Teak YN-30 - History

Teak YN-30 - History



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Teak
(YN-30: dp. 805 (lim.), 1. 163'2"; b. 30'6" dr. 11'8" s. 12.5 k. (tl.); cpl. 48; a. 1 3", 4 20mm. 4 .60 mg.,cl. Aloe)

Teak (YN-30) was laid down on 25 October 1940 at Camden, N.J., by John H. Mathias & Co., launched on 7 July 1941, sponsored by Mrs. E. L. Patch, placed in service on 7 May 1942, and commissioned on 10 December 1942 at Colon, Canal Zone, Lt. Harl Stanley Day, USNR, in command.

At the time of her commissioning, the net tender was assigned to the nets guarding the west gate of the Panama Canal. Teak transited the canal on 15 December 1942; departed Balboa on Christmas Eve; and arrived at San Francisco on 6 January 1943. Based at Tiburon Naval Net Depot on West San Francisco Bay, she began tending the harbor's antisubmarine nets on the 10th.

Throughout 1943 and into 1944, Teak patrolled and maintained the nets which protected the anchorages and harbor of San Francisco Bay. She inspected the nets, repaired and replaced worn parts and buoys, and freed mooring anchors and an occasional ship fouled in the nets. These routine but vital duties were varied by repairs at Alameda, with gunnery drills in October, and with a voyage to San Pedro in December.

Reclassified a net laying ship and redesignated AN35 on 20 January 1944, Teak passed under the Golden Gate Bridge shortly before sunset on 2 March and set her course for the South Pacific. Proceeding via Samoa, she reached New Guinea on 4 April and began operating out of Milne Bay and the nearby Trobriand Islands. For the next six months, she provided towing services in nearby waters, carried cargoes, placed sonar buoys, and took up unneeded buoys and moorings.

Reassigned to the Leyte Gulf Service Unit of the 7th Fleet Service Force, she departed Humboldt Bay in convoy on 18 October and entered Leyte Gulf on the 24th. For the next few weeks, despite frequent calls to general quarters, she laid net moorings and marker buoys in Leyte Gulf, aided grounded small craft, and made tows. Late in November, she began sonar buoy station duties between Samar and Homohon Islands. On 17 January 1945, she returned to tending and laying moorings. In mid-March, she proceeded to Luzon and operated in Manila Bay, primarily occupied in raising submerged barges, sampans, diesel boats, and steamboats. During this period-while assigned to the Ship Salvage, Fire Fighting and Rescue Unit, Service Force, Pacific-she won the Navy Unit Commendation.

She remained in the Philippines until late in November, when she headed, via the Marianas and Pearl Harbor, for the California coast and arrived at San Pedro on 4 January 1946. She was towed to Astoria by Mimosa (AN-26) in June and was decommissioned and placed in reserve on 30 August 1946. She was placed in custody of the Maritime Administration in June 1961, but remained under Navy ownership. Teak was sold to Levin Metals Corp., San Jose, Calif., on 16 March 1976.


The .35 Whelen was developed in 1922 as a wildcat cartridge. Remington Arms Company standardized the cartridge as a regular commercial round and first made it available in the Remington model 700 Classic in 1988. [1] It has since been chambered by other arms makers in bolt-action, semi-automatic and single shot rifles. It has a modest but steady following among big game hunters in North America.

One version of its origin is that it was designed by Colonel Townsend Whelen when he was commanding officer of the Frankford Arsenal. In a 1923 issue of American Rifleman Col. Whelen refers to it as "the first cartridge that I designed" and states that, "Mr. James V. Howe undertook this work of making dies, reamers, chambering tools, and of chambering the rifles, all in accordance with my design." James V. Howe was a toolmaker at the Arsenal and later a founder of Griffin & Howe.

In his 1940 book The Hunting Rifle: Design, Selection, Ballistics, Marksmanship, Col. Whelen gives a different version of its origin after describing the .400 Whelen.

