Clinical value of serum calcium in elderly patients with sepsis.

PURPOSE: To explore the clinical value of serum calcium (Ca) in elderly patients with sepsis. MATERIALS AND METHODS: The clinical data and laboratory data of elderly patients with sepsis (n = 165) and elderly population for physical examination (n = 67) in a tertiary hospital from January 2020 to November 2020 were collected. We analyzed serum Ca levels in sepsis and septic shock firstly, and then continued to investigate them in the survival group and the death group. Meanwhile, we also assessed the correlation between serum Ca and PCT. RESULTS: The serum Ca levels of the elderly patients with sepsis were lower than that of the control group (median 1.98 vs 2.31 mmol/L, P < 0.001), and the more severe the sepsis, the lower the serum Ca levels. Sepsis patients with decreased serum Ca had higher shock rate and mortality. There was a negative correlation between serum Ca and PCT (r = -0.2957, P < 0.001). CONCLUSION: Serum Ca has a certain value for the early recognition of elderly patients with sepsis and the judgment of the severity of the disease.

Expression changes of serum LINC00941 and LINC00514 in HBV infection-related liver diseases and their potential application values.

BACKGROUND: Long non-coding RNAs (LncRNAs) are considered as potential diagnostic markers for a variety of tumors. Here, we aimed to explore the changes of LINC00941 and LINC00514 expression in hepatitis B virus (HBV) infection-related liver disease and evaluate their application value in disease diagnosis. METHODS: Serum levels of LINC00941 and LINC00514 were detected by qRT-PCR. Potential diagnostic values were evaluated by receiver operating characteristic curve (ROC) analysis. RESULTS: Serum LINC00941 and LINC00514 levels were elevated in patients with chronic hepatitis B (CHB), liver cirrhosis (LC), and hepatocellular carcinoma (HCC) compared with controls. When distinguishing HCC from controls, serum LINC00941 and LINC00514 had diagnostic parameters of an AUC of 0.919 and 0.808, sensitivity of 85% and 90%, and specificity of 86.67% and 56.67%, which were higher than parameters for alpha fetal protein (AFP) (all p < 0.0001). When distinguishing HCC from LC, CHB, or LC from controls, the combined detection of LINC00941 or LINC00514 can significantly improve the accuracy of AFP test alone (all p < 0.05). CONCLUSIONS: LINC00941 and LINC00514 were increased in the serum of HBV infection-associated liver diseases and might be independent markers for the detection of liver diseases.

Transcranial direct current stimulation relieves visceral hypersensitivity via normalizing GluN2B expression and neural activity in anterior cingulate cortex.

Irritable bowel syndrome (IBS) is one of the most common challenging diseases for clinical treatment. The aim of this study is to investigate whether transcranial direct current stimulation (tDCS) has analgesic effect on visceral hypersensitivity (VH) in an animal model of IBS as well as the underlying mechanism. As the activation of GluN2B in anterior cingulate cortex (ACC) takes part in VH, we examined whether and how GluN2B in ACC takes part in the effect of tDCS. Neonatal maternal deprivation (NMD), a valuable experimental model to study the IBS pathophysiology, was used to induce visceral hypersensitivity of rats. We quantified VH as colorectal distention threshold and performed patch-clamp recordings of ACC neurons. The expression of GluN2B were determined by RT-qPCR and Western blotting. The GluN2B antagonist Ro 25-6981 was microinjected into the rostral and caudal ACC. tDCS was performed for 7 consecutive days. It was found that NMD decreased expression of GluN2B, which could be obviously reversed by tDCS. Injection of Ro 25-6981 into rostral and caudal ACC of normal rats induced VH and also reversed the analgesic effect of tDCS. Our data sheds light on the nonpharmacological therapy for chronic VH in pathological states such as IBS.NEW & NOTEWORTHY Irritable bowel syndrome (IBS) is a gastrointestinal disease characterized by visceral hypersensitivity. This study showed a decrease of GluN2B expression and neural activity in ACC of IBS-model rats, which could be obviously reversed by tDCS. In addition, blockade of GluN2B in rostral and caudal ACC induced VH of normal rats. Furthermore, analgesic effect of tDCS on NMD rats was reversed by GluN2B antagonist.

