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Systemic lupus erythematosus (SLE) is a chronic, inflammatory, and progressive autoimmune disease. The unclear pathogenesis, high heterogeneity, and prolonged course of the disease present significant challenges for effective clinical management of lupus patients. Dysregulation of the immune system and disruption of immune tolerance, particularly through the abnormal activation of B lymphocytes and the production of excessive autoantibodies, lead to widespread inflammation and tissue damage, resulting in multi-organ impairment. Currently, there is no systematic review that examines the specificity of B cell characteristics and pathogenic mechanisms across various organs. This paper reviews current research on B cells in lupus patients and summarizes the distinct characteristics of B cells in different organs. By integrating clinical manifestations of organ damage in patients with a focus on the organ-specific features of B cells, we provide a new perspective on enhancing the efficacy of lupus-targeted B cell therapy strategies. [ABSTRACT FROM AUTHOR]

Introduction: In the rise of the modern era, which intensifies mental health issues, some individuals consider suicide using methods such as poison ingestion. Rodenticides, commonly used for pest control, including brodifacoum, bromadiolone and bromethalin, are often involved in these cases. In a retrospective study conducted by the National Poison Information Centre, it was found that death due to rodenticide poisoning accounted for about 17.06% when compared to other pesticides, indicating a rise in the global burden of rodenticide poisoning. Prompt medical intervention and hospitalisation are vital in cases of rodenticide poisoning. Hence, histomorphological examination of affected organs is essential to determine the damage to vital organs, thereby guiding clinicians in future perspectives to facilitate patient recovery. Aim: To study the histomorphological findings of various organs affected by rodenticide poisoning and to assess which organ is most commonly involved. Materials and Methods: This cross-sectional study investigated the effects of rodenticide poisoning through medicolegal autopsy specimens at Government Medical College and Hospital, Krishnagiri, Tamil Nadu, India from June 2023 to June 2024 over a duration of 12 months. The study utilised retrospective data from autopsies, focusing on cases where death resulted from rodenticide poisoning. Autopsy specimens, including the heart, lungs, kidneys, liver, spleen and brain, were preserved in formalin and subjected to gross and microscopic examination by a pathologist. Histopathological sections were stained with Haematoxylin and Eosin (H&E). The study employed a convenience sampling technique with a sample size of 30, determined using Solvin's formula. Data from crime history, clinical history and autopsy findings were recorded and analysed using Statistical Package for the Social Sciences (SPSS) version 25.0, and compiled to draw conclusions regarding the impact of rodenticide poisoning on organ damage. Results: During the one-year period of the study, 450 medicolegal autopsies were processed, of which 180 (40%) cases were due to poison consumption. Of these, 32 cases (17.78%) were from rodenticide intake. Male predominance was observed in this study, comprising 20 males (62.50%) and 12 females (37.50%), with a ratio of 5:3. Histopathology revealed congestion in most of the organs, with the liver showing steatosis and necrosis, kidneys exhibiting acute tubular necrosis, and lungs displaying haemorrhage and oedema. The heart showed features of atherosclerotic changes in seven cases, whereas the brain showed congestion in 11 cases and cerebral haemorrhage in one case out of the 32 cases, respectively. Conclusion: This study found a higher prevalence of poisoning among males and increased susceptibility in teenagers and elderly individuals. The study emphasises the histomorphological findings of various organs in rodenticide poisoning and concludes that the liver, kidneys and lungs appear to be the most affected organs. It also highlights the importance of yoga in preventing suicides. [ABSTRACT FROM AUTHOR]

Sepsis remains a complex clinical challenge, with experimental animal models being crucial for developing effective therapeutic strategies. Current approaches often struggle to establish clinically relevant animal models that accurately represent human sepsis pathogenesis. This study aimed to determine the optimal intraperitoneal Escherichia coli (E. coli) dose for inducing a reproducible sepsis state in male rats. A preliminary experimental study was conducted using male Rattus norvegicus rats divided into three groups: a control group and two sepsis groups induced with E. coli at doses of 1x106 and 1.5x106 CFU/kg. Biomarkers including neutrophils, procalcitonin (PCT), interleukin-6 (IL-6), and malondialdehyde (MDA) were measured at 24-, 48-, and 72-hours post-induction. Histopathological examinations of liver, kidney, spleen, and heart tissues were performed using hematoxylin and eosin staining. Both E. coli doses significantly increased inflammatory and infection biomarkers. Dose of 1.5x106 CFU/kg demonstrated higher biomarker levels and more severe organ damage compared to control group and 1x106 CFU/kg dose. In dose of 1.5x106 CFU/kg group, Neutrophil levels increased from baseline 1.4x10³ to 7.71x10³ mmol/dL, IL-6 from 20.72 to 77.49 pg/mL, MDA from 1.37 to 12.15 nmol/mL and PCT from a normal level of 3.1 to 5.79 ng/mL within 72 hours, meeting the criteria for sepsis. Histopathological examination revealed significant organ damage, with higher induction doses correlating with increased histopathological damage scores. Intraperitoneal E. coli induction at 1.5x106 CFU/kg effectively creates a reproducible sepsis model in rats, providing a valuable experimental approach for studying sepsis pathogenesis and potential interventions. [ABSTRACT FROM AUTHOR]

Hemorrhagic shock is a type of hypovolemic shock and a significant cause of trauma-related death worldwide. The innate immune system has been implicated as a key mediator in developing severe complications after shock. Inflammation from the innate immune system begins at the time of initial insult; however, its activation is exaggerated, resulting in early and late-stage complications. Hypoxia and hypoperfusion lead to the release of molecules that act as danger signals known as damage-associated molecular patterns (DAMPs). DAMPs continue to circulate after shock, resulting in excess inflammation and tissue damage. We recently discovered that cold-inducible RNA-binding protein released into the extracellular space acts as a DAMP. During hemorrhagic shock, hypoperfusion leads to cell necrosis and the release of CIRP into circulation, triggering both systemic inflammation and local tissue damage. In this review, we discuss extracellular cold-inducible RNA-binding protein (eCIRP)'s role in sterile inflammation, as well as its various mechanisms of action. We also share our more newly developed anti-eCIRP agents with the eventual goal of producing drug therapies to mitigate organ damage, reduce mortality, and improve patient outcomes related to hemorrhagic shock. Finally, we suggest that future preclinical studies are required to develop the listed therapeutics for hemorrhagic shock and related conditions. In addition, we emphasize on the challenges to the translational phase and caution that the therapy should allow the immune system to continue to function well against secondary infections during hospitalization. [ABSTRACT FROM AUTHOR]

