Res-NeuS: Deep Residuals and Neural Implicit Surface Learning for Multi-View Reconstruction.

Surface reconstruction using neural networks has proven effective in reconstructing dense 3D surfaces through image-based neural rendering. Nevertheless, current methods are challenging when dealing with the intricate details of large-scale scenes. The high-fidelity reconstruction performance of neural rendering is constrained by the view sparsity and structural complexity of such scenes. In this paper, we present Res-NeuS, a method combining ResNet-50 and neural surface rendering for dense 3D reconstruction. Specifically, we present appearance embeddings: ResNet-50 is used to extract the appearance depth features of an image to further capture more scene details. We interpolate points near the surface and optimize their weights for the accurate localization of 3D surfaces. We introduce photometric consistency and geometric constraints to optimize 3D surfaces and eliminate geometric ambiguity existing in current methods. Finally, we design a 3D geometry automatic sampling to filter out uninteresting areas and reconstruct complex surface details in a coarse-to-fine manner. Comprehensive experiments demonstrate Res-NeuS's superior capability in the reconstruction of 3D surfaces in complex, large-scale scenes, and the harmful distance of the reconstructed 3D model is 0.4 times that of general neural rendering 3D reconstruction methods and 0.6 times that of traditional 3D reconstruction methods.

The Role and Mechanism of Spinal NF-κB-CXCL1/CXCR2 in Rats with Nucleus Pulposus-induced Radicular Pain.

STUDY DESIGN: Experimental study of the role and mechanism of spinal NFκB-CXCL1/CXCR2 in rats with nucleus pulposus-induced radicular pain. OBJECTIVE: This study investigated the role and mechanism of spinal NFκB-CXCL1/CXCR2 in autologous nucleus pulposus-induced pain behavior in rats and to clarify the involvement and regulation of spinal NFκB as an upstream molecule of CXCL1 in autologous nucleus pulposus-induced radicular pain in rats. SUMMARY OF BACKGROUND DATA: The inflammatory response of nerve roots is an important mechanism for the occurrence of chronic pain. NFκB-CXCL1/CXCR2 pathway plays an important role in the development of radicular pain, but its regulatory mechanism in the model of radicular pain induced by autologous nucleus pulposus is still unclear. MATERIALS AND METHODS: We established a rat model of autologous medullary nucleus transplantation. We observed and recorded the changes in 50% mechanical withdrawal threshold and thermal withdrawal latency before and after the administration of CXCL1-neutralizing antibodies, CXCR2 inhibitor, and NFκB inhibitor in each group of rats and evaluated the expression of NFκB, CXCL1, and CXCR2 in the spinal dorsal horn using immunofluorescence and Western blot. To compare differences between groups in behavioral testing, analysis of variance was employed. Dunnett's method was used to compare differences at different time points within a group and between different groups at the same time point. A comparison of the relative concentration of protein, relative concentration of mRNA, and semiquantitative data from immunofluorescence staining was conducted utilizing one-way ANOVA and Dunnett's pairwise comparison. RESULTS: Autologous nucleus pulposus transplantation can induce radicular pain in rats and upregulate the expression of CXCL1, CXCR2, and NFκB in the spinal cord. CXCL1 is co-expressed with astrocytes, CXCR2 with neurons, and NFκB with both astrocytes and neurons. The application of CXCL1 neutralizing antibodies, CXCR2 inhibitors, and NFκB inhibitors can alleviate pain hypersensitivity induced by autologous nucleus pulposus transplantation in rats. Inhibitors of NFκB could downregulate the expression of CXCL1 and CXCR2. CONCLUSIONS: We found that spinal NFκB is involved in NP-induced radicular pain in rats through the activation of CXCL1/CXCR2, enriching the mechanism of medullary-derived radicular pain and providing a possible new target and theoretical basis for the development of more effective anti-inflammatory and analgesic drugs for patients with chronic pain following LDH.

How immune breakthroughs could slow disease progression and improve prognosis in COVID-19 patients: a retrospective study.

