Hypoxia-preconditioned bone marrow-derived mesenchymal stem cells protect neurons from cardiac arrest-induced pyroptosis

Cardiac arrest can lead to severe neurological impairment as a result of inflammation,mitochondrial dysfunction,and post-cardiopulmonary resuscitation neurological damage.Hypoxic preconditioning has been shown to improve migration and survival of bone marrow–derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest,but the specific mechanisms by which hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown.To this end,we established an in vitro co-culture model of bone marrow–derived mesenchymal stem cells and oxygen–glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis,possibly through inhibition of the MAPK and nuclear factor κB pathways.Subsequently,we transplanted hypoxia-preconditioned bone marrow–derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia.The results showed that hypoxia-preconditioned bone marrow–derived mesenchymal stem cells significantly reduced cardiac arrest–induced neuronal pyroptosis,oxidative stress,and mitochondrial damage,whereas knockdown of the liver isoform of phosphofructokinase in bone marrow–derived mesenchymal stem cells inhibited these effects.To conclude,hypoxia-preconditioned bone marrow–derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest,and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.

The compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one alleviates neuroinflammation and cognitive impairment in a mouse model of Alzheimer's disease

Previous studies have shown that the compound(E)-2-(3,4-dihydroxystyryl)-3-hydroxy-4H-pyran-4-one(D30),a pyromeconic acid derivative,possesses antioxidant and anti-inflammatory properties,inhibits amyloid-β aggregation,and alleviates scopolamine-induced cognitive impairment,similar to the phase Ⅲ clinical drug resveratrol.In this study,we established a mouse model of Alzheimer's disease via intracerebroventricular injection of fibrillar amyloid-β to investigate the effect of D30 on fibrillar amyloid-β-induced neuropathology.Our results showed that D30 alleviated fibrillar amyloid-β-induced cognitive impairment,promoted fibrillar amyloid-β clearance from the hippocampus and cortex,suppressed oxidative stress,and inhibited activation of microglia and astrocytes.D30 also reversed the fibrillar amyloid-β-induced loss of dendritic spines and synaptic protein expression.Notably,we demonstrated that exogenous fibrillar amyloid-βintroduced by intracerebroventricular injection greatly increased galectin-3 expression levels in the brain,and this increase was blocked by D30.Considering the role of D30 in clearing amyloid-β,inhibiting neuroinflammation,protecting synapses,and improving cognition,this study highlights the potential of galectin-3 as a promising treatment target for patients with Alzheimer's disease.

Pyroptosis,ferroptosis,and autophagy in spinal cord injury:regulatory mechanisms and therapeutic targets

Regulated cell death is a form of cell death that is actively controlled by biomolecules.Several studies have shown that regulated cell death plays a key role after spinal cord injury.Pyroptosis and ferroptosis are newly discovered types of regulated cell deaths that have been shown to exacerbate inflammation and lead to cell death in damaged spinal cords.Autophagy,a complex form of cell death that is interconnected with various regulated cell death mechanisms,has garnered significant attention in the study of spinal cord injury.This injury triggers not only cell death but also cellular survival responses.Multiple signaling pathways play pivotal roles in influencing the processes of both deterioration and repair in spinal cord injury by regulating pyroptosis,ferroptosis,and autophagy.Therefore,this review aims to comprehensively examine the mechanisms underlying regulated cell deaths,the signaling pathways that modulate these mechanisms,and the potential therapeutic targets for spinal cord injury.Our analysis suggests that targeting the common regulatory signaling pathways of different regulated cell deaths could be a promising strategy to promote cell survival and enhance the repair of spinal cord injury.Moreover,a holistic approach that incorporates multiple regulated cell deaths and their regulatory pathways presents a promising multi-target therapeutic strategy for the management of spinal cord injury.

