Objective To explore the effects of different serum potassium levels on the 28-day prognosis of elderly patients with sepsis. Methods A retrospective analysis was conducted on the clinical data and laboratory indicators within 24 hours after the diagnosis in 204 elderly patients with sepsis admitted to the Department of Critical Care Medicine, Zhongshan Hospital, Fudan University from January 2018 to January 2022. According to the potassium concentrations in the blood of the patients within 24 hours after admission to intensive care unit (ICU), the patients were divided into the hyperkalemia group (K^＋≥5.3 mmol/L), normokalemia group (K^＋ 3.5–＜5.3 mmol/L), and hypokalemia group (K^＋＜3.5 mmol/L). According to 28-day outcomes, the patients were divided into the death group and survival group. The acute physiological and chronic health evaluation (APACHE) Ⅱ score, sequential organ failure assessment (SOFA) score and laboratory indicators were analyzed. Multivariate logistic regression analysis was used to analyze the risk factors for 28-day mortality in elderly patients with sepsis. Results Compared with the normokalemia group (n＝99), patients in both the hyperkalemia (n＝61) and hypokalemia (n＝44) groups had significantly higher levels of C-reactive protein (CRP) and procalcitonin (PCT), longer duration of mechanical ventilation, longer length of hospital stay and ICU stay, and higher mortality (P ＜ 0.05). The death group (n＝49) had significantly higher APACHE Ⅱ score, SOFA score, white blood cell (WBC) counts, CRP level, and PCT level than the survival group (n＝155, P＜0.05). Multivariate logistic regression analysis showed that increased or decreased serum potassium level, higher SOFA score, and increased WBC counts were independent risk factors for 28-day mortality in elderly patients with sepsis (P＜0.05). Quadratic fitted curve showed a U-shaped association between serum potassium levels and 28-day mortality risk in elderly patients with sepsis, with the lowest mortality risk observed within the intermediate (normal) range, and both hypokalemia and hyperkalemia were associated with an increased mortality risk (P＝0.182). Conclusion Both increased and decreased serum potassium levels are independent risk factors for 28-day mortality in elderly patients with sepsis, which should be given particular attention in clinical management.

Objective: To investigate the sleep quality in patients with burning mouth syndrome (BMS) and its influencing factors, providing a basis for developing sleep intervention measures to reduce the impact of BMS symptoms. Methods: This study was reviewed and approved by the Medical Ethics Committee, and informed consent was obtained from patients. A total of 150 patients with BMS and 150 healthy volunteers were enrolled as subjects in this study. The Pittsburgh sleep quality index (PSQI) was used to assess the sleep quality of patients with BMS. Visual analog scale (VAS) was used to assess the degree of oral mucosal pain, generalized anxiety disorder 7-item scale (GAD-7) was used to assess the frequency of anxiety symptoms, and the patient health questionnaire depression questionnaire (PHQ-9) was used to assess the frequency of depression symptoms. Univariate analysis was performed to identify potential influencing factors affecting sleep quality in patients with BMS, and multiple linear regression analysis was employed to determine independent risk factors. Results: The PSQI score for patients with BMS was 7.61 ± 4.29, which was significantly higher than that of healthy controls (P = 0.016). In the PSQI subscale analysis, patients with BMS exhibited increased sleep latency, decreased sleep duration, and lower sleep efficiency compared to healthy controls (P<0.05). Patients with BMS and comorbid sleep difficulties had significantly higher scores on GAD-7 and PHQ-9 compared to the patients with BMS without sleep difficulties (P<0.001), but there was no significant difference in pain VAS scores between the two (P = 0.068). Multiple linear regression analysis revealed that longer disease duration (>6 months), the presence of systemic concomitant symptoms (such as headache and mental stress), and higher depression scores were identified as independent risk factors affecting sleep quality in patients with BMS. Conclusion For patients with BMS, long course of illness, presence of headaches, high mental stress, and depressive symptoms may be independent factors affecting their sleep quality.

