As a fundamental aspect of bone fracture treatment, fracture reduction plays a decisive role in restoring the structural integrity and function of bones. At present, fracture reduction techniques mostly rely on semi-automatic interaction methods or healthy-side bone templates for registration, which have many limitations in clinical practice. In order to enhance treatment efficiency and accuracy, an automatic fracture reduction algorithm is proposed. This algorithm utilizes the similarity of fracture cross-sections for registration, thereby reducing the workload of physicians and eliminating the need for a healthy-side bone template. Initially, the closed edge is identified and extracted by analyzing the differences in the fracture surface and the calorific value diagram of the roughness distribution. Next, the fracture section is determined by using the identified closed edge as a guideline for regional expansion and similarity matching. During the registration phase, the iterative closest point (ICP) algorithm is highly sensitive to distance. Therefore, the geometric features of point clouds are incorporated into the objective function of the registration algorithm to mitigate the influence of noise, and fracture section registration is implemented one by one. Finally, the algorithm is tested and compared on 180 simulated datasets and 16 publicly available datasets. The results show that the proposed algorithm significantly improves the registration accuracy, and the registration error of clinical bone fracture cases is controlled within 1.7 mm.
Algorithms ; Fractures, Bone/therapy* ; Humans

OBJECTIVE: To identify early potential risk factors for hospital-acquired pneumonia (HAP) in patients with mild traumatic brain injury (mTBI), construct a risk prediction model, and evaluate its predictive efficacy. METHODS: A case-control study was conducted using clinical data from mTBI patients admitted to the neurosurgery department of Changzhou Second People's Hospital from September 2021 to September 2023. The patients were divided into two groups based on whether they developed HAP. Clinical data within 48 hours of admission were statistically analyzed to identify factors influencing HAP occurrence through univariate analysis. Least absolute shrinkage and selection operator (LASSO) regression analysis was employed for feature selection to identify the most influential variables. The dataset was divided into training and validation sets in a 7:3 ratio. A multivariate Logistic regression analysis was then performed using the training set to construct the prediction model, exploring the risk factors for HAP in mTBI patients and conducting internal validation in the validation set. Receiver operator characteristic curve (ROC curve), decision curve analysis (DCA), and calibration curve were utilized to assess the sensitivity, specificity, decision value, and predictive accuracy of the prediction model. RESULTS: A total of 677 mTBI patients were included, with 257 in the HAP group and 420 in the non-HAP group. The significant differences were found between the two groups in terms of age, maximum body temperature (MaxT), maximum heart rate (MaxHR), maximum systolic blood pressure (MaxSBP), minimum systolic blood pressure (MinSBP), maximum respiratory rate (MaxRR), cause of injury, and laboratory indicators [C-reactive protein (CRP), procalcitonin (PCT), neutrophil count (NEUT), erythrocyte sedimentation rate (ESR), fibrinogen (FBG), fibrinogen equivalent units (FEU), prothrombin time (PT), activated partial thromboplastin time (APTT), total cholesterol (TC), lactate dehydrogenase (LDH), prealbumin (PAB), albumin (Alb), blood urea nitrogen (BUN), serum creatinine (SCr), hematocrit (HCT), hemoglobin (Hb), platelet count (PLT), glucose (Glu), K⁺, Na⁺], suggesting they could be potential risk factors for HAP in mTBI patients. After LASSO regression analysis, the key risk factors were enrolled in the multivariate Logistic regression analysis. The results revealed that the cause of injury being a traffic accident [odds ratio (OR) = 2.199, 95% confidence interval (95%CI) was 1.124-4.398, P = 0.023], NEUT (OR = 1.330, 95%CI was 1.214-1.469, P < 0.001), ESR (OR = 1.053, 95%CI was 1.019-1.090, P = 0.003), FBG (OR = 0.272, 95%CI was 0.158-0.445, P < 0.001), PT (OR = 0.253, 95%CI was 0.144-0.422, P < 0.001), APTT (OR = 0.689, 95%CI was 0.578-0.811, P < 0.001), Alb (OR = 0.734, 95%CI was 0.654-0.815, P < 0.001), BUN (OR = 0.720, 95%CI was 0.547-0.934, P = 0.016), and Na⁺ (OR = 0.756, 95%CI was 0.670-0.843, P < 0.001) could serve as main risk factors for constructing the prediction model. Calibration curves demonstrated good calibration of the prediction model in both training and validation sets with no evident over fitting. ROC curve analysis showed that the area under the ROC curve (AUC) of the prediction model in the training set was 0.943 (95%CI was 0.921-0.965, P < 0.001), with a sensitivity of 83.6% and a specificity of 91.5%. In the validation set, the AUC was 0.917 (95%CI was 0.878-0.957, P < 0.001), with a sensitivity of 90.1% and a specificity of 85.0%. DCA indicated that the prediction model had a high net benefit, suggesting practical clinical applicability. CONCLUSIONS The cause of injury being a traffic accident, NEUT, ESR, FBG, PT, APTT, Alb, BUN, and Na⁺ are identified as major risk factors influencing the occurrence of HAP in mTBI patients. The prediction model constructed using these parameters effectively assesses the likelihood of HAP in mTBI patients.
Humans ; Risk Factors ; Case-Control Studies ; Logistic Models ; Healthcare-Associated Pneumonia/epidemiology* ; Brain Injuries, Traumatic/complications* ; Male ; Female ; ROC Curve ; Pneumonia/etiology* ; Middle Aged ; Adult

