Pathophysiology of severe gallstone pancreatitis:A new paradigm

Severe gallstone pancreatitis(GSP)refractory to maximum conservative therapy has wide clinical variations,and its pathophysiology remains controversial.This Editorial aimed to investigate the pathophysiology of severe disease based on Opie’s theories of obstruction,the common channel,and duodenal reflux and describe its types.Severe GSP might be a hybrid disease with pathology polarized between acute cholangitis with mild pancreatitis(biliary type)and necrotizing pancreatitis uncomplicated with biliary tract disease(pancreatic type),in which hepatobiliary and pancreatic lesion severity is inversely related to the presence or absence of impacted ampullary stones.Severe GSP is caused by stones that are persistently impacted at the ampulla with biliopancreatic obstruction(biliary type),and probably,stones that are either temporarily lodged at the duodenal orifice or passed into the duodenum,thereby permitting reflux of bile or possible duodenal contents into the pancreas(pancreas type).When the status of the stones and the presence or absence of impacted ampullary stones with biliopancreatic obstruction are determined,the clinical course and outcome can be predicted.Gallstones represent the main cause of acute pancreatitis globally,and clinicians are expected to encounter GSP more often.Awareness of the etiology and pathogenesis of severe disease is mandatory.

Mpox and related poxviruses:A literature review of evolution,pathophysiology,and clinical manifestations

The recently re-emerged mpox(monkeypox)virus that causes mpox disease is a member of genus Orthopoxvirus and has unprecedentedly spread worldwide.Numerous studies have contributed to our understanding of its evolution,pathophysiology,and clinical manifestations.The current outbreak of the mpox virus depicts its novel route of transmission as a new variant.However,the exact reason for its transition from an epidemic to a pandemic remains unclear.Furthermore,other poxviruses such as vaccinia virus,variola virus,and cowpox virus,also belong to the same genus,Orthopoxvirus.In the present review,our objective was to summarize the evidence on evolution,pathophysiology,and clinical manifestations of mpox virus and its related poxviruses.The present review would aid in a better understanding of the current circulating mpox virus and its differences from other poxviruses.In addition,the shared genetic factors contributing to virulence in these Orthopoxvirus highlight their evolutionary connections and genetic similarities.While they exhibit differences in virulence,studying these genetic relationships is crucial for understanding their biology,pathogenicity,and the development of effective vaccines and antiviral therapeutics to curb mpox disease.

Recent Advances for Global Perspectives on Etiology, Pathophysiology, Clinical Presentations, and Management of Moyamoya Disease

Moyamoya disease (MMD) is a condition characterized by the gradual narrowing and blockage of blood vessels in the brain, specifically those in the circle of Willis and the arteries that supply it. This results in reduced blood flow and oxygen to the brain, leading to progressive symptoms and potential complications. The underlying pathophysiological mechanism remains elucidated. However, recent studies have highlighted numerous etiologic factors: abnormal immune complex responses, susceptibility genes, branched-chain amino acids, antibodies, heritable diseases, and acquired diseases, which may be the great potential triggers for the development of moyamoya disease. Its clinical presentation has varying degrees from transient asymptomatic events to significant neurological deficits. Moyamoya disease (MMD) shows different patterns in children and adults. Children with MMD are more susceptible to ischemic events due to decreased blood flow to the brain. Conversely, adults with MMD are more prone to hemorrhagic events involving brain bleeding. Children with MMD may experience a range of symptoms including motor impairments, sensory issues, seizures, headaches, dizziness, cognitive delays, or ongoing neurological problems. Although adults may present with similar clinical symptoms as children, they are more prone to experiencing sudden onset intraventricular, subarachnoid, or intracerebral hemorrhages. One of the challenges in moyamoya disease is the potential for misdiagnosis or delayed diagnosis, particularly when physicians fail to consider MMD as a possible cause in stroke patients. This review aims to provide a comprehensive overview of recent global studies on the pathophysiology of MMD, along with advancements in its management. Additionally, the review will delve into various surgical treatment options for MMD, as well as its rare occurrence alongside atrioventricular malformations. Exciting prospects include the use of autologous bone marrow transplant and the potential role of Connexin 43 protein treatment in the development of moyamoya disease.

