DeforT: Deformable transformer for visual tracking.

Most trackers formulate visual tracking as common classification and regression (i.e., bounding box regression) tasks. Correlation features that are computed through depth-wise convolution or channel-wise multiplication operations are input into both the classification and regression branches for inference. However, this matching computation with the linear correlation method tends to lose semantic features and obtain only a local optimum. Moreover, these trackers use an unreliable ranking based on the classification score and the intersection over union (IoU) loss for the regression training, thus degrading the tracking performance. In this paper, we introduce a deformable transformer model, which effectively computes the correlation features of the training and search sets. A new loss called the quality-aware focal loss (QAFL) is used to train the classification network; it efficiently alleviates the inconsistency between the classification and localization quality predictions. We use a new regression loss called α-GIoU to train the regression network, and it effectively improves localization accuracy. To further improve the tracker's robustness, the candidate object location is predicted by using a combination of online learning scores with a transformer-assisted framework and classification scores. An extensive experiment on six testing datasets demonstrates the effectiveness of our method. In particular, the proposed method attains a success score of 71.7% on the OTB-2015 dataset and an AUC score of 67.3% on the NFS30 dataset, respectively.

[Effect of gut microbiota homeostasis on hematopoiesis in a neonatal rat model of necrotizing enterocolitis]. / è‚ é“å¾®ç”Ÿç‰©ç¨³æ€å¯¹åæ­»æ€§å°è‚ ç»“è‚ ç‚Žæ–°ç”Ÿå¤§é¼ æ¨¡åž‹é€ è¡€ç³»ç»Ÿçš„å½±å“.

OBJECTIVES: To study the effect of gut microbiota on hematopoiesis in a neonatal rat model of necrotizing enterocolitis (NEC). METHODS: Neonatal Sprague-Dawley rats were randomly divided into a control group and a model group (NEC group), with 6 rats in each group. Formula milk combined with hypoxia and cold stimulation was used to establish a neonatal rat model of NEC. Hematoxylin and eosin staining was used to observe the pathological changes of intestinal tissue and hematopoiesis-related organs. Routine blood tests were conducted for each group. Immunohistochemistry was used to observe the changes in specific cells in hematopoiesis-related organs. Flow cytometry was used to measure the changes in specific cells in bone marrow. 16S rDNA sequencing was used to observe the composition and abundance of gut microbiota. RESULTS: Compared with the control group, the NEC group had intestinal congestion and necrosis, damage, atrophy, and shedding of intestinal villi, and a significant increase in NEC histological score. Compared with the control group, the NEC group had significantly lower numbers of peripheral blood leukocytes and lymphocytes (P<0.05), nucleated cells in the spleen, thymus, and bone marrow, and small cell aggregates with basophilic nuclei in the liver (P<0.05). The NEC group had significant reductions in CD71+ erythroid progenitor cells in the liver, CD45+ lymphocytes in the spleen and bone marrow, CD3+ T lymphocytes in thymus, and the proportion of CD45+CD3-CD43+SSChi neutrophils in bone marrow (P<0.05). There was a significant difference in the composition of gut microbiota between the NEC and control groups, and the NEC group had a significant reduction in the abundance of Ligilactobacillus and a significant increase in the abundance of Escherichia-Shigella (P<0.05), which replaced Ligilactobacillus and became the dominant flora. CONCLUSIONS: Multi-lineage hematopoietic disorder may be observed in a neonatal rat model of NEC, which may be associated with gut microbiota dysbiosis and abnormal multiplication of the pathogenic bacteria Escherichia-Shigella.

Satisfaction in population-based cancer screening in a Chinese rural high-risk population: the Yangzhong early diagnosis and treatment of upper gastrointestinal cancer.

