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

Antineoplastic drugs refer to the drugs that act at the cellular and molecular levels to inhibit tumor growth or eliminate tumors through pathways such as cell killing,immune regulation,and endocrine regulation.Antineoplastic drugs generally including chemotherapeutic drugs,molecular targeted therapeutic drugs,immunotherapeutic drugs,and endocrine therapeutic drugs.The management and rational application of antineoplastic drugs in medical institutions are related to the safety of patient treatment.The standard for management of antineoplastic drugs use in clinical is compiled by the Pharmaceutical Affairs Committee of China Hospital Association,which specification requirements 18 key elements in the organizational management and system,medication management,drug monitoring and evaluation of antineoplastic drug management in healthcare institutions.This standard is applicable to all levels and types of healthcare institutions carrying out oncology diagnosis and treatment.This paper describes the methodology and basic content of the standard,hoping to providing a reference for medical institutions to carry out relevant work.

Objective To investigate the effect of silencing alpha tubulin acetyltransferase 1(α-TAT1)on migration behavior of endothelial cells induced by hepatopulmonary syndrome(HPS).Methods Online database Tabula Muris was used to analyze the expression of α-TAT1 in various cell subsets in the lungs.Twenty-four male SD rats were randomly divided into control group(Sham group,n=6)and common bile duct ligation group(HPS group,n=18).The rats in HPS group were euthanasized at 2 and 4 weeks after modelling,and then the expression of α-TAT1 in pulmonary vascular endothelial cells was detected by immunofluorescence colocalization.The sera from the Sham and HPS rats were used to stimulate human umbilical vein endothelial cells(HUVECs)for 12 and 24 h,respectively.Then the obtained HUVECs were divided into 4 groups:Sham serum+siRNA NC group,Sham serum+siRNA α-TAT1 group,HPS serum+siRNA NC group,HPS serum+siRNA α-TAT1 group.The expression levels of α-TAT1 and Ace-α-tubulin in HUVECs were detected by Western blotting.Immunofluorescence assay was applied to observe the levels of polymerized microtubules of α-Tubulin in HUVECs after nocodazole(10 μmol/L)pretreatment to evaluate the stability of microtubule structure.Cell scratch assay combined with cell immunofluorescence assay was employed to observe the nuclear localization of Golgi apparatus and cell migration ability of HUVECs.The angiogenesis ability of HUVECs was tested by in vitro angiogenesis test.Results In vivo and in vitro experiments showed that the expression of α-TAT1 in endothelial cells was significantly increased after HPS inducement.The expression levels of α-TAT1 and Ace-α-tubulin were significantly down-regulated,and the stability of microtubules was weakened in the siRNA α-TAT1 interference group(P＜0.01).In addition,the distribution of GM 130 labeled Golgi apparatus in the protrusion of HUVECs was down-regulated in the siRNAα-TAT1 interference group,as well as the migration ability(P＜0.01).And the length of angiogenesis and network level were also significantly declined(P＜0.01).Conclusion Silencing α-TAT1 reduces the migrαtion and angiogenesis of endothelial cells in HPS,which was associated with weakened stabilization of microtubule.

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.

Objective To compare the effect of palliative mitral valve surgeries and medication therapies for secondary non-ischemic mitral regurgitation. Methods The clinical data of patients with non-ischemic functional mitral regurgitation treated in our hospital between 2009 and 2019 were retrospectively analyzed. Patients with a left ventricular ejection fraction (LVEF)＜40% underwent a dobutamine stress test, and a positive result was determined when the LVEF improved by more than 15% compared to the baseline value. Positive patients were divided into a surgery group and a medication group. The surgery group underwent surgical mitral valve repair or replacement, while the medication group received simple medication treatment. Follow-up on survival and cardiac function status through outpatient or telephone visits every six months after surgery, and patients underwent cardiac ultrasound examination one year after surgery. The main research endpoint was a composite endpoint of all-cause death, heart failure readmission, and heart transplantation, and the differences in cardiac function and cardiac ultrasound parameters between the two groups were compared. Results Ultimately 41 patients were collected, including 28 males and 13 females with an average age of 55.5±11.1 years. Twenty-five patients were in the surgery group and sixteen patients in the medication group. The median follow-up time was 16 months, ranging 1-96 months. The occurrence of all-cause death in the surgery group was lower than that in the medication group (HR=0.124, 95%CI 0.024-0.641, P=0.034). The difference between the two groups was not statistically significant in the composite endpoint (HR=0.499, 95%CI 0.523-1.631, P=0.229). The New York Heart Association (NYHA) grade of the surgery group was better (NYHA Ⅰ-Ⅱ accounted for 68.0% in the surgury group and 18.8% in the medication group, P<0.01) as well as the grade of mitral valve regurgitation (87.5% of the patients in the medication group had moderate or above regurgitation at follow-up, while all the patients in the surgery group had moderate below regurgitation, P<0.01). There was no statistical difference in preoperative and follow-up changes in echocardiograph parameters between the two groups (P＞0.05). Conclusion For non-ischemic functional mitral regurgitation, if the cardiac systolic function is well reserved, mitral valve surgery can improve survival and quality of life compare to simple medication therapy.