Objective:To investigate the effects of enolase 1(ENO1)on the proliferation,migration,and invasion of gastric cancer cells and its underlying molecular mechanisms.Methods:The expression levels of ENO1 in human gastric cancer cell lines(HGC27,MKN-45,N-87,MGC803,BGC-823)and human gastric mucosal epithelial cells(GES-1)were detected using WB assay.Gene editing tools such as CRISPR and overexpression system were used to construct ENO1 knockdown and knockdown-rescue cell lines.Both MKN-45 and BGC-823 cells were grouped into control(Ctrl)group,ENO1 knockdown(ENO1 KD)group,and ENO1 knockdown-rescue(ENO1 KD-OE)group.The effects of ENO1 knockdown or ENO1 knockdown-rescue on the proliferation,migration,invasion,and apoptosis of gastric cancer cells were evaluated using colony formation assay,EdU staining,scratch wound healing assay,Transwell chamber assay and flow cytometry.Additionally,a xenograft model was established in nude mice,and the effects of ENO1 on tumor growth were monitored using small animal in vivo imaging and tumor tissue block measurement.ENO1 was silenced in MKN-45 cells employing RNA interference technology,and the downstream target genes of ENO1 were identified using RNA co-immunoprecipitation sequencing(RIP-seq)and bioinformatics analysis.The molecular mechanisms by which ENO1 regulates the proliferation,migration and invasion of gastric cancer cells was also analyzed.Results:ENO1 was significantly upregulated in gastric cancer cell lines(P<0.01 or P<0.001).ENO1 knockdown significantly inhibited proliferation,migration,and invasion while promoting apoptosis in MKN-45 and BGC-823 cells(P<0.001,P<0.000 1).Rescue experiments showed that restoring ENO1 expression significantly enhanced cell proliferation,migration,invasion,and inhibited apoptosis(P<0.05,P<0.01,P<0.001,P<0.000 1).In vivo experiments demonstrated that ENO1 knockdown significantly inhibited tumor growth in nude mice(P<0.000 1).The differentially expressed genes interacting with ENO1 protein were primarily enriched in pathways related to RNA splicing.Additionally,ENO1 protein was found to interact with the PKM gene,and their expressions showed a positive correlation in gastric cancer tissues(r=0.886).Conclusion:ENO1 is highly expressed in gastric cancer cells.ENO1 interacts with precursor mRNA of PKM to influence its RNA splicing process,thereby regulating PKM2 expression and promoting gastric cancer progression.

Objective:To investigate endothelial cell heterogeneity in diabetic cardiomyopathy (DCM) and identify potential therapeutic targets of dapagliflozin in cardiac vascular endothelial cells.Methods:ePharmaLib reverse virtual screening was performed on 15 148 protein crystals to identified the binding interactions between human-derived proteins and dapagliflozin. Subsequently, single-cell RNA sequencing data (PRJNA1069235) from wild-type mice (control group) and db/db mice (DCM group) were integrated, then dimensionality reduction and clustering analysis were performed to identify endothelial cell subpopulations in the heart tissue of DCM mice, followed by functional annotation. Cell-cell communication analysis was explored to investigate fibroblast-endothelial cell interactions. The Agilent Mouse ceRNA Microarray chip was used to perform transcriptomic analysis of heart tissue from mice fed a high-fat diet and treated with dapagliflozin. Intersection analysis of reverse virtual screening results, single-cell RNA sequencing results and chip analysis data was performed to identify common differentially expressed genes. In vitro, human umbilical vein endothelial cells were divided into blank control group, tumor necrosis factor-α (TNF-α) group (TNF-α 10 mg/L), dapagliflozin low concentration group (TNF-α 10 mg/L+dagliazin 2 μmol/L), dapagliflozin medium concentration group (TNF-α 10 mg/L+dagliazin 5 μmol/L) and dapagliflozin high concentration group (TNF-α 10+dagliazin 10 μmol/L). Western blot and real-time reverse transcriptase polymerase chain reaction were used to detect the expression of inflammatory factors and differential genes.Results:ePharmaLib reverse virtual screening identified 168 human-derived proteins with potential binding affinity to dapagliflozin, and single-cell analysis identifiedf 6 types of endothelial cell subpopulations. Compared with the control group, the abundance of capillary endothelial cells was significantly lower in DCM group, while the abundance of microvascular and venous endothelial cells was significantly higher ( P all<0.05). Cell-cell communication analysis showed significant expression of Pgf-Vegfr1 ligand-receptor pair. In addition, 15 differentially expressed genes were identified by intersection analysis of 168 dapagliflozin-binding proteins. Including Bcl2, Baz2b, Nos3, Ephb4, Cdk8, Pparg, Pde2a, Fgfr2, Fto, Stk24, Dlg1, Gsk3b, Pdpk1, Fas and Tnks2. Notably, Baz2b, Pparg, Fto and Gsk3b were differentially expressed in all cell subpopulations. Six differential genes, including Pde7a, Dlg1, Gsk3b, Nampt, Met and Adk, were obtained by the intersection of the chip analysis data with the virtual screening results of dapagliflozin. In vitro, compared to the human umbilical vein endothelial cells of TNF-α group, the expression levels of interleukin-6, interleukin-1β and p-P65 proteins and messenger RNA of Bcl2, Nos3, Cdk8, Pde2a, Dlg1, Pdpk1, Tnks2, Baz2b, Pparg, Fas, Pde7a and Nampt were significantly lower than dapagliflozin high concentration group ( P all<0.05). Conclusions:Dapagliflozin may inhibit endothelial cell inflammatory responses and improve endothelial dysfunction in DCM by regulating key genes such as Dlg1, Bcl2, Nos3, Pde7a and Nampt.

