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Innovative Bio-Products for Agriculture - Katarzyna Chojnacka - Bog - Nova Science Publishers Inc - Plusbog.dk

Flax Lipids - Raja Ragupathy - Bog - Nova Science Publishers Inc - Plusbog.dk

New Technology of Deep Placement of Slow Release Nitrogen Fertilizers for Promotion of Soybean Growth & Seed Yield - Norikuni Ohtake - Bog - Nova

Outline of Russian Literature - Maurice Baring - Bog - Nova Science Publishers Inc - Plusbog.dk

Candida albicans - - Bog - Nova Science Publishers Inc - Plusbog.dk

Candida albicans - - Bog - Nova Science Publishers Inc - Plusbog.dk

Candida albicans is an opportunistic pathogenic yeast and it is a common member of the human gut flora. It does not proliferate outside the human body. It is detected in the gastrointestinal tract and mouth in 40-60% of healthy adults. It is usually a commensal organism but can become pathogenic in immunocompromised individuals under a variety of conditions. Yeast infection is caused by a specific strain of yeast known as Candida. Although a small amount of yeast is found in the body, yeast infection occurs when there is an overgrowth of Candida. Most yeast infections is caused by Candida albicans. Fungal that affects different areas of the body like skin, mouth, genitals, throat and blood. The yeast Candida albicans lives inside every one of us. Normally it presents no problems, but today's widespread use of broad-spectrum antibiotics, antacids, contraceptive pills, and steroids, as well as the all-too-common sugar-rich diet, can lead to a proliferation of this parasitic yeast within the body. Often overlooked by doctors, overgrowth of Candida has been linked to a wide variety of physical and mental problems such as: acne; heartburn; muscular pain; anxiety; irritable bowel syndrome (IBS); fibromyalgia; bloating and constipation; chronic fatigue; migraine; cystitis irritable bowel syndrome (IBS); allergies; menstrual problems; irritability Candida that causes the human infection candidiasis results from an overgrowth of the fungus is for example often observed in HIV-infected patients. C. albicans is the most common fungal species isolated from biofilms either formed on (permanent) implanted medical devices or on human tissue. C. albicans, C. tropicalis, C. parapsilosis, and C. glabrata are together responsible for 50 -- 90% of all cases of candidiasis in humans. A mortality rate of 40% has been reported for patients with systemic candidiasis due to C. albicans. Invasive candidiasis contracted in a hospital causes 2,800 to 11,200 deaths yearly in the U.S. C. albicans is commonly used as a model organism for biology. It is also known as sweet fungus and sugar inhibits its growth. It is generally referred to as a dimorphic fungus because it grows both as yeast and filamentous cells. However, it has several different morphological phenotypes. C. albicans was for a long time considered an obligate diploid organism without a haploid stage. This is, however, not the case. Next to a haploid stage C. albicans can also exist in a tetraploid stage. The latter is formed when diploid C. albicans cells mate when they are in the opaque form. Candida thrives well on sugar and needs an acidic environment to survive. Processed and refined foods high in gluten and sugar (including natural sugars) create an ideal home for Candida, so the most logical place to start battling the enemy is by restricting intake of alcohol, sweets, bread, vinegar and foods containing vinegar, peanuts and foods high in sugar - including sweet fruits such as bananas and dates. Include protein rich foods like avocados, chia seeds and wild-caught fish. Garlic and turmeric (also known as curcumin) is a natural anti-fungal that can kill Candida. The best potent and all-natural candida killer is coconut oil. It contains caprylic acid, which has anti-microbial properties that can kill yeasts and candida. Studies have shown that it is more effective in treating candidiasis than the prescription drug fluconazole. There are relatively few drugs that can successfully treat Candidiasis. Treatment commonly includes amphotericin B,echinocandin, or fluconazole for systemic infections. Nystatin for oral and esophageal infection and Clotrimazole for skin and genital yeast infections.

