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ANTI-AGING BIOMEDICINE.
HIGH TECH BIO-MEDICAL TECHNOLOGIES FOR DISEASE TREATMENT AND LIFE EXTENSION.
EXPERIMENTAL AND CLINICAL DATA.

 
 6.1 STROKE RISK 
   
 
Fatty acid binding protein as a serum marker for the early diagnosis of stroke: A pilot study.
Early diagnosis by diffusion-weighted MRI of pure motor stroke limited to finger weakness.
Can a clinical score aid in early diagnosis and treatment of various stroke syndromes?
Early diagnosis and endovascular interventions for ischemic stroke.
Ischemic stroke, Part 1: Early, accurate diagnosis.
Comparability and validity of two clinical scores in the early differential diagnosis of acute stroke.
 
   
   
Mol Cell Proteomics. 2003 Oct 26 [Epub ahead of print].
Fatty acid binding protein as a serum marker for the early diagnosis of stroke: A pilot study.
Zimmermann-Ivol CG, Burkhard PR, Le Floch-Rohr J, Allard L, Hochstrasser DF, Sanchez JC.
Geneva Proteomics Center, Geneva University Hospital, Geneva 14, Geneva 1211.

No biological marker is currently available for the routine diagnosis of stroke. The aim of this pilot study was to determine whether heart-fatty acid binding protein (H-FABP) could be used as a valid diagnostic biomarker for stroke, as compared to neuron specific enolase (NSE) and S100B proteins. Using two-dimensional gel electrophoresis (2-DE) separation of cerebrospinal fluid (CSF) proteins and mass spectrometry techniques, FABP was found elevated in the CSF of deceased patients, used as a model of massive brain damage. Since H-FABP, a FABP form present in many organs, is also localised in the brain, an enzyme-linked immunosorbant assay (ELISA) was developed to detect H-FABP in stroke vs. control plasma samples. However, H-FABP being also a marker of acute myocardial infarction (AMI), Troponin-I and creatine kinase-MB (CK-MB) levels were assayed at the same time in order to exclude any concomitant heart damage. NSE and S100B levels were assayed simultaneously. These assays were assessed in serial plasma samples from 22 control patients with no AMI nor stroke, 20 patients with AMI but no stroke and 22 patients with an acute stroke but no AMI. Twenty-two out of the 22 control patients and 15 out of the 22 stroke patients were correctly classified, figures much better than those obtained with NSE or S100B, in the same studys population. H-FABP appears to be a valid serum biomarker for the early diagnosis of stroke. Further studies on large cohorts of patients are warranted.

   
   

J Neuroimaging. 1998 Jul;8(3):179-81.
Early diagnosis by diffusion-weighted MRI of pure motor stroke limited to finger weakness.
Hochman MS, DePrima SJ, Leon BJ.
Department of Neurology, University of Miami School of Medicine, FL, USA.

Pure motor neurologic deficits occur among 3%-14% of all patients with ischemic stroke. Pure motor monoparesis occurs among 2%-22% of patients with pure motor stroke. The authors report the case of a 73-year-old woman with isolated finger weakness as the sole manifestation of a small cortical-subcortical pure motor stroke diagnosed within 4 hours of onset by means of diffusion-weighted echoplanar magnetic resonance imaging. To the authors' knowledge, the case of a patient with pure motor stroke with finger weakness as the only manifestation has not been previously reported. Increased awareness of this rare clinical presentation of pure motor stroke coupled with the promise of prompt diagnosis by means of diffusion-weighted MRI should lead to earlier stroke intervention.

   
   

Am J Med Sci. 1998 Mar;315(3):194-8.
Can a clinical score aid in early diagnosis and treatment of various stroke syndromes?
Akpunonu BE, Mutgi AB, Lee L, Khuder S, Federman DJ, Roberts C.
Department of Internal Medicine, Medical College of Ohio, Toledo 43699-0008, USA.

