中医针灸对慢性胃炎患者慢性疼痛的临床观察及效果分析

对慢性胃炎患者接受治疗后的效果,提升的胃肠动力水平,以及药物反应及复发率来做系统性的比较分析。方法 这是挑选了50位慢性胃炎患者,通过随机分组方法,分成两个组,每组有25人。一组按照常规的医药发方,另一组则除常规的医方外,引入中医的针灸疗法。结果 试验终结之后,引用针灸疗法的对照组别明显比常规组别更有优势,胃肠动力水平也明显上升。针灸组中药物引起的负面效应发生率(4.00%)、慢性胃炎复发率(4.00%)都明显比常规组低(分别为24.00%和32.00%)。结论 中医针灸治疗能有效改善慢性胃炎患者治疗后的病症反应,提升胃肠动力水平,同时降低了慢性胃炎的复发率以及用药不良反应发生率,对于慢性胃炎患者治疗具有显著效果。

中医治疗骨伤后期肢体肿胀的效果

目的:探讨对骨伤后期肢体肿胀患者给予中医治疗后获得临床效果。方法:对我院时间范围处于2023年6月—2023年11月阶段的90例骨伤后期肢体肿胀患者展开分组对比研究;所有肢体肿胀患者的分组依据为投掷硬币法;参照组(45例):采用的治疗方法为西医治疗;研究组(45例):采用的治疗方法为中医治疗;组间比较两组骨伤后期肢体肿胀患者的疾病疼痛评分、肢体肿胀程度、病症反应消失时间、骨伤恢复情况以及并发症总发生率。结果:治疗前,与参照组疾病疼痛评分、肢体肿胀程度比较,研究组差异不明显(P>0.05);治疗后,与参照组疾病疼痛评分、肢体肿胀程度比较,研究组降低程度明显(P<0.05);与参照组疼痛、患肢皮纹消失、肿胀、张力性水泡消失时间展开比较,研究组缩短程度明显(P<0.05);与参照组骨痂生长时间、患肢运动功能恢复时间、住院时间比较,研究组缩短程度明显(P <0.05);与参照组并发症(患肢肌肉痉挛、肌肉坏死以及血栓)总发生率比较,研究组降低程度明显(P<0.05)。结论:临床对骨伤后期肢体肿胀患者给予中医治疗,可将疼痛以及肢体肿胀缓解,将病症消失时间缩短,促进良好预后。

走出疑病性反应的阴霾

“这个学期的体育选修课，我选的是健美操，提起来我就有些生气，不知怎的，身体就是不灵活，手和腿只要同时做动作，我就不知东南西北，真没辙儿。但我现在很开心。……这封信是我上数学课写的，我会经常和您联系，希望您别忘了我这个学生。”我怎么能忘记她呢?看着小雨从大学寄给我的信，我的眼前仿佛又出现了校园中那个每天紧锁愁眉，拖着一条腿走路的女生。

Fenofibrate for patients with asymptomatic primary biliary cirrhosis

AIM:Primary biliary cirrhosis (PBC) is a chronic, cholestatic disease of autoimmune etiology,the histology of which shows a destruction of the intrahepatic bile duct and portal inflammation. Ursodeoxycholic acid (UDCA) is now used as a first-line drug for asymptomatic PBC (aPBC) because it is reported that UDCA decreases mortality and prolongs the time of liver transplantation.However, only 20-30% of patients respond fully to UDCA.Recently,lipoprotein-lowering agents have been found to be effective for PBC.The aim of this study was to examine the safety and efficacy of fenofibrate, a member of the fibrate class of hypolipidemic and anti-inflammatory agent via peroxysome proliferatory-activated receptor α,in patients with aPBC.METHODS:Fenofibrate was administered for twelve weeks in nine patients with aPBC who failed to respond to UDCA.UDCA was used along with fenofibrate during the study.The data from aPBC patients were analyzed to assess the biochemical effect of fenofibrate during the study.RESULTS: The serum levels of alkaline phosphatase (ALP)(285±114.8IU/L) and immunoglobulin M (IgM) (255.8±85.9mg/dl) significantly decreased to 186.9±76.2IU/L and 192.9±67.5mg/dL respectively, after fenofibrate treatment in patients with aPBC (P<0.05). Moreover,the titer of antimitochondrial antibody (AMA) also decreased in 4 of 9 patients with aPBC. No adverse reactions were observed in any patients.CONCLUSION:Fenofibrate appears to be significantly effective in treating patients with aPBC who respond incompletely to UDCA alone.Although the mechanism of fenofibrate on aPBC has not yet been fully clarified,combination therapy using fenofibrate and UDCA might be related to the anti-immunological effects, such as the suppression of AMA production as well as its antiinflammatory effect.