Causes and Counter Measure Analysis of Inpatients Unqualified Clinical Specimens from 2015 to 2019.

BACKGROUND: To improve the quality of pre-analytical phase and provide targeted suggestions, this study analyzed factors causing unqualified clinical specimens in patients of the Department of Clinical Laboratory of Renmin Hospital of WuHan University from 2015 to 2019. METHODS: Inpatient specimens from January 2015 to December 2019 were retrospectively analyzed. Unqualified specimens were identified by referring to the general principle of rejection. The analytical indicators included incidence rate of unqualified specimens and constituent ratio of reasons of unqualified specimens. These two indicators were analyzed according to the inpatient wards and types of specimens. RESULTS: From 2015 to 2019, 21,674 inpatient unqualified specimens were collected, the incidence rate of unqualified specimens was 0.22% (21,674/9,700,869), the number and rate of unqualified specimens decreased year by year. The main reasons of unqualified specimens were insufficient volume (29.67%, 6,430/21,674) and clotting (26.31%, 5,703/21,674). The number of unqualified specimens in the departments of cardiovascular, pediatrics, neurology, oncology, urinary surgery, and intensive care unit ranked the top each year. Clotting (39.29%, 5,682/14,462) was the main reason of unqualified blood specimens while insufficient volume (71.18%, 3,365/4,727) was for urine specimens. Wrong identification caused unqualified feces (62.65%, 728/1,162) and body fluid (40.74%, 539/1,323) specimens. CONCLUSIONS: Clinical laboratory could make effective measures to improve pre-analytical quality by retrospectively analyzing data of unqualified specimens.

Downregulation of GRK6 in arcuate nucleus promotes chronic visceral hypersensitivity via NF-κB upregulation in adult rats with neonatal maternal deprivation.

AIMS: The arcuate nucleus is a vital brain region for coursing of pain command. G protein-coupled kinase 6 (GRK6) accommodates signaling through G protein-coupled receptors. Studies have demonstrated that GRK6 is involved in inflammatory pain and neuropathic pain. The present study was designed to explore the role and the underlying mechanism of GRK6 in arcuate nucleus of chronic visceral pain. METHODS: Chronic visceral pain of rats was induced by neonatal maternal deprivation and evaluated by monitoring the threshold of colorectal distension. Western blotting, immunofluorescence, real-time quantitative polymerase chain reaction techniques, and Nissl staining were employed to determine the expression and mutual effect of GRK6 with nuclear factor κB (NF-κB). RESULTS: Expression of GRK6 in arcuate nucleus was significantly reduced in neonatal maternal deprivation rats when compared with control rats. GRK6 was mainly expressed in arcuate nucleus neurons, but not in astrocytes, and a little in microglial cells. Neonatal maternal deprivation reduced the percentage of GRK6-positive neurons of arcuate nucleus. Overexpression of GRK6 by Lentiviral injection into arcuate nucleus reversed chronic visceral pain in neonatal maternal deprivation rats. Furthermore, the expression of NF-κB in arcuate nucleus was markedly upregulated in neonatal maternal deprivation rats. NF-κB selective inhibitor pyrrolidine dithiocarbamate suppressed chronic visceral pain in neonatal maternal deprivation rats. GRK6 and NF-κB were expressed in the arcuate nucleus neurons. Importantly, overexpression of GRK6 reversed NF-κB expression at the protein level. In contrast, injection of pyrrolidine dithiocarbamate once daily for seven consecutive days did not alter GRK6 expression in arcuate nucleus of neonatal maternal deprivation rats. CONCLUSIONS: Present data suggest that GRK6 might be a pivotal molecule participated in the central mechanisms of chronic visceral pain, which might be mediated by inhibiting NF-κB signal pathway. Overexpression of GRK6 possibly represents a potential strategy for therapy of chronic visceral pain.

Development and multicenter performance evaluation of fully automated SARS-CoV-2 IgM and IgG immunoassays.

