) Coral Sea (May, 1942) Midway (June, 1942) Guadalcanal (August, 1942) Aleutian Islands (May-June, 1943) Makin Island (November, 1943) Marshall Islands (January-March, 1944) and Saipan (June, 1944). Also mentioned in the journals are the activities of the aircraft carriers USS ENTERPRISE (CV-6), USS HORNET (CV-8), USS LEXINGTON (CV-2), and USS YORKTOWN (CV-5), including the sinking of LEXINGTON and YORKTOWN and the sinking of the escort aircraft carrier USS LISCOME BAY (CVE-46). Specific entries detail battle damage to the PHELPS and assistance provided by the battle damage repair ship USS PHAON (ARB-3) during a battle near Saipan (June 18-22, 1944) sunken Japanese ships in Manila Bay and the city of Manila in ruins (May 17-20, 1945) a typhoon near Okinawa (August 30-September 2, 1945) and the capitulation of Japan and the destruction of mines (September, 1945-March, 1946). A post-war file concerning the LOS ANGELES contains information on the ship's participation in the President's People to People Program and a visit to Japan's Blackship Festival (May-June, 1959).

A large number of photographs are included in the collection and focus on the ships Martineau served on and the places they visited. A scrapbook of photographs taken while on board the MISSISSIPPI during a Caribbean cruise includes images of the ship crew and officers scenes in Cuba, Haiti, the Virgin Islands, and Panama and passage through the Panama Canal (1934-1935). Other photographs include various battleships, and of particular interest is an image of the USS OKLAHOMA (BB-37) following the Japanese attack on Pearl Harbor. The ship is shown raised and stripped of materials in the harbor. Further photographs include the ENTERPRISE and other aircraft carriers the LOS ANGELES and other heavy cruisers the PHELPS, METCALF, and other destroyers and the EVERGLADES and another destroyer tender. Of note are two series of pictures documenting battle damage to the PHELPS (June 1944) and the scrapping of the LOS ANGELES. Also included are many photographs depicting shipboard life, social functions, groups of crewmen and officers, and portraits.

Further records include Navy administrative and personnel reports (1949, 1953-1958, undated), speech transcripts by Martineau and others (1949-1959, 1974-1987, undated), publications, clippings, miscellaneous materials, and videotapes of the PHELPS (October 1986) and the METCALF (1987-1989, 1992-1994) reunions. Oversized items include awards, certificates, and photographs.


Following shakedown off San Diego, Calif., Metcalf was assigned to the Pacific Fleet for duty. The destroyer departed Bremerton, Wash., 19 February 1945 for the Carolines via Pearl Harbor, Hawaii, arriving Ulithi 16 March.

Just in time to join the armada of warships staging there for the Okinawa campaign, Metcalf operated with escort carrier Group 3. From 27 March her group furnished close air support for the landings at Kerama Retto (26 March) and Okinawa (1 April), and made raids on the neighboring Japanese-held islands until 20 April. During this period the ship rescued half a dozen pilots and crewmembers of downed carrier planes. She also performed radar picket and screen operations.

Metcalf departed on the 20th for the Philippines via Guam, reporting to commander, 7th Fleet, at Leyte 30 April. The destroyer spent May and June convoying the fast cruisers and transports being assembled for the Borneo invasion.

On 9 June Metcalf arrived off Brunei Bay, Borneo, for 2 days patrol of the South China Sea before beginning shore bombardment in support of the Australian landing at Brunei Bay the 10th. After action off Miri-Lutong, south of Brunei Bay, from 19 to 21 June, she reached Balikpapan on the 27th for operations with Task Force 74 (TF㻊) prior to the main landing by Australian troops 1 July.

Metcalf reported to commander, Philippine sea frontier, 4 August for duty escorting convoys between the Philippines and Okinawa. She was one day out of Okinawa in antisubmarine formation for Convoy 10K-204 when the Japanese capitulated.

Assigned to the newly formed North China Force, the destroyer departed Okinawa 4 September to participate in the landing of Army occupation forces at Korea. Metcalf joined Shields (DD-596), Hart (DD-594), and Conner (DD-582) in leading Task Unit 78.1.15 (TU 78.1.15) into Jinsen 8 September through the mine-infested Yellow Sea. She stood ready to provide fire support for the landing troops the next day if needed.

On 12 September Metcalf got underway through the Yellow Sea for operations supporting the occupation of China. Her ports of call included Dairen, Ching-wang-tao, Taku, Chefoo, Shanghai, and Hong Kong.

In early 1946 Metcalf steamed for the west coast, via Pearl Harbor, arriving San Diego to report in March to the 16th (Inactive Reserve) Fleet. She decommissioned March 1946, and entered the Pacific Reserve Fleet there. After berthing at Long Beach, Calif., from 1 July 1951 into 1960, Metcalf moved to Stockton, Calif..

Metcalf was stricken 2 January 1971 she was sold 6 June 1972 and broken up for scrap.


