Intra-abdominal Hernia with Bowel Obstruction Triggering Multi-organ Failure: The Role of Preoperative Enteritis This report details the clinical course of a 41-year-old male who developed fulminant multiple organ dysfunction syndrome following emergency surgery for a strangulated intra-abdominal hernia. Preoperative manifestations, including diarrhea and marked leukocytosis, pointed towards an underlying infectious enteritis. We posited that surgical release of the obstructed, ischemic bowel segment precipitated a massive systemic influx of endotoxins and inflammatory mediators, triggering septic shock and rapid sequential organ failure. This case underscored the critical need to suspect concomitant gastrointestinal infection in patients presenting with mechanical bowel obstruction accompanied by infectious signs. Aggressive perioperative sepsis management encompassing early empiric antimicrobial therapy, vigilant hemodynamic monitoring, and preparedness for advanced organ support is essential to mitigate this severe complication.

Atherosclerosis (AS) remains the core pathological basis underlying the high incidence and high rates of mortality and disability associated with cardiovascular disease (CVD) worldwide. Its essence is not merely lipid deposition, but rather an immune-mediated disease of the vascular wall characterized by an interplay of lipid metabolism disorders and chronic inflammation, with damage to vascular endothelial cells serving as the initiating event. As the disease progresses, it involves complex synergistic interactions among various cellular components, including endothelial cells, macrophages, and inflammatory cells, ultimately leading to plaque formation, instability, and even fatal thrombotic events. In recent years, the central driving role of lipid metabolic reprogramming in the progression of AS has garnered increasing attention from the scientific community. Among the vast array of lipid molecules, long-chain fatty acids (LCFAs) have become a primary focus of research due to their exceptional physiological functions. Traditional views have primarily emphasized the basic physiological functions of LCFAs: serving as highly efficient energy substrates through mitochondrial β-oxidation and acting as key structural components of cellular phospholipid membranes. However, emerging evidence clearly indicates that the functions of LCFAs extend far beyond those of mere metabolic fuel. They also act as potent bioactive signaling molecules, playing an indispensable multidimensional role in the pathogenesis of AS. Equally noteworthy and representing a paradigm shift in cardiovascular research is the emerging theory of the “gut-heart axis”. This theoretical framework views the human gut microbiota—comprising trillions of microorganisms—as a critical and metabolically active “bioreactor”. A wealth of clinical and multi-cohort epidemiological studies have conclusively demonstrated that imbalances in the composition and function of the gut microbiota are highly correlated with the clinical risk and severity of AS. Within this axis, the gut microbiota serves as the primary processing hub for dietary lipids. It actively participates in the digestion and biochemical remodeling of LCFAs, thereby altering their saturation and chemical structure and generating a wide variety of gut microbial metabolites. The effects of these gut-derived lipid metabolites extend far beyond the local intestinal microenvironment. Upon entering the bloodstream, these circulating microbiota metabolites act as endocrine signals. Given the extreme complexity of the underlying mechanisms, a comprehensive elucidation of the synergistic and bidirectional interactions between LCFAs and the gut microbiota in vascular pathology is particularly urgent. Therefore, this article aims to provide a systematic review of the multidimensional regulatory mechanisms of LCFAs and their associated gut microbiota metabolites in the onset, progression, and clinical manifestations of AS. By thoroughly exploring the interaction patterns within the “LCFAs-gut microbiota-AS” triad, this review seeks to fundamentally expand our understanding of the pathogenesis of CVDs. More importantly, translating these mechanistic insights into clinical practice holds tremendous promise. We hope to provide a solid theoretical foundation for the future development of novel AS prevention and treatment strategies based on non-traditional approaches. These include precision nutritional interventions (i.e., dietary lipid intake plans tailored to an individual’s unique microbiome profile) and targeted microbiome modulation therapies (such as next-generation probiotics, prebiotics, or specific metabolite supplements). Targeting the gut as a “reactor” to treat vascular wall lesions represents a promising direction for future cardiovascular medicine.

A 21-year-old unmarried female visited Obstetrics and Gynecology Hospital,Fudan University with the chief complaint,memory decline for more than 20 days and discovery of a pelvic mass for more than 10 days.Through systematic examination,she was diagnosed with teratoma-associated anti-N-methyl-D-aspartate receptor(NMDAR)encephalitis.The patient underwent bilateral ovarian teratoma enucleation,and postoperative pathology revealed immature teratoma grade Ⅰ in the left ovary and mature teratoma in the right ovary.Perioperative combined immunotherapy significantly improved her neuropsychiatric symptoms.The diagnosis and treatment of ovarian teratoma-associated anti-NMDAR encephalitis require multidisciplinary collaboration,with accurate diagnosis,timely surgical resection within 1 month,and early initiation of immunotherapy being critical factors for improving prognosis.Clinicians should remain vigilant to avoid missed or misdiagnosed cases,as this condition can lead to severe outcomes.

