自适应式与固定式生物反馈训练对出口梗阻型便秘患者肛直肠功能和心理状态的影响

目的:探讨自适应式与固定式生物反馈训练对出口梗阻型便秘(OOC)患者肛直肠功能和心理状态的影响。方法:选取2017年4月～2019年12月期间晋城大医院收治的OOC患者98例,根据随机数字表法将患者分为对照组(n=49,固定式生物反馈训练)和研究组(n=49,自适应式生物反馈训练),比较两组患者疗效、肛直肠功能、排便次数、排便困难评分和心理状态。结果:研究组治疗8周后的临床总有效率93.88%(46/49),高于对照组的77.55%(38/49)(P0.05)。两组治疗8周后排便次数增加,排便困难评分降低(P0.05),研究组治疗8周后排便次数多于对照组,排便困难评分低于对照组(P0.05)。两组治疗8周后直肠肛门抑制反射阈、肛管静息压均较治疗前下降,模拟排便时直肠肛管压力梯度较治疗前升高(P0.05)。两组治疗8周后焦虑自评量表(SAS)、抑郁自评量表(SDS)评分均较治疗前下降,且研究组低于对照组(P0.05)。结论:与固定式生物反馈训练相比,自适应式生物反馈训练可获得与之效果相当的肛直肠功能改善程度,并可进一步减轻患者症状及改善心理状态,疗效显著。     

Zinc deficiency aggravates tubulointerstitial nephropathy caused by ureteral obstruction

Ureteral ligation causes tubulointerstitial nephropathy characterized by the tubular dilatation, the interstitial expansion, and a leukocyte infiltration into the tubulointerstitium. The present study was designed to explore whether zinc (Zn) deficiency affects the development of unilateral ureteral obstruction (UUO)-induced tubulointerstitial nephropathy. Compared to rats fed a standard diet, rats fed a Zn-deficient diet exhibited a greater influx of leukocytes into the tubulointerstitium of the cortex of the obstructed kidney 3 d following UUO. Furthermore, rats fed a Zn-deficient diet showed a slight invasion of leukocytes into the tubulointerstitium of the cortex of the contralateral nonobstructed kidney (CLK), although there was no infiltration of leukocytes into the CLK of rats fed a standard diet. These histological changes, however, were ameliorated by administration of enalapril, an angiotensin (ANG) I-converting enzyme inhibitor. Thus, it is suggested that Zn deficiency aggravates UUO-induced tubulointerstitial nephropathy via an increase in the action of ANG II.     

Melatonin attenuates monocrotaline-induced hepatic sinusoidal obstruction syndrome in rats via activation of Sirtuin-3

Melatonin possesses potent hepatoprotective properties, but it remains to be elucidated whether melatonin has a therapeutic effect on monocrotaline (MCT)-induced hepatic sinusoidal obstruction syndrome (HSOS). In this study, male Sprague Dawley rats were intraperitoneally injected with melatonin or the same volume of vehicle at 0 and 24 h after MCT intragastric administration. Next, hematoxylin–eosin staining and electron microscopy were performed to evaluate the hepatic sinusoidal injury of rats. Endothelial cell marker RECA-1 was observed by immunohistochemistry. Hepatic oxidative stress was analyzed by detecting malondialdehyde, glutathione S-transferase, and reactive oxygen species. Assessment of liver function was carried out by analysis of serum aspartate aminotransferase, alanine aminotransferase, total bilirubin, and albumin levels. Real-time polymerase chain reaction and Western blot analysis were used to identify liver Sirtuin-3 (SIRT3) and active matrix metallopeptidase 9 (MMP-9) expression. Besides, liver sinusoidal endothelial cells (LSECs) were used for the in vitro functional verification experiment. Specifically, liver histology of the melatonin-treated groups showed that the pathological damages caused by MCT were significantly attenuated, total HSOS scores were decreased, and the elevation of serum hyaluronic acid observed in the model group was also reduced. Moreover, melatonin treatment also improved the survival of rats after partial hepatectomy. Administration of melatonin ameliorated MCT-induced LSECs injury, hepatic oxidative stress, and hepatic dysfunction. Furthermore, melatonin treatment increased SIRT3 expression while attenuating MMP-9 activity in liver tissues. Cell experiment also demonstrated that SIRT3 might mediate the protective effect of melatonin on LSECs. Collectively, our study provided the potential rationale for the application of melatonin for the prevention of MCT-induced HSOS.     

Expression of stress proteins (HSP-70 and HSP-90) in the rabbit urinary bladder subjected to partial outlet obstruction

Partial obstruction of the rabbit bladder outlet induces a rapid hypertrophy characterized by increased bladder mass, increased smooth muscle content, and increased collagen deposition. In addition, partial outlet obstruction induces decreased contractile responses to both field stimulation and postsynaptic receptor stimulation. Although the morphological and contractile responses to partial outlet obstruction have been well characterized, there is little information on the cellular and molecular mechanisms of these changes. In a previous study, we demonstrated that one of the earliest genes to be expressed following partial outlet obstruction in rabbits was the gene expressing stress protein-70 (HSP-70). In order to further define the genetic and molecular basis of these responses, the expression of stress gene products HSP-70 and HSP-90 in rabbit urinary bladder subjected to partial outlet obstruction has been quantitatively evaluated by Western blot coupled with laser densitometry using anti-HSP-70 and-90 monoclonal antibodies. The data show that stress gene products HSP-70 and HSP-90 are constitutively expressed in control rabbit bladder tissue and transiently increased following partial outlet obstruction. Increased content of HSP-70 was detected at 6 hr after obstruction and reached a maximum (2.7-fold over the control level) at 24 hr. Increased HSP-90 was also detected at 6 hr but reached a maximum (4.5-fold over the control level) at 12 hr. By 7 day post-obstruction, the content of these two proteins returned to the control levels. This study suggests that alterations of stress gene expression resulting in increased HSP-70 and 90 may play an important role in the response of the bladder to partial outlet obstruction.     