Background: Previous infections and vaccinations have produced preexisting immunity, which differs from primary infection in the organism immune response and may lead to different disease severities and prognoses when reinfected. Objectives: The purpose of this retrospective cohort study was to investigate the impact of immune breakthroughs on disease progression and prognosis in patients with COVID-19. Methods: A retrospective cohort study was conducted on 1513 COVID-19 patients in Chengdu Public Health Clinical Medical Center from January 2020 to November 2022. All patients were divided into the no immunity group (primary infection and unvaccinated, n=1102) and the immune breakthrough group (previous infection or vaccination, n=411). The immune breakthrough group was further divided into the natural immunity subgroup (n=73), the acquired immunity subgroup (n=322) and the mixed immunity subgroup (n=16). The differences in clinical and outcome data and T lymphocyte subsets and antibody levels between two groups or between three subgroups were compared by ANOVA, t test and chi-square test, and the relationship between T lymphocyte subsets and antibody levels and the disease progression and prognosis of COVID-19 patients was assessed by univariate analysis and logistic regression analysis. Results: The total critical rate and the total mortality rate were 2.11% and 0.53%, respectively. The immune breakthrough rate was 27.16%. In the no immunity group, the critical rate and the mortality rate were all higher, and the coronavirus negative conversion time was longer than those in the immune breakthrough group. The differences in the critical rate and the coronavirus negative conversion time between the two groups were all statistically significant (3.72% vs. 0.24%, 14.17 vs. 11.90 days, all p<0.001). In addition, in the no immunity group, although lymphocyte counts and T subsets at admission were higher, all of them decreased consistently and significantly and were significantly lower than those in the immune breakthrough group at the same time from the first week to the fourth week after admission (all p<0.01). The total antibody levels and specific Immunoglobulin G (IgG) levels increased gradually and were always significantly lower than those in the immune breakthrough group at the same time from admission to the fourth week after admission (all p<0.001). Moreover, in the natural immunity subgroup, lymphocyte counts and T subsets at admission were the highest, and total antibody levels and specific IgG levels at admission were the lowest. Then, all of them decreased significantly and were the lowest among the three subgroups at the same time from admission to one month after admission (total antibody: from 546.07 to 158.89, IgG: from 6.00 to 3.95) (all p<0.001). Those in the mixed immunity subgroup were followed by those in the acquired immunity subgroup. While lymphocyte counts and T subsets in these two subgroups and total antibody levels (from 830.84 to 1008.21) and specific IgG levels (from 6.23 to 7.51) in the acquired immunity subgroup increased gradually, total antibody levels (from 1100.82 to 908.58) and specific IgG levels (from 7.14 to 6.58) in the mixed immunity subgroup decreased gradually. Furthermore, T lymphocyte subsets and antibody levels were negatively related to disease severity, prognosis and coronavirus negative conversion time. The total antibody, specific IgM and IgG levels showed good utility for predicting critical COVID-19 patients and dead COVID-19 patients. Conclusion: Among patients with COVID-19 patients, immune breakthroughs resulting from previous infection or vaccination, could decelerate disease progression and enhance prognosis by expediting host cellular and humoral immunity to accelerate virus clearance, especially in individuals who have been vaccinated and previously infected. Clinical trial registry: Chinese Clinical Trial Register ChiCTR2000034563.

Nutritional risk and a high NRS2002 score are closely related to disease progression and poor prognosis in patients with COVID-19.

Background: Organism can lead to excessive nutrient consumption in the infected state and increase nutritional risk, which is detrimental to the control of the infection and can further aggravate the disease. Objectives: To investigate the impact of nutritional risk and the NRS2002 score on disease progression and prognosis in patients with COVID-19. Methods: This was a retrospective cohort study including 1,228 COVID-19 patients, who were divided into a with-nutritional risk group (patients with NRS2002 score ≥ 3) and a without-nutritional risk group (patients with NRS2002 score < 3) according to the NRS2002 score at admission. The differences in clinical and outcome data between the two groups were compared, and the relationship between the NRS2002 score and the disease progression and prognosis of COVID-19 patients was assessed. Results: Of 1,228 COVID-19 patients, including 44 critical illness patients and 1,184 non-critical illness patients, the rate of harboring nutritional risk was 7.90%. Compared with those in the without-nutritional risk group, patients in the with-nutritional risk group had a significantly longer coronavirus negative conversion time, significantly lower serum albumin (ALB), total serum protein (TP) and hemoglobin (HGB) at admission, discharge or 2 weeks, a significantly greater proportion with 3 or more comorbidities, and a significantly higher rate of critical illness and mortality (all p < 0.001). Multiple regression analysis showed that nutritional risk, NRS2002 score and ALB at admission were risk factors for disease severity. In addition, nutritional risk, NRS2002 score and TP at admission were risk factors for prognosis. The NRS2002 score showed the best utility for predicting critical illness and death in COVID-19 patients. Conclusion: Nutritional risk and a high NRS2002 score are closely related to disease progression and poor prognosis in COVID-19 patients. For patients with NRS2002 score > 0.5, early intervention of malnutrition is needed to reduce the occurrence of critical disease. Additionally, for patients with NRS2002 score > 5.5, continuous nutritional support therapy is needs to reduce mortality and improve prognosis.Clinical Trial registration: [https://www.chictr.org.cn/historyversionpub.aspx?regno=ChiCTR2000034563], identifier [Chinese Clinical Trial Register ChiCTR2000034563].

High Number and Specific Comorbidities Could Impact the Immune Response in COVID-19 Patients.

