No abstract available.
Autopsy* ; Cardiomyopathies* ; Humans ; Infant, Newborn*

A relationship between preceding acute paralytic poliomyelitis and the later development of motor neuron disease has only occasionally been suggested since it was first postulated by Charcot in 1875. The authors recently experienced a 20-year-old male who was considered to have postpoliomyelitis muscular atrophy. We report this case in view of its rarity and necessity of differential diagnosis from other neuromuscular disorders. Clinical presentation included slowly progressive muscle wasting of left thigh for 4 years, mild weakness of left arm and both thigh, intermittent fasciculation, and previous history of acute paralytic poliomyelitis. Electromyographic findings showed fibrillation potentials, positive sharp waves, fasciculations, giant motor unit potentials and reduced interference patterns. Muscle biopsy revealed scattered small angulated fibers, individual myofiber degeneration and mild inflammatory cell infiltration.
Arm ; Biopsy ; Diagnosis, Differential ; Fasciculation ; Humans ; Male ; Motor Neuron Disease ; Poliomyelitis ; Postpoliomyelitis Syndrome* ; Thigh ; Young Adult

No abstract available.
Cytomegalovirus Infections*

No abstract available.
Autopsy* ; Down Syndrome* ; Leukemia* ; Megakaryocyte Progenitor Cells*

No abstract available.
Autopsy* ; Down Syndrome* ; Leukemia* ; Megakaryocyte Progenitor Cells*

No abstract available.
Arthroplasty, Replacement, Hip* ; Ceramics* ; Hip*

No abstract available.
Cervix Uteri* ; Female ; Health Expenditures*

BACKGROUND: The goal of successful resuscitation is not only to stop the process of ischemia as soon as possible but also to overcome the secondary injury process after resuscitation, which involves a complex interplay of mechanisms. Brain damage accompanying cardiac arrest and resuscitation is frequent and devastating. Cells die by one of two mechanisms: necrosis or delayed neuronal death. Delayed neuronal death may require protein synthesis. Neurons in the CA1 subfield of the hippocampus are selectively vulnerable to death after injury by ischemia and reperfusion. Death of these neurons occurs after an interval of 1 or 2 days. We assessed the effects of a protein synthesis inhibitor, cycloheximide(CHX), on hippocampal neuronal death of rats by using the ventricular fibrillation cardiac arrest(VFCA) model. METHODS: The effect of CHX(3mg/kg, s.c.) on hippocampal neuronal death was studied in two groups of 18 rats each, one group being subjected to a 2-min VFCA and the other to a 3-min VFCA. Each group was divided into three subgroups: control(group I,II) without subcutaneous injection of CHX, 'exp-12' of group I/II treated with CHX 12 hours after return of spontaneous circulation (ROSC), and 'exp-24' of group I/II treated with CHX 24 hours after ROSC. The coronal sections of the hippocampus levels were stained with hematoxylin-eosin after 72 hours of survival. The histologic damage score(HDS) was used to assign a score to the total number of damaged neurons counted in each of the hippocampal CA1 subfields. RESULTS: 1. There were not significan differences in heart rates, blood pressures, blood sugar, and blood gas in group I & II during the pre-arrest steady state or at 5 min and 30 min after ROSC. 2. In group I & II, the HDS, were significantly reduced in rats(I exp-12, 1.1+/-0.6; I exp-24, 1.3+/-0.5; II exp-12, 1.4+/-0.7; and II exp-24, 1.8+/-0.8) treated with CHX 12 hours or 24 hours after ROSC than control rats(I, 2.5+/-0.9, II, 2.9+/-0.8)(p<0.05). CONCLUSION: These results suggest that delayed hippocampal neuronal death from ischemic insult after ventricular fibrillation cardiac arrest followed by resuscitation can be prevented by a protein synthesis inhibitor, CHX. Further experimental studies of the action mechanism of protein synthesis inhibitors to delayed neuronal death and clinical applications are required.
Animals ; Blood Glucose ; Brain ; Heart Arrest* ; Heart Rate ; Hippocampus ; Injections, Subcutaneous ; Ischemia ; Necrosis ; Neurons* ; Protein Synthesis Inhibitors ; Rats* ; Reperfusion ; Resuscitation ; Ventricular Fibrillation*

No abstract available.

The prevalence of autoimmune, infectious and metabolic diseases is different for men and women owing to the respective ability of their immune systems to respond to self and foreign antigens. Although several factors, including hormones and the X-chromosome, have been suggested to contribute to such sex-specific immune responses, the underlying factors remain poorly defined. Recent studies using peroxisome proliferator-activated receptor (PPAR) ligands and knockout mice have identified sex-dimorphic expression of PPARs, and have shown that the inhibitory functions of PPAR in T cells are substantially affected by the sex hormones. In this review, we consider the sex-specific differences in PPARs and summarize the diverse PPAR-mediated, sex-specific properties of effector T-cell responses, such as T-cell activation, survival and differentiation, as well as their involvement in T-cell-related autoimmune diseases, including colitis, graft-versus-host disease and experimental autoimmune encephalomyelitis. Understanding PPAR-mediated sex differences in immune responses will provide more precise insights into the roles of PPARs in effector T cells.
Animals ; Autoimmune Diseases ; Colitis ; Encephalomyelitis, Autoimmune, Experimental ; Female ; Gonadal Steroid Hormones ; Graft vs Host Disease ; Humans ; Immune System ; Ligands ; Male ; Metabolic Diseases ; Mice ; Mice, Knockout ; Peroxisome Proliferator-Activated Receptors* ; Peroxisomes ; Prevalence ; Sex Characteristics ; T-Lymphocytes