Impact of early myocardial injury on patients with severe pneumonia.

Pneumonia often causes myocardial damage. This study sought to understand how early myocardial injury affects severe pneumonia patients' prognoses. This multi-center prospective cohort study from March 2020 to October 2023 comprised severe pneumonia patients. Binary logistic regression analysis examined how myocardial damage affects cardiac complications and acute renal injury (AKI). We used Spearman correlation analysis to examine the relationship between troponin I levels and the vasoactive inotropic score (VIS) in shock patients with myocardial injury. We used the Kaplan-Meier survival curve to evaluate the impact of myocardial injury on 30-day and 1-year survival rates. Mediation investigations examined how AKI and cardiac complications mediate myocardial injury and death. This study included 363 severe pneumonia patients, of whom 204 (56.2%) developed myocardial damage, 132 (36.4%) had cardiac problems, and 146 (40.2%) had AKI. Myocardial damage independently elevated the incidence of cardiac complications (OR = 2.548, 95% CI = 1.404-4.303, P = 0.002) and AKI (OR = 1.946, 95% CI = 1.177-3.219, P = 0.009). There was a positive link between troponin I and VIS in myocardial injury and shock patients (r = 0.43, P < 0.001). COX regression found myocardial injury to be a death risk (HR = 1.472, 95% CI = 1.043-2.077, P = 0.028). Adjusted Kaplan-Meier survival analysis showed significantly decreased short-term and long-term survival rates with myocardial injury (log-rank test P < 0.05). The mediation study showed that cardiac complications and AKI mediated myocardial injury and death by 19.30% and 17.18%, respectively. Early myocardial injury in severe pneumonia patients raises the likelihood of cardiac problems, AKI, and refractory shock, reducing short- and long-term survival.

Clinical relevance of neutrophil/lymphocyte ratio combined with APACHEII for prognosis of severe heatstroke.

We evaluated clinical implication of neutrophil-lymphocyte ratio (NLR) for severe heatstroke and predictive value of combined acute physiology and chronic health evaluation (APACHEII) score for prognosis of severe heatstroke. Retrospectively, we studied 185 individuals that have been admitted at emergency department for severe heatstroke. On the basis of their prognosis, we sorted the patients into two categories, namely non-survival (n = 43) and survival groups (n = 142). The primary outcome was 30-day mortality. A considerably higher NLR was observed among the non-survivors compared to survivors (P < 0.05). After correction for confounders, statistical analysis using multi-variable Cox regression indicated NLR as an independent risk factor for patient death (HR = 1.167, 95%CI = 1.110-1.226, P < 0.001). Through receiver-operating characteristics (ROC) curve, we estimated area-under the curve (AUC) of NLR to be 0.7720 (95% CI [0.6953, 0.8488]). Also, transformation of NLR into a profile type analysis showed that the marker remained a risk factor for death, which showed trend variation (P for trend <0.001). Subgroup forest plot analysis showed robustness in the predictive ability of NLR after exclusion of confounders. Besides, we demonstrated through Kaplan-Meier (KM) survival analysis curve that high risk NLR mortality substantially exceeded low risk NLR. The combined prediction of NLR and APACHEII achieved higher efficacy than NLR and APACHEII alone (AUC = 0.880, 95% CI [0.8280, 0.9290]). Additionally, Delong test indicated that the combined prediction demonstrated a significantly greater ROC than NLR and APACHEII alone, while DCA showed a considerably higher clinical net benefit rate. Increased NLR is a high risk factor and has predictive value for death in individuals with severe heatstroke. Suggestively, combination of NLR and APACHEII have greater predictive value.

A NOMOGRAM FOR PREDICTING PATIENTS WITH SEVERE HEATSTROKE.

ABSTRACT: Background: No predictive models are currently available to predict poor prognosis in patients with severe heatstroke. We aimed to establish a predictive model to help clinicians identify the risk of death and customize individualized treatment. Methods: The medical records and data of 115 patients with severe heatstroke hospitalized in the intensive care unit of Changzhou No. 2 People's Hospital between June 2013 and September 2019 were retrospectively analyzed for modeling. Furthermore, data of 84 patients with severe heatstroke treated at Jintan No. 1 People's Hospital from June 2013 to 2021 were retrospectively analyzed for external verification of the model. We analyzed the hematological parameters of the patients recorded within 24 h of admission, which included routine blood tests, liver function, renal function, coagulation routine, and myocardial enzyme levels. Risk factors related to death in patients with severe heatstroke were screened using Least Absolute Shrinkage and Selection Operator regression. The independent variable risk ratio for death was investigated using the Cox univariate and multivariate regression analyses. The nomogram was subsequently used to establish a suitable prediction model. A receiver operating characteristic curve was drawn to evaluate the predictive power of the prediction model and the Acute Physiology and Chronic Health Evaluation (APACHE II) score. In addition, decision curve analysis was established to assess the clinical net benefit. The advantages and disadvantages of both models were evaluated using the integrated discrimination improvement and Net Reclassification Index. A calibration curve was constructed to assess predictive power and actual conditions. The external data sets were used to verify the predictive accuracy of the model. Results: All independent variables screened by Least Absolute Shrinkage and Selection Operator regression were independent risk factors for death in patients with severe heatstroke, which included neutrophil/lymphocyte ratio, platelet (PLT), troponin I, creatine kinase myocardial band, lactate dehydrogenase, human serum albumin, D-dimer, and APACHE-II scores. On days 10 and 30, the integrated discrimination improvement of the prediction model established was 0.311 and 0.364 times higher than that of the APACHE-II score, respectively; and the continuous Net Reclassification Index was 0.568 and 0.482 times higher than that of APACHE-II, respectively. Furthermore, we established that the area under the curve (AUC) of the prediction model was 0.905 and 0.918 on days 10 and 30, respectively. Decision curve analysis revealed that the AUC of this model was 7.67% and 10.67% on days 10 and 30, respectively. The calibration curve showed that the predicted conditions suitably fit the actual requirements. External data verification showed that the AUC on day 10 indicated by the prediction model was 0.908 (95% confidence interval, 82.2-99.4), and the AUC on day 30 was 0.930 (95% confidence interval, 0.860-0.999). Conclusion: The survival rate of patients with severe heatstroke within 24 h of admission on days 10 and 30 can be effectively predicted using a simple nomogram; additionally, this nomogram can be used to evaluate risks and make appropriate decisions in clinical settings.