About the time we completed development of this cartridge, I went on a long hunting trip in the Northwest, and when I returned, Mr. Howe showed me another cartridge he had developed. The .30-06 case was necked to .35 caliber to use existing .35-caliber bullets. Mr. Howe asked my permission to call this cartridge the .35 Whelen, but he alone deserves credit for its development. [2] [3]

35 Whelen Edit

The 35 Whelen has an interesting history. It was designed by James Howe, of Griffin and Howe, partially in response to letters from Leslie Simpson and Stewart Edward White, suggesting that a good all-round rifle for African use would be one of 333 to 350 caliber, with a bullet of 250- to 300 grains (ideally 275 at 2500 fps. Both men (along with Roy Chapman Andrews and the Rev. Dr. Harry Caldwell, who were active in Asia,) perhaps the finest big game shots our country has produced, were aware of the outstanding performance of the 318 Westley-Richards with a 250-grain bullet, the 333 Jeffrey with a 300-grain bullet and the 350 Rigby with a 310-grain bullet on thin-skinned dangerous and non-dangerous game in Africa. It is of passing interest that the bullet for the old British 333 Jeffery is much like the 300-grain copper tube bullet which Winchester introduced for the 338 Magnum. The 35 Whelen was the first of 3 (three) efforts by Griffin and Howe to produce a cartridge that would meet this ideal. All were in 35 caliber. The 35 Whelen is simply the 30-06 necked up to 35 caliber and it’s about as easy to form from '06 brass as is the 270. Later, an "improved" version of the 35 Whelen, with venturi shoulders like Weatherby cartridges, was made up, but it never caught on. The 35 Whelen, now available in several factory rounds, and factory chambered in several different rifles (although some gunsmiths still sell properly formed brass for it) has racked up a tremendous record all over the world, rivaling the 375 Holland and Holland in its effectiveness. It was originally designed, partially, as a substitute for the 375 H & H, since rifles for it could be made up using inexpensive 30-06 actions rather than costly magnum-length Mauser Actions It has killed, with aplomb and efficiency, all of the trophy animals in the world, with the possible exception of the “Big Three” (elephant, rhinoceros, and cape buffalo.) It can be loaded down to 35 Remington speeds for light recoil and pot-shooting, or loaded up to provide terrific stopping power--more than should ever be needed by a competent rifleman facing American big game. Although not legal in certain parts of Africa for dangerous game (some countries require that rifles of at least 375 or 400 caliber be used,) solid nose bullets are available so that, in a pinch, it would probably serve. It is easy to rebarrel an action to this cartridge-- it does not even require opening up the bolt face or free-boring the rimless brass for it, as with the 358, is cheaper and easier to manufacture than the belted brass necessary for the 350 Remington, 35 Griffin and Howe (or Holland and Holland, as it is sometimes known) and 358 Norma Magnum. There is still a great future awaiting the 35 Whelen and, now that the 22-250 has been legitimized, perhaps we can hope that the 35 Whelen will meet the same good fortune. [4]

Rifle: Win. Mod. 70

Custom Barrel: 24" in.

Twist: 1-16

CASES: Brass, Gov’t Issue

Most people think that the .35 Whelen cartridge, which is a .30/06 case necked up to .35 caliber, was designed by Colonel Townsend Whelen. As a matter of fact, it was only named for Colonel Whelen, but was designed by James Howe, who was then with the famous firm of Griffin and Howe.

The cartridge was designed in the early 1920s at a time when the only way to get a .375 Magnum was to have one built up on the long expensive Magnum Mauser action. The great advantage of the .35 Whelen was that this was a cartridge that could handle heavy bullets and yet could be used on short actions like 98 Mauser and the Springfield.

Because .30/06 cases are cheap and plentiful and because good bullets like those made by Speer Inc. in 35 caliber are available, the 35 Whelen still retains considerable popularity. However, there are probably fewer .35 Whelens in use today than there were back in the 1920s and early 1930s, because with a minimum of fuss and bother one can get a factory Winchester Model 70 in .375 caliber. That great cartridge, of course, will beat the .35 Whelen on every count.

However, the man who has a yen for a rifle using heavy bullets of fairly large diameter at good velocities can’t go wrong on a .35 Whelen, if he is a handloader—and of course, he is a handloader or he would not be reading this book.

There are two varieties of the .35 Whelen and maybe more. The original cartridge had a short shoulder with the same slope as that of the .30/06. The so-called improved version has a sharper shoulder which theoretically at least will maintain headspace against the blow of the firing pin better.

Suitable .358 in (9.1 mm) bullets range in weight from 150 to 300 grains (9.7 to 19.4 g). Using a 250-grain (16 g) bullet, the .35 Whelen will generate 3,500 ft⋅lbf (4,700 J) at the muzzle from a 24 in (61 cm) barrel.

