Parsonage-Turner Syndrome of Unclear Causation: A Case Report.

Parsonage-Turner syndrome (PTS), also referred to as idiopathic brachial plexopathy or neuralgic amyotrophy, is a rare disorder that classically presents with abrupt, patchy, unilateral shoulder pain followed by varying degrees of weakness and atrophy of the upper extremity musculature. PTS is a serious diagnosis that can result in irreversible atrophy with delayed diagnosis and treatment. Since there currently is no gold standard for diagnosis and the syndrome can present as many other possible pathologies, careful clinical examination and thorough review of relevant imaging and diagnostic studies are critical for proper diagnosis. Here, we present a case of PTS diagnosed in a 67-year-old male with extensive overlapping cervical and rotator cuff pathology following an apparent orthostatic episode with no known mechanism of injury. This case report not only adds to the literature regarding the importance of close examination and plausible etiologies of PTS but also emphasizes close collaboration among specialties to avoid misdiagnosis.

Platelet-associated IgAs and impaired GPVI responses in platelets lacking WIP.

The role of the Wiskott-Aldrich syndrome protein (WASp) in platelet function is unclear because platelets that lack WASp function normally. WASp constitutively associates with WASp-interacting protein (WIP) in resting and activated platelets. The role of WIP in platelet function was investigated using mice that lack WIP or WASp. WIP knockout (KO) platelets lack WASp and thus are double deficient. WIP KO mice have a thrombocytopenia, similar to WASp KO mice, resulting in part from enhanced platelet clearance. Most WIP KO, but not WASp KO, mice evolved platelet-associated immunoglobulins (Ig) of the IgA class, which normalize their platelet survival but diminish their glycoprotein VI (GPVI) responses. Protein tyrosine phosphorylation, including that of phospholipase C-gamma2, and calcium mobilization are impaired in IgA-presenting WIP KO platelets stimulated through GPVI, resulting in defects in alpha-granule secretion, integrin alphaIIbbeta3 activation, and actin assembly. The anti-GPVI antibody JAQ1 induces the irreversible loss of GPVI from circulating platelets in wild-type mice, but not in WIP KO mice that bear high levels of platelet-associated IgAs. Together, the data indicate that platelet-associated IgAs negatively modulate GPVI signaling and function in WIP KO mice.

Distinguishing between invasions and habitat changes as drivers of diversity loss among California's freshwater fishes.

Many of California's native populations of freshwater fish are in serious decline, as are freshwater faunas worldwide. Habitat loss and alteration, hydrologic modification, water pollution, and invasions have been identified as major drivers of these losses. Because these potential causes of decline are frequently correlated, it is difficult to separate direct from indirect effects of each factor and to appropriately rank their importance for conservation action. Recently a few authors have questioned the conservation significance of invasions, suggesting that they are "passengers" rather than "drivers" of ecological change. We compiled an extensive, watershed-level data set of fish presence and conservation status, land uses, and hydrologic modifications in California and used an information theoretic approach (Akaike's information criterion, AIC) and path analysis to evaluate competing models of native fish declines. Hydrologic modification (impoundments and diversions), invasions, and proportion of developed land were all predictive of the number of extinct and at-risk native fishes in California watersheds in the AIC analysis. Although nonindigenous fish richness was the best single predictor (after native richness) of fishes of conservation concern, the combined ranking of models containing hydrologic modification variables was slightly higher than that of models containing nonindigenous richness. Nevertheless, the path analysis indicated that the effects of both hydrologic modification and development on fishes of conservation concern were largely indirect, through their positive effects on nonindigenous fish richness. The best-fitting path model was the driver model, which included no direct effects of abiotic disturbance on native fish declines. Our results suggest that, for California freshwater fishes, invasions are the primary direct driver of extinctions and population declines, whereas the most damaging effect of habitat alteration is the tendency of altered habitats to support nonindigenous fishes.

Proliferation zones in the salmon telencephalon and evidence for environmental influence on proliferation rate.

Cell proliferation occurs in the brain of fish throughout life. This mitotic activity contributes new neurons to some brain subdivisions, suggesting potential for plasticity in neural development. Recently we found that the telencephalon in salmonids (salmon, trout) is significantly reduced in fish reared in hatcheries compared to wild fish, and that these differences resulted in part from rearing conditions. Here, we describe localized areas of cell proliferation in the telencephalon of juvenile coho salmon (Oncorhynchus kisutch) and begin to explore whether mitotic activity in these areas is sensitive to environmental conditions. Using the 5-bromo-2'-deoxyuridine (BrdU) cell birth-dating technique, we localized proliferating cells in the telencephalon to three distinct zones (proliferation zones 1a, 1b, and 2). We measured the volumes of these zones and showed that they grew at different rates relative to body size. We also found that variation in environmental rearing conditions altered the density of BrdU-labeled cells in proliferation zone 2, but not in zones 1a or 1b. However, this change in mitotic activity did not generate a difference in telencephalon size. These results suggest that environmental conditions, and associated changes in swimming activity or social structure, may influence rates of cell proliferation in the fish forebrain.