Mast cells and basophils as the source of many other mediators beyond histamine

In addition to the prompt release of preformed mediators stored in secretory granules including histamine, proteases, and proteoglycans, mast cells also rapidly upon activation form lipid mediators by enzymatic biosynthesis mainly from arachidonic acid, but also from several other fatty acids 37 . The main products of arachidonic acid are the prostaglandins and the leukotrienes, the latter first described as slow-reacting substances (SRS). Both products, or their activity, were described in the 1930s, prostaglandins by Ulf von Euler (1905–1983), and the SRS by Fedelberg and Kellaway 38, 39 . The initial work on SRS was performed using either cobra venom or antigen stimulation of sensitized rats or guinea pigs where the effect of histamine could be distinguished from that of SRS. It was discovered that in contrast to histamine that gives a rapid response, there was also a product that caused a contraction that was slow in onset but gave a sustained reaction. Hence, this product was named slow-reacting substance 39 . Work by Uvnäs in Sweden and Brocklehurst in the UK confirmed the release of SRS activity following anaphylactic challenge, and Brocklehurst named the activity slow-reacting substance of anaphylaxis (SRS-A) 40 . He also drew the conclusion that antigen–antibody activation of mast cells induced a series of enzymatic steps that resulted in the specific release pattern of SRS-A. In 1971, Uvnäs showed that SRS-A was not a prostaglandin 41 . More detailed studies of SRS-A as a mediator of immediate hypersensitivity reactions were performed by Priscilla Piper in the United Kingdom 42 and Frank Austen and colleagues in the USA 43 . The birth of the leukotriene family came from the work of Bengt Samuelsson and his coworkers at the Karolinska Institutet, Stockholm, who discovered LTB4 as a new lipoxygenase-catalyzed metabolite in leukocytes. The properties of LTB4 resembled those of SRS-A, and SRS-A from a mouse mastocytoma was subsequently identified as a glutathione-conjugated metabolite named LTC4 44 . Both mast cells and basophils synthesize leukotrienes, but in contrast to basophils, mast cells also have the capacity to synthesize PGD2 45 .

In addition to the release of preformed mediators, it was recognized at the end of the 1980s that mast cells and basophils are potent sources of cytokines and growth factors with multifunctional capacities. These discoveries put mast cells and basophils into a new context as multifunctional inflammatory cells acting not only as effector cells in allergy, but also as regulators affecting a diverse set of immunological and physiological functions. The first study that demonstrated mast cells to be a source of cytokines was published in 1987 by Brown et al. 46 who described mRNA expression and release of IL-4 in mouse mast cells. This study was followed by others that showed the capacity of mast cells to de novo synthesize and release other cytokines upon immunological stimuli, including IL-3, IL-5, and IL-6, chemokines, interferon γ, and GM-CSF 47, 48 . During this time, basophils were also identified as a source of IL-4 49 and, as shown by three laboratories a few years later, of large amounts of IL-13 50-52 . Mast cells and basophils not only produce cytokines upon stimulation, but also preform and store cytokines, for example, TNF in their granules 53 . Small amounts of IL-4 can also be detected in granules of human basophils 50 . This capacity to store preformed cytokines in granules from which they are released rapidly upon stimulation is in contrast to most other cells where a de novo protein synthesis of the cytokine is induced leading to cytokine secretion in a delayed fashion.

The first studies of cytokine expression and release from mast cells were performed on transformed mouse mast cell lines or bone marrow-derived cultured mast cells, but they were soon followed by studies on human mast cells as well. Over the last 20 years since the first paper was published on IL-4 released from mast cells, more than 30 different types of cytokines, chemokines, growth factors, and interferons have been shown to be released from mast cells 54 . The cytokine spectrum appears to be more restricted to a Th2-like phenotype for basophils 55 . For mast cells, the expression very much depends on the context, for example, species, source, type of stimulation, and pretreatment. It is noteworthy to point out that in human diseases, that is, asthma or atopic dermatitis, the percentage of mast cells expressing a specific set of cytokines is often increased and they express different type of cytokines depending on the type of inflammation 56-58 .


Metcalf DD- 595 - History

1. Ballmer-Weber BK, Vieths S, Luttkopf D, Heuschmann P, Wuthrich B (2000): Celery allergy confirmed by double-blind, placebo-controlled food challenge: a clinical study in 32 subjects with a history of adverse reactions to celery root. J Allergy Clin Immunol, 106(2): 373-8

2. Bindslev-Jensen C, Poulsen LK (1996): In vitro diagnostic tests. Chapter 7 In: Sampson HA, Simons E, Metcalfe DD: Food Allergy 2nd edition, Blackwell Scientific Publications: 137-150

3. Bock SA (1987): Prospective appraisal of complaints of adverse reactions to foods in children during the first three years of life . Paediatrics, 79: 683-688

4. Bock SA, Sampson HA, Atkins FM, Zeiger RS, Lehrer S, Sachs M, Bush RK, Metcalfe DD (1988): Double-blind, placebo-controlled food challenge ( DBPCFC ) as an office procedure: a manual. J Allergy Clin Immunol, 82(6): 986-97

5. Burks AW, Sampson H (1993): Food allergies in children. Current Problems in Paediatrics 23: 230-252

6. Bruijnzeel-Koomen C, Ortolani C, Aas K, Bindslev-Jensen C, Björksten B, Moneret-Vautrin D, Wütrich B (1995): Adverse reactions to food. Position Paper. Allergy, 50: 623-635

7. Dearman RJ, Caddick H, Basketter DA, Kimber I (2000): Divergent antibody isotope responses induced in mice by systemic exposure to proteins: a comparison of ovalbumin with bovine serum albumin . Food Chem Toxicol, 38: 351-360

8. EPA (2000): A Set of Scientific Issues Being Considered by the Environmental Protection Agency Regarding Assessment of Scientific Information Concerning StarLink Corm. FIFRA Scientific Advisory Panel Meeting, Environmental Protection Agency of the United States

9. European Commission (1998): Consideration of the Epidemiological Basis for appropriate Measures for the Protection of the Public Heath in Respect of Food Allergy , SCOOP/NUTR/REPORT/2, European Commission, Brussels

10. FAO (1996): Biotechnology and food safety, Report of a joint FAO/WHO consultation. FAO Food and Nutrition Paper 61 , Food and Agriculture Organisation of the United Nations, Rome

11. Gendel SM (1998a): Sequence databases for assessing the potential allergenicity of proteins used in transgenic foods . Adv. Food Nutr. Res. 42: 63-92

12. Gendel SM (1998b): The use of amino acid sequence alignments to assess potential allergenicity of proteins used in genetically modified foods : Adv. Food Nutr. Res. 42: 45-62

13. Hefle SL, Nordlee JA, Taylor SL (1996): Allergenic foods . Critical Reviews in Food Science and Nutrition 36: S69-S89

