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Objective: The high hemoglobin, albumin, lymphocyte, and platelet (HALP) score has been reported to be a good prognostic indicator for several malignancies. However, more evidence is needed before it can be introduced into clinical practice. Here, we systematically evaluated the predictive value of HALP for survival outcomes in patients with solid tumors. Methods: This study was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Assessing the Methodological Quality of Systematic Reviews (AMSTAR) Guidelines. In March 2024, an electronic literature search was performed for articles regarding the prognostic role of HALP in solid tumors. Data from studies with reported risk ratios (HRs) and 95% confidence intervals (CIs) were pooled in a meta-analysis. Study bias was assessed using the QUIPS tool. Results: Of the 729 articles reviewed, 45 cohorts including data from 17,049 patients with cancer were included in the pooled analysis. The pooled results demonstrated that elevated HALP score was significantly associated with favorable overall survival (HR = 0.60, 95% CI 0.54-0.67, p < 0.01), cancer-specific survival (HR = 0.53, 95% CI 0.44- 0.64, p < 0.01), progression-free survival (HR = 0.62, 95% CI 0.54-0.72, p < 0.01), recurrence-free survival (HR = 0.48, 95% CI 0.30-0.77, p < 0.01), and disease-free survival (HR = 0.72, 95% CI 0.57-0.82, p < 0.01). Subgroup analyses based on various confounding factors further revealed the consistent prognostic impact of HALP on overall survival in patients with solid tumors. Conclusions: Our findings suggest that high HALP is associated with better survival outcomes in patients. The HALP score is a potential prognostic biomarker in solid tumors, but it needs to be further studied whether it can improve the established prognostic model. [ABSTRACT FROM AUTHOR]

Background: Periodontitis is among the most prevalent inflammatory conditions and greatly impacts oral health. This study aimed to elucidate the role of basement membrane-related genes in the pathogenesis and diagnosis of periodontitis. Methods: GSE10334 was used for identification of hub genes via the differential analysis, protein-protein interaction network, MCC and DMNC algorithms, and evaluation via LASSO regression and support vector machine analysis to identify basement membrane-related markers in patients with periodontitis. Findings were validated by analysis of the GSE16134 dataset and quantitative reverse transcription PCR. The regulatory interplay among lncRNAs, miRNAs, and mRNAs was investigated through multiple databases. Immune infiltration analysis was performed to assess the immune landscape in periodontitis. Results: ITGA7 was identified as a key gene for periodontitis, as supported by machine learning analysis, validation of expression, and receiver operating characteristic analysis from external datasets. Immune infiltration analysis revealed significant associations between ITGA7 expression and the infiltration of numerous immune cells implicated in periodontitis. Additionally, our findings suggest that the expression of the lncRNA LINC-PINT is significantly increased in periodontitis, and that it can modulate ITGA7 expression through hsa-miR-1293. Conclusion: ITGA7 is a potential diagnostic and therapeutic target for periodontitis. The LINC-PINT/hsa-miR-1293/ITGA7 axis and the relationship between ITGA7 and immune infiltration provide new insights into the molecular mechanisms underlying periodontitis and highlight potential avenues for clinical intervention. [ABSTRACT FROM AUTHOR]

Abstract Background Periodontitis is among the most prevalent inflammatory conditions and greatly impacts oral health. This study aimed to elucidate the role of basement membrane-related genes in the pathogenesis and diagnosis of periodontitis. Methods GSE10334 was used for identification of hub genes via the differential analysis, protein-protein interaction network, MCC and DMNC algorithms, and evaluation via LASSO regression and support vector machine analysis to identify basement membrane-related markers in patients with periodontitis. Findings were validated by analysis of the GSE16134 dataset and quantitative reverse transcription PCR. The regulatory interplay among lncRNAs, miRNAs, and mRNAs was investigated through multiple databases. Immune infiltration analysis was performed to assess the immune landscape in periodontitis. Results ITGA7 was identified as a key gene for periodontitis, as supported by machine learning analysis, validation of expression, and receiver operating characteristic analysis from external datasets. Immune infiltration analysis revealed significant associations between ITGA7 expression and the infiltration of numerous immune cells implicated in periodontitis. Additionally, our findings suggest that the expression of the lncRNA LINC-PINT is significantly increased in periodontitis, and that it can modulate ITGA7 expression through hsa-miR-1293. Conclusion ITGA7 is a potential diagnostic and therapeutic target for periodontitis. The LINC-PINT/hsa-miR-1293/ITGA7 axis and the relationship between ITGA7 and immune infiltration provide new insights into the molecular mechanisms underlying periodontitis and highlight potential avenues for clinical intervention.

Cardiovascular diseases (CVD) are a global medical, social and economic problem. Currently, the search and study of new biological markers that can provide early diagnosis of CVD, serve as a laboratory tool for evaluating the effectiveness of treatment or be used as prognostic markers and criteria for risk stratification continues. The interest of scientists is focused on the study of the type 1 lectin-like receptor for oxidized low-density lipoproteins (LOX-1) as a diagnostic and prognostic marker in CVD. The presented literature review highlights the potential significance of the LOX-1 study as a diagnostic and prognostic laboratory tool in CVD. It is expected that future clinical and experimental studies will confirm the possibility of using LOX-1 as an additional non-invasive tool for diagnosis and prognosis assessment in patients with CVD. Modulation of LOX-1 levels and expression using pharmacological drugs may prove to be a promising direction for the treatment of CVD.

Abstract Cervical cancer is one of the most common malignant tumors that seriously threaten women's health. Persistent infection with high risk human papillomavirus (HPV) is closely related to the progression of cervical cancer. Cervical cancer screening is an effective measure to reduce the incidence and mortality of cervical cancer. The two most common screening strategies are cytology and HPV testing, but they easily lead to missed diagnosis or overdiagnosis. To overcome such limitations, a new triage method needs to be explored. The World Health Organization second edition guideline includes DNA methylation testing as a new method to be evaluated. DNA methylation is a common epigenetic modification and is considered to be closely related to the occurrence and development of tumors. In recent years, many methylated genes have been found to be biomarkers for cervical cancer and precancerous lesions diagnosis. In this paper, we focus on the role and application of host DNA methylation, HPV DNA methylation, as well as combined host and HPV DNA methylation in the screening of cervical cancer and precancerous lesions.

ObjectiveThe high hemoglobin, albumin, lymphocyte, and platelet (HALP) score has been reported to be a good prognostic indicator for several malignancies. However, more evidence is needed before it can be introduced into clinical practice. Here, we systematically evaluated the predictive value of HALP for survival outcomes in patients with solid tumors.MethodsThis study was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Assessing the Methodological Quality of Systematic Reviews (AMSTAR) Guidelines. In March 2024, an electronic literature search was performed for articles regarding the prognostic role of HALP in solid tumors. Data from studies with reported risk ratios (HRs) and 95% confidence intervals (CIs) were pooled in a meta-analysis. Study bias was assessed using the QUIPS tool.ResultsOf the 729 articles reviewed, 45 cohorts including data from 17,049 patients with cancer were included in the pooled analysis. The pooled results demonstrated that elevated HALP score was significantly associated with favorable overall survival (HR = 0.60, 95% CI 0.54-0.67, p < 0.01), cancer-specific survival (HR = 0.53, 95% CI 0.44- 0.64, p < 0.01), progression-free survival (HR = 0.62, 95% CI 0.54-0.72, p < 0.01), recurrence-free survival (HR = 0.48, 95% CI 0.30-0.77, p < 0.01), and disease-free survival (HR = 0.72, 95% CI 0.57-0.82, p < 0.01). Subgroup analyses based on various confounding factors further revealed the consistent prognostic impact of HALP on overall survival in patients with solid tumors.ConclusionsOur findings suggest that high HALP is associated with better survival outcomes in patients. The HALP score is a potential prognostic biomarker in solid tumors, but it needs to be further studied whether it can improve the established prognostic model.

