As the impact of early albumin infusion on the prognosis of elderly individuals diagnosed with sepsis remains uncertain, this study aimed to investigate this effect in elderly patients with sepsis in the intensive care unit (ICU). We identified the information of elderly patients with sepsis requiring ICU admission from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database. They were divided into hypoalbuminemia group and control group, and the primary outcome was 90-d mortality. A multivariate logistic regression model and a multivariate Cox proportional-hazards model were used to analyze the correlation between hypoalbuminemia and patient prognosis. Kaplan-Meier survival curve and log-rank test were performed to analyze the survival outcomes. Propensity score matching (PSM) was implemented to determine the precise effect of early albumin infusion on the prognosis of elderly ICU patients with sepsis, and subgroups of patients were identified to explore the factors influencing the relationship. Early hypoalbuminemia was strongly associated with an increased risk of adverse clinical outcomes in elderly patients with sepsis in the ICU. In-hospital mortality (28.6% vs. 19.1%, P<0.001) and 90-d mortality (48.8% vs. 33.4%, P<0.001) were both significantly higher in the early hypoalbuminemia group than in the control group. PSM analysis showed that early albumin infusion was associated with lower in-hospital mortality and 90-d mortality in elderly patients with sepsis combined with hypoalbuminemia in the ICU. Early infusion of albumin could improve patient prognosis and reduce in-hospital mortality and 90-d mortality.

Respiratory injury caused by the inhalation of toxic gases represents a common and clinically significant form of chemical exposure.

Glyphosate(GLY),a widely used herbicide,has been extensively applied in both the agricultural and non-agricultural sectors worldwide.The rate of GLY use varies considerably depending on the crop type and local farming practices,which can be up to approximately 53.5％of agricultural land in certain regions.[1] Metabolic products of GLY,including aminomethylphosphonic acid,a primary degradation product of GLY,may induce oxidative stress and inflammation,both of which play key roles in the pathogenesis of renal injury.

Baicalein, a naturally occurring flavonoid with well-documented anti-inflammatory and neuroprotective effects, has shown therapeutic promise in multiple models of neurological disorders. However, whether baicalein can counteract diquat-induced neurotoxicity remains uncertain. This study reveals that baicalein alleviates diquat-induced neuroinflammation and microglial pyroptosis in mice in a gut microbiota (GM)-dependent manner. In the in vivo experiments, multi-omics analyses demonstrated that baicalein elevates the GM-derived metabolite indole-3-propionic acid (IPA), which was sufficient to suppress pyroptosis. In parallel, IPA was identified as a critical mediator of baicalein's neuroprotective effects, as exogenous IPA administration recapitulated baicalein's protection, and baicalein treatment significantly elevated IPA levels. Mechanistically, through inhibiting the DEAD-box helicase 3 X-linked / GTPase-activating protein (SH3 domain) binding protein 1 pathway by in vitro experiments. Our study demonstrated that baicalein mitigates diquat-induced neuroinflammation, underscoring the therapeutic potential of targeting the GM to counteract herbicide-related neurotoxicity.

Exogenous lipoid pneumonia (ELP) following hydrocarbon aspiration is an unusual but severe condition. This study aimed to summarize the cases of pneumonitis following fuel aspiration from a single center to serve as a useful reference for clinicians in the future. The clinical courses and outcomes of 11 patients with pneumonitis following fuel aspiration were collected and presented. Among them, four representative cases were described in detail to summarize the management experience of this disease, and these cases were analyzed to better understand the clinical features and management strategies of hydrocarbon pneumonitis following fuel aspiration. Almost all patients were found to present with cough and dyspnea, and the most common symptoms were dyspnea and chest pain. A high proportion (90.9%) of patients presented with bilateral lower pulmonary field involvement, and half of the patients showed pneumonic consolidation. One patient with irreversible lung injury received extracorporeal membrane oxygenation (ECMO) and a lung transplant. The other patients received oxygen support, antibiotics, steroids, and other supportive care. Antibiotics and steroids were the most commonly used treatments. While bronchoalveolar lavage (BAL) was beneficial for removing irritants, its utility could also be reduced due to significant risks. Finally, all patients had favorable outcomes. In conclusion, ELP was definitely harmful to patients' health, and hypoxemia was common among these patients. Supportive care, including antibiotics, steroids, and respiratory support, was the main treatment modality. It is recommended that the decision to employ BAL is made selectively. ECMO serves as a critical bridge to recovery or transplantation, and patients with timely and efficient treatment usually have a positive outcome.