Gut microbiota shifts in hepatitis B-related portal hypertension after transjugular intrahepatic portosystemic shunt:Mechanistic and clinical implications

In this article,we provide commentary on the recent article by Zhao et al.We focus on the shifts in the gut microbiota of patients with hepatitis B virus(HBV)-associated cirrhosis/portal hypertension(PH)following transjugular intrahepatic portosystemic shunt(TIPS)and the implications for understanding the mechanisms,diagnosis,and treatment.By comparing the gut microbiota composition and dynamic changes before and after TIPS in patients with and without hepatic encephalopathy,the authors found an increase in non-probiotic bacteria in those who developed hepatic encephalopathy post-TIPS,with Morganella species present only in the hepatic encephalopathy group.The gut microbiota changes post-TIPS among patients without the occurrence of hepatic encephalopathy suggest potential therapeutic benefits through prophylactic microbiome therapies.Furthermore,the specific gut microbiota alterations may hold promise to predict the risk of hepatic encephalopathy in individuals undergoing TIPS for HBVrelated PH.Despite these promising findings,future studies are needed to address limitations,including a small sample size,a relatively short evaluation period for gut microbiota alterations,the absence of data on dynamic alterations in gut microbiota post-TIPS and their correlation with blood ammonia levels,and the lack of validation in animal models.In conclusion,Zhao et al's study has shed new light on the link of gut microbiota with post-TIPS hepatic encephalopathy,potentially through the intricate gut-liver axis,and has important clinical implications for improving the management of patients with HBV-related PH.

Drosophila models used to simulate human ATP1A1 gene mutations that cause Charcot-Marie-Tooth type 2 disease and refractory seizures

Certain amino acids changes in the human Na^(+)/K^(+)-ATPase pump,ATPase Na^(+)/K^(+)transporting subunit alpha 1(ATP1A1),cause Charcot-Marie-Tooth disease type 2(CMT2)disease and refractory seizures.To develop in vivo models to study the role of Na^(+)/K^(+)-ATPase in these diseases,we modified the Drosophila gene homolog,Atpα,to mimic the human ATP1A1 gene mutations that cause CMT2.Mutations located within the helical linker region of human ATP1A1(I592T,A597T,P600T,and D601F)were simultaneously introduced into endogenous Drosophila Atpαby CRISPR/Cas9-mediated genome editing,generating the Atpα^(TTTF)model.In addition,the same strategy was used to generate the corresponding single point mutations in flies(Atpα^(I571T),Atpα^(A576T),Atpα^(P579T),and Atpα^(D580F)).Moreover,a deletion mutation(Atpα^(mut))that causes premature termination of translation was generated as a positive control.Of these alleles,we found two that could be maintained as homozygotes(Atpα^(I571T)and Atpα^(P579T)).Three alleles(Atpα^(A576T),Atpα^(P579)and Atpα^(D580F))can form heterozygotes with the Atpαmut allele.We found that the Atpαallele carrying these CMT2-associated mutations showed differential phenotypes in Drosophila.Flies heterozygous for Atpα^(TTTF)mutations have motor performance defects,a reduced lifespan,seizures,and an abnormal neuronal morphology.These Drosophila models will provide a new platform for studying the function and regulation of the sodium-potassium pump.

Prediction and stratification for the surgical adverse events after minimally invasive esophagectomy:A two-center retrospective study

BACKGROUND Minimally invasive esophagectomy(MIE)is a widely accepted treatment for esophageal cancer,yet it is associated with a significant risk of surgical adverse events(SAEs),which can compromise patient recovery and long-term survival.Accurate preoperative identification of high-risk patients is critical for improving outcomes.AIM To establish and validate a risk prediction and stratification model for the risk of SAEs in patients with MIE.METHODS This retrospective study included 747 patients who underwent MIE at two centers from January 2019 to February 2024.Patients were separated into a train set(n=549)and a validation set(n=198).After screening by least absolute shrinkage and selection operator regression,multivariate logistic regression analyzed clinical and intraoperative variables to identify independent risk factors for SAEs.A risk stratification model was constructed and validated to predict the probability of SAEs.RESULTS SAEs occurred in 10.2%of patients in train set and 13.6%in the validation set.Patients with SAE had significantly higher complication rate and a longer hospital stay after surgery.The key independent risk factors identified included chronic obstructive pulmonary disease,a history of alcohol consumption,low forced expiratory volume in the first second,and low albumin levels.The stratification model has excellent prediction accuracy,with an area under the curve of 0.889 for the training set and an area under the curve of 0.793 for the validation set.CONCLUSION The developed risk stratification model effectively predicts the risk of SAEs in patients undergoing MIE,facilitating targeted preoperative interventions and improving perioperative management.

