Search

Objective: To solve the problems of poor accuracy and low sorting efficiency of the existing string fruits in robot sorting. Methods: Based on the structure of the high-speed parallel food sorting system, the improved SURF algorithm and the improved RANSAC algorithm were combined to locate the grab points of the food sorting robot, and a three-dimensional grab model was established to realize the automatic and stable grab of string fruits. Taking grapes as an example, the superiority and accuracy of the proposed method were verified by experiments. Results: Compared with the conventional method, the proposed method improved the average capture success rate by about 15.00% and the average capture time by 0.101 s. Conclusion: The food sorting robot can effectively improve the accuracy of the positioning of the holding points of string fruits, and has a high success rate.

Objective To investigate the role of proline-rich protein tyrosine kinase (Pyk2) in angiotensin Ⅱ(Ang Ⅱ)-induced cardiac hypertrophy and the underlying mechanism in rat. Methods Primary rat cardio-myocytes were isolated from rats and randomly divided into control group, Ang Ⅱ induction group (the dose of Ang Ⅱ was 100 nmol/L, cardiomyocytes were stimulated in the cell culture dish for 24 hours), Pyk2 inhibitor PF-431396 group (the dose of PF-431396 was 10 μmol/L, added to the cell culture dish 30 minutes in advance before Ang Ⅱ stimulation) and Ang Ⅱ induction group intervened by PF-431396 (the dose of Ang Ⅱ was 100 nmol/L, the dose of PF-431396 was 10 μmol/L). The size of cardiomyocytes was measured by α-actinin fluorescence staining. RT-qPCR was performed to detect the mRNA level of hypertrophic markers (ANP and β-MHC) in cardiomyocytes. The expressions of p-Pyk2, Pyk2 and p53 in cardiomyocytes were detected by Western blot analysis. Results Ang Ⅱ stimulation increased the surface area of cardiomyocytes and the mRNA level of hypertrophic markers(P＜0.05). In addition, the proteins of p-Pyk2 and p53 were increased(P＜0.05). However, after treatment of Pyk2 inhibitor PF-431396, moycardial hypertrophy was significantly improved and the protein level of Pyk2 and p53 decreased(P＜0.05). Conclusions Pyk2 promotes cardiomyocyte hypertrophy in rat induced by Ang Ⅱ through the p53 signaling pathway.

Intrahepatic cholangiocarcinoma (ICC) is an aggressive type of cancer, and its incidence and mortality rates are increasing worldwide. Mortalin is a highly conserved chaperone protein involved in multiple pathological and physiological processes, including anti-apoptosis, carcinogenesis and metastasis. The Bcl-2 family of proteins can be divided into pro-survival and pro-apoptotic members, including B-cell lymphoma 2 (Bcl-2) and Bcl-2-like protein 4 (Bax). The aim of the present study was to investigate the association between mortalin, Bcl-2 and Bax, as well as the prognostic significance of the combined expression of mortalin, Bcl-2 and Bax in ICC. Immunohistochemistry was used to determine the expression of mortalin, Bcl-2 and Bax in 116 ICC samples and to assess the association between expression of 3 markers and clinicopathological features of ICC patients. This revealed that ICC tumor tissues overexpressed mortalin and Bcl-2 and exhibited low expression of Bax in ICC tumor tissues compared with that in corresponding peritumoral samples. According to Pearson's correlation coefficient analysis, high expression of mortalin in ICC was positively correlated with Bcl-2 expression and negatively correlated with Bax expression. Furthermore, multiple linear regression analysis demonstrated that mortalin was positively associated with Bcl-2, but not with Bax, in patients with ICC. Patients with ICC exhibiting high expression of mortalin/Bcl-2 or low expression of Bax were closely associated with a malignant ICC phenotype, a relatively low overall survival rate and a high recurrence rate. Multivariate analysis indicated that mortalin and Bcl-2 were independent prognostic indicators for ICC patients. Meanwhile, the concomitant overexpression of mortalin and Bcl-2 and the low expression of Bax were independent markers for predicting a relatively poor prognosis of ICC. The overexpression of mortalin and Bcl-2 and/or the low expression of Bax are implicated in the anti-apoptotic effect and tumor progression of ICC. Mortalin or Bcl-2, or a combination of mortalin, Bcl-2 and Bax may be used to predict the prognosis of ICC, as well as potential therapeutic targets. [ABSTRACT FROM AUTHOR]