Objective:To explore the spousal correlations of total cholesterol(TC),total triglyceride(TG),low-density lipoprotein cholesterol(LDL-C),and high-density lipoprotein cholesterol(HDL-C),and to investigate the reasons behind these spousal correlations.Methods:Participants and data were from the baseline survey of family-based cohort studies in Fangshan,Beijing and Tulou,Fujian.The ori-gin of spousal correlations were explored from perspectives of convergence,assortative mating,social ho-mogamy.Pearson's correlation and generalized linear models(GLM)were used to estimate the spousal correlation.Convergence was assessed by Pearson's correlation between the phenotypic differences be-tween couples and the duration of marriage,with GLM used for further validation.Pearson's correlation of genetic risk scores(GRS)and couple-specific Mendelian randomization(MR)were calculated to assess the genetic correlation and possible causal relationships between spouses.Two-independent-sample t-tests were used to compare GRS consistency across subgroups divided by education attainment,couple-specific MR and Q statistics used to test assortative mating in subgroups and intergroup differences.Results:In the study,342 couples(287 couples from Fangshan and 55 couples from Fujian)were included,with the average age of(64.91±8.76)years.Spousal correlations of TC,TG,HDL-C,and LDL-C showed statistically significant associations both before and after adjusting for covariates,with effect sizes of 0.229(95％CI:0.125-0.327),0.257(95％CI:0.155-0.354),0.179(95％CI:0.074-0.280),and 0.181(95％CI:0.076-0.282).For convergence,for each additional year of marriage,ΔTC increased by 0.016 mmol/L(95％CI:0.001-0.033 mmol/L),and ΔLDL-C increased by 0.017 mmol/L(95％CI:0.002-0.031 mmol/L).For assortative mating,GRS correlations and results of couple specific MR didn't show any statistical significance.For social homogamy,no differences in GRS or assortative mating were found between subgroups stratified by education attainment.Conclusion:The blood lipid in participants exhibit spousal phenotypic correlations,however,no effects of convergence,assortative mating or social homogamy were observed.More independent studies with larger sample sizes are warranted to further validate these findings in the future.

BACKGROUND:Cellular pyroptosis is an important pathological mechanism of cerebral ischemia/reperfusion injury.Buyang Huanwu Tang is a classic formula for the clinical treatment of ischemic stroke in traditional Chinese medicine,and cellular pyroptosis may be an effective target of Buyang Huanwu Tang in the treatment of cerebral ischemia/reperfusion injury.OBJECTIVE:To observe the effect and mechanism of Buyang Huanwu Tang on pyroptosis in brain tissues of middle cerebral artery occlusion/reperfusion rats.METHODS:Forty-eight Sprague-Dawley rats were randomly divided into sham operation group,model group,Astragalus membranaceus group and Buyang Huanwu Tang group.Except for the sham operation group,all groups were subjected to middle cerebral artery occlusion for ischemia for 2 hours and reperfusion for 72 hours.The rats in the Astragalus membranaceus group and Buyang Huanwu Tang group were continuously gavaged with the corresponding volume of drugs until ischemia and reperfusion for 72 hours after awakening from the modeling,once in the morning and once in the evening.Zea Longa score was used to observe the neurological deficits of rats.TTC staining was performed to observe cerebral infarct size in rats.Hematoxylin-eosin staining was used to observe the pathological changes of the brain tissue.Immunofluorescence was used to observe the co-expression of Tunel and Cleaved-Caspase-1 in the brain tissue and the expression of the junction protein ASC.Immunohistochemistry and western blot were used to detect the expression of pyroptosis-related proteins in rat brain tissues.RESULTS AND CONCLUSION:(1)Compared with the sham operation group,the neurological deficit score of rats was significantly higher in the model group(P<0.01),and compared with the model group,the neurological deficit score of rats was significantly lower in the Buyang Huanwu Tang group and the Astragalus membranaceus group(P<0.01).(2)Compared with the model group,the volume ratio of cerebral infarction was lower in the Astragalus membranaceus group and Buyang Huanwu Tang group(P<0.01).(3)In the model group,the nuclei of neuronal cells in the brain tissue were deeply stained or lysed,and arrangement of the cells was disorganized.Compared with the model group,the pathologic damage of the brain was less severe in the Buyang Huanwu Tang group and the Astragalus membranaceus group.(4)Compared with the sham operation group,the number of Tunel and Cleaved-Caspase-1 double-positive cells and immunofluorescence intensity of ASC in the brain tissue was significantly increased in the model group,and the expression of Cleaved-Caspase-1,NLRP3,interleukin 18,and interleukin 1β was significantly elevated in the model group(P<0.01).Compared with the model group,the number of Cleaved-Caspase-1 and Tunel double-positive cells,immunofluorescence intensity of ASC,and the expression of Cleaved-Caspase-1,NLRP3,interleukin 18,and interleukin 1β were all significantly decreased in the Buyang Huanwu Tang group and the Astragalus membranaceus group(P<0.01).The results indicate that Buyang Huanwu Tang and its monarch drug Astragalus membranaceus can effectively alleviate brain tissue injury in rats with middle cerebral artery occlusion and reperfusion,and its mechanism may be related to the inhibition of neuronal cell pyroptosis.

