Our interest in development of hyaluronidase inhibitors as male antifertility agents led to identification of Terminalia chebula (T. chebula) plant with hyaluronidase (HAase) inhibitory activity of human spermatozoa ( approximately 93% inhibition) and rat caudal epididymal spermatozoa ( approximately 86% inhibition) in vitro at 30 mg/ml.
Journal of the Medical Association of Thailand = Chotmaihet Thangphaet
BACKGROUND: Tri-sa-maw recipe is a botanical preparation comprised of equal proportions ofthe three herbalfruits, namely Terminalia chebula Retz., Tenninalia sp. and Terminalia bellirica Roxb. This recipe is used for antipyretic, expectorant, periodic maintenance, and relieving stomach tight. OBJECTIVE: To evaluate the acute and sub-chronic toxicities of Tri-sa-maw recipe extract in rats. MATERIAL AND METHOD: In the present study of acute toxicity, a single oral dose 5,000 mg/kg of Tri-sa-maw recipe extract was administered to rats.
A comparison of the data published in anatomy textbooks and anthropological tables does not reveal any change in basic heart dimensions during the period since the beginning of the 20th century to nowadays. However, normal values of many other parameters have changed up to 30% over the same period. These changes may be caused by the acceleration phenomenon or the extension of average lifespan.
Amyotrophic lateral sclerosis (ALS) is a progressive disease which is caused by degeneration of motor neurons in the central nervous system. The incidence of ALS is higher in men than women, but the female advantage disappears with increased age. Here, we report evidence that the female advantage is due to the protective role of estrogen. In an ALS mouse model carrying the human Cu/Zn superoxide dismutase (hSOD1) G93A transgene, ovariectomy did not alter the onset age of the disease while reducing the female lifespan by 7 days and making it comparable to that of the male transgenic mice.
Spinal muscular atrophy (SMA) is the most common genetic cause of infant mortality. SMA is caused by loss of functional survival motor neuron 1 (SMN1), resulting in death of spinal motor neurons. Current therapeutic research focuses on modulating the expression of a partially functioning copy gene, SMN2, which is retained in SMA patients. However, a treatment strategy that improves the SMA phenotype by slowing or reversing the skeletal muscle atrophy may also be beneficial. Myostatin, a member of the TGF-beta super-family, is a potent negative regulator of skeletal muscle mass.
Atrophy is one of the major age-related changes in the brain. The absence of brain atrophy in elderly individuals reflects deceleration in the process of biological aging. Moreover, results from human twin studies suggest a large genetic influence on the variance of human brain tissue volumes. To investigate the association of brain volumes with exceptional longevity, we tested whether middle-aged to elderly offspring of nonagenarian siblings have larger brain volumes than their spouses using magnetic resonance imaging.
Life's timekeeper is a 'free-running' intracellular oscillator synchronised across all cells. It runs throughout life splitting lifespan into equal length phases. During the maturational period it controls the overall rate of progression whereas in the post-maturational period it controls the overall rate of ageing. This includes the rate of senescence and hence time to death. As such life's timekeeper equates maturational and post-maturational time, hence explains the tight correlation between these time periods that has existed throughout mammalian evolution.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons in the spinal cord, brain stem, and motor cortex. Mutations in superoxide dismutase (SOD1) are associated with familial ALS and lead to SOD1 protein misfolding and aggregation. Here we show that the molecular chaperone, HSJ1 (DNAJB2), mutations in which cause distal hereditary motor neuropathy, can reduce mutant SOD1 aggregation and improve motor neuron survival in mutant SOD1 models of ALS.