Objective:To investigate endothelial cell heterogeneity in diabetic cardiomyopathy (DCM) and identify potential therapeutic targets of dapagliflozin in cardiac vascular endothelial cells.Methods:ePharmaLib reverse virtual screening was performed on 15 148 protein crystals to identified the binding interactions between human-derived proteins and dapagliflozin. Subsequently, single-cell RNA sequencing data (PRJNA1069235) from wild-type mice (control group) and db/db mice (DCM group) were integrated, then dimensionality reduction and clustering analysis were performed to identify endothelial cell subpopulations in the heart tissue of DCM mice, followed by functional annotation. Cell-cell communication analysis was explored to investigate fibroblast-endothelial cell interactions. The Agilent Mouse ceRNA Microarray chip was used to perform transcriptomic analysis of heart tissue from mice fed a high-fat diet and treated with dapagliflozin. Intersection analysis of reverse virtual screening results, single-cell RNA sequencing results and chip analysis data was performed to identify common differentially expressed genes. In vitro, human umbilical vein endothelial cells were divided into blank control group, tumor necrosis factor-α (TNF-α) group (TNF-α 10 mg/L), dapagliflozin low concentration group (TNF-α 10 mg/L+dagliazin 2 μmol/L), dapagliflozin medium concentration group (TNF-α 10 mg/L+dagliazin 5 μmol/L) and dapagliflozin high concentration group (TNF-α 10+dagliazin 10 μmol/L). Western blot and real-time reverse transcriptase polymerase chain reaction were used to detect the expression of inflammatory factors and differential genes.Results:ePharmaLib reverse virtual screening identified 168 human-derived proteins with potential binding affinity to dapagliflozin, and single-cell analysis identifiedf 6 types of endothelial cell subpopulations. Compared with the control group, the abundance of capillary endothelial cells was significantly lower in DCM group, while the abundance of microvascular and venous endothelial cells was significantly higher ( P all<0.05). Cell-cell communication analysis showed significant expression of Pgf-Vegfr1 ligand-receptor pair. In addition, 15 differentially expressed genes were identified by intersection analysis of 168 dapagliflozin-binding proteins. Including Bcl2, Baz2b, Nos3, Ephb4, Cdk8, Pparg, Pde2a, Fgfr2, Fto, Stk24, Dlg1, Gsk3b, Pdpk1, Fas and Tnks2. Notably, Baz2b, Pparg, Fto and Gsk3b were differentially expressed in all cell subpopulations. Six differential genes, including Pde7a, Dlg1, Gsk3b, Nampt, Met and Adk, were obtained by the intersection of the chip analysis data with the virtual screening results of dapagliflozin. In vitro, compared to the human umbilical vein endothelial cells of TNF-α group, the expression levels of interleukin-6, interleukin-1β and p-P65 proteins and messenger RNA of Bcl2, Nos3, Cdk8, Pde2a, Dlg1, Pdpk1, Tnks2, Baz2b, Pparg, Fas, Pde7a and Nampt were significantly lower than dapagliflozin high concentration group ( P all<0.05). Conclusions:Dapagliflozin may inhibit endothelial cell inflammatory responses and improve endothelial dysfunction in DCM by regulating key genes such as Dlg1, Bcl2, Nos3, Pde7a and Nampt.