AIM To investigate the effects of Xuesaitong Capsules(Panax notoginseng saponins)on ischemia/reperfusion injury in a mouse model of skin frostbite.METHODS The mice were randomly divided into the control group,the model group,the dexamethasone group(1 mg/kg),and the low-dose,medium-dose,and high-dose Xuesaitong Capsules groups(0.036,0.072,and 0.144 g/kg),with eight mice in each group.A frostbite model was established using a dry ice-cooled ceramic(ferrite)magnet.On the 2nd day after modeling,each group started its corresponding dosing by gavage for 14 consecutive days.The wound healing,histopathological changes,and serum levels of high-sensitivity C-reactive protein(hs-CRP),thromboxane B2(TXB2),6-keto-prostaglandin F1α(6-K-PGF1α),nitric oxide(NO)and endothelin(ET)were assessed using ELISA.The superoxide dismutase(SOD)activity and malondialdehyde(MDA)levels in skin tissues were measured biochemically.The protein expressions of tumor necrosis factor(TNF)-α,interleukin(IL)-1β,IL-6,Toll-like receptor(TLR)4 and phosphorylated nuclear factor-KB p65(p-NF-κB p65)in skin tissues were determined by Western blot.Additionally,LncRNA H19 mRNA expression in skin tissues was evaluated using RT-qPCR.RESULTS After the final administration,compared with the control group,the model group exhibited partial scab detachment,wound healing,and larger wound areas;hyperkeratosis with incomplete keratinization,detachment of the dermis and subcutaneous tissue,partial loss of appendages,subcutaneous edema,and dilated,congested,and hemorrhagic stromal vessels with extensive lymphocyte infiltration revealed by the histopathological examination;elevated serum levels of hs-CRP,TXB2,and ET(P＜0.05,P＜0.01);decreased 6-K-PGF1α and NO levels(P＜0.05,P＜0.01);reduced SOD activity in skin tissues(P＜0.01);increased MDA levels(P＜0.01);and upregulated protein expressions of TNF-α,IL-1β,IL-6,TLR4 and p-NF-κB p65,as well as LncRNA H19 mRNA expression(P＜0.05,P＜0.01).Compared with the model group,the group intervened with high-dose Xuesaitong Capsules displayed reduced wound areas(P＜0.01);decreased serum levels of hs-CRP,TXB2 and ET(P＜0.05,P＜0.01);increased 6-K-PGF1α and NO levels(P＜0.05,P＜0.01);enhanced SOD activity(P＜0.05,P＜0.01);reduced MDA level in skin tissues(P＜0.05,P＜0.01);and down-regulated TNF-α,IL-1β,IL-6,TLR4 and p-NF-κB p65 protein expressions and suppressed LncRNA H19 mRNA expression in skin tissues as well(P＜0.05,P＜0.01).CONCLUSION Xuesaitong Capsules alleviate ischemia/reperfusion injury in frostbite-injured mice by exerting anti-inflammatory and anti oxidative stress effects and restoring vascular endothelial function mediated by the downregulation of LncRNA H19 expression and inhibition of the TLR4/NF-κB signaling pathway.

