全程系统化护理干预对慢性前列腺炎病人治疗效果及依从性的影响

[目的]探讨全程系统化护理干预对慢性前列腺炎(CP)病人治疗依从性的影响.[方法]将100例确诊为慢性前列腺炎病人随机分为对照组和观察组,时照组给予常规护理;观察组除接受常规护理外,同时给予全程系统化护理干预(包括建立信赖基础、认知干预、心理干预、行为干预及跟踪随访).护理干预前后用CP症状积分指数表(NIH-CPSI)、自制的病人健康行为问卷调查表、自制的病人治疗依从性问卷调查表进行评价.[结果]两组干预前后CP症状、焦虑情绪均有改善;观察组疼痛不适、生活质量、焦虑评分、健康行为、治疗依从性改善明显优于对照组(P<0.05).[结论]对CP病人实施全程系统化护理干预,能帮助病人知晓CP的相关知识,改善认知态度,选择有益的生活方式,坚持遵医嘱用药、体格检查,提高CP病人的治疗依从性及生活质量.     

腓肠神经营养血管皮瓣在足部皮肤缺损中的应用

目的探讨腓肠神经营养血管皮瓣在足部皮肤缺损中的应用。方法于2002年3月-2008年3月应用腓肠神经营养血管皮瓣修复因各种原因引起的足部皮肤缺损,共修复52例56处缺损,对照同期其余皮瓣修复效果,进行分析比较。结果52例56处皮瓣修复,54处皮瓣完全成活,一处出现血肿,经清除血肿,皮瓣成活;另一处出现皮瓣远端部分坏死,经换药,坏死组织清除,遗留少许创面,予直接缝合关闭创面,伤口愈合好。52例病人均得到随访,时间半年至2年,皮瓣外形满意,功能良好。结论腓肠神经营养血管皮瓣修复足部皮肤缺损简单易行,手术时间短,皮瓣切取容易,不臃肿,肢体外形功能满意,是修复足部皮肤缺损的理想皮瓣。     

机械纺织工人畸变产物耳声发射的临床研究

目的研究畸变产物耳声发射(distortion product otoacoustic emissions,DPOAE)在监测和早期发现噪声性聋(noise induced hearingloss,NIHL)方面的应用价值。方法检测160名(285耳)机械纺织工人(其中噪声性聋组125例224耳,有噪声接触史但纯音听阈正常者为对照组,共35例61耳)和75名听力正常人(正常对照组)的鼓室导抗图、镫骨肌反射、纯音听阈及DPOAE,比较三组的DPOAE幅值和引出率。结果①噪声性聋组DPOAE幅值及引出率均较正常对照组明显下降(P<0.05);②对照组与正常对照组比较,对照组的DPOAE幅值在4kHz处、引出率在3~6kHz处明显下降(P<0.05);③随着接触噪声工龄的延长,DPOAE引出率逐渐下降(P<0.05)。结论DPOAE可以客观地监测和早期发现噪声性聋,较纯音测听更有意义。     

NLRP3 deficiency protects from type 1 diabetes through the regulation of chemotaxis into the pancreatic islets