Objective:To investigate the protective effect of folic acid on melanocytes under oxidative stress.Methods:The normal human melanocyte cell line (PIG1) was cultured in vitro and divided into 5 groups to receive corresponding treatments: control group (normal culture for 48 hours without other treatment), H 2O 2 treatment group (normal culture for 24 hours followed by the treatment with 1 mmol/L H 2O 2 for another 24 hours), and 3 folic acid pretreatment groups (pretreatment with folic acid at concentrations of 50, 125, and 250 μmol/L for 24 hours followed by the treatment with 1 mmol/L H 2O 2 for another 24 hours). The cell viability was assessed using the cell counting kit 8 (CCK8) assay, the intracellular melanin content was measured by the sodium hydroxide solubilization method, cell apoptosis rates were detected by annexin V-fluorescein isothiocyanate/propidium iodide double staining, levels of intracellular reactive oxygen species (ROS) were detected using the fluorescent probe CM-H2DCFDA, the mitochondrial membrane potential was determined using the fluorescent probe JC-1, and the mitochondrial ultrastructure was observed by transmission electron microscopy. Comparisons among multiple groups were performed using one-way analysis of variance, and multiple comparisons were performed using Tukey test. Results:Compared with the control group, the H 2O 2 treatment group showed decreased cell viability (83.62% ± 3.77% vs. 99.99% ± 5.06%, P = 0.031), intracellular melanin content (68.48% ± 4.17% vs. 100.11% ± 2.30%, P < 0.001) and mitochondrial membrane potential (2.96 ± 0.26 vs. 5.86 ± 0.56, P = 0.002), but increased cell apoptosis rate (16.35% ± 1.20% vs. 6.45% ± 1.34%, P = 0.001) and intracellular ROS level (138.98% ± 2.74% vs. 100.00% ± 0.64%, P = 0.004). Compared with the H 2O 2 treatment group, the 125-μmol/L and 250-μmol/L folic acid pretreatment groups showed increased cell viability (106.21% ± 6.34%, 101.64% ± 6.77%, respectively; both P < 0.05) and intracellular melanin content (77.24% ± 3.85%, 88.34% ± 2.65%, respectively; both P < 0.05) ; the 50-μmol/L, 125-μmol/L and 250-μmol/L folic acid pretreatment groups all showed decreased cell apoptosis rates (9.40% ± 0.99%, 9.00% ± 1.13%, 6.50% ± 0.28%, P = 0.007, 0.005, 0.001, respectively) ; the 125-μmol/L and 250-μmol/L folic acid pretreatment groups showed decreased intracellular ROS levels (112.99% ± 4.21%, 101.36% ± 10.60%, P = 0.023, 0.005, respectively), but increased mitochondrial membrane potential (4.93 ± 0.25, 5.67 ± 0.35, P = 0.012, 0.003, respectively). Transmission electron microscopy showed damaged mitochondrial ultrastructure in melanocytes in the H 2O 2 treatment group, characterized by a substantial number of vacuolated mitochondria, intimal swelling, and reduced ridges, compared with the control group; compared with the H 2O 2 treatment group, the 250-μmol/L folic acid pretreatment group exhibited decreased degree of mitochondrial damage, manifesting as reduced mitochondrial vacuolization, clearer mitochondrial ultrastructure, and slight swelling of mitochondrial ridges. Conclusion:Folic acid could reduce the oxidative stress level in melanocytes, thus protecting melanocytes from oxidative stress.