14. Hourihane JO’B, Kilburn SA, Nordlee J, Hefle S, Taylor SL, Warner JO (1997): An evaluation of the sensitivity of subjects with peanut allergy to very low doses of peanut protein: a randomized, double-blind, placebo-controlled food challenge study. J. Allergy Clin. Immunol, 100: 596-600

15. Jarvinen KM, Makinen-Kiljunen S, Suomalainen H (1999): Cow’s milk challenge through human milk evokes immune responses in infants with cow’s milk allergy. J. Pediatr, 135:506-512

16. Knippels et al. (1998): Oral sensitization to food proteins: a Brown Norway rat model. Clin Exp Allergy, 28: 368-375

17. Mekori YA (1996): Introduction to allergic diseases . Critical Reviews in Food Science and Nutrition 36: S1-S18

18. Metcalfe DD, Astwood JD, Townsend R, Sampson HA, Taylor SL, Fuchs RL (1996): Assessment of the allergenic potential of foods derived from genetically engineered crop plants . Critical Reviews in Food Science and Nutrition 36: S165-S186

19. Ortolani C, Ispano M, Pastorello E, Bigi A, Ansaloni R (1988) : The oral allergy syndrome. Ann Allergy 61(6 Pt 2): 47-52

20. Rance F, Dutau G (1997): Labial food challenge in children with food allergy. Pediatr Allergy Immunol 8: 41-44

21. Sampson HA (1990a): Food Allergy . Current Opinion in Immunology 2: 542-547

22. Sampson HA (1990b): Immunologic mechanisms in adverse reactions to foods . Immunology and Allergy Clinics of North America 11: 701-706

23. Sampson HA, Burks AW (1996): Mechanisms of food allergy . Annual Review of Nutrition 16: 161-177

24. Sorva R, Makinien-Kiljunen S, Juntunen-Backman K (1994): B-Lactoglobulin secretion in human milk varies widely after cow’s milk ingestion in mothers of infants with cow’s milk allergy : J Allergy Clin Immunol 93: 787-792

25. Taylor, S. L. (1997): Food from genetically modified organisms and potential for food allergy. Environ Toxicol Pharmacol 4: 121-126

26. WHO (1991): Strategies for assessing the safety of foods produced by biotechnology. Report of a Joint FAO/WHO Consultation, World Health Organization, Geneva

27. WHO (2000): Safety aspects of genetically modified foods of plant origin. Report of a Joint FAO/WHO Expert Consultation, World Health Organization, Geneva


Hereditary Alpha Tryptasemia

1. Tryptase:
Tryptase is an enzyme found almost exclusively in mast cells. It is used as a marker for identifying mast cells and is increased when mast cells are activated or increased in number. Examples of mast cell activation include severe allergic-type reactions causing anaphylaxis.

2. Tryptase Genes:
The genes that encode tryptase are located on human chromosome 16. There are mainly two forms of the gene, alpha (α) and beta (β). A third form, gamma tryptase (γ) is bound to the membrane of the granule and is not released from mast cells. 1 The α/β tryptase locus normally contains two genes, TPSB2, expressing only β-tryptase, and TPSAB1, expressing either α- or β- tryptase. 2 Each is expressed as a 275 amino acid pretryptase (before tryptase) that is broken down to a 257 amino acid protryptase (primitive tryptase). One portion of these protryptases is continuously secreted by unstimulated mast cells, and is the form detected in serum or plasma collected under non-anaphylactic conditions for both healthy people and patients with mastocytosis and other mast cell diseases. Another portion of the protryptases is changed to a 245 amino acid mature proteins (final protein), which is stored in mast cell granules. 3,4 Mature tryptase is stored as four chains associated with heparin in the granule, those four chains are called tetramers. α/β-Tryptases are primarily produced by mast cells. However, there is another cell that produces tryptase, and that is the basophil. Basophils contain only about 0.2% of the tryptase found in mast cells. 5

3. Levels of Tryptase in Serum:
In the general population baseline serum tryptase level is 5.1 ng/mL with a range from &lt1 to 31 ng/mL. In healthy twins tryptase level is related to genetics. 6 Levels of serum tryptase are affected by many factors, those include age, obesity, smoking, or alcohol consumption. Tryptase level is, however, not affected by the allergic status, 7 but can be increased in patients with active severe hives. Elevated baseline levels of total tryptase are also seen with malignancies that affect white blood cells related to the lineage of mast cells called myeloid neoplasms. 8-12 Other conditions in which tryptase is elevated include those with increased eosinophils (Hypereosinophilia) associated the FIP1L1-PDGFRA mutation. 13 End stage kidney disease, 14,15 treatment of some parasite infections (onchocerciasis), 16 systemic mastocytosis, 17 and rare familial lysosomal storage disorders such as Gaucher’s disease, 18. In clinical practice, levels above 10-11.5 ng/mL are generally considered high. For children serum tryptase level is 3.3 ng/mL (range 2.4-4.4) and is higher in younger children. 19 The baseline serum tryptase level has been utilized in diagnostic algorithms for the presence of mastocytosis in patients having or lacking typical skin lesions. 20-23 A tryptase level consistently above 20 ng/mL is one of the 2 criteria used in the diagnosis of systemic mastocytosis 23 when the patient does not have another blood neoplasm.

4. Risks Associated with High Basal Serum Tryptase Levels:
In the general population, people with elevated tryptase levels have a higher risk of anaphylaxis and food allergic reactions, reactions to drugs, contrast dye, insect stings 24-26 , and to allergy prophylactic injections for treatment of stinging insect allergies. 1,27 Tryptase in and by itself does not increase this risk high tryptase seems to be a bystander marker for other factors involved in those reactions, such as the presence of mast cell clones. Mature tryptases are released during episodes of mast cell activation, such as anaphylaxis caused by insect stings. The severity of clinical anaphylaxis resulting from insect stings directly correlates with the increase in the level of tryptase. 28-30 However, this dramatic correlation is not found in all types of anaphylaxis, for example, food-induced anaphylaxis is associated with lower increase in serum tryptase.