Emodin alleviates sepsis-mediated lung injury via inhibition and reduction of NF-kB and HMGB1 pathways mediated by SIRT1.

Inflammation plays an important role during sepsis, and excessive inflammation can result in organ damage, chronic inflammation, fibrosis, and scarring. The study aimed to investigate the specific mechanism of emodin by constructing in vivo and in vitro septic lung injury models via inhibition and reduction of NF-kB and high mobility group box 1 (HMGB1) pathways. A cecal ligation and puncture (CLP) model was built for adult male Sprague-Dawley rats. Concentrations of TNF-α, IL-1ß, and IL-6 in bronchoalveolar lavage fluid were determined using commercially available ELISA kits. Hematoxylin and eosin staining was used for the right lung inferior lobes. Myeloperoxidase (MPO) activity of the lung tissue was detected by using the MPO kit. Murine alveolar epithelial cell line (MLE-12) cells were used for flow cytometry and Western blot to analyze the apoptosis rate and protein expression. Emodin significantly decreased CLP-induced cell apoptosis, upregulated expression of sirtuin 1 (SIRT1), and inhibited p-p65/p65 and HMGB1. In lipopolysaccharide (LPS) treated cell model, emodin treatment markedly decreased LPS-induced release of IL-1, IL-6, and tumor necrosis factor (TNF)-α, inhibited LPS-induced cell apoptosis and suppressed protein levels of P-P65/P65 and HMGB1. However, science of SIRT1 reversed the above effects by treatment of emodin. In summarize, this study found that emodin can alleviate sepsis-induced lung injury in vivo and in vitro through regulation of SIRT1.

N-Alkylation of Amines with Alcohols Catalyzed by Manganese(II) Chloride or Bromopentacarbonylmanganese(I).

A manganese-catalyzed N-alkylation reaction of amines with alcohols via hydrogen autotransfer strategy has been demonstrated. The developed practical catalytic system including an inexpensive, nontoxic, commercially available MnCl2 or MnBr(CO)5 as the metal salt and triphenylphosphine as a ligand provides access to diverse aromatic, heteroaromatic, and aliphatic secondary amines in moderate-to-high yields. In addition, this operationally simple protocol is scalable to the gram level and suitable for synthesizing heterocycles such as indole and resveratrol-derived amines known to be active for Alzheimer's disease.

Effects of stromal interaction molecule 1 or Orai1 overexpression on the associated proteins and permeability of podocytes.

AIM: The present study was conducted to determine whether two important signalling molecules of store-operated channel (SOC), stromal interaction molecule 1 (STIM1) and Orai1, were involved in glomerular podocyte injury. We explored the effects of STIM1/Orai1 overexpression on podocyte associated proteins and cell permeability. METHODS: The expression of STIM1 and Orai1 were examined in the renal cortex of adriamycin-induced nephropathy mice by real-time RT-PCR. The recombinant plasmid of STIM1/Orai1, identified by restriction enzyme digestion and PCR, was transfected into MPC5 cells via lipofectamine 2000. The transfecting efficiency was observed by a fluorescence microscope. RT-PCR and Western blotting were used to evaluate the expression levels of STIM1, Orai 1 and some podocyte-associated molecules in the transfected MPC5 cells. In addition, we examined the diffusion of FITC-dextran across the podocyte monolayer to investigate whether STIM1/Orai1 overexpression could affect cell permeability. RESULTS: We found that the mRNA levels of STIM1 and Orai1 were increased in adriamycin-induced nephropathy mice. STIM1/Orai1 overexpression significantly decreased the expression of podocin and CD2-associated protein (CD2AP), whereas it increased the expression of α-actinin-4. The permeability was significantly increased in the STIM1/Orai1 overexpression group. CONCLUSION: Our findings suggested that STIM1/Orai1 overexpression could affect the cell permeability and the expression of partial podocyte-associated proteins, which may ultimately result in podocyte injury.