Rhabdomyolysis (RM) frequently gives rise to diverse complications, ultimately leading to an unfavorable prognosis for patients. Consequently, there is a pressing need for early prediction of survival rates among RM patients, yet reliable and effective predictive models are currently scarce. All data utilized in this study were sourced from the MIMIC-IV database. A multivariable Cox regression analysis was conducted on the data, and the performance of the new model was evaluated based on the Harrell's concordance index (C-index) and the area under the receiver operating characteristic curve (AUC). Furthermore, the clinical utility of the predictive model was assessed through decision curve analysis (DCA). A total of 725 RM patients admitted to the intensive care unit (ICU) were included in the analysis, comprising 507 patients in the training cohort and 218 patients in the testing cohort. For the development of the predictive model, 37 variables were carefully selected. Multivariable Cox regression revealed that age, phosphate max, RR mean, and SOFA score were independent predictors of survival outcomes in RM patients. In the training cohort, the AUCs of the new model for predicting 28-day, 60-day, and 90-day survival rates were 0.818 (95% CI: 0.766-0.871), 0.810 (95% CI: 0.761-0.855), and 0.819 (95% CI: 0.773-0.864), respectively. In the validation cohort, the AUCs of the new model for predicting 28-day, 60-day, and 90-day survival rates were 0.840 (95% CI: 0.772-0.900), 0.842 (95% CI: 0.780-0.899), and 0.842 (95% CI: 0.779-0.897), respectively. This study identified crucial demographic factors, vital signs, and laboratory parameters associated with RM patient prognosis and utilized them to develop a more accurate and convenient prognostic prediction model for assessing 28-day, 60-day, and 90-day survival rates. This study specifically targets patients with RM admitted to ICU and presents a novel clinical prediction model that surpasses the conventional SOFA score. By integrating specific prognostic indicators tailored to RM, the model significantly enhances prediction accuracy, thereby enabling a more targeted and effective approach to managing RM patients.
Diabetic wounds are a common complication in diabetes patients. Due to peripheral nerve damage and vascular dysfunction, diabetic wounds are prone to progress to local ulcers, wound gangrene and even to require amputation, bringing huge psychological and economic burdens to patients. However, the current treatment methods for diabetic wounds mainly include wound accessories, negative pressure drainage, skin grafting and surgery; there is still no ideal treatment to promote diabetic wound healing at present. Appropriate animal models can simulate the physiological mechanism of diabetic wounds, providing a basis for translational research in treating diabetic wound healing. Although there are no animal models that can fully mimic the pathophysiological mechanisms of diabetic wounds in humans, it is vital to explore animal simulation models used in basic research and preclinical studies of diabetic wounds. In addition, hydrogel materials are regarded as a promising treatment for diabetic wounds because of their good antimicrobial activity, biocompatibility, biodegradation and appropriate mechanical properties. Herein, we review and discuss the different animal models used to investigate the pathological mechanisms of diabetic wounds. We further discuss the promising future application of hydrogel biomaterials in diabetic wound healing.
Primary mucinous lung adenocarcinoma, a subtype of lung adenocarcinoma, is extremely rare. Currently, as there are no specific diagnostic features, it is easy to delay the diagnosis or even to misdiagnose when atypical symptoms are present.This case details a patient with primary mucinous lung adenocarcinoma and metastasis to the femoral head. The sole symptom was left hip pain and the initial diagnosis was isolated femoral head necrosis.By presenting this rare case report and the experiences learned from it, we hope to assist clinicians to identify bone metastasis cases with non-typical symptoms in order to make the correct diagnosis as soon as possible.