Indian perspective on childhood malnutrition:Prevalence,pathophysiology,risk factors,and prevention

BACKGROUND Childhood malnutrition contributes over half of the childhood mortality around the world,predominantly in South-Asian and sub-Saharan countries.AIM To summarize the childhood malnutrition epidemiology along with the comorbid factors associated with it and its management within the community.METHODS The data collection process involved conducting a comprehensive search using specific keywords such as child nutrition disorders and India with Boolean operators.The search was conducted in the Scopus and PubMed electronic databases.RESULTS Inadequate energy consumption initiates pathological alterations in the form of growth retardation,fat,visceral,and muscle loss,a reduction in basal metabolic rate,and a significant reduction in total energy expenditure.It has become evident that malnutrition shows an increased prevalence and incidence rate,despite available guidelines for the management of malnutrition.CONCLUSION Malnutrition can be a major player in the establishment of severe infections that result in significant post discharge mortalities in children.Future trials are required to fill the prime gaps in knowledge regarding the identification of other contributory factors in the pathogenesis of malnutrition and postdischarge infection.New biomarkers for early detection of malnutrition should be the priority of the scientific community for the early management of malnutrition.

Research and Exploration of Ideological and Political Education in the Course of Pathophysiology

Course based ideological and political education (CIPE) is an important way to improve the quality of ideological and political work and talent cultivation. This study explores for the first time the implementation of ideological and political education in the teaching of pathophysiology courses, and also analyzes the evaluation of student psychological status and the importance of mental health education in the implementation of IPE courses. A survey was conducted on 211 students at Yangtze University to understand their motivation and behavior towards learning ideological, political, and pathophysiological courses. In addition, a questionnaire survey was used to explore the relationship between pathophysiology and ideological and political courses, as well as the importance of their satisfaction with the implementation of ideological and political courses in pathophysiology and mental health education. The research results indicate that factors such as educational background and gender differences affect the learning of CIPE. Graduate students are more interested in ideological and political courses, while female students find it difficult to study pathophysiology;In addition, the results of one-way ANOVA indicate that the implementation effect of IPE in pathophysiology courses depends on the level of interest in IPE and pathophysiology courses, the level of consideration for the importance of professional courses, the professional gains after studying pathophysiology, and the level of understanding of the relationship between IPE and CIPE. 81.04% of students believe that in the CIPE process, telling stories by teachers themselves is the most popular way of communication and education. This reflects the importance of mental health education from the perspective of CIPE. In addition, this study also indicates that PBL and flipped classroom teaching models are popular teaching models in CIPE. This study is beneficial for promoting the improvement and implementation of CIPE and mental health education in higher education curricula, thus providing valuable insights for educational decision-makers.

血清CEA、CA242、CA199、PGR联合检验在早期胃癌辅助诊断中的临床价值

目的探讨血清CEA、CA242、CA199、PGR联合检验在早期胃癌中的诊断价值。方法选取我院2022年1月至2023年1月收治的胃癌患者82例作为观察组,另选同期健康体检者50例作为对照组。检测两组的CEA、CA242、CA199、PGR水平,绘制ROC曲线分析血清CEA、CA242、CA199、PGR及联合检验诊断胃癌的临床价值。结果观察组血清CEA、CA242、CA199水平高于对照组,PGR水平低于对照组(P<0.05)。绘制ROC曲线显示,血清CEA、CA242、CA199、PGR联合检验诊断胃癌的AUC为0.960,高于单项检验的0.762、0.796、0.757、0.773。结论血清CEA、CA242、CA199、PGR联合检验在胃癌早期诊断中具有一定价值,诊断效能更高,便于早期确诊与治疗。