BACKGROUND: Accurate and timely diagnosis of hemorrhagic and nonhemorrhagic strokes helps in patient management. Neuroimaging studies are useful in diagnosis and distinction of hemorrhagic (HS) and nonhemorrhagic (NHS) strokes. The use of clinical variables, such as Siriraj stroke scores (SSS), has shown good sensitivity, specificity and predictive values (distinguishing stroke types). The aim of our study was to evaluate the use of SSS in a U.S. population and assess whether it could aid to expedite treatment decisions. METHODS: Levels of consciousness, vomiting, headache and atheroma markers used in SSS were applied to patients who met the criteria for stroke. RESULTS: Of the 302 patients identified, the SSS classified 254 with sensitivity of 36% (HS) and 90% (NHS) and positive predictive values of 77% and 61%, respectively. CONCLUSION: Our results suggest that SSS is not reliable in distinguishing stroke types (in a US population). Definite neuroimaging studies are needed prior to thrombolytic therapy.

   
   

New Horiz. 1997 Nov;5(4):316-31.
Early diagnosis and endovascular interventions for ischemic stroke.
Hacein-Bey L, Kirsch CF, DeLaPaz R, Duong HD, Mayer SA, Pile-Spellman J, Mohr JP.
Department of Radiology, Columbia-Presbyterian Medical Center, New York, NY, USA.

In recent years there have been formidable advances in the war against stroke. The understanding and detection of stroke have undergone major progress at a rate previously unseen, partly due to major contributions from neuroradiology. Current routine neuroradiologic evaluation of acute stroke relies mainly on computed tomography scanning, although a number of radiologic modalities are becoming available that are based on various physical and chemical tissue properties, such as magnetic resonance imaging, single photon emission computed tomography, positron emission tomography, and magnetic resonance spectroscopy. All these new techniques allow the study of nervous tissue at the cellular and biochemical levels. A review of current diagnostic techniques for stroke follows in the first part of this article. The current status of endovascular therapy for ischemic stroke is reviewed in the second part of this article.

   
   

Geriatrics. 1993 Mar;48(3):26-8, 31-4.
Ischemic stroke, Part 1: Early, accurate diagnosis.
Bruno A.
Department of Neurology, University of New Mexico School of Medicine, Albuquerque.

To be consistent with a diagnosis of TIA or stroke, a focal neurologic deficit must have occurred suddenly. The differential diagnosis of TIA includes migraine aura (possibly without a headache), a hypotensive episode, radiculopathy, and an unusual seizure. Vascular risk factors (eg, hypertension, diabetes, smoking) and the extent of their control should be determined. Cardiac examination and ECG may provide important clues, as atrial fibrillation and valvular heart disorders are well recognized potential sources of emboli. During an acute stroke, CT is the best test to reliably distinguish between ischemic and hemorrhagic stroke. Other tests that may be indicated on an individual basis include MRI,, echocardiography, carotid duplex ultrasound, and arteriography.

   
   

BMJ. 1994 Jun 25;308(6945):1674-6.
Comparability and validity of two clinical scores in the early differential diagnosis of acute stroke.
Celani MG, Righetti E, Migliacci R, Zampolini M, Antoniutti L, Grandi FC, Ricci S.
Clinica Neurologica, Perugia, Italy.

