Gender differences and risk factors for acute kidney injury following cardiac surgery: A single center retrospective cohort study

Background: We studied AKI incidence and prognosis in cardiac surgery patients under and over 60 years old. Methods: We studied AKI in patients who underwent cardiac surgery at the First Affiliated Hospital of Wenzhou Medical University between Jan 2020 and Dec 2021, using improved global prognostic criteria for diagnosis. Results: After analyzing 781 patients (402 males, 379 females), AKI incidence after surgery was 30.22 %. Adjusting for propensity scores revealed no significant difference in AKI incidence between young males (24.1 %) and females (19.3 %). However, young females had higher AKI stages. Among older patients, AKI incidence was comparable between males (43.4 %) and females (42.2 %), but females had longer intubation times. Independent risk factors for AKI included age, male gender, and BMI, while intraoperative hemoglobin level was protective. Conclusions: No gender gap in AKI frequency for <60 years old and ≥60 years old post-cardiac surgery, yet women display increased AKI severity and extended intubation duration

Calcium/Calmodulin-Dependent Protein Kinase IV Mediates IFN-γ-Induced Immune Behaviors in Skeletal Muscle Cells

Background/Aims: Whether calcium/calmodulin-dependent protein kinase IV (CaMKIV) plays a role in regulating immunologic features of muscle cells in inflammatory environment, as it does for immune cells, remains mostly unknown. In this study, we investigated the influence of endogenous CaMKIV on the immunological characteristics of myoblasts and myotubes received IFN-γ stimulation. Methods: C2C12 and murine myogenic precursor cells (MPCs) were cultured and differentiated in vitro, in the presence of pro-inflammatory IFN-γ. CaMKIV shRNA lentivirus transfection was performed to knockdown CaMKIV gene in C2C12 cells. pEGFP-N1-CaMKIV plasmid was delivered into knockout cells for recovering intracellular CaMKIV gene level. CREB1 antagonist KG-501 was used to block CREB signal. qPCR, immunoblot analysis, or immunofluorescence was used to detect mRNA and protein levels of CaMKIV, immuno-molecules, or pro-inflammatory cytokines and chemokines. Co-stimulatory molecules expression was assessed by FACS analysis. Results: IFN-γ induces the expression or up-regulation of MHC-I/II and TLR3, and the up-regulation of CaMKIV level in muscle cells. In contrast, CaMKIV knockdown in myoblasts and myotubes leads to expression inhibition of the above immuno-molecules. As well, CaMKIV knockdown selectively inhibits pro-inflammatory cytokines/chemokines, and co-stimulatory molecules expression in IFN-γ treated myoblasts and myotubes. Finally, CaMKIV knockdown abolishes IFN-γ induced CREB pathway molecules accumulation in differentiated myotubes. Conclusions: CaMKIV can be induced to up-regulate in muscle cells under inflammatory condition, and positively mediates intrinsic immune behaviors of muscle cells triggered by IFN-γ

Basic Perforator Flap Hemodynamic Mathematical Model.

BACKGROUND: A mathematical model to help explain the hemodynamic characteristics of perforator flaps based on blood flow resistance systems within the flap will serve as a theoretical guide for the future study and clinical applications of these flaps. METHODS: There are 3 major blood flow resistance network systems of a perforator flap. These were defined as the blood flow resistance of an anastomosis between artery and artery of adjacent perforasomes, between artery and vein within a perforasome, and then between vein and vein corresponding to the outflow of that perforasome. From this, a calculation could be made of the number of such blood flow resistance network systems that must be crossed for all perforasomes within a perforator flap to predict whether that arrangement would be viable. RESULTS: The summation of blood flow resistance networks from each perforasome in a given perforator flap could predict which portions would likely survive. This mathematical model shows how this is directly dependent on the location of the vascular pedicle to the flap and whether supercharging or superdrainage maneuvers have been added. These configurations will give an estimate of the hemodynamic characteristics for the given flap design. CONCLUSIONS: This basic mathematical model can (1) conveniently determine the degree of difficulty for each perforasome within a perforator flap to survive; (2) semiquantitatively allow the calculation of basic hemodynamic parameters; and (3) allow the assessment of the pros and cons expected for each pattern of perforasomes encountered clinically based on predictable hemodynamic observations