Objective To analyse interrater reliability of four RheuMetric checklist 0–10 visual numerical scales (VNSs) of physician global assessment (DOCGL), inflammation or reversible findings (DOCINF), organ damage or irreversible findings (DOCDAM) and patient distress or findings explained by fibromyalgia, depression or anxiety (DOCDIS). Methods A retrospective study was performed of data from a rheumatology fellows' continuity clinic at Rush University. Each rheumatology patient seen in routine care with any diagnosis completed a multidimensional health assessment questionnaire (MDHAQ). Both the rheumatology fellow and attending rheumatologist independently completed RheuMetric estimates at the same visit for DOCGL, DOCINF, DOCDAM, DOCDIS and the proportion of DOCGL explained by each subglobal estimate (totalling 100%). Agreement between the two assessors was compared using paired t -tests, Spearman correlation coefficients, intraclass correlation coefficients (ICCs), Lin's concordance correlation coefficients (LCCCs) and Bland–Altman plots. Results In 112 patients, mean levels of DOCINF were highest in inflammatory diseases, DOCDAM in osteoarthritis (OA) and DOCDIS in primary fibromyalgia (FM). However, mean DOCDAM was as high as DOCINF in inflammatory diseases. No statistically significant differences were seen between scores from attending rheumatologists and fellows. Agreement within 2/10 ranged from 60% for DOCGL to 71% for DOICINF and DOCDAM. Spearman correlations were 0.49–0.65, ICCs were 0.46–0.63 and LCCCs were 0.46–0.62 between rheumatologist and fellow, indicating moderate agreement; reliability was slightly higher for each subglobal VNS than for DOCGL. Conclusion RheuMetric 0–10 DOCGL, DOCINF, DOCDAM and DOCDIS have moderate interrater reliability and are feasible in routine care to estimate patient status beyond DOCGL for improved management decisions. [ABSTRACT FROM AUTHOR]

Simple Summary: With global warming, heat stress has become an increasingly serious problem for poultry because of their abundant feathers, limited sweat glands, and fast metabolism. To alleviate the losses caused by poultry heat stress, it is important to investigate the mechanisms and control strategies for poultry heat stress. When heat stress occurs, the neuroendocrine system in poultry will be disrupted, while several organs in the body will be damaged, affecting the poultry's production performance and health. Adding nutrients to feed is a mild and effective means of heat stress management and holds significant implications for the poultry farming industry. Heat stress (HS) due to high temperatures has adverse effects on poultry, including decreased feed intake, lower feed efficiency, decreased body weight, and higher mortality. There are complex mechanisms behind heat stress in poultry involving the neuroendocrine system, organ damage, and other physiological systems. HS activates endocrine glands, such as the pituitary, adrenal, thyroid, and gonadal, by the action of the hypothalamus and sympathetic nerves, ultimately causing changes in hormone levels: HS leads to increased corticosterone levels, changes in triiodothyronine and thyroxine levels, decreased gonadotropin levels, reduced ovarian function, and the promotion of catecholamine release, which ultimately affects the normal productive performance of poultry. Meanwhile, heat stress also causes damage to the liver, lungs, intestines, and various immune organs, severely impairing organ function in poultry. Nutrient additives to feed are important measures of prevention and treatment, including natural plants and extracts, probiotics, amino acids, and other nutrients, which are effective in alleviating heat stress in poultry. Future studies need to explore the specific mechanisms through which heat stress impacts the neuroendocrine system in poultry and the interrelationships between the axes and organ damage so as to provide an effective theoretical basis for the development of preventive and treatment measures. [ABSTRACT FROM AUTHOR]

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Background/Objectives: Neutrophils, as the first line of defense in the immune response, produce neutrophil extracellular traps (NETs) upon activation, which are significant in the pathogenesis and organ damage in sepsis. This study aims to explore the clinical value of myeloperoxidase-DNA (MPO-DNA) and cell-free DNA (cf-DNA) in sepsis patients. Methods: Clinical data were collected from 106 sepsis patients, 25 non-sepsis patients, and 51 healthy controls. Sequential Organ Failure Assessment (SOFA) scores were calculated, and levels of MPO-DNA) complexes and cf-DNA were measured using specific kits. Correlation analyses assessed relationships between indicators, while logistic regression identified independent risk factors. Receiver operating characteristic (ROC) curves calculated the area under the curve (AUC) to evaluate the diagnostic value of the biomarkers. Results: Sepsis patients exhibited significantly elevated levels of MPO-DNA and cf-DNA compared to non-sepsis patients and healthy controls. In sepsis patients, MPO-DNA and cf-DNA levels correlated with inflammation, coagulation, and organ damage indicators, as well as procalcitonin (PCT) levels and SOFA scores. Both C-reactive protein (CRP) and cf-DNA were identified as independent risk factors for sepsis, demonstrating moderate diagnostic value. ROC analysis showed that the combination of MPO-DNA and CRP (AUC: 0.837) enhances the AUC value of CRP (0.777). Conclusions: In summary, elevated serum levels of MPO-DNA and cf-DNA in sepsis patients correlate with SOFA scores and PCT levels, providing reference value for sepsis diagnosis in clinical settings. [ABSTRACT FROM AUTHOR]

Pasteurella multocida toxin (PMT) is one of the most important virulence factors of Pasteurella multocida type D. Pasteurella multocida infection has caused enormous economic losses in the pig farming industry. Although it is well known that this bacterial infection causes progressive atrophic rhinitis, its effects on other organ tissues in pigs are unclear. In this study, PMT was expressed and purified, and the cytotoxic effects of PMT on four types of swine cells, LLC-PK1, PAM, IPEC, and ST, were investigated. LLC-PK1 exhibited the highest sensitivity to the cytotoxic effects of PMT. Our studies revealed that a PMT concentration of 0.1 µg/kg can lead to weight loss, whereas a PMT concentration of 0.5 µg/kg can lead to death in mice. PMT causes damage to the intestines, kidneys, lungs, livers, and spleens of mice. Furthermore, PMT caused acute death in pigs at treatment concentrations greater than 5 µg/kg; at PMT concentration of 2.5 µg/kg, weight loss occurred until death. PMT mainly caused damage to the hearts, lungs, livers, spleens and kidneys of pigs. The organ coefficient showed that damage to the heart and kidneys was the most severe and caused the renal pelvis and renal pyramid to dissolve and become cavitated. Pathology revealed hemorrhage in the lungs, liver, and spleen, and the kidneys were swollen and vacuolated, which was consistent with the damaged target organs in the mice. In conclusion, these findings demonstrate that PMT is extremely toxic in vitro and in vivo, causing damage to various organs of the body, especially the kidneys and lungs. This study provides a theoretical basis for the in-depth exploration of the cytotoxic effects of PMT on target organs. [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is a chronic, inflammatory, and progressive autoimmune disease. The unclear pathogenesis, high heterogeneity, and prolonged course of the disease present significant challenges for effective clinical management of lupus patients. Dysregulation of the immune system and disruption of immune tolerance, particularly through the abnormal activation of B lymphocytes and the production of excessive autoantibodies, lead to widespread inflammation and tissue damage, resulting in multi-organ impairment. Currently, there is no systematic review that examines the specificity of B cell characteristics and pathogenic mechanisms across various organs. This paper reviews current research on B cells in lupus patients and summarizes the distinct characteristics of B cells in different organs. By integrating clinical manifestations of organ damage in patients with a focus on the organ-specific features of B cells, we provide a new perspective on enhancing the efficacy of lupus-targeted B cell therapy strategies.

