Objective To explore the clinical characteristics and prognostic outcomes of patients with acute myocardial infarction complicated by Coronavirus Disease 2019 (COVID-19). Methods A retrospective study was conducted in 76 patients with acute myocardial infarction. Based on the presence of COVID-19, they were divided into the COVID-19 group (n=42) and the control group (n=34). General clinical conditions, laboratory examination indicators, interventional treatment characteristics, incidence of complications during hospitalization and prognosis were compared between the two groups. Independent influencing factors for coronary thrombotic lesions in acute myocardial infarction patients were analyzed. Results The diastolic blood pressure, left ventricular ejection fraction and lymphocyte count were significantly lower, while lipoprotein a, C-reactive protein, serum ferritin, fibrinogen, and D-dimer were significantly higher in the COVID-19 group than those in the control group (P < 0.05). The proportions of coronary thrombotic lesions, baseline TIMI flow of grade 0 to 1, thrombus burden of grade 4 to 5, use of GP Ⅱb/Ⅲa inhibitors and thrombus aspiration in the COVID-19 group were significantly higher than those in the control group (P < 0.05). Multivariate Logistic regression analysis revealed that COVID-19 and increased D-dimer were independent risk factors for coronary thrombotic lesions in acute myocardial infarction patients. The average length of hospital stay was significantly longer in the COVID-19 group than that in the control group (P < 0.05). A 6-month follow-up showed that the incidence of major adverse cardiac events (MACEs) was significantly higher in the COVID-19 group than that in the control group (P=0.014). Conclusion Patients with acute myocardial infarction complicated by COVID-19 exhibit a higher coronary thrombus load and have a poor prognosis.

Aim To investigate the induction of ferroptosis of Triapine in non-small cell lung cancer cells A549, and its mechanism. Methods The effects of Triapine on the proliferation of A549 cells were assessed by MTT assay and colony formation assay; the effect of intracellular ROS levels of Triapine treated A549 cells was studied by DCFH-DA probe; the intracellular glutathione (GSH) and lipid peroxides (LPO) levels of A549 cells were detected by the kits after treating with Triapine; the effects of Triapine on the expression of glutathione peroxidase 4 (GPX4) in A549 cells were analyzed by Western blot; the changes of GPX4 level and cell viability were evaluated for the cells intervened with ROS inhibitor. Results Triapine could inhibit the proliferation of A549 cells, and the IC

AIM: To investigate the anesthetic effect of remimazolam tosilate combined with remifentanil in elderly patients undergoing spinal surgery, and its impacts on hemodynamics, serum interleukin-1β (IL-1β) and C-X-C motif chemokine ligand 8 (CXCL8) level. METHODS: A total of 88 elderly patients who underwent spinal surgery in our hospital from May 2022 to May 2023 were randomly separated into an experimental group and a control group. The control group was given remifentanil, and the experimental group was anesthetized with remimazolam tosilate on the basis of the control group. The anesthesia effect, hemodynamic indicators, serum IL-1β and CXCL8 levels, and complication rate were compared between two groups. RESULTS: After different anesthesia regimens, the recovery time of spontaneous respiration, extubation time, and recovery time of the two groups were compared, and the experimental group were obviously shorter than the control group (P<0.05); compared with pre administration (T0), the fluctuation ranges of hemodynamic indexes, including heart rate (HR) and mean arterial pressure (MAP), in the experimental group after 1 min (T1), 5 min (T2), 10 min (T3) and after extubation (T4) of administration were obviously lower than those in the control group (P<0.05). After surgery, the levels of IL-1β and CXCL8 in the serum of the two groups obviously increased (P<0.05), but the experimental group showed a obvious decrease compared to the control group (P<0.05); there was no significant difference in the incidence of complications between the two groups (P>0.05). CONCLUSION: The combined anesthesia of remimazolam tosilate and remifentanil has an ideal effect and high clinical application value for elderly patients undergoing spinal surgery.

