Acute pulmonary embolism (APE) is a very common and important medical emergency in intensive care units with an unfavorable prognosis. This study aims to explore the prognostic factors of APE and to construct a prognostic prediction model. A retrospective analysis was conducted on 252 APE patients in the emergency department of our hospital from January 2020 to March 2024. The initial observation endpoint was set as the mortality status of patients within 30 days of admission. Cox multivariate regression analysis was used to identify independent risk factors for prognosis. Based on these factors, a nomogram predictive model was constructed and evaluated using R software. Within 30 days of admission, 42 patients died with an overall mortality rate of 16.6% (42/252). Binary Cox multivariate regression analysis indicated that age ≥ 62.5 (HR: 2.64, 95% CI: 1.23-5.63, p = 0.012), right ventricular dysfunction (RVD) (HR: 4.58, 95% CI: 1.76-11.96, p = 0.002), white blood cell count (WBC) ≥ 13.1 (HR: 2.35, 95% CI: 1.20-4.60, p = 0.013), albumin/fibrinogen ratio (AFR) < 9.15 (HR: 3.36, 95% CI: 1.76-6.42, p < 0.001), Prognostic Nutritional Index (PNI) < 50.3 (HR: 4.35, 95% CI: 1.62-11.71, p = 0.004), and Systemic Inflammation Response Index (SIRI) ≥ 1.05 (HR: 7.21, 95% CI: 3.38-15.37,p < 0.001) were independent risk factors for mortality. The nomogram model based on these factors demonstrated a good predictive value for 30-day mortality, with an AUC of 0.908. The nomogram model based on age, RVD, WBC, AFR, PNI, and SIRI has a well prognostic value for APE patients.

Background While some studies have suggested better outcomes for critically ill patients with balanced solutions over normal saline, the best type of intravenous fluid to use for stroke patients remains unknown.Objective To determine if balanced solutions or normal saline are associated with risk of hemorrhagic transformation or 90-day disability in patients with acute ischemic stroke treated with intravenous thrombolysis.Methods This was a retrospective review of the 2015-2019 Get with the Guidelines® data at a single academic medical center. Exposure was type of intravenous fluid and outcomes were modified Rankin scale (mRS) ≤2 at 90 days and hemorrhagic transformation. Multivariate analysis controlled for age, demographics, medical history, time to tPA, and admission stroke scale.Results We included 302 patients who received thrombolysis, of which 166 patients had mRS data at 90 days. In univariate analysis, exposure to any balanced solution was associated with increased 90-day disability (OR 4.3, 95% CI 3.8-4.9) and hemorrhagic transformation (OR 2.0, 95% CI 1.3-2.2). In multivariate analysis, exposure to a balanced solution at any time was associated with increased 90-day disability (OR 6.3, 95% CI 2.4-17.0, p<0.01), but not hemorrhagic transformation.Conclusion This observational trial demonstrated that exposure to balanced solutions is associated with increased risk of disability at 90 days and possibly hemorrhagic transformation in patients with acute ischemic stroke treated with intravenous thrombolysis. This data would suggest that normal saline is a preferred solution in these patients, though larger future trials are needed.

Hepatocellular carcinoma (HCC) ranks as the fifth most common neoplasm and the third leading cause of cancer-related deaths worldwide. Current serum biomarkers for HCC surveillance and early diagnosis, particularly alpha-fetoprotein (AFP) the most commonly used marker, lack satisfactory sensitivity and specificity, highlighting an urgent need for more effective markers with higher accuracy for early HCC detection. The downregulation of melanoma-associated antigen D1 (MAGE-D1) transcription plays a crucial role in apoptosis and inhibits cancer cell proliferation when expressed ectopically. Moreover, reduced MAGE-D1 expression correlates with improved prognosis in many cancers. Therefore, this study aims to evaluate the diagnostic role of MAGE-D1 in HCC, proposing it as a novel biomarker for early diagnosis and monitoring of tumor progression. Serum MAGE-D1 expression was measured using RT-qPCR on 198 subjects, divided into three groups: 88 with HCC, 56 with chronic liver conditions, and 54 as healthy controls. With a sensitivity of 93.3% and a specificity of 97.5%, MAGED-1 shows strong potential as a diagnostic marker for HCC. The performance of serum MAGED-1 expression in discrimination between HCC and chronic liver condition revealed an area under the curve (AUC) of 0.939 using the cutoff (0.752) yielded a sensitivity of 90%, specificity of 85%, and an accuracy of 91%. Evaluation of the diagnostic significance of MAGED-1 demonstrated an AUC value of 0.726, with a sensitivity of 63.6% and a specificity of 73.5%. In conclusion, MAGED-1 might be a specific and sensitive biomarker for HCC, potentially improving the malignancy diagnosis and prognosis.