Objectives: The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly spread globally. The laboratory diagnosis of SARS-CoV-2 infection has relied on nucleic acid testing; however, it has some limitations, such as low throughput and high rates of false negatives. Tests of higher sensitivity are needed to effectively identify infected patients. Methods: This study has developed fully automated chemiluminescent immunoassays to determine IgM and IgG antibodies to SARS-CoV-2 in human serum. The assay performance has been evaluated at 10 hospitals. Clinical specificity was evaluated by measuring 972 hospitalized patients and 586 donors of a normal population. Clinical sensitivity was assessed on 513 confirmed cases of SARS-CoV-2 by RT-PCR. Results: The assays demonstrated satisfied assay precision with coefficient of variation of less than 4.45%. Inactivation of specimen did not affect assay measurement. SARS-CoV-2 IgM showed clinical specificity of 97.33 and 99.49% for hospitalized patients and the normal population respectively, and SARS-CoV-2 IgG showed clinical specificity of 97.43 and 99.15% respectively. SARS-CoV-2 IgM showed clinical sensitivity of 82.54, 92.93, and 84.62% before 7 days, 7-14 days, and after 14 days respectively, since onset of symptoms, and SARS-CoV-2 IgG showed clinical sensitivity of 80.95, 97.98, and 99.15% respectively at the same time points above. Conclusions: We have developed fully automated immunoassays for detecting SARS-CoV-2 IgM and IgG antibodies in human serum. The assays demonstrated high clinical specificity and sensitivity, and add great value to nucleic acid testing in fighting against the global pandemic of the SARS-CoV-2 infection.

Comparison of Application Biological Variation and Patient Data for Selecting Delta Check Limits.

BACKGROUND: This study aimed to evaluate delta check limits set by reference change value (RCV) and patient data. METHODS: Patient data of 11 clinical chemistry analytes from June 2018 to May 2019 were collected. RCV with 95% or 99% levels of probability were calculated based on biological variation. The corresponding delta check limits for outpatients and inpatients were calculated by 95% or 99% central range of delta% which was the difference of two consecutive results within thirty days of the same patient for each analyte. Patient data in June 2019 were used to analyze the utility of delta check limits. RESULTS: In total, 434,927 paired results for these 11 analytes were included. The delta check limits were different between outpatients and inpatients, but were wider than those established by RCV. The difference between Glu's outpatient and inpatient boundaries was the largest, 95% central range from the outpatient (inpatients) was from -32.29% (-56.97%) to 38.78% (106.00%) while 99% central range from the outpatient (inpatients) was from -56.86% (-90.56%) to 89.96% (262.54%). The RCV is mainly determined by within-individual biological variation so that the RCV of each analyte varied from each other. As for RCV, Na had the lowest value and BUN had the highest one. In addition, the main reason for delta% exceeding delta check limits was a clinically significant change. CONCLUSIONS: Laboratories could use delta check procedure to find out errors in sample collection and monitor clinical significance. When delta% of patients exceed corresponding delta check limits in a short time, clinicians and personnel of clinical laboratory should pay more attention. Delta check limits should be reviewed regularly to check the utility of procedure.

Downregulation of glucose-6-phosphate dehydrogenase contributes to diabetic neuropathic pain through upregulation of toll-like receptor 4 in rats.