The .35 Whelen is not the ballistic twin of the .350 Remington Magnum and falls about 500 foot pounds short. With the correct bullet choice this cartridge is suitable for virtually all thin-skinned large and dangerous game. The European designation for this cartridge would be 9 × 63 mm with its wide bullet selection and high muzzle energy it is in the same echelon as the 9.3×62mm.


Contents

CKD is initially without symptoms, and is usually detected on routine screening blood work by either an increase in serum creatinine, or protein in the urine. As the kidney function decreases:

    is increased due to fluid overload and production of vasoactive hormones created by the kidney via the renin–angiotensin system, increasing the risk of developing hypertension and heart failure. accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to its high systemic concentration, urea is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates ("uremic frost"). accumulates in the blood (hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20–25 ml/min/1.73 m 2 , at which point the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin. [20] symptoms may range from mild edema to life-threatening pulmonary edema. results from poor phosphate elimination in the kidney. Hyperphosphatemia contributes to increased cardiovascular risk by causing vascular calcification. [21] Circulating concentrations of fibroblast growth factor-23 (FGF-23) increase progressively as the kidney capacity for phosphate excretion declines which may contribute to left ventricular hypertrophy and increased mortality in people with CKD . [22][23] results from 1,25 dihydroxyvitamin D3 deficiency (caused by high FGF-23 and reduced kidney mass) [24] and resistance to the action of parathyroid hormone. [25] Osteocytes are responsible for the increased production of FGF-23, which is a potent inhibitor of the enzyme 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol into 1,25 dihydroxyvitamin D3). [26] Later, this progresses to secondary hyperparathyroidism, kidney osteodystrophy, and vascular calcification that further impairs cardiac function. An extreme consequence is the occurrence of the rare condition named calciphylaxis. [27]
  • Changes in mineral and bone metabolism that may cause 1) abnormalities of calcium, phosphorus (phosphate), parathyroid hormone, or vitamin D metabolism 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (kidney osteodystrophy) and 3) vascular or other soft-tissue calcification. [10]CKD-mineral and bone disorders have been associated with poor outcomes. [10] may result from decreased capacity to generate enough ammonia from the cells of the proximal tubule. [20] Acidemia affects the function of enzymes and increases excitability of cardiac and neuronal membranes by the promotion of hyperkalemia. [28] is common and is especially prevalent in those requiring haemodialysis. It is multifactorial in cause, but includes increased inflammation, reduction in erythropoietin, and hyperuricemia leading to bone marrow suppression. Hypoproliferative anemia occurs due to inadequate production of erythropoietin by the kidneys. [29]
  • In later stages, cachexia may develop, leading to unintentional weight loss, muscle wasting, weakness and anorexia. [30] is very common in both men and women with CKD. A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common. [31] uerques M, Jannini EA, Strippoli GF | display-authors = 6 | title = Interventions for treating sexual dysfunction in patients with chronic kidney disease | journal = The Cochrane Database of Systematic Reviews | issue = 12 | pages = CD007747 | date = December 2010 | pmid = 21154382 | doi = 10.1002/14651858.CD007747.pub2 | url = https://espace.library.uq.edu.au/view/UQ:238403/UQ238403_OA.pdf >></ref>
  • People with CKD are more likely than the general population to develop atherosclerosis with consequent cardiovascular disease, an effect that may be at least partly mediated by uremic toxins. [32] [unreliable medical source?] People with both CKD and cardiovascular disease have significantly worse prognoses than those with only cardiovascular disease. [33]

The three most common causes of CKD in order of frequency as of 2015 are diabetes mellitus, hypertension, and glomerulonephritis. [34] About one of five adults with hypertension and one of three adults with diabetes have CKD. If the cause is unknown, it is called idiopathic. [35]

By anatomical location Edit

    disease includes large vessel disease such as bilateral kidney artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome, and vasculitis.
  • Glomerular disease comprises a diverse group and is classified into:
    • Primary glomerular disease such as focal segmental glomerulosclerosis and IgA nephropathy (or nephritis)
    • Secondary glomerular disease such as diabetic nephropathy and lupus nephritis

    Other Edit

    • Genetic congenital disease such as polycystic kidney disease or 17q12 microdeletion syndrome. , is "a new form of kidney disease that could be called agricultural nephropathy". [36] A high and so-far unexplained number of new cases of CKD, referred to as the Mesoamerican nephropathy, has been noted among male workers in Central America, mainly in sugar cane fields in the lowlands of El Salvador and Nicaragua. Heat stress from long hours of piece-rate work at high average temperatures [37][38][39][40] of about 36 °C (96 °F) is suspected, as are agricultural chemicals [41]

    Diagnosis of CKD is largely based on history, examination and urine dipstick combined with the measurement of the serum creatinine level (see above). It is important to differentiate CKD from acute kidney injury (AKI) because AKI can be reversible. One diagnostic clue that helps differentiate CKD from AKI is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). In many people with CKD, previous kidney disease or other underlying diseases are already known. A significant number present with CKD of unknown cause.