乳腺X线征象、ADC值联合血清CA125、CEA水平预测乳腺癌新辅助化疗后腋窝淋巴结病理状态的价值

目的:探讨联合应用乳腺X线征象、磁共振表观扩散系数(ADC)值与血清CA125、CEA水平预测乳腺癌新辅助化疗后转移性腋窝淋巴结病理状态的价值。方法:前瞻性纳入2020年1月-2022年12月在我院接受全程新辅助化疗及腋窝淋巴结清扫术的152例女性乳腺癌患者作为研究对象,根据腋窝淋巴结清扫术后病理结果将所有患者分为腋窝病理完全缓解(PCR)组(55例)和非PCR组(97例)。于新辅助化疗前一周内,对所有患者进行乳腺X线和磁共振扩散加权成像检查及血清CA125、CEA水平检测。结果:乳腺癌新辅助化疗后腋窝PCR与非PCR患者的Ki-67表达状态差异有统计学意义(P<0.05)。新辅助化疗后腋窝非PCR患者治疗前乳腺X线征象中血管增多、增粗及边缘毛刺的发生比例显著高于PCR患者(P<0.05)。新辅助化疗后腋窝非PCR患者的治疗前ADC值显著低于PCR患者(t=4.372,P<0.001),而血清CA125、CEA水平显著高于PCR患者(P<0.05)。多因素Logistic回归分析结果显示,Ki-67高表达(X1)、血管增多、增粗(X2)、较高的ADC值(X4)、血清CA125水平(X5)是乳腺癌新辅助化疗后腋窝非PCR的独立危险因素(P<0.05),构建Logistic回归模型为Logit(P)=-3.206+0.792X1+0.953X2+1.199X4+0.845X5。ROC曲线分析结果显示,Logistic回归模型预测新辅助化疗后转移性腋窝淋巴结病理状态的曲线下面积为0.856(95%CI:0.794~0.917),敏感度和特异度分别为73.2%和85.5%。结论:乳腺X线特征、ADC值、血清CA125水平及Ki67表达状态与伴有转移性腋窝淋巴结的乳腺癌患者新辅助化疗后腋窝淋巴结病理状态有关,联合以上特征具有一定预测价值。

血清CA125、CA724、CEA水平与胃癌临床病理特征的关系研究

目的探讨血清糖类抗原(CA)125、CA724、癌胚抗原(CEA)水平与胃癌(GC)患者临床病理特征的关系。方法选取80例GC患者作为观察组,另选取同期80例胃部良性病变患者作为对照组。检测并比较两组患者血清CA125、CA724、CEA水平及其阳性检出率,并分析GC患者血清CA125、CA724、CEA水平与其临床病理特征的关系。结果观察组CA125、CA724、CEA水平及其阳性检出率均明显高于对照组(P<0.05);且TNM分期为Ⅲ~Ⅳ期、分化程度低、浸润深度在黏膜下层以及有淋巴结转移的GC患者血清CA125、CA724、CEA水平均明显增高,差异均具有统计学意义(P<0.05)。结论CA125、CA724、CEA在GC中呈高表达状态,且与TNM分期、分化程度、浸润深度和淋巴结转移关系密切,可为GC患者病情发展的进一步评估提供有力的参考,也可作为GC预后的评估指标。