Helicobacter pylori infection and respiratory diseases:a review

In the past few years,a variety of extradigestive disorders, including cardiovascular,skin,rheumatic and liver diseases, have been associated with Helicobacter pylori(H.pylori) infection.The activation of inflammatory mediators by H.pylori seems to be the pathogenetic mechanism underlying the observed associations.The present review summarizes the current literature,including our own studies,concerning the association between H.pyloriinfection and respiratory diseases. A small number of epidemiological and serologic,case- control studies suggest that H.pylori infection may be associated with the development of chronic bronchitis.A frequent coexistence of pulmonary tuberculosis and H.pylori infection has also been found.Moreover,recent studies have shown an increased H.pyloriseroprevalence in patients with bronchiectasis and in those with lung cancer.On the other hand,bronchial asthma seems not to be related with H.pylori infection. All associations between H.pylori infection and respiratory diseases are primarily based on case-control studies, concerning relatively small numbers of patients.Moreover, there is a lack of studies focused on the pathogenetic link between respiratory diseases and H.pylori infection. Therefore,we believe that larger studies should be undertaken to confirm the observed results and to clarify the underlying pathogenetic mechanisms.

Importance of nutrition in inflammatory bowel disease

Inflammatory bowel disease （IBD） results from the interaction between an individual＇s immune response and precipitant environmental factors, which generatean anomalous chronic inflammatory response in thosewho are genetically predisposed. Various feeding practices have been implicated in the origin of IBD based on epidemiological observations in developed countries, but we do not have solid evidence for the etiological role played by specific food types. IBD is associated with frequent nutritional deficiencies, thepattern and severity of which depends on the extent,duration and activity of the inflammation. Nutritional support allows these deficiencies in calories, macro and micronutrients to be rectified. Enteral nutrition is also aprimary therapy for IBD, especially for Crohn＇s disease,as it allows the inflammatory activity to be controlled,kept in remission, and Drevents or delays the need forsurgery. Nutritional support is especially important in childhood IBD as an alternative to pharmacological treatment. This report discusses the complex relationship between diet and IBD.

T cell immune response is correlated with fibrosis and inflammatory activity in hepatitis B cirrhotics

AIM： TO explore the relationship among interferon-γ （IFN-γ） activity, fibrogenesis, T cell immune responses and hepatic inflammatory activity. METHODS： Peripheral blood samples from a total of 43 hepatitis B cirrhotic patients （LC） and 19 healthy controls （NC） were collected to measure their serum levels of IFN-γ, interleukin-2 （IL-2）, soluble interleukin-2 receptor （sIL-2R）, interleukin-10 （IL-10） and three serological markers of fibrosis including hyaluronic acid （HA）, procollagen type III peptide （PIIIP）, and type iV collagen were measured using a double antibody sandwich ELISA. Also, serum total bilirubin （TB） and alanine aminotransferase （ALT） were measured by routine measures. RESULTS： The concentrations of serological markers of fibrosis in patients with active cirrhosis （ALC） were significantly higher than those in stationary liver cirrhosis （SLC） or NC groups. The levels of serological markers in HBeAg-positive patients were significantly higher than those in HBeAg-negative patients. In SLC and ALC patients, a negative linear correlation was found between IFN-γ levels and the serological markers of fibrosis. IFN-γ and IL-2 levels in the ALC group were significantly higher than those in the SLC and NC groups, but the statistical difference was not significant between the latter two. In contrast, IL-10 levels in the SLC group were significantly higher than that in the NC group, but no significant difference was found between SLC and ALC groups. The sIL-2R level was elevated gradually in all these groups, and the differences were significant. Positive linear correlations were seen between IFN-γ activity and ALT levels （r = 0.339, P 〈 0.05）, and IL-2 activity and TB levels （r = 0.517, P 〈 0.05）. sIL-2R expression was positively correlated with both ALT and TB levels （r = 0.324, 0.455, P 〈 0.05）, whereas there was no statistically significant correlation between IL-10 expression and serum ALT and TB levels （r = -0.102, -0.093, P 〉 0.05）. Finally, there was a positive correlation between IFN-γ and IL-2 levels. CONCLUSION： T cell immune responses are correlated with fibrosis and hepatic inflammatory activity and may play an important role in liver cirrhosis.