Background: Gallstones are common lesions that often require surgical intervention. Laparoscopic cholecystectomy is the treatment of choice for symptomatic gallstones. Preoperatively, the anatomical morphology of the cystic duct (CD), needs to be accurately recognized, especially when anatomical variations occur in the CD, which is otherwise prone to bile duct injury. However, at present, there is no optimal classification system for CD morphology applicable in clinical practice, and the relationship between anatomical variations in CDs and gallstones remains to be explored., Aim: To create a more comprehensive clinically applicable classification of the morphology of CD and to explore the correlations between anatomic variants of CD and gallstones., Methods: A total of 300 patients were retrospectively enrolled from October 2021 to January 2022. The patients were divided into two groups: The gallstone group and the nongallstone group. Relevant clinical data and anatomical data of the CD based on magnetic resonance cholangiopancreatography (MRCP) were collected and analyzed to propose a morphological classification system of the CD and to explore its relationship with gallstones. Multivariate analysis was performed using logistic regression analyses to identify the independent risk factors using variables that were significant in the univariate analysis., Results: Of the 300 patients enrolled in this study, 200 (66.7%) had gallstones. The mean age was 48.10 ± 13.30 years, 142 (47.3%) were male, and 158 (52.7%) were female. A total of 55.7% of the patients had a body mass index (BMI) ≥ 24 kg/m 2 . Based on the MRCP, the CD anatomical typology is divided into four types: Type I: Linear, type II: n-shaped, type III: S-shaped, and type IV: W-shaped. Univariate analysis revealed differences between the gallstone and nongallstone groups in relation to sex, BMI, cholesterol, triglycerides, morphology of CD, site of CD insertion into the extrahepatic bile duct, length of CD, and angle between the common hepatic duct and CD. According to the multivariate analysis, female, BMI (≥ 24 kg/m 2 ), and CD morphology [n-shaped: Odds ratio (OR) = 10.97, 95% confidence interval (95%CI): 5.22-23.07, P < 0.001; S-shaped: OR = 4.43, 95%CI: 1.64-11.95, P = 0.003; W-shaped: OR = 7.74, 95%CI: 1.88-31.78, P = 0.005] were significantly associated with gallstones., Conclusion: The present study details the morphological variation in the CD and confirms that CD tortuosity is an independent risk factor for gallstones., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflicts of interest., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Background: Cattle encephalon glycoside and ignotin injection (CEGI), a multitargeted neurotrophic drug, has been widely used in the treatment of central and peripheral nerve injuries, such as stroke, hypoxic ischemic encephalopathy, and diabetic neuropathy in the People's Republic of China. However, data regarding the effect of CEGI on Alzheimer's disease (AD) remain scarce. The present study aimed to investigate the effect of CEGI on learning and memory in an APPswe/PS1dE9 double-transgenic mouse model, a suitable animal model of AD, and elucidate its possible mechanisms., Materials and Methods: Five-month-old APP/PS1 mice were intraperitoneally administered 6.6 mL/kg or 13.2 mL/kg of CEGI for 1 month. After 1 month of administration, all mice received Morris water maze training and a probe test. Mouse brain sections were detected by standard biochemical and immunohistochemical measures., Results: CEGI treatment significantly improved the spatial learning and memory deficits and decreased cerebral amyloid-β42 levels in brain homogenates of APP/PS1 mice. CEGI treatment elevated the activities of superoxide dismutase, and reduced the levels of malondialdehyde. CEGI attenuated neuronal damage in the hippocampus of APP/PS1 mice and upregulated protein and gene expression of Bcl-2 and the ratio of Bcl-2/Bax. CEGI treatment decreased the number of Iba1(+) activated microglia in the cortex of the APP/PS1 mice., Conclusion: Our results showed that CEGI prevents memory impairment, possibly by decreasing the amyloid-β42 levels in APP/PS1 mice and inhibiting oxidative stress, apoptosis, and inflammation, making CEGI a promising therapeutic agent for AD.