BACKGROUND AND AIM: Diabetic neuropathic pain is a refractory and disabling complication of diabetes mellitus. The pathogenesis of the diabetic neuropathic pain is still unclear, and treatment is insufficient. The aim of this study is to investigate the roles of glucose-6-phosphate dehydrogenase (G6PD) and toll-like receptor 4 (TLR4) in neuropathic pain in rats with diabetes. METHODS: Type 1 diabetes model was induced by intraperitoneal injection of streptozotocin (STZ, 75 mg/kg) in adult female Sprague-Dawley rats. Paw withdrawal threshold and paw withdrawal latency of rats were measured by von Frey filaments and thermal radiation, respectively. The expressions of G6PD and TLR4 in L4-L6 dorsal root ganglions (DRGs) were measured by western blotting and quantitative real-time polymerase chain reaction analysis. Fluorescent immunohistochemistry was employed to detect expressions of G6PD and TLR4 and co-location of G6PD with TLR4. RESULTS: The mRNA and protein expression levels of G6PD in DRGs were significantly decreased in diabetic rats when compared with age-matched control rats. Upregulation of G6PD by intrathecal injection of G6PD overexpression adenovirus markedly attenuated hindpaw pain hypersensitivity of diabetic rats. The mRNA and protein expression levels of TLR4 in DRGs of diabetic rats were significantly increased when compared with control rats. Intrathecal injection of TLR4-selective inhibitor CLI-095 attenuated diabetic pain in dose- and time-dependent manners. Furthermore, G6PD and TLR4 were co-localized in DRG neurons. Intrathecal injection of G6PD overexpression adenovirus greatly reduced TLR4 expression, while intrathecal injection of CLI-095 had no significant effect on G6PD expression in diabetic rats. CONCLUSIONS: Our results suggest that decrease in G6PD expression was involved in diabetic peripheral neuropathic pain, which was most likely through upregulation of TLR4 expression in the DRGs of rats.

Relationship Between Diabetes Mellitus and Cirrhosis Risk in Chronic Hepatitis B Patients in Wuhan, China.

BACKGROUND The objective of our research was to assess the possible link between diabetes mellitus (DM) and liver cirrhosis in chronic hepatitis B (CHB) patients in Wuhan, China. MATERIAL AND METHODS Individuals with a diagnosis of both liver cirrhosis and chronic HBV infection (n=257), and CHB-only patients (n=514) were matched 1: 2 by age and sex. Demographic, lifestyle, laboratory, and clinical characteristics were reviewed. Univariate and the multiple logistic regression analysis were conducted to investigate the association between DM and HBV-related liver cirrhosis. RESULTS The prevalence of DM was higher among CHB patients with liver cirrhosis than in those without liver cirrhosis (22.2% vs. 12.8%, P=0.001), yielding an adjusted odds ratio (AOR) of 2.317 and a 95% confidence interval (CI) of 1.528-3.513. Among them, 87.7% of liver cirrhosis patients were diagnosed with DM before liver cirrhosis diagnosis, yielding an AOR (95% CI) of 2.386 (1.533-3.714). In comparison to patients with a DM duration of 2-5 years, the AOR (95% CI) for those with a DM duration >5 years was 2.073 (0.701-6.132). In DM treatment, the AOR (95% CI) for those treated with insulin was 4.746 (1.329-16.949). CONCLUSIONS DM was associated with cirrhosis risk in CHB patients in Wuhan, China.

Sensitization of P2X3 receptors in insular cortex contributes to visceral pain of adult rats with neonatal maternal deprivation.

Aims Insular cortex is a brain region critical for processing of the sensation. Purinergic receptors are involved in the formation of chronic pain. The aim of the present study was to explore the role and mechanism of P2X3 receptors (P2X3Rs) in insular cortex in chronic visceral pain. Methods Chronic visceral pain in adult rats was induced by neonatal maternal deprivation and measured by detecting the threshold of colorectal distension. Western blotting, immunofluorescence, and real-time quantitative polymerase chain reaction techniques were used to detect the expression and distribution of P2X3Rs. Synaptic transmission in insular cortex was recorded in brain slices by patch clamp techniques. Results Expression of P2X3Rs both at mRNA and protein levels in right hemisphere of insular cortex was significantly increased in neonatal maternal deprivation rats. In addition, P2X3Rs were expressed with NeuN or synaptophysin but not with glial fibrillary acidic protein and CD11b. The co-localization of P2X3Rs with NeuN or synaptophysin was greatly enhanced in right hemisphere of insular cortex in neonatal maternal deprivation rats. Furthermore, neonatal maternal deprivation markedly increased both the frequency and amplitude of miniature excitatory postsynaptic current in right hemisphere of insular cortex. Incubation of A347091 significantly decreased the frequency of spontaneous excitatory postsynaptic current and miniature excitatory postsynaptic current of insular cortex neurons of neonatal maternal deprivation rats. Incubation of P2X3Rs agonists α,ß-mATP remarkably increased the frequency of spontaneous excitatory postsynaptic current and miniature excitatory postsynaptic current of the right hemisphere of insular cortex neurons of healthy control rats. Importantly, injection of A317491 significantly enhanced the colorectal distension threshold of neonatal maternal deprivation rats, while injection of α,ß-mATP into right but not left insular cortex markedly decreased the colorectal distension threshold in healthy control rats. Conclusions Overall, our data provide integrated pharmacological, biochemical, and functional evidence demonstrating that P2X3Rs are physically and functionally interconnected at the presynaptic level to control synaptic activities in the right insular cortex, thus contributing to visceral pain of neonatal maternal deprivation rats.