Immunotherapy with checkpoint inhibitors has improved the outcomes of patients with metastatic lung cancer in recent years. Despite improved prognosis, not all patients respond to treatment. Therapeutic interventions to build on the success of immune checkpoint inhibitors are needed.

Kidney transplantation is a pivotal treatment for end-stage renal disease. However, renal ischemia-reperfusion injury (IRI) during surgery significantly impacts graft function. Despite unclear molecular mechanisms, no specific therapies or preventative measures are available. Gene expression profiles from renal biopsies before and after IRI were downloaded from public databases. Differentially expressed genes were identified using the Wilcoxon rank-sum test and weighted gene co-expression network analysis. Ferroptosis-associated genes were screened using the FerrDb database. The genes with the highest connectivity were identified via the protein-protein interaction (PPI) network and upstream regulatory miRNAs were found through the gene-miRNA network. A mouse renal IRI model was constructed for transcriptome sequencing and quantitative real-time polymerase chain reaction (qRT-PCR) validation to elucidate the relationship between key ferroptosis genes and regulatory miRNAs in renal IRI. Differential analysis identified 15 ferroptosis-associated genes (, , , , , , , , , , , , , , and ) involved in renal IRI regulation. In animal experiments, ferroptosis-related genes were also upregulated in the model group. Enrichment analysis and hematoxylin-eosin pathological staining suggested these genes are primarily involved in renal inflammatory responses. PPI network analysis revealed as the gene with the highest connectivity, and the gene-miRNA network indicated might be regulated by Animal experiments revealed decreased and increased levels in the model group, identifying potential therapeutic targets. regulates ferroptosis in renal IRI by targeting , highlighting as a crucial gene in the ferroptosis process of renal IRI.

Extrapulmonary tuberculosis (EPTB) is an important public health problem due to its diverse clinical presentations, diagnostic complexities and significant impact on patient outcomes and public health. Our study aimed to understand the sociodemographic, clinical and laboratory characteristics as well as diagnostic and treatment modalities of adult patients with EPTB. This is a multicentric retrospective study that covers patients with EPTB cases followed up from January 2015 to December 2022 among TB dispensaries and Infectious Diseases and Clinical Microbiology clinics of 15 hospitals located in various regions of Turkey. The study included 64.6% women with a mean age of 44 years and a mortality rate of 3.5% within one year of diagnosis. Initial constitutional symptoms were predominantly fatigue (57%), anorexia (53.7%). The most commonly affected sites were the lymph nodes (49.1%) and pleura (9.7%). The lumbar region was particularly involved in cases with spinal TB. Diagnostic findings included acid-fast bacilli positivity in 27.5% of cases, TB PCR positivity in 41%, elevated adenosine deaminase levels in 91.2% (especially in pleural and peritoneal fluids) and mycobacterial culture positivity in 40.9%. Pathology slides showed granulomatous inflammation in 97.7%. Increased C-reactive protein levels correlated with the number of organs affected. Anti-TB treatment-related hepatotoxicity was detected in 8.9% of patients. In this study, it is important to note that the lumbar region is predominantly affected with involment in spinal region. C-reactive protein level was consistent with the number of organ involvements was one of the most critical results of this study.

