84 research outputs found

    Soviet Illegal Whaling: The Devil and the Details

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    In 1948, the U.S.S.R. began a global campaign of illegal whaling that lasted for three decades and, together with the poorly managed β€œlegal” whaling of other nations, seriously depleted whale populations. Although the general story of this whaling has been told and the catch record largely corrected for the Southern Hemisphere, major gaps remain in the North Pacific. Furthermore, little attention has been paid to the details of this system or its economic context. Using interviews with former Soviet whalers and biologists as well as previously unavailable reports and other material in Russian, our objective is to describe how the Soviet whaling industry was structured and how it worked, from the largest scale of state industrial planning down to the daily details of the ways in which whales were caught and processed, and how data sent to the Bureau of International Whaling Statistics were falsified. Soviet whaling began with the factory ship Aleut in 1933, but by 1963 the industry had a truly global reach, with seven factory fleets (some very large). Catches were driven by a state planning system that set annual production targets. The system gave bonuses and honors only when these were met or exceeded, and it frequently increased the following year’s targets to match the previous year’s production; scientific estimates of the sustainability of the resource were largely ignored. Inevitably, this system led to whale populations being rapidly reduced. Furthermore, productivity was measured in gross output (weights of whales caught), regardless of whether carcasses were sound or rotten, or whether much of the animal was unutilized. Whaling fleets employed numerous people, including women (in one case as the captain of a catcher boat). Because of relatively high salaries and the potential for bonuses, positions in the whaling industry were much sought-after. Catching and processing of whales was highly mechanized and became increasingly efficient as the industry gained more experience. In a single day, the largest factory ships could process up to 200 small sperm whales, Physeter macrocephalus; 100 humpback whales, Megaptera novaeangliae; or 30–35 pygmy blue whales, Balaenoptera musculus brevicauda. However, processing of many animals involved nothing more than stripping the carcass of blubber and then discarding the rest. Until 1952, the main product was whale oil; only later was baleen whale meat regularly utilized. Falsified data on catches were routinely submitted to the Bureau of International Whaling Statistics, but the true catch and biological data were preserved for research and administrative purposes. National inspectors were present at most times, but, with occasional exceptions, they worked primarily to assist fulfillment of plan targets and routinely ignored the illegal nature of many catches. In all, during 40 years of whaling in the Antarctic, the U.S.S.R. reported 185,778 whales taken but at least 338,336 were actually killed. Data for the North Pacific are currently incomplete, but from provisional data we estimate that at least 30,000 whales were killed illegally in this ocean. Overall, we judge that, worldwide, the U.S.S.R. killed approximately 180,000 whales illegally and caused a number of population crashes. Finally, we note that Soviet illegal catches continued after 1972 despite the presence of international observers on factory fleets

    Humpback and Fin Whaling in the Gulf of Maine from 1800 to 1918

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    The history of whaling in the Gulf of Maine was reviewed primarily to estimate removals of humpback whales, Megaptera novaeangliae, especially during the 19th century. In the decades from 1800 to 1860, whaling effort consisted of a few localized, small-scale, shore-based enterprises on the coast of Maine and Cape Cod, Mass. Provincetown and Nantucket schooners occasionally conducted short cruises for humpback whales in New England waters. With the development of bomb-lance technology at mid century, the ease of killing humpback whales and fin whales, Balaenoptera physalus, increased. As a result, by the 1870’s there was considerable local interest in hunting rorquals (baleen whales in the family Balaenopteridae, which include the humpback and fin whales) in the Gulf of Maine. A few schooners were specially outfitted to take rorquals in the late 1870’s and 1880’s although their combined annual take was probably no more than a few tens of whales. Also in about 1880, fishing steamers began to be used to hunt whales in the Gulf of Maine. This steamer fishery grew to include about five vessels regularly engaged in whaling by the mid 1880’s but dwindled to only one vessel by the end of the decade. Fin whales constituted at least half of the catch, which exceeded 100 animals in some years. In the late 1880’s and thereafter, few whales were taken by whaling vessels in the Gulf of Maine

    Whaling dispute continues

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    Podocyte-Specific Overexpression of Wild Type or Mutant Trpc6 in Mice Is Sufficient to Cause Glomerular Disease

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    Mutations in the TRPC6 calcium channel (Transient receptor potential channel 6) gene have been associated with familiar forms of Focal and Segmental Glomerulosclerosis (FSGS) affecting children and adults. In addition, acquired glomerular diseases are associated with increased expression levels of TRPC6. However, the exact role of TRPC6 in the pathogenesis of FSGS remains to be elucidated. In this work we describe the generation and phenotypic characterization of three different transgenic mouse lines with podocyte-specific overexpression of the wild type or any of two mutant forms of Trpc6 (P111Q and E896K) previously related to FSGS. Consistent with the human phenotype a non-nephrotic range of albuminuria was detectable in almost all transgenic lines. The histological analysis demonstrated that the transgenic mice developed a kidney disease similar to human FSGS. Differences of 2–3 folds in the presence of glomerular lesions were found between the non transgenic and transgenic mice expressing Trpc6 in its wild type or mutant forms specifically in podocytes. Electron microscopy of glomerulus from transgenic mice showed extensive podocyte foot process effacement. We conclude that overexpression of Trpc6 (wild type or mutated) in podocytes is sufficient to cause a kidney disease consistent with FSGS. Our results contribute to reinforce the central role of podocytes in the etiology of FSGS. These mice constitute an important new model in which to study future therapies and outcomes of this complex disease

    Stromal Down-Regulation of Macrophage CD4/CCR5 Expression and NF-ΞΊB Activation Mediates HIV-1 Non-Permissiveness in Intestinal Macrophages

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    Tissue macrophages are derived exclusively from blood monocytes, which as monocyte-derived macrophages support HIV-1 replication. However, among human tissue macrophages only intestinal macrophages are non-permissive to HIV-1, suggesting that the unique microenvironment in human intestinal mucosa renders lamina propria macrophages non-permissive to HIV-1. We investigated this hypothesis using blood monocytes and intestinal extracellular matrix (stroma)-conditioned media (S-CM) to model the exposure of newly recruited monocytes and resident macrophages to lamina propria stroma, where the cells take up residence in the intestinal mucosa. Exposure of monocytes to S-CM blocked up-regulation of CD4 and CCR5 expression during monocyte differentiation into macrophages and inhibited productive HIV-1 infection in differentiated macrophages. Importantly, exposure of monocyte-derived macrophages simultaneously to S-CM and HIV-1 also inhibited viral replication, and sorted CD4+ intestinal macrophages, a proportion of which expressed CCR5+, did not support HIV-1 replication, indicating that the non-permissiveness to HIV-1 was not due to reduced receptor expression alone. Consistent with this conclusion, S-CM also potently inhibited replication of HIV-1 pseudotyped with vesicular stomatitis virus glycoprotein, which provides CD4/CCR5-independent entry. Neutralization of TGF-Ξ² in S-CM and recombinant TGF-Ξ² studies showed that stromal TGF-Ξ² inhibited macrophage nuclear translocation of NF-ΞΊB and HIV-1 replication. Thus, the profound inability of intestinal macrophages to support productive HIV-1 infection is likely the consequence of microenvironmental down-regulation of macrophage HIV-1 receptor/coreceptor expression and NF-ΞΊB activation
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