Supplemental L-Arginine Improves the Embryonic Intestine Development and Microbial Succession in a Chick Embryo Model

Early colonization of intestinal microbiota plays an important role in intestinal development. However, the microbial succession at an embryonic stage and its assembly patterns induced by prenatal nutrition are unknown. In the present study, we used a chick embryo model to investigate the effects of in ovo feeding (IOF) of L-arginine (Arg) on the intestinal development and microbial succession of embryos. A total of 216 fertile eggs were randomly distributed into 2 groups including the non-injected control group and IOF of Arg group with 7 mg/egg. The results showed that IOF Arg increased the intestinal index, absolute weight of jejunum, and improved jejunal morphology in terms of villus width and surface area (p < 0.05). The relative mRNA expressions of mTOR and 4E-BP1 were up-regulated and accompanied by higher contents of Mucin-2 in the Arg group (p < 0.05). There was a significant elevation in contents of serum glucose and high-density lipoprotein cholesterol, whereas there was a decreased low-density lipoprotein cholesterol in the Arg group (p < 0.05). Additionally, Proteobacteria and Firmicutes were major intestinal bacteria species at the embryonic stage. However, Arg supplementation targeted to shape assembly patterns of microbial succession and then changed microbial composition (p = 0.05). Meanwhile, several short-chain fatty acids (SCFAs)-producing bacteria, such as Roseburia, Blautia, and Ruminococcus were identified as biomarkers in the Arg group (LDA > 3, p < 0.05). Accordingly, significant elevated concentrations of SCFAs, including lactic acid and formic acid, were observed in the Arg group (p < 0.05), accompanied by the higher concentration of butyric acid (0.05 < p < 0.10). In conclusion, prenatal Arg supplementation improved embryonic intestine development by regulating glucose and lipid homeostasis to supply more energy for chick embryos. The possible mechanism could be the roles of Arg in shaping the microbial assembly pattern and succession of the embryonic intestine, particularly the enrichment of potential probiotics. These findings may contribute to exploring nutritional strategies to establish health-promoting microbiota by manipulating prenatal host-microbe interactions for the healthy development of neonates.

On the Driver of Blood Circulation Beyond the Heart

The heart is widely acknowledged as the unique driver of blood circulation. Recently, we discovered a flow-driving mechanism that can operate without imposed pressure, using infrared (IR) energy to propel flow. We considered the possibility that, by exploiting this mechanism, blood vessels, themselves, could propel flow. We verified the existence of this driving mechanism by using a three-day-old chick-embryo model. When the heart was stopped, blood continued to flow, albeit at a lower velocity. When IR was introduced, flow increased, by ~300%. When IR energy was diminished under otherwise physiological conditions, blood failed to flow. Hence, this IR-dependent, vessel-based flow-driving mechanism may indeed operate in the circulatory system, complementing the action of the heart.

IN-VITRO SCREENING OF THEAFLAVIN AND GINKGETIN ON A549 LUNG CANCER CELL LINE

Cancer is a complex, multi-gene, multi-step disease occurring as a result of a sequential accumulation of genetic and epigenetic changes. Death due to cancer rank second among all cause of death globally. Dysregulation of signaling pathway e.g. HGF/c-MET which were otherwise activated during embryonic development contributes to malignant transformation and metastasis in later phase of life. Phytochemicals due to their safety, low toxicity, and general availability are either taken as supplement or through dietary sources for cancer chemoprevention or supportive agent during the treatment of cancer. The present study therefore aim to screen in-silico inspired c-MET antagonist Theaflavin & Ginkgetin in-vitro on against A549 cell line along with their antiangiogenesis effect on chick embryo model.

Scoliotic disease: report to the teacher

It is with gratitude that I dedicate my work to the teacher, Ya.L. Tsivyan, who not only provided a subject for research, but also, on his own example of a person devoted to his work, brought up a generation of scholars for whom life and science are inseparable.The paper presents the results of many years of research on idiopathic scoliosis in the form of a report to the teacher. Several fundamental topics were considered:1) for the first time in world practice, it was established, on the basis of a study of 50 patients with idiopathic scoliosis, that the etiological factor of scoliosis is ectopic localization of neural crest derivatives, which are not genetically determined to chondrogenic differentiation and the growth process, in the vertebral body growth plate;2) a local disturbance of chondrogenesis in the vertebral body growth plate is the cause of the growth asymmetry and formation of spinal deformity in idiopathic scoliosis;3) the degree of structural changes in the spine and the prognosis of the deformity progression depend on the level of disturbance of the morphogenetic processes in the vertebral body growth plate embedded in embryogenesis;4) it is supposed to confirm the proposed hypotheses by inhibition of the PAX3 gene in the chick embryo model of idiopathic scoliosis and to get answers to many more unclear questions concerning scoliotic disease.