Effects of Time Point of Pre-Competitions Peaking on Performance in Major-Competitions.

Objectives: To study the effects of the time points of pre-competition peaking (TPCP, the time point when an athlete's peaking shows up before a major-competition) on the athletes' performances in the major-competition (M-Performance). Design: Mixed design. Methods: We used cluster analysis to classify 892 elite track and field athletes who participated in the 2017 and 2019 IAAF World Championships in Athletics, based on their TPCP and other related factors. Furthermore, we used a fixed-effects model and a mixed-effects model to analyze the relationship between the TPCP and M-Performance. Results: The TPCP of elite track and field athletes were divided into four categories: late, slightly late, slightly early, and early. In speed/power events, athletes in the slightly late category had better M-Performance. In endurance events, athletes in the slightly early category had better M-Performance. In speed/power events, delaying the TPCP did not improve the athletes' M-Performance. In endurance events, advancing the TPCP effectively improved the athletes' M-Performance. Conclusions: To improve M-Performance, athletes in speed/power events should be peaking 2-8 weeks before a major-competition, and athletes in endurance events should be peaking 8-14 weeks before a major-competition. Future research should aim to identify individual factors affecting TPCP, such as the time for the body's adaptation to training and the residual training effect.

Antibody-labeled gold nanoparticle based resonance Rayleigh scattering detection of S100B.

Traumatic brain injury (TBI) is a sudden brain injury due to an external force that causes a large number of deaths and permanent disabilities every year. S100B has been recognized as a potential objective quantitative biomarker for screening the prognosis of TBI and severe head injury. In this article, an anti-S100B monoclonal antibody was immobilized on cysteamine (Cy) functionalized gold nanoparticles (AuNPs) by EDC-NHS chemistry, which enabled S100B resonance Rayleigh scattering (RRS) detection based on antibody-labeled gold nanoparticles. The prepared conjugates were characterized by ultraviolet-visible spectroscopy (UV-vis), transmission electron microscopy (TEM), Fourier transform infrared spectroscopy (FTIR), dynamic light scattering (DLS) and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Based on the specific binding of the antibody and antigen, the RRS intensities at 381 nm and 541 nm wavelengths were significantly enhanced, and thus a dual wavelength overlapping resonance Rayleigh scattering (DWO-RRS) method was established. The scattering intensity of the two overlapping peaks was proportional to the concentration of S100B in the range of 0.05-4.5 ng mL-1 with a detection limit of 0.002 ng mL-1. The proposed DWO-RRS method is time-saving, simple, sensitive, and can be used to determine the concentration of S100B in human serum with satisfactory results, which has a promising application in the early diagnosis of TBI.

An efficient lightweight network for image denoising using progressive residual and convolutional attention feature fusion.

While deep learning has become the go-to method for image denoising due to its impressive noise removal capabilities, excessive network depth often plagues existing approaches, leading to significant computational burdens. To address this critical bottleneck, we propose a novel lightweight progressive residual and attention mechanism fusion network that effectively alleviates these limitations. This architecture tackles both Gaussian and real-world image noise with exceptional efficacy. Initiated through dense blocks (DB) tasked with discerning the noise distribution, this approach substantially reduces network parameters while comprehensively extracting local image features. The network then adopts a progressive strategy, whereby shallow convolutional features are incrementally integrated with deeper features, establishing a residual fusion framework adept at extracting encompassing global features relevant to noise characteristics. The process concludes by integrating the output feature maps from each DB and the robust edge features from the convolutional attention feature fusion module (CAFFM). These combined elements are then directed to the reconstruction layer, ultimately producing the final denoised image. Empirical analyses conducted in environments characterized by Gaussian white noise and natural noise, spanning noise levels 15-50, indicate a marked enhancement in performance. This assertion is quantitatively corroborated by increased average values in metrics such as Peak Signal-to-Noise Ratio (PSNR), Structural Similarity Index (SSIM), and Feature Similarity Index for Color images (FSIMc), outperforming the outcomes of more than 20 existing methods across six varied datasets. Collectively, the network delineated in this research exhibits exceptional adeptness in image denoising. Simultaneously, it adeptly preserves essential image features such as edges and textures, thereby signifying a notable progression in the domain of image processing. The proposed model finds applicability in a range of image-centric domains, encompassing image processing, computer vision, video analysis, and pattern recognition.

Clinical prognostic evaluation of immunocytes in different molecular subtypes of breast cancer.