Objective: By comparing viral sepsis caused by SARS CoV-2 with pneumosepsis caused by other pathogens, we aimed to compare the pathogen– host relationship, organ damage affecting the clinic, and similar and different features of the two types of sepsis. Materials and Methods: A total of 414 patients diagnosed with critical COVID-19 between 2019 and 2021 and 303 pneumosepsis cases that met the diagnostic criteria for sepsis-3 between 2016 and 2019 admitted to the Anesthesiology and Reanimation Intensive Care Unit (ICU) were retrospectively screened. The patient’s demographic data, mortality rates, length of stay in the intensive care unit, development of secondary organ dysfunction, presentation values of laboratory and mechanical ventilation, and changes within the 1-week follow-up were compared. Results: The SOFA scores were significantly higher in the COVID-19 sepsis group at presentation (8.2±2.9 vs.7.2±3.7; p

Objectives: We aim to independently assess the validity of the damage index for antiphospholipid syndrome (DIAPS) in thrombotic antiphospholipid syndrome (APS) patients by exploring the prevalence and risk factors of organ damage and evaluating its impact on health-related quality of life (HR-QoL). Methods: Cross-sectional study including all thrombotic APS patients (Sydney criteria) attending a Portuguese tertiary centre. Damage was assessed using the DIAPS, and HR-QoL using the 3- and 5-level EuroQol HR-QoL (EQ-D5-3L and 5L), and Visual Analogue Scale (VAS) applied via a phone questionnaire. Spearman's correlation between DIAPS and the HR-QoL scales was performed. Risk factors for damage accrual and HR-QoL impairment were explored using univariate and multivariate logistic regression. Results: Among the 108 patients (female, 65.7%; white, 90.7%; primary APS, 75.9%; median disease duration, 6 years), damage (DIAPS≥1) developed in 48.2% of patients (mean ± SD DIAPS, 3.08 ± 1.83). DIAPS's neuropsychiatric domain was the most affected (24.2%), followed by the peripheral vascular domain (20.3%). No clinical, demographic nor laboratory parameters were significantly associated with damage. Regarding HR-QoL, pain/discomfort, anxiety/depression and usual activities domains were the most frequently impaired in both scales. DIAPS's domains correlated similarly with the EQ-5D-3L and 5L scales' individual domains. Female sex, medical disorders, secondary APS and type of presenting thrombosis (arterial) increased the risk of HR-QoL impairment. Total DIAPS was associated with higher odds of mobility, self-care and pain/discomfort impairment in both EQ-5D-3L and 5L scales but lost its independent risk in multivariable analysis. Conclusion: This external validation of DIAPS reinforces the ability of the score to correlate with HR-QoL while also highlighting risk factors for HR-QoL impairment other than damage accrual. [ABSTRACT FROM AUTHOR]

This article presents a case study of a 29-year-old man who arrived at the emergency department with extremely high blood pressure and kidney dysfunction. The patient experienced symptoms such as headache and weakness, and further examination revealed retinopathy and left ventricular hypertrophy. These findings indicated a hypertensive emergency, specifically malignant hypertension associated with thrombotic microangiopathy. The article emphasizes the need for timely diagnosis and treatment in cases of this condition, and discusses the challenges of accurately diagnosing it. [Extracted from the article]

Objective: By comparing viral sepsis caused by severe acute respiratory syndrome coronavirus-2 with pneumosepsis caused by other pathogens, we aimed to compare the pathogen-host relationship, organ damage affecting the clinic, and similar and different features of the two types of sepsis. Materials and Methods: A total of 414 patients diagnosed with critical coronavirus disease-2019 (COVID-19) between 2019 and 2021 and 303 pneumosepsis cases that met the diagnostic criteria for sepsis-3 between 2016 and 2019 admitted to the anesthesiology and reanimation intensive care unit (ICU) were retrospectively screened. The patient's demographic data, mortality rates, length of stay in the ICU, development of secondary organ dysfunction, presentation values of laboratory and mechanical ventilation, and changes within the 1-week follow-up were compared. Results: The sequential organ failure assessment scores were significantly higher in the COVID-19 sepsis group at presentation (8.2±2.9 vs. 7.2±3.7; p<0.0001) and during follow-up (8.9±4.9 vs. 7.8±3.7; p=0.002). The mean age of the patients was 65.4±17.2 years in the non-COVID-19 sepsis group and 57.9±17.1 years in the COVID-19 sepsis group (p<0.0001). The number of days on mechanical ventilation was significantly higher in the COVID-19 sepsis group (p=0.018). Mortality was detected in 299 patients (41.7%) in total, with no significant difference being observed between the two groups (p=0.592). Conclusion: Despite the patient population having a lower mean age and fewer comorbidities, organ dysfunction was higher in COVID-19 sepsis patients during admission to the ICU and follow-up. While the pathogen causing sepsis can be brought under control with rapid diagnosis and appropriate antimicrobial treatment, organ damage cannot be controlled with appropriate antiviral treatment in COVID-19 sepsis. In COVID-19 sepsis, secondary organ damage may be more evident as a result of damage and immunomicrothrombosis, which causes high mortality and morbidity, the mechanism of which has not yet been fully elucidated. [ABSTRACT FROM AUTHOR]

