The accurate and timely detection of biochemical coagulation indicators is pivotal in pulmonary and critical care medicine. Despite their reliability, traditional laboratories often lag in terms of rapid diagnosis. Point-of-care testing (POCT) has emerged as a promising alternative, which is awaiting rigorous validation. We assessed 226 samples from patients at the First Affiliated Hospital of Guangzhou Medical University using a Beckman Coulter AU5821 and a PUSHKANG POCT Biochemistry Analyzer MS100. Furthermore, 350 samples were evaluated with a Stago coagulation analyzer STAR MAX and a PUSHKANG POCT Coagulation Analyzer MC100. Metrics included thirteen biochemical indexes, such as albumin, and five coagulation indices, such as prothrombin time. Comparisons were drawn against the PUSHKANG POCT analyzer. Bland-Altman plots (MS100: 0.8206‒0.9995; MC100: 0.8318‒0.9911) evinced significant consistency between methodologies. Spearman correlation pinpointed a potent linear association between conventional devices and the PUSHKANG POCT analyzer, further underscored by a robust correlation coefficient (MS100: 0.713‒0.949; MC100: 0.593‒0.950). The PUSHKANG POCT was validated as a dependable tool for serum and whole blood biochemical and coagulation diagnostics. This emphasizes its prospective clinical efficacy, offering clinicians a swift diagnostic tool and heralding a new era of enhanced patient care outcomes.
Humans ; Point-of-Care Testing ; Critical Care ; Blood Coagulation Tests/methods* ; Male ; Blood Coagulation ; Female ; Middle Aged ; Reproducibility of Results ; Prothrombin Time ; Aged ; Adult ; Point-of-Care Systems

Objective ToanalyzethecharacteristicmanifestationsandearlydiagnosticvalueofCTinsolitarypulmonarynodules (SPNs)lessthan2cmusing L o g istic regressionanalysis.Methods 156patientswithSPNlessthan2cmconfirmedbypathology werecollected.Statisticalassignment was performed and binary L o g istic regression wasimplemented for CT manifestations.Those features,whichmightbesignsoflungcancer,wereextractedfromtheCTimagesandtheirrisklevelswerealsoanalyzed.Results SixCTsignsincluding "ground-glasssign"(8.12),"lobulationsign"(6.72),"vascularconvergencesign"(6.02),"spiculesign"(5.07),"necrosis and cavitation "(3.41 ),and "vacuole sign (1.02 )" were enrolled in the L o g istic equation.Conclusion "Ground-glass sign "is associated with the highest risk level for lung cancer nodules.T he L o g istic m odel constructed fro m C T m anifestations is helpful for identifyingsolitarylungcancernodules.

OBJECTIVETo evaluate the enhanced effect of gemcitabine by emodin and the possible mechanisms of the enhancement.

METHODBased on the model of SW1990 cell xenograft on athymic mouse, the mice were randomized to four groups with intraperitoneal (IP) injections of different drugs: group N (injecting 0.9% sodium chloride), group E (emodin, 40 mg x kg(-1)), group G (gemcitabine, 125 mg x kg(-1)), and group E + G (emodin 40 mg x kg(-1) and gemcitabine 80 mg x kg(-1) in combination). The tumor volume, tumor weight and body weight of mice were measured during the drug therapy. The mice were sacrificed one week after last injection of drug. Tunel assay were used used to detect the apoptosis of tumor cells. And immunohistochemistry (IHC) and Western blot (WB) were used to detect the variance of the apoptosis relative protein expression of Bax, Bcl-2, and Cytochrome C .

RESULTOne week after the last administration, the mean tumor volume and tumor weight in group E + G were significantly decreased compared to the other groups. Tunel assay showed group E + G presented apparently more apoptosis than the other groups. Immunohistochemistry (IHC) and Western blot (WB) analysis showed the expression of Cytochrome C in cytoplasmin and Bax in group E + G was apparently upregulated while the expression of Bcl-2 was apparently downregulated compared to the other groups. As a result, Bcl-2/Bax ratio was significantly decreased in group E + G.

CONCLUSIONEmodin can significantly improve the antitumor effect of gemcitabine on transplanted tumor of SW1990 cell line through apparently enhancing the tumor cell apoptosis by gemcitabine. Downregulation of Bcl-2/Bax ratio and promoting release of Cytochrome C from mitochondria is possibly one of the mechanisms of the augmented apoptosis.

Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Cytochromes c ; metabolism ; Deoxycytidine ; analogs & derivatives ; pharmacology ; Drug Synergism ; Emodin ; pharmacology ; Female ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Mice ; Mice, Nude ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Tumor Burden ; drug effects ; Xenograft Model Antitumor Assays ; bcl-2-Associated X Protein ; metabolism