    Screening Edit

    Screening those who have neither symptoms nor risk factors for CKD is not recommended. [42] [43] Those who should be screened include: those with hypertension or history of cardiovascular disease, those with diabetes or marked obesity, those aged > 60 years, subjects with African American ancestry, those with a history of kidney disease in the past, and subjects who have relatives who had kidney disease requiring dialysis.

    Screening should include calculation of the estimated GFR (eGFR) from the serum creatinine level, and measurement of urine albumin-to-creatinine ratio (ACR) in a first-morning urine specimen (this reflects the amount of a protein called albumin in the urine), as well as a urine dipstick screen for hematuria. [44]

    The glomerular filtration rate (GFR) is derived from the serum creatinine and is proportional to 1/creatinine, i.e. it is a reciprocal relationship:the higher the creatinine, the lower the GFR. It reflects one aspect of kidney function: how efficiently the glomeruli - the filtering units - work. Normal GFR is 90-120 mLs/min. The units of creatinine vary from country to country. But since the glomeruli make up <5% of the mass of the kidney, the GFR does not indicate all aspects of kidney health and function. This can be done by combining the GFR level with the clinical assessment of the person, including fluid status, and measuring the levels of hemoglobin, potassium, phosphate and parathyroid hormone (PTH).

    Ultrasound Edit

    Kidney ultrasonography is useful for diagnostic and prognostic purposes in chronic kidney disease. Whether the underlying pathologic change is glomerular sclerosis, tubular atrophy, interstitial fibrosis or inflammation, the result is often increased echogenicity of the cortex. The echogenicity of the kidney should be related to the echogenicity of either the liver or the spleen (Figure 22 and Figure 23). Moreover, decreased kidney size and cortical thinning are also often seen and especially when disease progresses (Figure 24 and Figure 25). However, kidney size correlates to height, and short persons tend to have small kidneys thus, kidney size as the only parameter is not reliable. [45]

    Chronic renal disease caused by glomerulonephritis with increased echogenicity and reduced cortical thickness. Measurement of kidney length on the US image is illustrated by '+' and a dashed line. [45]

    Nephrotic syndrome. Hyperechoic kidney without demarcation of cortex and medulla. [45]

    Chronic pyelonephritis with reduced kidney size and focal cortical thinning. Measurement of kidney length on the US image is illustrated by '+' and a dashed line. [45]

    End-stage chronic kidney disease with increased echogenicity, homogenous architecture without visible differentiation between parenchyma and renal sinus and reduced kidney size. Measurement of kidney length on the US image is illustrated by '+' and a dashed line. [45]

    Additional imaging Edit

    Additional tests may include nuclear medicine MAG3 scan to confirm blood flow and establish the differential function between the two kidneys. Dimercaptosuccinic acid (DMSA) scans are also used in kidney imaging with both MAG3 and DMSA being used chelated with the radioactive element technetium-99. [46]

    Stages Edit

    A glomerular filtration rate (GFR) ≥ 60 ml/min/1.73 m 2 is considered normal without chronic kidney disease if there is no kidney damage present.

    Kidney damage is defined signs of damage seen in blood, urine, or imaging studies which includes lab albumin/creatinine ratio (ACR) ≥ 30. [48] All people with a GFR <60 ml/min/1.73 m 2 for 3 months are defined as having chronic kidney disease. [48]

    Protein in the urine is regarded as an independent marker for worsening of kidney function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if protein loss is significant. [49]

    1. Stage 1: Slightly diminished function kidney damage with normal or relatively high GFR (≥90 ml/min/1.73 m 2 ) and persistent albuminuria. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. [48]
    2. Stage 2: Mild reduction in GFR (60–89 ml/min/1.73 m 2 ) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. [48]
    3. Stage 3: Moderate reduction in GFR (30–59 ml/min/1.73 m 2 ):. [48] British guidelines distinguish between stage 3A (GFR 45–59) and stage 3B (GFR 30–44) for purposes of screening and referral. [49]
    4. Stage 4: Severe reduction in GFR (15–29 ml/min/1.73 m 2 ) [48] Preparation for kidney replacement therapy.
    5. Stage 5: Established kidney failure (GFR <15 ml/min/1.73 m 2 ), permanent kidney replacement therapy, [48] or end-stage kidney disease.