Chronic pancreatitis (CP) is a progressive and irreversible fibroinflammatory disorder, accompanied by pancreatic exocrine insufficiency and dysregulated gut microbiota. Recently, accumulating evidence has supported a correlation between gut dysbiosis and CP development. However, whether gut microbiota dysbiosis contributes to CP pathogenesis remains unclear. Herein, an experimental CP was induced by repeated high-dose caerulein injections. The broad-spectrum antibiotics (ABX) and ABX targeting Gram-positive (G⁺) or Gram-negative bacteria (G^-) were applied to explore the specific roles of these bacteria. Gut dysbiosis was observed in both mice and in CP patients, which was accompanied by a sharply reduced abundance for short-chain fatty acids (SCFAs)-producers, especially G⁺ bacteria. Broad-spectrum ABX exacerbated the severity of CP, as evidenced by aggravated pancreatic fibrosis and gut dysbiosis, especially the depletion of SCFAs-producing G⁺ bacteria. Additionally, depletion of SCFAs-producing G⁺ bacteria rather than G^- bacteria intensified CP progression independent of TLR4, which was attenuated by supplementation with exogenous SCFAs. Finally, SCFAs modulated pancreatic fibrosis through inhibition of macrophage infiltration and M2 phenotype switching. The study supports a critical role for SCFAs-producing G⁺ bacteria in CP. Therefore, modulation of dietary-derived SCFAs or G⁺ SCFAs-producing bacteria may be considered a novel interventive approach for the management of CP.

Functional membrane microdomains (FMMs) that are mainly composed of scaffold proteins and polyisoprenoids play important roles in diverse cellular physiological processes in bacteria. The aim of this study was to identify the correlation between MK-7 and FMMs and then regulate the MK-7 biosynthesis through FMMs. Firstly, the relationship between FMMs and MK-7 on the cell membrane was determined by fluorescent labeling. Secondly, we demonstrated that MK-7 is a key polyisoprenoid component of FMMs by analyzing the changes in the content of MK-7 on cell membrane and the changes in the membrane order before and after destroying the integrity of FMMs. Subsequently, the subcellular localization of some key enzymes in MK-7 synthesis was explored by visual analysis, and the intracellular free pathway enzymes Fni, IspA, HepT and YuxO were localized to FMMs through FloA to achieve the compartmentalization of MK-7 synthesis pathway. Finally, a high MK-7 production strain BS3AT was successfully obtained. The production of MK-7 reached 300.3 mg/L in shake flask and 464.2 mg/L in 3 L fermenter.
Bacillus subtilis/metabolism* ; Vitamin K 2/metabolism* ; Bioreactors/microbiology* ; Membrane Microdomains/metabolism*

OBJECTIVE: To evaluate the clinical outcomes of reverse total shoulder arthroplasty as a revision procedure for the failed fixation of proximal humeral fractures in the elderly patients. METHODS: A retrospective analysis was performed on 8 patients with failed internal fixation of proximal humeral fractures from May 2014 to March 2020, including 3 males and 5 females, aged from 65 to 75 years old. All 8 patients underwent reverse total shoulder arthroplasty, and the mean time between initial fixation and reverse total shoulder arthroplasty ranged from 8 to 16 months. Range of motion(ROM), University of California at Los Angeles(UCLA) shoulder score, visual analogue scale (VAS), self-rating anxiety scale(SAS), and Constant-Murley score of shoulder function were assessed pre-operatively and at the last follow-up. Complications relating to the surgery were recorded. RESULTS: All 8 patients successfully followed up. The mean follow-up after reverse total shoulder arhroplasty ranged from 16 to 28 months. The range of motion (forward flexion, external rotation, abduction and internal rotation) of the affected shoulder was significantly improved after surgery, and the post-operative VAS, SAS and UCLA scores were also significantly improved. For the Constant-Murley score of shoulder joint function, the total scores and the subscores of pain, daily activities, range of motion and strength test at the last follow-up were all significantly improved. Scapular glenoid notch was observed in patient, which was evaluated as grade 1 on imaging. All the other patients did not develop specific or non-specific complications. CONCLUSION Reverse total shoulder arhroplasty is an appropriate treatment as a revision surgery for failed fixation of proximal humeral fractures. It has shown satisfactory clinical outcomes, accelerating the rehabilitation of shoulder function and improving the quality of life.
Male ; Female ; Humans ; Aged ; Shoulder/surgery* ; Arthroplasty, Replacement, Shoulder/methods* ; Retrospective Studies ; Treatment Outcome ; Quality of Life ; Shoulder Joint/surgery* ; Shoulder Fractures/surgery* ; Humerus/surgery* ; Range of Motion, Articular