Objectives:To evaluate the clinical outcome of acute respiratory distress syndrome (ARDS) in patients with Stanford Type A aortic dissection (AAD).Methods:A total of 212 patients diagnosed with AAD and receiving surgical treatment in the Affiliated Hospital of Jining Medical University from January 2016 to December 2021 were included. The patients were divided into ARDS group and non-ARDS group based on the definition of ARDS Berlin after surgery. The preoperative general clinical data of the two groups were compared by univariate analysis, and the preference-matching variables were screened. The patients were divided into ARDS group ( n=63) and non-ARDS group ( n=63) by using propensity matching score, and the clinical outcome indexes of ARDS group and non-ARDS group were compared after matching. Results:A total of 63 patients (29.7%) were diagnosed with ARDS after AAD. A total of 63 pairs of patients were successfully matched using propensity score to adjust preoperative confounding factors. After matching, the proportion of total arch surgery, operation time, perioperative blood loss, red blood cell transfusion and plasma transfusion in the ARDS group were significantly higher than those in the non-ARDS group, with statistical significance (all P<0.05). After the match, In the ARDS group, Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score [18(14-24)points vs 13(12-15)points], mechanical ventilation time [86.0(57.3-158.0)h vs 41.5(23.8-60.4)h], intensive care unit (ICU) stay time [7.0(6.0-11.5)d vs 4.0(3.0-6.0)d] and hospital stay [18.0(14.0-24.5)d vs 13.5(10.8-18.0)d] were significantly higher than those in the non-ARDS group, with statistical significance (all P<0.05). There was no significant difference in in-hospital mortality (3.2% vs 1.6%) or within 30 days after discharge (6.3% vs 3.2%) between the two groups (all P>0.05). Conclusions:The incidence of ARDS is higher in patients diagnosed with AAD based on the Berlin definition, but there is no increase in the mortality rate within 30 days of hospital and discharge in ARDS group. The Berlin definition of ARDS may have some limitations in the application of ARDS in patients with AAD after surgery.

Objectives:To evaluate the clinical outcome of acute respiratory distress syndrome (ARDS) in patients with Stanford Type A aortic dissection (AAD).Methods:A total of 212 patients diagnosed with AAD and receiving surgical treatment in the Affiliated Hospital of Jining Medical University from January 2016 to December 2021 were included. The patients were divided into ARDS group and non-ARDS group based on the definition of ARDS Berlin after surgery. The preoperative general clinical data of the two groups were compared by univariate analysis, and the preference-matching variables were screened. The patients were divided into ARDS group ( n=63) and non-ARDS group ( n=63) by using propensity matching score, and the clinical outcome indexes of ARDS group and non-ARDS group were compared after matching. Results:A total of 63 patients (29.7%) were diagnosed with ARDS after AAD. A total of 63 pairs of patients were successfully matched using propensity score to adjust preoperative confounding factors. After matching, the proportion of total arch surgery, operation time, perioperative blood loss, red blood cell transfusion and plasma transfusion in the ARDS group were significantly higher than those in the non-ARDS group, with statistical significance (all P<0.05). After the match, In the ARDS group, Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score [18(14-24)points vs 13(12-15)points], mechanical ventilation time [86.0(57.3-158.0)h vs 41.5(23.8-60.4)h], intensive care unit (ICU) stay time [7.0(6.0-11.5)d vs 4.0(3.0-6.0)d] and hospital stay [18.0(14.0-24.5)d vs 13.5(10.8-18.0)d] were significantly higher than those in the non-ARDS group, with statistical significance (all P<0.05). There was no significant difference in in-hospital mortality (3.2% vs 1.6%) or within 30 days after discharge (6.3% vs 3.2%) between the two groups (all P>0.05). Conclusions:The incidence of ARDS is higher in patients diagnosed with AAD based on the Berlin definition, but there is no increase in the mortality rate within 30 days of hospital and discharge in ARDS group. The Berlin definition of ARDS may have some limitations in the application of ARDS in patients with AAD after surgery.