OBJECTIVE--To compare two available clinical scores for the differential diagnosis of cerebral ischaemia and haemorrhage in acute stroke patients. DESIGN--Prospective, multicentre study of acute stroke patients evaluated with computed tomography and Allen and Siriraj scores; the scores were tested for comparability (kappa statistic) and validity (sensitivity, specificity, positive and negative predictive values, diagnostic gain). The effect of a policy of using Allen and Siriraj scores to determine pathological type of stroke before computed tomography was calculated. SETTING--Three hospitals in Italy, all participating in the international stroke trial, with different access facilities to computed tomography. SUBJECTS--231 consecutive patients who were screened in the three hospitals for possible inclusion in the international stroke trial from 1 November 1991 to 31 May 1993. RESULTS--The prevalence of haemorrhage (diagnosed with computed tomography) was 14.7% (95% confidence interval 10.1% to 19.3%). Allen scores were "uncertain" in 44 cases and Siriraj scores in 38 cases; in the 164 cases with both the scores in the range of "certainty" kappa was 0.72. Sensitivity, specificity, positive and negative predictive values, and diagnostic gain for haemorrhage were 0.38, 0.98, 0.71, 0.91, and 0.58 for Allen scores and 0.61, 0.94, 0.63, 0.93, and 0.48 for Siriraj scores; positive predictive values for infarction were 91% for Allen scores and 93% for Siriraj scores. According to these data, of 1000 patients with acute stroke, 680 would be correctly and 70 wrongly diagnosed as "ischaemic" with the Allen score; the figures would be 671 and 48 with Siriraj score. CONCLUSION--When computed tomography is not immediately available and the clinician wishes to start antithrombotic treatment (or randomise patients in a clinical trial), the Siriraj score (and possibly the Allen score) can be useful to identify patients at low risk of intracerebral haemorrhage.

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FASTING / LOW CALORIE PROGRAMS
on the Adriatic Coast
The Anti-Aging Fasting Program consists of a 7-28 days program (including 3 - 14 fasting days). 7-28-day low-calorie diet program is also available .
More information
    The anti-aging story (summary)
Introduction. Statistical review. Your personal aging curve
  Aging and Anti-aging. Why do we age?
    2.1  Aging forces (forces that cause aging
     
Internal (free radicals, glycosylation, chelation etc.) 
External (Unhealthy diet, lifestyle, wrong habits, environmental pollution, stress, poverty-change "poverty zones", or take it easy. etc.) 
    2.2 Anti-aging forces
     
Internal (apoptosis, boosting your immune system, DNA repair, longevity genes) 
External (wellness, changing your environment; achieving comfortable social atmosphere in your life, regular intake of anti-aging drugs, use of replacement organs, high-tech medicine, exercise)
    2.3 Aging versus anti-aging: how to tip the balance in your favour!
 
    3.1 Caloric restriction and fasting extend lifespan and decrease all-cause mortality (Evidence)
      Human studies
Monkey studies
Mouse and rat studies
Other animal studies
    3.2 Fasting and caloric restriction prevent and cure diseases (Evidence)
        Obesity
Diabetes
Hypertension and Stroke
Skin disorders
Mental disorders
Neurogical disorders
Asthmatic bronchitis, Bronchial asthma
Bones (osteoporosis) and fasting
Arteriosclerosis and Heart Disease
Cancer and caloric restriction
Cancer and fasting - a matter of controversy
Eye diseases
Chronic fatigue syndrome
Sleeping disorders
Allergies
Rheumatoid arthritis
Gastrointestinal diseases
Infertility
Presbyacusis
    3.3 Fasting and caloric restriction produce various
      biological effects. Effects on:
        Energy metabolism
Lipids metabolism
Protein metabolism and protein quality
Neuroendocrine and hormonal system
Immune system
Physiological functions
Reproductive function
Radio-sensitivity
Apoptosis
Cognitive and behavioral functions
Biomarkers of aging
    3.4 Mechanisms: how does calorie restriction retard aging and boost health?
        Diminishing of aging forces
  Lowering of the rate of gene damage
  Reduction of free-radical production
  Reduction of metabolic rate (i.e. rate of aging)
  Lowering of body temperature
  Lowering of protein glycation
Increase of anti-aging forces
  Enhancement of gene reparation
  Enhancement of free radical neutralisation
  Enhancement of protein turnover (protein regeneration)
  Enhancement of immune response
  Activation of mono-oxygenase systems
  Enhance elimination of damaged cells
  Optimisation of neuroendocrine functions
    3.5 Practical implementation: your anti-aging dieting
        Fasting period.
Re-feeding period.
Safety of fasting and low-calorie dieting. Precautions.
      3.6 What can help you make the transition to the low-calorie life style?
        Social, psychological and religious support - crucial factors for a successful transition.
Drugs to ease the transition to caloric restriction and to overcome food cravings (use of adaptogenic herbs)
Food composition
Finding the right physician
    3.7Fasting centers and fasting programs.
  Food to eat. Dishes and menus.
    What to eat on non-fasting days. Dishes and menus. Healthy nutrition. Relation between foodstuffs and diseases. Functional foods. Glycemic index. Diet plan: practical summary. "Dr. Atkins", "Hollywood" and other fad diets versus medical science
     