血清LAIR2联合CYFRA21-1、NSE、CEA对肺癌的辅助诊断价值

目的探究血清白细胞关联免疫球蛋白样受体2(LAIR2)联合细胞角蛋白19片段(CYFRA21-1)、神经特异性烯醇化酶(NSE)、癌胚抗原(CEA)对肺癌的辅助诊断价值。方法回顾性选取86例肺癌患者作为观察组,另外选取同时期进行相关检查的健康体检人群57例作为对照组。比较2组一般资料、LAIR2、CYFRA21-1、NSE、CEA水平,评价LAIR2、CYFRA21-1、NSE、CEA对肺癌的诊断价值。结果2组性别、年龄、体质量指数比较差异无统计学意义(P<0.05)。观察组LAIR2、CYFRA21-1、NSE、CEA水平均显著高于对照组(P均<0.001)。将观察组=1,对照组=0作为因变量,LAIR2、CYFRA21-1、NSE、CEA作为自变量,进行回归分析,结果显示,LAIR2、CYFRA21-1、NSE、CEA均是肺癌发生的独立危险因素。LAIR2的预测阈值为5.770 ng/ml,灵敏度76.7%,特异度89.5%;CYFRA21-1的预测阈值为3.765 ng/ml,灵敏度80.2%,特异度96.5%;NSE的预测阈值为7.975 ng/ml,灵敏度79.1%,特异度87.7%;CEA的预测阈值为3.120 ng/ml,灵敏度90.7%,特异度100.0%。LAIR2、CYFRA21-1、NSE、CEA以及四者联合的AUC面积分别为0.867、0.925、0.889、0.939以及0.997,四者联合的AUC面积最大,灵敏度为96.5%,特异度为100.0%,预测效能较好。结论肺癌患者血清LAIR2、CYFRA21-1、NSE、CEA水平均异常增加。血清LAIR2联合CYFRA21-1、NSE、CEA对肺癌的辅助诊断有一定积极意义。

血清CEA、AFP与FOLR1联合检测在卵巢癌中的意义

目的 探讨血清癌胚抗原(CEA)、甲胎蛋白(AFP)与叶酸受体1(FOLR1)联合检测在卵巢癌中的诊断价值。方法 选取97例卵巢癌患者为观察组,同期97例卵巢良性病变患者为对照组。比较2组研究参与者入院时血清CEA、AFP、FOLR1水平,分析血清CEA、AFP、FOLR1水平与卵巢癌患者病理学参数的相关性,受试者操作特征(ROC)曲线分析血清CEA、AFP、FOLR1联合检测对卵巢癌的诊断价值。结果 入院时,观察组血清CEA、AFP、FOLR1水平较对照组高,差异有统计学意义(P<0.05);不同病理学参数卵巢癌患者血清CEA、AFP、FOLR1水平比较:中高分化低于低分化,Ⅰ~Ⅱ期低于Ⅲ~Ⅳ期,肌层浸润程度<1/2低于肌层浸润程度≥1/2,差异有统计学意义(P<0.05);血清CEA、AFP、FOLR1水平与卵巢癌分化程度呈负相关,与FIGO分期、肌层浸润程度呈正相关,差异有统计学意义(P<0.05);血清CEA、AFP、FOLR1联合检测诊断卵巢癌的曲线下面积(AUC)为0.815,最佳诊断敏感度、特异度分别为94.85%、68.01%。结论 血清CEA、AFP与FOLR1联合检测在卵巢癌中具有良好的诊断效能,可进一步提高肿瘤标志物联合检测在临床诊断中的参考价值。

超声弹性成像联合癌胚抗原CEA、CA153和CA125对乳腺癌患者的早期诊断价值

目的探讨超声弹性成像与肿瘤标志物CEA、CA153和CA125对乳腺癌的早期诊断价值,为临床诊治提供指导。方法将秦皇岛市第一医院收治早期乳腺癌患者归为A组,良性病变患者为B组,正常体检者为C组,均为48例女性。均行弹性超声诊断并采用CLIA法测定血清CEA、CA153、CA125水平,评估超声及血清检测的联合诊断价值。结果A组弹性评分与血清检测水平和阳性率均高于另外两组(P均<0.05),另外两组之间无统计学意义;联合检测敏感性、特异性、诊断符合率均高于其余单项检测结果(P均<0.05)。结论超声弹性成像、CA153、CA125和CEA联合检测有助于鉴别诊断良恶性病变,提高早期检出率,能够指导治疗方案和监测病情,值得临床推广。

