Archives of Medical Research最新文献

Background and objective

Disturbed autonomic nervous system (ANS) may promote inflammatory, immune, and oxidative stress responses, which may increase the risk of acute coronary events. S100β has been proposed as a biomarker of neuronal injury that would provide an insightful understanding of the crosstalk between the ANS, immune-inflammatory cells, and plaques that drive atherosclerosis. This study investigates the correlation between S100β, and functional coronary stenosis as determined by quantitative flow ratio (QFR).

Methods

Patients with unstable angina pectoris (UAP) scheduled for coronary angiography and QFR were retrospectively enrolled. Serum S100β levels were determined by enzyme-linked immunosorbent assay. The Gensini score was used to estimate the extent of atherosclerotic lesions and the cumulative sum of three-vessel QFR (3V-QFR) was calculated to estimate the total atherosclerotic burden.

Results

Two hundred thirty-three patients were included in this study. Receiver operator characteristic (ROC) curve indicated that S100β>33.28 pg/mL predicted functional ischemia in patients with UAP. Multivariate logistic analyses showed that a higher level of S100β was independently correlated with a functional ischemia-driven target vessel (QFR ≤0.8). This was also closely correlated with the severity of coronary lesions, as measured by the Gensini score (OR = 5.058, 95% CI: 2.912–8.793, p <0.001). According to 3V-QFR, S100β is inversely associated with total atherosclerosis burden (B = –0.002, p <0.001).

Conclusions

S100β was elevated in the functional ischemia stages of UAP. It was independently associated with coronary lesion severity as assessed by Gensini score and total atherosclerosis burden as estimated by 3V-QFR in patients with UAP.

Background

Ulipristal acetate (UPA) and levonorgestrel are used as emergency hormonal contraceptives. Although both are highly effective in preventing pregnancy, UPA shows efficacy even when taken up to 120 h after unprotected sexual intercourse.

Aims

To investigate whether the mechanism of UPA's contraceptive action involves post-fertilization effects.

Methods

In vitro and in vivo studies using cultured human endometrial cells and a pre-clinical rat model.

Results

Endometrial cells treated with UPA showed changes in the expression of receptivity gene markers and a significant decrease in trophoblast spheroids attached to the cultured cells. In addition, administration of UPA to female unmated rats decreased the expression of implantation-related genes in the endometrium and inhibited the number of implantation sites in the mated group compared to the non-treated group.

Conclusions

These results support that UPA as an emergency contraceptive might have post-fertilization effects that may affect embryo implantation.

Purpose

Sarcopenia or age-associated muscle loss is common in patients with Alzheimer's disease (AD). We have previously demonstrated the contribution of a leaky gut to sarcopenia in AD. Here, we asked whether resistant exercise (RE) reduces the sarcopenia phenotype by repairing intestinal leakage in patients with AD.

Method

A prospective, single-center study of older adults, including healthy controls and patients with AD (n = 44–51/group), was conducted to measure plasma zonulin and claudin-3 (markers of intestinal leakage), handgrip strength (HGS), and short physical performance battery (SPPB) as a measure of functional capacity. Measurements in patients with AD were performed at baseline and after 12 weeks of RE.

Results

At baseline, patients with AD had higher plasma zonulin and claudin-3 and lower HGS, gait speed, and SPPB scores than controls. RE reduced plasma zonulin and claudin-3 levels and improved HGS, SPPB scores, and gait speed. Regression analysis revealed robust relationships between changes in plasma zonulin and claudin-3 with HGS. Plasma zonulin was also positively associated with SPPB scores. In addition, RE downregulated plasma markers of inflammation and oxidative stress. However, the prevalence of sarcopenia based on low HGS and muscle atrophy or low SPPB was not affected by RE.

Conclusion

Taken together, disruption of the intestinal mucosal barrier may contribute to functional decline and sarcopenia in AD, which is incompletely recovered by RE. Circulating levels of zonulin and claudin-3 may be valuable in predicting sarcopenia and functional capacity in older adults with AD.

Aim

To evaluate the progress of the Mexican Institute of Social Security Recovery Policy (IMSS-RP) in addressing the decline in essential health services caused by the COVID-19 pandemic.

Methods

We analyzed eleven indicators of essential health services from 35 IMSS state delegations. The assessment included ambulatory and hospital care indicators such as breast and cervical cancer screening, family medicine, dental and specialty visits, diabetes and hypertension visits and health outcomes, deliveries, and elective surgeries. We analyzed the period before (January 2018–March 2021) and during (April 2021–June 2023) the implementation of the IMSS-RP. Statistical analysis to determine the association of the policy with service indicators and the change in their trends included an interrupted time series analysis and Poisson Generalized Estimating Equation models.