With the increasing maturity of neonatal intensive care technology， the survival rate of premature infants has been increased significantly. At the same time， the incidence of brain injury has also been elevated year by year， and most of the affected children are complicated with early clinical manifestations and long-term sequelae of nervous system injury. Therefore， finding a simple and effective diagnostic method to improve the quality of life of premature infants has become a key problem to be solved urgently in the current field. In recent years， more and more biological markers of brain injury have been studied and applied to the early diagnosis and prognosis assessment of brain injury in premature infants. This article reviews the domestic and international research progress on these biological markers， aiming to provide reference for the early diagnosis and prognosis assessment of brain injury in premature infants.

Long non-coding RNAs (lncRNAs), defined as RNA molecules exceeding 200 nucleotides in length, have been implicated in the regulation of various biological processes and the progression of tumors. Among them, LINC00518, a recently identified lncRNA encoded by a gene located on chromosome 6p24.3, consists of three exons and is predicted to positively regulate the expression of specific genes. LINC00518 has emerged as a key oncogenic lncRNA in multiple cancer types. It exerts its tumor-promoting effects by modulating the expression of several target genes, primarily through acting as a sponge for microRNAs (miRNAs). Additionally, LINC00518 influences critical signaling pathways, including the Wnt/β-catenin, JAK/STAT, and integrin β3/FAK pathways. Elevated levels of LINC00518 in tumor tissues are associated with increased tumor size, advanced clinical stage, metastasis, and poor survival prognosis. This review provides a comprehensive summary of the genetic characteristics, expression patterns, biological functions, and underlying mechanisms of LINC00518 in human diseases. [ABSTRACT FROM AUTHOR]

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Chronic heart failure (CHF) is a global medical, social and economic problem. Currently, the search and study of new biomarkers that can provide early diagnosis of CHF, serve as a laboratory tool for assessing the effectiveness of treatment, or be used as prognostic markers and risk stratification criteria are ongoing. Scientists' interest is focused, in particular, on studying the role of fibroblast growth factor 21 (FGF21) in CHF. There is increasing evidence highlighting the value of FGF21 as a new marker for the diagnosis and assessment of prognosis in patients with CHF. The role of FGF21 in CHF is very interesting due to its cardioprotective aspects. Final confirmation of the diagnostic, prognostic and therapeutic roles of FGF21 will come from future studies.

This document is a compilation of research articles that explore the role of arachidonic acid and its metabolites in various types of cancer, with a specific focus on ovarian cancer. The articles discuss the effects of arachidonic acid on cancer progression, its metabolism pathways, and its potential as a therapeutic target and biomarker. The document also includes references on the role of cytochrome P450 enzymes in cancer, the anti-inflammatory properties of epoxyeicosatrienoic acids, and the impact of arachidonic acid on the tumor microenvironment. Overall, this document provides valuable information for researchers studying the relationship between arachidonic acid metabolism and cancer. [Extracted from the article]

Previous research has demonstrated that stretching can enhance athletic performance and induce cardiovascular adaptations. This study aims to assess whether a 4-week preventative stretching routine can enhance heart rate variability and heart rate recovery, faster blood lactate clearance, and improve performance following submaximal strength exercises. Twenty-four healthy adults were recruited and randomly allocated to either the experimental group or the control group. Both groups engaged in submaximal strength exercises (5 sets to voluntary failure at 60% of 1RM) comprising bench press and back squat exercises under baseline conditions and after stretching protocol. The experimental group followed the Stretching Protocol, while the control group adhered to their regular training routine. ANOVA analysis revealed a significant pre-post interaction effect between groups in the variable of squat repetitions, although no notable pre- or post-differences were observed in heart rate variability, heart rate recovery, blood lactate concentration, or bench repetitions in either group. A 4-week preventative stretching program does not appear adequate to enhance lactate clearance and cardiovascular adaptation after submaximal strength exercises in resistance-trained individuals compared to the control group. However, it is plausible that such a stretching routine may mitigate muscle fatigue, though further investigation is warranted to substantiate this hypothesis.

Abstract Background and objectives We explored the prognostic usefulness of the pan-immune-inflammation value (PIV) in patients with stage IIIB/C non-small-cell lung cancer (NSCLC) who underwent concurrent chemoradiotherapy (CCRT). Methods and patients For all patients, the PIV was calculated using platelet (P), monocyte (M), neutrophil (N), and lymphocyte (L) measures obtained on the first day of CCRT: PIV = P × M × N ÷ L. Using receiver operating characteristic (ROC) curve analysis, we searched for the existence of an ideal cutoff that may partition patients into two groups with unique progression-free- (PFS) and overall survival (OS) results. The primary endpoint of this retrospective cohort research was to determine whether there were any significant relationships between pretreatment PIV measures and post-CCRT OS outcomes. Results The present research included a total of 807 stage IIIB/C NSCLC patients. According to ROC curve analysis, the ideal PIV cutoff was 516 [area under the curve (AUC): 67.7%; sensitivity: 66.4%; specificity: 66.1%], which divided the whole cohort into two: low PIV (L-PIV: PIV

Background Recently, machine learning algorithms have identified preprocedural γ‐glutamyl transferase (GGT) as a significant predictor of long‐term mortality after coronary revascularization in the SYNTAX (Synergy Between PCI [Percutaneous Coronary Intervention] With Taxus and Cardiac Surgery) trial. The aim of the present study is to investigate the impact of preprocedural GGT on 10‐year all‐cause mortality in patients with complex coronary artery disease after revascularization. Methods and Results The SYNTAX trial was a randomized trial comparing PCI with coronary artery bypass grafting in 1800 patients with complex coronary artery disease. The present report is a post hoc subanalysis of the SYNTAXES (Synergy Between PCI With Taxus and Cardiac Surgery Extended Survival) trial, an investigator‐driven extended 10‐year follow‐up of the SYNTAX trial. The association between preprocedural GGT and 10‐year all‐cause mortality was investigated. The mean values of GGT for men and women were 43.5 (SD, 48.5) and 36.4 (SD, 46.1) U/L, respectively. In multivariable Cox regression models adjusted by traditional risk factors, GGT was an independent predictor for all‐cause death at 10‐year follow‐up, and each SD increase in log‐GGT was associated with a 1.24‐fold risk of all cause death at 10‐year follow‐up (95% CI, 1.10–1.40). According to previously reported sex‐related GGT thresholds, patients with higher GGT level had a 1.74‐fold risk of all‐cause death at 10‐year follow‐up (95% CI, 1.32–2.29) compared with patients with lower GGT level. Conclusions Preprocedural GGT is an independent predictor of 10‐year mortality after coronary revascularization in patients with complex coronary artery disease. In patients with elevated GGT, strong secondary prevention may be required after revascularization and must be studied prospectively. Registration URL: https://clinicaltrials.gov/study/NCT03417050.

