Background: Overcrowding, poor hygiene and scarcity of portable water are common features of population growth in a resource poor nation especially with rising cost of living from inflation. This is the often the state of many underdeveloped nations such as Nigeria. Such environments encourage the spread of communicable diseases. This study assess the pattern, trend, and at-risk population of Entamoeba histolytica (E. histolytica), implicated in intestinal Amoebiasis in South-South Nigeria. Method: This retrospective study was conducted using hospital data obtained from the laboratory department of a general hospital clinic in Warri and covered a period of four years from January 2015 - December 2018. The record of 4,169 laboratory results of stool samples examined by direct smear and concentration technique, were recovered from a designed computer database. Trend of infection over the period as well as variations in distribution patterns between sex, age and seasons were determined using appropriate statistical tools. Results: Out of the 4,169 stool samples 365 (8.8%) had E. histolytica with decreasing trend of infection from 2015 – 2018 as 135 of 1210 (11%); 118 of 1114 (10.6%); 57 of 792 (7.2%); 55 of 1053 (5.2%) respectively. Prevalence of infections was higher in females, 57.5% (95CI%, 51.7-59.7, n= 210) than males (n=155, 42.5%, 95%CI, 40.3-48.6). The prevalence of infections was highest among Age brackets 1-5years, 6-15 years and 35+ years; but lowest in the 26-35 years with peak season of infections at first and last quarters of each year. Conclusions: Children are more vulnerable to E. histolytica infestation and the dry seasons of the year place them at risk. This information underscores the need for local surveillance to evaluate the effectiveness of control and preventive health measures with a view of reducing the prevalence and morbidity of parasitic infections in our locality.
Backgrounds Obesity has been recognised as a risk factor for poor asthma control. There is clinical evidence showing a poorer response to steroid therapy in obese asthmatic patients. However, the treatments to restore the poor corticosteroid sensitivity have not been established yet. Our objective was to establish a potential treatment for obese asthmatic patients. Methods: Total 74 asthmatic patients (Obesity (OB), n= 52), Non-obesity (NOB) n=22) were recruited for this study. Peripheral blood mononuclear cells (PBMCs) were obtained and incubated with or without metformin and serial dilutions of dexamethasone for 1 hr, followed by stimulation with TNF-α. After overnight incubation, supernatants were harvested and CXCL8 in the supernatants was measured by ELISA. Then, IC50-Dex was calculated using the data. Results: The IC50-Dex of PBMC obtained from the OB was significantly higher than that obtained from the NOB (p=0.002). The IC50-Dex of PBMC obtained from the OB significantly correlated with the number of acute exacerbations per year (ρ=0.310, p=0.028). In both groups, TNF-α-induced CXCL-8 releases were not affected by metformin treatments. In the OB, the metformin treatment significantly decreased the IC50-Dex of PBMC (p<0.001), but it did not in the NOB (p=0.926). Conclusions: Metformin might be a drug candidate to restore poor corticosteroid sensitivity in obese asthmatic subjects.
A 24-year-old woman presented with an abnormal sound in her neck. She had no history of previous surgery, endotracheal intubation or neck trauma. She had been aware of this abnormal sound since she was 12 years old, but paid no attention to it. She had been recommended to visit a hospital for a neck examination. Stridor was heared in the neck ["coming from the throat"?]. Peak flow was markedly suppressed in pulmonary function tests, and the flow volume loop indicated upper airway stenosis. Bronchoscopy revealed subglottic tracheal stenosis, and magnetic resonance imaging showed that the cricoid cartilage was normal. Nd-YAG laser treatment was performed in Mitsui Memorial Hospital and her symptoms were improved. Biopsy of the stenotic area of the trachea showed dense fibrous tissue proliferation in the submucosa. Neither granuloma nor vasculitis was found in the biopsy specimen. No systemic disease capable of inducing tracheal stenosis was found on systemic examination. From these clinical and pathological findings, we diagnosed idiopathic subglottic stenosis.
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