Neuropsychological alterations in hepatitis C infection:The role of inflammation

About 50% of patients with hepatitis C virus(HCV)infection complain of neuropsychiatric symptoms,"brain fog",weakness,fatigue,and exhibit some degree of quality of life impairment,irrespective of the severity of liver disease.Since the first observation of HCV-related cognitive deficits,10 studies have been published that have evaluated neuropsychiatric performance in patients with HCV infection and different degrees of hepatic impairment.Unfortunately,these have often included patients with cirrhosis,patients who had acquired the infection through previous intravenous drug misuse,who had a history of relatively recent treatment with interferon,or were on psychoactive medication.In addition,different neuropsychological batteries and tests that explored different cognitive domains were used,which makes the results of the studies difficult to compare.Finally,limited information is available on the pathogenesis of HCV-related cognitive impairment.Cerebral and/or systemic inflammation may be important players but their potential role has not been substantiated by experimental data.The present review outlines the available evidence of the presence of cognitive impairment in patients with HCV infection,with a focus on the potential relationship with cerebral and/or systemic inflammation.

Protective Effect of Emodin against Lipopolysaccharides-induced Corneal Injury in Rats

Objective To investigate the effect of emodin on lipopolysaccharides （LPS）-induced corneal injury in rats. Methods Three parallel incisions on the central surface of corneal epithelium were made and LPS was applied on them to induce corneal injury in Wistar rats. All rats were randomly divided into emodin group （n=40） and keratitis group （n=40）. Rats in the emodin group received subconjunctival injection of emodin and rats in the keratitis group received its vehicle 30 minutes before LPS exposure. At different time points-1 3, 6, 12, and 24 hours after LPS exposure, the symptoms of all rats were observed and the severity of their ocular inflammation was examined with a slit lamp microscope, then 8 rats in each group were killed through cervical dislocation and their eyes were enucleated and prepared to observe pathological changes of corneal tissue under a light microscope. The activation of nuclear factor-loB （NF-κB） under different condi- tions was determined by Western blot. Immunocytochemistry staining with an antibody against intercellular adhesion molecule-1 （ICAM-1） was performed to identify positive cells in corneal tissues. Results The model of acute keratitis was successfully established in Wistar rats. LPS could induce a typical corneal inflammatory response, such as hyperemia, corneal edema and opacity, which were observed in model rats. Compared with keratitis group, both ocular behaviors and damages of the corneal structure were improved in emodin group. Furthermore, the activation of NF-κB and the expression of ICAM-1 induced by LPS were markedly inhibited in emodin group. Conclusion Emodin can inhibit the activation of NF-κB and the expression of ICAM-I induced by LPS in corneas, protect against acute corneal injury, and improve symptoms in rats.

Potential role of Th17 cells in the pathogenesis of inflammatory bowel disease

The etiopathology of inflammatory bowel disease （IBD） remains elusive. Accumulating evidence suggests that the abnormality of innate and adaptive immunity responses plays an important role in intestinal inflam- mation. IBD including Crohn＇s disease （CD） and ulcerative colitis （UC） is a chronic inflammatory disease of the gastrointestinal tract, which is implicated in an inappropriate and overactive mucosal immune response to luminal flora. Traditionally, CD is regarded as a Thl- mediated inflammatory disorder while UC is regarded as a Th2-1ike disease. Recently, Th17 cells were identified as a new subset of T helper cells unrelated to Thl or Th2 cells, and several cytokines [e.g. interleukin （IL）-21, IL-23] are involved in regulating their activation and differentiation. They not only play an important role in host defense against extracellular pathogens, but are also associated with the development of autoimmunity and inflammatory response such as IBD. The identification of Th17 cells helps us to explain some of the anomalies seen in the Thl/Th2 axis and has broadened our understanding of the immunopathological effects of Th17 cells in the development of IBD.