Objective:To analyze micromorphological changes in psoriatic lesions before and after short-term treatment with secukinumab by dermoscopy and reflectance confocal microscopy (RCM), and to provide reliable microscopic indicators for monitoring the treatment efficacy.Methods:Nineteen patients with moderate to severe plaque psoriasis treated with secukinumab were collected from the Department of Dermatology, Wuhan No. 1 Hospital between July and December 2021. Dermoscopy and RCM were performed on same lesions in every patients at weeks 0, 2, and 4 after the start of treatment, and clinical evaluation was conducted at the same time. The changes in clinical scores, dermoscopic scores, and RCM characteristics before and after treatment were analyzed.Results:Dermoscopy showed that the bright red background of psoriatic lesions gradually lightened, pigmentation gradually increased, scales markedly decreased, and dotted/globular vessels changed from a uniform and regular distribution pattern to a clustered distribution pattern or completely disappeared after 2 to 4 weeks of treatment. As RCM revealed, after 2 and 4 weeks of treatment, the epidermal thickness decreased; the thicknesses from the stratum corneum to the dermal papilla at weeks 0, 2, and 4 were 76.85 ± 21.08 μm, 56.93 ± 16.58 μm, and 52.45 ± 15.76 μm, respectively; epidermal parakeratosis was alleviated or disappeared, inflammatory cells also decreased in number or disappeared in the epidermis and dermis, vascular dilatation was alleviated in the dermal papilla, and the structure of dermal papillary rings gradually became brighter in color after the treatment; the diameters of the dermal papillae decreased, measuring 53.96 ± 4.65 μm, 45.54 ± 5.11 μm, and 41.47 ± 4.54 μm at weeks 0, 2, and 4, respectively.Conclusion:The changes of microscopic indicators in psoriatic lesions are closely related to clinical efficacy, and the recovery of the dermal papillary ring structure by RCM can serve as an early observational indicator for the control of inflammation in psoriatic lesions and as an early predictive indicator for the effectiveness of subsequent treatment.

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.

From birth to adulthood, we often align our behaviors, attitudes, and opinions with a majority, a phenomenon known as social conformity. A seminal framework has proposed that conformity behaviors are mainly driven by three fundamental motives: a desire to gain more information to be accurate, to obtain social approval from others, and to maintain a favorable self-concept. Despite extensive interest in neuroimaging investigation of social conformity, the relationship between brain systems and these fundamental motivations has yet to be established. Here, we reviewed brain imaging findings of social conformity with a componential framework, aiming to reveal the neuropsychological substrates underlying different conformity motivations. First, information-seeking engages the evaluation of social information, information integration, and modification of task-related activity, corresponding to brain networks implicated in reward, cognitive control, and tasks at hand. Second, social acceptance involves the anticipation of social acceptance or rejection and mental state attribution, mediated by networks of reward, punishment, and mentalizing. Third, self-enhancement entails the excessive representation of positive self-related information and suppression of negative self-related information, ingroup favoritism and/or outgroup derogation, and elaborated mentalizing processes to the ingroup, supported by brain systems of reward, punishment, and mentalizing. Therefore, recent brain imaging studies have provided important insights into the fundamental motivations of social conformity in terms of component processes and brain mechanisms.
Humans ; Social Conformity ; Motivation ; Brain ; Social Behavior ; Brain Mapping

