AGRANULOCYTIC ANGINA (SCHULTZ) AND F-UNCTIONAL GRANULOCYTOPENIA

Schultz (1) in 1922 dcscribed what appeared to be a new syndro me characterized by an ulcerative angina, extre-me leukopenia with complete or almost cornplcte disappearance of the polymorphonuclear cells, its occurrence in middle-aged women, with marked prostration, a rapidly fatal outcome, and unknown etiology. This symptom-com- plex was given the name of agranulocytosis, later described as agranu. locytic angina and believed to be a new clinical entity. Since then some 150 cases have been reported chiefiyin Germany, Austria, and the United States. Many of the cascs conform to the originaldes- cription and others do not. It was soon discovered that the disease is not peculiar to women nor always fatal. Kastlin {2) reviewing the literature in 1927 found 43 cascs of which t4 were in women. Includ- ing his two cases there were in the series 42 deaths and 3 recoveries. In the same year Haken (3) reported 3 cases occurring in children aged 4, 6, and 8 years respectiveIy and.Weiss (3) reported the occur- rence of agranulocytosis in a child 6 years old. Potts (3) in the latter part of 1928 reviewed 38 additional cases including the 4 juvenile patients already mentioned. Of these 38 patients, 33 died. Women were attacked about three and a balf times as frcqucntly as men and children combined.     

Relationship between insomnia and pain in major depressive disorder: A sleep diary and actigraphy study

ObjectivesInsomnia and pain are frequent complaints during the course of a major depressive episode. We analyzed the association between insomnia and pain symptoms using subjective and objective sleep measures.MethodsThis is a prospective, naturalistic follow-up study in a university-based psychiatric unit. Ninety-one Chinese patients were enrolled during an acute episode of major depressive disorder (mean age = 48 years, 73 women); 82 of them were reassessed 3 months later using the same assessment on sleep, pain, depressive, and anxiety symptoms. Clinician-rated insomnia symptoms were obtained using the insomnia items of the Hamilton Rating Scale for Depression. Subjective sleep disturbances were assessed using the Insomnia Severity Index (ISI). Detailed sleep pattern was acquired using sleep diary and actigraphy. Pain intensity was evaluated using a verbal rating scale, a visual analog scale, and a multidimensional pain scale.ResultsCross-sectional analyses found that insomnia symptoms and quantitative sleep parameters were related to pain symptoms. The correlations between sleep and pain scores were more significant after 3 months of pharmacotherapy as compared to baseline. After controlling for the severity of anxiety and depression, the ISI total score and actigraphy-derived wake after sleep onset and total sleep time remained significant in predicting pain.ConclusionThis study supports specific role of subjective sleep disturbances and actigraphic measures in predicting pain symptoms in major depressive disorder. Further studies using a micro-longitudinal design are necessary to find out the causal relationship between sleep and pain in depressed patients.     

Dexamethasone ameliorates retinal photic injury in albino rats.

The effect of dexamethasone in two regimens on retinal photic injury was studied in Lewis albino rats that were exposed to 24 hr of continuous green fluorescent light. Under regimen 1, dexamethasone was given at a daily dosage of 1 mg kg-1 for 8 days, starting 6 days before light exposure. Under regimen 2, dexamethasone was given at the same daily dosage for 3 days, started 1 day before light exposure. Pathologic study of the light-exposed retina, morphometric evaluation of the photoreceptor cell loss, cell counts of the macrophages in the subretinal space, and measurements of rhodopsin levels were undertaken in the dexamethasone-treated and control retinas at various times. The administration of dexamethasone in both regimens did not produce pathologic changes in the retina before light exposure, but rhodopsin levels were significantly lowered in both treated groups when compared to corresponding vehicle treated control animals. Under regimen 1, at 6 hr after light exposure, both the treated and the control groups showed comparable loss of photoreceptor cells, degeneration of the photoreceptor elements and retinal pigment epithelium, but a significantly lowered level of rhodopsin in the treated group was noted. At 6 days after exposure, the outer nuclear layer thickness, and the outer and inner segments showed significant preservation in the treated group. Also in the treated group, the number of macrophages was significantly reduced and the retinal pigment epithelial (RPE) vacuolation was markedly less. However, there was no difference in rhodopsin levels. At 14 days after exposure, the outer nuclear layer thickness and rhodopsin levels of the treated rats had significantly higher values than the controls. Under regimen 2, however, at 6 days after exposure, an ameliorative effect in the RPE was observed but there were no differences of rhodopsin levels, the outer nuclear thickness and number of macrophages between the treated and control groups. Regimen 1 was associated with a significantly higher retinal level of dexamethasone when compared with regimen 2. The ameliorative effect of dexamethasone on rat retinal photic injury may be through inhibition of lipid peroxidation, in which a high retinal level of the steroid is required.     

Localization of leptin receptor immunoreactivity in the lean and obese Zucker rat brain

Leptin, a product of the obese (ob) gene, is secreted by adipocytes and appears to act as a hormone to regulate food intake, metabolism and body weight. Subcutaneous administration of leptin causes reductions in food intake and body and fat-depot weights in both lean and genetically obese (ob/ob) mice, and leptin infusion into the lateral cerebral ventricles decreases feeding with short latency, suggesting a central site of action. A gene defect in the Zucker obese rat causes an amino acid substitution in the leptin receptor and reduced leptin binding at the cell surface. An antiserum to a portion of the mouse leptin receptor (AA 877–894) located within the intracellular domain was used to label Zucker lean (Fa/?) and obese (fa/fa) rat brain sections. At optimal dilution (1:8000), only cells in the basal forebrain, preoptic area, hypothalamus and brainstem were moderately or intensely labeled. The most intensely-labeled nuclei, the anterior commissural, magnocellular paraventricular, supraoptic, circularis in the anterior hypothalamus and fornical in the lateral hypothalamus contain large neurons that synthesize and secrete vasopressin or oxytocin and their respective neurophysins. Diminished leptin transport into the central nervous system or defective signal transduction in Zucker obese rats may sufficiently compromise leptin regulation of the HPA axis, NPY-immunoreactive neurons or other hypothalamic elements to cause obesity.     

The diagnostic and treatment characteristics of El Tor cholera and its combinations with other infectious diseases in an outbreak of multiple intestinal infection]

The article summarizes the experience of diagnosis and treatment of El Tor cholera in servicemen during an outbreak of intestinal polyinfection in the conditions of dry hot climate in desert and mountainous terrain of Afghanistan. The authors describe the clinical course of El Tor cholera which is stipulated by the mixed character of dehydration, polymorphism of clinical symptoms and more severe forms of concomitant infections.