Effects of Venous Superdrainage and Arterial Supercharging on Dorsal Perforator Flap in a Rat Model

<div><p>Objective</p><p>To comparatively assess the effects of venous superdrainage and arterial supercharging on dorsal perforator flap survival.</p><p>Materials and Methods</p><p>Sixty male Sprague-Dawley rats (450–550g) were randomly divided into three groups (n = 20), including control group (Control) and experimental groups A (venous superdrainage, Exp. A) and B (arterial supercharging, Exp. B). At postoperative day 7, survival areas of the flaps were evaluated and all animals underwent angiography. Laser Doppler was used to evaluate flap perfusion from 0h to 7days after surgery. Histology with hematoxylin and eosin staining was used to count microvessels. Tissue of “Choke vessels”was excised for quantification of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) by western blot assay at 6h and 7days after surgery.</p><p>Results</p><p>In the Exp. A group, almost all flaps survived (98.2±1.6%); in the Exp. B and control group, survival areas accounted for 78.8±8.5% and 60.3±7.8%, respectively (P <0.001). In addition, Exp. A animals showed improved <i>anastomosis</i> of choke vessels 2 compared with the Exp. B and Control groups. Furthermore, flap blood flow and <i>partial pressure of oxygen</i> in the Exp. A group were significantly higher compared with values obtained for the Exp. B and Control groups, from 6 hours to 7 days after surgery. <i>More microvessels</i> were found in the Exp. A group <i>(11</i>.<i>65±1</i>.<i>33) than in</i> Exp. B (<i>9</i>.<i>25±0</i>.<i>34)</i> and control (<i>7</i>.<i>25±0</i>.<i>91) animals on POD 7</i>. The relative expression level of HIF-1α and VEGF were significant at 6h and 7days after surgery.</p><p>Conclusions</p><p>Venous superdrainage in rat dorsal perforator flap is more effective than arterial supercharging in promoting flap survival, and could effectively alter hemodynamics in the microcirculation and stimulate blood vessel formation.</p></div

Average microvessel count in each group (AMC) at POD 7.

<p>Average microvessel count in each group (AMC) at POD 7.</p

Flap survival.

<p>Comparison of the flap survival, survival area was showed as means±SD.</p

Skin flap design and surgical procedure.

<p>Right dorsal perforator flap model measured 3×12 cm (Fig 1A), Experimental group A, posterior intercostal artery (PIA) was ligated while accompanying vein was preserved (Fig 1B); Experimental group B, posterior intercostal vein (PIV) was ligated while accompanying artery was preserved (Fig 1C); Control group, posterior intercostal artery and vein were ligated, only vascular pedicle (iliolumbar artery and vein, IAV) was preserved (Fig 1D). Finally, the flap was sutured back into its location (Fig 1E). “Choke vessels”: anastomosis area of perforator vessels, IAV: iliolumbar artery and vein, PIAV: posterior intercostal artery and vein, TDAV: thoracodorsal artery and vein.</p

Metastasis organotropism in colorectal cancer: advancing toward innovative therapies

Abstract Distant metastasis remains a leading cause of mortality among patients with colorectal cancer (CRC). Organotropism, referring to the propensity of metastasis to target specific organs, is a well-documented phenomenon in CRC, with the liver, lungs, and peritoneum being preferred sites. Prior to establishing premetastatic niches within host organs, CRC cells secrete substances that promote metastatic organotropism. Given the pivotal role of organotropism in CRC metastasis, a comprehensive understanding of its molecular underpinnings is crucial for biomarker-based diagnosis, innovative treatment development, and ultimately, improved patient outcomes. In this review, we focus on metabolic reprogramming, tumor-derived exosomes, the immune system, and cancer cell-organ interactions to outline the molecular mechanisms of CRC organotropic metastasis. Furthermore, we consider the prospect of targeting metastatic organotropism for CRC therapy

The schematic drawing of grouping.

<p>The schematic drawing of grouping.</p