Cisplatin (DDP) resistance represents a pivotal contributing factor to chemotherapy failure and adverse patient outcomes in gastric cancer (GC). The objective of the present study was to investigate the roles and underlying mechanisms of myocyte enhancer factor 2A (MEF2A) in DDP resistance in GC. GC cell line AGS and MKN-45 cells were applied to construct DDP-resistant cells. CCK-8, colony formation, and flow cytometry methods were validated for determining the IC50 value of DDP and cell survival of GC cells. qRT-PCR and western blotting analysis quantified the molecular levels at mRNA and protein, respectively. Chromatin immunoprecipitation and dual-luciferase assays validated the molecular relationship between MEF2A and NF-κB inhibitor alpha (NFKBIA). Roles of MEF2A in in vivo were performed employing a xenograft model. The results showed that NFKBIA was greatly decreased in DDP-resistant AGS and MKN-45 cells compared to their respective parental cells. Increasing NFKBIA expression impaired the IC50 value of DDP and cell survival in DDP-resistant cells, while these alterations were rescued upon TNF-α treatment. Mechanistically, MEF2A acts as a transcriptional activator of NFKBIA, which led to the reduction of phosphorylation of p65 and cytoplasmic retention. Moreover, MEF2A overexpression promoted the sensitivity of GC cells to DDP and tumor growth, whereas these effects were partially reversed by NFKBIA silence. Collectively, MEF2A mitigated the DDP resistance in GC cells by modulatory actions on the NFKBIA/NF-κB signaling, shedding light on MEF2A/NFKBIA might be a promising intervention target for improving DDP resistance in GC.

NKG2D chimeric antigen receptor (CAR)-modified T cells (NKG2D CAR-T cells) have been reported to be preclinically efficient in several tumors, but little is known whether NKG2D CAR-T cells co-expressing IL21 (IL21-NKG2D CAR-T cells) display greater antitumor activity in multiple myeloma (MM). In this study, the lentivirus has been produced for expression of the IL21 sequence linked to the extracellular NKG2D sequence with the signal peptide linked through the CD8α hinge-transmembrane domain to the 4-1BB molecule fused with the CD3-ζ chain signaling domain, and the engineered IL21-NKG2D CAR-T cells and NKG2D CAR-T cells were constructed. The CAR expression on CAR-T cells was assessed by flow cytometry, and the killing effects of CAR-T cells on MM were assessed by the cytotoxicity assay and ELISA assay. Moreover, xenograft models were also established to evaluate the ability of IL21-NKG2D-CAR-T cells to eliminate MM in vivo. Our results indicated that NKG2D CAR-T cells had dramatic cytotoxicity on MM cells in vitro, and co-expression of IL-21 significantly increased the cytotoxicity of NKG2D CAR-T cells on MM cells. Remarkably, we found that dexamethasone enhanced the cytotoxicity of IL21-NKG2D CAR-T cells on MM cells. Furthermore, IL21-NKG2D CAR-T cells also displayed significant anti-myeloma activity in vivo. In conclusion, IL21-NKG2D CAR-T cells had dramatic cytotoxicity on MM cells in vitro and in vivo, and a system to apply IL21-NKG2D CAR-T cells and low dosage of dexamethasone for the future study of the targeted therapy for MM has been established.

Early onset colorectal cancer (EO-CRC) is increasing. We investigated the risk factors for ER-CRC compared to late onset colorectal cancer (LO-CRC). CRC patients between the years 1999 and 2021 were retrospectively evaluated. Data regarding demographics, comorbidities, malignancies, and mortality were collected. Data were retrieved using the MdClone platform from a large Health Maintenance Organization. The cohort was subdivided into EO-CRC (age ≤ 50 years) and LO-CRC (age ≥ 51 years) groups. 61,679 patients diagnosed with CRC were included in our analysis, 30,456 (49.4%) males, and 4891 (7.9%) Arabs, with an average age at diagnosis of 70.1 ± 13.1 years. 5561 (9%) patients were included in the EO-CRC group. Over the last decades, higher rates of EO-CRC were diagnosed compared to the previous decade, 9.8% vs 8.3%, p < 0.001. A higher percentage of EO-CRC patients were females (52.8% vs 50.4%), had a family history of CRC (9.9% vs 5.5%), were Arabs (18.7% vs 6.9%), and were smokers (32.7% vs 30.2%) compared to LO-CRC patients. Significantly lower rates of comorbidities such as ischemic heart disease, diabetes mellitus, hypertension, obesity, and iron deficiency anemia were found among EO-CRC patients, with a lower all-cause mortality (27.7% vs 63.1%, p < 0.001). 348 (6.3%) of the EO-CRC patients had another Lynch-related cancer until age 50 years compared to 45 (0.1%) at the LO-CRC. Young individuals with increased risk for CRC need special consideration and should be referred early for screening and endoscopic investigation, particularly those with a family history of CRC, smokers, and those of Arab ethnicity.