DKK 624.00
1

Adaptive Mechanisms in Migraine - Vinod Kumar Gupta - Bog - Nova Science Publishers Inc - Plusbog.dk

Adaptive Mechanisms in Migraine - Vinod Kumar Gupta - Bog - Nova Science Publishers Inc - Plusbog.dk

Migraine has evolved into a giant puzzle and its literature comprises a vast loosely-linked enterprise challenging human problem-solving capacity. There is no central idea in migraine to elaborate a general theory which in turn could ultimately lead to creation of a unifying hypothesis that collects the various strands of evidences into a coherent and logically defensible intelligible synthesis. Current pathogenetic concepts of migraine, in particular cortical spreading depression (CSD), do not focus on the precise onset of the attack. Neither the aura nor the headache represents the true beginning of a migraine attack. The primary or causal physiological alteration underlying migraine lies in the ''pre-prodromal'' phase, the variable interim between exposure to the headache-provoking stimulus or situation and the onset of the migraine prodrome. The migraine prodrome itself can last several hours to a few days. Since CSD is believed to underlie both the migrainous scintillating scotoma as well as the headache, it cannot be regarded as an early or initial ''pre-prodromal'' physiological event. The biology of migraine is not the study of laboratory ''markers'' but the elucidation of physiological forces (trait and/or state factors) that push (precipitate) or pull (predispose) patients towards aura/headache or aura/headache-free state. The pathophysiology of migraine has been hitherto confined to analyses of diverse precipitating and remitting factors and uncertain postulations about recorded laboratory aberrations into presumptive causal algorithms. The key cranial physiological system involved in migraine remains unidentified. Migraine attacks occur during stress and, more commonly, after cessation of stress. The author has earlier proposed that a physiological neuroendocrine ''system'' comprised of well-regulated parallel activation of the vasopressinergic, intrinsic brain serotonergic, and intrinsic brain noradrenergic systems constitutes an important adaptive mechanism that governs vascular integrity, antinociception, behaviour and overall function during stressful occasions, including migraine attacks. Such a conceptual template can be used to segregate the vast phenomenology of migraine into primary pathogenetic or secondary non-pathogenetic divisions; non-pathogenetic migrainous phenomena can be further subdivided into adaptive and concomitant (epiphenomenal) physiological events. Nausea and/or vomiting, facial pallor, Raynaud''s phenomenon, episodic daytime sleepiness, and relative hypotension (both spontaneous as well as induced by prophylactic anti-migraine pharmacologic agents) likely reflect the non-pathogenetic (adaptive or epiphenomenal) clinical components of migraine. The pathophysiological basis of aura/headache and nausea/vomiting of migraine is very unlikely to be identical. Exogenous magnesium does not readily cross the intact blood-brain barrier and decreases the permeability of the blood-brain barrier. Magnesium depletion appears to serve an important adaptive function; its utility in migraine management is not convincing. Magnesium depletion, platelet activation, peripheral alterations in serotonin and catecholamine metabolism, hyper-responsiveness of brain noradrenergic, serotonergic, vasopressinergic, and dopaminergic systems, parasympathetic nevous system activation, pupillary miosis, and cutaneous allodynia probably represent some of the secondary adaptive physiological mechanisms operative in migraine. A critical or central role for brain neuronal involvement in migraine pathogenesis appears unikely as established migraine preventive agents like atenolol, nadolol, and verapamil do not readily cross the intact blood-brain barrier or influence brain neuronal function. Antidepressants, including amitriptyline, induce brain noradrenergic and serotonergic hyperfunction, rendering highly unlikely that such brain states underlie migraine. Elucidation of adaptive physiological mechanisms in migraine can rationalise important epidemiological, clinical, and pharmacological features and sow the seeds for evolution of an integrative synthesis which process, in turn, might herald the creation of a comprehensive thought framework and research vision for migraine.

DKK 405.00
1