Excessive N-acetyl-p-benzoquinone imine(NAPQI)formation is a starting event that triggers oxidative stress and subsequent hepatocyte necrosis in acetaminophen(APAP)overdose caused acute liver failure(ALF).S-glutathionylation is a reversible redox post-translational modification and a prospective mechanism of APAP hepatotoxicity.Glutaredoxin-1(Glrx1),a glutathione-specific thioltransferase,is a primary enzyme to catalyze deglutathionylation.The objective of this study was to explored whether and how Glrx1 is associated with the development of ALF induced by APAP.The Glrx1 knockout mice(Glrx1-/-)and liver-specific overexpression of Glrx1(AAV8-Glrx1)mice were produced and underwent APAP-induced ALF.Pirfenidone(PFD),a potential inducer of Glrx1,was administrated preceding APAP to assess its protective effects.Our results revealed that the hepatic total protein S-glutathionylation(PSSG)increased and the Glrx1 level reduced in mice after APAP toxicity.Glrx1-/- mice were more sensitive to APAP overdose,with higher oxidative stress and more toxic metabolites of APAP.This was attributed to Glrx1 deficiency increasing the total hepatic PSSG and the S-glutathionylation of cytochrome p450 3a 11(Cyp3a11),which likely increased the activity of Cyp3a11.Conversely,AAV8-Glrx1 mice were defended against liver damage caused by APAP overdose by inhibiting the S-glutathionylation and activity of Cyp3a11,which reduced the toxic metabolites of APAP and oxidative stress.PFD precede administration upregulated Glrx1 expression and alleviated APAP-induced ALF by decreasing oxidative stress.We have identified the function of Glrx1 mediated PSSG in liver injury caused by APAP overdose.Increasing Glrx1 expression may be investigated for the medical treatment of APAP-caused hepatic injury.

