Developed by the co-inventor of the pacemaker at London University, Arasys Effortless Fitness technology has been known for its significant inch loss and muscle building. New clinical studies are presently designed to provide evidence that Arasys has the same health benefits as regular exercise by virtue of resonating the brain signal given to the nerve in charge of the muscle.
Xanya Sofra Weiss
Xanya Sofra-Weiss. Ph.D, (2008)
Ionic Currents: The Spark of Life and Directional Force in Cellular Metabolism and Energetics.
The aging process cannot be conceptualized by examining a single gene or a single pathway, but can best be addressed at the systems level. Aging is not only the sum total of shortened telomeres, denatured proteins and DNA molecules, or oxidative damage in the mitochondria. Aging attacks key regulatory nodes crucial for the biological network stability. It is the dynamic process of increasing imbalances in the systemic organization of degenerating biological processes. DNA and stem cells engineering have successfully reversed certain individual components of time attrition resulting in rejuvenation and aging delay. So far, research has merely followed a sequential process that goes from the part to the whole, identifying aging genes and engineering stem cells, etc. However, discovering pieces of the puzzle still requires identification of the interconnections between matching pieces before the solution emerges. The old, the ill, and the injured all suffer from misarranged patterns of atoms. A single substitution an A for a G in a DNA molecule can cause a significant change in the conductance of the molecule leading to cancer. Such research findings demonstrate how the sequence and interrelations of amino acids in a protein, or the sequence of base pairs in a DNA molecule can become determining factors between health and disease, aging and youth. Gene expression is stronger when the gene is attached to the nuclear envelope (the membrane that surrounds the nucleus) than when it moves away from the nuclear envelope (see image). In other words, cells make use of the nuclear architecture to code epigenetic information. The DNA sequence alone doesn’t determine everything. The importance of the spatial organization or nuclear architecture in regulating gene expression begs for scientific observation that does not merely focus on the study of atoms and molecules, (the basic components of a Gestalt); but on the interrelations, sequence, orientation and spatial organization of these atoms and molecules (the dynamic whole or Gestalt). Recent research has shown that DNA, proteins, cells, including stem cells, appear to be electrical in that they demonstrate conductivity or the presence of ionic currents. Since electricity is a dynamic entity emerging out of the interactions of atoms and molecules, we propose that perhaps the simplest way of focusing on the entire system is by decoding the complex electrical signals that map biological interactions with respect to spatial organization. Biological signals must be analyzed in terms of their amperage, frequency, voltage, interactions, orientation, spatial organization. Next will be their translation into electronic signals that comply with the specifications of amperage, frequency, voltage or biological signals. Electronic signals will then be intertwined to orchestrate a Gestalt waveform built on the basis of information attained from observations of biological interactions and architecture – a process similar to that done in Pollock’s lab (1990-2004). This Gestalt waveform will act as an electronic diplomat to awaken biological processes that have diminished with aging or disease by signaling the recuperation and activation of biological reparative mechanisms leading to extended longevity.
Xanya Sofra Weiss
NEWS RELEASE spacer Print Version APRIL 24, 2009
New Target for Maintaining Healthy Blood Pressure Discovered by Penn Scientists
PHILADELPHIA – In trying to understand the role of prostaglandins – a family of fatty compounds key to the cardiovascular system – in blood pressure maintenance, researchers at the University of Pennsylvania School of Medicine and colleagues discovered that mice that lack the receptor for one type of prostaglandin have lower blood pressure and less atherosclerosis than their non-mutant brethren.
Prostaglandin F2-alpha receptor expression depicted in blue in renal artery.
Prostaglandin F2-alpha receptor expression depicted in blue in renal artery.
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The results indicate that the normal role for the type of prostaglandin studied, PGF2α, is to increase blood pressure and accelerate atherosclerosis, at least in rodents, and suggest that targeting this pathway could represent a novel therapeutic approach to cardiovascular disease.
