Heparin binding epidermal growth factor in renal ischaemia/reperfusion injury

The epidermal growth factor (EGF) receptor and its ligands are crucially involved in the renal response to ischaemia. We studied the heparin binding‐epidermal growth factor (HB‐EGF), a major ligand for the EGF receptor, in experimental and human ischaemia/reperfusion injury (IRI). HB‐EGF mRNA and protein expression was studied in rat kidneys and cultured human tubular (HK‐2) cells that were subjected to IRI and in human donor kidneys during transplantation. The effect of EGF receptor inhibition was investigated in vivo and in vitro. Furthermore, urinary HB‐EGF protein excretion was studied after renal transplantation. Finally, HB‐EGF KO and WT mice were subjected to IRI to study the role of HB‐EGF in renal injury. HB‐EGF mRNA was significantly up‐regulated in the early phase of IRI in rats, cells, and human donor biopsies. Treatment with PKI‐166 reduces macrophage accumulation and interstitial α‐SMA in the early phase of IRI in rats. In vitro, PKI‐166 causes a marked reduction in HB‐EGF‐induced cellular proliferation. Urinary HB‐EGF is increased after transplantation compared with control urines from healthy subjects. HB‐EGF KO mice subjected to IRI revealed significantly less morphological damage after IRI, compared with WT mice. We conclude that IRI results in early induction of HB‐EGF mRNA and protein in vivo and in vitro. Absence of HB‐EGF and inhibition of the EGF receptor in the early phase of IRI has protective effects, suggesting a modulating role for HB‐EGF. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.     

Serum hepatitis B surface antigen correlates with fibrosis and necroinflammation: A multicentre perspective in China

The kinetics of serum hepatitis B surface antigen (HBsAg) during the natural history of hepatitis B virus (HBV) infection has been studied, but the factors affecting them remain unclear. We aimed to investigate the factors affecting HBsAg titres, using data from multicentre, large‐sized clinical trials in China. The baseline data of 1795 patients in 3 multicentre trials were studied, and the patients were classified into 3 groups: hepatitis B early antigen (HBeAg)‐positive chronic HBV infection (n = 588), HBeAg‐positive chronic hepatitis B (n = 596), and HBeAg‐negative chronic hepatitis B (n = 611). HBsAg titres in the different phases were compared, and multiple linear progression analyses were performed to investigate the implicated factors. HBsAg titres varied significantly in different phases (P = .000), with the highest (4.60 log10 IU/mL [10%‐90% confidence interval: 3.52 log10 IU/mL‐4.99 log10 IU/mL]) in patients with HBeAg‐positive chronic HBV infection. In all phases, age and HBV DNA were correlated with serum HBsAg level. In HBeAg‐positive chronic hepatitis B patients, a negative correlation between HBsAg titres and fibrosis stage was observed. Alanine amonitransferase or necroinflammatory activity was also correlated with HBsAg titres in HBeAg‐negative chronic hepatitis B patients. In conclusion, decreased HBsAg titres may be associated with advancing fibrosis in HBeAg‐positive chronic hepatitis B patients or increased necroinflammation in those with HBeAg‐negative chronic hepatitis B. Our findings may help clinicians better understand the kinetics of HBsAg and provide useful insights into the management of this disease.     

Consumption of milk with added casein phosphopeptide-amorphous calcium phosphate remineralizes enamel subsurface lesions in situ

Background:  Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) is an anticariogenic agent that is suitable to be added to foods. The aim of this double-blind, three-way crossover randomized study was to investigate the capacity of CPP-ACP, when added to bovine milk, to remineralize enamel subsurface lesions in situ .
Methods:  Ten subjects drank 100 mL of bovine milk containing no added CPP-ACP (control milk), 0.2% (w/v) CPP-ACP or 0.3% (w/v) CPP-ACP, for 30 seconds once daily for 15 days, whilst wearing removable appliances with attached slabs of enamel containing subsurface enamel lesions. After each treatment and a one-week washout period, subjects crossed over to another treatment and this was repeated until they had consumed each of the three milk products. At the completion of each treatment the enamel slabs were removed and remineralization was determined using microradiography.
Results:  The results demonstrated that all three milk samples remineralized enamel subsurface lesions in situ . However, the two milk samples containing added CPP-ACP each produced significantly greater remineralization than the control milk.
Conclusions:  The remineralizing effect of CPP-ACP in milk was dose-dependent with milk containing 0.2% CPP-ACP and 0.3% CPP-ACP producing an increase in mineral content of 81% and 164%, respectively, relative to the control milk.     

