Measurement of RudsR_{\text{uds}} and RR between 3.12 and 3.72 GeV at the KEDR detector

Using the KEDR detector at the VEPP-4M $e^+e^-$ collider, we have measured the values of $R_{\text{uds}}$ and $R$ at seven points of the center-of-mass energy between 3.12 and 3.72 GeV. The total achieved accuracy is about or better than $3.3\%$ at most of energy points with a systematic uncertainty of about $2.1\%$. At the moment it is the most accurate measurement of $R(s)$ in this energy range

Search for narrow resonances in e+ e- annihilation between 1.85 and 3.1 GeV with the KEDR Detector

We report results of a search for narrow resonances in e+ e- annihilation at center-of-mass energies between 1.85 and 3.1 GeV performed with the KEDR detector at the VEPP-4M e+ e- collider. The upper limit on the leptonic width of a narrow resonance Gamma(R -> ee) Br(R -> hadr) < 120 eV has been obtained (at 90 % C.L.)

Measurement of main parameters of the \psi(2S) resonance

A high-precision determination of the main parameters of the \psi(2S) resonance has been performed with the KEDR detector at the VEPP-4M e^{+}e^{-} collider in three scans of the \psi(2S) -- \psi(3770) energy range. Fitting the energy dependence of the multihadron cross section in the vicinity of the \psi(2S) we obtained the mass value M = 3686.114 +- 0.007 +- 0.011 ^{+0.002}_{-0.012} MeV and the product of the electron partial width by the branching fraction into hadrons \Gamma_{ee}*B_{h} = 2.233 +- 0.015 +- 0.037 +- 0.020 keV. The third error quoted is an estimate of the model dependence of the result due to assumptions on the interference effects in the cross section of the single-photon e^{+}e^{-} annihilation to hadrons explicitly considered in this work. Implicitly, the same assumptions were employed to obtain the charmonium leptonic width and the absolute branching fractions in many experiments. Using the result presented and the world average values of the electron and hadron branching fractions, one obtains the electron partial width and the total width of the \psi(2S): \Gamma_{ee} =2.282 +- 0.015 +- 0.038 +- 0.021 keV, \Gamma = 296 +- 2 +- 8 +- 3 keV. These results are consistent with and more than two times more precise than any of the previous experiments

Cellular and molecular mechanisms of inflammation of esophageal mucosa under different

The review presents modern data on the cellular and molecular mechanisms of inflammatory changes of esophageal mucosa exposed to different types of reluctate (gastric, biliary or duodenal/mixed). The authors describe data on key mediators of inflammation in gastroesophageal reflux disease (GERD) and their major cellular sources, changes of the immune profile of patients. Discusses the possible impact of changes in the cellular and molecular components in the development of the inflammatory response in the esophagus on the clinical features of GERD and its therapy-refractory forms

Possible use of adaptation to hypoxia in Alzheimer's disease: A hypothesis

Disorders in memory and other cognitive functions in Alzheimer's disease (AD) may result from an exhaustion of adaptive reserves in the brain. Therefore it is a challenge to find methods to increase the adaptive reserve of the organism to combat AD. Excitotoxicity, Ca2+ homeostasis disruptions, oxidative stress, disturbed synthesis of NO, and impaired cerebral circulation are suggested as key pathogenic factors of AD. At present it appears that stimulation of the self-defense systems in neural cells is a promising strategy in restricting the progression of AD. These systems include those of antioxidants, heat shock proteins (HSPs), NO, and other so-called stress-limiting systems. Non-drug activation of these systems can be achieved most efficiently by adaptation of the organism to environmental challenges, such as hypoxia. In this paper the potential of methods used in adaptive medicine is explored. The protective mechanisms of adaptation to hypoxia may be related to restriction of oxidative stress in the hippocampus, the limitation of a decrease in NO production induced by β-amyloid, and increased density of the vascular network in the brain. In this review we selectively present data that support the idea that adaptation to hypoxia is a possible non-drug means in the prevention of AD. In our opinion this strategy may provide a break-through in the clinical approach of this disease. © Med Sci Monit, 2005

Prospects of non-drug approaches to Alzheimer's disease

Despite the urgency of the problem of prevention and treatment of neurodegenerative processes underlying Alzheimer's disease (AD) and other severe disorders of the central nervous system, therapeutic and prophylactic potential of drugs is yet insufficient. Numerous adverse effects of the drugs, which might improve cognitive function in patients with AD substantiate serious consideration of measures enhancing adaptive potential and mobilizing self-defense of the body. It is clear now that endogenous defense systems of the brain can limit progression of AD long after the onset of the disease. The measures mobilizing the self-defense include administration of natural adaptogens and various types of adaptation, such as adaptation to dietary restrictions, promotion of physical and mental activity, and adaptation to hypoxia. This review presents data supporting a hypothesis that non-drug activation of self-defense of the body can prevent cognitive decline induced by neurodegenerative processes in the brain by targeting key points of AD pathogenesis

Possible use of adaptation to hypoxia in Alzheimer's disease: A hypothesis

Disorders in memory and other cognitive functions in Alzheimer's disease (AD) may result from an exhaustion of adaptive reserves in the brain. Therefore it is a challenge to find methods to increase the adaptive reserve of the organism to combat AD. Excitotoxicity, Ca2+ homeostasis disruptions, oxidative stress, disturbed synthesis of NO, and impaired cerebral circulation are suggested as key pathogenic factors of AD. At present it appears that stimulation of the self-defense systems in neural cells is a promising strategy in restricting the progression of AD. These systems include those of antioxidants, heat shock proteins (HSPs), NO, and other so-called stress-limiting systems. Non-drug activation of these systems can be achieved most efficiently by adaptation of the organism to environmental challenges, such as hypoxia. In this paper the potential of methods used in adaptive medicine is explored. The protective mechanisms of adaptation to hypoxia may be related to restriction of oxidative stress in the hippocampus, the limitation of a decrease in NO production induced by β-amyloid, and increased density of the vascular network in the brain. In this review we selectively present data that support the idea that adaptation to hypoxia is a possible non-drug means in the prevention of AD. In our opinion this strategy may provide a break-through in the clinical approach of this disease. © Med Sci Monit, 2005

Prospects of non-drug approaches to Alzheimer's disease

Despite the urgency of the problem of prevention and treatment of neurodegenerative processes underlying Alzheimer's disease (AD) and other severe disorders of the central nervous system, therapeutic and prophylactic potential of drugs is yet insufficient. Numerous adverse effects of the drugs, which might improve cognitive function in patients with AD substantiate serious consideration of measures enhancing adaptive potential and mobilizing self-defense of the body. It is clear now that endogenous defense systems of the brain can limit progression of AD long after the onset of the disease. The measures mobilizing the self-defense include administration of natural adaptogens and various types of adaptation, such as adaptation to dietary restrictions, promotion of physical and mental activity, and adaptation to hypoxia. This review presents data supporting a hypothesis that non-drug activation of self-defense of the body can prevent cognitive decline induced by neurodegenerative processes in the brain by targeting key points of AD pathogenesis