To retrospectively analyze the relationship between preoperative blood parameters and postoperative clinical outcomes in patients with different molecular subtypes of breast cancer (BC), a cohort of 601 patients with BC in the Third Affiliated Hospital, Sun Yat-sen University, was retrospectively reviewed. They were categorized into four subtypes according to the expression of ER, PR, HER-2, and KI-67%. White blood cell, neutrophil, lymphocyte, monocyte, eosinophil, basophil, and platelet counts, the neutrophil-to-lymphocyte ratio (NLR), the neutrophil-to-monocyte ratio (NMR), the lymphocyte-to-monocyte ratio (LMR), and the platelet-to-lymphocyte ratio (PLR) were recorded. Univariate and multivariate analyses were performed to identify the relationship between parameters and ratios and disease-free survival (DFS) and overall survival (OS). Luminal subtypes of BC had smaller tumor volume, better differentiation degree of invasive ductal carcinoma, less lymph node metastasis, and better clinical outcome than the HER-2 overexpression and triple-negative BC (TNBC) subtypes. In multivariate analysis, age and LMR were the independent prognostic factors of DFS in patients with luminal A (age, p = 0.005; LMR, P = 0.026); PLR in patients with luminal B (DFS; p = 0.032; OS, p= 0.012); LMR in patients with HER-2 overexpression (DFS; p = 0.008; OS, p = 0.017); and NLR for DFS (p = 0.014); and WBC for OS (p = 0.008) in patients with TNBC. LMR was the benign predictor of luminal A and HER-2 overexpression. PLR was the adverse predictor of luminal B. WBC and NLR were the adverse predictors of TNBC. Therefore, these peripheral blood parameters can play an important role in the diagnosis and treatment of patients with different molecular subtypes of BC.

Ethylene carbodiimide-fixed donor splenocytes combined with cordycepin induce long-term protection to mice cardiac allografts.

Infusion of ethylene carbodiimide-fixed donor splenocytes (ECDI-SPs) is an effective method to induce donor-specific protection to allografts. However, the ischemia reperfusion (I/R) injury during transplant leads to abundant of pro-inflammatory cytokines, which negates the effect of ECDI-SPs. Therefore, suppressing pro-inflammatory cytokine secretion while promoting anti-inflammatory cytokine release would enhance the graft protective efficacy of ECDI-SPs. In this study, we aimed to determine the effect of ECDI-SPs combined with a short course of cordycepin (an anti-inflammatory agent) on the long-term outcomes of mice cardiac allografts. Our results demonstrated that ECDI-SPs combined with cordycepin significantly promoted mice cardiac allograft survival compared with ECDI-SPs monotherapy. This effect was accompanied by decreased production of pro-inflammatory cytokines (IL-1ß, IL-6, IL-17 and TNFα), increased secretion of anti-inflammatory cytokines (IL-10 and TGFß), inhibition of Th17 and expansion of Tregs, and prevention of I/R injury. We concluded that cordycepin appeared to enhance the effect of modulating cytokine profile and regulate the Teff:Treg balance so as to strengthen the graft protective effect of ECDI-SPs. Our study of ECDI-SPs combined with cordycepin may provide a promising approach for prolong allograft survival.

Glycyrrhizin Ameliorate Ischemia Reperfusion Lung Injury through Downregulate TLR2 Signaling Cascade in Alveolar Macrophages.

This experiment was conducted to study whether pretreatment with Glycyrrhizin (GL) could ameliorate ischemia-reperfusion (I/R) lung injury and investigate the mechanisms of its protective effects in a mice model. Six-eight weeks male BALB/C mice were randomly assigned to four groups (n = 6): Control, Glycyrrhizin, I/R and I/R+Glycyrrhizin. Lung I/R was achieved by clamping the left hilus pulmonis. GL (200 mg/kg) was injected intraperitoneally 30 min before anesthesia. Measurement of pathohistological lung injury score, pulmonary permeability, isolated alveolar macrophages, inflammatory mediators, TLR2 and its downstream factors (MyD88, NF-κB) were performed. The results were as anticipated. Pathohistological evaluation indicated that GL significantly ameliorated I/R-induced lung injury, pulmonary permeability and edema. Pretreatment with GL significantly inhibited I/R-induced inflammation in lung tissues and BALF. In addition, GL significantly decreased I/R-induced isolated alveolar macrophages and suppressed I/R-induced expression of TLR2 and its downstream factors in lung tissues and alveolar macrophages. Collectively, our data indicated that pretreatment with GL could ameliorate I/R lung injury. The mechanisms of its protective effects might be inhibit I/R-induced inflammatory response through downregulate TLR2 signaling cascade in alveolar macrophages.