Prenatal maternal stress induces visceral hypersensitivity of adult rat offspring through activation of cystathionine-ß-synthase signaling in primary sensory neurons.

Irritable bowel syndrome is a disorder of unknown etiology characterized by widespread, chronic abdominal pain associated with altered bowel movements. Increasing amounts of evidence indicate that stressors presented during gestational periods could have long-term effects on the offspring's tissue structure and function, which may predispose to gastrointestinal diseases. The aim of the present study is to determine whether prenatal maternal stressis a adverse factor affecting gastrointestinal sensitivity and to investigate possible mechanisms underlying prenatal maternal stress-induced visceral hypersensitivity in adult offspring. Prenatal maternal stress was induced in pregnant Sprague-Dawley rats by exposure to heterotypic intermitent stress from gestational day 7 to delivery. Prenatal maternal stress significantly increased visceromotor response to colorectal distention in adult offspring from the age of 6 weeks to 10 weeks. Prenatal maternal stress also enhanced neuronal excitability including depolarization of resting membrane potentials, reduction in rheobase, and an increase in the number of action potentials evoked by 2× and 3× rheobase current stimultion of colon-specific dorsal root ganglion neurons. Prenatal maternal stress remarkably enhanced expression of cystathionine-ß-synthase and Nav1.7 in T13-L2 thoracolumbar dorsal root ganglions both at protein and mRNA levels. Intraperitoneal injection of aminooxyacetic acid, an inhibitor of cystathionine-ß-synthase, attenuated prenatal maternal stress-induced visceral hypersensitivity in a dose-dependent manner. A consecutive seven-day administration of aminooxyacetic acid reversed the hyperexcitability of colon-specific dorsal root ganglion neurons and markedly reduced Nav1.7 expression. These results indicate that the presence of multiple psychophysical stressors during pregnancy is associated with visceral hypersensitivity in offspring, which is likely mediated by an upregualtion of cystathionine-ß-synthase and Nav1.7 expression. Prenatal maternal stress might be a significant contributor to irritable bowel syndrome, and cystathionine-ß-synthase might be a potential target for treatment for chronic visceral hypersensitivity in patients with irritable bowel syndrome.

Synthesis and characterization of a new soy protein isolate/Polyamic acid salt blend films.

In this study, a new method was developed to produce biodegradable material using soy protein isolate (SPI) as matrix. The blend films were successfully prepared by casting the aqueous dispersions of SPI and polyamic acid salt (PAS) solution. The effects of blending and PAS content on the structure of the resultant films were investigated by Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), differential scanning calorimetry (DSC) analyses, scanning electron microscopy (SEM). Furthermore, film thickness, water vapor permeability (WVP), water barrier and mechanical properties were measured. The result showed that there exists strong intermolecular interactions between SPI and PAS, which played an important role in forming a homogeneous structure of the blend films. Moreover, the incorporation of PAS enhanced the water barrier and mechanical properties of the films. This is a simple way to prepare biodegradable films compared with other methods and the blend films have the potentiality to be used as food packaging and biomedical materials instead of synthetic polymer.

Protein expression profiling during wallerian degeneration after rat sciatic nerve injury.

