ABSTRACT
Castleman's disease is a rare atypical lymphoproliferative disorder. Although HHV-8 has been reported to be a cause of Castleman's disease, the etiology and pathogenesis of the disease remains mostly unknown. We experienced a 51-year-old female patient who was concurrently diagnosed with Castleman's disease and systemic lupus erythematosus. Castleman's disease has been rarely reported in patients with systemic lupus erythematosus. Thus, we report the case and briefly discuss relevant articles.
Subject(s)
Female , Humans , Castleman Disease , Herpesvirus 8, Human , Lupus Erythematosus, Systemic , Lymphoproliferative DisordersABSTRACT
Developmental disability shows life-long behavioral abnormality with no significant physical malformation. This study was undertaken to develop an animal model for developmental disability by using two-factor approach. Lipopolysaccharide (LPS), a bacterial toxin, and NAN-190, a 5-HT1A receptor antagonist, were administered to Sprague-Dawley rats on postnatal day (PND) 5 to induce inflammation and an altered 5-HT system, respectively. Long-term alteration of behavior occurred in the drug-treated groups. The LPS-treated group showed impaired motor coordination in the Rota-rod test. The LPS- treated or both LPS and NAN-190-treated groups showed impaired fore-paw muscle power in the wire maneuver test. These groups also showed decreased white matter volume and increased serotonergic fibers. The LPS and NAN-190-treated group also exhibited neurologic deficit in the placing reaction test and impaired equilibrium function in the tilt table test. The results showed that a variety of altered behaviors can be generated by two factor model, and suggested that combination of important etiologic factors and possible underlying defects is a promising strategy of establishing an animal model for developmental disabilities.
Subject(s)
Animals , Developmental Disabilities , Inflammation , Models, Animal , Neurologic Manifestations , Rats, Sprague-Dawley , Receptor, Serotonin, 5-HT1A , Serotonin , Tilt-Table TestABSTRACT
We report a 54-year old female who had mild dyspnea, coughing, abdominal distension, tightening and thickening of the skin, and Raynaud's phenomenon. Clinical manifestations, laboratory and radiologic examinations were compatible with systemic sclerosis. She was also diagnosed to have ovarian cancer on histopathologic study. The possible causative relation between systemic sclerosis and malignant neoplasms is a controversial issue, but several studies have demonstrated an increased frequency of cancer in patients with systemic sclerosis, especially lung and breast cancers. Ovarian cancer was rarely reported in association with systemic sclerosis. We present this case with a review of literatures.
Subject(s)
Female , Humans , Middle Aged , Breast , Cough , Dyspnea , Lung , Ovarian Neoplasms , Scleroderma, Systemic , SkinABSTRACT
This study was conducted to define the molecular mechanism of fasting-induced down-regulation of neuronal nitric oxide synthase (nNOS) expression in the hypothalamic paraventricular nucleus (PVN). Rats were adrenalectomized (ADX), and then either underwent food deprivation or received varying doses of dexamethasone for 48 h. The brain tissues were processed for NADPH-diaphorase (NADPH-d) staining, a histochemical marker of nNOS enzyme activity. Both the ADX and the sham operated rats showed a significant weight loss after 48 h of food deprivation. Food deprivation decreased the number of NADPH-d containing cells in the PVN of sham rats, however, not in the ADX rats. Dexamethasone dose- dependently decreased NADPH-d cells in the PVN of ADX rats. The effect of ADX or dexamethasone was limited to the parvocellular subdivision of PVN. These results suggest that the adrenal glucocorticoids may down-regulate nNOS expression in the PVN during food deprivation.
Subject(s)
Animals , Male , Rats , Adrenalectomy , Biomarkers , Dexamethasone/blood , Down-Regulation/physiology , Fasting/physiology , Food Deprivation/physiology , Glucocorticoids/blood , NADPH Dehydrogenase/metabolism , Nitric Oxide Synthase/metabolism , Paraventricular Hypothalamic Nucleus/enzymology , Rats, Sprague-DawleyABSTRACT
The role of 5-hydroxytryptamine (5-HT)1A receptor activity in prenatal ischemia was studied, by injecting 8-hydroxy-dipropylaminotetraline (8-OH-DPAT; 50 microgram/kg, s.c.), a 5-HT1A agonist on gestation day 17, and 30 min later inducing transient ischemia by ligating the uterine vessels for 30 min. On postnatal day 95, rats that had experienced prenatal ischemia showed impaired motor coordination and reduced concentration of 5-HT in the cerebellum compared with Sham-operated controls. In addition, they showed increased 5-HT1A receptor densities in the cerebral cortex. Pretreatment with 8-OH-DPAT ameliorated the behavioral and neurochemical sequelae measured in the present study. The results suggest that 5-HT1A receptors protect the brain from ischemic insult and/or facilitate recovery after prenatally experienced ischemia.