Postoperative delirium (POD) has become a critical challenge with severe consequences and increased incidences as the global population ages. However, the underlying mechanism is yet unknown. Our study aimed to explore the changes in metabolites in three specific brain regions and saliva of older mice with postoperative delirium behavior and to identify potential non-invasive biomarkers. Eighteen-month-old male C57/BL6 mice were randomly assigned to the anesthesia/surgery or control group. Behavioral tests were conducted 24 h before surgery and 6, 9, and 24 h after surgery. Complement C3 (C3) and S100 calcium-binding protein B protein (S100beta) levels were measured in the hippocampus, and a metabolomics analysis was performed on saliva, hippocampus, cortex, and amygdala samples. In total, 43, 33, 38, and 14 differential metabolites were detected in the saliva, hippocampus, cortex, and amygdala, respectively. "Pyruvate" "alpha-linolenic acid" and "2-oleoyl-1-palmitoy-snglycero-3-phosphocholine" are enriched in one common pathway and may be potential non-invasive biomarkers for POD. Common changes were observed in the three brain regions, with the upregulation of 1-methylhistidine and downregulation of D-glutamine. Dysfunctions in energy metabolism, oxidative stress, and neurotransmitter dysregulation are implicated in the development of POD. The identification of changes in the level of salivary metabolite biomarkers could aid in the development of noninvasive diagnostic methods for POD. [ABSTRACT FROM AUTHOR]

The prediction of outcomes following cardiac arrest continues to provide significant difficulties. A preferred strategy involves adopting a multimodal approach, which encompasses the careful evaluation of the biomarker neuron-specific enolase (NSE). This systematic review and meta-analysis aimed to gather and summarize new and existing evidence on the prediction effect of neuron-specific enolase for survival to hospital discharge among adult patients with cardiac arrest. We searched PubMed Central, Scopus, EMBASE databases, and the Cochrane Library without language restrictions from their inceptions until 30 October 2023 and checked the reference lists of the included studies. Pooled results were reported as standardized mean differences (SMDs) and were presented with corresponding 95% confidence intervals (CIs). The primary outcome was survival to hospital discharge (SHD). Eighty-six articles with 10,845 participants were included. NSE showed a notable degree of specificity in its ability to predict mortality as well as neurological status among individuals who experienced cardiac arrest (p < 0.05). This study demonstrates the ability to predict fatality rates and neurological outcomes, both during the time of admission and at various time intervals after cardiac arrest. The use of NSE in a multimodal neuroprognostication algorithm has promise in improving the accuracy of prognoses for persons who have undergone cardiac arrest. [ABSTRACT FROM AUTHOR]

Background and objectives: We explored the prognostic usefulness of the pan-immune-inflammation value (PIV) in patients with stage IIIB/C non-small-cell lung cancer (NSCLC) who underwent concurrent chemoradiotherapy (CCRT). Methods and patients: For all patients, the PIV was calculated using platelet (P), monocyte (M), neutrophil (N), and lymphocyte (L) measures obtained on the first day of CCRT: PIV = P × M × N ÷ L. Using receiver operating characteristic (ROC) curve analysis, we searched for the existence of an ideal cutoff that may partition patients into two groups with unique progression-free- (PFS) and overall survival (OS) results. The primary endpoint of this retrospective cohort research was to determine whether there were any significant relationships between pretreatment PIV measures and post-CCRT OS outcomes. Results: The present research included a total of 807 stage IIIB/C NSCLC patients. According to ROC curve analysis, the ideal PIV cutoff was 516 [area under the curve (AUC): 67.7%; sensitivity: 66.4%; specificity: 66.1%], which divided the whole cohort into two: low PIV (L-PIV: PIV < 516; N = 436) and high PIV (H-PIV: PIV ≥ 516; N = 371). The comparisons between the PIV groups indicated that either the median PFS (9.2 vs. 13.4 months; P < 0.001) or OS (16.7 vs. 32.7 months; P < 0.001) durations in the H-PIV group were substantially inferior to their L-PIV counterpart. Apart from the H-PIV (P < 0.001), the N3 nodal stage (P = 0.006), IIIC disease stage (P < 0.001), and receiving only one cycle of concurrent chemotherapy (P = 0.005) were also determined to be significant predictors of poor PFS (P < 0.05, for each) and OS (P < 0.05, for each) outcomes in univariate analysis. The multivariate analysis findings revealed that all four variables had independent negative impacts on PFS (P < 0.05, for each) and OS (P < 0.05, for each). Conclusions: The findings of this hypothesis-generating retrospective analysis claimed that the novel PIV was an independent and steadfast predictor of PFS and OS in stage IIIB/C NSCLC patients. [ABSTRACT FROM AUTHOR]

Objective: Reduced hemispheric asymmetry has been identified as a potential risk factor for schizophrenia, characterized by diminished brain lateralization and a lack of dominance in the left hemisphere. Moreover, there is growing evidence of disrupted connectivity between various cortical regions. This study aimed to investigate gender differences in left-footedness as a potential biological marker for neuronal dysontogenesis in individuals with schizophrenia and control subjects. Materials and methods: A New Combined Foot Dominance Scale (14 foot tests), comprising a Modified Chapman & Chapman Subscale (10 foot tests) and a Complex Tasks Subscale (four foot tests) was administered as performance tasks in 180 subjects [98 schizophrenia patients with mean age 34.45  years (SD  =  15.67, range 23–79) for men and 42.20  years (SD  =  11.38, range 21–63) for women and 82 controls with a mean age 34.70  years (SD  =  16,82, range 18–79) for men and 44.50  years (SD  =  10.73, range 23–67)]. As our data are not continuous and lacks normal distribution, the non-parametric Mann–Whitney test was used for comparing categorical data. Results: The mean left-footedness, as assessed by the New Combined Foot Dominance Scale, is significantly higher in individuals with schizophrenia compared to control subjects. Our findings from inter-gender comparisons reveal that female schizophrenia patients exhibit a significantly greater average left-footedness than female control subjects, while in males no such a statistical significant difference is detected. Conclusion: Left foot dominance is higher in patients with schizophrenia than in control subjects and women contribute significantly more to this difference. [ABSTRACT FROM AUTHOR]

Abstract Background Osteoarthritis is a very common clinical disease in middle-aged and elderly individuals, and with the advent of ageing, the incidence of this disease is gradually increasing. There are few studies on the role of basement membrane (BM)-related genes in OA. Method We used bioinformatics and machine learning methods to identify important genes related to BMs in OA patients and performed immune infiltration analysis, lncRNA‒miRNA-mRNA network prediction, ROC analysis, and qRT‒PCR. Result Based on the results of machine learning, we determined that LAMA2 and NID2 were the key diagnostic genes of OA, which were confirmed by ROC and qRT‒PCR analyses. Immune analysis showed that LAMA2 and NID2 were closely related to resting memory CD4 T cells, mast cells and plasma cells. Two lncRNAs, XIST and TTTY15, were simultaneously identified, and lncRNA‒miRNA‒mRNA network prediction was performed. Conclusion LAMA2 and NID2 are important potential targets for the diagnosis and treatment of OA.