miR-506-3p、sST2和CEA在恶性胸腔积液患者中表达水平及诊断价值分析

目的分析miR-506-3p、可溶性生长刺激表达基因2蛋白(sST2)和癌胚抗原(CEA)在恶性胸腔积液患者中表达水平及其诊断价值。方法选取108例胸腔积液患者作为研究组,根据超声检查及病理检查结果,将32例结核性胸腔积液患者纳入结核性组,41例癌性胸腔积液患者和35例淋巴瘤性胸腔积液患者纳入恶性组。另随机抽取54例本院健康体检者纳入对照组。比较研究组患者及对照组健康体检者的血清sST2、CEA水平;比较恶性组与结核性组患者胸水miR-506-3p、sST2和CEA水平。采用ROC分析各指标对恶性胸腔积液的诊断价值。结果血清sST2和CEA水平,恶性组>结核性组>对照组(P<0.05)。与结核性组比较,恶性组胸水miR-506-3p水平降低(P<0.05),而sST2和CEA水平升高(P<0.05)。ROC结果显示,血清sST2、CEA及胸水miR-506-3p、sST2、CEA对恶性胸腔积液均具有诊断价值,且联合诊断的灵敏度最高。结论在恶性胸腔积液患者中,胸水miR-506-3p低表达,而血清和胸水sST2、CEA高表达;对恶性胸腔积液具有一定诊断价值,且联合诊断的灵敏度最高。

Irritable bowel syndrome:Emerging paradigm in pathophysiology

Irritable bowel syndrome(IBS)is one of the most common gastrointestinal disorders,characterized by abdominal pain,bloating,and changes in bowel habits.These symptoms cannot be explained by structural abnormalities and there is no specific laboratory test or biomarker for IBS.Therefore,IBS is classified as a functional disorder with diagnosis dependent on the history taking about manifested symptoms and careful physical examination.Although a great deal of research has been carried out in this area,the pathophysiology of IBS is complex and not completely understood.Multiple factors are thought to contribute to the symptoms in IBS patients;altered gastrointestinal motility,visceral hypersensitivity,and the brain-gut interaction are important classical concepts in IBS pathophysiology.New areas of research in this arena include inflammation,postinfectious low-grade inflammation,genetic and immunologic factors,an altered microbiota,dietary factors,and enteroendocrine cells.These emerging studies have not shown consistent results,provoking controversy in the IBS field.However,certain lines of evidence suggest that these mechanisms are important at least a subset of IBS patients,confirming that IBS symptoms cannot be explained by a single etiological mechanism.Therefore,it is important to keep in mind that IBS requires a more holistic approach to determining effective treatment and understanding the underlying mechanisms.

Pathophysiology of colorectal peritoneal carcinomatosis: Role of the peritoneum

Colorectal cancer(CRC) is the third most common cancer and the fourth most common cause of cancerrelated death worldwide. Besides the lymphatic and haematogenous routes of dissemination,CRC frequently gives rise to transcoelomic spread of tumor cells in the peritoneal cavity,which ultimately leads to peritoneal carcinomatosis(PC). PC is associated with a poor prognosis and bad quality of life for these patients in their terminal stages of disease. A loco-regional treatment modality for PC combining cytoreductive surgery and hyperthermic intraperitoneal peroperative chemotherapy has resulted in promising clinical results. However,this novel approach is associated with significant morbidity and mortality. A comprehensive understanding of the molecular events involved in peritoneal disease spread is paramount in avoiding unnecessary toxicity. The emergence of PC is the result of a molecular crosstalk between cancer cells and host elements,involving several well-defined steps,together known as the peritoneal metastatic cascade. Individual or clumps of tumor cells detach from the primary tumor,gain access to the peritoneal cavity and become susceptible to the regular peritoneal transport. They attach to the distant peritoneum,subsequently invade the subperitoneal space,where angiogenesis sustains proliferation and enables further metastatic growth. These molecular events are not isolated events but rather a continuous and interdependent process. In this manuscript,we review current data regarding the molecular mechanisms underlying the development of colorectal PC,with a special focus on the peritoneum and the role of the surgeon in peritoneal disease spread.