外科动物实验中猪的麻醉问题

猪作为重要的实验动物,在外科实验中运用传统的麻醉方法时易引起呼吸道阻塞而死亡,我们使用全麻插管技术,并辅以术前术后各种对症处理,成功地解决了手术中猪因呼吸道阻塞而死亡的问题。     

Surgery for hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a genetically determined cardiac disease characterised by otherwise unexplained myocardial hypertrophy of the left ventricle, and may result in left ventricular outflow tract obstruction. It is the most common cause of sudden cardiac death in young adults due to arrhythmias. Septal myectomy is a surgical treatment for HCM with moderate to severe outflow tract obstruction, and is indicated for patients with severe symptoms refractory to medical therapy. The surgical approach involves obtaining access to the interventricular septum via transaortic, transapical or transmitral approaches, and excising a portion of the hypertrophied myocardium to relieve the outflow tract obstruction. Large, contemporary series from centres experienced in septal myectomy patients have demonstrated a low early mortality of <2 %, excellent long-term survival that matches the general population, and durable relief of symptoms.     

Urine as a source for clinical proteome analysis: From discovery to clinical application

The success of clinical proteome analysis should be assessed based on the clinical impact following implementation of findings. Although there have been several technological advancements in mass spectrometry in the last years, these have not resulted in similar advancements in clinical proteomics. In addition, application of proteomic biomarkers in clinical diagnostics and practical improvement in the disease management is extremely rare. In this review, we discuss the relevant issues associated with identification of robust biomarkers of clinical value. Urine appears to be an ideal source of biomarkers, for theoretical, methodological, and practical reasons. Therefore, this review is focused on the search for biomarkers in urine within the last decade. Urine can be used for non-invasive assessment of a variety of diseases including those affecting the urogenital tract and also other pathologies such as cardiovascular disease or appendicitis. We also discuss the importance of data validation, an essential step in translating biomarkers into the clinical practice. Furthermore, we examine several examples of apparently successful proteomic biomarker discovery studies and their implications for disease diagnosis, prognosis, and therapy evaluation. We also discuss some current challenges in this field and reflect on future research prospects. This article is part of a Special Issue entitled: Biomarkers: A Proteomic Challenge.     

Plasma carbonyls do not correlate with lung function or computed tomography measures of lung density in older smokers

Abstract

Oxidative stress and inflammation are hallmarks of chronic obstructive pulmonary disease (COPD). A critical byproduct of oxidative damage is the introduction of carbonyl groups into amino acid residues. We hypothesize that plasma carbonyl content is inversely correlated with lung function and computed tomography (CT) measures of lung density among smokers and is elevated in COPD. Carbonyl was measured in plasma of participants aged 60 years and older by ELISA. Generalized linear and additive models were used to adjust for potential confounders. Among 541 participants (52% male, mean age 67 years, 41% current smokers), mean plasma carbonyl content was 17.9±2.9 nmol ml^?1 and mean forced expiratory volume in one second (FEV₁) was 80.7±20.9% of predicted. Plasma carbonyl content was inversely associated with FEV₁, but this relationship was largely explained by age. Multivariate analyses ruled out clinically meaningful associations of plasma carbonyl content with FEV₁, FEV₁/FVC (forced vital capacity) ratio, severity of airflow obstruction, and CT lung density. Plasma carbonyl content is a poor biomarker of oxidative stress in COPD and emphysema.     

Up‐regulation of the human‐specific CHRFAM7A gene protects against renal fibrosis in mice with obstructive nephropathy

Renal fibrosis is a major factor in the progression of chronic kidney diseases. Obstructive nephropathy is a common cause of renal fibrosis, which is also accompanied by inflammation. To explore the effect of human‐specific CHRFAM7A expression, an inflammation‐related gene, on renal fibrosis during obstructive nephropathy, we studied CHRFAM7A transgenic mice and wild type mice that underwent unilateral ureteral obstruction (UUO) injury. Transgenic overexpression of CHRFAM7A gene inhibited UUO‐induced renal fibrosis, which was demonstrated by decreased fibrotic gene expression and collagen deposition. Furthermore, kidneys from transgenic mice had reduced TGF‐β1 and Smad2/3 expression following UUO compared with those from wild type mice with UUO. In addition, the overexpression of CHRFAM7A decreased release of inflammatory cytokines in the kidneys of UUO‐injured mice. In vitro, the overexpression of CHRFAM7A inhibited TGF‐β1‐induced increase in expression of fibrosis‐related genes in human renal tubular epithelial cells (HK‐2 cells). Additionally, up‐regulated expression of CHRFAM7A in HK‐2 cells decreased TGF‐β1‐induced epithelial‐mesenchymal transition (EMT) and inhibited activation f TGF‐β1/Smad2/3 signalling pathways. Collectively, our findings demonstrate that overexpression of the human‐specific CHRFAM7A gene can reduce UUO‐induced renal fibrosis by inhibiting TGF‐β1/Smad2/3 signalling pathway to reduce inflammatory reactions and EMT of renal tubular epithelial cells.