Background: Osteoarthritis (OA) and rheumatoid arthritis (RA) are both joint diseases with many different causes. Inflammatory arthritis, also known as rheumatoid arthritis, is one of the most complex types of arthritis. Non-inflammatory arthritis, also known as osteoarthritis, is a disease caused when the cartilage between the joints begins to be damaged. Considering the different treatment approaches for OA and RA, an accurate diagnosis of the type of arthritis is very important. The present study was conducted with the aim of finding gene expression and introducing reliable molecular biomarkers for RA and OA. Methods: The microarray dataset was obtained under the GSE27390 number. The samples included nine samples of mononuclear cells obtained from the bone marrow of RA patients, 10 samples of mononuclear cells obtained from the bone marrow of OA patients. Differential expression analysis between the OA and RA groups was performed using GEO2R, and genes with differential expression were separated by examining two factors such as logFC#1 and p.adj. Value

HOXC cluster antisense RNA 3 (HOXC-AS3) is a novel long noncoding RNA (lncRNA) that exhibits aberrant expression patterns in various cancer types. Its expression is closely related to clinicopathological features, demonstrating significant clinical relevance across multiple tumors. And HOXC-AS3 plays multifaceted roles in tumor progression, impacting cell proliferation, apoptosis, migration, invasion, epithelial-mesenchymal transition (EMT), autophagy, senescence, tumor growth, and metastasis. In this review, we summarized and comprehensively analyzed the expression and clinical significance of HOXC-AS3 as a diagnostic and prognostic biomarker for malignancies. Additionally, we presented an in-depth update on HOXC-AS3's functions and regulatory mechanisms in cancer pathogenesis. This narrative review underscores the importance of HOXC-AS3 as a promising lncRNA candidate in cancer research and its potential as a predictive biomarker and therapeutic target in clinical applications. [ABSTRACT FROM AUTHOR]

Simple Summary: We investigated the prognostic significance of the newly created Global Immune-Nutrition-Inflammation Index (GINI) in IIIC non-small cell lung cancer (NSCLC) patients who received definitive concurrent chemoradiotherapy (CCRT). A total of 802 newly diagnosed stage IIIC NSCLC patients were included. The optimal pre-CCRT GINI cutoff was 1562 (area under the curve: 76.1%; sensitivity: 72.4%; specificity: 68.2%; Youden index: 0.406). GINI ≥ 1562 was associated with significantly shorter median locoregional progression-free (p < 0.001), progression-free (p < 0.001), and overall survival (p < 0.001) than GINI < 1562. For each survival endpoint, the association between GINI and survival outcomes appeared independent of other confounding variables (p < 0.05 for each). The novel GINI index effectively stratified patients with stage IIIC NSCLSC into two distinct subgroups, demonstrating significant differences in both median and long-term survival rates. Background: We sought to determine the prognostic value of the newly developed Global Immune-Nutrition-Inflammation Index (GINI) in patients with stage IIIC non-small cell lung cancer (NSCLC) who underwent definitive concurrent chemoradiotherapy (CCRT). Methods: This study was conducted on a cohort of 802 newly diagnosed stage IIIC NSCLC patients who underwent CCRT. The novel GINI created first here was defined as follows: GINI = [C-reactive protein × Platelets × Monocytes × Neutrophils] ÷ [Albumin × Lymphocytes]. The receiver operating characteristic (ROC) curve analysis was used to determine the optimal pre-CCRT GINI cut-off value that substantially interacts with the locoregional progression-free (LRPFS), progression-free (PFS), and overall survival (OS). Results: The optimal pre-CCRT GINI cutoff was 1562 (AUC: 76.1%; sensitivity: 72.4%; specificity: 68.2%; Youden index: 0.406). Patients presenting with a GINI ≥ 1562 had substantially shorter median LRPFS (13.3 vs. 18.4 months; p < 0.001), PFS (10.2 vs. 14.3 months; p < 0.001), and OS (19.1 vs. 37.8 months; p < 0.001) durations than those with a GINI < 1562. Results of the multivariate analysis revealed that the pre-CCRT GINI ≥ 1562 (vs. <1562), T4 tumor (vs. T3), and receiving only 1 cycle of concurrent chemotherapy (vs. 2–3 cycles) were the factors independently associated with poorer LRPS (p < 0.05 for each), PFS (p < 0.05 for each), and OS (p < 0.05 for each). Conclusion: The newly developed GINI index efficiently divided the stage IIIC NSCLSC patients into two subgroups with substantially different median and long-term survival outcomes. [ABSTRACT FROM AUTHOR]

Treatment of bipolar disorder is prone to prolongation despite various treatments, including medication. The efficacy of exercise treatment (i.e., interventions involving physical exercise and sports intervention) for major depressive disorders has been reported for depressive symptoms, cognitive function, and sleep disturbances. However, its efficacy for bipolar disorder has yet to be established. We designed a randomized, controlled, double-blind clinical trial that includes 100 patients with bipolar disorder aged 20–65 years. This will be a cluster-randomized, two-group trial that will be conducted in ten psychiatric hospitals. The hospitals will be randomly assigned to an exercise intervention + treatment as usual (exercise) group or a placebo exercise intervention (stretching) + treatment as usual (control) group. Patients will be assessed using an extensive battery of clinical tests, physical parameters, sleep status, biological parameters (cytokines, neurotrophic factors), and genetic parameters (DNA and RNA) at baseline after a 6-week intervention period, at 10-week follow-up, and at 6-month follow-up. This innovative study may provide important evidence for the effectiveness of exercise in the treatment of bipolar depression based on clinical, biological, genetic, and physiological markers. [ABSTRACT FROM AUTHOR]

ObjectivesWhen examining the relationship between smoking intensity and toxicant exposure biomarkers in an effort to understand the potential risk for smoking-related disease, individual biomarkers may not be strongly associated with smoking intensity because of the inherent variability in biomarkers. Structural equation modeling (SEM) offers a powerful solution by modeling the relationship between smoking intensity and multiple biomarkers through a latent variable.MethodsBaseline data from a randomized trial (N = 1250) were used to estimate the relationship between smoking intensity and a latent toxicant exposure variable summarizing five volatile organic compound biomarkers. Two variables of smoking intensity were analyzed: the self-report cigarettes smoked per day and total nicotine equivalents in urine. SEM was compared with linear regression with each biomarker analyzed individually or with the sum score of the five biomarkers.ResultsSEM models showed strong relationships between smoking intensity and the latent toxicant exposure variable, and the relationship was stronger than its counterparts in linear regression with each biomarker analyzed separately or with the sum score.ConclusionsSEM is a powerful multivariate statistical method for studying multiple biomarkers assessing the same class of harmful constituents. This method could be used to evaluate exposure from different combusted tobacco products.

Research into new biological markers may help early diagnosis and effective therapy for cardiology patients. The use of biomarkers to evaluate patients has made a major impact in oncology, but is still in its infancy in the cardiology field. Studies on secreted frizzled-related protein 5 (SFRP5) have revealed its potential use as a marker of cardiovascular pathology. Preclinical studies have highlighted the important role this protein plays in many biological processes. It reduces the proliferation and migration of cardiac fibroblasts and suppresses the Wnt5A/JNK signaling pathway thus reducing the severity of oxidative stress and inflammation. It normalizes nitric oxide production and has several other effects. However, recent clinical studies of SFRP5 have produced conflicting data. Nevertheless, this protein shows promise as a marker for several metabolic and cardiovascular diseases. Preliminary data also suggest SFRP5 may be a therapeutic target. Further study of SFRP5 and its role in cardiovascular pathology is necessary, and will create new diagnostic and prognostic possibilities for this biological marker.