Pathophysiology of chronic pancreatitis induced by dibutyltin dichloride joint ethanol in mice

AIM: To search for a new chronic pancreatitis model in mice suitable for investigating the pathophysiological processes leading to pancreatic fibrosis.METHODS: The mice were randomly divided into 2 groups(n = 50), control group and model group. The mice in model group were given ethanol(10%) in drinking water after injection of dibutyltin dichloride(DBTC)(8 mg/kg BW) in tail vein. The mice in control group were injected with only solvent into tail vein( 60 % ethanol, 20% glycerine and 20% normal saline) and drank common water. At days 1, 7, 14, 28, and 56 after application of DBTC or solvent, 10 mice in one group were killed at each time point respectively. Blood was obtained by inferior vena cava puncture. The activity of amylase, concentration of bilirubin and hyaluronic acid in serum were assayed. The pancreas was taken to observe the pancreatic morphology by HE staining, and to characterize the pancreatic fibrosis by Masson staining. The expression of F4/80, CD3 and fibronectin(FN) were assayed by immuno-histochemistry or Immunofluorescence technique. Collagen typeⅠ(COL1A1) in pancreas were detected by Western blot. The expression of matrix metalloproteinase-1(MMP-1) and tissue inhibitor of metalloproteinases-1(TIMP-1) m RNA in the pancreas was assessed by real time PCR.RESULTS: DBTC induced an acute edematous pancreatitis within 1 d. The dilated acini, scattered acinar cell necrosis, and inflammatory cells were found at day 7. Extensive infiltration with inflammatory cells following deposition of connective tissue was observed at day 14. At day 28, level of pancreatic fibrosis was aggravated. The pancreatic tissue was replaced by an extended interstitial fibrosis at the end of 2 mo. There was significant difference in the level of amylase, bilirubin and hyaluronic acid in serum between control group and model group(P < 0.05). The level of COL1A1 and FN in pancreas increased. The expression of MMP-1 m RNA in pancreas decreased, but TIMP-1 m RNA increased at model group.CONCLUSION: DBTC joint Ethanol drinking can induce chronic pancreatitis in accordance with the pathophysiological modification of human. DBTC joint Ethanol-induced pancreatitis in mice is an effective and handy experimental method. The model is suitable to study the mechanism of pancreatic fibrosis in chronic pancreatitis.

Gastroesophageal reflux disease:From pathophysiology to treatment

This review focuses on the pathophysiology of gastroesophageal reflux disease (GERD) and its implications for treatment. The role of the natural anti-reflux mechanism (lower esophageal sphincter, esophageal peristalsis, diaphragm, and trans-diaphragmatic pressure gradient), mucosal damage, type of refluxate, presence and size of hiatal hernia, Helicobacter pylori infection, and Barrett’s esophagus are reviewed. The conclusions drawn from this review are: (1) the pathophysiology of GERD is multifactorial; (2) because of the pathophysiology of the disease, surgical therapy for GERD is the most appropriate treatment; and (3) the genesis of esophageal adenocarcinoma is associated with GERD.

Solitary rectal ulcer syndrome:Clinical features,pathophysiology,diagnosis and treatment strategies

Solitary rectal ulcer syndrome (SRUS) is an uncommon benign disease, characterized by a combination of symptoms, clinical findings and histological abnormalities. Ulcers are only found in 40% of the patients; 20% of the patients have a solitary ulcer, and the rest of the lesions vary in shape and size, from hyperemic mucosa to broad-based polypoid. Men and women are affected equally, with a small predominance in women. SRUS has also been described in children and in the geriatric population. Clinical features include rectal bleeding, copious mucus discharge, prolonged excessive straining, perineal and abdominal pain, feeling of incomplete defecation, constipation, and rarely, rectal prolapse. This disease has well-described histopathological features such as obliteration of the lamina propria by fibrosis and smooth muscle fibers extending from a thickened muscularis mucosa to the lumen. Diffuse collage deposition in the lamina propria and abnormal smooth muscle fiber extensions are sensitive markers for differ-entiating SRUS from other conditions. However, the etiology remains obscure, and the condition is frequently associated with pelvic floor disorders. SRUS is difficult to treat, and various treatment strategies have been advocated, ranging from conservative management to a variety of surgical procedures. The aim of the present review is to summarize the clinical features, pathophysiology, diagnostic methods and treatment strategies associated with SRUS. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.