Hyperglycemia, one of the major risk factors for atherosclerosis, leads to the accumulation of advanced glycation end products (AGEs), contributing to cardiovascular complications. Such accumulation may accelerate the progression of vascular disease in patients with diabetes. Reverse cholesterol transport (RCT) protein, ATP-binding membrane cassette transporters A1 and G1 (ABCA1 and ABCG1) and cholesterol 27-hydroxylase facilitate cholesterol removal from macrophages. AGE inhibits RCT by reducing the expression of ABCA1 and ABCG1. This study aimed to evaluate whether plasma from poorly controlled adolescents with type 1 diabetes (T1D) disrupts cholesterol homeostasis in human monocytes/macrophages. Twenty healthy controls (HCs) and 20 patients with type 1 diabetes mellitus (T1DM), 10-19 years old, were enrolled. Naïve THP-1 macrophages were exposed to plasma from each HC and patient with T1D. Following incubation, mRNA for cholesterol efflux (ABCA1, ABCG1, and 27-hydroxylase) and cholesterol uptake (CD36, ScR-A1, lectin oxidized low-density lipoprotein (LOX)-1, and CXCL16) were isolated. Foam cell formation was quantified to confirm the pro-atherogenic effects of T1D plasma on macrophages. Results showed that T1D plasma had an elevated level of N-(carboxymethyl)-lysine-modified proteins and upregulated CXCL16 and, to a lesser degree, ScR-A1. This change in gene expression in the presence of T1D plasma is associated with increased lipid accumulation and foam cell formation by THP-1 macrophages. In our study, these cells' uptake of an AGE product occurred mainly through the SR-A1 and CXCL16 receptors, leading to increased intracellular oxidized low-density lipoprotein. We conclude that AGEs may contribute to accelerated atherosclerosis in diabetes through effects on both forward and reverse cholesterol movement.

The current study was conducted aimed at exploring the clinical characteristics and distinguishing factors of patients with the novel coronavirus pneumonia (COVID-19) complicated with active pulmonary tuberculosis. A total of 354 patients with COVID-19 in our hospital from November 2022 to February 2023 were included in the present study, of whom 87 patients were also combined with active pulmonary tuberculosis. Significant differences were found in fever, fatigue, nasal congestion, nasal discharge, sore throat, expectoration, and weight loss between the two groups (p < 0.05). There were significant differences in the levels of leukocyte, neutrophil, lymphocyte count, monocyte, hemoglobin, C-reactive protein, and CD4/CD8 between the two groups (p < 0.05). There were significant differences in pulmonary consolidation, multifocal ground-glass opacities in both lungs and infiltrating shadows, "cavity" by CT imaging between the two groups (p < 0.05). The independent variables were set as the indicators with different results of clinical characteristics and CT imaging, including fever, fatigue, nasal congestion, nasal discharge, sore throat, expectoration, weight loss, leukocytes, count neutrophils and lymphocytes, monocytes, hemoglobin, C-reactive protein, CD4/CD8, pulmonary consolidation, multifocal ground-glass opacities in both lungs and infiltration shadows. Our findings have revealed that fever, fatigue, expectoration, leukocytes, neutrophils, monocytes, hemoglobin, C-reactive protein, lymphocytes, CD4/CD8, pulmonary consolidation, multifocal ground-glass opacities in both lungs, and infiltration shadows were the risk factors responsible for the patients with COVID-19 complicated with active pulmonary tuberculosis.

