Gastro-oesophageal reflux in children: surgical management

Gastro-oesophageal reflux disease (GORD) is symptomatic reflux of gastric contents into the oesophagus. Factors predisposing to GORD are loss of the physiological antireflux barrier and anatomic abnormalities of the oesophagus or diaphragm. Conservative measures and medical management results in resolution of symptoms in a majority of children. Surgery is indicated in the event of failure of medical management or severe complications. Surgical procedures include open or laparoscopic fundoplication in children with normal neurology; fundoplication with or without vagotomy and pyloroplasty; surgical feeding jejunostomy and oesophago-gastric dissociation in the severely neurologically impaired children.     

Increase in Temperature Induces the Malathion Toxicity in <Emphasis Type="Italic">Pangasianodon hypophthalmus</Emphasis>: A Short Term Acute Test

The study was conducted to evaluate the effect of higher temperature beyond optimum range on acute toxicity for malathion (effective concentration 50 %) in Pangasianodon hypophthalmus. A 2 days renewal bioassay system for 96 h was used to determine LC₅₀ value of malathion at three different regimes of temperature that is 30, 32 and 34 °C considering as T1, T2 and T3, respectively. The physico-chemical parameters of water of different treatment groups were estimated during pre and post-exposure of test chemical, following standard methods. The result of short term acute toxicity test at 96 h LC₅₀ values through probit analysis was found to be 7.76, 6.45 and 4.46 µL L^?1 for T1, T2, and T3, respectively. The 96 h LC₅₀ of malathion at 34 °C was found to be significantly (p < 0.01) lower as compared with estimated LC₅₀ for malathion at 30 and 32 °C. High temperature and free carbon dioxide coupled with low dissolved oxygen were significantly noticed in T3 group when compared to T1 and T2 groups. Lower LC₅₀ of malathion at 34 °C as compared to 30 and 32 °C showed that at a higher temperature, the toxicity of malathion increased, signifying diminished fish protective response to malathion toxicity. The current study reflects the impact of increased temperature on pesticide toxicity in the aquatic ecosystem, alarming the aqua farmers to judiciously use malathion in ponds.     

Long-term sequelae of herpes simplex virus encephalitis–related white matter injury: correlation of neuropsychological outcome and diffusion tensor imaging

Journal of NeuroVirology - The pathophysiology of the memory impairment following Herpes Simplex virus encephalitis is not yet established and understood. This study attempts to elucidate the role...     

Fetuin-A levels are increased in the adipose tissue of diabetic obese humans but not in circulation

Background

The hepatokine fetuin-A is linked to obesity and type 2 diabetes, but its presence and expression in adipose tissue remain unclear. In this study, we aimed to assess the circulating levels of fetuin-A and its expression in subcutaneous adipose tissue (SAT) from diabetic and non-diabetic obese subjects and their modulation by exercise.

Methods

SAT and blood were obtained from adults obese (diabetic, n=118 and non-diabetic, n=166) before and after a 3-month exercise program (diabetic, n=40 and non-diabetic, n=36, respectively). Plasma fetuin-A was assayed using ELISA. The presence and expression of fetuin-A in SAT, peripheral blood mononuclear cells (PBMCs) and cell lines (3T3-L1, THP-1, HepG2, RAW 264.7) were analysed using confocal microscopy, immunoblotting and qRT-PCR.

Results

Plasma fetuin-A level did not significantly differ between diabetic and non-diabetic obese subjects. However, when the non-diabetic group was divided into metabolically healthy and unhealthy phenotypes, significantly higher fetuin-A level was observed in the unhealthy sub-group. Circulating fetuin-A was mainly associated with glycaemic markers. In SAT, fetuin-A protein level was significantly higher in the diabetic obese subjects but its mRNA was not detected. Similarly, fetuin-A protein was detected in PBMCs, but its mRNA was not. In line with this, the use of various cell lines and culture media indicated that the presence of fetuin-A in SAT and PBMCs was due to its uptake from circulation rather than its endogenous expression. Finally, physical exercise decreased fetuin-A levels in both plasma and SAT in both groups.

Conclusions

Fetuin-A levels increased in association with diabetes in SAT but not in circulation in the obese subjects. Moreover, physical exercise decreased fetuin-A level. Fetuin-A potentially acts as a hepatokine taken up by other tissues, such as adipose tissue.

     

Founder effects of the homogentisate 1,2-dioxygenase (HGD) gene in a gypsy population and mutation spectrum in the gene among alkaptonuria patients from India

Clinical Rheumatology - Alkaptonuria (AKU) is a rare metabolic disease. The global incidence is 1:100,000 to 1:250,000. However, identification of a founder mutation in a gypsy population from...     

