A rare case of massive gastrointestinal hemorrhage caused by Meckel's diverticulum in a 53-year-old man.

A 53-year-old man with a history of lung cancer mestastic to the brain and pelvis presented with hypotension and massive GI bleeding. He had no past history of gastrointestinal disease or bleeding. The patient was found to have an unusual focal source of bleeding--a large ulcerated Meckel's diverticulum with acute hemorrhage.

Deficiency in Cardiac Dystrophin Affects the Abundance of the $\alpha$ -/ $\beta$ -Dystroglycan Complex.

Although Duchenne muscular dystrophy is primarily categorised as a skeletal muscle disease, deficiency in the membrane cytoskeletal protein dystrophin also affects the heart. The central transsarcolemmal linker between the actin membrane cytoskeleton and the extracellular matrix is represented by the dystrophin-associated dystroglycans. Chemical cross-linking analysis revealed no significant differences in the dimeric status of the $\alpha$ -/ $\beta$ -dystroglycan subcomplex in the dystrophic mdx heart as compared to normal cardiac tissue.

Subproteomics analysis of Ca+-binding proteins demonstrates decreased calsequestrin expression in dystrophic mouse skeletal muscle.

Duchenne muscular dystrophy represents one of the most common hereditary diseases. Abnormal ion handling is believed to render dystrophin-deficient muscle fibres more susceptible to necrosis. Although a reduced Ca(2+) buffering capacity has been shown to exist in the dystrophic sarcoplasmic reticulum, surprisingly no changes in the abundance of the main luminal Ca(2+) reservoir protein calsequestrin have been observed in microsomal preparations.

Drastic reduction in the luminal Ca2+ -binding proteins calsequestrin and sarcalumenin in dystrophin-deficient cardiac muscle.

Luminal Ca2+ -binding proteins play a central role in mediating between Ca2+ -uptake and Ca2+ -release during the excitation-contraction-relaxation cycle in muscle fibres. In the most commonly inherited neuromuscular disorder, Duchenne muscular dystrophy (DMD), the reduced expression of key Ca2+ -binding proteins causes abnormal Ca2+ -buffering in the sarcoplasmic reticulum (SR) of skeletal muscle. The heart is also affected in dystrophinopathies, as manifested by the pathological replacement of cardiac fibres by connective and fatty tissue.

Iatrogenic pseudoaneurysms: comparison of treatment modalities, including duplex-guided thrombin injection.

The purpose of our study was to review the results of the three treatment modalities currently used at Charleston Area Medical Center (CAMC) for iatrogenic pseudoaneuryms. Retrospective records were reviewed of patients treated for pseudoaneurysms (PSA) from July 1, 2001 to June 30, 2002. In the 12-month period, 69 psedoaneurysms were treated with either ultrasound-guided compression (UGC), duplex-guided thrombin injection, or open operative repair.

Comparative analysis of Dp427-deficient mdx tissues shows that the milder dystrophic phenotype of extraocular and toe muscle fibres is associated with a persistent expression of beta-dystroglycan.

The cell biological hypothesis of Duchenne muscular dystrophy assumes that deficiency in the membrane cytoskeletal element dystrophin triggers a loss in surface glycoproteins, such as beta-dystroglycan, thereby rendering the sarcolemmal membrane more susceptible to micro-rupturing. Secondary changes in ion homeostasis, such as increased cytosolic Ca2+ levels and impaired luminal Ca2+ buffering, eventually lead to Ca2+-induced myonecrosis. However, individual muscle groups exhibit a graded pathological response during the natural time course of x-linked muscular dystrophy.