Multiple bladder calculi: a rare cause of irreducible uterine prolapse

Background A vesical calculus in a prolapsed cystocele is rare. Objective To highlight bladder calculi as a cause of irreducible uterine prolapse. Case Report A case of irreducible total uterine prolapse caused by multiple vesical calculi is presented. Bladder stones were removed through vaginal cystolithotomy followed by vaginal hysterectomy. Conclusion In cases of acute irreducible pelvic organ prolapse, the possibility of bladder stones should be kept in mind and X-ray pelvis including the prolapsed mass should be done to confirm the diagnosis.     

Acute laryngeal stridor — Controversies in current management

Conclusion The successful management of acute laryngeal stridor in infants and small children depends upon a close cooperation and team work of pediatrician, otolaryngologist and specialised nursing care in a pediatric intensive care unit. The overall opinion is in favour of steroid, racemic epinephrine and intubation or tracheostomy in severe croup. Endoscopy should be performed in all the cases, either immediately, prior to or con-commitant with the establishment of airways. This helps in achieving correct diagnosis and rationalising the treatment. Mortality and morbidity has been significantly reduced by close monitoring and quality nursing of intubated or tracheostomised child. Early extubation can be achieved by regular examination of laryngeal mucosa by direct laryngoscopy in an intensive care unit. Cases of severe croup should be followed up, as they have increased susceptibility to develop bronchial asthma.     

EnteropathognicEscherichia coli diarrhea in hospitalized children at Delhi

Prevalence of enteropathogenicE. coli (EPEC) in 4178 cases of acute diarrhea in hospitalised children of <2 years old admitted during 1980–1985 was studied.E. coli in pure culture was obtained from 15·5% of the stool samples. Of the isolates 58·8% were typable, however, only 43·2% belonged to known EPEC serotypes. The commonest serotype, was 020 (21·1%), followed by 018 (20·7%), 026 (8·8%), 0119 (8·4%), 0125 (7·7%), 086 (6·1%) and others. Majority of the serotypes were obtained from males and in the age group >6–12 months.     

Working area and angle of attack in three cranial base approaches: pterional, orbitozygomatic, and maxillary extension of the orbitozygomatic approach

OBJECTIVE: This study was designed to quantify the operative exposure obtained in the pterional, orbitozygomatic, and modified orbitozygomatic with maxillary extension surgical approaches. METHODS: The pterional and orbitozygomatic approaches and a variation of the orbitozygomatic osteotomy that included an extra centimeter of bone resection in the inferior direction ("maxillary extension") were performed on cadaveric heads. For each surgical exposure, the working area was determined by using triangles defined with anatomic points. The "angle of attack" of the approaches for the same target point was determined with the use of a robotic microscope. RESULTS: The maximum allowable angle of attack was significantly greater with the orbitozygomatic approach (37.2 +/- 4.7 degrees) than that with the pterional approach (27.1 +/- 4.3 degrees) (P < 0.001). The angle of attack with the maxillary extension (42.0 +/- 4.9 degrees) was significantly greater than that with the orbitozygomatic approach (P < 0.001). The working areas were 281, 343, and 371 mm(2) for the pterional, orbitozygomatic, and maxillary extension approaches, respectively. The orbitozygomatic approach with maxillary extension had a significantly larger working area than the pterional approach (P = 0.011). CONCLUSION: Increments in bony removal open a wider angle in which to work more than they increase the actual amount of working area. Increasing the amount of bone removed by using an orbitozygomatic approach instead of a pterional approach converts a narrow space into a wide portal, allowing surgeons to work closer to the surgical target while decreasing the need for brain retraction. Extending the orbitozygomatic approach into the maxillary region also improves the exposure area and angle, but less significantly.     