Studies in animal models and human subjects have shown that both innate and adaptive immunity contribute to the pathogenesis of type 1 diabetes (T1D). Whereas the role of TLR signaling pathways in T1D has been extensively studied, the contribution of the nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein (NLRP) 3 inflammasome pathway remains to be explored. In this study, we report that NLRP3 plays an important role in the development of T1D in the nonobese diabetic (NOD) mouse model. NLRP3 deficiency not only affected T-cell activation and Th1 differentiation, but also modulated pathogenic T-cell migration to the pancreatic islet. The presence of NLRP3 is critical for the expression of the chemokine receptors CCR5 and CXCR3 on T cells. More importantly, NLRP3 ablation reduced the expression of chemokine genes CCL5 and CXCL10 on pancreatic islet cells in an IRF-1–dependent manner. Our results suggest that molecules involved in chemotaxis, accompanied by the activation of the NLRP3 inflammasome, may be effective targets for the treatment of T1D.Type 1 diabetes (T1D) is a T-cell–mediated autoimmune disease characterized by the destruction of insulin-producing pancreatic beta cells in genetically predisposed individuals. Studies in animal models and human subjects have shown that both innate and adaptive immunity play a role in disease pathogenesis. Strategies targeting either T or B cells have shown some efficacy in T1D in both animal and human studies (1–4). Recently, the role of innate immunity in T1D has been increasingly appreciated. We, and others, have demonstrated that Toll-like receptor (TLR) signaling pathways are essential for the development of T1D. Nonobese diabetic (NOD) mice deficient in TLR2, TLR9, or MyD88 showed delayed disease development or were protected from diabetes (5–9). However, the development of autoimmune diabetes was accelerated in TLR4^−/− NOD mice (5–7, 10). Whereas the role of TLR signaling has been intensively studied, the contribution of the nucleotide binding domain-like receptor (NLR) signaling pathway to the pathogenesis of T1D remains to be explored.Nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein (NLRP) 3 is a NLR family member, together with ASC and caspase-1, forms protein complexes that are responsible for the innate immune response to pathogens and/or “danger” signals (11). Increasing evidence indicates that the NLRP3 inflammasome plays an important role in obesity and type 2 diabetes (12–14). However, little is known about the role of NLRP3 in autoimmune diabetes. Whereas the inflammasome has been extensively studied in the control of infection, only recently has the role of the NLRP inflammasome in autoimmune disease been recognized. Polymorphisms in inflammasome genes are involved in the predisposition to systemic lupus erythematosus (15). NLRP3 deficiency dramatically delayed the course and reduced severity of experimental autoimmune encephalomyelitis by suppression of Th1 and Th17 responses (16). Mice deficient in ASC, the adaptor protein of the NLRP3 inflammasome pathway, were also less susceptible to collagen-induced arthritis (17). Nevertheless, the role of the inflammasome pathway in the pathogenesis of T1D is unclear. Although caspase-1 or IL-1β deficiency did not protect NOD mice from T1D (18, 19), IL-1 blockade showed a synergistic protective effect when combined with anti-CD3 therapy for T1D in a mouse model (20). Interestingly, recent genetic association studies suggested that polymorphisms in inflammasome genes might be involved in the predisposition to T1D. A coding polymorphism in NLRP1 was demonstrated to confer susceptibility to T1D (21). Furthermore, two single-nucleotide polymorphisms in NLRP3 were identified in a separate association study as a predisposing factor for T1D (22).Thus, we generated NLRP3-deficient (NLRP3^−/− or KO) NOD mice to understand the role of NLRP3 in the pathogenesis of T1D. Here, we show that NOD mice deficient in NLRP3 were protected from T1D development. Mechanistic studies suggested that the expression of NLRP3, in both hematopoietic and nonhematopoietic cells, was important for diabetes development. Whereas NLRP3 deficiency in the hematopoietic compartment reduced the diabetogenicity of immune cells, its ablation in nonhematopoietic cells, particularly in the pancreatic islets, compromised the migration of immune cells into the target tissue. Destruction of beta cells was reduced via the down-regulation of chemokine gene expression in the pancreatic islets leading to protection from diabetes.     

Protective effects of berberine on high fat-induced kidney damage by increasing serum adiponectin and promoting insulin sensitivity

Berberine (BBR) has been reported in several studies in cell and animal models. However, the mechanism of actions is not fully understood. The present study was therefore aimed to explore the effects of berberine on insulin sensitivity and kidney damage in a high fat diet rat model. Impaired glucose tolerance rats induced by injection of berberine while fed with high fat laboratory chow. After rats were treated for 4 weeks, OGTT and IPITT were determined. Mass and PAS were used to study the kidney tissue. ELISA was used to detect the protein concentration of CRP and TNF-α. Western blot was used to detect the proteins adiponectin, adipoR1, adipoR2 and p-AMPK expression level. These encouraging findings suggest that berberine has excellent pharmacological potential to prevent kidney damage.     

Development of a diabetes mobile healthcare system and clinical application in China: a narrative review

Journal of Public Health - With the rapid development and spread of information technology, mobile healthcare (M-healthcare) is emerging as a feasible option for improved monitoring and treatment...     

创意经济时代高等院校文化创意人才培养方式探析

资本的时代已经过去,创意的时代已经来临,创意产业已经成了新的经济增长点。但目前高等院校的人才教育培养方式与创意经济时代的发展还存在一些不相适应的地方,本文旨在初步探析创意经济时代高等院校文化创意人才培养方式。     

1例阴茎异常勃起症病人的护理

阴茎异常勃起症是一种与性刺激和性欲无关的阴茎持续性痛性勃起[1]。临床较少见,大部分原因不清,少部分与阴茎或会阴部外伤、白血病、服用抗精神病药、镰状细胞贫血、阴茎背静脉栓塞等有关[2]。2005年9月我科收治1例阴茎异常勃起症病人行阴茎头、阴茎海绵体分流术,效果满意。现报告如下。1病例简介病人,男,36岁,因阴茎无性欲持续勃起10余天入院。查体:阴茎极度勃起,表面暗红,明显触痛,呈持续性,病人感阴茎胀痛伴排尿困难。病人10年前患精神分裂症,长期服用氯丙嗪等抗精神病药物,诊断为阴茎异常勃起症。立即给予阴茎海绵体冲洗法治疗,效果不…     

实验性肝硬化血浆内源性阿片肽含量的变化及其意义

目的：通过检测实验性肝硬化变各阶段三种内源性阿片肽（ＥＯＰ）血浆浓度变化，探讨其与肝硬化高动力循环状态及腹水形成的关系，方法：应用放射免疫法测定了四氯化碳（ＣＣｌ４）诱发大鼠肝硬化过程中血浆三种ＥＯＰ的含量变化。结果：结果显示肝硬化腹水组及肝硬化无腹水线血浆亮啡肽（Ｌ－ＥＮＫ）强啡肽（ＤｙｎＡｌ－１３）含量均显著高于正常对照组（Ｐ〈０．０１，Ｐ〈０．０５），而且升高的水平与肝功能损害的程度呈显著正