INTRODUCTION: Wallerian degeneration (WD) is an important area of research in modern neuroscience. Many protein expressions are regulated by differentially expressed genes in WD, but the precise mechanisms are elusive. METHODS: In this study, we profiled differentially expressed proteins in WD after rat sciatic nerve injury using an antibody array. RESULTS: Functional analysis positively identified cell proliferation, regulation of cell proliferation, and immune system processes. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed molecular networks related mainly to cytokine-cytokine receptor interaction, the mitogen-activated proteinkinase (MAPK) signaling pathway, apoptosis, the toll-like receptor (TLR) signaling pathway, and the Janus kinase (Jak) - signal transducer and activator of transcription (STAT) signaling pathway. Interactions between these differential proteins were well established and regulated by the key factors transforming growth factor beta 1 (TGF-ß1), toll-like receptor 4 (TLR4), Fas ligand (FasL), and 5'-AMP-activated protein kinase catalytic subunit alpha-1 (PRKAA1). CONCLUSIONS: These results provide information related to functional analysis of differentially expressed genes during WD.

Analysis of Serum Anti-HBs Levels and HBsAg/HBeAg Markers in Children and Adolescents: A Cross-Sectional Study.

Hepatitis B virus (HBV) is a global public health concern, and China continues to face a high burden of HBV cases. Vaccination plays a critical role in controlling and eradicating HBV. However, studies have shown that some individuals may experience waning immunity over time, highlighting the importance of enhanced immunization strategies. This study aimed to investigate the relationship between age, gender, and anti-HBs antibody levels, as well as the prevalence of serum hepatitis B surface antigen (HBsAg)/HBV e antigen (HBeAg) positivity. This retrospective study included 43,609 pediatric patients who visited the outpatient department between January 2013 and December 2022. Serum biomarkers (HBsAg, anti-HBs, HBeAg, anti-HBe, and anti-HBc) were measured using Roche Cobas 8000. There is a significant difference in anti-HBs titer between genders and across different age groups (p < 0.05). The serological markers HBsAg/HBeAg exhibited the highest positivity rate in the age group of 15-18 years. The findings demonstrate a gradual decrease in anti-HBs levels following HBV vaccination. The prevalence of serum markers HBsAg/HBeAg is higher among adolescents aged 15-18 years, which should be a matter of concern and attention.

Analysis of the diagnostic and prognostic value of serum PAD2 in patients with sepsis in the intensive care unit.

BACKGROUND: Sepsis is a common disease in the intensive care unit (ICU). In recent years, the incidence rate and mortality rate remain high. Early diagnosis of sepsis is crucial for treatment and can effectively reduce mortality. So far, the ability of serum peptidylarginine deaminase 2 (PAD2) in the diagnosis and prognosis of sepsis patients is still unclear. We conducted this study to reveal the clinical value of PAD2 as a biomarker for sepsis patients. METHODS: A prospective study method was used to select 207 patients in the ICU of Renmin Hospital of Wuhan University from May 2022 to May 2023. They were divided into the sepsis group (n = 135) and control group (n = 72), and data were collected within 24 h of hospitalization. Sepsis patients were divided into a survival group (n = 80) and a non-survival group (n = 55) based on their 28-day survival status. Using statistical methods to evaluate the diagnostic and prognostic value of PAD2 in sepsis. RESULTS: The serum PAD2 concentrations in the sepsis group were significantly higher than in the control group (median 16.70 vs 35.32 ng/ml, P < 0.001). Multivariate logistic regression analysis showed that the Quick Sequential Organ Failure Assessment (qSOFA), C-reactive protein (CRP), procalcitonin (PCT), and PAD2 were independent risk factors for sepsis. The Receiver operating characteristic (ROC) curve showed that the combined diagnostic value of qSOFA, CRP, PCT, and PAD2 was the highest. The serum PAD2 concentrations in the non-survival group of patients with sepsis were significantly higher than those in the survival group (median 29.26 vs 50.08 ng/ml, P < 0.05). The COX regression analysis showed that PAD2, sequential organ failure score Assessment (SOFA) score, and Acute Physiology and Chronic Health Evaluation (APACHE II) score were independent factors affecting the prognosis of sepsis patients. The ROC analysis showed that the combined prognostic value of PAD2, SOFA, and APACHE II scores was significantly higher than any single indicator. The Kaplan-Meier survival analysis showed that patients with PAD2 ≤ 48.62 ng/ml had a better prognosis. CONCLUSION: The significant increase in serum PAD2 concentrations in patients is an independent risk factor affecting the occurrence of sepsis and 28-day mortality. The combination of PAD2 and other indicators can further improve the diagnostic and prognostic value for ICU sepsis patients.