The development in diagnosis and treatment of myocardial infarction has significantly improved the prognosis of some patients, while the overall survival rate of patients remains much room for improvement. Further research of the mechanism of injury after myocardial ischemia and reperfusion may explore new directions of research. As a newly discovered form of regulated cell death, ferroptosis, an iron-dependent cell death caused by lipid peroxidation, which has been characterized by cell death involving the accumulation of lipid peroxides and reactive oxygen species. Ferroptosis, which has been acknowledged to play an important role in ischemia-reperfusion injury. Studies suggest that iron death-related marker changes after myocardial infarction (MI), including hiatus of mitochondrial ferritin (FtMt) in intracellular iron metabolism, decreased levels of glutathione peroxidase 4 (Gpx4), a terminal molecule of glutathione metabolism pathway, insufficient use of antiporter cystine/glutathione synthesis (SXc-) in glutathione synthesis, and overexpression of Acyl-CoA synthetase long-chain family member 4 (ACSL4) can lead to oxidative stress, inflammatory response, cardiomyocyte injury after myocardial infarction, and can aggravate the myocardial ischemia-reperfusion injury. The four biological markers mentioned above, FtMt, Gpx4, SXc- and ACSL4, are important research targets for the diagnosis and treatment of iron death after MI, which may deserve further study.

Objectives: We aimed to determine serum PGs (serum pepsinogens) and H. Pylori IgG in atrophic gastritis and gastric cancer patients and evaluate the gastric cancer risk. Method: We enrolled 40 gastric cancer patients, 40 chronic atrophic gastritis patients and 40 healthy control subjects. Serum PGI, PGII, and H. pylori IgG levels were measured by ELISA. The PGI to PGII ratio was calculated. Results: The mean age of the subjects was 60±10.9 years, We found that 52.6% (n=60) were male. H. Pylori IgG was positive in 67 subjects. The serum PGI and PGR levels were significantly decreased in gastric cancer and atrophic gastritis groups compared to the healthy control. According to classification ABC (D), group D had higher proportion of atrophic gastritis cases, group C had higher proportion of gastric cancer cases than others. Additionally, we evaluated all subjects by giving one point to each of the age ≤40, positive family history of gastric cancer, positive previous gastric disease history, PGI ≤75.07 ng/ml, PGR ≤6.25, or two point to each of PGI ≤35.25 ng/ml, and PGR ≤5.27, with score ranging between 0-7. As score increased, the risk of atrophic gastritis or gastric cancer increased. Conclusion: A combination of methods involving PGs and other risk factors may predict the probability of gastric cancer and could identify individuals who may need upper endoscopy.

Abstract Background Elevated levels of S-100B in serum are increasingly considered a potential biochemical marker of nervous system damage. To our knowledge, limited number of research studies have tested the serum S-100B protein levels in children with epilepsy. The objective of our study is to measure the serum levels of S-100B protein in pediatric cases with epilepsy. Results The mean serum concentration of S-100B protein was 0.135 ± 0.014 mg/L in the patient group and 0.082 ± 0.018 mg/L in the control group. The patients showed significantly high S-100B protein levels compared with healthy controls (P

Crude oil samples recovered from three oilfields distributed within the central Niger Delta were used to investigate biological marker fingerprints, sources of organic matter, conditions of deposition, and thermal maturation. This was achieved by the application of gas chromatography-mass spectrometric (GC-MS) analyses on the saturated components of the crude oils. The biological marker ratios show low sterane/hopane (steranes/hopane ˂ 1) in the scope of 0.29 to 0.61 indicating that the crude oils initiated from rocks containing high terrigenous biota (mainly land plants). The n-alkanes distribution and the pristane/phytane ratios (0.63 to 2.08) suggested source deposition under oxic to suboxic environmental conditions. The percentage composition of C27, C28, and C29 steranes and oleanane index (18α (H)-oleanane/ C30 17α (H)-hopane) also indicated major contributions from terrigenous organic biota with minor marine source input. The studied crude oils have C32:22S/ (22S+22R) ratios in the scope of 0.55 to 0.64, and these values suggested high maturation level. This agrees with the oleanane index (0.64 to 0.95), CPI (0.92 to 1.06), C29: 20S/ (20S + 20R) sterane ratios (0.29 to 0. 61), Ts/(Ts+Tm) ratio (0.45 to 0.83) and moretane/C30 hopane proportion (0.16 to 0.24).

Inflammation is a universal response of a living organism to various damaging factors and is aimed at restoring tissue integrity and minimizing cell death. Proinflammatory cytokines, in particular interleukins, are active participants in the inflammatory response. In patients with heart failure, inflammatory reactions lead to damage to cardiomyocytes, their apoptosis and activation of neurohumoral systems, which contribute to the initiation of myocardial hibernation and mechanisms of its remodeling. The purpose of this review is to consider IL-1 as a diagnostic and prognostic marker in heart failure, as well as the effect of treatment with a recombinant form of IL-1R on the course of the disease.

ObjectiveReduced hemispheric asymmetry has been identified as a potential risk factor for schizophrenia, characterized by diminished brain lateralization and a lack of dominance in the left hemisphere. Moreover, there is growing evidence of disrupted connectivity between various cortical regions. This study aimed to investigate gender differences in left-footedness as a potential biological marker for neuronal dysontogenesis in individuals with schizophrenia and control subjects.Materials and methodsA New Combined Foot Dominance Scale (14 foot tests), comprising a Modified Chapman & Chapman Subscale (10 foot tests) and a Complex Tasks Subscale (four foot tests) was administered as performance tasks in 180 subjects [98 schizophrenia patients with mean age 34.45 years (SD = 15.67, range 23–79) for men and 42.20 years (SD = 11.38, range 21–63) for women and 82 controls with a mean age 34.70 years (SD = 16,82, range 18–79) for men and 44.50 years (SD = 10.73, range 23–67)]. As our data are not continuous and lacks normal distribution, the non-parametric Mann–Whitney test was used for comparing categorical data.ResultsThe mean left-footedness, as assessed by the New Combined Foot Dominance Scale, is significantly higher in individuals with schizophrenia compared to control subjects. Our findings from inter-gender comparisons reveal that female schizophrenia patients exhibit a significantly greater average left-footedness than female control subjects, while in males no such a statistical significant difference is detected.ConclusionLeft foot dominance is higher in patients with schizophrenia than in control subjects and women contribute significantly more to this difference.

Background: Osteoarthritis is a very common clinical disease in middle-aged and elderly individuals, and with the advent of ageing, the incidence of this disease is gradually increasing. There are few studies on the role of basement membrane (BM)-related genes in OA. Method: We used bioinformatics and machine learning methods to identify important genes related to BMs in OA patients and performed immune infiltration analysis, lncRNA‒miRNA-mRNA network prediction, ROC analysis, and qRT‒PCR. Result: Based on the results of machine learning, we determined that LAMA2 and NID2 were the key diagnostic genes of OA, which were confirmed by ROC and qRT‒PCR analyses. Immune analysis showed that LAMA2 and NID2 were closely related to resting memory CD4 T cells, mast cells and plasma cells. Two lncRNAs, XIST and TTTY15, were simultaneously identified, and lncRNA‒miRNA‒mRNA network prediction was performed. Conclusion: LAMA2 and NID2 are important potential targets for the diagnosis and treatment of OA. [ABSTRACT FROM AUTHOR]