Background: Cellular immunodeficiency and comorbidities are common in COVID-19 patients. Aim: The purpose of this study was to investigate comorbidities impacting on the cellular immunity in COVID-19 patients. Methods: The research objects included 55 healthy controls and 718 COVID-19 patients who divided into the control group and the COVID-19 group, respectively. Those in the COVID-19 group were divided into subgroups on the basis of the number and types of comorbidities present. Lymphocyte itself and its subsets were compared between the control group and the COVID-19 group, the groups with comorbidities based on the different number and types of comorbidities, and the relationship between the lymphocyte counts and subsets with the number and types of comorbidities was investigated. Results: Compared with the control group, the lymphocyte counts and T cell subsets were significantly increased in the groups with comorbidities, but both B and NK cell subsets were significantly decreased in the no comorbidity group and in most of the groups with comorbidities (all P<0.05). In the three comorbidities group, the lymphocyte counts and T cell subsets were all significantly decreased, but the CD56+ percentage was obviously increased (all P<0.05). The number of comorbidities was negatively correlated with the lymphocyte counts and the T and NK cell subsets. A negative correlation also existed between cancer and both the lymphocyte counts and the T cell subsets, between chronic hepatitis B and the lymphocyte counts, and between chronic kidney disease and the CD3+ counts. A positive correlation existed between nonalcoholic fatty liver disease (NAFLD) disease and both lymphocyte and CD3+ counts. The risk factors were number of comorbidities for the lymphocyte count, CD3+CD4+ and CD3+CD8+ percentages, NAFLD for the lymphocyte and CD3+ counts, cardiovascular diseases for CD3+CD4+ and CD3+CD8+ percentages, diabetes mellitus for the CD3+CD8+ percentage, and cancer for the CD3+ percentage, respectively. Conclusions: High numbers of comorbidities and specific comorbidities could impact the immune response of COVID-19 patients. This study provides a reference for clinicians in the identification of suitable and timely immunotherapy for COVID-19 patients. Clinical Trial Registry: https://www.chictr.org.cn/enindex.aspx, identifier ChiCTR2000034563.

Osthole-Mediated Inhibition of Neurotoxicity Induced by Ropivacaine via Amplification of the Cyclic Adenosine Monophosphate Signaling Pathway.

Background: Ropivacaine is widely used for clinical anesthesia and postoperative analgesia. However, the neurotoxicity induced by ropivacaine in a concentration- and duration-dependent manner, and it is difficult to prevent neurotoxicity. Osthole inhibits phosphodiesterase-4 activity by binding to its catalytic site to prevent cAMP hydrolysis. The aim of this present study is to explore the precise molecular mechanism of osthole-mediated inhibition of neurotoxicity induced by ropivacaine. Methods: SH-SY5Y cell viability and apoptosis were measured in different concentration and duration. Protein concentration was determined in each signaling pathway. The molecular mechanism of osthole-mediated inhibition of ropivacaine-caused neurotoxicity was evaluated. Results: The study demonstrated that osthole inhibits SH-SY5Y cells neurotoxicity in a duration- and concentration-dependent manner. Moreover, ropivacaine significantly increased the expression of caspase-3 by promoting the phosphorylation of p38. Osthole-induced upregulation of cAMP activated cAMP-dependent signaling pathway, sequentially leading to elevated cyclic nucleotide response element-binding protein levels, which inhibits P38-dependent signaling and decreases apoptosis of SH-SY5Y. Conclusions: This study display the evidence confirmed the molecular mechanism by which osthole amplification of cAMP-dependent signaling pathway, and overexpression of cyclic nucleotide response element-binding protein inhibits P38-dependent signaling and decreases ropivacaine-induced SH-SY5Y apoptosis.

Gradual increasing dyslipidemia in treatment-naive male patients with human immunodeficiency virus and treated with tenofovir plus lamivudine plus efavirenz for 3 years.

INTRODUCTION: Since the development of antiretroviral therapy (ART) with TDF plus 3TC plus EFV, this specific regimen has not been studied enough with long-term lipid and uric acid monitoring. METHODS: A prospective follow-up cohort study was performed. Sixty-one treatment-naive male patients with human immunodeficiency virus (HIV) were divided into three groups based on their baseline CD4+ cell count (26, 12, and 23 patients in the < 200, 200 to 350, and > 350 groups, respectively). The lipid and purine metabolism parameters of the patients over 144 weeks were analyzed. RESULT: Within 144 weeks, TG, LDL-c, TC and HDL-c gradually increased, especially TC and HDL-c (P = 0.001, 0.000, respectively). Moreover, the percentages of hyper-cholesterolemia, hyper LDL cholesterolemia, hyper-triglyceridemia and low HDL cholesterolemia also gradually increased, especially low HDL cholesterolemia significantly increased (P = 0.0007). The lower the baseline CD4+ cell counts were, the higher the TG levels and the lower the TC, LDL-c and HDL-c levels were. But there was significant difference of only baseline LDL-c levels between the three groups (P = 0.0457). No significant difference of the UA level and the percentages of hyperuricemia was found between the different follow-up time point groups or between the three CD4+ cell counts groups (all P > 0.05). The risk factors for dyslipidemia included age, anthropometric parameters and follow-up weeks, and for hyperuricemia was virus load. CONCLUSIONS: Gradual increasing dyslipidemia was found in male patients with human immunodeficiency virus primarily treated with tenofovir plus lamivudine plus efavirenz for 3 years. There-fore lipid metabolism parameters should be closely monitored during long-term ART with the TDF plus 3TC plus EFV regimen.