    The term "non-dialysis-dependent chronic kidney disease" (NDD-CKD) is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for kidney failure known as kidney replacement therapy (RRT, including maintenance dialysis or kidney transplantation). The condition of individuals with CKD, who require either of the two types of kidney replacement therapy (dialysis or transplant), is referred to as the end-stage kidney disease (ESKD). Hence, the start of the ESKD is practically the irreversible conclusion of the NDD-CKD. Even though the NDD-CKD status refers to the status of persons with earlier stages of CKD (stages 1 to 4), people with advanced stage of CKD (stage 5), who have not yet started kidney replacement therapy, are also referred to as NDD-CKD.

    Apart from controlling other risk factors, the goal of therapy is to slow down or halt the progression of CKD. Control of blood pressure and treatment of the original disease are the broad principles of management.

    Blood pressure Edit

    Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are recommended as first-line agents since they have been found to slow the decline of kidney function, relative to a more rapid decline in those not on one of these agents. [13] They have also been found to reduce the risk of major cardiovascular events such as myocardial infarction, stroke, heart failure, and death from cardiovascular disease when compared to placebo in individuals with CKD. [13] ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD. [13] Aggressive blood pressure lowering decreases people's risk of death. [50]

    Other measures Edit

    • Aggressive treatment of high blood lipids is recommended. [51]
    • A low-protein, low-salt diet may result in slower progression of CKD and reduction in proteinuria as well as controlling symptoms of advanced CKD to delay dialysis start. [52] A tailored low-protein diet, designed for low acidity, may help prevent damage to kidneys for people with CKD. [53]
    • Anemia - A target hemoglobin level of 9–12 g/dL is recommended [54][55] raising hemoglobin levels to the normal range has not been found to be of benefit. [56]
      • Guidelines recommend treatment with parenteral iron prior to treatment with erythropoietin.
      • Replacement of erythropoietin is often necessary in people with advanced disease. [57]
      • It is unclear if androgens improve anemia. [58]

      Referral to a nephrologist Edit

      Guidelines for referral to a nephrologist vary between countries. Most agree that nephrology referral is required by Stage 4 CKD (when eGFR/1.73m 2 is less than 30 ml/min or decreasing by more than 3 ml/min/year). [59]

      It may also be useful at an earlier stage (e.g. CKD3) when urine albumin-to-creatinine ratio is more than 30 mg/mmol, when blood pressure is difficult to control, or when hematuria or other findings suggest either a primarily glomerular disorder or secondary disease amenable to specific treatment. Other benefits of early nephrology referral include proper education regarding options for kidney replacement therapy as well as pre-emptive transplantation, and timely workup and placement of an arteriovenous fistula in those people with chronic kidney disease opting for future hemodialysis.

      Renal replacement therapy Edit

      At stage 5 CKD, kidney replacement therapy is usually required, in the form of either dialysis or a kidney transplant.

      In CKD numerous uremic toxins accumulate in the blood. Even when ESKD (largely synonymous with CKD5) is treated with dialysis, the toxin levels do not go back to normal as dialysis is not that efficient. Similarly, after a kidney transplant, the levels may not go back to normal as the transplanted kidney may not work 100%. If it does, the creatinine level is often normal. The toxins show various cytotoxic activities in the serum and have different molecular weights, and some of them are bound to other proteins, primarily to albumin. Uremic toxins are classified into three groups as small water-soluble solutes, middle molecular-weight solutes, and protein-bound solutes. [60] Hemodialysis with high-flux dialysis membrane, long or frequent treatment, and increased blood/dialysate flow has improved removal of water-soluble small molecular weight uremic toxins. Middle molecular weight molecules are removed more effectively with hemodialysis using a high-flux membrane, hemodiafiltration and hemofiltration. However, conventional dialysis treatment is limited in its ability to remove protein-bound uremic toxins. [61]

      CKD increases the risk of cardiovascular disease, and people with CKD often have other risk factors for heart disease, such as high blood lipids. The most common cause of death in people with CKD is cardiovascular disease rather than kidney failure.