Background: Osteoarthritis (OA) and rheumatoid arthritis (RA) are both joint diseases with many different causes. Inflammatory arthritis, also known as rheumatoid arthritis, is one of the most complex types of arthritis. Non-inflammatory arthritis, also known as osteoarthritis, is a disease caused when the cartilage between the joints begins to be damaged. Considering the different treatment approaches for OA and RA, an accurate diagnosis of the type of arthritis is very important. The present study was conducted with the aim of finding gene expression and introducing reliable molecular biomarkers for RA and OA. Methods: The microarray dataset was obtained under the GSE27390 number. The samples included nine samples of mononuclear cells obtained from the bone marrow of RA patients, 10 samples of mononuclear cells obtained from the bone marrow of OA patients. Differential expression analysis between the OA and RA groups was performed using GEO2R, and genes with differential expression were separated by examining two factors such as logFC#1 and p.adj. Value<0.05. Signaling pathways were determined using Enrichr databases. Next, the genes with the most expression changes were introduced. This study is a bioinformatics analysis and was conducted jointly at Bam University of Medical Sciences and Rajaie Cardiovascular, Medical and Research Institute from September 2022 to March 2023. Results: The results showed that, 5083 genes had significant expression differences. Analysis of signaling pathways showed that antigen processing and presentation, natural killer cell-mediated cytotoxicity, the, IL-17 signaling pathway, Th17 cell differentiation and cytokine-cytokine receptor interaction, as inflammatory pathways, were important in this disease. It was also determined that CH25H (upregulated in RA samples) and GYPE (downregulated in RA samples) genes can distinguish rheumatoid arthritis from osteoarthritis. Conclusion: Since accurate diagnosis helps with better disease treatment, it is very important to obtain new biological diagnostic markers. Overall, our data showed that genes can act as novel biomarkers with potential utility in the diagnosis of RA and OA and can be considered novel molecular biomarkers for the diagnosis of these two diseases. [ABSTRACT FROM AUTHOR]

Introduction: The aim of this study was to observe the diagnostic role of procalcitonin to evaluate sepsis and assess the level of inflammation for the patients of Critical Care Unit of different departments. Methods: This cross sectional, prospective and observational study was conducted at Armed Forces Institute of Pathology on the patients at Critical Care Unit of Paediatric, Surgery, Gynae and Medicine department in a tertiary care hospital (Combined Military Hospital, Dhaka) from June, 2020 to May, 2021. Total 106 patients were enrolled in this study. As the study was conducted during corona pandemic, RT-PCR test for Corona virus disease 2019 (COVID-19) along with serum procalcitonin and bacterial culture and sensitivity tests for different samples were prescribed for all 106 patients. Result: Out of 106 patients, 30.2% (32) patients were found positive and 69.69% (74) were found negative for COVID-19 and 14.15% (15) patients had clinical documentation of bacterial co-infection, confirmed by blood, respiratory, or urine culture. After PCT test, 20.75 % (22) samples were found with severe sepsis or septic shock, 7.54% (08) samples were found with systemic infection, 18.06% (20) samples were with possible systemic infection, 31.13 % (33) samples were with local infections and 21.69% (23) were found within normal ranges of PCT. Conclusion: This study supports the importance of the diagnostic role of PCT to assess the level of sepsis as well as presence of co-infection which suggests that PCT level is a good biomarker for early diagnosis, assessment and treatment of patients in CCU. [ABSTRACT FROM AUTHOR]

Min Wen,1– 3 Zhen Dong,2 Lili Zhang,2 Bing Li,2,3 Yunshu Zhang,2,3 Keqing Li2,3 1School of Psychology and Mental Health, North China University of Science and Technology, Tangshan, People’s Republic of China; 2Hebei Provincial Mental Health Center, Baoding, People’s Republic of China; 3Hebei Provincial Key Laboratory of Major Mental and Behavioral Disorders, Baoding, People’s Republic of ChinaCorrespondence: Keqing Li; Yunshu Zhang, Email like1002@sina.com; yunshucoffee@sina.comBackground: Eye movement is critical for obtaining precise visual information and providing sensorimotor processes and advanced cognitive functions to the brain behavioral indicator.Methods: In this article, we present a narrative review of the eye-movement paradigms (such as fixation, smooth pursuit eye movements, and memory-guided saccade tasks) in major depression.Results: Characteristics of eye movement are considered to reflect several aspects of cognitive deficits regarded as an aid to diagnosis. Findings regarding depressive disorders showed differences from the healthy population in paradigms, the characteristics of eye movement may reflect cognitive deficits in depression. Neuroimaging studies have demonstrated the effectiveness of different eye movement paradigms for MDD screening.Conclusion: Depression can be distinguished from other mental illnesses based on eye movements. Eye movement reflects cognitive deficits that can help diagnose depression, and it can make the entire diagnostic process more accurate.Keywords: depressive disorder, cognitive impairment, eye movement, biological marker, neurology

Antiseizure medication (ASM) is the primary treatment for epilepsy. In clinical practice, methods to assess ASM efficacy (predict seizure freedom or seizure reduction), during any phase of the drug treatment lifecycle, are limited. This scoping review identifies and appraises prognostic electroencephalographic (EEG) biomarkers and prognostic models that use EEG features, which are associated with seizure outcomes following ASM initiation, dose adjustment, or withdrawal. We also aim to summarize the population and context in which these biomarkers and models were identified and described, to understand how they could be used in clinical practice. Between January 2021 and October 2022, four databases, references, and citations were systematically searched for ASM studies investigating changes to interictal EEG or prognostic models using EEG features and seizure outcomes. Study bias was appraised using modified Quality in Prognosis Studies criteria. Results were synthesized into a qualitative review. Of 875 studies identified, 93 were included. Biomarkers identified were classed as qualitative (visually identified by wave morphology) or quantitative. Qualitative biomarkers include identifying hypsarrhythmia, centrotemporal spikes, interictal epileptiform discharges (IED), classifying the EEG as normal/abnormal/epileptiform, and photoparoxysmal response. Quantitative biomarkers were statistics applied to IED, high‐frequency activity, frequency band power, current source density estimates, pairwise statistical interdependence between EEG channels, and measures of complexity. Prognostic models using EEG features were Cox proportional hazards models and machine learning models. There is promise that some quantitative EEG biomarkers could be used to assess ASM efficacy, but further research is required. There is insufficient evidence to conclude any specific biomarker can be used for a particular population or context to prognosticate ASM efficacy. We identified a potential battery of prognostic EEG biomarkers, which could be combined with prognostic models to assess ASM efficacy. However, many confounders need to be addressed for translation into clinical practice. [ABSTRACT FROM AUTHOR]

Combination of bovine serum albumin with microemulsions as constituting ingredient biopolymer has long been regarded an innovative method to address the surface functionalization and stability issues in the targeted payload deliveries, thereupon producing effectively modified microemulsions, which are superior in loading capacity, transitional and shelf-stability, as well as site-directed/site-preferred delivery, has become a favored option. The current study aimed to develop an efficient, suitable and functional microemulsion system encapsulating sesame oil (SO) as a model payload towards developing an efficient delivery platform. UV-VIS, FT-IR, and FE-SEM were used to characterize, and analyze the developed carrier. Physicochemical properties assessments of the microemulsion by dynamic light scattering size distributions, zeta-potential, and electron micrographic analyses were performed. The mechanical properties for rheological behavior were also studied. The HFF-2 cell line and hemolysis assays were conducted to ascertain the cell viability, and in vitro biocompatibility. The in vivo toxicity was determined based on a predicted median lethal dose (LD50) model, wherein the liver enzymes' functions were also tested to assess and confirm the predicted toxicity. [ABSTRACT FROM AUTHOR]

It has been proven that in patients with heart failure (HF), there is an increased level of adrenomedullin (ADM) in plasma. Biomarker indices correlate with the severity of hemodynamic dysfunction, as well as with neurohumoral indices, which are activated depending on the severity of congestive circulatory failure. In addition, the expression of the ADM gene in the heart and kidneys is increased in experimental and clinical HF. A small number of studies have examined the effect of ADM infusion. These studies have generally shown that hormone infusion has beneficial hemodynamic effects and promotes the maintenance/improvement of renal function, but most of the studies have been short-lived. The available results suggest that increasing ADM levels reduce the negative effects of vasoconstriction and sodium retention. A better understanding of the role of a biological marker in congestive circulatory failure may lead to the development of drugs that target ADM receptors.