5. Alpha Tryptasemia:
In 2014, Lyons et al. from NIH, published a report of a multiple families with high levels of serum tryptase. 31 The inheritance pattern was consistent with an autosomal dominant Mendelian inheritance. Autosomal dominant inheritance means that if a parent has one gene causing a high tryptase level, each child has a 50% chance of having high tryptase regardless of the gender of the child. The patients and their blood relatives, described in this report also had problems with connective tissues. About 87% of
the patients with high tryptase suffered from episodic hives, flushing, and/or abdominal pain with diarrhea. One third of those patients had a history of anaphylaxis, 94% had a history of environmental allergies or asthma, and about 70% had problems with connective tissues some with hypermobile joint disorder. One third of the patients with elevated tryptase experienced chronic musculoskeletal pain, another third experienced orthostatic hypotension with tachycardia (POTS), and half had a neuropsychiatric diagnosis. There was a direct correlation of the symptoms from each organ system (skin, gastrointestinal tract, connective tissue and allergic disorders) with the level of tryptase. In a separate report, familial hypertryptasemia in one family was also described. One of the affected family members in this report had clonal mutation of c-KIT (Asp816Val) consistent with clonal mast cell activation syndrome. 32 Calculations based on the referral pattern suggested that about 4-6% of the general population have elevated tryptase. In this report, Lyons et. al. identified duplications and triplications (increase in the copy number of the α-tryptase gene by two or three times) in the TPSAB1 gene encoding alpha-tryptase. This increase in gene copy number was associated in increase of serum tryptase level. Thirty five families were presented with this multi-organ symptom complex. The higher the number of gene copies, the higher the basal serum levels of tryptase and the worse the symptoms. Two additional family groups were identified in this report totaling 172 individuals. Findings from the NIH group showed direct link between duplications in TPSAB1 with irritable bowel syndrome, skin complaints, connective tissue abnormalities, and autonomic dysfunction. 333

In 2017, Lyons et. al. reported an overlap between a gene that encodes a calcium channel and alpha tryptase. This calcium channel contributes to sensations of pain and itching. It is related to movement in the intestinal wall, anxiety, and control of blood pressure. The gene for this calcium channel is called CACNA1H. Because it overlaps with the human tryptase locus (site) it could explain the symptoms associated with increased copies of the tryptase gene. However, even though a link in the genetic inheritance between this calcium channel and tryptase gene was identified, no clinical differences were observed in association with the CACNA1H haplotype. This means that we still do not know the cause of symptoms related to different organ systems in patients with alpha-tryptasemia 34

6. Summary:
In summary, hereditary alpha tryptasemia is an autosomal dominant genetic disorder caused by increase in number of copies of genes encoding alpha-tryptase. Individuals with this trait have increased basal serum tryptase levels. Some have symptoms associated related to other organ systems that do not appear directly caused by tryptase. The higher tryptase gene copy number (TPSAB1) is associated with higher levels of basal serum tryptase and also associated with more severe the clinical symptoms. 35
Finally, a patient with five copies of the tryptase gene TPSAB1 was found recently found to have a clonal mast cell disorder. 36