Results

The volume of services showed substantial declines during the first year of the COVID-19 pandemic, reaching between 11 and 81% of pre-pandemic levels. All services increased significantly during the first 27 months of the IMSS-RP implementation; specialty visits, cervical and breast cancer screening, and diabetes control exceeded pre-pandemic levels (103%,112%,103%, and 138%, respectively). However, only deliveries and the percentage of patients with controlled diabetes and hypertension showed a stable increase following the IMSS-RP implementation, whereas the remaining services showed an initial increase but began to decrease over time.

Conclusions

After 27 months of implementation, IMSS-RP achieved progress in increasing the volume of essential health services and improving chronic disease control. However, declining trends in several services signal the need to focalize the policy.

Background

Cognitive impairment is defined as a neurological condition that alters multiple cerebral functions such as reasoning, memory, concentration, and association, among others. It has found to be widely correlated with several factors such as oxidative stress. The latter could be induced by numerous pathological conditions characterized by increased levels of free radicals and decreased levels of antioxidants. Pregnancy is a period when women undergo a physiological state of oxidative stress due to hormonal changes and increased oxygen requirements to maintain pregnancy. However, when oxidative stress exceeds antioxidant capacity, this leads to cellular damage that promotes a diabetogenic state. Recent studies suggest a possible association between gestational diabetes and cognitive impairment, but the underlying mechanisms remain unclear.

Aims

We aim to explore the pathophysiological relationship between cognitive impairment and oxidative stress, focusing on the possible involvement of oxidative stress as the inducing mechanism.

Methods

We performed a comprehensive literature review through PubMed and Google Scholar. Our keywords were “neuroinflammation”, “cognitive impairment”, “gestational diabetes”, “oxidative stress”, “antioxidants”, and “free radicals”.

Results

From the initial 400 records identified, a total of 78 studies were analyzed and included in our study.

Conclusion

Oxidative stress plays a fundamental role in the development of cognitive impairment. Understanding this correlation is essential to the development of targeted medical interventions and, ultimately, promote research and prevention that will benefit the mother-child binomial in the short and long term.

The rise in life expectancy has significantly increased the occurrence of age-related chronic diseases, leading to escalating expenses for both society and individuals. Among the main factors influencing health and lifespan, lifestyle takes a forefront position. Specifically, nutrition, mental activity, and physical exercise influence the molecular and functional mechanisms that contribute to the prevention of major age-related diseases. Gaining deeper insights into the mechanisms that drive the positive effects of healthy lifestyles is valuable for creating interventions to prevent or postpone the development of chronic degenerative diseases. This review summarizes the main mechanisms that underlie the positive effect of lifestyle factors in counteracting the major age-related diseases involving brain health, musculoskeletal function, cancer, frailty, and cardiovascular diseases, among others. This knowledge will help to identify high-risk populations for targeted intervention trials and discover new biomarkers associated with healthy aging.

Background and aim

Autoimmunity refers to the presence of autoantibodies and autoreactive lymphocytes against the structural molecules of an individual's cells or tissues, known as self-antigens or autoantigens. It might exist in the absence of autoimmune disease. However, how autoimmunity develops remains a mystery, despite the discovery of autoantibodies in human cord blood.

Methods

Murine fetuses on day 14 of gestation were subjected to intraperitoneal injection of murine thyroid peroxidase (TPO) peptides or collagen type II (CII) at graded doses via transuterine approach. Postnatally, the recipients were examined for autoantibodies by ELISA and autoreactive lymphocytes by in vitro incorporation of tritium and for the development of autoimmune thyroiditis or arthritis.

Results

At one month of age, the recipients did not secrete significant levels of anti-TPO or CII IgG_2a in sera until a dose of 0.5 µg TPO or 5.0 µg CII was injected in utero. Serum anti-TPO or CII IgG_2a persisted for at least two to four months postnatally. In recipients with elevated autoantibodies, their lymphocytes also showed proliferative responses specifically to TPO or CII. However, the development of autoantibodies and autoreactive lymphocytes was not associated with inflammatory cell infiltration of thyroid glands or paw joints even though anti-TPO or CII IgG_2a was enhanced by postnatal TPO or CII challenge.

Conclusion

Fetal exposure to free autoantigens could be immunogenic, shedding new light on the in utero origin of autoantibodies and autoreactive lymphocytes. The development of autoimmunity requires a threshold intensity of autoantigen exposure in the fetus.