Potassium and calcium channels in different nerve cells act as therapeutic targets in neurological disorders

The central nervous system, information integration center of the body, is mainly composed of neurons and glial cells. The neuron is one of the most basic and important structural and functional units of the central nervous system, with sensory stimulation and excitation conduction functions. Astrocytes and microglia belong to the glial cell family, which is the main source of cytokines and represents the main defense system of the central nervous system. Nerve cells undergo neurotransmission or gliotransmission, which regulates neuronal activity via the ion channels, receptors, or transporters expressed on nerve cell membranes. Ion channels, composed of large transmembrane proteins, play crucial roles in maintaining nerve cell homeostasis. These channels are also important for control of the membrane potential and in the secretion of neurotransmitters. A variety of cellular functions and life activities, including functional regulation of the central nervous system, the generation and conduction of nerve excitation, the occurrence of receptor potential, heart pulsation, smooth muscle peristalsis, skeletal muscle contraction, and hormone secretion, are closely related to ion channels associated with passive transmembrane transport. Two types of ion channels in the central nervous system, potassium channels and calcium channels, are closely related to various neurological disorders, including Alzheimer's disease, Parkinson's disease, and epilepsy. Accordingly, various drugs that can affect these ion channels have been explored deeply to provide new directions for the treatment of these neurological disorders. In this review, we focus on the functions of potassium and calcium ion channels in different nerve cells and their involvement in neurological disorders such as Parkinson's disease, Alzheimer's disease, depression, epilepsy, autism, and rare disorders. We also describe several clinical drugs that target potassium or calcium channels in nerve cells and could be used to treat these disorders. We concluded that there are few clinical drugs that can improve the pathology these diseases by acting on potassium or calcium ions. Although a few novel ion-channelspecific modulators have been discovered, meaningful therapies have largely not yet been realized. The lack of target-specific drugs, their requirement to cross the blood–brain barrier, and their exact underlying mechanisms all need further attention. This review aims to explain the urgent problems that need research progress and provide comprehensive information aiming to arouse the research community's interest in the development of ion channel-targeting drugs and the identification of new therapeutic targets for that can increase the cure rate of nervous system diseases and reduce the occurrence of adverse reactions in other systems.

Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

Background:Long noncoding RNA,LINC01106 exhibits high expression in lung adenocarcinoma(LUAD)tumor tissues,but its functional role and regulatory mechanism in LUAD cells remain unclear.Methods:LINC01106 expression was analyzed in LUAD tissues and its functional impact on LUAD cells was assessed.LUAD cells were silenced with sh-LINC01106 and injected into nude mice to investigate tumor growth.The downstream transcription factors and molecular mechanism were determined using the Human transcription factor database(TFDB)database and Gene Expression Profiling Interactive Analysis(GEPIA)database.Additionally,the impact of linc01106 on autophagy was analyzed by determining the expression of autophagy-related genes(ATGs)in LUAD cells.Results:Our results showed that LINC01106 exhibited upregulation in both LUAD tissues and cell lines.The silencing of LINC01106 demonstrated a suppressive effect on tumorigenesis in a xenograft mouse model of LUAD.Additionally,LINC01106 was found to recruit TATA-binding protein-associated factor 15(TAF15),an RNA-binding protein,thereby enhancing the mRNA stability of TEA domain transcription factor 4(TEAD4).In turn,TEAD4 served as a transcription factor that bound to the LINC01106 promoter and regulated its expression.Further assays indicated that LINC01106 promoted autophagy in LUAD cells by upregulating the expression of autophagy-related genes(ATGs).The silencing of LINC01106 in LUAD cells inhibited autophagy,and cell proliferation,and promoted apoptosis,which all were effectively reversed by ATG5 overexpression.Conclusions:Overall,LINC01106,transcriptionally activated by TEAD4,interacts with TAF15 to promote the stability of TEAD4 and upregulates the expression of ATGs,promoting malignancy of LUAD cells.

Hydroxyurea-related ileocecal region ulcers as a rare complication:A case report

BACKGROUND Hydroxyurea,an antimetabolite,is frequently prescribed for various hemato-logical disorders,and its common side effects include gastrointestinal problems,cutaneous or mucosal lesions and pyrexia/fever.CASE SUMMARY This study reports the case of a 67-year-old woman who developed recurrent abdominal pain after 10 years of continuous hydroxyurea therapy for primary thrombocythemia.Colonoscopy revealed an ileocecal ulcer.After discontinuing hydroxyurea therapy for 6 months,follow-up colonoscopy showed a significant reduction in the ulceration.CONCLUSION We consider cecal ulcers as a rare complication of hydroxyurea therapy which typically resolves upon stopping the drug.