BACKGROUND: Screening for upper gastrointestinal cancer (UGC) effectively reduces morbidity and mortality in gastric and esophageal cancers. It is considered one of the effective measures for cancer control in China, but studies on its functional quality are lacking. Our study assessed the quality of screening service funded by Upper Gastrointestinal Cancer Early diagnosis and treatment (UGCEDAT) and its correlation in Yangzhong People's hospital, China. METHODS: A cross-sectional study was conducted among 516 screening users at a screening centre in Yanghzong People's hospital from April to July 2021. The service quality questionnaire (SERVQUAL) based on the service quality gap (SQG) model was adopted. We calculated the mean scores of perceptions and expectations and their gap. To determine the association between overall SQG and related features of participants, we used a multivariate logistic regression. RESULTS: The average scores of screening service users' perceptions and expectations were 4.05 and 4.55, respectively. The SQG of five dimensions (tangibles, reliability, responsiveness, assurance and empathy) were negative, and the overall SQG was -0.51. The responsiveness dimension had the largest gap, and tangibles had the smallest gap. Occupation status (AOR: 0.57; CI: 0.37-0.89), health self-assessment (AOR: 4.97; CI: 1.35-18.23), endoscopy experience (AOR: 0.55; CI: 0.38-0.81), distance from screening hospital (AOR: 1.85; CI: 1.25-2.73) and frequency of visit (AOR: 1.65; CI: 1.10-2.46) were associated with the overall SQG. CONCLUSIONS: We observed a negative gap between perceptions and expectations of the function quality of screening service, implying a high dissatisfaction across different dimensions. Service providers should take adequate measures to bridge the dimension with the largest quality gap. Meanwhile, attention should be paid to identifying the influencing factors of the overall SQG and the characteristics of dimensional expectations and perceptions to improve the effectiveness of the screening program.

Prevalence and coprevalence of modifiable risk factors for upper digestive tract cancer among residents aged 40-69 years in Yangzhong city, China: a cross-sectional study.

OBJECTIVES: To describe the prevalence of modifiable risk factors for upper digestive tract cancer (UDTC) and its coprevalence, and investigate relevant influencing factors of modifiable UDTC risk factors coprevalence among residents aged 40-69 years in Yangzhong city, China. DESIGN: Cross-sectional study. PARTICIPANTS: A total of 21 175 participants aged 40-69 years were enrolled in the study. 1962 subjects were excluded due to missing age, marital status or some other selected information. Eventually, 19 213 participants were available for the present analysis. MAIN OUTCOMES MEASURES: Prevalence and coprevalence of eight modifiable UDTC risk factors (overweight or obesity, current smoking, excessive alcohol consumption, insufficient vegetables intake, insufficient fruit intake and the consumption of pickled, fried and hot food) were analysed. RESULTS: The prevalence of overweight/obesity, current smoking, excessive alcohol consumption, insufficient vegetables intake, insufficient fruit intake and the consumption of pickled, fried and hot food in this study was 45.3%, 24.1%, 16.2%, 66.1%, 94.5%, 68.1%, 36.0% and 88.4%, respectively. Nearly all (99.9%) participants showed one or more UDTC risk factors, 98.6% of the participants showed at least two risk factors, 92.2% of the participants had at least three risk factors and 69.7% of the participants had four or more risk factors. Multivariate logistic regression analysis revealed that men, younger age, single, higher education, higher annual family income and smaller household size were more likely to present modifiable UDTC risk factors coprevalence. CONCLUSIONS: The prevalence and coprevalence of modifiable UDTC risk factors are high among participants in Yangzhong city. Extra attention must be paid to these groups who are susceptible to risk factors coprevalence during screening progress. Relative departments also need to make significant public health programmes that aim to decrease modifiable UDTC risk factors coprevalence among residents aged 40-69 years from high-risk areas of UDTC.

Decidual mesenchymal stem/stromal cell-derived extracellular vesicles ameliorate endothelial cell proliferation, inflammation, and oxidative stress in a cell culture model of preeclampsia.