The results appeared this week in the Proceedings of the National Academy of Sciences.
“Blocking this prostaglandin receptor may provide a strategy for controlling blood pressure and its attendant vascular disease,” notes senior author Garret A. FitzGerald, MD, Director of the Institute for Translational Medicine and Therapeutics at Penn.
To address prostaglandins’ role in maintaining blood pressure, FitzGerald and his team, including researchers from the University of Southern Denmark, created strains of mice in which both the maternal and paternal copies of the gene for the PGF2α receptor were deleted. They did this in mice with a normal genetic background and in ones that contained an additional mutation in the low-density lipoprotein receptor gene. These manipulations effectively rendered the mice unable to respond to the prostaglandins.
The delicate balance the body maintains to keep blood pressure stable involves not only the prostaglandin system, but another biological pathway, the renin-angiotensin-aldosterone system, or RAAS. Under conditions of low blood pressure, the liver secretes a protein called angiotensiogen. Renin, an enzyme produced by the kidneys, cleaves angiotensiogen into a peptide called angiotensin I. Angiotensin I is cleaved again to form angiotensin II, which stimulates blood vessels to narrow, thereby increasing blood pressure. At the same time, angiotensin II induces the release of the hormone aldosterone, which further elevates blood pressure by promoting retention of water and sodium in the kidneys.
Many conventional therapies for high blood pressure target components of the RAAS pathway. For instance, ACE inhibitors such as captopril (Capoten) target the formation of angiotensin II, while aliskiren (Tekturna) targets renin.
The team assessed the impact of the PGF2α receptor mutations on both blood pressure and RAAS activity. They found that under a variety of circumstances deletion of the PGF2α receptor lowered blood pressure coincident with suppression of RAAS activity.
“Precisely how these two observations are connected is the focus of our current research,” says FitzGerald.
Blood pressure was reduced in both types of genetically engineered mice relative to control littermates. The RAAS molecules renin, angiotensin I, and aldosterone were also reduced, a biological situation leading to lower blood pressure.
The team found that the PGF2α receptor is expressed in the smooth muscle surrounding arteries in the kidneys. However, it was absent in the muscle surrounding the aorta, in the atherosclerotic lesions of mice with their PGF2α receptors knocked out, as well as in the macrophages that inhabit those lesions. Importantly, these atherosclerotic lesions were smaller and less abundant in mice that had both the low-density lipoprotein and PGF2α receptors knocked out, as was macrophage infiltration and inflammatory cytokine production, both of which are indicators of the inflammatory response that marks these plaques.
Prostaglandins are produced during the oxidation of certain cell molecules by cyclooxygenases, the COX enzymes targeted by COX inhibitors, but how remains unclear. FitzGerald’s group had previously shown that blockading cyclooxygenase 1 and its major prostaglandin product, thromboxane, also lowers blood pressure, slowing atherosclerosis, but in this previous study, the relevant genes are present in the aorta and its atherosclerotic lesions. PGF2α, by contrast, acts via the kidney and represents a distinct therapeutic opportunity.
“The picture is emerging that PGF2α controls blood pressure by a mechanism unique among the prostaglandins,” says FitzGerald. “Besides the case of thromboxane, two other types of prostaglandins, PGI2 and PGE2, stimulate renin secretion, which is part of the RAAS pathway.”
Assuming these findings can be translated to humans, targeting the PGF2α pathway could represent a novel opportunity for therapeutic control of blood pressure in cardiovascular patients.
The research was funded by the National Heart, Lung, and Blood Institute and the American Heart Association.
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PENN Medicine is a $3.6 billion enterprise dedicated to the related missions of medical education, biomedical research, and excellence in patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation’s first medical school) and the University of Pennsylvania Health System.
Penn’s School of Medicine is currently ranked #3 in the nation in U.S.News & World Report’s survey of top research-oriented medical schools; and, according to the National Institutes of Health, received over $366 million in NIH grants (excluding contracts) in the 2008 fiscal year. Supporting 1,700 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.
