A Case Report of Ruptured Popliteal Aneurysm in the Setting of Blunt Trauma.

INTRODUCTION: Popliteal artery aneurysms are in most cases asymptomatic but cause significant complications if ruptured. An acute popliteal aneurysm rupture is relatively rare, and few cases have been documented secondary to blunt trauma. Common presenting signs and symptoms include distal limb ischemia and absent dorsalis pedis pulses. Timely management and recognition of this rare presentation are crucial as this condition can result in limb loss or death if not treated in a timely manner. CASE REPORT: An 80-year-old man with history of hypertension presented to the emergency department complaining of inability to feel sensation below his left knee after falling from ground level. Physical examination was pertinent for bounding radial and femoral pulses bilaterally, although absent dorsalis pedis and posterior tibial pulses to the left lower extremity. Computed tomography angiography identified occlusion of the left superficial femoral arterial lumen associated with a ruptured popliteal aneurysm, approximately eight centimeters in size. He immediately received unfractionated heparin and was admitted to the hospital for left medial thigh exploration and decompressive dermatofasciotomy. CONCLUSION: After confirmation of popliteal aneurysmal rupture with advanced imaging, heparinization and vascular surgery consultation are critical steps that should be taken to prevent limb loss.

Zinc regulates a switch between primary and alternative S18 ribosomal proteins in Mycobacterium tuberculosis.

The Mycobacterium tuberculosis genome encodes five putative 'alternative' ribosomal proteins whose expression is repressed at high Zn(2+) concentration. Each alternative protein has a primary homologue that is predicted to bind Zn(2+). We hypothesized that zinc triggers a switch between these paired homologous proteins and therefore chose one of these pairs, S18-1/S18-2, to study mechanisms of the predicted competition for their incorporation into ribosomes. Our data show that Zn(2+)-depletion causes accumulation of both S18-2 mRNA and protein. In contrast, S18-1 mRNA levels are unchanged to slightly elevated under Zn(2+)-limited conditions. However, the amount of S18-1 protein is markedly decreased. We further demonstrate that both S18 proteins interact with ribosomal protein S6, a committed step in ribosome biogenesis. Zn(2+) is absolutely required for the S18-1/S6 interaction while it is dispensable for S18-2/S6 dimer formation. These data suggest a model in which S18-1 is the dominant ribosome constituent in high zinc conditions, e.g. inside of phagosomes, but that it can be replaced by S18-2 when zinc is deficient, e.g. in the extracellular milieu. Consequently, Zn(2+)-depletion may serve as a signal for building alternative ribosomes when M. tuberculosis is released from macrophages, to allow survival in the extracellular environment.

Quantitative neuropathology associated with chronic manganese exposure in South African mine workers.

Manganese (Mn) is a common neurotoxicant associated with a clinical syndrome that includes signs and symptoms referable to the basal ganglia. Despite many advances in understanding the pathophysiology of Mn neurotoxicity in humans, with molecular and structural imaging techniques, only a few case reports describe the associated pathological findings, and all are in symptomatic subjects exposed to relatively high-level Mn. We performed an exploratory, neurohistopathological study to investigate the changes in the corpus striatum (caudate nucleus, putamen, and globus pallidus) associated with chronic low-level Mn exposure in South African Mn mine workers. Immunohistochemical techniques were used to quantify cell density of neuronal and glial components of the corpus striatum in eight South African Mn mine workers without clinical evidence of a movement disorder and eight age-race-gender matched, non-Mn mine workers. There was higher mean microglia density in Mn mine workers than non-Mn mine workers in the globus pallidus external and internal segments [GPe: 1.33 and 0.87 cells per HPF, respectively (p=0.064); GPi: 1.37 and 0.99 cells per HPF, respectively (p=0.250)]. The number of years worked in the Mn mines was significantly correlated with microglial density in the GPi (Spearman's rho 0.886; p=0.019). The ratio of astrocytes to microglia in each brain region was lower in the Mn mine workers than the non-Mn mine workers in the caudate (7.80 and 14.68; p=0.025), putamen (7.35 and 11.11; p=0.117), GPe (10.60 and 16.10; p=0.091) and GPi (9.56 and 12.42; p=0.376). Future studies incorporating more detailed occupational exposures in a larger sample of Mn mine workers will be needed to demonstrate an etiologic relationship between Mn exposure and these pathological findings.