Abstract Background Systemic lupus erythematosus (SLE), a chronic multisystem autoimmune disease, carries high risk of organ damage and burden to healthcare systems. SLE disease modification aims to reduce disease activity with minimal treatment toxicity and preventing or minimizing organ damage development. This real-world study utilizing healthcare administrative claims data assessed organ damage development, associated costs and healthcare resource utilization (HCRU) in patients with SLE in Germany. Methods Claims data from January 1, 2007, to December 31, 2017, were obtained from the Betriebskrankenkassen German Sickness Fund Database. Adults (> 18 years) with a confirmed SLE diagnosis between January 1, 2009, and December 31, 2014, (inclusion period) were included. The index date was calculated based on the first recorded SLE diagnosis during this period. Patients were propensity score–matched (1:3) to a comparator cohort without SLE by age, sex, and comorbidities (Charlson comorbidity index). Organ damage was identified using an algorithm developed based on conditions described in the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI), using ICD-10-GM diagnostic codes, healthcare procedures, and/or treatments. Results 2121 patients with SLE and 6308 comparator patients were included (mean follow-up time: 6.4 years). Organ damage prevalence increased from 60.5% at baseline to 83.0% during 6 years of follow-up in all patients with SLE, while 17.0% of patients with SLE did not develop organ damage. Patients with newly confirmed SLE diagnosis without organ damage at baseline were nearly twice as likely to develop organ damage within 5 years versus the comparator cohort (52.0% vs. 27.0%). Total annual costs per patient-year for patients with SLE with organ damage were more than double those of patients with SLE without organ damage; both the number of inpatient admissions and length of stay were higher. Conclusions The application of a recently developed algorithm allowed us to use claims data to elucidate SLE organ damage, and its associated high clinical and economic burden, in a large, representative sample in Germany. To our knowledge, this is the first European analysis of its kind involving a broad cohort of patients with SLE treated in the routine care setting.

Objective To explore the possibility of rhabdomyolysis and related organ damage in new recruits training in high temperature and high humidity environment by comparing the effects of different training environments on the laboratory indicators and electrocardiogram. Methods A total of 250 new recruits from a unit in Beijing and another 250 ones from a unit in Hainan were recruited and assigned into conventional environment group and high temperature and high humidity environment group, respectively. All of them were male, with an average age of 21.36±2.59 years. Before and in 4 weeks after training in the same subjects, their general information, blood and urine indicators, and electrocardiogram were collected. All data were statistically analyzed. Results The incidences of inflammatory reaction, myocardial injury, muscle injury, liver injury, and kidney injury were 45.76%, 3.39%, 12.71%, 25.42%, and 12.71%, respectively, in the high temperature and high humidity environment group, which were all significantly higher than those in the conventional environment group (P < 0.05). The former group had an incidence rate of 6.78%, 5.93%, 8.47%, 6.78%, and 2.54%, respectively, in sinus bradycardia, atrial premature beats, unspecific ST-T changes, left ventricular hypertension and short PR interval, and all of the rates were higher than those of the conventional environment group (P < 0.05). Conclusion The incidences of inflammatory reaction, myocardial injury, muscle injury, liver injury, kidney injury, and ECG abnormalities are more common in new recruits after military training in high temperature and high humidity environment.

Abstract Background Temperature control plays a pivotal role in patients with heat stroke (HS), but little work has been done sufficiently on the use of temperature control to reflect disease progression. Here, we defined and analyzed the concrete role of controlling time for core temperature to physiological level (CTTP), in order to explore a potential index to guide the treatment of HS. Method This is a retrospective cohort study. From three hospitals located in Sichuan province, China, we collected a total of 179 HS cases with clinical diagnosis and treatment records. We defined CTTP as the time interval of HS onset to stabilization of core temperature (rectal temperature) below 37.7°C and analyzed the correlation between CTTP and inpatient death of HS patients. Results Of all the cases, 64.80% were male and 53.07% were exertional heat stroke (EHS). The median (IQR) age was 59 (23.5–73) years old, and the median (IQR) onset temperature was 42 (40.4–42)°C. Multivariable analysis demonstrated significantly high inpatient death in the highest CTTP tertile (>18 h) (hazard ratio: 18.75; 99% confidence interval: 4.06–86.59; p = .0002). In addition, compared with patients in lowest CTTP tertile, patients in highest CTTP tertile were at significantly higher risk of organ damage: 3.48‐fold for respiratory failure (95% CI: 1.41–8.59, p = .0069); 3.18‐fold for shock (95% CI: 1.37–7.39, p = .0071); 4.09‐fold for rhabdomyolysis (95% CI: 1.73–9.64, p = .0013); 4.64‐fold for renal damage (95% CI: 2.12–10.14, p = .0001). Conclusion Long of CTTP predicts inpatient death of HS patients with a CTTP tertile >18 h associated with the highest rate of inpatient death.

Hemorrhagic shock is a type of hypovolemic shock and a significant cause of trauma-related death worldwide. The innate immune system has been implicated as a key mediator in developing severe complications after shock. Inflammation from the innate immune system begins at the time of initial insult; however, its activation is exaggerated, resulting in early and late-stage complications. Hypoxia and hypoperfusion lead to the release of molecules that act as danger signals known as damage-associated molecular patterns (DAMPs). DAMPs continue to circulate after shock, resulting in excess inflammation and tissue damage. We recently discovered that cold-inducible RNA-binding protein released into the extracellular space acts as a DAMP. During hemorrhagic shock, hypoperfusion leads to cell necrosis and the release of CIRP into circulation, triggering both systemic inflammation and local tissue damage. In this review, we discuss extracellular cold-inducible RNA-binding protein (eCIRP)’s role in sterile inflammation, as well as its various mechanisms of action. We also share our more newly developed anti-eCIRP agents with the eventual goal of producing drug therapies to mitigate organ damage, reduce mortality, and improve patient outcomes related to hemorrhagic shock. Finally, we suggest that future preclinical studies are required to develop the listed therapeutics for hemorrhagic shock and related conditions. In addition, we emphasize on the challenges to the translational phase and caution that the therapy should allow the immune system to continue to function well against secondary infections during hospitalization.

Introduction Obesity has became a significant health concern over the past decade. According to a higher body mass index (BMI), obesity enhances the probability of malignancy, type 2 diabetes mellitus, cardiac disorders, and musculoskeletal diseases. Bariatric surgery, a typical and effective surgical intervention for patients with excess body weight with concurrent medical conditions, achieves significant weight loss over a long period. Numerous studies have been conducted on the effectiveness of various bariatric surgery techniques for improving glycemic homeostasis and helping patients lose weight. However, little is known about how bariatric surgery affects the lipid profile. The study aims to determine how patients' altered BMI affects lipid parameters following OAGB/MGB surgery. Methods To achieve this, the longitudinal observational study was conducted from January 2021 to January 2022 among 150 patients scheduled to undergo Anastomosis Gastric Bypass Surgery. The mean age of the patients was 41.7 years, with a standard deviation of 14.7 years (mean±SD: 41.7±14.7). Among the study participants, 56 individuals (37.3%) were male, while 94 (62.7%) were female. Objectives Regarding comorbidities, hypertension was identified as the most prevalent condition among the enrolled patients, affecting 49.3% of them. Results It was observed that the levels of S. Cholesterol and S. Triglyceride showed a significant decrease after one month (Visit-1) of the bypass surgery, with a reduction of 21.8 mg/dl (95% CI=-31.9, -11.6, p=<0.001) and 14 mg/dl (95% CI=-25.5, -2.51, p=0.017), respectively Conclusion OAGB outcome is associated with a healthier lipid profile and enhanced weight management. [ABSTRACT FROM AUTHOR]