Objective:To investigate the effect of gallic acid on the morphology, proliferation and cell cycle of keloid fibroblasts, as well as on collagen contraction and the transforming growth factor-β (TGF-β) /Sma- and Mad-related proteins (Smads) signaling pathway, and to explore the role and mechanisms of action of gallic acid in the treatment of keloids.Methods:From August to December 2022, 3 keloid tissue samples were collected from 3 patients with clinically and pathologically confirmed keloids after surgery in the Department of Dermatologic Surgery, Wuhan No.1 Hospital. Primary fibroblasts were isolated and cultured by using the tissue culture method, and 3- to 8-passage fibroblasts were used for subsequent experiments. Cultured keloid fibroblasts were divided into 4 groups: low-, medium- and high-dose gallic acid groups treated with 0.025, 0.05 and 0.1 mg/ml gallic acid respectively, and a control group cultured with Dulbecco′s modified Eagle′s medium (DMEM) containing 10% fetal calf serum. After 24-, 48-, and 72-hour treatment, cellular proliferative activity was evaluated by cell counting kit 8 (CCK8) assay, and collagen contraction by using a three-dimensional culture method. After 24-hour treatment in the above groups, pictures were taken using a differential interference inverted fluorescence microscope, and changes in the cell cycle were analyzed by flow cytometry. Some keloid fibroblasts were divided into 2 groups: an experimental group (high-dose gallic acid group) treated with 0.1 mg/ml gallic acid, and a control group cultured with DMEM containing 10% fetal calf serum. After 24-hour treatment, enzyme-linked immunosorbent assay (ELISA) was performed to determine the changes in supernatant concentrations of TGF-β1, TGF-β2, and TGF-β3 in the two groups, real-time fluorescence-based quantitative PCR to detect the relative mRNA expression levels of TGF-β1, TGF-β2, TGF-β3, Smad2, Smad3, Smad4, and α-smooth muscle actin (α-SMA). Statistical analysis was carried out using t test, one-way analysis of variance and two-way analysis of variance, and least significant difference (LSD) - t test was used for multiple comparisons. Results:Compared with the control group, the gallic acid groups showed gradual changes in the shape of keloid fibroblasts under the microscope as the dose of gallic acid increased, including gradually shrinking cell bodies, enlarged intercellular spaces, cell atrophy, increased number of apoptotic cells, etc. CCK8 assay showed that the cellular proliferative activity changed significantly as the dose of gallic acid increased and the treatment time was prolonged ( Fgroup = 78.31, P < 0.001; Ftime = 4.17, P = 0.037), and the proliferative activity of keloid fibroblasts was significantly lower in the high-dose gallic acid group than in the control group at 24, 48, and 72 hours (all P < 0.05). The three-dimensional culture showed that different degrees of collagen contraction occurred in all groups over time, marked collagen contraction was observed in the control group, and a lower degree of collagen contraction in the gallic acid groups; the collagen contraction indices were significantly lower in the medium- and high-dose gallic acid groups than in the control group at 24, 48, and 72 hours (all P < 0.05). Flow cytometry showed that the cell apoptosis rates were significantly higher in the low-, medium- and high-dose gallic acid groups (38.68% ± 3.05%, 41.82% ± 2.19%, 43.56% ± 3.58%, respectively) than in the control group (12.58% ± 1.56%, all P < 0.001) after 24-hour treatment; compared with the control group, the medium- and high-dose gallic acid groups showed significantly decreased proportions of cells in the G0/G1 phase (both P < 0.01), but significantly increased proportions of cells in the S phase and G2/M phase (all P < 0.05). ELISA revealed that the TGF-β1 concentration was significantly lower in the high-dose gallic acid group (758.58 ± 31.42 pg/ml) than in the control group (1 081.30 ± 44.72 pg/ml, t = 11.81, P<0.001), there was no significant difference in the TGF-β2 concentration between the high-dose gallic acid group (71.05 ± 7.40 pg/ml) and the control group (76.43 ± 6.51 pg/ml, t = 1.09, P = 0.317), while the TGF-β3 concentration was significantly higher in the high-dose gallic acid group (5.70 ± 3.87 pg/ml) than in the control group (0.00 ± 0.00 pg/ml, t = 2.94, P = 0.026). As real-time fluorescence-based quantitative PCR revealed, the high-dose gallic acid group showed significantly decreased mRNA expression levels of TGF-β1, Smad2, Smad3, Smad4, and α-SMA (all P < 0.05), but significantly increased mRNA expression level of TGF-β3 ( t = 6.78, P = 0.002) compared with the control group; however, there was no significant difference in the TGF-β2 mRNA expression level between the above two groups ( t = 0.05, P = 0.962) . Conclusion:Gallic acid could change the cell cycle, inhibit the proliferative activity, promote apoptosis and change the shape of keloid fibroblasts, and thus inhibit scar formation and contraction, which may be related to the inhibition of TGF-β/Smads signaling pathway.