Vegetables
Fruits
Bread, cereals, pasta, fiber
Glycemic index
Fish
Meat and poultry
Sugar and sweet
Legumes
Fats and oils
Dairy and eggs
Mushrooms
Nuts and seeds
Alcohol
Coffee
Water
Food composition

  Anti-aging drugs and supplements
    5.1 Drugs that are highly recommended
      (for inclusion in your supplementation anti-aging program)
        Vitamin E
Vitamin C
Co-enzyme Q10
Lipoic acid
Folic acid
Selenium
Flavonoids, carotenes
DHEA
Vitamin B
Carnitin
SAM
Vinpocetine (Cavinton)
Deprenyl (Eldepryl)
    5.2 Drugs with controversial or unproven anti-aging effect, or awaiting other evaluation (side-effects)
        Phyto-medicines, Herbs
HGH
Gerovital
Melatonin
      5.3 Drugs for treatment and prevention of specific diseases of aging. High-tech modern pharmacology.
        Alzheimer's disease and Dementia
Arthritis
Cancer
Depression
Diabetes
Hyperlipidemia
Hypertension
Immune decline
Infections, bacterial
Infections, fungal
Memory loss
Menopause
Muscle weakness
Osteoporosis
Parkinson's disease
Prostate hyperplasia
Sexual disorders
Stroke risk
Weight gaining
    5.4 The place of anti-aging drugs in the whole
      program - a realistic evaluation
 
    6.1 Early diagnosis of disease - key factor to successful treatment.
      Alzheimer's disease and Dementia
Arthritis
Cancer
Depression
Diabetes
Cataracts and Glaucoma
Genetic disorders
Heart attacks
Hyperlipidemia
Hypertension
Immune decline
Infectious diseases
Memory loss
Muscle weakness
Osteoporosis
Parkinson's disease
Prostate hyperplasia
Stroke risk
Weight gaining
    6.2 Biomarkers of aging and specific diseases
    6.3 Stem cell therapy and therapeutic cloning
    6.4 Gene manipulation
    6.5 Prosthetic body-parts, artificial organs
        Blood
Bones, limbs, joints etc.
Brain
Heart & heart devices
Kidney
Liver
Lung
Pancreas
Spleen
    6.6 Obesity reduction by ultrasonic treatment
  Physical activity and aging. Experimental and clinical data.
        Aerobic exercises
Stretching
Weight-lifting - body-building
Professional sport: negative aspects
 
  Conclusion: the whole anti-aging program
    9.1 Modifying your personal aging curve
      Average life span increment. Expert evaluation.
     
Periodic fasting and caloric restriction can add 40 - 50 years to your lifespan
Regular intake of anti-aging drugs can add 20-30 years to your lifespan
Good nutrition (well balanced, healthy food, individually tailord diet) can add 15-25 years to your lifespan
High-tech bio-medicine service can add 15-25 years to your lifespan
Quality of life (prosperity, relaxation, regular vocations) can add 15-25 years to your lifespan
Regular exercise and moderate physical activity can add 10-20 years to your lifespan
These approaches taken together can add 60-80 years to your lifespan, if you start young (say at age 20). But even if you only start later (say at 45-50), you can still gain 30-40 years


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    9.2 The whole anti-aging life style - brief summary 
    References eXTReMe Tracker
        The whole anti-aging program: overview
         
       

       
     
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