Objective To verify that lncRNA-C21orF96 regulates the expression of miRNA-875-5p and USF2 genes and promotes the invasion and metastasis of gastric cancer.Methods RT-PCR was used to measure the expression of lncRNA-C21orF96 related miRNA in gastric cancer cells.pcDNA3.1 plasmid was used to over-express lncRNA-C21orF96 in KATO-Ⅲ and siRNA was used to knockdown the expression of lncRNA-C21orF96 in SGC-7901,and RT-PCR was used to measure the expression of miRNA-875-5p and USF2 genes;By overexpressing lncRNA-C21orF96 in MKN45,transwell was used to observe changes of cells invasion and migration.Results LncRNA-C21orF96 showed a significant inverse relationship with miR-875-5p,(SGC-7901:21.19 ±1.09 vs.3.28 ±0.06,P＜0.01;SNU-16:24.76 ±2.09 vs.8.16 ±0.07,P ＜ 0.01).In KATO-Ⅲ over-expressing lncRNA-C21 orF96,miR-875-5p expression decreased significantly while USF2 expression increased (P ＜0.01);In SGC-7901 with lncRNA-C21orF96 knockdown,miR-875-5p expression increased significantly while USF2 expression decreased (P ＜ 0.05).The number of cells passing through the artificial basement membrane in the experimental group was significantly different from that in the control group (migration:216.19 ± 2.30 vs.89.19 ± 4.60,P＜0.001;invasion:146.18 ±5.3 vs.59.18 ± 2.60,P ＜ 0.001).Conclusions The overexpression of lncRNA-C21orF96 significantly reduces the expression of miR-875-5p and promotes the expression of USF2,hence promoting the invasion and metastasis of gastric cancer.

Objective To evaluate the efficacy of liraglutide in the treatment of Nonalcoholic Fatty Liver Disease(NAFLD).Methods Randomized controlled trials(RCTs)that evaluated the efficacy of liraglutide for NAFLD treatment were searched in multiple databases,including Pubmed,EMBASE,the Cochrane library,CNKI,Wanfang database and VIP.Literature identification and data extraction were based on the inclusion and exclusion criteria.RevMan 5.3 software was used for Meta-analysis.Results A total of 7 RCTs with 500 patients of NAFLD were included.Improved liver histology,or improved the level of alanine aminotransferase[WMD=-25.32,95％CI(-37.22,-13.41),P<0.01] and aspartate aminotransferase[WMD=-24.56,95％CI(-35.10,-14.03),P<0.01] were seen in 12-48 weeks liraglutide treatment.However,liraglutide could not decreased the level of serum cholesterol[WMD=-14.38,95％CI(-48.95,-20.20),P=0.42] and triglyceride[WMD=-15.55,95％CI(-36.20,-5.10),P=0.14].Conclusion liraglutide has the therapeutic effect of NAFLD.

Objective To investigate pulmonary capillary changes in patients with diabetes mellitus. Meth-otis Fifty-eight patients with diabetes mellitus were enrolled and forty-seven healthy subjects were taken as control. Diffusion capacity of carbonmonoxide (DLCO) and pulmonary ventilatory function were measured. DM and Vc were measured in twenty-one patients and twelve healthy subjects among them. Results FEV1/FVC was (81.02± 6.40) % in patients with diabetes mellitus and ( 81.20±6.96 ) % in controls, and FEV 1% was ( 102.03±14.40) in patients with diabetes mellitus and 103.94±11.42 in controls ,with no significant difference between patients with DLCO% was ( 72.79±19.85 ) % in patients with diabetes mellitus and ( 90.60±13.25 ) % in controls with a sig-patients whose course of disease was less than ten years,and DLCO% was (64.69±17.49)% in patients with dia-betes mellitus whose course of disease is equal or more than ten years and (80.90±18.98)% in patients whose course of disease is less than ten years,with significant difference between these two groups (t = 4.435, -3. 381, 13.88)% in patients with diabetes mellitas and (83.58±26.79)% in controls with a significant difference (t = 4. 612, P < 0.001 ). Vc was ( 61.40±52.84 ) ml in patients with diabetes mellitus and ( 66.99±19.63 ) ml in con-trols with no significant difference (P > 0.05 ), and Vc% was (78.05±64. 40)% in patients with diabetes mellitus and (79.33±23.32) % in controls, with no significant difference ( P > 0.05 ). Conclusions Diffusing capacity is decreased in patients with diabetes mellitus, which is related to the course of disease . DM decline is the main cause of DLCO decrease in patients with diabetes mellitus.