Application of a nomogram from coagulation-related biomarkers and C1q and total bile acids in distinguishing advanced and early-stage lung cancer.

BACKGROUND: This study aimed to establish a nomogram to distinguish advanced- and early-stage lung cancer based on coagulation-related biomarkers and liver-related biomarkers. METHODS: A total of 306 patients with lung cancer and 172 patients with benign pulmonary disease were enrolled. Subgroup analyses based on histologic type, clinical stage, and neoplasm metastasis status were carried out and multivariable logistic regression analysis was applied. Furthermore, a nomogram model was developed and validated with bootstrap resampling. RESULTS: The concentrations of complement C1q, fibrinogen, and D-dimers, fibronectin, inorganic phosphate, and prealbumin were significantly changed in lung cancer patients compared to benign pulmonary disease patients. Multiple regression analysis based on subgroup analysis of clinical stage showed that compared with early-stage lung cancer, female (P < 0.001), asymptomatic admission (P = 0.001), and total bile acids (P = 0.011) were negatively related to advanced lung cancer, while C1q (P = 0.038), fibrinogen (P < 0.001), and D-dimers (P = 0.001) were positively related. A nomogram model based on gender, symptom, and the levels of total bile acids, C1q, fibrinogen, and D-dimers was constructed for distinguishing advanced lung cancer and early-stage lung cancer, with an area under the receiver operating characteristic curve of 0.919. The calibration curve for this nomogram revealed good predictive accuracy (P-Hosmer-Lemeshow = 0.697) between the predicted probability and the actual probability. CONCLUSIONS: We developed a nomogram based on gender, symptom, and the levels of fibrinogen, D-dimers, total bile acids, and C1q that can individually distinguish early- and advanced-stage lung cancer.

Diagnostic and Prognostic Value of C1q in Sepsis-Induced Coagulopathy.

Early identification of biomarkers that can predict the onset of sepsis-induced coagulopathy (SIC) in septic patients is clinically important. This study endeavors to examine the diagnostic and prognostic utility of serum C1q in the context of SIC. Clinical data from 279 patients diagnosed with sepsis at the Departments of Intensive Care, Respiratory Intensive Care, and Infectious Diseases at the Renmin Hospital of Wuhan University were gathered spanning from January 2022 to January 2024. These patients were categorized into two groups: the SIC group comprising 108 cases and the non-SIC group consisting of 171 cases, based on the presence of SIC. Within the SIC group, patients were further subdivided into a survival group (43 cases) and non-survival group (65 cases). The concentration of serum C1q in the SIC group was significantly lower than that in the non-SIC group. Furthermore, A significant correlation was observed between serum C1q levels and both SIC score and coagulation indices. C1q demonstrated superior diagnostic and prognostic performance for SIC patients, as indicated by a higher area under the curve (AUC). Notably, when combined with CRP, PCT, and SOFA score, C1q displayed the most robust diagnostic efficacy for SIC. Moreover, the combination of C1q with the SOFA score heightened predictive value concerning the 28-day mortality of SIC patients.

Serum ApoB/ApoA1 ratio in patients with CHB and the occurrence of HBV related cirrhosis and HBV related hepatocellular carcinoma.