INTRODUCTION:Diquat-induced toxic brain injury is a challenging clinical issue, characterized by oxidative stress and neuroinflammation, which causes extensive damage to the central nervous system and has a poor prognosis. METHODS:We conducted a retrospective analysis of three patients diagnosed with diquat-induced toxic brain injury who underwent hyperbaric oxygen therapy in the subacute or chronic phase. Clinical data, laboratory findings, and neuroimaging were reviewed to assess their response to treatment. RESULTS:Three young adults were admitted following ingestion of diquat solution (20 g/L) and developed transient multiorgan dysfunction, managed with supportive interventions. All patients exhibited altered consciousness, such as somnolence or coma, elevated intracranial pressure, and central nervous system lesions on imaging. After stabilization of vital signs and oxygenation, hyperbaric oxygen therapy was administered. Post-treatment neuroimaging demonstrated lesion reduction. At final follow-up, two patients showed improvements in their Neurofunctional Scores and modified Barthel Indices, achieving clinical independence, while the third patient discontinued treatment for financial reasons. DISCUSSION:These observations suggest a potential association between hyperbaric oxygen therapy and neurological improvement in the subacute or chronic phase of diquat-induced toxic brain injury. Possible underlying mechanisms may include improved tissue oxygenation and modulation of inflammatory responses. CONCLUSIONS:These preliminary findings suggest a possible benefit of hyperbaric oxygen therapy in the subacute or chronic phase of diquat-induced toxic brain injury. However, due to the limited sample size and lack of a control group, larger and prospective studies are needed to verify its efficacy and safety.

Chlorfenapyr poisoning is associated with high mortality due to the absence of evidence-based treatment strategies or specific antidotes.

Purpose:With the increasing incidence of acute diquat (DQ) poisoning, this study aims to analyze immune biomarkers in patients and explore their impact on outcomes. Methods:A retrospective multicenter cohort study included 145 patients with acute DQ poisoning from six hospitals in Zhejiang Province, China. Immune-inflammatory parameters were compared between DQ patients and healthy controls. Patients were then grouped according to their 28-day survival status for prognostic analysis. Clinical, laboratory, and immune parameters were collected. Least absolute shrinkage and selection operator (LASSO) regression, multivariate logistic regression, and receiver operating characteristic analysis were used to identify predictors of mortality. Bioinformatics analysis was performed to explore potential molecular targets and pathways. Results:Of 145 patients, 72 died within 28 days. Non-survivors showed higher procalcitonin (PCT), lactate, and organ injury markers, as well as elevated interleukin-6 and interleukin-10, compared with survivors. Compared with healthy controls, patients with DQ poisoning exhibited increased white blood cells (WBC), neutrophils, monocytes, and cytokines, alongside reduced lymphocytes and T-cell subsets (all P < 0.0001). LASSO and logistic regression identified PCT, WBC, and lactate as independent predictors of mortality, with PCT providing the greatest discriminative value (AUC = 0.88). Bioinformatics analysis further indicated enrichment of immune-related pathways and hub genes associated with immune dysregulation. Conclusion:Acute DQ poisoning causes pronounced immune-inflammatory disturbances that are more severe in non-survivors. PCT is the strongest independent predictor of 28-day mortality, while exploratory bioinformatics highlights immune pathways with potential prognostic and therapeutic relevance.