Pathophysiology and biology of peritoneal carcinomatosis

Peritoneal carcinomatosis represents a devastating form of cancer progression with a very poor prognosis.Its complex pathogenesis is represented by a dynamic process comprising several steps.To the best of our knowledge pathogenesis can be partly explained by 3 major molecular pathways: (1) dissemination from the primary tumor;(2) primary tumor of peritoneum;and (3) independent origins of the primary tumor and peritoneal implants.These are not mutually exclusive and combinations of different mechanisms could occur inside a single case.There are still several aspects which need explanation by future studies.A comprehensive understanding of molecular events involved in peritoneal carcinomatosis is of paramount importance and should be systematically pursued not only to identify novel strategies for the prevention of the condition,but also to obtain therapeutic advances,through the identification of surrogate markers of prognosis and development of future molecular targeted therapies.

Efficacy of prone position in acute respiratory distress syndrome patients: A pathophysiology-based review

Acute respiratory distress syndrome(ARDS) is a syndrome with heterogeneous underlying pathological processes. It represents a common clinical problem in intensive care unit patients and it is characterized by high mortality. The mainstay of treatment for ARDS is lung protective ventilation with low tidal volumes and positive end-expiratory pressure sufficient for alveolar recruitment. Prone positioning is a supplementary strategy available in managing patients with ARDS. It was first described 40 years ago and it proves to be in alignment with two major ARDS pathophysiological lung models; the "sponge lung"- and the "shape matching"-model. Current evidence strongly supports that prone positioning has beneficial effects on gas exchange, respiratory mechanics, lung protection and hemodynamics as it redistributes transpulmonary pressure, stress and strain throughout the lung and unloads the right ventricle. The factors that individually influence the time course of alveolar recruitment and the improvement in oxygenation during prone positioning have not been well characterized. Although patients' response to prone positioning is quite variable and hard to predict, large randomized trials and recent meta-analyses show that prone position in conjunction with a lung-protective strategy, when performed early and in sufficient duration, may improve survival in patients with ARDS. This pathophysiology-based review and recent clinical evidence strongly support the use of prone positioning in the early management of severe ARDS systematically and not as a rescue maneuver or a last-ditch effort.

MMP-9、CEA与NLR对胃癌患者腹膜转移的预测价值分析

目的探讨MMP-9、CEA与NLR对胃癌患者腹膜转移的预测价值。方法选取2020年01月-2022年12月在枣阳市第一人民医院治疗的110例胃癌患者作为研究对象,根据临床诊断腹膜是否发生转移的情况将其分成转移组(n=38)和未转移组(n=72),检测两组受检者的血清MMP-9、CEA与NLR表达水平,分析MMP-9、CEA、NLR和胃癌转移的相关性,采用受试者工作特征曲线(ROC)分析MMP-9、CEA与NLR对胃癌腹膜转移的诊断价值,比较两组患者的一般资料和MMP-9、CEA与NLR表达。结果(1)单因素分析结果显示:转移组较未转移组的肿瘤分化、MMP-9、CEA与NLR更高(P<0.05)。(2)多因素Logistic回归分析显示:MMP-9、CEA和NLR是胃癌患者腹膜转移的独立危险因素。(3)ROC曲线分析显示:MMP-9、CEA与NLR对胃癌患者腹膜转移有一定的预测作用(MMP-9:AUC=0.660,95%CI为0.554~0.776,其敏感度、特异度分别为0.684、0.597。CEA:AUC=0.831,95%CI为0.752~0.910,其敏感度、特异度分别为0.789、0.736。NLR:AUC=0.798,95%CI为0.710~0.887,其敏感度、特异度分别为0.711、0.778);且联合预测具有较高的敏感度(0.763)和特异度(0.889),AUC(0.899)高于单个变量的AUC,提示联合预测胃癌患者腹膜转移的价值和准确度更高。结论MMP-9、CEA和NLR是胃癌患者腹膜转移的独立危险因素,MMP-9、CEA和NLR联合预测胃癌患者腹膜转移的准确度高于单个变量,诊断价值更高。