Introduction. Currently, the search and study of new biological markers that can help early diagnosis of heart failure, serve as a laboratory tool for assessing the effectiveness of therapy, be a predictive marker of possible adverse clinical outcomes and a significant criterion for risk stratification is very relevant. While cardiospecific markers, including natriuretic peptides, their precursors, and highly sensitive troponins, are widely used in clinical practice, the need to use other markers does not have sufficient evidence. aspect of a biological marker of heart failure.Gamma-glutamyl transpeptidase is an enzyme localized on the outer side of cell membranes and involved in the metabolism of glutathione and cysteine. This enzyme is a dimeric glycoprotein (68 kDa), consisting of 2 subunits – a large and a small (46 and 22 kDa). Gamma-glutamyl transpeptidase is encoded by a multigene family consisting of at least 7 different genes located on chromosome 22; however, only 1 of these genes is involved in the formation of a functional enzyme. Gamma-glutamyl transpeptidase was found in all cells except erythrocytes. There is a significant variability in enzyme activity, which is especially high in tissues with a secretory and absorptive function, such as the kidneys, biliary tract, intestines, and epididymis.Purpose of the review is to present an overview of current publications devoted to the study of γ-glutamyl transpeptidase in the aspect of a biological marker of heart failure.Materials and methods. The analysis of literature sources (foreign and domestic articles) was carried out in the databases: PubMed, RSCI, MedLine, Google Scholar, Science Direct. The search was performed according to the following keywords: biological markers, heart failure, γ-glutamyl transpeptidase, biological markers, heart failure, γ-glutamyl transpeptidase.Results. In addition to its clinical use as a test for liver disease, biliary tract disease, and alcohol abuse, γ-glutamyl transpeptidase is of great interest because of its association with cardiovascular disease, diabetes, metabolic syndrome, and cancer. In the literature available to us, we found a small number of works devoted to the study of γ-glutamyl transpeptidase in patients with heart failure. In the review, we have presented data from experimental and clinical studies indicating a clear link between γ-glutamyl transpeptidase and heart failure. The pathogenetic mechanism of the possible relationship between γ-glutamyl transpeptidase and heart failure is not completely clear. The localization of this enzyme in tissues with a transport function has led to the assumption that it is involved in the transport of amino acids through the γ-glutamyl cycle.Conclusion. Further deeper understanding of the structure and function of the enzyme is needed, as well as future clinical studies to determine the diagnostic, prognostic and possibly therapeutic significance of this biological marker.

Zhixian Wu,1,2,&ast; Hongwei Cheng,1,&ast; Jie Liu,1,&ast; Shuaishuai Zhang,1 Minda Zhang,1 Fangzhou Liu,1 Yinghui Li,2 Qian Huang,2 Yi Jiang,3 Shaohua Chen,3 Lizhi Lv,3 Dongliang Li,2 Jin-Zhang Zeng1 1Fujian Provincial Key Laboratory of Innovative Drug Target Research and State Key Laboratory of Cellular Stress Biology, School of Pharmaceutical Sciences, Xiamen University, Xiamen, People’s Republic of China; 2Department of Hepatobiliary Disease, Dongfang Hospital, Xiamen University, Fuzhou, People’s Republic of China; 3Department of Hepatobiliary Surgery, Dongfang Hospital, Xiamen University, Fuzhou, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Jin-Zhang Zeng; Dongliang Li, Email jzzeng@xmu.edu.cn; dongliangli93@163.comPurpose: Early detection and prognostic prediction of hepatocellular carcinoma (HCC) remain a great challenge. In this study, we explored the role and diagnostic significance of stanniocalcin 2 (STC2), recently identified as a secretory protein, in HCC.Methods: STC2 mRNA and protein in HCC tissues were examined by qRT-PCR and immunohistochemistry. The regulatory role of HCC growth by STC2 was evaluated in vitro and in vivo. Serum STC2 levels were determined in HCC patients and compared to those with liver cirrhosis (LC) and normal controls (NC). The difference and significance of STC2 levels between groups were analyzed by Mann–Whitney U-test. The diagnostic value of serum STC2 in detecting early HCC was assayed with receiver operating characteristics (ROC). The association of STC2 with overall survival (OS) was determined with Kaplan–Meier method.Results: STC2 was elevated in about 77.1% HCC patients and correlated with advanced tumor progression. Overexpression or knockdown of STC2 stimulated or suppressed HCC colony formation and xenograft tumor growth. AKT activation played a critical role in tumor-promoting effect of STC2. The median level of serum STC2 in HCC patients (n = 98, 2086.6 ng/L) was 2.6-fold and 4.2-fold that in LC patients (n = 42, 801.9 ng/L) and NC (n = 26, 496.9 ng/L), respectively. A cut-off value 1493 ng/L for STC2 could distinguish early HCC from LC with a sensitivity of 76.9% and a specificity of 76.2%, both of which were superior to AFP at 20 μg/L (sensitivity 69.2%, specificity 52.4%). STC2 was positive in 77.8% (14/18) AFP-negative patients. High STC2 level was correlated with poor overall and disease specific survival.Conclusion: STC2 is upregulated in both tumor and serum of HCC patients, and its overexpression promotes HCC via AKT pathway. STC2 possesses a diagnostic significance and may serve as an auxiliary biomarker of AFP for detecting early HCC.Keywords: biological marker, serological diagnosis, early diagnosis, prognosis

Abstract Background With the growing practice of home mechanical ventilation, there is a need to identify biological markers for adequate follow-up. Red cell distribution width (RDW) is a promising candidate because it is convenient, objective and may reflect treatment effect over a long period of time. The aim of this study was to explore the possible role of RDW as a marker for home mechanical ventilation in real-life, unselected chronic respiratory patient populations. Methods First, we identified characteristic RDW values for mixed case, unselected chronic respiratory failure and home mechanical ventilated patients through retrospective review within our institutional database. Next, we conducted a prospective observational study to identify RDW changes during the first six months of optimized home mechanical ventilation treatment. Adult patients starting home mechanical ventilation were included. Factors affecting RDW change during the first 6 months of treatment were analysed. Results RDW was elevated in both chronic respiratory failure and home mechanical ventilation patients compared to healthy individuals in the retrospective review. In the prospective study of 70 patients, we found that 55.4% of patients starting home mechanical ventilation have abnormal RDW values which are reduced from 14.7 (IQR = 13.2–16.2)% to 13.5 (IQR = 13.1–14.6)% during the first 6 months of HMV treatment (p

