Electrophoresis of isolated secretory granules from guinea-pig submaxillary gland

1 The nature of the surface charge on secretory granules from the submaxillary gland of the guinea-pig has been studied by electrophoresis of the isolated granules. The granules suspended in buffered sucrose solutions move to the anode.2 Divalent ions reduce the anodal movements of the granules. Calcium and magnesium neutralize the net surface charge of the granules. This result supports the hypothesis that the electrostatic surface charge which can be reduced by calcium ions may be a major factor in controlling the fusion of secretory granules to the cell membrane, before release by exocytosis.3 The mechanisms which couple membrane events with enzyme or hormone release from secretory glands are considered.     

Properties of kallikrein-containing granules isolated from the submaxillary gland of the guinea-pig

1. Granular fractions of high purity consisting of subcellular kallikrein- and amylase-storing organelles have been isolated from homogenates of guinea-pig submaxillary gland.2. The isolated kallikrein- and amylase-containing granules closely resembled secretory granules observed in situ in serous acinar cells in intra-granular appearance, size and histochemical reaction.3. The subcellular, histochemical and ultrastructural studies indicate that the serine protease, kallikrein, is like amylase an exocrine enzyme with a functional role in saliva.     

幽门螺杆菌感染患者血清可溶性幽门螺杆菌抗原及其 IgG,IgA型免疫复合物测定

目的　测定血清可溶性幽门螺杆菌抗原(S-Hp)和其特异性免疫复合物(Hp-IC)并评价它们对幽门螺杆菌感染诊断的意义.方法　采用双抗体夹心式酶免疫测定法.结果　66例Hp感染患者血清S-Hp阳性率90.91%,显著高于28例阴性对照组阳性率0%,P<0.001.S-Hp含量与Hp感染菌量呈成比,但43例Hp阳性患者治疗前后S-Hp 含量无显著改变（P>0.05）.血清 S-Hp抗原均以IgG和/或IgA型特异性免疫复合物形式存在,Hp-IC对Hp感染诊断特异性85.71%,敏感性77.23%. 结论　S-Hp和Hp-IC测定可用于临床Hp感染诊断,对阐明Hp致病机理有重要意义.     

Global infant mortality trends and attributable determinants – an ecological study using data from 192 countries for the period 1990–2011

Background

Infant mortality rate (IMR) is regarded as an important indicator of population health. IMR rates vary substantially with the highest found in sub-Saharan Africa (SSA) compared to the lowest in Europe. Identifying spatial disparities in IMR and quantifying attributable risk factors is essential for policymakers when tailoring time-appropriate interventions at a global, regional, and country level.

Methods

Data for 192 countries were extracted from the World Bank Development Indicator database for the period 1990–2011. Spatial clustering was used to identify significant higher-risk IMR countries. A robust ecological generalized linear negative binomial regression model was used to quantify risk factors and associated decomposition values (Shapley).

Results

Significant reductions were observed in IMR for all of the World Health Organization regions for the period 1990–2011 except for SSA, which indicated a reversal of this trend in the 1990s due to HIV. Significant high-risk clustering of IMR is also indicated in SSA countries and parts of Asia. Maternal mortality (survival), lack of water and sanitation and female education were confirmed as prominent and high attributable risk factors for IMR. Distinct temporal changes in the attributability of these factors were observed, as well as significant heterogeneity with regards to the most attributable factor by region and country.

Conclusions

Our study suggests that maternal mortality is the most prominent attributable risk factor for infant mortality, followed by lack of access to sanitation, lack of access to water, and lower female education. Variation exists across regions and countries with regards to the most attributable factor. Our study also suggests significant underestimation of IMR in regions known for poorer data quality. The results will aid policymakers in re-tailoring time-appropriate interventions to more effectively reduce IMR in line with Millennium Development Goal 4.

