Hypervirulent and multidrug resistant Klebsiella pneumoniae strains pose a significant threat to the public health. In the present study, 21 carbapenem-resistant K. pneumoniae isolates (CRKP) were determined by the string test as hypermucoviscous K. pneumoniae (HMKP), with the prevalence of 15.0% (21/140) among CRKP, and 1.1% (21/1838) among all K. pneumoniae isolates. Among them, 7 (33.3%), and 1 (4.76%) isolate belonged to capsular serotype K20 and K2 respectively, while 13 (61.9%, 13/21) weren't successfully typed by capsular serotyping. All the 21 isolates were carbapenemase-producers and were positive for bla_KPC-2. In addition to bla_KPC-2, all the 21 isolates except one harbor bla_SHV-11, and 15 carry extended-spectrum β-lactamase gene bla_CTX-M-65. The virulence-associated genes with more than 90% of positive rates among 21 isolates included ureA (100%, 21/21), wabG (100%, 21/21), fimH (95.2%, 20/21), entB (95.2%, 20/21), ycf (95.2%, 20/21), ybtS (95.2%, 20/21), and iutA (90.5%, 19/21). rmpA and aerobactin were found in 57.1% (12/21) isolates. Five sequence types (STs) were identified by multilocus sequence typing (MLST), including ST11 (11 K-non capsule typable and 5 K20 isolates), ST268 (1 K20 isolate and 1 K-non capsule typable isolate), ST65 (1 K2 isolate), ST692 (1 K-non capsule typable isolate), and ST595, a novel sequence type (1 K-non capsule typable isolate). Pulsed-field gel electrophoresis (PFGE) results showed two major PFGE clusters, of which cluster A accounts for 6 ST11 isolates (28.6%) and cluster B includes 8 ST11 isolates (38.1%, 8/21). Ten and six ST11 isolates were isolated from 2014 and 2015, respectively, while 8 were isolated from the same month of December in 2014. Ten isolates were collected from the intensive care unit (ICU), and all except one belonged to ST11. Additional 4 ST11 isolates were collected from patients in non-ICU wards, who had more than 10 days of ICU stay history in 2014 prior to transfer to their current wards where the isolates were recovered. Taken together, the present study showed a hospital outbreak and dissemination of ST11 HMKP with carbapenem resistance caused by KPC-2. Effective surveillance and strict infection control strategies should be implemented to prevent outbreak by HMKP with carbapenem resistance in hospitals.

Background: This study aimed to explore the association between the triglyceride-glucose (TyG) index and the risk of in-hospital mortality in critically ill patients with sepsis. Methods: This was a retrospective observational cohort study and data were obtained from the Medical Information Mart for Intensive Care-IV (MIMIC IV2.2) database. The participants were grouped into three groups according to the TyG index tertiles. The primary outcome was in-hospital all-cause mortality. Multivariable logistics proportional regression analysis and restricted cubic spline regression was used to evaluate the association between the TyG index and in-hospital mortality in patients with sepsis. In sensitivity analysis, the feature importance of the TyG index was initially determined using machine learning algorithms and subgroup analysis based on different subgroups was also performed. Results: 1,257 patients (56.88% men) were included in the study. The in-hospital, 28-day and intensive care unit (ICU) mortality were 21.40%, 26.17%, and 15.43% respectively. Multivariate logistics regression analysis showed that the TyG index was independently associated with an elevated risk of in-hospital mortality (OR 1.440 [95% CI 1.106–1.875]; P = 0.00673), 28-day mortality (OR 1.391; [95% CI 1.52–1.678]; P = 0.01414) and ICU mortality (OR 1.597; [95% CI 1.188–2.147]; P = 0.00266). The restricted cubic spline regression model revealed that the risks of in-hospital, 28-day, and ICU mortality increased linearly with increasing TyG index. Sensitivity analysis indicate that the effect size and direction in different subgroups are consistent, the results is stability. Additionally, the machine learning results suggest that TyG index is an important feature for the outcomes of sepsis. Conclusion: Our study indicates that a high TyG index is associated with an increased in-hospital mortality in critically ill sepsis patients. Larger prospective studies are required to confirm these findings.