The typical manifestations of primary aldosteronism (PA) are hypertension with or without hypokalemia, high aldosterone, and low renal level. However, PA with normal blood pressure is rare in clinical practice. This article reported the diagnosis and treatment of a patient with subclinical PA, admitted for "adrenal accidental tumor" with normal blood pressure and serum potassium. We summarized and analyzed the clinical characteristics and treatment strategies, in order to provide some reference for clinicians.

Liver is the central hub regulating energy metabolism during feeding-fasting transition. Evidence suggests that fasting and refeeding induce dynamic changes in liver size, but the underlying mechanisms remain unclear. Yes-associated protein (YAP) is a key regulator of organ size. This study aims to explore the role of YAP in fasting- and refeeding-induced changes in liver size. Here, fasting significantly reduced liver size, which was recovered to the normal level after refeeding. Moreover, hepatocyte size was decreased and hepatocyte proliferation was inhibited after fasting. Conversely, refeeding promoted hepatocyte enlargement and proliferation compared to fasted state. Mechanistically, fasting or refeeding regulated the expression of YAP and its downstream targets, as well as the proliferation-related protein cyclin D1 (CCND1). Furthermore, fasting significantly reduced the liver size in AAV-control mice, which was mitigated in AAV Yap (5SA) mice. Yap overexpression also prevented the effect of fasting on hepatocyte size and proliferation. Besides, the recovery of liver size after refeeding was delayed in AAV Yap shRNA mice. Yap knockdown attenuated refeeding-induced hepatocyte enlargement and proliferation. In summary, this study demonstrated that YAP plays an important role in dynamic changes of liver size during fasting-refeeding transition, which provides new evidence for YAP in regulating liver size under energy stress.

Objective:To develop an illness perception scale of somatization symptom and complete the reliability and validity test, so as to provide a new tool for illness perception evaluation of somatization symptom in patients with non-psychotic mental disorders.Methods:Form May 2020 to January 2022, 473 non-psychotic patients with somatization symptom were selected from the outpatient and inpatient department of the Sichuan Provincial People′s Hospital and Sichuan Psychiatric Medicine Center. According to the literature research method, semi-structured interview method, the existing illness perception scale and the clinical experience of psychiatrists, the total item pool of the scale was obtained ( n=46), consequently, the item pool was modified by a discussion of the research group and Delphi expert consultation method was used to form a predictive scale. Two hundred and three patients were invited to complete the measuring scale, and the items of the predictive scale were screened according to the results of item analysis to form a formal scale. Exploratory factor analysis was used to construct the scale dimension. The formal scale was tested in 270 patients, Cronbach α coefficient was used to evaluate the reliability of the total scale and each dimension, and Pearson correlation analysis was used to verify the retest reliability. AMOS equation model verifies the structural validity of the scale, and Pearson correlation analysis is used to verify the criterion validity of the scale with PHQ-15, GAD-7 and PHQ-9 as criteria. Results:A total of 443 patients′ valid information was collected. According to the results of discussion by the research group and letters from experts, the prediction scale with 36 items was finally obtained, and 20 items were removed according to the results of item analysis. There were 16 items in the formal scale, including four dimensions: disease distress, symptom understanding, treatment attitude and medication attitude, which could explain the variation rate of 57.702%. The correlation coefficient between the total score of the scale and PHQ-15, GAD-7 and PHQ-9 was 0.395-0.506. Confirmatory factor analysis indicates that the model is ideal (χ 2/ df=1.719, GFI=0.922, CFI=0.937, NFI=0.865, IFI=0.939, RMSEA=0.055) and has good validity. The internal consistency coefficient and test-retest reliability correlation coefficient of the total scale and the four dimensions are 0.683-0.831 and 0.746-0.836, respectively, and the reliability results are satisfactory. Conclusion:The scale has good reliability and validity, and can be used to measure the disease cognition of patients with non-psychotic mental disorders on somatization symptoms.