Oxidative stress and endothelial dysfunction contribute substantially to the pathogenesis of preeclampsia (PE). Decidual mesenchymal stem/stromal cells (DMSC), reportedly reduce endothelial cell dysfunction and alleviate PE-like symptoms in a murine model. However, as a therapeutic strategy, the use of whole DMSC presents significant technical limitations, which may be overcome by employing DMSC-secreted extracellular vesicles (DMSC_EV). DMSC_EV restoration of endothelial dysfunction through a paracrine effect may alleviate the clinical features of PE. OBJECTIVE: To determine whether DMSC-secreted, extracellular vesicles (DMSC_EV) restore endothelial cell function and reduce oxidative stress. METHODS: DMSC were isolated from the placentae of uncomplicated term pregnancies and DMSC_EV prepared by ultracentrifugation. Human umbilical vein endothelial cells (HUVEC) were treated with bacterial lipopolysaccharide (LPS), or with serum from PE patients, to model the effects of PE. DMSC_EV were then added to treated HUVEC and their growth profiles, inflammatory state, and oxidative stress levels measured. RESULTS: DMSC_EV displayed characteristic features of extracellular vesicles. In both LPS- and PE serum-treatment models, addition of DMSC_EV significantly increased HUVEC cell attachment and proliferation, and significantly reduced production of pro-inflammatory cytokine IL-6. The addition of DMSC_EV to LPS-treated HUVEC had no significant effect on total antioxidant capacity, superoxide dismutase levels or on lipid peroxidation levels. In contrast, the addition of DMSC_EV to PE serum-treated HUVEC resulted in a significant reduction in levels of lipid peroxidation. CONCLUSION: Addition of DMSC_EV had beneficial effects in both LPS- and PE serum- treated HUVEC but the two treatment models to induce endothelial cell dysfunction showed differences. The LPS treatment of HUVEC model may not accurately model the endothelial cell dysfunction characteristic of PE. Human cell culture models of PE show that DMSC_EV improve endothelial cell dysfunction in PE, but testing in in vivo models of PE is required.

Genetic Susceptibility to Gestational Diabetes Mellitus in a Chinese Population.

Introduction: New genetic variants associated with susceptibility to obesity and metabolic diseases have been discovered in recent genome-wide association (GWA) studies. The aim of this study was to investigate the association of theses risk variants with gestational diabetes mellitus (GDM). Methods: We performed a case-control study including 964 unrelated pregnant women with GDM and 1,021 pregnant women with normal glucose tolerance (as controls). A total of 33 genetic variants confirmed by GWA studies for obesity and metabolic diseases were selected and measured. Results: We observed that FTO rs1121980 and KCNQ1 rs163182 conferred a decreased GDM risk in the dominant and additive model [additive model: OR (95% CI) = 0.79 (0.67-0.94), P = 0.007 for rs1121980; OR(95%CI) = 0.84 (0.73-0.96), P = 0.009 for rs163182], whereas MC4R rs12970134 and PROX1 rs340841 conferred an increased GDM risk in the dominant, recessive, and additive model [additive model: OR(95%CI) = 1.25 (1.07-1.46), P = 0.006 for rs12970134; OR(95%CI) = 1.22 (1.07-1.39), P = 0.002 for rs340841). With the increasing number of risk alleles of the four significant SNPs, GDM risk was significantly increased in a dose-dependent manner (Ptrend < 0.001). And the significant positive associations between the weighted genetic risk score and risk of GDM persisted. Further function annotation indicated that these four SNPs may fall on the functional elements of human pancreatic islets. The genotype-phenotype associations indicated that these SNPs may contribute to GDM by affecting the expression levels of their nearby or distant genes. Conclusion: Our study suggests that FTO rs1121980, KCNQ1 rs163182, MC4R rs12970134, and PROX1 rs340841 may be markers for susceptibility to GDM in a Chinese population.

Genetic Variants in AC092159.2 and Risk of Gestational Diabetes Mellitus in a Chinese Population.

Long-noncoding RNA AC092159.2, located ∼247 bp upstream of the TMEM18 gene, may play integral roles in metabolic processes, including adipocyte differentiation and glycometabolism. AC092159.2 may be an important regulator of TMEM18, which is an important susceptibility gene related to obesity and type 2 diabetes. We designed a case-control study (including 964 gestational diabetes mellitus [GDM] cases and 1021 controls) to assess the associations of 14 single-nucleotide polymorphisms (SNPs) in AC092159.2 with the GDM risk. Logistic regression analyses showed that rs11127496 A > G, rs12714417 C > T, and rs1320334 A > G conferred a decreased GDM risk in the recessive and additive model, whereas rs11691220 T > C conferred an increased GDM risk in the dominant and additive model. Also, with increasing number of protective alleles of the four SNPs, the risk of GDM was significantly decreased in a dose-dependent manner (ptrend = 0.007). Further function annotation indicated that these four SNPs may fall on the function elements of human pancreatic islets. The genotype-phenotype associations suggested that these SNPs may contribute to GDM by affecting TMEM18 expression. AC092159.2 SNPs (rs11127496 A > G, rs11691220 T > C, rs12714417 C > T, and rs1320334 A > G) may be susceptibility makers for risk of GDM in Chinese females.