Translational research moves scientific discoveries and innovations across the development spectrum for a particular target or disease, trying to bridge in a multidisciplinary fashion the gap between laboratory scientific discoveries and practical, real-world applications in medicine and in healthcare. Translational research aims to move research findings across settings, specific languages, methodologies, and study designs, from laboratory to clinical practice and ultimately into community- and population-level health benefits. In contrast, translational science is a distinct field, which evolved over time toward a systematic study and practice of operationalizing the translation of content from one language, ecosystem, environment, contextual landscape, culture, discipline, area, or domain into another. It involves systematic and transdisciplinary integration of knowledge from basic science, clinical research and population science to improve human health, better longevity, and to ensure disease- and disability-free lives. Translational science often uses knowledge, operational frameworks, and specific capabilities borrowed from other specialties, disciplines, and fields such as operations management, implementation and dissemination science, quality improvement and management, project management, public health, intervention science, change management and leadership, decision science, design thinking, functional design, data science, communication and marketing science, etc. The main goal of this article is to open a series of thematic reviews in this journal, introducing the reader to the main definitions, contingencies, touchpoints, and overlapping areas between translational science and these related specialties, disciplines, and fields of study. Transdisciplinary capabilities borrowing from these related specialties can create a robust translational science machinery for health systems, research organizations, and innovation hubs.

Triple-positive breast cancer (TPBC) is a type of breast cancer that overexpresses estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2). Dysregulation of estrogen receptor signaling has been implicated in the pathogenesis of breast cancer. ERα activation triggers the production of second messengers, including cAMP, leading to the activation of signals such as PI3K/AKT or Ras/MAPK. Ruxolitinib is a specific inhibitor of JAK1/JAK2. MK-2206 is an allosteric inhibitor of the Akt. The limitations of the use of ruxolitinib and MK-2206 as single agents necessitate the development of combination therapies with other drugs. This study is the first to investigate the effects of combining ruxolitinib with MK-2206 on MAPK and PI3K/AKT signaling in BT474 breast cancer cells. Additionally, this work aimed to increase the anticancer effects of cotreatment with MK-2206 and ruxolitinib. Ruxolitinib, MK-2206, and their combination reduced cell viability in a dose- and time-dependent manner, as determined by MTT assays after 48 hours of treatment. Colony formation and wound healing assays demonstrated that MK-2206 exhibited a synergistic anti-proliferative effect. The effects of ruxolitinib, MK-2206, and their combination on PI3K/AKT and MAPK signaling were assessed via western blotting. Ruxolitinib and MK-2206 combined treatment inhibits cell death in BT474 cells by downregulating ERα, Src-1, ERK1/2, SAPK/JNK, and c-Jun. Our results revealed the relationships among the ERα, PI3K/AKT, and MAPK signaling pathways in ER+ breast cancer cells. Understanding the interactions among ERα, PI3K-AKT-mTOR, and MAPK could lead to novel combination therapies.

In this retrospective cohort study, we investigated the prognostic value of sarcopenia evaluated by Computed Tomography (CT)-based indices for adverse hospitalization outcomes in patients with acute infections. We analyzed data from 225 patients admitted to the hospital for acute infections between 2019 and 2020. Patients who had undergone an abdominal CT scan either up to 1 month before or within the first 3 days of hospitalization were included. CT image analysis was used to evaluate skeletal muscle mass (by skeletal muscle index (SMI)) and muscle quality (by psoas muscle density, pMD). Low pMD was associated with higher in-hospital mortality (31% vs 11.4% p < 0.001) as well as higher longer-term mortality rates (p = 0.008 for 30 days and <0.001 for 90- and 1-year mortality). Low pMD remained an independent poor prognostic factor after controlling for confounders, with an adjusted odds ratio (aOR) of 2.74, (95% CI 1.33-5.67, p = 0.006) for 1-year mortality, and aOR of 2.61, (95% CI 1.23-5.55) for a prolonged hospital stay. Low SMI was associated with adverse outcomes, although this association was not independent after controlling for confounders. Notably, patients with both low SMI and pMD exhibited the poorest hospitalization outcomes: aOR for 1-year mortality 5.015 (95% CI 1.767-14.23, p = 0.002), and prolonged length of stay aOR 3.197, (95% CI 1.159-8.821, p = 0.025). CT-based muscle indices serve as independent prognostic factors in medical patients admitted with acute infection. Incorporating radiological assessments of sarcopenia into routine care for hospitalized patients with acute infection may enable risk stratification and early intervention in reversible conditions.