Mizagliflozin ameliorates diabetes induced kidney injury by inhibitor inhibit inflammation and oxidative stress

BACKGROUND Mizagliflozin(MIZ)is a specific inhibitor of sodium-glucose cotransport protein 1(SGLT1)originally developed as a medication for diabetes.AIM To explore the impact of MIZ on diabetic nephropathy(DN).METHODS Diabetic mice were created using db/db mice.They were administered either a low dose(0.5 mg/kg)or a high dose(1.0 mg/kg)of the SGLT1 inhibitor MIZ via stomach gavage for 8 weeks.Subsequently,mesangial cells(MCs)were isolated and subjected to high glucose conditions in culture to assess the effects of MIZ on DN.RESULTS The results showed that low doses of MIZ significantly reduced albuminuria to a level comparable to that achieved with high doses in db/db mice.High doses of MIZ led to a substantial increase in body weight in mice,along with decreased blood glucose levels and food intake.Moreover,the intervention with high-dose MIZ notably decreased the expression of extracellular matrix genes,such as collagen type 1 alpha 1 mRNA levels.While the expression of SGLT1 increased after exposure to high glucose,it decreased following treatment with MIZ.Furthermore,MIZ intervention was more effective in improving lactate dehydrogenase levels in MCs induced by high glucose compared to canagliflozin.MIZ also significantly elevated levels of antioxidant enzymes superoxide dismutase,catalase,and glutathione,while reducing malondialdehyde levels.CONCLUSION These findings indicate that MIZ can ameliorate DN by inhibiting SGLT1,inflammation,and oxidative stress.

Tranylcypromine upregulates Sestrin 2 expression to ameliorate NLRP3-related noise-induced hearing loss

Noise-induced hearing loss is the primary non-genetic factor contributing to auditory dysfunction.However,there are currently no effective pharmacological interventions for patients with noise-induced hearing loss.Here,we present evidence suggesting that the lysine-specific demethylase 1 inhibitor–tranylcypromine is an otoprotective agent that could be used to treat noise-induced hearing loss,and elucidate its underlying regulatory mechanisms.We established a mouse model of permanent threshold shift hearing loss by exposing the mice to white broadband noise at a sound pressure level of 120 d B for 4 hours.We found that tranylcypromine treatment led to the upregulation of Sestrin2(SESN2)and activation of the autophagy markers light chain 3B and lysosome-associated membrane glycoprotein 1 in the cochleae of mice treated with tranylcypromine.The noise exposure group treated with tranylcypromine showed significantly lower average auditory brainstem response hearing thresholds at click,4,8,and 16 k Hz frequencies compared with the noise exposure group treated with saline.These findings indicate that tranylcypromine treatment resulted in increased SESN2,light chain 3B,and lysosome-associated membrane glycoprotein 1 expression after noise exposure,leading to a reduction in levels of 4-hydroxynonenal and cleaved caspase-3,thereby reducing noise-induced hair cell loss.Additionally,immunoblot analysis demonstrated that treatment with tranylcypromine upregulated SESN2 expression via the autophagy pathway.Tranylcypromine treatment also reduced the production of NOD-like receptor family pyrin domaincontaining 3(NLRP3)production.In conclusion,our results showed that tranylcypromine treatment ameliorated cochlear inflammation by promoting the expression of SESN2,which induced autophagy,thereby restricting NLRP3-related inflammasome signaling,alleviating cochlear hair cell loss,and protecting hearing function.These findings suggest that inhibiting lysine-specific demethylase 1 is a potential therapeutic strategy for preventing hair cell loss and noise-induced hearing loss.