     

Enhanced transcription factor DNA binding and gene expression induced by arsenite or arsenate in renal slices

Although the kidney represents a target for the accumulation and toxicity of arsenic, little is known about the molecular targets of arsenic in this organ. Therefore, these studies were designed to examine the molecular impact of arsenite [As(III)] and arsenate [As(V)] at low (nanomolar) concentrations. Precision-cut rabbit renal cortical slices were challenged with As(III) or As(V) for up to 8 h. Neither form of the metal induced overt cytotoxicity as assessed by intracellular K+ levels over this time period at concentrations from 0.01-10 microM. In addition, no alterations in the expression of Hsp 60, 70, or 90 were observed. However, induction of heme oxygenase-1 (Hsp 32) was seen following a 4-h challenge with As(III), but not with As(V). As(III) and As(V) induced DNA binding of AP-1 at 2- and 4-h exposure; following a 6-h exposure there was no difference. Although no alteration in the DNA binding activity of ATF-2 was induced by As(III) or As(V), both forms enhanced the DNA binding activity of Elk-1. Enhanced DNA binding activity of AP-1 and Elk-1 correlated with increased gene expression of c-fos, but not c-jun, at 2 h. c-myc gene expression was also induced by As(III) and As(V), albeit at a later time point (6 h). These results suggest that acute arsenic challenge, by either As(III) or As(V), is associated with discrete alterations in the activity of signaling pathways and gene expression in renal tissue.      

Outcomes of Stage I/II vulvar cancer patients after negative superficial inguinal lymphadenectomy

OBJECTIVES: To investigate the patterns of recurrence associated with superficial inguinal lymphadenectomy (SupIL) and vulvectomy for patients with Stage I/II vulvar cancer. METHODS: A retrospective chart review identified patients from 1990-2001 with Stage I/II vulvar cancer that underwent SupIL and vulvectomy. Survival was analyzed using the Kaplan-Meier method with Fisher Exact and Chi-square tests for comparisons between groups. RESULTS: 65 patients with Stage I/II vulvar cancer with a pathologically negative SupIL were identified (30 Stage I, 35 Stage II). Three patients recurred in the inguinal region, (4.6%) and 11 patients (16.9%) recurred on the vulva. Two of the 11 patients died of disease, six patients are alive without evidence of disease after additional therapy. Five-year disease-free survival and overall survival were 66% and 97%, respectively. Risk of recurrence was not associated with smoking status, stage, or margin status. CONCLUSIONS: SupIL and vulvectomy for Stage I/II vulvar cancer have a low recurrence rate in the inguinal region when nodes are negative. The local recurrence rate (17%) is acceptable, and overall survival is good using this conservative approach.     

PDLA/PLLA and PDLA/PCL nanofibers with a chitosan‐based hydrogel in composite scaffolds for tissue engineered cartilage

Osteoarthritis (OA) is the most prevalent musculoskeletal disease in humans, causing pain, loss of joint motility and function, and severely reducing the standard of living of patients. Cartilage tissue engineering attempts to repair the damaged tissue of individuals suffering from OA by providing mechanical support to the joint as new tissue regenerates. The aim of this study was to create composite three dimensional scaffolds comprised of electrospun poly(D,L‐lactide)/poly(L‐lactide) (PDLA/PLLA) or poly(D,L‐lactide)/polycaprolactone (PDLA/PCL) with salt leached pores and an embedded chitosan hydrogel to determine the potential of these scaffolds for cartilage tissue engineering. PDLA/PLLA‐hydrogel scaffolds displayed the largest compressive moduli followed by PDLA/PCL‐hydrogel scaffolds. Dynamic mechanical tests showed that the PDLA/PLLA scaffolds had no appreciable recovery while PDLA/PCL scaffolds did exhibit some recovery. Primary canine chondrocytes produced both collagen type II and proteoglycans (primary components of extracellular matrix in cartilage) while being cultured on scaffolds composed of electrospun PDLA/PCL. As a result, a composite electrospun embedded hydrogel scaffold shows promise for treating individuals suffering from OA. Copyright © 2012 John Wiley & Sons, Ltd.