References:
1. Vitte J. Human mast cell tryptase in biology and medicine. Mol Immunol. 201563(1):18-24.
2. Trivedi NN, Caughey GH. Mast cell peptidases: chameleons of innate immunity and host defense. Am J Respir Cell Mol Biol. 201042(3):257-267.
3. Schwartz LB, Sakai K, Bradford TR, et al. The alpha form of human tryptase is the predominant type present in blood at baseline in normal subjects and is elevated in those with systemic mastocytosis. J Clin Invest. 199596(6):2702-2710.
4. Kanthawatana S, Carias K, Arnaout R, Hu J, Irani AM, Schwartz LB. The potential clinical utility of serum alpha-protryptase levels. J Allergy Clin Immunol. 1999103(6):1092-1099.
5. Jogie-Brahim S, Min HK, Fukuoka Y, Xia HZ, Schwartz LB. Expression of alpha-tryptase and beta- tryptase by human basophils. J Allergy Clin Immunol. 2004113(6):1086-1092.
6. Sverrild A, van der Sluis S, Kyvik KO, et al. Genetic factors account for most of the variation in serum tryptase–a twin study. Ann Allergy Asthma Immunol. 2013111(4):286-289.
7. Gonzalez-Quintela A, Vizcaino L, Gude F, et al. Factors influencing serum total tryptase concentrations in a general adult population. Clin Chem Lab Med. 201048(5):701-706.
8. Valent P, Sperr WR, Samorapoompichit P, et al. Myelomastocytic overlap syndromes: biology, criteria, and relationship to mastocytosis. Leuk Res. 200125(7):595-602.
9. Sperr WR, Drach J, Hauswirth AW, et al. Myelomastocytic leukemia: evidence for the origin of mast cells from the leukemic clone and eradication by allogeneic stem cell transplantation. Clin Cancer Res. 200511(19 Pt 1):6787-6792.
10. Horny HP, Sotlar K, Stellmacher F, et al. The tryptase positive compact round cell infiltrate of the bone marrow (TROCI-BM): a novel histopathological finding requiring the application of lineage specific markers. J Clin Pathol. 200659(3):298-302.
11. Sperr WR, El-Samahi A, Kundi M, et al. Elevated tryptase levels selectively cluster in myeloid neoplasms: a novel diagnostic approach and screen marker in clinical haematology. Eur J Clin Invest. 200939(10):914-923.4
12. Valent P, Orazi A, Busche G, et al. Standards and impact of hematopathology in myelodysplastic syndromes (MDS). Oncotarget. 20101(7):483-496.
13. Klion AD, Noel P, Akin C, et al. Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness. Blood. 2003101(12):4660-4666.
14. Sirvent AE, Gonzalez C, Enriquez R, et al. Serum tryptase levels and markers of renal dysfunction in a population with chronic kidney disease. J Nephrol. 201023(3):282-290.
15. Jesky MD, Stringer SJ, Fenton A, et al. Serum tryptase concentration and progression to end-stage renal disease. Eur J Clin Invest. 201646(5):460-474.
16. Cooper PJ, Schwartz LB, Irani AM, Awadzi K, Guderian RH, Nutman TB. Association of transient dermal mastocytosis and elevated plasma tryptase levels with development of adverse reactions after treatment of onchocerciasis with ivermectin. J Infect Dis. 2002186(9):1307-1313.
17. Valent P, Akin C, Arock M, et al. Definitions, criteria and global classification of mast cell disorders with special reference to mast cell activation syndromes: a consensus proposal. Int Arch Allergy Immunol. 2012157(3):215-225.
18. Schussler E, Yang A, Lyons JJ, Milner JD, Wang J. Persistent tryptase elevation in a patient with Gaucher disease. J Allergy Clin Immunol Pract. 20186(2):697-699.
19. Sahiner UM, Yavuz ST, Buyuktiryaki B, et al. Serum basal tryptase levels in healthy children: correlation between age and gender. Allergy Asthma Proc. 201435(5):404-408.
20. van Doormaal JJ, van der Veer E, van Voorst Vader PC, et al. Tryptase and histamine metabolites as diagnostic indicators of indolent systemic mastocytosis without skin lesions. Allergy. 201267(5):683-690.
21. Alvarez-Twose I, Gonzalez-de-Olano D, Sanchez-Munoz L, et al. Validation of the REMA score for predicting mast cell clonality and systemic mastocytosis in patients with systemic mast cell activation symptoms. Int Arch Allergy Immunol. 2012157(3):275-280.
22. Valent P, Escribano L, Broesby-Olsen S, et al. Proposed diagnostic algorithm for patients with suspected mastocytosis: a proposal of the European Competence Network on Mastocytosis. Allergy. 201469(10):1267-1274.
23. Arber DA, Orazi A, Hasserjian R, et al. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016127(20):2391-2405.
24. Fellinger C, Hemmer W, Wohrl S, Sesztak-Greinecker G, Jarisch R, Wantke F. Clinical characteristics and risk profile of patients with elevated baseline serum tryptase. Allergol Immunopathol (Madr). 201442(6):544-552.
25. Sahiner UM, Yavuz ST, Buyuktiryaki B, et al. Serum basal tryptase may be a good marker for predicting the risk of anaphylaxis in children with food allergy. Allergy. 201469(2):265-268.
26. Aberer E, Savic S, Bretterklieber A, Reiter H, Berghold A, Aberer W. Disease spectrum in patients with elevated serum tryptase levels. Australas J Dermatol. 201556(1):7-13.
27. Dugas-Breit S, Przybilla B, Dugas M, et al. Serum concentration of baseline mast cell tryptase: evidence for a decline during long-term immunotherapy for Hymenoptera venom allergy. Clin Exp Allergy. 201040(4):643-649.
28. Schwartz LB, Metcalfe DD, Miller JS, Earl H, Sullivan T. Tryptase levels as an indicator of mast-cell activation in systemic anaphylaxis and mastocytosis. N Engl J Med. 1987316(26):1622-1626.
29. Schwartz LB, Yunginger JW, Miller J, Bokhari R, Dull D. Time course of appearance and disappearance of human mast cell tryptase in the circulation after anaphylaxis. J Clin Invest. 198983(5):1551-1555.
30. Schwartz LB, Min HK, Ren S, et al. Tryptase precursors are preferentially and spontaneously released, whereas mature tryptase is retained by HMC-1 cells, Mono-Mac-6 cells, and human skin-derived mast cells. J Immunol. 2003170(11):5667-5673.5
31. Lyons JJ, Sun G, Stone KD, et al. Mendelian inheritance of elevated serum tryptase associated with atopy and connective tissue abnormalities. J Allergy Clin Immunol. 2014133(5):1471-1474.
32. Sabato V, Van De Vijver E, Hagendorens M, et al. Familial hypertryptasemia with associated mast cell activation syndrome. J Allergy Clin Immunol. 2014134(6):1448-1450 e1443.
33. Lyons JJ, Yu X, Hughes JD, et al. Elevated basal serum tryptase identifies a multisystem disorder associated with increased TPSAB1 copy number. Nat Genet. 201648(12):1564-1569.
34. Lyons JJ, Stotz SC, Chovanec J, et al. A common haplotype containing functional CACNA1H variants is frequently coinherited with increased TPSAB1 copy number. Genet Med. 2017.
35. Lyons JJ. Hereditary Alpha Tryptasemia: Genotyping and Associated Clinical Features. Immunol Allergy Clin North Am. 201838(3):483-495.
36. Sabato V, Chovanec J, Faber M, Milner JD, Ebo D, Lyons JJ. First Identification of an Inherited TPSAB1 Quintuplication in a Patient with Clonal Mast Cell Disease. J Clin Immunol. 201838(4):457-459.

Hereditary Alpha Tryptasemia Testing

Commercial testing is now available for Hereditary Alpha Tryptasemia through Gene by Gene laboratory.
Info Here
*This test is not offered direct to consumer and must be authorized by a qualified medical professional.
*This test is not currently available for New York State residents.

This test is used to determine alpha tryptase copy number. Alpha tryptase is encoded by the TPSAB1 gene, which is on chromosome 16. The primary gene products of this gene are β-tryptase, which can be produced by TPSAB1 and TPSB2, and α-tryptase, which is only produced by the TPSAB1 gene.

Individuals who inherited one copy of α-tryptase–encoding sequence on both have normal serum tryptase levels.
This test measures both α- and β-tryptase. A normal result is any combination of α- and β-tryptase that adds up to 4.
A positive result – which means there is a duplication or triplication of α-tryptase – is a combination of α and β-tryptase that is 5 or higher.


What Ever Happened to Jackie's Son Andy on "Roseanne"?

The character was played by two different sets of twins.

All of the Conner kids made a comeback on the much-anticipated Roseanne reboot (except for Jerry), but fans will remember that Roseanne Barr wasn't the only mother on the show. Laurie Metcalf's character Jackie Harris gave birth to a son named Andy Harris during Season 6, but will he make an appearance on the new show?