Obesity and metabolic syndrome: long-term benefits of central leptin gene therapy

The recent rapid rise in the incidence of obesity has prompted investigations into understanding the hormonal and neuronal pathways involved in body weight homeostasis in order to devise novel therapeutic strategies. The early enthusiasm for the adipocyte hormone leptin as a regulator of fat mass was largely discarded because of the apparent development of leptin resistance, as seen in obese subjects with elevated blood leptin levels. We postulated that this leptin ineffectiveness may be caused by a lack of leptin availability at target sites in the hypothalamus. To test this hypothesis, we used viral vectors to introduce the leptin gene into the brain for a sustained supply of leptin in the hypothalamus. A single injection of recombinant adeno-associated virus encoding the leptin gene (rAAV-lep) into the third cerebroventricle prevented the aging-associated gradual increase in body weight and adiposity in adult rats for 6 months of the experiment. When administered to prepubertal rats, significantly lower body weight gain and adiposity were maintained for up to 10 months of the experiment. In addition, obesity was prevented in rats introduced to a high-fat diet and also reversed in obese-prone rats maintained on a high-fat diet. Body weight homeostasis and loss of adiposity by leptin gene therapy was achieved by an increase in energy expenditure, and when the rAAV-lep titer was increased, there was also a voluntary reduction in food intake. Importantly, this therapy reduced blood levels of insulin, triglycerides and free fatty acids, the pathophysiologic correlates of the metabolic syndrome. Thus, the long-term beneficial effects of central leptin gene therapy may herald the development of newer therapeutic strategies to control the epidemic of obesity and related metabolic disorders.     

Complete genome sequence and analysis of Wolinella succinogenes

To understand the origin and emergence of pathogenic bacteria, knowledge of the genetic inventory from their nonpathogenic relatives is a prerequisite. Therefore, the 2.11-megabase genome sequence of Wolinella succinogenes, which is closely related to the pathogenic bacteria Helicobacter pylori and Campylobacter jejuni, was determined. Despite being considered nonpathogenic to its bovine host, W. succinogenes holds an extensive repertoire of genes homologous to known bacterial virulence factors. Many of these genes have been acquired by lateral gene transfer, because part of the virulence plasmid pVir and an N-linked glycosylation gene cluster were found to be syntenic between C. jejuni and genomic islands of W. succinogenes. In contrast to other host-adapted bacteria, W. succinogenes does harbor the highest density of bacterial sensor kinases found in any bacterial genome to date, together with an elaborate signaling circuitry of the GGDEF family of proteins. Because the analysis of the W. succinogenes genome also revealed genes related to soil- and plant-associated bacteria such as the nif genes, W. succinogenes may represent a member of the epsilon proteobacteria with a life cycle outside its host.     

Central leptin gene therapy blocks high-fat diet-induced weight gain,hyperleptinemia, and hyperinsulinemia: increase in serum ghrelin levels

Recombinant adeno-associated virus (rAAV), encoding either rat leptin (rAAV-lep) or green fluorescent protein (rAAV-GFP, control), was injected intracerebroventricularly in rats consuming a high-fat diet (HFD; 45 kcal%). Caloric consumption and body weight were monitored weekly until the rats were killed at 9 weeks. Untreated control rats consuming regular rat diet (RCD; 11 kcal%) were monitored in parallel. Body weight gain was accelerated in rAAV-GFP + HFD control rats relative to those consuming RCD, despite equivalent kcal consumption. At 9 weeks, serum leptin, free fatty acids, triglycerides, and insulin were elevated in HFD control rats. In contrast, rAAV-lep treatment reduced intake and blocked the HFD-induced increase in weight, adiposity, and metabolic variables. Blood glucose was slightly reduced but within the normal range, and serum ghrelin levels were significantly elevated in rAAV-lep + HFD rats. Uncoupling protein-1 (UCP1) mRNA in brown adipose tissue (BAT), an index of energy expenditure through nonshivering thermogenesis, was decreased in rats consuming HFD. Treatment with rAAV-lep significantly augmented BAT UCP1 mRNA expression, indicating increased thermogenic energy expenditure. These findings demonstrate that central leptin gene therapy efficiently prevents weight gain, increased adiposity, and hyperinsulinemia in rats consuming an HFD by decreasing energy intake and increasing thermogenic energy expenditure.