      Chronic kidney disease results in worse all-cause mortality (the overall death rate) which increases as kidney function decreases. [62] The leading cause of death in chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5. [62] [63] [64]

      While kidney replacement therapies can maintain people indefinitely and prolong life, the quality of life is negatively affected. [65] [66] Kidney transplantation increases the survival of people with stage 5 CKD when compared to other options [67] [68] however, it is associated with an increased short-term mortality due to complications of the surgery. Transplantation aside, high-intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three-times-a-week hemodialysis and peritoneal dialysis. [69]

      People with ESKD are at increased overall risk for cancer. [70] This risk is particularly high in younger people and gradually diminishes with age. [70] Medical specialty professional organizations recommend that physicians do not perform routine cancer screening in people with limited life expectancies due to ESKD because evidence does not show that such tests lead to improved outcomes. [71] [72]

      About one in ten people have chronic kidney disease. In Canada 1.9 to 2.3 million people were estimated to have CKD in 2008. [56] CKD affected an estimated 16.8% of U.S. adults aged 20 years and older in the period from 1999 to 2004. [73] In 2007 8.8% of the population of Great Britain and Northern Ireland had symptomatic CKD. [74]

      Chronic kidney disease was the cause of 956,000 deaths globally in 2013, up from 409,000 deaths in 1990. [19]

      Chronic kidney disease of unknown aetiology Edit

      The cause of chronic kidney disease is in some cases not known it is referred to as chronic kidney disease of unknown aetiology (CKDu). As of 2020 [update] a rapidly progressive chronic kidney disease, unexplained by diabetes and hypertension, had increased dramatically in prevalence over a few decades in several regions in Central America and Mexico, a CKDu referred to as the Mesoamerican nephropathy (MeN). It was estimated in 2013 that at least 20,000 men had died prematurely, some in their 20s and 30s a figure of 40,000 per year was estimated in 2020. In some affected areas CKD mortality was five times the national rate. MeN primarily affects men working as sugarcane labourers. [38] The cause is unknown, but in 2020 the science found a clearer connection between heavy labour in high temperatures and incidence of CKDu improvements such as regular access to water, rest and shade, can significantly decrease the potential CKDu incidence. [75] CKDu also affects people in Sri Lanka where it is the 8th largest cause of in-hospital mortality. [76]

      Although CKDu was first documented among sugar cane workers in Costa Rica in the 1970s, it may well have affected plantation labourers since the introduction of sugar cane farming to the Caribbean in the 1600s. In colonial times the death records of slaves on sugar plantations was much higher than for slaves forced into other labour. [75]

      Race Edit

      African, Hispanics, and South Asians, particularly those from Pakistan, Sri Lanka, Bangladesh, and India, are at high risk of developing CKD. Africans are at greater risk due to the number of people affected with hypertension among them. As an example, 37% of ESKD cases in African Americans can be attributed to high blood pressure, compared with 19% among Caucasians. [77] Treatment efficacy also differs between racial groups. Administration of antihypertensive drugs generally halts disease progression in white populations but has little effect in slowing kidney disease among black people, and additional treatment such as bicarbonate therapy is often required. [77] While lower socioeconomic status contributes to the number of people affected with CKD, differences in the number of people affected by CKD are still evident between Africans and Whites when controlling for environmental factors. [77]

      The International Society of Nephrology is an international body representing specialists in kidney diseases.

      United States Edit

      • The National Kidney Foundation is a national organization representing people with chronic kidney diseases and professionals who treat kidney diseases.
      • The American Kidney Fund is a national nonprofit organization providing treatment-related financial assistance to one of every five people undergoing dialysis each year.
      • The Renal Support Network is a nonprofit, patient-focused, patient-run organization that provides nonmedical services to those affected by CKD.
      • The American Association of Kidney Patients is a nonprofit, patient-centric group focused on improving the health and well-being of CKD and people undergoing dialysis .
      • The Renal Physicians Association is an association representing nephrology professionals.

      United Kingdom Edit

      It was said to be costing the NHS about £1.5 billion a year in 2020. [78]

      The UK National Kidney Federation and British Kidney Patient Association (BKPA) represents people with chronic kidney disease. The Renal Association represents Kidney physicians and works closely with the National Service Framework for kidney disease.