At the 2018 Winter TCA press tour, Roseanne explained to PopSugar why Andy would not be returning to the reboot for the first season. "We haven't dealt with Andy, Laurie's son, yet," she said. "But we had so many stories to tell over the arc of these nine episodes that we were hoping for another season to bring more clarity to those characters."

And another season they did get, but without Roseanne. The spinoff show, The Conners, premiered on October 16, but there's still has yet to be a mention of Andy, although Jackie was front and center in the first episode.

In case you forgot, inn the "Labor Day" episode of Roseanne, which aired in 1994, Jackie's son was born and played by two sets of infant twins. Andy was later shown as a toddler until the show's end in 1997.

Fraternal twins Garrett and Kent Hazen were the first brothers to play Andy for three seasons, People reported in 2000. &ldquoWhen they were tiny babies, Kent liked it more, and as they got older Garrett enjoyed it more,&rdquo the Hazen's real-life mother, Karen Hazen, told People. &ldquoHe did a speaking part. He got to say, &lsquoGrandma&rsquos crazy.&rsquo That was a highlight. I look at the show as such a blessing.&rdquo

Garrett Hazen spoke with GoodHousekeeping.com about what he and his brother have been up to since their time on the show. "I became obsessed with the guitar at a young age, and for the last few years have dove pretty deep into writing and recording music under my name," Garrett shares. "I just released my second EP, 'Gold.'"

His brother has taken on a completely new career path. "My twin brother Kent is a twitch streamer for live role playing games like Dungeons and Dragons, and other video game content on his channel," Garrett says.

When asked whether he would reprise the role of Andy on the original Roseanne reboot, Garrett told us in April that he would definitely consider it. "I would be so open to it," he says. "I love film/tv and binge watch as many shows as I can. Being on the stage has always been where I feel the most like myself, and acting is another extension of the stage for me."

However, producers did not contact Hazen or his brother for the part. Identical twins Tyler and Trevor Battaglia, who took on the role just before the series ended, are no longer in the entertainment business, Tyler told GoodHousekeeping.com.

"My brother and I aren't acting anymore, but we also were wondering what would happen to our part when the show returned," Tyler said.


Metcalf DD- 595 - History

Mossberg Shotgun Models & Specifications

.410 Bolt Action Repeater

4 Shot, Takedown, .410 bore only (2 1/2 inch), 4 shell fixed top loading magazine. Weight 5 1/2 lbs, barrel 26" with metal bead front and inverted leaf rear sights. Walnut finished stock with finger flutes in fore-end, steel butt plate, swivels and chrome plated bolt leaver and trigger. Made 1933-?

Model 70 Bolt Action Single Shot

Single shot, Takedown, .410 bore only (2 1/2 inch). Weight 4 3/4 lbs, barrel 24" with metal bead front and inverted leaf rear sights. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate. Made 1933-1934.

Model 73 Bolt Action Single Shot

Single Shot, Takedown, .410 bore only (2 1/2 & 3 inch). Weight 4 3/4 lbs, barrel 24", full choke, with metal bead front and inverted leaf rear sights. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate & swivels. Replaced Model 70. Made 1935-1936.

Model 73A Bolt Action Single Shot

Single Shot, Takedown, .410 bore only (2 1/2" & 3 inch). Weight 5 3/4 lbs, barrel 24", full choke, with metal bead front and inverted leaf rear sights. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate , chrome plated bolt lever & trigger, swivels. Made 1936-1939.

Model 73B Bolt Action Single Shot

Single shot, Takedown, .410 bore only (2 1/2 & 3 inch). Weight 5 1/2 lbs, barrel 24", full choke, with metal bead front and inverted leaf rear sights. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate , chrome plated bolt lever & trigger, swivels. Made 1939-1940.

Model 75 Bolt Action Single Shot

Single Shot, Takedown, 20 gauge only (2 1/2 & 2 3/4 inch). Weight 6 1/4 lbs, barrel 26", full choke, with metal bead front sight. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate & chrome plated bolt lever and trigger. Made ?-?

Model 75A Bolt Action Single Shot

Single Shot, Takedown, 20 gauge only (2 1/2 & 2 3/4 inch). Weight 6 lbs, barrel 26", full choke, metal bead front sight. Walnut finished pistol grip stock, chrome plated bolt lever and trigger. Same as 85A except single shot. Made ?-?

Model 75B Bolt Action Single Shot

Single Shot, Takedown, 20 gauge only (2 1/2 & 2 3/4 inch). Weight 6 1/4 lbs, barrel 26", full choke, metal bead front sight. Walnut finished pistol grip stock, chrome plated bolt lever and trigger.. Made 1939-1940.

Model 80 Bolt Action Repeater

4-Shot, Takedown, .410 bore only (2 1/2 inch), 4 shell fixed top loading magazine. Weight 5 1/2 lbs, barrel 24", full choke, with metal bead front and inverted leaf rear sights. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate , chrome plated bolt lever & trigger, swivels. Made 1933-1936.

Model 83 Bolt Action Repeater

4-Shot, Takedown, .410 bore only (2 1/2 & 3 inch), 4 shell fixed top loading magazine. Weight 5 3/4 lbs, barrel 24", full choke, with metal bead front and inverted leaf rear sights. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate , chrome plated bolt lever & trigger, swivels. Made 1936-1938.

Model 83B Bolt Action Repeater

3-Shot, Takedown, .410 bore only (2 1/2 & 3 inch), 3 shell fixed top loading magazine. Weight 5 1/2 lbs, barrel 24", full choke, with metal bead front and inverted leaf rear sights. Walnut finished pistol grip stock with finger flutes in fore-end, steel butt plate , chrome plated bolt lever & trigger, swivels. Made 1939-1940.