The occurrence of sepsis-associated acute kidney injury (SA-AKI) predicts a worse prognosis. We aimed to assess the impact of acetaminophen use on short-term mortality in patients with SA-AKI. A total of 6563 patients diagnosed with SA-AKI from the 2008 to 2019 Medical Information Mart for Intensive Care IV (MIMIC-IV) database were enrolled in this retrospective cohort study. The Cox regression model was utilized to analyze the associations of acetaminophen with 30-day mortality and in-hospital mortality. Additional propensity score matching (PSM) analysis was performed regarding patients with acetaminophen use versus those without. Of these patients, 30-day mortality occurred in 1421 (21.65%) patients and in-hospital mortality in 1246 (18.99%) patients. Patients who used acetaminophen were associated with a reduced risk of 30-day mortality (hazard ratio (HR) = 0.80, 95% confidence interval (CI): 0.71-0.90) and in-hospital mortality (HR = 0.72, 95% CI: 0.63-0.82). The PSM analysis demonstrated that acetaminophen use was still related to a reduced risk of 30-day mortality and in-hospital mortality. Subgroup analysis showed that the relationships between acetaminophen and 30-day mortality and in-hospital mortality were consistent across subgroups (p < 0.05). The use of acetaminophen has an association with lower short-term mortality in patients with SA-AKI.

Immunothrombosis has emerged as a potential mechanistic link underlying the development and progression of acute respiratory distress syndrome (ARDS), but understanding its specific profile in patients, both locally and systemically, is limited. The objective of this study was to characterize and compare the immunothrombotic signatures in patients diagnosed with pneumonia-related ARDS (p-ARDS) at both the pulmonary and systemic levels and to evaluate their clinical relevance. The study included 23 consecutive patients diagnosed with p-ARDS admitted to the intensive care unit at a tertiary university hospital from July 2022 to May 2023, alongside 40 concurrently hospitalized patients with common pneumonia as controls. Paired bronchoalveolar lavage fluid (BALF) and serum samples were collected from the participants for the analysis of 15 biomarkers to assess and quantify the pulmonary and systemic immunothrombotic signatures. The study results revealed significant pulmonary inflammation and systemic endothelial injury in p-ARDS patients compared to pneumonia controls. These observations were maintained after adjustment for severity of illness (Acute Physiology and Chronic Health Evaluation II scores). In terms of clinical relevance, inflammatory biomarkers (interleukin [IL]-6, IL-8) in BALF were found to correlate with PaO/FiO ratio, while serum levels of a disintegrin and metalloproteinase with thrombospondin type 1 motif 13 (ADAMTS-13) and thrombomodulin showed associations with Sequential Organ Failure Assessment and Disseminated Intravascular Coagulation scores. In conclusion, this preliminary investigation identified compartment-specific variations in the immunothrombotic signature between patients with p-ARDS and those with pneumonia alone, with inflammatory responses predominantly localized in the alveolar compartments and coagulation/endothelial injury biomarkers more pronounced in peripheral blood.

Infection with can spread and cause central nervous system involvement, known as neuroborreliosis. Microglia phagocytose bacteria, mediate inflammation, and elicit an immune response toward the spirochete. Like other tissue macrophages, microglia can polarize into two different modulatory phenotypes, M1 and M2. We explored human microglial polarization changes upon infection with . HMC3 human microglia cell line was infected with for 24 h. Expression of polarization markers was evaluated via flow cytometry at 4 and 24 h. Secreted immunological mediators were evaluated using a multiplex ELISA system at 4, 18, and 24 h. An early decrease followed by a later increase in expression of M1 polarization marker iNOS was observed at 4 h, and 24 h, respectively. A decrease in M2 marker CX3CR1 occurred at 24 h. There were no changes in expression of M1 markers CD14, or in M2 markers CD163 and CD206. Multiplex ELISA evidenced an increase in secretion of activation markers MIP-1α, MIP- 1β, IP-10, chemotactic factor MCP-1, M1 polarization cytokine IL-8, and VEGF, at 4, 18, and 24 h. A decrease of iNOS at 4 h of infection suggests a diminished production of reactive nitrogen species that are a critical component of innate defense against infection. Increased iNOS and simultaneously decreased expression of CX3CR1 at 24 h, may suggest initiation of neuroprotective regulation of microglia recruitment to neuroinflammation. The dynamics of major inflammatory cytokines appear to be important in the microglial response to and should be further studied as these could become therapeutic targets in neuroborreliosis.