      Australia Edit

      Kidney Health Australia serves that country.

      The incidence rate of CKD in dogs was 15.8 cases per 10,000 dog years at risk. The mortality rate of CKD was 9.7 deaths per 10,000 dog years at risk. (rates developed from a population of 600,000 insured Swedish dogs one dog year at risk is one dog at risk for one year)The breeds with the highest rates were the Bernese mountain dog, miniature schnauzer and boxer. The Swedish elkhound, Siberian husky and Finnish spitz were the breeds with the lowest rates. [79] [80]

      Currently, several compounds are in development for the treatment of CKD. These include the angiotensin receptor blocker (ARB) olmesartan medoxomil and sulodexide, a mixture of low molecular weight heparin and dermatan sulfate. [81] [82]

      Unbiased research with complete reporting is required to determine the safety and effectiveness of acupuncture to treat depression, pain, sleep problems, and uraemic pruritus in people who are undergoing dialysis treatments on a regular basis. [83]


      Our 100-Year History

      Victor Tyrie joined the Royal Marines as a drummer boy in 1912, aged 14 years. This studio photograph was taken just before he deployed to the Western Front in 1917. Victor was eventually invalided from the service in 1919 following the loss of his left thumb, still clearly evident here.

      In 1919 following service in the First World War, Victor Tyrie and Frederick Barlow were employed by The Castles Shipbreaking Company on a government subsidized training scheme making outdoor furniture from Teak, which was sourced from the breaking of old timber ships, the foundation of the teak outdoor furniture industry. This employment ceased when the subsidy finished after one year. Further interesting information is available on the Castles Shipbreaking website, in particular chapter 8.

      In 1920 Victor and Frederick together with a few others started their own business in London, initially in Walthamstow and shortly afterwards moving to a small horse stable no longer required behind a terrace of Victorian houses in Leytonstone.

      In the early years our outdoor furniture was made almost entirely by hand with the only machine being a saw-bench we made ourselves from an electric motor, steel shaft, bearings and with a wooden table. Production, including planing the teak and cutting the mortice and tenon joints was all performed using hand tools and it took the most efficient worker at least a full day to make one teak seat.

      The business prospered based on a quickly earned reputation for quality and value. The following pages from our catalogue in the 1920s shows the Rothesay and London design seats that we still make today. The retail prices shown evidences the inflation since that time of more than 200 times.


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      Mid-Century Modern Danish Teak Furniture

      Furnish Me Vintage carries one of the Florida’s largest teak furniture collections including beds, tables, chairs, and desks by mid century modern designers.

      After WWII ships returned from Asia with as much teak as they could, not wanting to return without goods. This is one reason why this particular wood was so cost effective for Scandinavian countries, beginning in the late 40’s. There was an abundance and Scandinavian designers began building teak furniture at a low cost to be mass produced. However, this wasn’t the first time this wood had been utilized. Teak, or Tectona grandis, is native to the tropics. It was used as early as the 7th century, adorning homes of wealthy and powerful people. As early as the 1600’s Indonesia was colonized by the dutch, who began using teak wood for shipbuilding for its ability to ward off dry rot. Teak has an abundance of natural oils and rubber locked within the tight grain of the wood. They also protect the wood from dry rot, which can happen to older wood furniture. What’s more, the oils and rubber protect the heart of the wood from invaders like fungi and parasites, even termites that can destroy other woods. Protecting wooden furniture from such intruders requires applications of weatherproof oils and treatments not so with teak. You’ll find an abundance of natural oils and rubber locked right into the tight grain of the wood. All woods contain oils that protect the tree — think maple, sap or tea tree oil. Teak, however, can retain these oils and its rubber even after being felled and processed. Because of this, teak has greater naturally weather-resistant properties than just about any other type of wood. When dried to a proper moisture level the oils and rubber weatherproof the wood. If well cared for, teak pieces can last for a hundred plus years.


      Can Teak Wood Be Used in a Shower?

      Teak wood is enjoyed because of its beauty and because of its high oil content, which makes it more moisture-resistant than most other types of wood. Teak is sometimes used in swim platforms on boats, and has been used in shipbuilding for centuries. It requires little maintenance even in the dampest conditions, making it a viable option for shower use.