Model 83D Bolt Action Repeater

3-Shot, Takedown, .410 bore only (2 1/2 & 3-inch), 2 shell fixed top loading magazine. Weight 5 1/2 lbs, barrel, 23" with two interchangeable choke tubes, Modified & Full. Plain one piece pistol grip stock. Made 1940-1946. Production suspended in 1942 for war efforts.

Model 85 Bolt Action Repeater

3-Shot, Takedown, 20 gauge only (2 1/2 & 2 3/4 inch), 2 shell top loading magazine. Weight 6 1/4 lbs, barrel 26", full choke, metal bead front sight. Walnut finished pistol grip stock, chrome plated bolt lever and trigger. Made 1934-1937.

Model 85A Bolt Action Repeater

3-Shot, Takedown, 20 gauge only (2 1/2 & 2 3/4 inch), 2 shell top loading magazine. Weight 6 lbs, barrel 26", full choke, metal bead front sight. Walnut finished pistol grip stock, chrome plated bolt lever and trigger. Made 1937-1939.

Model 85B Bolt Action Repeater

3-Shot, Takedown, 20 gauge only (2 1/2 & 2 3/4 inch), 2 shell detachable magazine. Weight 6 1/4 lbs, barrel 26", full choke, metal bead front sight. Walnut finished pistol grip stock, chrome plated bolt lever and trigger. Made 1939-1940.

Model 85D Bolt Action Repeater

3-Shot, Takedown, 20 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 6 1/4 lbs, barrel, 25" with three interchangeable choke tubes, Modified, Full & Improved Cylinder. Plain one piece pistol grip stock. Made 1940-1946. Production suspended in 1942 for war efforts.

Model 173 Bolt Action Single Shot

Single Shot, Takedown, .410 bore only (2 1/2 & 3-inch). Weight 5 1/2 lbs, Barrel 24", standard barrel full choke, front bead sight. Genuine American walnut Monte Carlo stock, later models walnut finish. Same as 183K except single shot and no C-Lect-Choke. Made 1957-1960.

Model 173-A Bolt Action Single Shot, Slimmer barrel than 173. Made 1960-1963.

Model 173-B Bolt Action Single Shot, change to trigger and safety lever 1963-1971.

Model 173Y Bolt Action Single Shot

Single Shot, Takedown, .410 bore only (2 1/2 & 3-inch). Weight 5lbs, Barrel 22". Youth gun, short barrel and stock. Plain pistol grip, Walnut finish stock. Made 1961-1963.

Model 173Y-A Bolt Action Single Shot, change to trigger and safety lever. Made 1963-1968.

Model 183D Bolt Action Repeater

3-Shot, Takedown, .410 bore only (2 1/2 & 3-inch), 2 shell fixed top loading magazine. Weight 5 1/2 lbs, barrel, 23" with two interchangeable choke tubes, Modified & Full. Plain one piece pistol grip stock. Made 1947-1948.

Model 183D-A Bolt Action Shotgun, left hand extractor added. Made 1948-1950.

Model 183D-B Bolt Action Repeater, firing pin design change. Made 1950-1953.

Model 183D-C Bolt Action Repeater, ejector interrupter added. Made 1953-1956.

Model 183D-D Bolt Action Repeater, change to ejector interrupter. Made 1956-1960.

Model 183D-E Bolt Action Repeater, Slimmer barrel. Made 1960-1963.

Model 183D-F Bolt Action Repeater, change to trigger and safety lever. Made 1968-1971.

Model 183D-G Bolt Action Repeater, change to barrel and front sight. Made 1968-1971

Model 183K Bolt Action Repeater

3-Shot, Takedown, .410 bore only (2 1/2 & 3-inch), 2 shell fixed top loading magazine. Weight 5 1/2 lbs, barrel, 25" with variable C-Lect-Choke. Genuine walnut one piece Monte Carlo stock, later models walnut finish. Made 1953-1956.

Model 183K-A Bolt Action Repeater, firing pin design change. Made 1956-1960.

Model 183K-B Bolt Action Repeater, Slimmer barrel. Made 1960-1963.

Model 183K-C Bolt Action Repeater, change to trigger and safety lever. Made 1963-1986.

Model 183K-D Bolt Action Repeater, change to barrel and front sight. Made 1968-1986.

Model 185D Bolt Action Repeater

3-Shot, Takedown, 20 gauge only (2 1/2 & 2 3/4-inch), 2 shell detachable magazine. Weight 6 1/4 lbs, barrel, 25" with three interchangeable choke tubes, Modified, Full & Improved Cylinder. Plain one piece Monte Carlo pistol grip stock. Made 1947-1950.

Model 185D-A Bolt Action Repeater. Made 1950-1950.

Model 185D-B Bolt Action Repeater, firing pin design change. Made 1950-1955.

Model 185D-C Bolt Action Repeater, redesign of magazine bottom plate. Made 1955-1958.

Model 185K Bolt Action Repeater

3-Shot, Takedown, 20 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 6 1/4 lbs, barrel, 26" with variable C-Lect-Choke with ventilated barrel. Genuine AmericanWalnut Monte Carlo one piece pistol grip stock with recoil pad. Made 1950-1950.

Model 185K-A Bolt Action Repeater. Made 1950-1955.

Model 185K-B Bolt Action Repeater. Made 1955-1963.

Model 185K-C Bolt Action repeater, change to trigger and safety lever. Made 1963-1964.

Model 185K-E Bolt Action Repeater, change to butt plate. Made 1964-1964.

Thanks JP for the photo.

Model 190 Bolt Action Repeater

3-Shot, Takedown, 16 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 6 1/4 lbs, barrel, 26" with variable C-Lect-Choke. Genuine Walnut Monte Carlo one piece pistol grip stock. Made 1950-1955.

Thanks JP for the photo.

Model 190A Bolt Action Repeater

3-Shot, Takedown, 16 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight ? lbs, barrel, ?" Made 1955-1956.

Model 190D Bolt Action Repeater

3-Shot, Takedown, 16 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 6 lbs, barrel, 28" with two interchangeable choke tubes, Full & Improved Cylinder. Genuine American walnut Monte Carlo stock with recoil pad. Made 1955-1958.