Helicobacter pylori infection and endocrine disorders:Is there a link?

Helicobacter pylori(H pylori) infection is a leading world-wide infectious disease as it affects more than half of the world population and causes chronic gastritis,peptic ulcer disease and gastric malignancies.The infection elicits a chronic cellular inflammatory response in the gastric mucosa.However,the effects of this local inflammation may not be confi ned solely to the digestive tract but may spread to involve extraintestinal tissues and/or organs.Indeed,H pylori infection has been epidemiologically linked to extra-digestive conditions and diseases.In this context,it has been speculated that H pylori infection may be responsible for various endocrine disorders,such as autoimmune thyroid diseases,diabetes mellitus,dyslipidemia,obesity,osteoporosis and primary hyperparathyroidism.This is a review of the relationship between H pylori infection and these endocrine disorders.

Nutritional stimulation of the autonomic nervous system

Disturbance of the inflammatory response in the gut is important in several clinical diseases ranging from inflmmatory bowel disease to postoperative ileus. Several feedback mechanisms exist that control the inflammatory cascade and avoid collateral damage. In the gast rointestinal tract, it is of particular importance tocontrol the immune response to maintain the balance that allows dietary up take and utilization of nutrientson one hand, while preventing invasion of bacteria and toxins on the other hand. The process of digestion and absorption of nutrients requires a relative hyporesponsiveness of the immune cells in the gut to luminacontents which is not yet fully understood. Recentlythe autonomic nervous system has been identifi ed asan important pathway to control local and systemic inflammation and gut barrier integrity. Activation of thepathway is possible via electrical or via pharm acological interventions, but is also achieved in a physiologicamanner by ingestion of dietary lipids. Administration of dietary lipids has been shown to be very effectivein reducing the inflammatory cascade and maintaining intestinal barrier integrity in several experimental studies. This beneficial effect of nutrition on the inflammatory response and intestinal barrier integrity opens new therapeutic opportunities for treatment of certain gastrointestinal disorders. Furthermore, this neural feedback mechanism provides more insight in the relative hyporesponsiveness of the immune cells in the gut. Here, we will discuss the regulatory function of the autonomic nervous system on the inflammatory response and gut barrier function and the potential benefit in a clinical setting.

Exceptionally rare cause of a total stomach resection

The first-ever case of a 54-year-old woman who overdosed on non-steroidal anti-inflammatory drugs in an attempt at suicide.Before that incident,she had not been treated for coexisting diseases such as rheumatoid arthritis or depression.At the time of admission to the General Surgery Department,the patient reported pains in the epigastric region with accompanying nausea and vomiting with mucous content as well as the inability to ingest food orally.Despite parenteral and enteral feeding,the patient exhibited a drop in body mass.The histopathologic examination of a sample taken from the stomach during gastroscopy showed some non-specific necrotic and inflammatory masses with granulation.Intraoperatively,a very small,infiltrated stomach with an initial section of duodenum was identified.A total stomach resection together with the reconstruction of digestive tract continuity was performed using the Roux-Y method.Histopathologic examination of the stomach revealed a deep,chronic and exacerbated inflammatory condition with an extensive ulceration over the entire length of the stomach,reaching up to the pylorus.Additionally,numerous lymphatic glands with inflammatory reaction changes were observed.

按摩治疗疾病过程中触诊的必要性

经络反应病症,多反应在体表筋肉,有的在经、在穴,有的非经非穴.有的是疾病反应,有的本身就是疾病.随疾病的发生发展和治疗过程中消长.所以按摩者在施术的过程中必须把触诊贯穿始终,以掌握病情的发展变化.

