The discrepancy in timing between synchronous signals and visual stimulation should not be underestimated.

Response latency is a critical parameter in studying human behavior, representing the time interval between the onset of stimulus and the response. However, different time between devices can introduce errors. Serial port synchronization signal can mitigate this, but limited information is available regarding their accuracy. Optical signals offer another option, but the difference in the positioning of optical signals and visual stimuli can introduce errors, and there have been limited reports of error reduction. This study aims to investigate methods for reducing the time errors. We used the Psychtoolbox to generate visual stimuli and serial port synchronization signals to explore their accuracy. Subsequently, we proposed a calibration formula to minimize the error between optical signals and visual stimuli. The findings are as follows: Firstly, the serial port synchronization signal presenting precedes visual stimulation, with a smaller lead time observed at higher refresh rates. Secondly, the lead time increases as the stimulus position deviates to the right and downwards. In Linux and IOPort(), serial port synchronization signals exhibited greater accuracy. Considering the poor accuracy and the multiple influencing factors associated with serial port synchronization signals, it is recommended to use optical signals to complete time synchronization. The results indicate that under the darkening process, the time error is - 0.23 ~ 0.08 ms (mean). This calibration formula can help measure the response latency accurately. This study provides valuable insights for optimizing experimental design and improving the accuracy of response latency. Although it only involves visual stimuli, the methods and results of this study can still serve as a reference.

Glycine prevents pressure overload induced cardiac hypertrophy mediated by glycine receptor.

As a major amino acid, glycine has multiple functions in metabolism, growth, immunity, cytoprotection, and survival. The aim of this study was to determine the effects of glycine on pathologic cardiac hypertrophy and the mechanism underlying it. Pre-treatment with glycine significantly attenuated murine cardiac hypertrophy induced by transverse aortic constriction or by administration of angiotensin II (Ang II). This action was associated with a suppressive extracellular signal-regulated kinase 1/2 phosphorylation in myocardium. The cardioprotective effect of glycine disappeared when endogenous glycine receptor α2 was knocked down by mRNA interference in rats. Co-culture experiments revealed that glycine could also antagonize Ang II stimulated release of transforming growth factor ß and endothelin-1 by cardiomyocytes, which prevented an over-production of collagens in rat fibroblasts. These results, for the first time, demonstrate that glycine may be a novel cardioprotector against pressure overload induced cardiac hypertrophy. Thus, glycine would be useful in the prevention of cardiac hypertrophy and heart failure.

Breast cancer risk in rheumatoid arthritis: an update meta-analysis.

BACKGROUND: The incidence of breast cancer in RA patients remains controversial. Thus we performed a meta-analysis to investigate the impact of RA on breast cancer. METHODS: Published literature was available from PubMed, Embase, and Cochrane Library. Pooled standardized incidence rate (SIR) was computed by random-effect model analysis. RESULTS: We identified 16 separate studies in the present study, in which the number of patients ranged from 458 to 84,475. We did not find the increased cancer risk in RA patients (SIR=0.86, 95% CI=0.72-1.02). However, subgroup analysis showed that breast cancer risk in RA patients was positively different in Caucasians (SIR=0.82, 95% CI=0.73-0.93) and non-Caucasians (SIR=1.21, 95% CI=1.19-1.23), respectively. In subgroup analysis by style, a reduced incidence was found in hospital-based case subjects (SIR=0.82, 95% CI=0.69-0.97). Similarly, subgroup analysis for adjusted factors indicated that in A3 (age and sex) and A4 (age, sex, and race/ethnicity) the risk was decreased (SIR=0.87, 95% CI=0.76-0.99; SIR=0.63, 95% CI=0.59-0.67). CONCLUSIONS: The meta-analysis revealed no increased breast cancer risk in RA patients. However, in the subgroup analysis, the risk of breast cancer is increased in non-Caucasians patients with RA while it decreased in Caucasian population, hospital-based case subjects, and A3 group. Such relationship may provide preference for risk of breast cancer in different population.

Class A scavenger receptor deficiency augments angiotensin II-induced vascular remodeling.

Class A scavenger receptor (SR-A) is a multifunctional molecule that participates in macrophage-mediated inflammation. Here we evaluated the role of SR-A in angiotensin II (Ang II)-induced hypertensive vascular remodeling. Chronic infusion of Ang II leads to an increased systolic blood pressure both in SR-A knockout (SR-A(-/-)) and wild type (SR-A(+/+)) mice with no significant difference between these two groups. SR-A(-/-) hypertensive mice, however, exhibited a marked augmentation of arterial wall thickening and vascular cell proliferation compared with SR-A(+/+) hypertensive mice. M1 macrophage markers were increased whereas M2 macrophage markers were decreased in vascular tissues of SR-A(-/-) mice. Co-culture experiments revealed that more pro-inflammatory cytokines like TNF-α were produced by SR-A(-/-) peritoneal macrophages leading to a stronger proliferation of primary vascular smooth muscle cells in vitro. In addition, SR-A(-/-) macrophages were more prone to lipopolysaccharide-induced M1 differentiation while resisting interleukin-4-induced M2 differentiation. Importantly, transplantation of SR-A(-/-) bone marrow into SR-A(+/+) mice significantly augmented Ang II-induced vascular remodeling. These results show that SR-A is critical for Ang II-induced vascular remodeling by regulating macrophage polarization. Therefore, SR-A may be a useful therapeutic target for the intervention of hypertensive vascular remodeling.