New classification of gastric polyps:An in-depth analysis and critical evaluation

With the widespread use of upper gastrointestinal endoscopy,more and more gastric polyps(GPs)are being detected.Traditional management strategies often rely on histopathologic examination,which can be time-consuming and may not guide immediate clinical decisions.This paper aims to introduce a novel classification system for GPs based on their potential risk of malignant transformation,categorizing them as"good","bad",and"ugly".A review of the literature and clinical case analysis were conducted to explore the clinical implications,management strategies,and the system's application in endoscopic practice.Good polyps,mainly including fundic gland polyps and inflammatory fibrous polyps,have a low risk of malignancy and typically require minimal or no intervention.Bad polyps,mainly including hyperplastic polyps and adenomas,pose an intermediate risk of malignancy,necessitating closer monitoring or removal.Ugly polyps,mainly including type 3 neuroendocrine tumors and early gastric cancer,indicate a high potential for malignancy and require urgent and comprehensive treatment.The new classification system provides a simplified and practical framework for diagnosing and managing GPs,improving diagnostic accuracy,guiding individualized treatment,and promoting advancements in endoscopic techniques.Despite some challenges,such as the risk of misclassification due to similar endoscopic appearances,this system is essential for the standardized management of GPs.It also lays the foundation for future research into biomarkers and the development of personalized medicine.

Research hotspots and trends in gut microbiota and nonalcoholic fatty liver disease: A bibliometric study

BACKGROUND Recent research indicates that the intestinal microbial community,known as the gut microbiota,may play a crucial role in the pathogenesis of nonalcoholic fatty liver disease(NAFLD).To understand this relationship,this study used a compre-hensive bibliometric analysis to explore and analyze the currently little-known connection between gut microbiota and NAFLD,as well as new findings and possible future pathways in this field.AIM To provide an in-depth analysis of the current focus issues and research deve-lopments on the interaction between gut microbiota and NAFLD.METHODS In this study,all data were collected from the Web of Science Core Collection,and the related searches were completed on one day(February 21,2024).The data were stored in plain text format to facilitate subsequent analysis.VOSviewer 1.6.20 and CiteSpace 6.1R6 Basic were used for knowledge graph construction and bibliometric analysis.RESULTS The study included a total of 1256 articles published from 2013 to 2023,and the number of published papers demonstrated an upward trend,reaching a peak in the last two years.The University of California,San Diego held the highest citation count,while Shanghai University of Traditional Chinese Medicine in China led in the number of published works.The journal"Nutrients"had the highest publication count,while"Hepatology"was the most frequently cited.South Korean author Suk Ki Tae was the most prolific researcher.The co-cited keyword cluster labels revealed ten major clusters,namely cortisol,endothelial dysfunction,carbohydrate metabolism,myocardial infarction,non-alcoholic steatohepatitis,lipotoxicity,glucagon-like peptide-1,non-islet dependent,ethnicity,and microRNA.Keyword outbreak analysis highlighted metabolic syndrome,hepatic steatosis,insulin resistance,hepatocellular carcinoma,cardiovascular disease,intestinal permeability,and intestinal bacterial overgrowth as prominent areas of intense research.CONCLUSION Through the quantitative analysis of relevant literature,the current research focus and direction of gut microbiota and NAFLD can be more clearly understood,which helps us better understand the pathogenesis of NAFLD,and also opens up innovative solutions and strategies for the treatment of NAFLD.

Transcriptome and single-cell profiling of the mechanism of diabetic kidney disease

BACKGROUND The NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome may play an important role in diabetic kidney disease(DKD).However,the exact link remains unclear.AIM To investigate the role of the NLRP3 inflammasome in DKD.METHODS Using datasets from the Gene Expression Omnibus database,30 NLRP3 inflammasome-related genes were identified.Differentially expressed genes were selected using differential expression analysis,whereas intersecting genes were selected based on overlapping differentially expressed genes and NLRP3 inflammasome-related genes.Subsequently,three machine learning algorithms were used to screen genes,and biomarkers were identified by overlapping the genes from the three algorithms.Potential biomarkers were validated by western blotting in a db/db mouse model of diabetes.RESULTS Two biomarkers,sirtuin 2(SIRT2)and caspase 1(CASP1),involved in the Leishmania infection pathway were identified.Both biomarkers were expressed in endothelial cells.Pseudo-temporal analysis based on endothelial cells showed that DKD mostly occurs during the mid-differentiation stage.Western blotting results showed that CASP1 expression was higher in the DKD group than in the control group(P<0.05),and SIRT2 content decreased(P<0.05).CONCLUSION SIRT2 and CASP1 provide a potential theoretical basis for DKD treatment.

