Dual Function of Hydrogen Bond and CEI to Enhanced Lithium-Ion Battery Performance.

The stability of the commercial electrolyte is linked to the internal solvent molecule, particularly in enhancing the stability of these molecules. Hereby, we introduce a dual function strategy involving hydrogen bond induced solvent molecules and the in situ fabrication cathode-electrolyte interphase (CEI) to address this issue. The additive N-(4-(2,5-dioxo-4-oxazolidinyl)butyl)-2,2,2-trifluoroacetamide (DOTFA), with its oxazolidinyl and trifluoroacetamide functional units, establishes hydrogen bonds with the solvent, forming CEI films on the cathode surface that enhance the antioxidation ability of the electrolyte. These hydrogen bonds contribute to enhancing the high-pressure structural stability of the solvent molecule. Additionally, the uniform and robust in situ constructed CEI films act as a shield, protecting the cathode from various side reactions and enhancing interface compatibility. By incorporation of the DOTFA additive in the electrolyte, lithium-ion batteries with NCM811 cathodes exhibit excellent cycling performance. The work highlights the significance of dual function in solvent molecules and provides an effective method for enhancing the antioxidation ability of the electrolyte.

Relationship between stress hyperglycaemic ratio and incidence of in-hospital cardiac arrest in patients with acute coronary syndrome: a retrospective cohort study.

BACKGROUND: The stress hyperglycaemic ratio (SHR), a new marker that reflects the true hyperglycaemic state of patients with acute coronary syndrome (ACS), is strongly associated with adverse clinical outcomes in these patients. Studies on the relationship between the SHR and in-hospital cardiac arrest (IHCA) incidence are limited. This study elucidated the relationship between the SHR and incidence of IHCA in patients with ACS. METHODS: In total, 1,939 patients with ACS who underwent percutaneous coronary intervention (PCI) at the Affiliated Hospital of Zunyi Medical University were included. They were divided into three groups according to the SHR: group T1 (SHR ≤ 0.838, N = 646), group T2 (0.838< SHR ≤ 1.140, N = 646), and group T3 (SHR3 > 1.140, N = 647). The primary endpoint was IHCA incidence. RESULTS: The overall IHCA incidence was 4.1% (N = 80). After adjusting for covariates, SHR was significantly associated with IHCA incidence in patients with ACS who underwent PCI (odds ratio [OR] = 2.6800; 95% confidence interval [CI] = 1.6200-4.4300; p<0.001), and compared with the T1 group, the T3 group had an increased IHCA risk (OR = 2.1800; 95% CI = 1.2100-3.9300; p = 0.0090). In subgroup analyses, after adjusting for covariates, patients with ST-segment elevation myocardial infarction (STEMI) (OR = 3.0700; 95% CI = 1.4100-6.6600; p = 0.0050) and non-STEMI (NSTEMI) (OR = 2.9900; 95% CI = 1.1000-8.1100; p = 0.0310) were at an increased IHCA risk. After adjusting for covariates, IHCA risk was higher in patients with diabetes mellitus (DM) (OR = 2.5900; 95% CI = 1.4200-4.7300; p = 0.0020) and those without DM (non-DM) (OR = 3.3000; 95% CI = 1.2700-8.5800; p = 0.0140); patients with DM in the T3 group had an increased IHCA risk compared with those in the T1 group (OR = 2.4200; 95% CI = 1.0800-5.4300; p = 0.0320). The restriction cubic spline (RCS) analyses revealed a dose-response relationship between IHCA incidence and SHR, with an increased IHCA risk when SHR was higher than 1.773. Adding SHR to the baseline risk model improved the predictive value of IHCA in patients with ACS treated with PCI (net reclassification improvement [NRI]: 0.0734 [0.0058-0.1409], p = 0.0332; integrated discrimination improvement [IDI]: 0.0218 [0.0063-0.0374], p = 0.0060). CONCLUSIONS: In patients with ACS treated with PCI, the SHR was significantly associated with the incidence of IHCA. The SHR may be a useful predictor of the incidence of IHCA in patients with ACS. The addition of the SHR to the baseline risk model had an incremental effect on the predictive value of IHCA in patients with ACS treated with PCI.

Association of the triglyceride glucose-body mass index with the extent of coronary artery disease in patients with acute coronary syndromes.

BACKGROUND: Studies have shown that insulin resistance is strongly associated with the development of cardiovascular disease, and the triglyceride glucose-body mass index (TyG-BMI index) is considered to be a reliable surrogate marker of insulin resistance. There are limited studies on the relationship between TyG-BMI index and the extent of coronary artery disease in patients with acute coronary syndrome (ACS). This study aimed to investigate the relationship between TyG-BMI index and the extent of coronary artery disease in patients with ACS. METHODS: Overall, 2,317 patients with ACS who underwent percutaneous coronary intervention at the Affiliated Hospital of Zunyi Medical University were included in this study. The TyG-BMI index was grouped according to the tertile method. The extent of coronary artery disease in patients with ACS was quantitatively assessed using the SYNTAX score, which was categorised as low (≤ 22), intermediate (23-32), and high risk (≥ 33). RESULTS: In the overall population, multivariate logistic regression analyses showed that TyG-BMI index was associated with mid/high SYNTAX score in patients with ACS (odds ratio [OR] = 1.0041; 95% confidence interval [CI] = 1.0000-1.0079; p = 0.0310). Subgroup analyses showed that TyG-BMI index was an independent risk factor for mid/high SYNTAX score in female ACS patients after adjusting for multiple confounders (OR = 1.0100; 95% CI = 1.0000-1.0200; p = 0.0050), and that the risk of mid/high SYNTAX score was 2.49 times higher in the T3 group (OR = 2.4900; 95% CI = 1.2200-5.0600; p = 0.0120). Restricted cubic spline analysis showed a linear correlation between TyG-BMI index and complex coronary artery disease (SYNTAX score > 22) in women with ACS. In female ACS patients, inclusion of the TyG-BMI index did not improve the predictive power of the underlying risk model (net reclassification improvement: 0.0867 [-0.0256-0.1989], p = 0.1301; integrated discrimination improvement: 0.0183 [0.0038-0.0329], p = 0.0135). CONCLUSIONS: TyG-BMI index is linearly associated with the degree of complex coronary artery disease in female ACS patients. However, the inclusion of the TyG-BMI index did not improve the predictive power of the underlying risk model for female ACS patients.

