In recent years, the hemoglobin, albumin, lymphocyte, and platelet (HALP) score has emerged as a potential marker of immunological and nutritional status. This study aimed to evaluate the association between the HALP score and prognosis in patients with sepsis. This retrospective cohort study analyzed sepsis patients using clinical data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Patients were classified into Low-score and High-score groups. Confounding factors were controlled through propensity score matching (PSM) analysis. The primary outcome was 28-day mortality in individuals with sepsis. Survival probabilities between groups were compared using Kaplan-Meier curves. Multivariable Cox regression analysis and a smoothing spline fitting curve were employed to investigate the relationship between the HALP score and 28-day mortality. ROC curve analysis and subgroup analysis were performed to evaluate the predictive ability of the HALP score and its components. A total of 2,968 sepsis patients were included, with 809 (27.26%) deaths within 28 days. After PSM analysis, the High-score group had a 24% lower risk of 28-day mortality compared to the Low-score group (HR, 0.76; 95% CI, 0.64–0.91). In the unmatched cohort, the multivariable Cox regression model also indicated that the High-score group had a lower 28-day mortality risk (HR, 0.78; 95% CI, 0.67–0.91). The smoothing spline fitting curve showed a nonlinear relationship between the HALP score and 28-day mortality, with an inflection point at 24.69. When the HALP score was below 24.69, an increase of one point in the HALP score was associated with a 2% reduction in 28-day mortality (HR, 0.98; 95% CI, 0.97–0.99). The HALP score provided incremental predictive value for 28-day mortality when combined with the SOFA score. Albumin was identified as the most influential component of the HALP score. Among patients with sepsis, the HALP score exhibited a nonlinear relationship with 28-day mortality. An elevated HALP score is associated with reduced 28-day, 90-day, 360-day, and in-hospital mortality among sepsis patients.

Numerous studies have explored the suitability of biocompatible materials in regenerative medicine. Platelet concentrates are derived from centrifuged blood and are named according to their biological characteristics, such as platelet-rich plasma, platelet-rich fibrin and concentrated growth factor. Platelet concentrates have gained considerable attention in soft and hard tissue engineering. Indeed, multiple components of autologous platelet concentrates, such as growth factors, fibrin matrix and platelets, serve essential roles in wound healing. Current studies are focused on cutting-edge strategies to meet the requirements for tissue restoration by improving the properties of autologous platelet concentrates. In the present review, applications of platelet concentrates for tissue engineering are discussed, presenting a selection of recent advances and novel protocols. In addition, several aspects of these strategies, such as the advantages of lyophilized platelet concentrates and the combination of platelet concentrates with biomaterials, stem cells or drugs are discussed. The present review aims to summarize novel strategies using platelet concentrates to improve the outcomes of wound healing.

Background: Despite novel advances in screening, targeting and immunotherapies, early diagnosis and satisfactory treatments against hepatocellular carcinoma (HCC) remain formidable challenges. Given the unique advantages, carbon quantum dots (CQDs) become a smart theranostic nanomaterial for cancer diagnosis and therapy. Results: In this work, a type of bio-friendly CQDs, trichrome-tryptophan-sorbitol CQDs (TC-WS-CQDs), is synthesized from natural biocompatible tryptophan via the one-pot hydrothermal method. Compared with normal hepatocytes, a much stronger green fluorescence is detected in HCC cells, indicating the ability of TC-WS-CQDs to target HCC cells. Furthermore, green-emitting TC-WS-CQDs generate large amounts of reactive oxygen species (ROS), leading to autophagy of HCC cells. Additionally, the green-emitting TC-WS-CQDs perform significant tumor inhibition by inducing autophagy via p53-AMPK pathway in vitro and in vivo studies with almost no systemic toxicity. Conclusions: The results may highlight a promising anticancer nanotheranostic strategy with integration of diagnosis, targeting, and therapy. Graphical

Background: Serum calcium levels disorder have been reported to be associated with poor prognosis in different diseases. Studies on the association between serum calcium and outcomes of septic patients remained limited. The aim of this study is to investigate the association between serum calcium and 28-day mortality in septic patients. Method: Patients diagnosed with sepsis in the Medical Information Mart for Intensive Care III database were included. Patients were divided into five groups according to the quintiles of serum calcium levels, and their baseline characteristics were compared. Multivariate Cox regression models were used to assess the association between serum calcium and 28-day mortality. Smooth curve fitting and segmented regression models were used to visualize the association between serum calcium levels and 28-day mortality risk. The 28-day survival probability between five groups was analyzed using Kaplan-Meier curves. Results: A total of 3,016 patients with sepsis were enrolled, and the 28-day mortality rate was 35.64%. After adjusting for confounders, compared with the reference quintile (Q4: 9.00–9.50), the lowest serum calcium level quintile (Q1: 5.70–8.20) was independently associated with an increased risk of 28-day mortality (hazard ratio [HR], 2.12; 95% CI, 1.76–2.56). Smooth spline fitting revealed a U-shaped association between serum calcium and 28-day mortality. When serum calcium was 9.0 mg/dL, the 28-day mortality risk increased by 12% per unit increase in serum calcium (HR, 1.12; 95% CI, 1.04–1.20). Conclusion: A U-shaped association was observed between serum calcium levels and 28-day mortality in septic patients. Lower or higher serum calcium levels were associated with increased risk of 28-day mortality in septic patients.

A high recurrence rate and easy metastasis are two prominent clinical features of hepatocellular carcinoma (HCC), which is also the most common cause of cancer-related death. However, the molecular pathogenesis of HCC remains unclear. Soluble resistance-related calcium-binding protein (Sorcin) is highly expressed in a variety of tumor cell lines and multidrug-resistant cell lines and participates in the malignant progression of tumors by regulating apoptosis. Pyroptosis is also a form of programmed cell death that plays a crucial role in exerting tumor suppression function and evoking anti-tumor immune responses. However, there is no consensus that Sorcin promotes HCC progression by regulating pyroptosis. Our study manifested that Sorcin was considerably upregulated, whereas pyroptosis-associated proteins were significantly decreased in HCC tissues and cells. Sorcin silencing attenuated the proliferation, migration, and invasion of HCC cells. Knockdown of Sorcin activates pyroptosis, and overexpression of Sorcin inhibits pyroptosis, yet has no significant effect on apoptosis, ferroptosis, and autophagy in HCC cells. Furthermore, coimmunoprecipitation and immunofluorescence assays revealed that Sorcin interacted with NLRP3 inflammasome to regulate pyroptosis in HCC cells. Then, the NLRP3 inhibitor MCC950 inhibited the activation of Sorcin knockdown-induced pyroptosis and reversed the effect of Sorcin silencing-induced weakening of malignant biological behavior in HCC. Similarly, suppression of Caspase-1 reversed the inhibitory effect of Sorcin knockdown on the malignant progression of HCC via knockdown of Caspase-1 or the inhibitor VX765. Consistent with the in vitro results, the nude mouse experiment showed that Sorcin knockdown inhibited the growth of HCC by activating pyroptosis, while Caspase-1 knockdown partially restored the growth inhibition caused by Sorcin knockdown. Collectively, high Sorcin expression in HCC negatively regulates pyroptosis by interacting with the NLRP3 inflammasome to promote HCC proliferation, migration, and invasion. The results of this study provide a scientific basis for Sorcin as a new biomarker and potential therapeutic target for HCC.