Manganese (Mn) is a neurotoxin that has been etiologically linked to the development of neurodegenerative diseases in the case of overexposure. It is widely accepted that overexposure to Mn leads to manganism, which has clinical symptoms similar to Parkinson’s disease (PD), and is referred to as parkinsonism. Astrocytes have been reported to scavenge and degrade extracellular α-synuclein (α-Syn) in the brain. However, the mechanisms of Mn-induced neurotoxicity associated with PD remain unclear. Serpina3n is highly expressed in astrocytes and has been implicated in several neuropathologies. The role Serpina3n plays in Mn neurotoxicity and PD pathogenesis is still unknown. Here, we used wild-type and Serpina3n knockout (KO) C57BL/6 J mice with i.p. injection of 32.5 mg/kg MnCl2 once a day for 6 weeks to elucidate the role of Serpina3n in Mn-caused neurotoxicity regarding parkinsonism pathogenesis. We performed behavioral tests (open field, suspension and pole-climbing tests) to observe Mn-induced motor changes, immunohistochemistry to detect Mn-induced midbrain changes, and Western blot to detect Mn-induced changes of protein expression. It was found that Serpina3n KO markedly alleviated Mn neurotoxicity in mice by attenuating midbrain dopaminergic neuron damage and ameliorating motor deficits. Furthermore, using immunofluorescence colocalization analysis, Western blot and quantitative real-time PCR on Mn-treated C8-D1A cells, we found that Serpina3n KO significantly improved astrocytic α-Syn clearance by suppressing Mn-induced lysosomal dysfunction. Reduced transcription factor EB (TFEB)-v/p-ATPase signaling is responsible for the impairment of the lysosomal acidic environment. These novel findings highlight Serpina3n as a detrimental factor in Mn neurotoxicity associated with parkinsonism, capture the novel role of Serpina3n in regulating lysosomal function, and provide a potential target for antagonizing Mn neurotoxicity and curing parkinsonism in humans.

BACKGROUND:Diquat, a commonly employed bipyridyl herbicide, is recognized for its hepatotoxic effects attributed to the generation of reactive oxygen species. Baicalin (BAI), a flavonoid derivative, has garnered significant research interest for its hepatoprotective properties. Nevertheless, the clinical application of BAI is constrained by its limited water solubility and poor bioavailability. To address these challenges, BAI-nanoliposome (BAI-NL) has emerged as a novel drug delivery platform aimed at enhancing therapeutic outcomes. METHODS:We used diquat-induced liver injury mouse model and AML12 hepatocytes to test the protective effect of BAI and BAI-NL on liver inflammation, oxidative stress, and mitochondrial function. The parameters included histological, biochemical, and molecular biological analyses. RESULTS:In the diquat-induced model, both BAI and BAI-NL exhibited effectiveness on attenuating liver inflammation. Ex vivo analyses further indicated that BAI-NL was superior to BAI in preserving mitochondrial membrane potential, reducing oxidative stress, and modulating the phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin RBR E3 ubiquitin-protein ligase (Parkin) signaling pathway. These findings enhanced mitophagy and facilitated the removal of damaged mitochondria. CONCLUSIONS:BAI-NL exhibited superior hepatoprotective effects compared to free BAI, possibly by reducing inflammation, preserving mitochondrial homeostasis, and reinstating autophagic balance through modulation of the PINK1/Parkin signaling pathway. These outcomes indicate a groundbreaking method for addressing liver diseases and underscore the potential of nanoliposome technology in augmenting the efficacy of natural compounds.

In order to synthesize available results regarding human immunodeficiency virus (HIV) infection and inflammatory bowel disease (IBD), we conducted a systematic review and meta-analysis to provide quantitative estimates of associated risk. A systematic search of four scientific databases, PubMed, the Cochrane Library, EMBASE, and Scopus, was performed. The overall odds ratio (OR) with the corresponding 95

The aim of this study was to develop a model for early prediction of adverse events and treatment effectiveness in patients with hyperkalemia. We collected clinical data from patients with hyperkalemia in the First Hospital of Zhejiang University School of Medicine between 2015 and 2021. The least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression were used to analyze the predictors on the full dataset. We randomly divided the data into a training group and a validation group, and used LASSO to filter variables in the training set. Six machine learning methods were used to develop the models. The best model was selected based on the area under the curve (AUC). Shapley additive exPlanations (SHAP) values were used to explain the best model. A total of 1074 patients with hyperkalemia were finally enrolled. Diastolic blood pressure (DBP), breathing, oxygen saturation (SPO2), Glasgow coma score (GCS), liver disease, oliguria, blood sodium, international standardized ratio (ISR), and initial blood potassium were the predictors of the occurrence of adverse events; peripheral edema, estimated glomerular filtration rate (eGFR), blood sodium, actual base residual, and initial blood potassium were the predictors of therapeutic effect. Extreme gradient boosting (XGBoost) model achieved the best performance (adverse events: AUC = 0.87; therapeutic effect: AUC = 0.75). A model based on clinical characteristics was developed and validated with good performance.