Pancreatic carcinoma underlying a complex presentation in late pregnancy: a case report.

BACKGROUND: Gestational diabetes mellitus is strongly related to the risk of pancreatic cancer in pregnant women, but gestational diabetes can precede a diagnosis of pancreatic cancer by many years. Women with a history of gestational diabetes showed a relative risk of pancreatic cancer of 7.1. Pancreatic adenocarcinoma is one of the most common malignancies associated with thromboembolic events. A clinical study showed that thromboembolic events were detected in 36% of patients diagnosed as having pancreatic cancer. Studies showed that gestational diabetes mellitus could be one of the important risk factors for pancreatic cancer. CASE PRESENTATION: Gestational diabetes mellitus is associated with increased risk of breast and pancreatic cancer. This case report describes a 29-year-old Chinese woman who presented with: gestational diabetes mellitus; International Society on Thrombosis and Haemostasis criteria suggested disseminated intravascular coagulation with a score of 5; hemolysis, elevated liver enzymes, low platelet count syndrome; and pulmonary hypertension. After an intravenous injection of fibrinogen, she gave birth to a normal baby and following delivery, her blood pressure reached 180/110 mmHg. Laboratory analysis results showed elevated lactic dehydrogenase, decreased platelets and fibrinogen, and urine protein was positive. She was transfused with fresh frozen plasma, blood coagulation factor, and fibrinogen. Subsequently, she was transferred to a maternity intensive care unit, where magnesium sulfate seizure prophylaxis was continued for 24 hours to keep her magnesium level at a low therapeutic range. However, continuous oxygen therapy was needed to maintain her oxygenation. Further laboratory investigations revealed elevated carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 72-4. Positron emission tomography-computed tomography showed malignant carcinoma in the head of her pancreas with lymph node involvement along with bone, peritoneal, and left adrenal metastasis, as well as double lung lymphangitic carcinomatosis. CONCLUSION: A differential diagnosis of digestive system neoplasm should be considered when a pregnant patient presents with gestational diabetes mellitus and disseminated intravascular coagulation, where the disseminated intravascular coagulation has no specific cause and cannot be readily resolved.

Genetic variants in vitamin D signaling pathways and risk of gestational diabetes mellitus.

Vitamin D (VD) deficiency during pregnancy has been repeatedly linked to an increased gestational diabetes mellitus (GDM) risk. We sought to determine the influences of genetic variants in vitamin D signaling pathways on the risk of GDM. In this study, we genotyped 15 single nucleotide polymorphisms (SNPs) within 8 representative genes (CYP27A1, CYP27B1, CYP24A1, VDR, RXRA, RXRB, RXRG and GC) of the vitamin D signaling pathways in a case-control study with 964 GDM cases and 1,021 controls using the Sequenom MassARRAY iPLEX platform. Logistic regression analyses in additive model showed that GC rs16847024 C>T, RXRG rs17429130 G>C and RXRA rs4917356 T>C were significantly associated with the increased risk of GDM (adjusted OR = 1.31, 95% CI = 1.10-1.58 for rs16847024; adjusted OR = 1.28, 95% CI = 1.04-1.57 for rs17429130; adjusted OR = 1.28, 95% CI = 1.06-1.54 for rs4917356). And GDM risk significantly increased with the increasing number of variant alleles of the three SNPs in a dose-dependent manner (P for trend < 0.001). Moreover, the combined effect of the three SNPs on GDM occurrence was more prominent in older women (age > 30). Further interactive analyses also detected a significantly multiplicative interaction between the combined variant alleles and age on GDM risk (P = 0.035). Together, these findings indicate that GC rs16847024, RXRG rs17429130 and RXRA rs4917356 were candidate susceptibility markers for GDM in Chinese females. Further validation studies with different ethnic background and biological function analyses were needed.

Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway.

Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Salidroside (SAL), one of the main effective constituents of Rhodiola rosea, has been reported to suppress oxidative stress-induced cardiomyocyte injury and necrosis by promoting transcription of nuclear factor E2-related factor 2 (Nrf2)-regulated genes such as heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase (quinone1) (NQO1). However, it has not been indicated whether SAL might ameliorate endothelial injury induced by oxidative stress. Here, our study demonstrated that SAL might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway. The results of our study indicated that SAL decreased the levels of intercellular reactive oxygen species (ROS) and malondialdehyde (MDA), and improved the activities of superoxide dismutase (SOD) and catalase (CAT), resulting in protective effects against oxidative stress-induced cell damage in HUVECs. It suppressed oxidative stress damage by inducing Nrf2 nuclear translocation and activating the expression of Nrf2-regulated antioxidant enzyme genes such as HO-1 and NQO1 in HUVECs. Knockdown of Nrf2 with siRNA abolished the cytoprotective effects against oxidative stress, decreased the expression of Nrf2, HO-1, and NQO1, and inhibited the nucleus translocation of Nrf2 in HUVECs. This study is the first to demonstrate that SAL suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.

Dehydration of fructose to 5-hydroxymethylfurfural by rare earth metal trifluoromethanesulfonates in organic solvents.

The catalytic dehydration of fructose to 5-hydroxymethylfurfural (HMF) was investigated by using various rare earth metal trifluoromethanesulfonates, that is, Yb(OTf)(3), Sc(OTf)(3), Ho(OTf)(3), Sm(OTf)(3), Nd(OTf)(3) as catalysts in DMSO. It is found that the catalytic activity increases with decreasing ionic radius of rare earth metal cations. Among the examined catalysts, Sc(OTf)(3) exhibits the highest catalytic activity. Fructose conversion of 100% and a HMF yield of 83.3% are obtained at 120°C after 2h by using Sc(OTf)(3) as the catalyst. Moreover, the catalytic dehydration of fructose was also carried out in different solvents, for example, DMA, 1,4-dioxane, and a mixture of PEG-400 and water. The results show that among the solvents DMSO is the most efficient in promoting the dehydration of fructose to HMF, and no rehydration byproducts such as levulinic acid and formic acid are detected.

Resveratrol-induced augmentation of telomerase activity delays senescence of endothelial progenitor cells.

BACKGROUND: Previous studies have shown that resveratrol increases endothelial progenitor cell (EPC) numbers and functional activity. Increased EPC numbers and activity are associated with the inhibition of EPC senescence. In this study, we investigated the effect of resveratrol on the senescence of EPCs, leading to potentiation of cellular function. METHODS: EPCs were isolated from human peripheral blood and identified immunocytochemically. EPCs were incubated with resveratrol (1, 10, and 50 µmol/L) or control for specified times. After in vitro cultivation, acidic ß-galactosidase staining revealed the extent of senescence in the cells. To gain further insight into the underlying mechanism of the effect of resveratrol, we measured telomerase activity using a polymerase chain reaction (PCR)-enzyme-linked immunosorbent assay (ELISA) technique. Furthermore, we measured the expression of human telomerase reverse transcriptase (hTERT) and the phosphorylation of Akt by immunoblotting. RESULTS: Resveratrol dose-dependently inhibited the onset of EPC senescence in culture. Resveratrol also significantly increased telomerase activity. Interestingly, quantitative real-time PCR analysis demonstrated that resveratrol dose-dependently increased the expression of the catalytic subunit, hTERT, an effect that was significantly inhibited by pharmacological phosphatidylinositol 3-kinase (PI3-K) blockers (wortmannin). The expression of hTERT is regulated by the PI3-K/Akt pathway; therefore, we examined the effect of resveratrol on Akt activity in EPCs. Immunoblotting analysis revealed that resveratrol led to dose-dependent phosphorylation and activation of Akt in EPCs. CONCLUSION: Resveratrol delayed EPCs senescence in vitro, which may be dependent on telomerase activation.