Inflammation plays an important role in the initiation and progression of acute kidney injury (AKI). However, evidence regarding the prognostic effect of the platelet-to-lymphocyte ratio (PLR), a novel systemic inflammation marker, among patients with AKI is scarce. In this study, we investigated the value of the PLR in predicting the outcomes of critically ill patients with AKI. Patient data were extracted from the Multiparameter Intelligent Monitoring in Intensive Care Database III version 1.3. PLR cutoff values were determined using smooth curve fitting or quintiles and were used to categorize the subjects into groups. The clinical outcomes were 30-day and 90-day mortality in the intensive care unit (ICU). Cox proportional hazards models were used to evaluate the association between the PLR and survival. A total of 10,859 ICU patients with AKI were enrolled. A total of 2277 thirty-day and 3112 ninety-day deaths occurred. A U-shaped relationship was observed between the PLR and both 90-day and 30-day mortality, with the lowest risk being at values ranging from 90 to 311. The adjusted HR (95% CI) values for 90-day mortality given risk values < 90 and > 311 were 1.25 (1.12–1.39) and 1.19 (1.08–1.31), respectively. Similar trends were observed for 30-day mortality or when quintiles were used to group patients according to the PLR. Statistically significant interactions were found between the PLR and both age and heart rate. Younger patients (aged < 65 years) and those with more rapid heart rates (≥89.4 beats per minute) tended to have poorer prognoses only when the PLR was < 90, whereas older patients (aged ≥ 65 years) and those with slower heart rates ( 311 (P < 0.001 for age and P < 0.001 for heart rate). The preoperative PLR was associated in a U-shaped pattern with survival among patients with AKI. The PLR appears to be a novel, independent prognostic marker of outcomes in critically ill patients with AKI.

The spread of the coronavirus (SARS-CoV-2, COVID-19 for short) has caused a large number of deaths around the world. We summarized the data reported in the past few months and emphasized that the main causes of death of COVID-19 patients are DAD (Diffuse Alveolar Damage) and DIC (Disseminated intravascular coagulation). Microthrombosis is a prominent clinical feature of COVID-19, and 91.3% of dead patients had microthrombosis.Endothelial damage caused by SARS-CoV-2 cell invasion and subsequent host response disorders involving inflammation and coagulation pathways play a key role in the progression of severe COVID-19. Microvascular thrombosis may lead to microcirculation disorders and multiple organ failure lead to death.The characteristic pathological changes of DAD include alveolar epithelial and vascular endothelial injury, increased alveolar membrane permeability, large numbers of neutrophil infiltration, alveolar hyaline membrane formation, and hypoxemia and respiratory distress as the main clinical manifestations. DAD leads to ARDS in COVID-19 patients. DIC is a syndrome characterized by the activation of systemic intravascular coagulation, which leads to extensive fibrin deposition in the blood. Its occurrence and development begin with the expression of tissue factor and interact with physiological anticoagulation pathways. The down-regulation of fibrin and the impaired fibrinolysis together lead to extensive fibrin deposition.DIC is described as a decrease in the number of platelets and an increase in fibrin degradation products, such as D-dimer and low fibrinogen. The formation of microthrombus leads to the disturbance of microcirculation, which in turn leads to the death of the patient. However, the best prevention and treatment of COVID-19 microthrombosis is still uncertain.This review discusses the latest findings of basic and clinical research on COVID-19-related microthrombosis, and then we proposed the theory of microcirculation perfusion bundle therapy to explore effective methods for preventing and treating COVID-19-related microthrombosis. Further research is urgently needed to clarify how SARS-CoV-2 infection causes thrombotic complications, and how it affects the course and severity of the disease. To cultivate a more comprehensive understanding of the underlying mechanism of this disease. Raise awareness of the importance of preventing and treating microthrombosis in patients with COVID-19.

Bacterial infection and scar formation remain primary challenges in wound healing. To address these issues, we developed a decellularized pomelo peel (DPP) functionalized with an adhesive PVA-TSPBA hydrogel and antibacterial gallic acid/copper MOFs. The hybrid wound dressing demonstrates favorable biocompatibility. It does not impede the proliferation of fibroblasts or immune cells and can stimulate fibroblast migration, endothelial angiogenesis, and M2 macrophage polarization. Additionally, the dressing can scavenge reactive oxygen species (ROS) and provide antioxidant effects. Furthermore, DPP + MOF@Gel effectively inhibits the viability of S. aureus and E. coli in vitro and in vivo. The histological observations revealed enhanced granulation tissue formation, re-epithelialization, and angiogenesis in the DPP + MOF@Gel group compared to other groups. The local immune response also shifted from a pro-inflammatory to a pro-regenerative status with DPP + MOF@Gel treatment. The skin incision stitching experiment further exhibits DPP + MOF@Gel could reduce scar formation during wound healing. Taken together, the hybrid DPP + MOF@Gel holds great promise for treating bacteria-infected skin wounds and inhibiting scar formation during wound healing.