Risk factors,monitoring,and treatment strategies for early recurrence after rectal cancer surgery

Early recurrence(ER)following surgery for rectal cancer is a significant factor impacting patient survival rates.Tsai et al identified age,preoperative neoadjuvant therapy,length of hospital stay,tumour location,and pathological stage as factors influencing the risk of ER.Postoperative monitoring for ER should encompass a thorough medical history review,physical examination,tumour marker testing,and imaging studies.Additionally,noninvasive circulating tumour cell DNA testing can be utilized to predict ER.Treatment strategies may involve radical surgery,radiation therapy,chemotherapy,and immunotherapy.Through a comprehensive analysis of risk factors,the optimization of monitoring methods,and the development of personalized treatment strategies,it is anticipated that both the efficacy of treatment and the quality of life for rectal cancer patients with postoperative recurrence can be significantly improved.

Effect of ligamentum teres uteri preservation in laparoscopic high hernia sac ligation in children with indirect inguinal hernia

BACKGROUND Routinely separating the ligamentum teres uteri(LTU)intraoperatively remains an unresolved issue for female children undergoing surgery for indirect inguinal hernia(IIH).AIM To identify the effect of LTU preservation in laparoscopic high hernia sac ligation(LHSL)in children with IIH.METHODS The participants were 100 female children with unilateral IIH admitted from April 2022 to January 2024 to the Pediatric Surgery Department of Zhangzhou Municipal Hospital of Fujian Province.They were categorized based on LTU retention into the control group(n=45 cases),which underwent LTU ligation intraoperatively,and the experimental group(55 cases),which had the LTU preserved intraoperatively.All children underwent LHSL.RESULTS This study comparatively analyzed the operation time,hospitalization time,blood loss,postoperative recurrence rate,and complications(repeated pain in the inguinal region,foreign body sensation in the inguinal region,bloody exudation at the inguinal incision,and incision infection),which were all comparable between the two groups.CONCLUSION The above results indicate that LTU preservation during LHSL exerts certain therapeutic benefits for children with IIH.LTU preservation does not increase hospitalization time,blood loss,postoperative recurrence rate,and complications,which is safe and feasible,compared with conventional LTU ligation.LHSL with LTU preservation should be performed if conditions permit,which is worth popularizing.

ICU-acquired weakness in critically ill patients at risk of malnutrition: risk factors, biomarkers, and early enteral nutrition impact

BACKGROUND: This study aimed to explore the risk factors associated with intensive care unitacquired weakness(ICU-AW) in critically ill patients at risk of malnutrition and to evaluate the efficacy of early enteral nutrition(EEN) and the role of biomarkers in managing ICU-AW.METHODS: This retrospective, observational cohort study included 180 patients at risk of malnutrition admitted to the emergency intensive care unit of the First Affiliated Hospital of Xiamen University Hospital from January 2022 to December 2023. Patients were divided into ICU-AW group and non-ICU-AW group according to whether they developed ICU-AW, or categorized into EEN and parenteral nutrition(PN) groups according to nutritional support. ICU-AW was diagnosed using the Medical Research Council score. The primary outcome was the occurrence of ICU-AW.RESULTS: The significant factors associated with ICU-AW included age, sex, type of nutritional therapy, mechanical ventilation(MV), body mass index(BMI), blood urea nitrogen(BUN), and creatinine(Cr) levels(P<0.05). The PN group developed ICU-AW earlier than did the EEN group, with a significant difference observed(log-rank P<0.001). Among biomarkers for ICU-AW, the mean prealbumin(PAB)/C-reactive protein(CRP) ratio had the highest diagnostic accuracy(area under the curve [AUC] 0.928, 95% confidence interval [95% CI] 0.892–0.946), surpassing the mean Cr/BUN ratio(AUC 0.740, 95% CI 0.663–0.819) and mean transferrin levels(AUC 0.653, 95% CI 0.574–0.733).CONCLUSION: Independent risk factors for ICU-AW include female sex, advanced age, PN, MV, lower BMI, and elevated BUN and Cr levels. EEN may potentially delay ICU-AW onset, and the PAB/CRP ratio may be an effective diagnostic marker for this condition.