Severe COVID-19 is a systemic disorder involving excessive inflammatory response, metabolic dysfunction, multi-organ damage, and several clinical features. Here, we performed a transcriptome meta-analysis investigating genes and molecular mechanisms related to COVID-19 severity and outcomes. First, transcriptomic data of cellular models of SARS-CoV-2 infection were compiled to understand the first response to the infection. Then, transcriptomic data from lung autopsies of patients deceased due to COVID-19 were compiled to analyze altered genes of damaged lung tissue. These analyses were followed by functional enrichment analyses and gene–phenotype association. A biological network was constructed using the disturbed genes in the lung autopsy meta-analysis. Central genes were defined considering closeness and betweenness centrality degrees. A sub-network phenotype–gene interaction analysis was performed. The meta-analysis of cellular models found genes mainly associated with cytokine signaling and other pathogen response pathways. The meta-analysis of lung autopsy tissue found genes associated with coagulopathy, lung fibrosis, multi-organ damage, and long COVID-19. Only genes DNAH9 and FAM216B were found perturbed in both meta-analyses. BLNK, FABP4, GRIA1, ATF3, TREM2, TPPP, TPPP3, FOS, ALB, JUNB, LMNA, ADRB2, PPARG, TNNC1, and EGR1 were identified as central elements among perturbed genes in lung autopsy and were found associated with several clinical features of severe COVID-19. Central elements were suggested as interesting targets to investigate the relation with features of COVID-19 severity, such as coagulopathy, lung fibrosis, and organ damage. [ABSTRACT FROM AUTHOR]

Objectives Patients with SLE have an increased risk of comorbidities and impaired survival. We aimed to assess whether various thresholds of oral CS (OCS) can predict development of infections, comorbidities, malignancies and survival in SLE using data from national health registries in Sweden. Methods All incident SLE cases, age >18 years, in Sweden (n  = 5309) between 2005 and 2020 and matched population controls (n  = 26 545) were included and followed until 2020, a total of 257 942 patient years. Data from national registers were retrieved including information from the National Prescribed Drug Register. Risk factors were analysed using time-dependent Cox regression models. Results Compared with no OCS, >0 to <5.0 mg/day, 5.0–7.5 mg/day as well as >7.5 mg/day OCS predicted development of infections (pneumonia, influenza, herpes zoster and urinary tract infection), osteoporosis, osteonecrosis, gastroduodenal ulcers, cataracts, hypertension and mortality (all P  < 0.05). OCS >0 to <5.0 mg/day was associated with lower hazard ratios for these comorbidities than higher doses of OCS. Fifteen years after diagnosis, 48% of patients were taking OCS at a median dose of 5.7 mg/day. A small reduction of OCS treatment 5 years after diagnosis in patients diagnosed with SLE 2006–10 compared with 2011–15 was observed, 49% vs 46% respectively (P  = 0.039). Conclusion Results highlight the potential harm associated with even low OCS dose treatment in SLE and the need to judiciously use OCS at the lowest possible dose to maximize efficacy and minimize harm. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of the serum HCQ concentration on clinical manifestations, disease activity and organ damage in a longitudinal cohort of SLE patients. Methods The 338 SLE patients were assessed with respect to their demographic data, clinical and laboratory findings, Physician's Global Assessment (PGA), adjusted mean SLEDAI-2000 (AMS) and SLICC Damage Index (SDI) annually for 5 consecutive years. Patients were divided into two groups according to their serum HCQ concentration at baseline: subtherapeutic (<500 ng/ml) and therapeutic (≥500 ng/ml) groups. The impact of the HCQ concentration on the clinical outcomes was evaluated in a longitudinal analysis using a generalized estimating equation (GEE). Results Of the 338 patients, 287 (84.9%) were in the subtherapeutic group at baseline. This group had a higher incidence of newly developed LN (P  = 0.036) and had been prescribed higher mean and cumulative doses of prednisolone (P  = 0.003 and P  = 0.013, respectively) than the therapeutic group. In multivariable analyses based on GEE, the subtherapeutic group had a higher AMS score (β = 1.398, 95% CI 0.607, 2.189; P  < 0.001), higher PGA score (β = 0.328, 95% CI 0.215, 0.441; P  < 0.001) and higher SDI score (β = 0.366, 95% CI 0.061, 0.671; P  = 0.019) across all 5 years. Conclusion The subtherapeutic HCQ concentration was associated with the development of new-onset LN, and had significant associations with disease activity and cumulative organ damage in SLE patients over time. [ABSTRACT FROM AUTHOR]

During the COVID-19 pandemic, there has been a resurgence of mucormycosis, a rare and opportunistic fungal infection, with India reporting a particularly notable increase in incidence. Mucormycosis is a life-threatening condition that requires prompt diagnosis and treatment to prevent high mortality rates and severe sequelae. It is caused by the inhalation of spores from ubiquitous filamentous fungi belonging to the order Mucorales. Individuals with compromised immune systems or underlying conditions, such as diabetes, ketoacidosis, and neutropenia, are particularly vulnerable to infection. The risk and severity of mucormycosis are exacerbated by several factors, including corticosteroid therapy, prolonged intensive care stay, and the use of ventilators. Additionally, contaminated oxygen humidifiers pose a significant risk. Effective management of mucormycosis in critically ill COVID-19 patients relies on early diagnosis, optimization of predisposing factors, timely antifungal treatment, surgical debridement, and adjuvant therapies. Imaging modalities such as contrast-enhanced CT scans and MRI are crucial for guiding surgical debridement and assessing disease extent. This review article provides a comprehensive overview of the clinical pathogenesis, risk factors, diagnosis, treatment, and challenges associated with mucormycosis in COVID-19 patients, summarizing the latest findings in this field. [ABSTRACT FROM AUTHOR]

The official recording outbreak COVID-19 virus was in Dec 2019. When it affects humans, it affects almost all age groups, especially aged people. COVID-19 becomes a Global pandemic within a short period. The primary consequence of this infection is that it targets the individual's respiratory system and causes severe acute respiratory syndrome (SARS-CoV-2). Research efforts were made internationally to find a proper vaccine. Here, with the mechanism of action, this review provides the infection mechanism, Immunological changes, and associated organ damage.