The aim of the present study was to investigate the expression levels of transforming growth factor-β (TGF-β) receptor type II (TβRII) and DPC4/Smad4 in the TGF-β signaling pathway and the importance of these expression levels in non-small cell lung cancer (NSCLC). The mRNA and protein expression levels of TβRII and DPC4/Smad4 were detected by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively, in NSCLC and control nonlesional lung tissues of 60 patients. The protein expression levels of DPC4/Smad4 were detected by immunohistochemistry in paraffin-embedded samples of NSCLC. In addition, the correlations among the expression levels of TβRII and DPC4/Smad4 and their association with the clinical and pathological features of NSCLC were analyzed. The expression levels of TβRII and DPC4/Smad4 in NSCLC tissues were significantly lower when compared with the control nonlesional lung tissues (P<0.05). In addition, the expression of TβRII and DPC4/Smad4 in poorly-differentiated NSCLC tissues was significantly lower compared with moderately- or well-differentiated NSCLC tissues (P<0.05). The expression levels of TβRII and DPC4/Smad4 were significantly lower in NSCLC tissues with metastatic lymph nodes compared with tissue without metastatic lymph nodes (P<0.05). Thus, the expression levels were demonstrated to significantly correlate with the clinical and pathological stages, and subsequently were shown to be associated with the occurrence and progression of NSCLC. In conclusion, TβRII and DPC4/Smad4 may play an important role in the tumorigenesis, differentiation and progression of NSCLC via the TGF-β signaling pathway.

Aim: To investigate the role and mechanism of insulin-like growth factor binding protein-related protein 1 (IGFBPrP1) in the development of liver fibrosis., Methods: An in vitro model using hepatic stellate cell (HSC)-T6 cells and an in vivo model of rat liver overexpressing IGFBPrP1 were established using an IGFBPrP1-expressing recombinant adenovirus. The expression of IGFBPrP1 was examined by immunofluorescence, and the expression of collagen I and fibronectin was measured by real-time reverse transcription-polymerase chain reaction and Western blot analysis. The expression of Smad2/3 and p-Smad2/3 was examined by Western blot and immunohistochemistry. A shSmad3-expressing recombinant adenovirus (AdshSmad3) was designed and used to knockdown the Smad3 gene in HSC-T6 cells and rat liver fibrosis transfected with IGFBPrP1. The expression of collagen I, fibronectin, and α-smooth muscle actin (α-SMA) was determined by Western blot analysis and immunohistochemistry. Hepatocyte apoptosis was assessed using TUNEL assay., Results: IGFBPrP1 overexpression induced collagen deposition and up-regulated the expression of α-SMA and p-Smad2/3, and AdshSmad3 inhibited IGFBPrP1-stimulated p-Smad2/3 activation and the expression of α-SMA, collagen I and fibronectin in HSC-T6 cells. Similarly, increased hepatocyte apoptosis (38.56% ± 3.42% vs 0.24% ± 0.03%, P < 0.05), α-SMA positive stained cells (29.84% ± 1.36% vs 5.83% ± 1.47%, P < 0.05), and increased numbers of Smad3 (35.88% ± 2.15% vs 10.24% ± 1.31%, P < 0.05) and p-Smad2/3 positive cells (28.87% ± 2.73% vs 8.23% ± 0.98%, P < 0.05) were detected in the livers of IGFBPrP1-overexpressing rats compared with the control group. Moreover, AdshSmad3 reduced IGFBPrP1-stimulated Smad3 expression and attenuated α-SMA expression (29.84% ± 1.36% vs 8.23% ± 1.28%, P < 0.05), hepatocyte apoptosis (38.56% ± 3.42% vs 6.75% ± 0.52%, P < 0.05), and both collagen I and fibronectin deposition in the livers of AdIGFBPrP1-treated rats., Conclusion: IGFBPrP1 induces liver fibrosis by mediating the activation of hepatic stellate cells and hepatocyte apoptosis in a Smad3-dependent mechanism.

