Release of noradrenaline from the ligated cat hypogastric nerve

After in vivo ligation for 24 h of the cat hypogastric nerve, large amounts of noradrenaline (NA) and dopamine β-hydroxylase (DBH) accumulated in the nerve segment immediately proximal to the ligature (P₁). In vitro incubation of 24-h-ligated nerves (segments P₁ and P₂) in oxygenated Krebs solution at 37% C in the presence of the ionophore X537A or high K⁺ concentrations caused a marked release of endogenously accumulated NA into the incubation medium. High-K⁺-evoked release was entirely dependent on extracellular Ca²⁺. Electrical nerve stimulation caused an 80% tissue NA loss, but the transmitter could not be found in the medium as intact NA. These results suggest that the in vivo ligated cat hypogastric nerve may serve as a useful model of adrenergic nerve terminals free of effector cells.     

Monitoring nutrient intakes in India

An attempt has been made to identify suitable indicators to monitor changes in nutritional status of population by using NNMB database from 1975 to 1980. Conventional indicators in this regard are nutrient intakes, clinical status and growth, particularly of children. Examination of the data revealed that average energy intake at household as well as that of preschoolers could be used for assessing changes overtime. One of the reliable indicators of nutritional status appears to be distribution of children according to body weight deficits rather than clinical deficiency signs. Based on these indicators, the results of the analysis suggested that in the 10 states where NNMB is operating, there has been an increase in average consumption of calories as well as improvement in body weight status of preschool children.     

Arterial embolization for traumatic hemobilia with hepato-portal fistula

A case of blunt liver trauma complicated by delayed upper gastrointestinal bleeding, probably hemobilia, was successfully treated by intra-arterial embolization. Laparotomy with liver resection or hepatic artery ligation—procedures that carry a high morbidity and mortality in a critically ill patient—were avoided. Embolization techniques can be a valuable alterantive to surgery in the mangement of hepatic trauma with delayed hemorrhage in selected, high-risk cases     

IM-133N modulates cytokine secretion by RAW264.7 and THP-1 cells

An indigenous herbal extract IM-133N containing extracts of Prosopis glandulosa Torr and Symplocos racemosa Roxb were evaluated for potential immunomodulatory effects using RAW264.7 and THP-1 cells. The incubation of the cells for 24?h with IM-133N over a dose range 0–125?µg/ml did not cause cytotoxicity that exceeded 10%. The results indicated that non-cytotoxic doses of IM-133N effectively up-regulated iNOS, TNFα, IL-6, IL-10, IL-8 and IFNγ gene expression in both the RAW264.7 and THP-1 cells. The results also indicated IM-133N elicited dose-related increases in nitric oxide (NO) and tumor necrosis factor (TNF)-α production by RAW264.7 or THP-1 cells. These results demonstrated that IM-133N could stimulate NO and induced pro-inflammatory cytokine expression by monocytes/macrophages. As clinical studies have shown IM-133N to be an effective immunomodulator without any adverse effects, the results of the present study provide further support for the potential use of this agent as an immunostimulant or as an immunotherapy adjuvant.     

草药复方Bresol？抵抗化合物48/80诱导的肥大细胞脱颗粒及组胺释放：促使肥大细胞稳定的一种非免疫机制

目的：研究一种草药复方制剂Bresol？对于肥大细胞脱颗粒以及组胺释放的保护作用。 方法：使用大鼠腹膜内肥大细胞,在体外经化合物48/80诱导肥大细胞脱颗粒及组胺释放,评估Bresol？稳定肥大细胞的作用。 结果：显微镜下正常对照组涂片显示较多完整的肥大细胞,有极少量的脱颗粒肥大细胞和微量的组胺释放。阳性对照组中用化合物48/80培养的肥大细胞出现了显著的肥大细胞脱颗粒现象以及高浓度的组胺释放。而100 mg/L浓度的Bresol？明显抑制了化合物48/80诱导的肥大细胞脱颗粒。此外,Bresol？可有效抑制化合物48/80诱导的组胺释放,且抑制效果与剂量有关。 结论：Bresol？能够在体外抑制化合物48/80诱导的肥大细胞脱颗粒和组胺释放。本研究的发现可解释Bresol？对多种过敏疾病有效可能是通过一种非免疫机制。     

Genomics of Postprandial Lipidomics in the Genetics of Lipid-Lowering Drugs and Diet Network Study

Postprandial lipemia (PPL) is an important risk factor for cardiovascular disease. Inter-individual variation in the dietary response to a meal is known to be influenced by genetic factors, yet genes that dictate variation in postprandial lipids are not completely characterized. Genetic studies of the plasma lipidome can help to better understand postprandial metabolism by isolating lipid molecular species which are more closely related to the genome. We measured the plasma lipidome at fasting and 6 h after a standardized high-fat meal in 668 participants from the Genetics of Lipid-Lowering Drugs and Diet Network study (GOLDN) using ultra-performance liquid chromatography coupled to (quadrupole) time-of-flight mass spectrometry. A total of 413 unique lipids were identified. Heritable and responsive lipid species were examined for association with single-nucleotide polymorphisms (SNPs) genotyped on the Affymetrix 6.0 array. The most statistically significant SNP findings were replicated in the Amish Heredity and Phenotype Intervention (HAPI) Heart Study. We further followed up findings from GOLDN with a regional analysis of cytosine-phosphate-guanine (CpGs) sites measured on the Illumina HumanMethylation450 array. A total of 132 lipids were both responsive to the meal challenge and heritable in the GOLDN study. After correction for multiple testing of 132 lipids (α = 5 × 10⁻⁸/132 = 4 × 10⁻¹⁰), no SNP was statistically significantly associated with any lipid response. Four SNPs in the region of a known lipid locus (fatty acid desaturase 1 and 2/FADS1 and FADS2) on chromosome 11 had p < 8.0 × 10⁻⁷ for arachidonic acid FA(20:4). Those SNPs replicated in HAPI Heart with p < 3.3 × 10⁻³. CpGs around the FADS1/2 region were associated with arachidonic acid and the relationship of one SNP was partially mediated by a CpG (p = 0.005). Both SNPs and CpGs from the fatty acid desaturase region on chromosome 11 contribute jointly and independently to the diet response to a high-fat meal.