The University of Pennsylvania Health System (UPHS) includes its flagship hospital, the Hospital of the University of Pennsylvania, rated one of the nation’s top ten “Honor Roll” hospitals by U.S.News & World Report; Pennsylvania Hospital, the nation’s first hospital; and Penn Presbyterian Medical Center. In addition UPHS includes a primary-care provider network; a faculty practice plan; home care, hospice, and nursing home; three multispecialty satellite facilities; as well as the Penn Medicine at Rittenhouse campus, which offers comprehensive inpatient rehabilitation facilities and outpatient services in multiple specialties.
Xanya Sofra Weiss
Xanya Sofra-Weiss
Aging is not just the sum total of individually deteriorating cells, shortened telomeres, denatured proteins and DNA molecules, or oxidative damage in the mitochondria. Aging is the dynamic process of increasing imbalances caused by: (1) cellular energy shortage, (2) incomplete cellular differentiation, (3) immune deficiency, (4) decreased systemic intelligence reflected in a/ defects in repair mechanisms, b/ inadequate spatial orientation and c/ poor network communication. International research has repeatedly shown that: (1)Electrons stabilize free radicals (2) Electron transport within DNA deflects oxidative damage; (3)Electrons provide a) direction information b) embryonic development c) cellular differentiation d) healing.(4) Electron transport chain results in Protons spinning the ATP-synthase in the mitochondria to produce ATP. Additionally, Proteins, the central intelligence mechanism of the cell are synthesized by aminoacids that are bound by virtue of their electric charge. A number of studies have shown that Protein synthesis occurs at specific frequencies below 1 Hz. Modern electronics and molecular biology research are combined to deduce the specifications for a technology that promotes Healthy Anti-aging. Resonating the firings, spatial organization and rhythms of electrically excitable cells leads to healing and rejuvenation in a completely safe, noninvasive method. However, to date, few devices pay attention to waveform formation that reflects the essence of cellular communications. There is a lot to be gained by developing a device that can emit signals capable of intertwining with those of signal transduction receptors (including G proteins, gene transcription and the activation of T cells). Such a device will not only become the protagonist in Anti-aging but it will have sufficient sophistication to heal disease and enhance overall immune efficiency.
Xanya Sofra Weiss
Giorgio Iervasi, MD; Alessandro Pingitore, MD, PhD; Patrizia Landi, BSc; Mauro Raciti, BSc; 2003
Background—Clinical and experimental data have suggested a potential negative impact of low-T3 state on the prognosis of cardiac diseases. The aim of the present prospective study was to assess the role of thyroid hormones in the prognosis of patient population with heart disease. Methods and Results—A total of 573 consecutive cardiac patients underwent thyroid function profile evaluation. They were divided in two subgroups: group I, 173 patients with low T3, ie, with free T3 (fT3) 3.1 pmol/L, and group II, 400 patients with normal fT3 ( 3.1 pmol/L). We considered cumulative and cardiac death events. During the 1-year follow-up, there were 25 cumulative deaths in group I and 12 in group II (14.4% versus 3%, P 0.0001); cardiac deaths were 13 in group I and 6 in group II (7.5% versus 1.5%, P 0.0006). According to the Cox model, fT3 was the most important predictor of cumulative death (hazard ratio [HR] 3.582, P 0.0001), followed by dyslipidemia (HR 2.955, P 0.023), age (HR 1.051, P 0.005), and left ventricular ejection fraction (HR 1.037, P 0.006). At the logistic multivariate analysis, fT3 was the highest independent predictor of death (HR 0.395, P 0.003). A prevalence of low fT3 levels was found in patients with NYHA class III-IV illness compared with patients with NYHA class I-II ( 2 5.65, P 0.019). Conclusions—Low-T3 syndrome is a strong predictor of death in cardiac patients and might be directly implicated in the poor prognosis of cardiac patients.
Xanya Sofra Weiss
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