Clinical research has suggested that chronic HBV infection exerts a certain effect on the occurrence of cardiovascular disease by regulating cholesterol metabolism in liver cells. High serum apolipoprotein B/apolipoprotein A1 (ApoB/ApoA1) ratio plays a certain role in the above regulation, and it serves as a risk factor for cardiovascular disease. However, whether the ApoB/ApoA1 ratio is correlated with chronic HBV infection and its disease progression remains unclear. In accordance with the inclusion and exclusion criteria, all 378 participants administrated at Renmin Hospital of Wuhan University from March 2021 to March 2022, fell into Healthy Control (HC) group (50 participants), Hepatocellular carcinoma (HCC) group (107 patients), liver cirrhosis (LC) group (64 patients), chronic hepatitis B (CHB) group (62 patients), chronic hepatitis C (CHC) group (46 patients) and Hepatitis E Virus (HEV) group (49 patients). Serum ApoA1 and ApoB concentrations were measured at admission, and the ApoB/ApoA1 ratio was determined. The levels of laboratory parameters in the respective group were compared and ApoB/ApoA1 ratios in HCC patients and LC patients with different severity were further analyzed. ROC curves were plotted to analyze the early diagnostic ability of ApoB/ApoA1 ratio for HBV-associated HCC. Logistic regression and restricted cubic spline analysis were used to explore the correlation between ApoB/ApoA1 ratio and LC and HCC risk. A comparison was drawn in terms of ApoB/ApoA1 ratio between the groups, and the result was expressed in descending sequence: HEV group > CHB group > LC group > HCC group > CHC group > HC group, early-stage HCC < middle-stage HCC < advanced-stage HCC, Class A LC < Class B LC < Class C LC. Serum ApoB/ApoA1 ratio combined diagnosis with AFP exhibited the capability of increasing the detection efficacy and specificity of AFP for HCC and AFP-negative HCC. The incidence of LC and HCC in the respective logistic regression model showed a negative correlation with the serum ApoB/ApoA1 ratio in CHB patients (P < 0.05). After all confounding factors covered in this study were regulated, the result of the restricted cubic spline analysis suggested that in a certain range, serum ApoB/ApoA1 ratio showed an inverse correlation with the prevalence of LC or HCC in CHB patients. Serum ApoB/ApoA1 ratio in CHB patients may be conducive to identifying high-risk patients for HCC or LC, such that LC and HCC can be early diagnosed and treated.

Analysis of Key Genes and miRNA-mRNA Networks Associated with Glucocorticoids Treatment in Chronic Obstructive Pulmonary Disease.

Background: Some patients with chronic obstructive pulmonary disease (COPD) benefit from glucocorticoid (GC) treatment, but its mechanism is unclear. Objective: With the help of the Gene Expression Omnibus (GEO) database, the key genes and miRNA-mRNA related to the treatment of COPD by GCs were discussed, and the potential mechanism was explained. Methods: The miRNA microarray dataset (GSE76774) and mRNA microarray dataset (GSE36221) were downloaded, and differential expression analysis were performed. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the differentially expressed genes (DEGs). The protein interaction network of the DEGs in the regulatory network was constructed with the STRING database, and the key genes were screened through Cytoscape. Potential downstream target genes regulated by differentially expressed miRNAs (DEMs) were predicted by the miRWalk3.0 database, and miRNA-mRNA regulatory networks were constructed. Finally, some research results were validated. Results: ① Four DEMs and 83 DEGs were screened; ② GO and KEGG enrichment analysis mainly focused on the PI3K/Akt signalling pathway, ECM receptor interaction, etc.; ③ CD2, SLAMF7, etc. may be the key targets of GC in the treatment of COPD; ④ 18 intersection genes were predicted by the mirwalk 3.0 database, and 9 pairs of miRNA-mRNA regulatory networks were identified; ⑤ The expression of miR-320d-2 and TFCP2L1 were upregulated by dexamethasone in the COPD cell model, while the expression of miR-181a-2-3p and SLAMF7 were downregulated. Conclusion: In COPD, GC may mediate the expression of the PI3K/Akt signalling pathway through miR-181a-2-3p, miR-320d-2, miR-650, and miR-155-5p, targeting its downstream signal factors. The research results provide new ideas for RNA therapy strategies of COPD, and also lay a foundation for further research.