Cardiopulmonary bypass (CPB) initiates an intense inflammatory response due to various factors: conversion from pulsatile to laminar flow, cold cardioplegia, surgical trauma, endotoxemia, ischemia-reperfusion injury, oxidative stress, hypothermia, and contact activation of cells by the extracorporeal circuit. Redundant and overlapping inflammatory cascades amplify the initial response to produce a systemic inflammatory response, heightened by coincident activation of coagulation and fibrinolytic pathways. When unchecked, this inflammatory response can become maladaptive and lead to serious postoperative complications. Concerted research efforts have been made to identify technical refinements and pharmacologic interventions that appropriately attenuate the inflammatory response and ultimately translate to improved clinical outcomes. Surface modification of the extracorporeal circuit to increase biocompatibility, miniaturized circuits with sheer resistance, filtration techniques, and minimally invasive approaches have improved clinical outcomes in specific populations. Pharmacologic adjuncts, including aprotinin, steroids, monoclonal antibodies, and free radical scavengers, show real promise. A multimodal approach incorporating technical, circuit-specific, and pharmacologic strategies will likely yield maximal clinical benefit.

AbstractContext Plantamajoside (PMS) possesses rich pharmacological characteristics that have been applied to remedy dozens of diseases. However, the understanding of PMS in sepsis remains insufficient.Objective Role of PMS in sepsis-regulated organ dysfunction and potential mechanisms were investigated.Materials and methods Thirty C57BL/6 male mice were adaptive fed for three days and used to establish acute sepsis model by caecal ligation and perforation (CLP). These experimental mice were divided into Sham, CLP, CLP + 25 mg PMS/kg body weight (PMS/kg), CLP + 50 mg PMS/kg and CLP + 100 mg PMS/kg (n = 6). The pathological and apoptotic changes of lung, liver and heart tissues were observed via HE and TUNEL staining. The injury-related factors of lung, liver and heart were detected by corresponding kits. ELISA and qRT-PCR were applied to assess IL-6/TNF-α/IL-1β levels. Apoptosis-related and TRAF6/NF-κB-related proteins were determined using Western blotting.Results All doses of PMS enhanced the survival rates in the sepsis-induced mouse model. PMS remitted sepsis-mediated lung, liver and heart injury through prohibiting MPO/BALF (70.4%/85.6%), AST/ALT (74.7%/62.7%) and CK-MB/CK (62.3%/68.9%) levels. Moreover, the apoptosis index (lung 61.9%, liver 50.2%, heart 55.7% reduction) and IL-6/TNF-α/IL-1β levels were suppressed by PMS. Furthermore, PMS lowered TRAF6 and p-NF-κB p65 levels, whereas TRAF6 overexpression reversed the protective influences of PMS in organ injury, apoptosis and inflammation triggered by sepsis.Discussion and conclusions PMS suppressed sepsis-induced organ dysfunction by regulating the TRAF6/NF-κB axis, and PMS treatment may be considered as a novel strategy for sepsis-caused damage in future.

Background/Objectives: Neutrophils, as the first line of defense in the immune response, produce neutrophil extracellular traps (NETs) upon activation, which are significant in the pathogenesis and organ damage in sepsis. This study aims to explore the clinical value of myeloperoxidase-DNA (MPO-DNA) and cell-free DNA (cf-DNA) in sepsis patients. Methods: Clinical data were collected from 106 sepsis patients, 25 non-sepsis patients, and 51 healthy controls. Sequential Organ Failure Assessment (SOFA) scores were calculated, and levels of MPO-DNA) complexes and cf-DNA were measured using specific kits. Correlation analyses assessed relationships between indicators, while logistic regression identified independent risk factors. Receiver operating characteristic (ROC) curves calculated the area under the curve (AUC) to evaluate the diagnostic value of the biomarkers. Results: Sepsis patients exhibited significantly elevated levels of MPO-DNA and cf-DNA compared to non-sepsis patients and healthy controls. In sepsis patients, MPO-DNA and cf-DNA levels correlated with inflammation, coagulation, and organ damage indicators, as well as procalcitonin (PCT) levels and SOFA scores. Both C-reactive protein (CRP) and cf-DNA were identified as independent risk factors for sepsis, demonstrating moderate diagnostic value. ROC analysis showed that the combination of MPO-DNA and CRP (AUC: 0.837) enhances the AUC value of CRP (0.777). Conclusions: In summary, elevated serum levels of MPO-DNA and cf-DNA in sepsis patients correlate with SOFA scores and PCT levels, providing reference value for sepsis diagnosis in clinical settings.

Abstract Hypoxic-ischemic injury is a common pathological dysfunction in clinical settings. Mitochondria are sensitive organelles that are readily damaged following ischemia and hypoxia. Dynamin-related protein 1 (Drp1) regulates mitochondrial quality and cellular functions via its oligomeric changes and multiple modifications, which plays a role in mediating the induction of multiple organ damage during hypoxic-ischemic injury. However, there is active controversy and gaps in knowledge regarding the modification, protein interaction, and functions of Drp1, which both hinder and promote development of Drp1 as a novel therapeutic target. Here, we summarize recent findings on the oligomeric changes, modification types, and protein interactions of Drp1 in various hypoxic-ischemic diseases, as well as the Drp1-mediated regulation of mitochondrial quality and cell functions following ischemia and hypoxia. Additionally, potential clinical translation prospects for targeting Drp1 are discussed. This review provides new ideas and targets for proactive interventions on multiple organ damage induced by various hypoxic-ischemic diseases.

Abstract Objective The aim of the current study was to determine the mechanism by which Zerumbone (ZER) ameliorates inflammation and organ damage in a rat model of severe acute pancreatitis (SAP). Methods Different concentrations of ZER (10, 20 and 40 mg/kg) were administered by femoral vein puncture 30 min prior to establishment of the SAP model. Hematoxylin and eosin (H&E) staining was used to assess pathological changes in the pancreatic tissue of SAP-induced rats. The lung wet/dry (W/D) ratio was assessed and serum levels of amylase (AMY), alanine aminotransferase (ALT), creatinine (Cr), aspartate aminotransferase (AST) and phospholipase A2 (PLA2) were measured. Western blot analysis was used to examine changes in the expression of ROS/NF-κB pathway-associated proteins. Results SAP was confirmed by significant histopathological damage to the pancreas. ZER (10, 20 and 40 mg/kg) was found to alleviate pancreatitis and decrease ascites volume, lung W/D ratio, pancreatic pathology score, oxidative stress and inflammatory damage. High concentrations (20 and 40 mg/kg) of ZER were shown to increase levels of hepatorenal toxicity. In contrast, 10 mg/kg ZER was found to attenuate liver enzyme levels, reduce pathological damage to the liver, and protect against extrapancreatic organ damage to the liver in SAP-induced rats. Moreover, ZER showed no significant side effects in normal rats. Finally, we demonstrated that ZER mediated its anti-inflammatory effects on SAP through the ROS/NF-κB signaling pathway. Conclusion ZER alleviated SAP-induced oxidative stress and inflammatory injury via the ROS/NF-κB pathway, and had a protective effect on lung injury and liver damage.