To investigate the impact of vaccines on sociodemographic characteristics, clinical profiles, and outcomes of SARS-CoV-2 infection among healthcare workers in South China during the period of Omicron variant dominance, a retrospective, analytical cross-sectional study was conducted. The findings revealed that while full vaccination could not prevent Omicron variant infection efficiently (26.51% uninfected vs 14.29% uninfected between vaccinated and unvaccinated participants, p = 0.506), it did substantially reduce the length of viral clearance significantly (p < 0.05), potentially facilitating quicker patient recovery. Unvaccination was found to be an independent risk factor for slow clearance when a linear regression analysis model was used (Coefficient: -3.516; 95% CI: -6.425 to -0.607; p = 0.020). Therefore, all eligible individuals should be fully vaccinated to get prepared for a potential wave of epidemic in the future.

Endocrine disruptive chemicals (EDCs) are considered as the potential attributes for the increasing trend in obesity and metabolic syndrome (MS) through disruption of sex hormones, particularly in women. We evaluated the association of understudied EDC compounds with total testosterone (TT), sex hormone-binding globulin (SHBG), obesity, and metabolic syndrome (MS). A population-based cross-sectional study was conducted using the National Health and Nutrition Examination Survey datasets collected during the years 2013-2016. Women of age ≥15 years with urinary measurements of non-persistent EDCs including bisphenol, triclosan, triclocarban, dichlorophenol, and paraben compounds were included in this study. Data were analyzed using the modified Poisson models to estimate the adjusted relative risk (RR) and 95% confidence interval (CI). The associations were also validated by considering TT and SHBG concentrations as the outcomes. The study included 1974 women with 11% high TT, 10.5% low SHBG, 40% obesity, and 46.2% MS. A medium to high exposure to bisphenol-A (RR=1.64; 95%CI: 1.14, 2.35, p=0.009), bisphenol-F (RR=1.83; 95%CI: 1.35, 2.49, p<0.001), bisphenol-S (RR=1.83; 95%CI: 1.35, 2.49, p=0.041) and 2, 4- dichlorophenol (RR=1.61; 95%CI: 1.06, 2.45, p=0.026) were associated with low SHBG but not with high TT. In addition, high exposure to triclosan was also inversely associated with lower SHBG concentrations (regression coefficient=-0.09; 95%CI: -0.15, -0.02, p=0.013). However, these EDCs were found to be associated with SHBG, obesity, and MS according to menopausal status. High exposure to certain non-persistent EDCs was associated with low SHBG, obesity, and MS according to menopausal status.

Peripheral T-cell lymphoma (PTCL) is an extensive class of heterogeneous diseases with dismal outcomes. Brentuximab vedotin (BV) is an antibody‒drug conjugate (ADC) comprising CD30-directed antibody. This review aimed to evaluate the efficacy and safety of BV for treating PTCL. We searched the PubMed, Embase, Cochrane Library and Web of Science databases for studies evaluating the efficacy of BV alone or in combination with other drugs for treating PTCL. The primary outcome measures included objective response rate (ORR), complete remission (CR), progression-free survival (PFS) and overall survival (OS). The secondary outcomes included 5-year OS, 5-year PFS and adverse events. 22 studies involving 1137 patients were included. These studies reported the use patterns of BV, ORR, CR, PFS, OS, and adverse events. The pooled ORR and CR rate were 68% (95% CI: 59%-75%) and 43% (95% CI: 34%-53%). For survival outcomes, the longest median PFS was 8.3 months, and the longest median OS was 26.3 months. The most common adverse event was peripheral neuropathy and neutropenia. The analysis suggested that BV alone or in combination with other drugs improved the response and survival rates in PTCL patients and was associated with tolerable adverse effects.