Glufosinate-ammonium herbicides are the most widely used broad-spectrum, non-selective herbicides in the world. Glufosinate-ammonium is a structural analogue of glutamate (Glu) which can irreversibly inhibit the activity of glutamine synthetase (GS) and Glu decarboxylase in plants, thereby blocking the synthesis of glutamine (Gln) from Glu and ammonia (Hoerlein, 1994). This causes the plants to die because of the nitrogen metabolism disorder and subsequent intracellular accumulation of ammonia. In humans, the characteristic features of glufosinate-ammonium herbicide poisoning include gastrointestinal symptoms and neurotoxicity (Watanabe and Sano, 1998). Currently, there are no antidotes for glufosinate-ammonium herbicide poisoning, and thus supportive care is the key treatment.

The worldwide spread of carbapenem-resistant Klebsiella pneumoniae (CRKP) has led to a major challenge to human health. The emergence and prevalence of transferable plasmid carrying carbapenemase encoding gene is undoubtedly a potential factor in increasing the burden of carbapenem resistance. In this study, we described the reginal dissemination of repB(1701) plasmid carrying blaNDM-4 in China, with the coexistence of blaNDM-4 and blaOXA-9 in two independent K. pneumoniae isolates for the first time. Whole-genome sequencing and plasmid characterization of isolates L2388 and L3835 showed both blaNDM-4 and blaOXA-9 genes are situated on the transferable plasmid, designated as pL2388-NDM-OXA [120,100 bp, IncFII(K)-repB(R1701)] and pL3835-NDM-OXA [127,486 bp, repB(R1701)]. Notably, two copies of blaNDM-4 were identified in different orientations within pL3835-NDM-OXA. The blaNDM-4 sequence is relatively conserved (blaNDM-4-ble-trpF-dsbD-cutA-groES-groL), with various mobile genetic elements (MEGs) surrounding it, particularly IS26, which may play a pivotal role in gene-level dissemination. The previously unrecognized distribution of these plasmids across select regions of Southern China and Vietnam suggests a potentially wider epidemiological range than initially presumed in the context of microbiology and epidemiology. This is the first report of transferable IncFII(K)-repB(R1701)/repB(R1701) plasmids carrying the blaNDM-4 gene, relevant detection and investigation measures should be taken to control the prevalence.

>Clinical practice has shown that kidney transplant recipients infected with COVID-19 are prone to developing critical illness and have a higher mortality rate. [1] Kidney transplant recipients require longterm oral anti-rejection drugs to suppress the immune response.This result may be related to the strong immunosuppression in kidney transplant recipients compared to the general population. [2] Therefore,the treatment of kidney transplant recipients infected with severe COVID-19 is a difficult problem.Here,we report the use of extracorporeal membrane oxygenation（ECMO）-assisted treatment for a kidney transplant recipient who was infected with severe COVID-19.

Copper sulfate is a frequently used copper compound in laboratory settings, with instances of poisoning being uncommon. A study conducted by the American Association of Poison Control Centers' National Poison Data System found that only 140 individuals were exposed to copper compounds over the course of a year, with five cases being intentional (Gummin et al., 2023). Severe poisoning from copper sulfate can result in isolated gastrointestinal injury (Galust et al., 2023), intravascular hemolysis (Adline et al., 2024), rhabdomyolysis (Richards et al., 2020), and other symptoms documented in the literature. However, there have been no reports of long-term uncontrolled hyperglycemia in patients with copper sulfate poisoning. This case study documents the treatment approach for a patient with unexplained, long-term, uncontrolled hyperglycemia, alongside multiple organ dysfunction resulting from intentional ingestion of a large dose of copper sulfate. This case report details the long-term complications in a patient's recovery from acute copper sulfate, highlighting the significance of ongoing monitoring and intervention.