A coronal comminuted femoral intertrochanteric fracture is a special type of fracture that easily leads to internal fixation failure, and the current internal fixation techniques remain controversial. This study aims to evaluate the effect of traction-bed-assisted reduction and double-plate internal fixation in the treatment of comminuted and coronally split intertrochanteric femoral fracture.Retrospective analyses of the clinical data of 83 patients diagnosed with, and treated for, comminuted and coronally split intertrochanteric femoral fracture from December 2017 to November 2019 were conducted. Among the total number of 83 patients, 40 patients received traction-bed-assisted reduction and PFNA fixation (the control group), whereas 43 patients received traction-bed-assisted reduction and double-plate internal fixation (the experimental group). The major indicators for the research analysis such as the general information of patients, perioperative data, and follow-up data of both groups were collected, sorted out, and meticulously analyzed.The time taken for traction-bed-assisted reduction and double-plate intern fixation in the experimental group was significantly shorter than that in the control group (P < .05). The post-operative Harris Hip Score (HHS) at 3 months and at the final follow-up after the surgery was significantly better in the experimental group compared with that in the control group, both of which were statistically significant (P < .05). However, there were statistically no significant differences between the two groups in terms of preoperative hemoglobin (Hb) level, amount of intraoperative total blood loss, immediate post-operative Hb level, incidence of wound infection within 14 days post-operatively, time taken to step up on the ground after surgery, HHS 2 weeks after surgery, time taken for fracture healing, and the incidence of complications (P > .05).The use of a traction bed to achieve adequate reduction, followed by internal fixation using double plates, comparatively takes less time for both reduction and operation in the treatment of comminuted and coronally split intertrochanteric femoral fractures, which also restores proper hip joint movements relatively early and hence provides better hip joint functions in the long run.
Abstract Background: We aimed to compare the efficacy and functional outcomes of using an acromioclavicular joint hook plate (AJHP) versus a locking plate (LP) in the treatment of anterior sternoclavicular joint dislocation. Methods: Seventeen patients with anterior sternoclavicular joint dislocation were retrospectively analyzed from May 2014 to September 2019. Six patients were surgically treated with an AJHP, and 11 were surgically treated with an LP. Five male and one female patients composed the AJHP group, and nine male and two female patients composed the LP group. The mean age of all patients was 49.5 years. Results: Reduction and fixation were performed with AJHP or LP in all 17 patients. All patients were followed up for a mean duration of 14.4 months. There were no reported complications, wound infections, or instances of plate or screw breakage. The mean operative blood loss, operative time, and length of incision in the AJHP group were significantly better than those in the LP group. Shoulder girdle movement of the AJHP group was significantly better than that of the LP group. Conclusions: This study revealed that AJHP facilitated glenohumeral joint motion, reduced the risk of rupture of mediastinal structures, required a shorter incision, and had lesser blood loss and a shorter duration of operation compared with LP. However, some deficiencies require further improvement.
Patients who suffered a traumatic brain injury (TBI) show a faster fracture healing than patients with isolated fractures. Prior studies have suggested that this process may be accelerated through the inhibition of key microRNAs. In this study, we aimed to explore the mechanisms underlying this phenomenon, with a special focus on miR-16-5p, which is markedly decreased in patients with TBI. In vitro, miR-16-5p over-expression significantly inhibited cell proliferation in MC3T3-E1 cells transfected with agomiR-16-5p. Flow cytometry analysis further demonstrated that the overexpression of miR-16-5p induced cell cycle G1/S phase arrest and apoptosis. Moreover, target prediction and luciferase reporter assay demonstrated that miR-16-5p could negatively regulate Bcl-2 and Cyclin-D1 expression. Meanwhile, Bcl-2 and Cyclin-D1 were up-regulated after osteogenic differentiation while the down-regulation of endogenous Bcl-2 and Cyclin-D suppressed the osteogenic differentiation of MC3T3-E1 cells. In vivo, PBS, agomiR-16-5p and antagomiR-16-5p were injected into fracture sites to assess any improvements in fracture healing, which further confirmed the negative effect of miR-16-5p on fracture healing. Together, these results demonstrate miR-16-5p downregulation may accelerate fracture healing by enhancing the proliferation and inhibiting the apoptosis of osteoblasts in patients with both fractures and TBI. These phenomena may be exploited in the treatment of fractures.