Bow-and-arrow sign on point-of-care ultrasound for diagnosis of pacemaker lead-induced heart perforation: A case report and literature review.

BACKGROUND: Pacemaker lead-induced heart perforation is a rare but life-threatening complication of pacemaker implantation, and timely diagnosis remains a challenge for clinicians. Here, we report a case of pacemaker lead-induced cardiac perforation rapidly diagnosed by a "bow-and-arrow" sign on point-of-care ultrasound (POCUS). CASE SUMMARY: A 74-year-old Chinese woman who had undergone permanent pacemaker implantation 26 d before suddenly developed severe dyspnea, chest pain, and hypotension. The patient had received emergency laparotomy for an incarcerated groin hernia and was transferred to the intensive care unit 6 d before. Computed tomography was not available due to unstable hemodynamic status, so POCUS was performed at the bedside and revealed severe pericardial effusion and cardiac tamponade. Subsequent pericardiocentesis yielded a large volume of bloody pericardial fluid. Further POCUS by an ultrasonographist revealed a unique "bow-and-arrow" sign indicating right ventricular (RV) apex perforation by the pacemaker lead, which facilitated the rapid diagnosis of lead perforation. Given the persistent drainage of pericardial bleeding, urgent off-pump open chest surgery was performed to repair the perforation. However, the patient died of shock and multiple organ dysfunction syndrome within 24 h post-surgery. In addition, we also performed a literature review on the sonographic features of RV apex perforation by lead. CONCLUSION: POCUS enables the early diagnosis of pacemaker lead perforation at the bedside. A step-wise ultrasonographic approach and the "bow-and-arrow" sign on POCUS are helpful for rapid diagnosis of lead perforation.

Hyperoxia Provokes Time- and Dose-Dependent Gut Injury and Endotoxemia and Alters Gut Microbiome and Transcriptome in Mice.

Background: Oxygen therapy usually exposes patients to hyperoxia, which induces injuries in the lung, the heart, and the brain. The gut and its microbiome play key roles in critical illnesses, but the impact of hyperoxia on the gut and its microbiome remains not very clear. We clarified the time- and dose-dependent effects of hyperoxia on the gut and investigated oxygen-induced gut dysbiosis and explored the underlying mechanism of gut injury by transcriptome analysis. Methods: The C57BL/6 mice were randomly divided into the control group and nine different oxygen groups exposed to hyperoxia with an inspired O2 fraction (FiO2) of 40, 60, and 80% for 24, 72, and 168 h (7 days), respectively. Intestinal histopathological and biochemical analyses were performed to explore the oxygen-induced gut injury and inflammatory response. Another experiment was performed to explore the impact of hyperoxia on the gut microbiome by exposing the mice to hyperoxia (FiO2 80%) for 7 days, with the 16S rRNA sequencing method. We prolonged the exposure (up to 14 days) of the mice to hyperoxia (FiO2 80%), and gut transcriptome analysis and western blotting were carried out to obtain differentially expressed genes (DEGs) and signaling pathways related to innate immunity and cell death. Results: Inhaled oxygen induced time- and dose-dependent gut histopathological impairment characterized by mucosal atrophy (e.g., villus shortening: 80% of FiO2 for 24 h: P = 0.008) and enterocyte death (e.g., apoptosis: 40% of FiO2 for 7 days: P = 0.01). Administered time- and dose-dependent oxygen led to intestinal barrier dysfunction (e.g., endotoxemia: 80% of FiO2 for 72 h: P = 0.002) and potentiated gut inflammation by increasing proinflammatory cytokines [e.g., tumor necrosis factor alpha (TNF-α): 40% of FiO2 for 24 h: P = 0.003)] and reducing anti-inflammatory cytokines [Interleukin 10 (IL-10): 80% of FiO2 for 72 h: P < 0.0001]. Hyperoxia induced gut dysbiosis with an expansion of oxygen-tolerant bacteria (e.g., Enterobacteriaceae). Gut transcriptome analysis identified 1,747 DEGs and 171 signaling pathways and immunoblotting verified TLR-4, NOD-like receptor, and apoptosis signaling pathways were activated in oxygen-induced gut injury. Conclusions: Acute hyperoxia rapidly provokes gut injury in a time- and dose-dependent manner and induces gut dysbiosis, and an innate immune response is involved in an oxygen-induced gut injury.