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Pseudo-pseudo Meigs' syndrome or Tjalma syndrome is a rare manifestation of patients with systemic lupus erythematosus defined by the presence of ascites, pleural effusions, and an elevated cancer antigen 125 level. In this case, we described a patient with lupus who presented with sudden impaired renal function and subsequent development of massive ascites with marked high serum ferritin. Hyperferritinemia is one of the abnormal laboratory findings in severe inflammation with ferritin functioning as an inflammatory marker. However, its correlation with lupus activity remains unclear. Therefore, a review of the literature regarding pseudo-pseudo Meigs' syndrome associated with lupus and high ferritin level in this disease was carried out.

Among the 14.6% of American households experiencing food insecurity, approximately 2 million are occupied by older adults. Food insecurity among older adults has been linked to poor health, lower cognitive function, and poor mental health outcomes. While evidence of the association between individual or household-level factors and food insecurity has been documented, the role of neighborhood-level factors is largely understudied. This study uses data from a representative sample of 1,870 New York City senior center participants in 2008 to investigate the relationship between three neighborhood-level factors (walkability, safety, and social cohesion) and food insecurity among the elderly. Issues relating to food security were measured by three separate outcome measures: whether the participant had a concern about having enough to eat this past month (concern about food security), whether the participant was unable to afford food during the past year (insufficient food intake related to financial resources), and whether the participant experienced hunger in the past year related to not being able to leave home (mobility-related food insufficiency). Unadjusted and adjusted logistic regression was performed for each measure of food insecurity. Results indicate that neighborhood walkability is an important correlate of mobility-related food insufficiency and concern about food insecurity, even after controlling the effects of other relevant factors.

Behçet's disease (BD) is a multisystem disorder characterized by vasculitis. Pulmonary vascular problems such as pulmonary artery aneurysms (PAA) are reported to indicate poor prognosis and high mortality. We describe a 43-year-old man who presented with life threatening bilateral PAA and thromboembolic disease due to BD. He was treated with prednisone and pulse cyclophosphamide and was poorly responsive to the conventional immunosuppression. The introduction of adalimumab therapy stabilized his PAA. We report that the inhibition of TNF-alpha using the neutralizing monoclonal antibody adalimumab has the potential to induce rapid, complete, and long-lasting remission in a life-threatening manifestation of BD.

It has been proposed that continuously generated hydrogen peroxide (H(2)O(2)) inhibits typical apoptosis and instead initiates an alternate, apoptosis-inducing factor (AIF)-dependent process. Aside from the role of AIF, however, the detailed morphological characterization of H(2)O(2)-induced cell death is not complete. This study examined the cellular mechanism(s) by which the continuous presence of H(2)O(2) induces cell death. We also further analyzed the precise role of AIF by inhibiting its expression with siRNA. Exposure of cells to H(2)O(2) generated by glucose oxidase caused mitochondrion-mediated, caspase-independent cell death. In addition, H(2)O(2) exposure resulted in cell shrinkage and chromatin condensation without nuclear fragmentation, indicating that H(2)O(2) stimulates a pyknotic cell death. Further analysis of AIF-transfected cells clearly demonstrated that nuclear translocation of AIF is the most important event required for nuclear condensation, phosphatidyl serine translocation, and ultimately cell death in H(2)O(2)-exposed cells. Furthermore, ATP was rapidly and severely depleted in cells exposed to H(2)O(2) generated by glucose oxidase but not by H(2)O(2) added as a bolus. Suppression of the H(2)O(2)-mediated ATP depletion by 3-aminobenzamide led to a significant increase of nuclear fragmentation in glucose oxidase-exposed cells. Collectively, these findings suggest that an acute energy reduction by H(2)O(2) causes caspase-independent and AIF-dependent cell death.

Calpeptin inhibits myoblast fusion by inhibiting the activity of calpain. However, the mechanism by which calpeptin inhibits myogenesis is not completely understood. This study examined how calpeptin affects the expression of the myogenic regulatory factors (MRFs) and the phosphorylation of p38 mitogen-activated protein kinase (MAPK) in differentiating C2C12 myoblasts. Consistent with previous reports, calpeptin inhibited the induction of mu-calpain and the formation of myotubes in these cells. In particular, calpeptin inhibited the expression of the early and mid differentiation markers including MyoD, Myf5, myogenin, and MRF4 as well as the expression of the late markers such as troponin T and myosin heavy chain (MyHC). Calpeptin also suppressed the phosphorylation of p38 MAPK in C2C12 cells. SB203580, a specific p38 inhibitor, prevented the expression of the muscle-specific markers and their fusion into myotubes in these cells, which was further accelerated in the presence of calpeptin. These findings suggest that calpeptin inhibits the myogenesis of skeletal muscle cells by down-regulating the MRFs and involving p38 MAPK signaling.

Mechanical stress leads to satellite cell activation, which is an important event in the development, growth, and remodeling of postnatal skeletal muscle. Although there is a considerable knowledge on the events involved in skeletal muscle regeneration and development, the precise role of mechanical stress on activation of satellite cells remains unclear. Previously, satellite cells were isolated from adult bovine muscle and it was shown that the cells are multipotent, i.e., capable of proliferating and to differentiating into both myoblasts and adipocytes. This study investigated the cellular mechanisms by which cyclic mechanical stretching modulates the proliferation and differentiation of adult bovine satellite cells. The application of cyclic stretch induced the proliferation of satellite cells and inhibited their differentiation into myotubes. This response is believed to be closely related to the stretch-mediated changes in the expression of myogenic and cell cycle regulatory factors. Cyclic stretching increased the level of extracellular signal-regulated kinase (ERK) phosphorylation, whereas a specific ERK inhibitor (PD98058) blocked the stretch-mediated inhibition of myogenesis in a dose-dependent manner. Overall, this study demonstrates for the first time that cyclic mechanical stretch induces the proliferation of bovine satellite cells and suppresses their myogenic differentiation through the activation of ERK.