Objective:To investigate the relationship between peripheral blood helper T cell 1/helper T cell 2 (Th1/Th2), helper T cell 17/regulatory T cell (Th17/Treg) and efficacy of programmed death receptor 1 (PD-1) inhibitor in patients with advanced non-small cell lung cancer (NSCLC) combined with chronic obstructive pulmonary disease (COPD).Methods:The clinical data of 107 patients with advanced NSCLC combined with COPD who were admitted to Suzhou Ninth Hospital Affiliated to Soochow University from April 2021 to September 2022 were retrospectively analyzed. The patients were treated with PD-1 inhibitor, and they were categorized into the disease control group (82 cases) and the disease progression group (25 cases) according to the clinical efficacy. Th1/Th2, Th17/Treg and clinical data of patients before treatment were compared between the two groups, and logistic regression was used to analyze the independent influencing factors of patients' PD-1 inhibitor efficacy.Results:Th1/Th2 and Th17/Treg before treatment in the disease control group were higher than those in the disease progression group (12.49±1.14 vs. 7.04±1.06, t = 21.26, P < 0.001; 0.14±0.03 vs. 0.09±0.04, t = 6.72, P < 0.001). The proportions of patients with TNM stage Ⅳ, lymph node metastasis and brain metastasis in the disease progression group were higher than those in the disease control group (all P < 0.01). The results of multivariate logistic regression analysis showed that pre-treatment Th1/Th2 ( OR = 0.744, 95% CI 0.685-0.799, P < 0.001), pre-treatment Th17/Treg ( OR = 0.514, 95% CI 0.465-0.552, P < 0.001), TNM stage ( OR = 1.258, 95% CI 1.049-1.656, P = 0.048), lymph node metastasis ( OR = 1.790, 95% CI 1.223-2.734, P = 0.005), and brain metastasis ( OR = 1.640, 95% CI 1.184-2.348, P = 0.005) were independent influencing factors of PD-1 inhibitor efficacy in patients with advanced NSCLC combined with COPD. Conclusions:Patients with advanced NSCLC combined with COPD who have high Th1/Th2 and Th17/Treg before treatment have good outcomes with PD-1 inhibitor therapy.

More than 150 glycosylphosphatidylinositol (GPI)-anchored proteins (GPI-APs) are expressed in mammalian cells and involved in various physiological processes such as immune recognition, cell communication and signal transduction. GPI is transferred to proteins in the endoplasmic reticulum (ER). When GPI-anchoring is impaired, precursor proteins are thought to be degraded through ER-associated degradation (ERAD). However, the mechanism of their degradation in ERAD remains unclear. To investigate the impact of ERAD pathways on degradation of GPI precursor proteins, we used series of knockout (KO) human embryonic kidney 293 (HEK293) cells defective in PIGS gene, which encodes a GPI transamidase complex subunit, combined with KO in HRD1 (PIGS-HRD1-KO) or GP78 (PIGSGP78-KO), which encodes the E3 ubiquitin ligases for the ERAD pathways. We compared the stability of 16 GPI precursor proteins in the ERAD-deficient cells with the parental PIGS-KO cells. Western blotting data showed that the GPI precursor proteins were stabilized in either PIGS-HRD1-KO (I