      History of Teak Wood

      Teak, also known as Tectona Grandis, is a tall, straight deciduous tree that grows with buttressing stems and a large crown. Teak is native to South East Asia and its natural distribution goes from the Indian subcontinent through Myanmar and Thailand to Laos. We do not know if the teak stands in Indonesia are native or the result of early cultivation by the Hindu settlers, quite possibly as early as the 7th century.

      Since the Middle Ages it has been used in ship building. Its durability and natural oils made it a perfect choice for the construction of ocean going vessels. Teak oil also creates a resistance to splitting and cracking and wards off termites and other insects.

      It is also easy to work with, and it is resistant to decay. The main advantage of teak for the building of ships is its unique ability to prevent rust and corrosion when in contact with metal. These qualities make it a valuable resource. Even today, teak wood is used in the construction of ships and expensive yachts and boats.

      When the ships were no longer sea worthy the ships decking was in such good condition that the teak wood was recycled and made into outdoor furniture. It is possible that the first outdoor teak benches were made of old ship decks. Teak wood is so durable and strong that there are century old teak park benches in England still in use today.

      The harvesting of teak wood is not an easy process. The logs are so heavy they will not float. Therefore, transporting the wood is not a particularly easy thing to do. In fact, elephants pull the logs through the jungle regions, just as they did a century ago. The elephants must pull the logs a long way through the jungles to the waterways. The trained elephants stack the logs in piles.

      Teak wood was admired for its beauty back in the 1800s in India. It was able to capture the romantic nature of the Victorian era making it a perfect complement to an English garden. The durable and versatile nature of teak wood make it well sought after throughout the world.

      Teak is grown today throughout Central America, parts of South America and Asia. Teak wood today is used for indoor wood flooring and other general construction. Teak is popular for durable and beautiful outdoor patio furniture. Its high oil content makes it ideal for outdoor furniture. Teak wood patio furniture is favored among high-end ski resorts. For construction projects requiring durability and elegance, teak wood is the wood of choice.


      Our History

      In 1998, Justine Stamen Arrillaga founded The TEAK Fellowship in memory of DeWitt White (1981 – 1997) and Teak Dyer (1970 – 1988), two people close to her whose lives were tragically cut short. Wanting to provide other young people with the opportunity for a brighter future, she created a program to help aspiring students use education to overcome economic hardships and achieve their potential.

      Starting with a pioneer class of 22 seventh grade students, Justine directed TEAK and managed its growth for eight years. In 2005, Lynn D. Sorensen succeeded Justine as TEAK’s Executive Director, and in 2015, John F. Green became TEAK’s third Executive Director. Starting with the first cohort, 100 percent of TEAK Fellows have been accepted into top independent, public, and parochial high schools. Every single Fellow has matriculated to 4-year colleges of these, 89 percent have entered top-tier schools, including an average of 30 percent into the Ivy League each year. Of the students who have completed the Fellowship, 89 percent are college graduates and leaders in multiple professions.

      While continuing its core work of preparing students to apply to and succeed at top high schools and colleges, TEAK has expanded its programming over the course of its history to better achieve and build upon these goals. In 2008, TEAK celebrated its first class of college graduates. In 2012, TEAK shifted the program’s entry point from 7th grade to 6th grade to increase student preparation prior to entering their rigorous high schools. In 2019, after a successful capital campaign, Glancing Back>Looking Forward, TEAK expanded its program by 50%, increasing enrollment from 30 students per cohort to 45 Fellows. Today, TEAK remains an enduring yet innovative program, opening doors to excellent educational opportunities and preparing students to succeed and lead in their schools, professions, and communities.


      In the Future

      Some researchers have predicted that lifestyle factors like obesity will halt or even reverse the rise in life expectancy for the first time in modern history.

      Epidemiologists and gerontologists such as S. Jay Olshanky warn that in the United States—where two-thirds of the population is overweight or obese—obesity and its complications, like diabetes, could very well reduce life expectancy at all ages in the first half of 21st century.  

      In the meantime, rising life expectancy in the West brings both good and bad news—it’s nice to be living longer, but you are now more vulnerable to the types of illnesses that hit as you get older. These age-related diseases include coronary artery disease, certain cancers, diabetes, and dementia.

      While they can affect quantity and quality of life, many of these conditions can be prevented or at least delayed through healthy lifestyle choices like following an anti-aging diet, maintaining a healthy weight, exercising regularly and keeping stress hormones like cortisol at bay.


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