Model 190K Bolt Action Repeater

3-Shot, Takedown, 16 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 6 3/4 lbs, barrel, 26" with variable C-Lect-Choke and ventilated barrel. Genuine American walnut Monte Carlo stock with recoil pad. Made 1956-1956.

Model 190K-A Bolt Action Repeater. Made1956-1957.

Model 190K-B Bolt Action Repeater. Made 1957-1962.

Model 190K-C Bolt Action Repeater, change to trigger and safety lever. Made 1963-1963.

Model 195 Bolt Action Repeater

3-Shot, Takedown, 12 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 7 1/2 lbs, barrel, 26" variable C-Lect-Choke, ventalated barrel, front and rear sight. Genuine walnut, Monte Carlo stock with rubber recoil pad. Made 1954-1955.

Model 195A Bolt Action Repeater

3-Shot, Takedown, 12 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight ? lbs, barrel, ?" Made 1955-1956.

Model 195D Bolt Action Repeater

3-Shot, Takedown, 12 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 6 3/4 lbs, barrel, 28" with two interchangeable choke tubes, Full & Improved Cylinder. Genuine American walnut Monte Carlo stock with rubber recoil pad. Made 1955-1958.

Model 195K Bolt Action Repeater

3-Shot, Takedown, 12 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 7 1/2 lbs, barrel, 26" with variable C-Lect-Choke. Plain one piece pistol grip stock. Made 1956-1963.

Model 195K-A Bolt Action Repeater, change to barrel. Made 1956-1963.

Thanks JP for the photo.

Model 200D Slide Action Shotgun

3 shot, 12 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 7 1/2 lbs, barrel 28" with two interchangeable choke tubes, Full & Improved Cylinder . Plain one piece pistol grip stock. Black nylon slide. Made 1955-1956.

Model 200D-A Slide Action Shotgun, change to barrel. Made 1956-1959.

Model 200K Slide Action Shotgun

3 shot, 12 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 7 1/2 lbs, barrel 28" with variable C-Lect-Choke. Plain one piece pistol grip stock. Black nylon slide. Made 1955-1956.

Model 200K-A Slide Action Shotgun, change to barrel. Made 1956-1959.

Model 385K Bolt Action Repeater

3 shot, Takedown, 20 gauge only (2 3/4 & 3-inch), 2 shell detachable magazine. Weight 6 1/4 lbs, barrel 26" with variable C-Lect-Choke. Genuine American walnut Monte Carlo stock with recoil pad, later models walnut finish. Same as 395K except 20 gauge. Made 1965-1968.

Model 385K-A Bolt Action Repeater, change to barrel. Made 1968-1983

Model 385K-B Bolt Action Repeater, change to takedown, added cross bolt. Made ?-?

Model 390K Bolt Action Repeater

3 shot, Takedown, 16 gauge only (2 3/4-inch), 2 shell detachable magazine. Weight 6 3/4 lbs, barrel 26" with variable C-Lect-Choke. Genuine American walnut Monte Carlo stock with recoil pad, later models walnut finish. Same as 385K except 16 gauge. Made 1965-1974.

Model 390K-A Bolt Action Repeater. Made ?-?.

Model 390K-B Bolt Action Repeater. Made ?-?.

Model 395 Bolt Action Repeater

3 shot, Takedown, 12 gauge only (2 3/4 & 3-inch), 2 shell detachable magazine. Weight 7 1/2 lbs, barrel 38" with a full choke, rear sight groove & front bead. Monte Carlo stock with recoil pad, walnut finish. Made 1982-1982.

Model 395K Bolt Action Repeater

3 shot, Takedown, 12 gauge only (2 3/4 & 3-inch), 2 shell detachable magazine. Weight 6 3/4 lbs, barrel 28" with variable C-Lect-Choke, rear sight groove & front bead. Genuine American walnut Monte Carlo stock with recoil pad, later models walnut finish. Made 1964-1983.

Model 395K-A Bolt Action Repeater, change to barrel. Made ?-?

Model 395K-B Bolt Action Repeater, change to takedown, added cross bolt. Made ?-?

3 shot, Takedown, 12 gauge only (2 3/4 & 3-inch), 2 shell detachable magazine. Weight 6 3/4 lbs, barrel 24" with cylinder bore, rifle sights, swivels & web sling. Monte Carlo stock with recoil pad, walnut finish. Made 1968-1977.

Model 595AP5 Bolt Action Repeater

5 shot, Takedown, 12 gauge only ( inch), 4 shell detachable magazine. Weight lbs, barrel ,swivels & web sling. Monte Carlo stock with recoil pad, walnut finish. Made 1983-?.

Model 585K Bolt Action Repeater

3 shot, Takedown, 20 gauge only (2 3/4 & 3-inch), 2 shell detachable magazine. Weight 6 3/8 lbs, barrel 28" with variable C-Lect-choke. Monte Carlo stock with recoil pad, walnut finish. Made 1984-?.

Model 595K Bolt Action Repeater

3 shot, Takedown, 12 gauge only (2 3/4 & 3-inch), 2 shell detachable magazine. Weight 7 1/2 lbs, barrel 38" with full choke or 28" with C-Lect-choke. Monte Carlo stock with recoil pad, walnut finish. Made 1984-?.

Model 695 Bolt Action Rifled Slug Gun

3 shot, 12 gauge only, 2 shell detachable magazine. 22", fully rifled and ported barrel. Black synthetic stock, adjustable sight, "Tasco style" scope bases. Made 1996-?

Model 695 Bolt Action Turkey Gun

3 shot, 12 gauge only, 2 shell detachable magazine. 22", Accu Choke barrel & extra full Turkey-Tube. OFM Woodland camo synthetic stock, rear U and front bead sights, "Tasco style" scope bases. Made 1996-?


Watch the video: India Alert. New Episode 595. Pehalwan - पहलवन. #DangalTVChannel