This paper discusses, from a mathematician's point of view, the thesis formulated by Israel Gelfand, one of the greatest mathematicians of the 20th century, and one of the pioneers of mathematical biology, about the unreasonable ineffectiveness of mathematics in biology as compared with the obvious success of mathematics in physics. The author discusses the limitations of the mainstream mathematics of today when it is used in biology. He suggests that some emerging directions in mathematics have potential to enhance the role of mathematics in biology.We compared the magnitude of muscular strength changes among older women occupants of different strength tertiles in response to progressive resistance-training (RT). Additionally, we examined the possibility of older women initially characterized as weak (occupants of the lower tertile of strength status) can achieve a higher muscular strength level to be inserted into a better category (middle or upper tertiles). The present investigation was attended by 113 physically independent older women (>60 years old). Muscular strength was assessed by one-repetition maximum (1RM) tests on chest press, preacher curl, leg extension exercises, and by the isokinetic (ISOK) peak torque of knee extension and flexion at 60 and 180°/s angular velocities. The RT lasted 12 weeks (3 x/week) and consisted of eight exercises for the whole body. The participants were divided into tertiles (LOWER, MIDDLE, and UPPER) according to the performance at baseline for each strength measure. After RT, the LOWER tertile showed more significant magnitude gains than the UPPER tertile to the 1RM in leg extension and preacher curl and isokinetic measurements (6.9-36.3%). A considerable number of older women increased muscular strength enough to move from LOWER to MIDDLE or UPPER tertiles. From our results, it can be inferred that older women occupants of the lower strength tertile show more significant muscular strength gains when compared to their stronger counterparts. Moreover, 12 weeks of RT seem to be sufficient to transfer older women previously characterized as "weak" to a better category.
Traditional Chinese Medicine (TCM) defined constitution as a health statue or physical fitness that determines individual susceptibility to diseases. Yin deficiency constitution (YinDC) is a type of constitution closely related to aging. Previous studies found that the characteristic genes of YinDC are part of the inflammatory aging signaling pathways (e.g., NF-kappa B). Therefore, the aim of the study was to further reveal the dysregulation of genes associated with inflammatory aging in YinDC women.

This study adopted the industrial standard of constitutional judgment, and screened YinDC (n=30) and Balanced constitution (BC) (n=30) from women between the ages of 35 to 49, a range categorized as the degenerating period by TCM. Five genes CCL4, BCL2A1, NFKBIA, TAK1, and IL-8 were analyzed by qRT-PCR.

Logistical regression revealed the correlation between body constitution and the expression of the five genes the expression of NFKBIA and CCL4 mRNA was significantly up-regulated, whereas the expression of BCL2A1 mRNA was significantly down-regulated in YinDC (P<0.05). Age or weight, when included in the model, did not affected the correlations.

Increased mRNA expression of CCL4 and NFKBIA and decreased mRNA expression of BCL2A1 may be the molecular basis of premature aging of YinDC women. These results provide a mechanistic basis for early conditioning of YinDC, anti-aging, and the prevention of aging-related diseases.
Increased mRNA expression of CCL4 and NFKBIA and decreased mRNA expression of BCL2A1 may be the molecular basis of premature aging of YinDC women. https://www.selleckchem.com/products/4sc-202.html These results provide a mechanistic basis for early conditioning of YinDC, anti-aging, and the prevention of aging-related diseases.
Mind-body integrative health (MBIH) interventions to improve adolescent sleep are lacking. The study characterized sleep quality and bedtime-related psychosocial stressors among urban minority adolescents, explored associations between demographics factors, stressors and sleep quality, and gauged interest in a MBIH sleep intervention.

167 school-based health center (SBHC) patients (mean age = 16.3; 64 % female; 68 % Latino) participated in a needs assessment as part of a quality improvement project. They reported bedtime-related psychosocial stressors using items from the Adolescent Sleep Hygiene Scale (ASHS), sleep quality using the Pittsburgh Sleep Quality Index (PSQI), and interest in a MBIH-based sleep intervention. Chi-square and logistic regression examined associations between demographics, stressors, sleep quality, and interest in the intervention.

67 % had poor sleep quality. Females, compared to males, had 2.23 higher odds (95 % Confidence Interval [CI] 1.12, 4.42) of having poor sleep qualityportunity for practitioners and complementary therapists to offer MBIH interventions to a population at high-risk for poor sleep quality.
Higenamine (HG), is one of the main active components in many widely used Chinese herbs, and a common ingredient of health products in Europe and North America. Several groups, including our own, have previously shown the beneficial effects of HG against cardiomyocyte death during acute ischemic damage. However, the effect of HG on chronic cardiac remodeling, such as cardiac fibrosis, remains unknown.

Herein, we aim to investigate the role of HG in cardiac fibrosis in vivo as well as its cellular and molecular mechanisms.

Chronic pressure overload with transverse aortic constriction (TAC) significantly increased cardiac hypertrophy, fibrosis, and cardiac dysfunction in mice, which were significantly attenuated by HG. Consistently, cardiac fibrosis induced by the chronic infusion of isoproterenol (ISO), was also significantly reduced by HG. Interestingly, our results showed that HG had no effect on adult mouse CM hypertrophy in vitro. However, HG suppressed the activation of cardiac fibroblasts (CFs) in vitro. Furthermore, TGF-β1-induced expression of ACTA2, a marker of fibroblast activation, was significantly suppressed by HG. Concomitantly, HG inhibited TGF-β1-induced phosphorylation of Smad2/3 in CFs. HG also reduced the expression of extracellular matrix molecules such as collagen I and collagen III. To our surprise, the inhibitory effect of HG on CFs activation was independent of the activation of the beta2 adrenergic receptor (β2-AR) that is known to mediate the effect of HG on antagonizing CMs apoptosis.

Our findings suggest that HG ameliorates pathological cardiac fibrosis and dysfunction at least partially by suppressing TGF-β1/Smad signaling and CFs activation.
Our findings suggest that HG ameliorates pathological cardiac fibrosis and dysfunction at least partially by suppressing TGF-β1/Smad signaling and CFs activation.