防治术后高龄肺癌患者心律失常47例

1 临床资料唐都医院胸腔外科自2000-01/2002-01年间共施行高龄肺癌手术216(男167,女49)例,年龄70～82岁,平均年龄75岁.术前心电图异常42例,低氧血症23例,阻塞性和限制性肺通气功能障碍32例.其中行全肺切除15例,肺叶切除163例,肺楔形切除38例.     

Surfactant protein B deficiency: Clinical, histological and molecular evaluation

Congenital alveolar proteinosis due to surfactant protein B deficiency is an inherited disease which results in severe respiratory failure in term infants soon after birth. The pathophysiologic basis of this disease is now known to be an inability to synthesise adequate quantities of normally functioning surfactant protein B. We report a male infant with fatal respiratory failure of neonatal onset, and histopathological features typical of those seen in congenital alveolar proteinosis. Molecular analysis of genomic DNA revealed two mutations, the 'common' 121ins2 mutation in exon 4, and a novel 2bp frameshift mutation in exon 5. We believe this is the first Australian case of surfactant protein B deficiency confirmed by molecular analysis.     

Benzodiazepines inhibit the rate of neutrophil apoptosis

Background Benzodiazepines, which are commonly administered perioperatively, can depress immune function. Neutrophil apoptosis plays a central role in the regulation of inflammation. This is particularly important during and after surgery. Aim To examine the effects of benzodiazepines (midazolam and diazepam) on neutrophil apoptosis. Methods Venous blood samples were withdrawn from patients scheduled to undergo elective surgery, (a) immediately prior to, and 10 minutes after administration of midazolam 0.2mg/kg intravenously (n=11) and (b) immediately prior to, and 60 minutes after administration of diazepam 10mg po (n=10). Neutrophil apoptosis was measured by Annexin VFITC after 1 and 12 hours in culture. Results The percentage of apoptotic cells was significantly less after midazolam at 12% (11.9) hours in culture compared to pre-midazolam 29.7% (13.3) (p<0.05). After diazepam, the rates of neutrophil apoptosis were also significantly less after 12 hours in culture (p<0.05). Conclusion Administration of benzodiazepines in clinically relevant doses inhibits neutrophil apoptosis. In the perioperative period, this may influence the inflammatory response to surgery.     

Prevalence of asymptomatic left ventricular systolic dysfunction in hypertensive Nigerians: echocardiographic study of 832 subjects

Background

We sought to determine the prevalence of echocardiographically determined left ventricular systolic dysfunction in asymptomatic hypertensive subjects seen in Abeokuta, Nigeria.

Methods

Echocardiography was performed in 832 consecutive hypertensive subjects referred for cardiac evaluation over a three-year period.

Results

Data were obtained in 832 subjects (50.1% women) aged 56.0 ± 12.7 years (men 56.9 ± 13.3 years, women 55.0 ± 12.0 years, range 15–88). The prevalence of left ventricular systolic dysfunction (LVSD) was 18.1% in the study population (mild LVSD = 9.6%, moderate LVSD = 3.7% and severe LVSD = 4.8%). In a multivariate analysis, male gender, body mass index and LV mass were the predictors of LVSD.

Conclusion

Significant numbers of hypertensive subjects in this study had varying degrees of left ventricular systolic dysfunction. Early introduction of disease-modifying drugs in these patients, such as angiotensin converting enzyme inhibitors or angiotensin receptor blockers may retard or prevent the progression to overt heart failure.