Heart failure (HF) remains a serious problem in Russian and world health care due to the growing morbidity and mortality from complications of heart failure, despite the development and implementation of programs for the early detection and treatment of heart failure in asymptomatic patients. Currently, a large number of new biological markers have been studied that could serve as a laboratory tool for diagnosing and predicting the course of heart failure, but only brain natriuretic peptides have found application in real clinical practice. Renalase is a recently discovered cytokine that is synthesized by the kidneys and released into the blood. To date, seven subtypes of renalase have been found, each of which plays a different physiological role in the human body. Renalase is usually positioned as a signaling molecule that activates cytoprotective intracellular signals, leading to a decrease in blood pressure and protection of the heart muscle. The concentration of renalase freely circulating in the bloodstream of an adult is approximately 3–5 ng / ml. Currently, the level of renalase is determined by the enzyme immunoassay with a detection range of 3.12 to 200 ng / ml, while the minimum detectable concentration of the marker is less than 1.38 ng / ml. The presence of missense polymorphism of renalase is associated with myocardial dysfunction. Data from animal and human studies have shown that renalase plays a key role in the metabolism of catecholamines and in cardioprotective processes. Studies have shown the contribution of renalase to the occurrence of cardiovascular diseases: ischemic heart disease, arterial hypertension, diabetes mellitus, and aortic stenosis. Moreover, detailed protocols of multicenter prospective studies have demonstrated that functional polymorphism of the renalase gene was associated with myocardial hypertrophy in patients with aortic stenosis, hypertension, metabolic syndrome, unstable angina pectoris and stable forms of coronary artery disease, as well as in patients receiving renal replacement therapy. Based on these data and further studies, renalase has been proposed as a predictive biomarker of ischemia in patients with coronary microvascular dysfunction, as well as a predictor of clinically significant progression of chronic kidney disease in patients with cardiovascular diseases.Our review presents data on the role of renalase in heart failure. Further study of the structure and function of renalase, as well as future clinical studies, will allow determining the diagnostic, prognostic and, possibly, therapeutic significance of this biological marker in HF and other cardiovascular diseases.

Background: Elevated levels of S-100B in serum are increasingly considered a potential biochemical marker of nervous system damage. To our knowledge, limited number of research studies have tested the serum S-100B protein levels in children with epilepsy. The objective of our study is to measure the serum levels of S-100B protein in pediatric cases with epilepsy. Results: The mean serum concentration of S-100B protein was 0.135 ± 0.014 mg/L in the patient group and 0.082 ± 0.018 mg/L in the control group. The patients showed significantly high S-100B protein levels compared with healthy controls (P < 0.001). Conclusion: Our data suggest that increased S-100B protein levels in the serum potentially indicate neuronal damage in the brains of children with epilepsy. [ABSTRACT FROM AUTHOR]

Yunqiang Liu,1,&ast; Mengjun Tu,2,3,&ast; Lingling Wang4,5 1School of Medical College, Guangdong Medical University, Zhanjiang, Guang Dong Province, 524023, People’s Republic of China; 2Eye Hospital and School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang Province, 325027, People’s Republic of China; 3National Clinical Research Center for Ocular Diseases, Wenzhou, Zhejiang Province, 325027, People’s Republic of China; 4Department of Clinical Laboratory Center of the Second Affiliated Hospital & Yu Ying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, 325027, People’s Republic of China; 5School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, 325035, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Lingling Wang, Department of Clinical Laboratory Center of The Second Affiliated Hospital & Yu Ying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, 325027, People’s Republic of China, Tel +8618867786629, Email ll77sky@163.comPurpose: Only a few studies have reported the role of FOXS1, a transcriptional factor, in the tumor development process. In this article, we investigate the function of FOXS1 in distinct neoplastic development and the tumor immune microenvironment (TIME).Patients and Methods: The latent roles of FOXS1 in various tumors were prospected based on TCGA, GTEx, CCLE, GEPIA2, cBioPortal, TIMER, ImmuCellAI databases, GSVA datasets, GSEA datasets, and R packages. The expression difference, gene alteration, clinical characteristics, prognostic values, biological mechanism, potential pathways, tumor microenvironment, and immune cell infiltration related to FOXS1 were appraised.Results: FOXS1 was strongly expressed in pan-cancer, and this gene was associated with low survival rates. FOXS1 was linked to many pathways that are cancer-promoting and immune-related. The expression of this transcriptional factor in cancers was positively related to immune cell infiltration, especially M2-like macrophages and Treg cells. In addition to that, FOXS1 demonstrated a positive relationship with many immune-suppression genes, such as TGFB1 and ARORA2A.Conclusion: Our study identified an oncogenic effect of FOXS1, which may play a vital role as a prognosticative biological marker in pan-cancer. Exorbitant expression of FOXS1 is associated with high TAMs and Treg cells infiltration. These cells have an immunosuppressive function and promote the development of the immunosuppressive tumor microenvironment. The research of FOXS1 provided a potential drug target for tumor immunotherapy.Keywords: FOXS1, pan-cancer, biological marker, M2-like macrophages, Treg cells, immunosuppressive microenvironment

Introduction: Due to the obvious adverse effects of exposure to free crystalline silica and the high exposure level in silica-related occupations, the present study aimed at the investigation of renal symptoms in cement factory workers. Materials and methods: For this reason, 128 workers who were working cement factory with a determined occupational exposure to crystalline-free silica were selected as the case group, and 143 workers who were working in the Hamedan Province Rural Water and Wastewater company without being exposed to crystalline free silica were selected as controls. Various kidney-related parameters were evaluated and compared between the selected case and control groups. Results: The results of urine analysis between cases and control showed that there was a statistical difference between the cases and controls regarding Red Blood Cell (RBC), epithelial count, and bacteria (p

BackgroundCerebral microbleeds (CMB) are MRI-demonstrable cerebral microhemorrhages (CMH) which commonly coexist with ischemic stroke. This creates a challenging therapeutic milieu, and a strategy that simultaneously protects the vessel wall and provides anti-thrombotic activity is an attractive potential approach. Phosphodiesterase 3A (PDE3A) inhibition is known to provide cerebral vessel wall protection combined with anti-thrombotic effects. As an initial step in the development of a therapy that simultaneously treats CMB and ischemic stroke, we hypothesized that inhibition of the PDE3A pathway is protective against CMH development.MethodsThe effect of PDE3A pathway inhibition was studied in the inflammation-induced and cerebral amyloid angiopathy (CAA)-associated mouse models of CMH. The PDE3A pathway was modulated using two approaches: genetic deletion of PDE3A and pharmacological inhibition of PDE3A by cilostazol. The effects of PDE3A pathway modulation on H&E- and Prussian blue (PB)-positive CMH development, BBB function (IgG, claudin-5, and fibrinogen), and neuroinflammation (ICAM-1, Iba-1, and GFAP) were investigated.ResultsRobust development of CMH in the inflammation-induced and CAA-associated spontaneous mouse models was observed. Inflammation-induced CMH were associated with markers of BBB dysfunction and inflammation, and CAA-associated spontaneous CMH were associated primarily with markers of neuroinflammation. Genetic deletion of the PDE3A gene did not alter BBB function, microglial activation, or CMH development, but significantly reduced endothelial and astrocyte activation in the inflammation-induced CMH mouse model. In the CAA-associated CMH mouse model, PDE3A modulation via pharmacological inhibition by cilostazol did not alter BBB function, neuroinflammation, or CMH development.ConclusionsModulation of the PDE3A pathway, either by genetic deletion or pharmacological inhibition, does not alter CMH development in an inflammation-induced or in a CAA-associated mouse model of CMH. The role of microglial activation and BBB injury in CMH development warrants further investigation.