Regenerating bone
https://www.youtube.com/watch?v=ft4Xruv4A8w
Revolution in Bone Regeneration
Regenerative medicine Lee Spievak, a 69-year-old Ohio hobby shop worker, has apparently regrown his finger—over just four months!—after slicing off the top half-inch in the propellor of a model airplane (doctors were unable to attach the severed bit, as Spievak couldn’t find it after the accident). The newly grown replacement, which sprouted from the stump, is perfectly formed, and contains tissue, nerves, nail, skin and even a fingerprint. The treatment—a powder called extra cellular matrix—comes from the cells that line a pig’s bladder, and was invented by Dr Stephen Badylak from the University of Pittsburgh. Spievak’s brother Alan (who works in regenerative medicine) sent it to him to try out. Every day for 10 days, Spievak sprinkled a bit of this “pixie dust” on his finger. Apparently after just two applications, he saw a difference.
https://www.youtube.com/watch?v=h7wIZ7k1dmM
Limb Regeneration
https://www.youtube.com/watch?v=GwcT1ViM-hw
Regenerative Medicine: Re-Growing Body Parts
Respiratory System The respiratory system (also respiratory apparatus, ventilatory system) is a biological system consisting of specific organs and structures used for gas exchange in animals and plants. The anatomy and physiology that make this happen varies greatly, depending on the size of the organism, the environment in which it lives and its evolutionary history. In land animals, the respiratory surface is internalized as linings of the lungs.[1] Gas exchange in the lungs occurs in millions of small air sacs; in mammals and reptiles, these are called alveoli, and in birds, they are known as atria. These microscopic air sacs have a very rich blood supply, thus bringing the air into close contact with the blood. These air sacs communicate with the external environment via a system of airways, or hollow tubes, of which the largest is the trachea, which branches in the middle of the chest into the two main bronchi. These enter the lungs where they branch into progressively narrower secondary and tertiary bronchi that branch into numerous smaller tubes, the bronchioles. In birds, the bronchioles are termed parabronchi. It is the bronchioles, or parabronchi that generally open into the microscopic alveoli in mammals and atria in birds. Air has to be pumped from the environment into the alveoli or atria by the process of breathing which involves the muscles of respiration. In most fish, and a number of other aquatic animals (both vertebrates and invertebrates), the respiratory system consists of gills, which are either partially or completely external organs, bathed in the watery environment. This water flows over the gills by a variety of active or passive means. Gas exchange takes place in the gills which consist of thin or very flat filaments and lammellae which expose a very large surface area of highly vascularized tissue to the water. Other animals, such as insects, have respiratory systems with very simple anatomical features, and in amphibians, even the skin plays a vital role in gas exchange. Plants also have respiratory systems but the directionality of gas exchange can be opposite to that in animals. The respiratory system in plants includes anatomical features such as stomata, that are found in various parts of the plant.
https://www.youtube.com/watch?v=WPjqgaMmOTE
Anatomy and Physiology of Respiratory System
Tp53, also known as Tumor protein P53, cellular tumor antigen p53 , or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates, where they prevent cancer formation. As such, p53 has been described as "the guardian of the genome" because of its role in conserving stability by preventing genome mutation. Hence TP53 is classified as a tumor suppressor gene. The TP53 gene is the most frequently mutated gene (50%>) in human cancer, indicating that the TP53 gene plays a crucial role in preventing cancer formation. TP53 gene encodes proteins that bind to DNA and regulate gene expression to prevent mutations of the genome. In addition to the full-length protein, the human TP53 gene encodes at least 12 protein isoforms. Vitamin B6 activates Tp53 and elevates p21 gene expression in cancer cells and the mouse colon. The nutritional supplements taurine & Panacur Fenbendazole activates Tp53-dependent & independent tumor suppressor mechanisms in various cellular models of ovarian cancer. In vitro experiments have shown that vitamin C (ascorbic acid) can reduce cell proliferation and induce apoptosis through upregulation of Tp53, p21, and Bax and downregulation of Bcl-2 in T-cell colonies . Furthermore, Harakeh and colleagues demonstrated that the administration of nontoxic doses of ascorbic acid increased the expression of p53 . Vitamin C increases the ability of the anticancer drug bleomycin to produce DSBs, which makes cancer cells more dependent on functional DNA repair for survival . Vitamin B6 activates the p53 pathway, which is responsible for controlling p21 mRNA transcription