Ginsenoside Rg1 promotes endothelial progenitor cell migration and proliferation.

AIM: To investigate the effect of ginsenoside Rg1 on the migration, adhesion, proliferation, and VEGF expression of endothelial progenitor cells (EPCs). METHODS: EPCs were isolated from human peripheral blood and incubated with different concentrations of ginsenoside Rg1 (0.1, 0.5, 1.0, and 5.0 micromol/L) and vehicle controls. EPC migration was detected with a modified Boyden chamber assay. EPC adhesion was determined by counting adherent cells on fibronectin-coated culture dishes. EPC proliferation was analyzed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In vitro vasculogenesis was assayed using an in vitro vasculogenesis detection kit. A VEGF-ELISA kit was used to measure the amount of VEGF protein in the cell culture medium. RESULTS: Ginsenoside Rg1 promoted EPC adhesion, proliferation, migration and in vitro vasculogenesis in a dose- and time-dependent manner. Cell cycle analysis showed that 5.0 micromol/L of ginsenoside Rg1 significantly increased the EPC proliferative phase (S phase) and decreased the resting phase (G(0)/G(1) phase). Ginsenoside Rg1 increased vascular endothelial growth factor production. CONCLUSION: The results indicate that ginsenoside Rg1 promotes proliferation, migration, adhesion and in vitro vasculogenesis.

Preparation and characterization of Prussian blue nanowire array and bioapplication for glucose biosensing.

Prussian blue nanowire array (PBNWA) was prepared via electrochemical deposition with polycarbonate membrane template for effective modification of glassy carbon electrode. The PBNWA electrode thus obtained was demonstrated to have high-catalytic activity for the electrochemical reduction of hydrogen peroxide in neutral media. This enabled the PBNWA electrode to show rapid response to H2O2 at a low potential of -0.1 V over a wide range of concentrations from 1x10(-7) M to 5x10(-2) M with a high sensitivity of 183 microA mM(-1) cm(-2). Such a low-working potential also substantially improved the selectivity of the PBNWA electrode against most electroactive species such as ascorbic acid and uric acid in physiological media. A detection limit of 5x10(-8) M was obtained using the PBNWA electrode for H2O2, which compared favorably with most electroanalysis procedures for H2O2. A biosensor toward glucose was then constructed with the PBNWA electrode as the basic electrode by crosslinking glucose oxidase (GOx). The glucose biosensor allowed rapid, selective and sensitive determination of glucose at -0.1 V. The amperometric response exhibited a linear correlation to glucose concentration through an expanded range from 2x10(-6) M to 1x10(-2) M, and the response time and detection limit were determined to be 3 s and 1 microM, respectively.

Platelet-derived growth factor BB modulates PCNA protein synthesis partially through the transforming growth factor beta signalling pathway in vascular smooth muscle cells.

PDGF-BB (Platelet-derived growth factor BB) and TGF-beta1(transforming growth factor beta1) are important growth factors in the modulation of vascular smooth muscle cell (VSMC) proliferation and PCNA (proliferating cell nuclear antigen) expression in VSMCs. PCNA expresses at a high level in proliferating cells. The present study aims to assess the effects of PDGF-BB-induced overexpression of TGF-beta1 on PCNA in VSMCs. The downstream proteins of the TGF-beta signalling system in VSMCs, including TGF-beta type I receptor (ALK-5 in VSMCs), Smurf2, Smad2, pSmad2/3, Smad4, and Smad7, were also investigated. Our results revealed that PDGF-BB significantly increased the expressions of TGF-beta1 and PCNA, and the increase in PCNA can be partially inhibited by neutralizing anti-TGF-beta1 antibody. Furthermore, PDGF-BB increased the expression of ALK-5, Smurf2, pSmad2/3, and Smad4, but lowered the levels of Smad2 and Smad7; these alterations were partially restored by neutralizing anti-TGF-beta1 antibody. These findings suggest that PDGF-BB promotes PCNA expression in VSMCs partially through TGF-beta1 overexpression, and that the TGF-beta signalling system involves the molecular mechanism of PDGF-BB in VSMCs.