Hexokinase (HXK) family proteins exert critical roles in catalyzing hexose phosphorylation, sugar sensing, and modulation of plant growth and stress adaptation. Nevertheless, a large amount remains unknown about the molecular profile of HXK enzymes in Populus trichocarpa, a woody model tree species. A genome-wide survey of HXK-encoding genes, including phylogenies, genomic structures, exon/intron organization, chromosomal distribution, and conserved features, was conducted, identifying six putative HXK isogenes (PtHXK1-6) in the Populus genome. The evolutionary tree demonstrated that 135 homologous HXKs between 17 plant species were categorized into four major subfamilies (type A, B, C, and D), clustering one plastidic (PtHXK3) and five mitochondrial PtHXKs grouped into type A and B, respectively. The in silico deduction prompted the presence of the conserved sugar-binding core (motif 4), phosphorylation sites (motif 2 and 3), and adenosine-binding domains (motif 7). The transcriptomic sequencing (RNA-seq) and the quantitative real-time PCR (qRT-PCR) assays revealed that three isogenes (PtHXK2, 3, and 6) were abundantly expressed in leaves, stems, and roots, while others appeared to be dominantly expressed in the reproductive tissues. Under the stress exposure, PtHXK2 and 6 displayed a significant induction upon the pathogenic fungi (Fusarium solani) infection and marked promotions by glucose feeding in roots. In contrast, the PtHXK3 and 6 are ABA-responsive genes, following a dose-dependent manner. The comprehensive analyses of the genomic patterns and expression profiling provide theoretical clues and lay a foundation for unraveling the physiological and signaling roles underlying the fine-tuned PtHXKs responding to diverse stressors.
Mesenchymal stem cells (MSCs) critically contribute to bone formation, and proper induction of osteogenic differentiation can lead to an increase in bone mass. In the present study, we reported that an increased miR-194-5p level in plasma is inversely related to the degree of bone formation in osteoporosis patients. We also noted that increased miR-194-5p in the MSCs of ovariectomized (OVX) mice and agomiR-194-5p manipulation of miR-194-5p significantly suppressed bone formation, both in aged and OVX mice. Furthermore, our in vitro study showed that overexpression of miR-194-5p suppresses osteogenic differentiation, as evidenced by the decreased bone formation marker genes and matrix mineralization. The luciferase assay indicated that Wnt family member 5a (Wnt5a) is a target gene of miR-194-5p that positively regulates osteogenic differentiation. Collectively, these data indicated that miR-194-5p inhibition may be a potential strategy for osteoporosis prevention. Mesenchymal stem cells (MSCs) critically contribute to bone formation, and proper induction of osteogenic differentiation can lead to an increase in bone mass. In the present study, we reported that an increased miR-194-5p level in plasma is inversely related to the degree of bone formation in osteoporosis patients. We also noted that increased miR-194-5p in the MSCs of ovariectomized (OVX) mice and agomiR-194-5p manipulation of miR-194-5p significantly suppressed bone formation, both in aged and OVX mice. Furthermore, our in vitro study showed that overexpression of miR-194-5p suppresses osteogenic differentiation, as evidenced by the decreased bone formation marker genes and matrix mineralization. The luciferase assay indicated that Wnt family member 5a (Wnt5a) is a target gene of miR-194-5p that positively regulates osteogenic differentiation. Collectively, these data indicated that miR-194-5p inhibition may be a potential strategy for osteoporosis prevention.
Although osteoporosis is one of the most common chronic age-related diseases, there is currently no gold standard for treatment. Evidence suggests resveratrol, a natural polyphenolic compound, may be helpful in the treatment of osteoporosis and other diseases. However, the molecular mechanisms underlying the anti-osteoporotic effects of resveratrol remain largely unknown. In the present study, KEGG pathway enrichment analysis of resveratrol-targeted genes identified 33 associated pathways, 12 of which were also involved in osteoporosis. In particular, the MDM2/p53 signaling pathway was identified as a potential key pathway among the shared pathways. In vitro experiments indicated that MDM2-mediated p53 degradation induced osteoblast differentiation, and resveratrol could partially reverse p53-dependent inhibition of osteogenic differentiation. These findings suggest resveratrol may alleviate osteoporosis at least in part by modulating the MDM2/p53 signaling pathway.
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