Objective:To explore the association between perceived social support,TMEM161B gene rs768705 polymorphism,and their interaction with incidence of depressive symptoms in the freshmen.Methods:A total of 9928 freshmen from two medical universities were investigated at baseline and follow-up two years later during 2018-2020 by cluster sampling.A self-report demographic characteristics questionnaire was used to collect information of general demographic characteristics.Perceived Social Support Scale,Beck Depression Inventory,Beck Anxiety Inventory and Adolescent Self-Rating Life Events Check List were used to measure the level of perceived social support,depressive symptoms,anxiety symptoms and the number of negative life events of individuals.Blood sam-ples were collected and typed for DNA by professionals.Results:Family support and other support were all nega-tively associated with depressive symptoms in the freshmen(OR=0.96,95％CI:0.93-0.99;OR=0.94,95％CI:0.91-0.98).There was no correlation between friend support and depressive symptoms in the freshmen(OR=0.99,95％CI:0.95-1.02).TMEM161B gene rs768705 polymorphism(AG)was positively associated with de-pressive symptoms in the freshmen(OR=1.58,95％CI:1.12-2.23).The interactions of friend support with TMEM161B gene rs768705 polymorphism(AG)(OR=1.13,95％CI:1.02-1.26)and other support with TMEM161B gene rs768705 polymorphism(AG)(OR=1.13,95％CI:1.02-1.25)had significant effects on the incidence of depressive symptoms in the females and no significant effect in the males.Conclusion:The perceived social support,TMEM161B gene rs768705 polymorphism and their interaction are associated with influence of de-pressive symptoms,and have sex difference in the freshmen.

OBJECTIVE To construct the drug utilization evaluation criteria for Dezocine injection,so as to provide reference for the rational drug use in medical institutions.METHODS On the basis of evidence methodology,relevant guidelines/expert consensus,systematic reviews/meta-analysis were consulted;the evaluation criteria framework for Dezocine injection was established after screening evidence.Delphi method was employed,whereby 28 clinicians and clinical pharmacists from secondary and above-level medical institutions across eight provinces,including Tianjin,Beijing and Shandong,were selected to participate in two rounds of questionnaire surveys.The final indicators were determined based on the experts'enthusiasm coefficient,authority coefficient,and degree of coordination.RESULTS The effective recovery rate of questionnaire was 100%in the first round and 92.86%in the second round;expert authority coefficient was 0.82 in the first round and 0.81 in the second round;the coordination degree of experts in the first round was 0.29,and in the second round was 0.31(P＜0.001).Drug utilization evaluation standard system for Dezocine injection was formed finally,including three dimensions of medication indications,medication process and medication results,with a total of 11 first-level indicators(such as indications,usage and dosage)and 33 second-level indicators(such as labor analgesia and the management of severe pain following major or moderate surgeries combined with other analgesic drugs).The average importance scores for each indicator ranged from 4.08 to 5.00 points,with an overall average score of 4.61 points and coefficient of variation ranging from 0 to 0.19.CONCLUSIONS The drug utilization evaluation criteria for Dezocine injection established based on evidence-based methodology and Delphi method is authoritative and scientific,which provides a reference for subsequent evaluation of the rationality of clinical medication.

Osteosarcoma(OS) is the most common primary bone malignancy with a high propensity for local infiltration and metastasis.c-Jun N-terminal kinases(JNK)is an extremely im-portant member of the mitogen-activated protein kinase(MAPK)family,and the JNK signaling pathway has been shown to be in-volved in regulating OS development.In this paper,we review the research progress on the JNK signaling pathway regulating biological behaviors such as proliferation,migration,invasion,an-giogenesis,autophagy,apoptosis and pyroptosis of OS,as well as the oxidative stress and non-coding RNA regulation of OS through the JNK signaling pathway,to further explore the intrin-sic regulatory mechanisms of the JNK signaling pathway,so as to provide a new way of thinking in searching for the treatment of OS.

Osteosarcoma(OS) is the most common primary bone malignancy with a high propensity for local infiltration and metastasis.c-Jun N-terminal kinases(JNK)is an extremely im-portant member of the mitogen-activated protein kinase(MAPK)family,and the JNK signaling pathway has been shown to be in-volved in regulating OS development.In this paper,we review the research progress on the JNK signaling pathway regulating biological behaviors such as proliferation,migration,invasion,an-giogenesis,autophagy,apoptosis and pyroptosis of OS,as well as the oxidative stress and non-coding RNA regulation of OS through the JNK signaling pathway,to further explore the intrin-sic regulatory mechanisms of the JNK signaling pathway,so as to provide a new way of thinking in searching for the treatment of OS.