Influence of Oxygen Vacancy Behaviors in Cooling Process on Semiconductor Gas Sensors: A Numerical Analysis.

The influence of oxygen vacancy behaviors during a cooling process in semiconductor gas sensors is discussed by the numerical analysis method based on the gradient-distributed oxygen vacancy model. A diffusion equation is established to describe the behaviors of oxygen vacancies, which follows the effects of diffusion and exclusion in the cooling process. Numerical analysis is introduced to find the accurate solutions of the diffusion equation. The solutions illustrate the oxygen vacancy distribution profiles, which are dependent on the cooling rate as well as the temperature interval of the cooling process. The gas-sensing characteristics of reduced resistance and response are calculated. Both of them, together with oxygen vacancy distribution, show the grain size effects and the re-annealing effect. It is found that the properties of gas sensors can be controlled or adjusted by the designed cooling process. The proposed model provides a possibility for sensor characteristics simulations, which may be beneficial for the design of gas sensors. A quantitative interpretation on the gas-sensing mechanism of semiconductors has been contributed.

A Hierarchical Building Segmentation in Digital Surface Models for 3D Reconstruction.

In this study, a hierarchical method for segmenting buildings in a digital surface model (DSM), which is used in a novel framework for 3D reconstruction, is proposed. Most 3D reconstructions of buildings are model-based. However, the limitations of these methods are overreliance on completeness of the offline-constructed models of buildings, and the completeness is not easily guaranteed since in modern cities buildings can be of a variety of types. Therefore, a model-free framework using high precision DSM and texture-images buildings was introduced. There are two key problems with this framework. The first one is how to accurately extract the buildings from the DSM. Most segmentation methods are limited by either the terrain factors or the difficult choice of parameter-settings. A level-set method are employed to roughly find the building regions in the DSM, and then a recently proposed 'occlusions of random textures model' are used to enhance the local segmentation of the buildings. The second problem is how to generate the facades of buildings. Synergizing with the corresponding texture-images, we propose a roof-contour guided interpolation of building facades. The 3D reconstruction results achieved by airborne-like images and satellites are compared. Experiments show that the segmentation method has good performance, and 3D reconstruction is easily performed by our framework, and better visualization results can be obtained by airborne-like images, which can be further replaced by UAV images.

[Role of p38 mitogen-activated protein kinase pathway in pathogenesis of ulcerative colitis].

OBJECTIVE: To elucidate the role of p38 mitogen-activated protein kinase (p38MAPK) in the pathogenesis of ulcerative colitis (UC) and DSS-induced colitis in mice. METHODS: (1) 27 Balb/c mice were divided randomly into three groups: DSS-induced colitis group, normal control group and SB203580 treatment group. In DSS-induced colitis group, mice were feed with 5% DSS solution. In SB203580 treatment group, mice were feed with 5%DSS solution for 72 hours, then treated with intraperitoneal injection of SB203580 (1 mg/kg) once daily. Disease activity index (DAI) was record to evaluate the severity of colitis. The mice were executed after 7 days. The levels of TNF-alpha and IL-1beta were measured by ELISA. (2) A total of 54 cases were included in the study. 36 cases were patients with active ulcerative colitis, 18 cases were normal mucosa from 18 colon cancer cases served as control. Effects of SB203580 (a selective p38MAPK inhibitor) on expression of TNF-alpha and IL-1beta in intestinal mucosal biopsy specimens from patients with ulcerative colitis were determined on condition of tissue culture. RESULTS: (1) The DAI scores, the levels of TNF-alpha and IL-1beta in SB203580 group were lower significantly compared with DSS group (P < 0.05), and were increased significantly compared with normal control group (P < 0.05). (2) The levels of TNF-alpha and IL-1beta in intestinal mucosal biopsy specimens in SB203580 treatment group were lower significantly than those in UC group (P < 0.05). CONCLUSION: SB203580 can inhibit p38MAPK signal transduction pathway, then reduce the expression of pro-inflammatory cytokine TNF-alpha and IL-1beta.