Hepatitis C comorbidities affecting the course and response to therapy

Several studies have demonstrated that the outcome of chronic hepatitis C (CHC) infection is profoundly influenced by a variety of comorbidities. Many of these comorbidities have a significant influence on the response to antiviral therapy. These comorbidities negatively affect the course and outcome of liver disease, often reducing the chance of achieving a sustained virological response with PEGylated interferon and ribavirin treatments. Comorbidities affecting response to antiviral therapy reduce compliance and adherence to inadequate doses of therapy. The most important comorbidities affecting the course of CHC include hepatitis B virus coinfection, metabolic syndrome, and intestinal bacterial overgrowth. Comorbidities affecting the course and response to therapy include schistosomiasis, iron overload, alcohol abuse, and excessive smoking. Comorbidities affecting response to antiviral therapy include depression, anemia, cardiovascular disease, and renal failure.

Human endogenous retroviruses and cancer

Human endogenous retroviruses(HERVs) are retroviruses that infected human genome millions of years ago and have persisted throughout human evolution. About 8% of our genome is composed of HERVs, most of which are nonfunctional because of epigenetic control or deactivating mutations. However, a correlation between HERVs and human cancer has been described and many tumors, such as melanoma, breast cancer, germ cell tumors, renal cancer or ovarian cancer, express HERV proteins, mainly HERV-K(HML6) and HERV-K(HML2). Although the causative role of HERVs in cancer is controversial, data from animal models demonstrated that endogenous retroviruses are potentially oncogenic. HERV protein expression in human cells generates an immune response by activating innate and adaptive immunities. Some HERV-derived peptides have antigenic properties. For example, HERV-K(HML-6) encodes the HER-K MEL peptide recognized by CD8+ lymphocytes. In addition, HERVs are twoedged immunomodulators. HERVs show immunosuppressive activity. The presence of genomic retroviral elements in host-cell cytosol may activate an interferon type I response. Therefore, targeting HERVs through cellular vaccines or immunomodulatory drugs combined with checkpoint inhibitors is attracting interest because they could be active in human tumors.

EXPERIENCE IN THE POINT-SELECTION FOR ELECTRO-ACUPUNCTURE

Point selection along the course of meridians is the basic principle for acupuncture prescription and selection of points. In application, there are three categories of point selection: selection of local and adjacent points; selection of distant points, and selection of symptomatic points. Based on the

精细化护理对胸部创伤患者预防肺部感染的效果分析

胸部发生创伤易导致多重并发症的发生，使患者的生活质量受严重影响。针对此病症，医护人员多主张实施手术方法治疗。但由于胸部创伤术具有一定的特殊性，易造成肺部感染的发生，再加上患者受伤后其机体免疫能力相对较差，从而容易引发不良病症反应的发生，如急性呼吸功能缺乏等。

Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy

Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac 1 and Epac2, are cAMP mediators playing important roles in maintenance of endothelial barrier and neuronal functions To investigate the roles of Epacs in the pathogenesis of ischemic retinopathy, transient middle cerebral artery occlusion （tMCAO） was performed on Epacl-deficient （Epacl-/- ） mice, Epac2-deficient （Epac2-/-） mice, and their wild type counter-parts （Epacl＋/＋ and Epac2＋/＋）. Two-hour occlusion and 22-hour reperfusion were conducted to induce ischemia/reperfusion injury to the retina. After tMCAO, the contralateral retinae displayed similar morphology between different genotypes. Neu-ronal loss, retinal edema and increase in immunoreactivity for aquaporin 4 （AQP4）, glial fibrillary acidic protein （GFAP）, peroxiredoxin 6 （Prx6） were observed in ipsilateral retinae. Epac2 / ipsilateral retinae showed more neuronal loss in retinal ganglion cell layer, increased retinal thickness and stronger immunostaining of AQP4, GFAP, and Prx6 than those of Epac2＋/＋. However, Epacl-/- ipsilateral retinae displayed similar pathology as those in Epacl＋/＋ mice. Our observations suggest that Epac2-deficiency led to more severe ischemic retinopathy after retinal ischemia/reperfusion injury.