BackgroundPreeclampsia (PE) is associated with subsequent higher risk of cardiovascular and kidney disease. Serum copeptin, as a proxy for vasopressin, and urinary uromodulin, were associated with PE physiopathology and kidney functional mass respectively. We describe concentrations of these proteins in the post-partum period and characterize their association with persistent hypertension (HTN) or albuminuria.MethodsPatients with PE and healthy controls with uncomplicated pregnancy were prospectively included at two teaching hospitals in Switzerland. Clinical parameters along with serum copeptin and urinary uromodulin were measured at 6 weeks post-partum. PE patients were further characterized based on presence of HTN (defined as either systolic BP (SBP) ≥140 mmHg or diastolic (BP) ≥90 mmHg) or albuminuria [defined as urinary albumin to creatinine ratio (ACR) ≥3 mg/mmol].ResultsWe included 226 patients with 35 controls, 120 (62.8%) PE with persistent HTN/albuminuria and 71 (37.1%) PE without persistent HTN/albuminuria. Median serum copeptin concentration was 4.27 (2.9–6.2) pmol/L without differences between study groups (p > 0.05). Higher copeptin levels were associated with higher SBP in controls (p = 0.039), but not in PE (p > 0.05). Median urinary uromodulin concentration was 17.5 (7.8–28.7) mg/g with lower levels in PE patients as compared to healthy controls (p 0.05). Higher uromodulin levels were associated with lower albuminuria in PE as well as control patients (p = 0.040).ConclusionSerum copeptin levels at 6 weeks post-partum are similar between PE patients and healthy controls and cannot distinguish between PE with or without residual kidney damage. This would argue against a significant pathophysiological role of the vasopressin pathway in mediating organ damage in the post-partum period. On the opposite, post-partum urinary uromodulin levels are markedly lower in PE patients as compared to healthy controls, potentially reflecting an increased susceptibility to vascular and kidney damage that could associate with adverse long-term cardiovascular and kidney outcomes.

Introduction: Excessive weight gain in individuals leads to various metabolic disorders, such as diabetes mellitus, contributing to a further increase in body mass index (BMI). Thus, the patient enters a vicious cycle that leads to irreversible health damage. Bariatric surgery has displayed positive outcomes of weight loss with the return of BMI towards normal, which may reduce blood glucose levels to near normal. The remission of diabetes mellitus may be attributed to the reduction in inflammation, improvement of insulin resistance, lowering of peptide YY, and overall improved metabolic state of the body. Methods: One fifty patients, both female and male, in the age group of 20-60 years with grade II and grade III obesity having mean BMI of 45.63±6.54 (male) and 41.81± 5.93kg/m2 (female) were randomly selected for this study. Hemoglobin, Fasting Blood sugar (FBS), 2 hours postprandial blood sugar (PP2BS). Hemoglobin A1c (HbA1c) serum insulin was assessed at the visit, marked as a baseline, then again at the visit 3 months, and finally at the visit by the patient 6 months after bariatric surgery. Results: Hemoglobin level increased significantly from baseline at the 3rd-month post-surgery visit. FBS increased substantially from baseline at the 3rd-month postsurgery visit, which decreased considerably at the 6th-month visit following surgery. HbA1c showed a significant decrease in level from baseline following surgery. Conclusion: Improvement in BMI following bariatric surgery may have a positive impact on blood glucose levels in diabetic patients who may hope to see better management of their condition and may enjoy a better quality of life. [ABSTRACT FROM AUTHOR]

Objective: This study was conducted to characterize the clinical presentation, results of serological and immunological tests and sociodemographic factors in the Pakistani Lupus population. Methods: This prospective, cross-sectional study was undertaken at the Clinic for Arthritis and Rheumatic Diseases, Rawalpindi Teaching Hospital, Rawalpindi, Pakistan between January 2020 and June 2023, involving adult patients with SLE (classified based on 1997 revised ACR criteria). Demographic data, clinical and laboratory features, auto-antibody profile, disease duration, treatment history and organ damage (calculated by SLICC/ACR-DI) were recorded for all patients. Descriptive statistics and logistic regression analysis were performed for statistical assessment. Results: A total of 98 patients (94.9% females and 5.1% males) were enrolled in the study. The mean age of patients was 30.93±11.09 years while the mean duration of illness was 3.27±3.01years. The most commonly observed clinical manifestations were neuropsychiatric systemic lupus erythematosus in 84% of patients and mucocutaneous involvement (photosensitivity, mucosal ulcers, facial rash, alopecia and discoid lupus in 63.92%, 56.70%, 48.45%, 37.11% and 13.40% patients respectively). They were followed by serositis, arthralgias and renal involvement in 60.42%, 33.67% and 25% of patients respectively. Antinuclear antibody by indirect immunofluorescence was positive in all while anti-dsDNA was positive in 50% of patients. Conclusions: Fatigue was the most commonly recorded symptom while Neuropsychiatric SLE was the most commonly observed systemic manifestation in the Pakistani population followed by mucocutaneous involvement, serositis, arthralgias and renal involvement. Reasons for serious manifestations at initial presentation include deficiency of healthcare professionals trained in the field of Rheumatology and lack of awareness among patients. [ABSTRACT FROM AUTHOR]

Objective: Black/African American women with systemic lupus erythematosus (SLE) experience greater organ damage and at younger ages than white women. The objective of this study was to advance research on SLE inequities by identifying sociodemographic risk profiles associated with organ damage accrual specifically among Black/African American women. Methods: Latent profile analysis was conducted among 438 Black/African American women with SLE living in Atlanta, GA and enrolled in the Black Women's Experiences Living with Lupus (BeWELL) Study (May 2015 to April 2017). Proportional hazard and Poisson regression models examined prospective associations between sociodemographic profiles and the timing and degree of organ damage accrual over 2 years. Results: Four profiles emerged: (1) "Younger/Lower SES with Uncontrolled SLE" (44.8%), (2) "Older/Lower SES with Uncontrolled SLE" (23.3%), (3) "Mid-SES with Controlled SLE" (19.6%), and (4) "Higher SES with Controlled SLE" (11.2%). Approximately 42% of participants experienced new organ damage during the follow-up period. Proportional hazard models indicated that "Older/Lower SES with Uncontrolled SLE" participants were at greatest risk of new organ damage (HR = 2.41; 95% CI = 1.39, 4.19), followed by "Younger/Lower SES with Uncontrolled SLE" participants (HR = 1.56; 95% CI = 0.92, 2.67), compared to those in the "Higher SES with Controlled SLE" profile. Poisson regression models revealed that these two groups also exhibited greater organ damage accrual (b = 0.98, SE = 0.24, 95% CI = 0.52, 1.44 and b = 0.72, SE = 0.23, 95% CI = 0.27, 1.17, respectively). Conclusions: Black/African American women with fewer socioeconomic resources and uncontrolled SLE are at greatest risk for increasing disease severity over time. Social inequities likely contribute to racial inequities in SLE progression. [ABSTRACT FROM AUTHOR]