Modified formulation of CPDA for storage of whole blood, and of SAGM for storage of red blood cells, to maintain the concentration of 2,3-diphosphoglycerate

BACKGROUND AND OBJECTIVES: A dramatic decrease in the level of 2,3-diphosphoglycerate (2,3-DPG) takes place during the storage of whole blood (WB) in CPDA (citrate-phosphate-dextrose-adenine) and a similar decrease occurs during the storage of red blood cells (RBCs) in SAGM (saline-adenine-glucose-mannitol). The aim of the present study was to prevent this decrease by modifying CPDA and SAGM. MATERIALS AND METHODS: The pH of WB anticoagulant or RBC preservative solution was maintained at 7.6 by autoclaving the dextrose solution separately, by incorporating ascorbic acid and nicotinic acid into both CPDA and SAGM (to produce modified CPDA and SAGM solutions), and by reducing the concentration of adenine and adding citrate to the modified SAGM solution. The concentration of 2,3-DPG in WB after 28 days of storage in modified CPDA, and in RBCs stored in modified SAGM, was compared with that in WB or RBCs stored in unmodified solutions. RESULTS: The initial 2,3-DPG levels were maintained after 28 days in the modified formulations [10.63 +/- 2.58 microM/g of haemoglobin (Hb) in the case of modified CPDA and 12.07 +/- 1.47 microM/g of Hb in the case of modified SAGM], whereas in standard CPDA and SAGM solutions, the concentration of 2,3-DPG decreased to very low levels (0.86 +/- 0.97 microM/g Hb for CPDA and 0.12 +/- 0.008 for SAGM). CONCLUSIONS: Our modification in the formulation of CPDA or SAGM is effective in arresting the dramatic decrease in the level of 2,3-DPG that occurs during storage of WB and RBCs in unmodified solutions.     

Determination of relationships among non-toxigenic Vibrio cholerae O1 biotype El Tor strains from housekeeping gene sequences and ribotype patterns

Sequencing of three housekeeping genes, mdh, dnaE and recA, and ribotyping for seven non-toxigenic Vibrio cholerae O1 strains isolated from different geographic sources indicate a phylogenetic relationship among the strains. Results of MLST and ribotyping indicate a clear difference between three toxigenic strains (N16961, O395, and 569B) and three non-toxigenic strains from India (GS1, GS2, and GW87) and one Guam strain (X392), the latter of which were similar in both MLST and ribotyping, while two other non-toxigenic strains from the USA and India (2740-80 and OR69) appeared to be more closely related to toxigenic strains than to non-toxigenic strains, although this was not supported by ribotyping. These results provide clues to the emergence of toxigenic strains from a non-toxigenic progenitor by acquisition of virulence gene clusters. Results of split decomposition analysis suggest that widespread recombination occurs among the three housekeeping genes and that recombination plays an important role in the emergence of toxigenic strains of V. cholerae O1.     

Anastomotic Healing in a Small Bowel Transplantation Model in the Rat

Anastomotic healing is impaired after intestinal surgery because of ischemia and reperfusion injury (IRI), which can result in intestinal leaks leading to increased mortality. The objective of this study was to determine the effects of transplant IRI and immune mechanisms on intestinal graft anastomotic healing. Orthotopic intestinal transplantations (OIT) were performed in rats. The experimental design consisted of six groups A–F (n = 5/group): A, allogeneic OIT treated with tacrolimus (1mg/kg/day); B, syngeneic OIT treated with tacrolimus; C, syngeneic OIT; D, allogeneic OIT; E, proximal and distal anastomoses performed in nontransplanted animals; F, same as in group E but treated with tacrolimus. Anastomotic bursting pressure (ABP), hydroxyproline content (HPC), and mucosal inflammatory infiltrate (MII) were determined at the anastomotic sites (proximal and distal) and compared between groups. ABP was significantly (p < 0.001) reduced in OIT groups A, B, C, and D compared to control groups E and F at both the proximal and distal anastomotic sites. HPC was 1 g/mg of tissue in groups A, B, C, and D, and 5g/mg of tissue in groups E and F. This demonstrates a significant (p < 0.001) reduction in HPC after OIT. MII was significantly (p < 0.001) increased in OIT groups when compared to nontransplanted control groups. MII was also significantly (p < 0.05) increased in allogeneic OIT groups A and D compared to syngeneic OIT groups B and C. Generally, ABP and HPC were inversely proportional to MII in both nontransplanted control and OIT groups. Reduced anastomotic strength was demonstrated in both syngeneic and allogeneic OIT anastomotic sites irrespective of immunosuppressive therapy, and is probably related to IRI.