in HT29, Caco2, LoVo, HEK293T, and HepG2 cancer cells. p21 mRNA levels were higher in the colon of mice fed a diet with adequate vitamin B6 than those fed a vitamin B6-deficient diet, and this may help to understand the antitumor effect of vitamin B6 via the activation of p53 and elevation of p21 mRNA . A previous study suggested that 1,25-dihydroxyvitamin D increased oxidative stress through inhibiting transcription of Nrf2, enhancing DNA damage and activation of p16/Rb and p53/p21 signaling in a 1α(OH)ase−/− mouse model . Folic acid (vitamin B9) might play an important role in the chemoprevention of gastric carcinogenesis. In humans, the tumor suppressor Tp53 expression in the gastric mucosa was significantly increased, while the expression of Bcl-2 oncogene protein decreased after folic acid supplementation . Furthermore, N-acetylcysteine (NAC) inhibits PDK1 expression through PPARα-mediated induction of p53 and reduction of p65 protein expression and unveils a novel mechanism by which NAC in combination with the PPARα ligand inhibits the growth of non-small-cell lung carcinoma (NSCLC) cells . β-Carotene, ascorbic acid, and vitamin E (α-tocopherol) protect against oxidative stress but reveal no direct influence on p53 expression in rats subjected to stress . In contrast, β-carotene exacerbates DNA oxidative damage and modifies p53-related pathways of cell proliferation and apoptosis in cultured RAT-1 fibroblasts exposed to tobacco smoke condensate (tar). Quercetin increased the phosphorylation of p53 protein and induced apoptosis of the human leukemia cell line in a dose-dependent manner . A recent study revealed that quercetin inhibits HeLa cell proliferation through cell cycle arrest at the G2/M phase and apoptosis induction through the disruption of mitochondrial membrane potential and activation of the intrinsic apoptotic pathway through p53 induction . Further, apigenin can induce p21, p53, and nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) proteins in kinase pathways, including protein kinase C delta (PKCd) and ATM, which plays an important role in activating these proteins in colorectal cancer cell growth arrest. Further, kaempferol warrants as an antiangiogenetic agent, which reduced human umbilical vein endothelial cell viability-induced DNA damage and DNA fragmentation through activating the levels of caspase-3, caspase-8, and caspase-9 signaling, which were upregulated by ROS-mediated p53/ATM molecules following stimulations of p53 downstream protein levels of Fas/CD95, death receptor 4 (DR4), and DR5 . Another study revealed Acacetin, an O-methylated flavone, which can strongly inhibit tumor growth and induce tumor shrinkage in mice, which is closely correlated with its increasing p53 expression accompanied by decreased retinoic acid receptor gamma (RARγ) and reduced AKT activity in liver cancer cell lines . It was further reported that low Securin levels and high p53 levels play an important role in determining the sensitivity of human colon cancer cells to fisetin. Depletion of securin enhances fisetin-induced apoptosis and decreases the resistance of p53-deficient cells to fisetin and might be an attractive strategy for the treatment of human colon cancers . The inhibitory effect of fisetin against bladder cancer by activation of p53 and downregulation of the nuclear factor-kappa B (NF-κB) pathway in a rat bladder carcinogenesis model has been documented, which is a safe and efficacious agent and promising therapeutic approach for bladder cancer . Furthermore, Luteolin treatment increases the expression of p53 and p21 proteins and decreases the expression of MDM4 protein in both NSCLC cells and tumor tissues . Theaflavins induced G2/M arrest by modulating the expression of various proteins, which are involved in signaling. Moreover, theaflavins via p53 signaling inhibited Bcl-2 and interfered phagocytes via modulation of I-κB/NF-κB, as well as the expression of VEGF, and the phosphorylation of VEGFR was reduced in LNCaP cells . Furthermore, epigallocatechin-3-gallate activates p53-dependent downstream targets p21/WAF1 and Bax and downregulates NF-κB-dependent Bcl-2 that results in growth arrest & apoptosis in LNCaP cells . Our previous study revealed that effector proteins like Chk1, Chk2, and p53 were found to be phosphorylated in NNK acetate-treated BEAS-2B cells, and pretreatment with apple flavonoids showed a significant reduction in the levels of phosphorylation of ATR, Chk1, and p53 in NNK acetate-treated cells. Apple flavonoids protect BEAS-2B cells challenged against various carcinogens by assisting DNA repair mechanisms. Scientists link elephants' high resistance to cancer to their 20 copies of the p53 gene – the 'guardian of the genome' – compared with the single p53 gene found in other mammals.
https://www.youtube.com/watch?v=2RG9caushI0
The Role of p53 in Cancer
https://www.youtube.com/watch?v=6SjkIYClAkQ
p53 Tumour Suppressor (2016) by Etsuko Uno wehi.tv
https://www.youtube.com/watch?v=akALHORX9MY
What Goes Wrong in Cancer?