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The research paper extensively covers the phenomenon of bioaccumulation, focusing on its impact in freshwater ecosystems, particularly on fish. It details how heavy metals like mercury, lead, cadmium, and arsenic, originating from industrial pollution, agricultural runoff, and atmospheric deposition, accumulate in fish tissues over time. The abstract highlights the adverse effects of such bioaccumulation on fish health, including reproduction issues, growth abnormalities, and organ damage. It also underscores the consequent risks to human health when these contaminated fish are consumed. The study emphasizes the importance of addressing heavy metal pollution in aquatic ecosystems through effective waste management, reduction of industrial discharges, sustainable agricultural practices, and regular monitoring of fish populations. This approach is crucial to manage and mitigate the risks of heavy metal bioaccumulation in freshwater fish, thereby protecting both aquatic life and human health. [ABSTRACT FROM AUTHOR]

BACKGROUND Emerging evidence suggests that a hypertensive response to exercise (HRE) during dynamic or isometric stress tests assessing cardiac function is predictive of hypertension and cardiovascular events such coronary artery disease, heart failure and stroke. Whether HRE represents a marker of masked hypertension (MH) in individuals with no prior history of hypertension is still unclear. This is also the case for the association between MH and hypertension-mediated organ damage (HMOD) in the HRE setting. METHODS We addressed this issue through a review and a meta-analysis of studies providing data on this topic in normotensive individuals undergone both to dynamic or static exercise and to 24-h blood pressure monitoring (ABPM). A systematic search was performed using Pub-Med, OVID, EMBASE and Cochrane library databases from inception up to February 28th 2023. RESULTS Six studies including a total of 1,155 untreated clinically normotensive individuals were considered for the review. Data provided by the selected studies can be summarized as follows: (i) HRE is a BP phenotype linked to a high prevalence of MH (27.3% in the pooled population); (ii) MH is, in turn, associated with a greater, consistent likelihood of echocardiographic left ventricular hypertrophy (OR: 4.93, CI: 2.16–12.2, P  < 0.0001) and vascular organ damage, as assessed by pulse wave velocity, (SMD: 0.34 ± 0.11, CI: 0.12–0.56, P  = 0002). CONCLUSIONS On the basis of this, albeit limited, evidence, the diagnostic work-up in individuals with HRE should primarily be addressed to look for MH as well as for markers of HMOD, a highly prevalent alteration in MH. [ABSTRACT FROM AUTHOR]

Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease with limited therapeutic targets or clinical outcome predictors. This study aimed to gain more insights into the underlying immunological pathways and prognostic biomarkers of SLE. Integrated analyses of RNA-seq data from 64 SLE and 62 healthy controls, examining 27 immune cell types to explore the key pathways and driver genes in SLE pathogenesis. Single-cell RNA sequencing data from the skin and kidney were used to determine the association of COX5A expression with organ damage. The associations of COX5A with SLE phenotypes were further evaluated in two independent cohorts, and receiver operating characteristic (ROC) curves were constructed to assess the value of COX5A as a biomarker for disease activity and organ damage in SLE. We found that oxidative phosphorylation (OXPHOS) is the most significantly altered metabolic pathway in SLE, especially in effector T cells. Notably, we identified an OXPHOS-related enzyme, COX5A, whose expression was significantly higher in effector T cells than in naïve T cells and showed associations with disease activity, organ damage, and steroid treatment of SLE. Furthermore, ROC curves showed that COX5A is a robust biomarker for disease activity, kidney involvement, and new-onset skin lesions, with the area under the curve (AUC) values of 0.880, 0.801, and 0.805, respectively. Our results identified the OXPHOS signature as a prominent feature in SLE T cells, and COX5A as a potential candidate biomarker for disease activity and organ damage in SLE. [ABSTRACT FROM AUTHOR]

Plantamajoside (PMS) possesses rich pharmacological characteristics that have been applied to remedy dozens of diseases. However, the understanding of PMS in sepsis remains insufficient. Role of PMS in sepsis-regulated organ dysfunction and potential mechanisms were investigated. Thirty C57BL/6 male mice were adaptive fed for three days and used to establish acute sepsis model by caecal ligation and perforation (CLP). These experimental mice were divided into Sham, CLP, CLP + 25 mg PMS/kg body weight (PMS/kg), CLP + 50 mg PMS/kg and CLP + 100 mg PMS/kg (n = 6). The pathological and apoptotic changes of lung, liver and heart tissues were observed via HE and TUNEL staining. The injury-related factors of lung, liver and heart were detected by corresponding kits. ELISA and qRT-PCR were applied to assess IL-6/TNF-α/IL-1β levels. Apoptosis-related and TRAF6/NF-κB-related proteins were determined using Western blotting. All doses of PMS enhanced the survival rates in the sepsis-induced mouse model. PMS remitted sepsis-mediated lung, liver and heart injury through prohibiting MPO/BALF (70.4%/85.6%), AST/ALT (74.7%/62.7%) and CK-MB/CK (62.3%/68.9%) levels. Moreover, the apoptosis index (lung 61.9%, liver 50.2%, heart 55.7% reduction) and IL-6/TNF-α/IL-1β levels were suppressed by PMS. Furthermore, PMS lowered TRAF6 and p-NF-κB p65 levels, whereas TRAF6 overexpression reversed the protective influences of PMS in organ injury, apoptosis and inflammation triggered by sepsis. PMS suppressed sepsis-induced organ dysfunction by regulating the TRAF6/NF-κB axis, and PMS treatment may be considered as a novel strategy for sepsis-caused damage in future. [ABSTRACT FROM AUTHOR]

Purpose of Review: Review parenteral therapeutic choices in treatment of hypertensive crises by mechanism of action and summarize recent literature on the management of hypertensive crises. Recent Findings: Recent data have documented the safety and efficacy of labetalol and nicardipine in treatment of hypertensive crises as well as characterized the hypertensive emergency population to a much greater extent. Summary: Based on recent data, hypertensive emergencies are seen in 0.5% of all emergency room visits. Ischemic stroke and heart failure/pulmonary edema are the most common forms of organ damage seen in hypertensive emergencies. There are many therapeutic choices in treatment of hypertensive crises with varied mechanisms of action. Large randomized, controlled trial evidence is lacking in this therapeutic area; however, recent data have documented the safety and efficacy of labetalol and nicardipine. [ABSTRACT FROM AUTHOR]