Diquat (DQ) is a widely utilized nonselective herbicide that is primarily used to control a wide range of weeds and crop residues. It also has significant environmental implications. DQ exposure can cause severe damage to the central nervous system (CNS), a critical symptom of acute poisoning that endangers patients. Despite its severity, the underlying mechanisms of DQ-induced toxic encephalopathy remain unclear, hindering the development of precise treatments. Our research demonstrated that acute DQ exposure in mice significantly increases oxidative stress and triggers neuroinflammation in the hippocampus. Furthermore, in vitro findings indicate that the detrimental effects of DQ are mediated by its disruption of autophagic processes, leading to exacerbated neural damage. DQ initially promotes autophagy in BV2 microglia for self-protection against oxidative stress and inflammation. However, this process is subsequently blocked, intensifying neural damage. Crucially, our results show that the activation of autophagy can reverse these adverse effects. This study not only sheds light on the intricate mechanisms of DQ neurotoxicity but also provides potential therapeutic targets for mitigating DQ-induced toxic encephalopathy.

Paraquat poisoning results in significant pulmonary damage, but current treatments are only minimally effective in repairing the injured lung tissues. Recent research has highlighted the promise of using stem cell therapy, namely mesenchymal stem cells, as a new method for treating paraquat toxicity. These cells have shown effectiveness in decreasing inflammation, apoptosis, and fibrosis in the mice lungs subjected to paraquat. The therapeutic implications of mesenchymal stem cells are believed to arise from their release of bioactive proteins and their capacity to regulate inflammatory responses. However, additional clinical study is required to validate these therapies' efficacy. This review thoroughly explores the pathophysiology of paraquat poisoning and the properties of mesenchymal stem cells. Additionally, it critically assesses the long-term safety and effectiveness of mesenchymal stem cell therapies, which is crucial for developing more dependable and effective treatment protocols. In summary, although mesenchymal stem cells offer promising prospects for treating lung injuries, more investigations are required to optimize their therapeutic promise and ensure their safe clinical application in the context of paraquat poisoning.

Parishin, a natural compound, has demonstrated significant potential in mitigating age-related phenotypes and improving outcomes in age-associated diseases. Given that aging is a major risk factor for numerous chronic conditions, including pulmonary fibrosis, we investigated parishin's effects on cellular senescence and lung health. In our study, we treated mouse lung epithelial cells with parishin and observed a reduction in cellular senescence markers alongside an upregulation of sirtuin 1 (SIRT1). Building on these in vitro findings, we administered parishin to naturally aged mice. The treatment resulted in decreased pulmonary fibrosis and reduced DNA damage in lung tissue. Notably, we found that parishin treatment led to a reduction in Cluster of differentiation 38 (CD38) levels, concomitant with an increase in SIRT1 expression. These findings indicate that parishin may enhance lung function in aged mice, suggesting its potential as a therapeutic agent for treating age-related pulmonary disorders.

A 54-year-old woman in good health was admitted to our hospital with diquat poisoning. The patient drank an unknown dose of diquat, and acute kidney injury developed early. However, there were no obvious pulmonary abnormalities and no signs of central nervous system toxicity in the early stage. The woman underwent active treatment, which resulted in a significant decrease in blood diquat levels, but her lung condition progressively worsened and neurological symptoms developed. Fortunately, the patient survived after intensive hemoperfusion combined with continuous renal replacement therapy (CRRT), intracranial pressure reduction, and anti-infective treatment. This case report highlights the importance of being aware of the development of delayed pulmonary symptoms and neurologic complications when caring for patients poisoned with diquat, even in those with low diquat blood concentrations. Interestingly, we also detected the concentration of diquat in the cerebrospinal fluid (CSF) of patients with diquat poisoning, and found that the rate of decrease of diquat concentration in the CSF was considerably slower than that in the blood.Notably, a specific correlation was observed between the concentration of diquat in the CSF, rather than in the blood, and both the intracranial pressure (ICP) and the severity of cerebral edema in this patient.