Prevalence and clinical characteristics of chronic kidney disease among patients with newly diagnosed ketosis-onset diabetes

BACKGROUND The prevalence and clinical characteristics of chronic kidney disease(CKD)among patients with ketosis-onset diabetes(also known as ketosis-prone diabetes)remain unclear.Furthermore,the classification of ketosis-onset diabetes remains controversial and requires further investigation.AIM To investigate the prevalence and clinical features of CKD in patients with newly diagnosed ketosis-onset diabetes.METHODS This real-world study included 217 patients with type 1 diabetes mellitus(T1DM),698 with ketosis-onset diabetes,and 993 with non-ketotic T2DM.The prevalence and clinical characteristics of CKD were compared among the three groups.Risk factors associated with CKD were evaluated using binary logistic regression for each group.RESULTS After adjusting for age and sex,the prevalence of CKD among patients with ketosis-onset diabetes(17.8%)was significantly higher than that in those with T1DM(8.3%,P=0.007),but was not statistically different compared to those with non-ketotic T2DM(21.7%,P=0.214).Furthermore,some risk factors for CKD,including age,and serum uric acid and C-reactive protein levels,in patients with ketosis-onset diabetes were similar to those with T2DM,but significantly different from those with T1DM.CONCLUSION The prevalence,clinical characteristics,and risk factors for CKD among patients with ketosis-onset diabetes were more similar to those with non-ketotic T2DM but considerably different from those with T1DM.These findings further support the classification of ketosis-onset diabetes as a subtype of T2DM rather than idiopathic T1DM.

Helicobacter pylori infection and risk of gastric cancer in Changle County,Fujian Province,China

AIM To evaluate the effects of Helicobacterpylori infection and other environmental factorson the development of gastric cancer.METHODS A population-based case-controlstudy was conducted in Changle County,FujianProvince.The primary gastric cancer cases werehistologically confirmed or diagnosed by surgerybetween,January 1996 and March 1998.Healthycontrols were randomly selected and matched byage,sex,and neighborhood of residence.Atotal of 101 pairs were included in the study.Specially trained interviewers conducted face-to-face interviews with the subjects according toa standardized questionnaire.Helicobacterpylori infections were measured by serum IgGantibody to Helicobacter pylori.ConditionalLogistic Regression analysis was used.RESULTS The presence of IgG antibody toHelicobacter pylori was 63.7% in studysubjects,56.0% in patients with cardiac cancer,and 60.5% in patients with non-cardiac gastriccancer.The risk factors of gastric cancer inChangle County were identified such as loweducational level[OR=3.864;95% confidenceinterval(95% CI)1.604-9.311],lowconsumption of fresh vegetables(OR=4.925;95%Cl 1.356-17.885),high intake of fish sauce(OR=10.587;95% Cl 2.821-39.738),unscheduled meals(OR=4.254;95%Cl 1.445- 12.552),and Helicobacter pylori infection(OR=3.453;95%Cl 0.901-13.224).CONCLUSION Helicobacter pylori infectionmay be important in the etiology of gastriccancer,but major risk factors other thanHelicobacter pylori are responsible for the highgastric morbidity in Changle County.

Fish sauce and gastric cancer:an ecological study in Fujian Province,China

AIM To explore the relationship betweenconsumption of fish sauce and the risk of gastriccancer in Fujian Province.METHODS An ecological study was carriedout.A total of 11000 subjects from 55 townshipswere randomly selected from 10 counties withinFujian Province.All subjects were localresidents who had been living in Fujian Provincefor more than 20 years,within the age group of45-74 years.Trained interviewers conductedface-to-face interviews with a standardizedquestionnaire,which covered the frequency andamount of food intake,dietary habit,tobaccoand alcohol consumption and history of chronicgastric diseases.Univariate and multivariateanalyses were performed using Epi-info and SASstatistical packages,respectively.RESULTS A significant correlation betweenmonthly consumption of fish sauce and mortalityof gastric cancer was found.Pearson’scoefficient of correlation was statisticallysignificant with r=0.7356 for males,r=0.5246for females(P【0.01).In the multivariateanalysis,consumption of fish sauce still showedan association with the risk of gastric cancer.No significant positive correlation betweenesophagus cancer,liver cancer,colon cancerand consumption of fish sauce were observed.CONCLUSION Long-term intake of fish saucemay be related to high mortality of gastriccancer.Consumption of fish sauce might be oneof important and unique etiologic factors ofgastric cancer in Fujian Province.Furtherstudies are needed to confirm this ecologicalstudy.