In the title coordination polymer, [Na(C(4)H(2)N(3)O(4))(H(2)O)(2)](n), the Na(I) atom is six-coordinated by one O atom and one N atom from a 2H-1,2,3-triazole-4-carb-oxy-5-carboxyl-ate ligand and four O atoms from four water mol-ecules, forming a distorted octa-hedal geometry. The Na(I) atoms are bridged by water mol-ecules into a chain structure along [100]. Inter-molecular N-H⋯O, O-H⋯N and O-H⋯O hydrogen bonds connect the chains. An intra-molecular O-H⋯O hydrogen bond between the carboxyl-ate groups is observed.

Background: During hepatectomy, a period of ischemia and restoration of the blood supply can result in hepatic ischemia-reperfusion injury (IRI). Current research indicates that erythropoietin (EPO) has a protective effect in animal models of cerebral ischemia, myocardial infarction, and renal IRI. However there is lack of research into the role of EPO in hepatic IRI. This study aimed to explore the role of EPO in hepatic IRI and its possible mechanism of action., Methods: Thirty male Sprague-Dawley rats were divided into three groups: (1) ten rats in the experimental group were given 1000 IU/kg EPO one day before the operation; (2) ten rats in a control group were given normal saline preoperatively as a placebo; and (3) ten rats served as a sham-operated group. Hepatic IRI was induced by occluding the hepatic arteries of the three cephalad hepatic segments and the portal vein for about 45 minutes, while in the sham-operated group only laparotomy was performed. The levels of ALT and AST were tested 24 hours pre- and post-operation. All rats were sacrificed 24 hours after the operation to assess the pathologic changes in the liver and measure the expression of heme oxygenase-1 (HO-1) through Western blotting and RT-PCR., Results: Hepatic IRI was markedly mitigated in the experimental group as compared with the control group. Moreover, the expression of HO-1 at the level of both transcription and protein increased prominently (P<0.05) in the experimental group., Conclusion: These results demonstrate that EPO can up-regulate HO-1 in liver tissues and accordingly decrease hepatic injury through its anti-inflammatory property.

Objective: To study the correlations of mannose-binding lectin (MBL) gene promoter polymorphisms and plasma MBL concentrations to the susceptibility to HIV infection in northern Chinese Han population., Methods: This case-control study included 115 HIV-infected patients and 115 non-infected healthy individuals, in whom the MBL gene promoter polymorphisms were detected using pyrosequencing technique and plasma MBL concentrations measured using enzyme-linked immunosorbent assay (ELISA)., Results: The MBL promoter genotypes of LY/LY, LY/LX, HY/LY, HY/HY and LX/LX were detected in 66 (57.40%), 25 (21.70%), 17 (14.80%), 5 (4.30%) and 2 (1.70%) among the HIV-infected patients, and in 77 (67.00%), 23(20.00%), 12 (10.40%), 0 (0.00%), and 3 (2.60%) among the healthy individuals, respectively. The frequencies of haplotypes LY, HY and LX were 75.70%, 11.70% and 12.60% among the patients, and 82.20%, 5.20% and 12.60% among the healthy individuals, respectively, showing significant difference in the halpotype between the two groups (P=0.041). The average plasma MBL concentration was significantly lower in HIV-infected group than in the healthy individuals (1775.14-/+786.31 vs 3672.21-/+597.13 microg/L, P=0.001)., Conclusion: The genotypes of LY/LY and LY/LX and the haplotypes of LY and HY are predominant in northern Chinese Han population, and the plasma MBL concentration in HIV infected patients is generally only 50% of that in healthy individuals. We therefore presume that MBL promoter polymorphisms and plasma MBL concentration can be associated with the susceptibility to HIV infection in this population, and individuals with low plasma MBL concentration are more susceptible to HIV infection.