The document discusses a study on the effects of a complex herbal formulation called CIRCULAT in treating chronic ischemic heart disease. The study found that 85% of the initial 20 patients showed good responses to CIRCULAT therapy as measured by imaging and stress tests over periods of 6 months to 1 year. The treatment was associated with reductions in perfusion damage percentages on imaging and increases in functional capacity on stress tests for most patients.
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Manejo de la diabetes en el anciano
Dr. Guillermo E. Umpierrez
Professor of Medicine in the Division of Endocrinology at Emory University School of Medicine, Section Head, Diabetes and Endocrinology. USA. Editor en Jefe del BJM Open Diabetes Research and Care.
Memorias Conferencia Científica Anual sobre Síndrome Metabólico 2017 - Programa Científico
Manejo de la diabetes en el anciano
Dr. Guillermo E. Umpierrez
Professor of Medicine in the Division of Endocrinology at Emory University School of Medicine, Section Head, Diabetes and Endocrinology. USA. Editor en Jefe del BJM Open Diabetes Research and Care.
- Recorded videos of the lecture:
English Language version of this lecture is available at: https://youtu.be/-Ynxvhbcl7U
Arabic Language version of this lecture is available at: https://youtu.be/QpK_toctVlw
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Journal Club about the Phase 2 study of Selonsertib in Diabetic Kidney Disease to Our Division on 12/9/19.
Also an intro about the Phase 3 study (MOSAIC) we will be launching before the end of the year
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/NQMiLXb0AXk
Arabic Language version of this lecture is available at:
https://youtu.be/o_I9bzxcJoQ
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Nocturnal GERD may be more important than daytime GERD in the development of severe GERD-related complications; and up to 80% of refluxers describe nocturnal symptoms. Nighttime reflux is associated with a 11x risk of esophageal adenocarcinoma, as well as sleep disturbance and respiratory symptoms.
Perhaps you don’t need to know the details of nocturnal GERD… but ask yourself-
“Do you feel lucky?”
- Recorded videos of the lecture:
English Language version of this lecture is available at: https://youtu.be/-Ynxvhbcl7U
Arabic Language version of this lecture is available at: https://youtu.be/QpK_toctVlw
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Journal Club about the Phase 2 study of Selonsertib in Diabetic Kidney Disease to Our Division on 12/9/19.
Also an intro about the Phase 3 study (MOSAIC) we will be launching before the end of the year
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/NQMiLXb0AXk
Arabic Language version of this lecture is available at:
https://youtu.be/o_I9bzxcJoQ
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Nocturnal GERD may be more important than daytime GERD in the development of severe GERD-related complications; and up to 80% of refluxers describe nocturnal symptoms. Nighttime reflux is associated with a 11x risk of esophageal adenocarcinoma, as well as sleep disturbance and respiratory symptoms.
Perhaps you don’t need to know the details of nocturnal GERD… but ask yourself-
“Do you feel lucky?”
My Nephrology Registrar Seminar Talk from September 2013
Topics Covered
Pathogenesis of Diabetic Nephropathy
Other Renal Disease in Diabetes
Treatment of Diabetic Kidney Disease + The Joint Renal Diabetic Clinic
Deciding When Hospice Care is Needed | VITAS HealthcareVITAS Healthcare
The goal of this webinar is to help healthcare professionals address the specific challenges of end-of-life care when determining a terminal prognosis, so they can provide the optimum care for the patient and family during the final stages of life.
Аллопуринол и прогрессирование ХБП и кардиоваскулярные события. РКИ / Allopur...hivlifeinfo
Allopurinol and Progression of CKD and Cardiovascular Events- Long-term Follow-up of a Randomized Clinical Trial.Am J Kidney Dis. 2015 Apr
Background:Asymptomatic hyperuricemia increases renal and cardiovascular (CV) risk. We previously
conducted a 2-year, single-blind, randomized, controlled trial of allopurinol treatment that showed improved
estimated glomerular filtration rate and reduced CV risk.
Study Design:Post hoc analysis of a long-term follow-up after completion of the 2-year trial.
Setting & Participants:113 participants (57 in the allopurinol group and 56 in the control group) initially
followed up for 2 years and 107 participants followed up to 5 additional years.
Intervention: Continuation of allopurinol treatment, 100 mg/d, or standard treatment.
Outcome:Renal event (defined as starting dialysis therapy and/or doubling serum creatinine and/or$50%
decrease in estimated estimated glomerular filtration rate) and CV events (defined as myocardial infarction,
coronary revascularization or angina pectoris, congestive heart failure, cerebrovascular disease, and peripheral vascular disease).
Results:During initial follow-up, there were 2 renal and 7 CV events in the allopurinol group compared with
6 renal and 15 CV events in the control group. In the long-term follow-up period, 12 of 56 participants taking
allopurinol stopped treatment and 10 of 51 control participants received allopurinol. During long-term follow-up,
an additional 7 and 9 participants in the allopurinol group experienced a renal or CV event, respectively, and an
additional 18 and 8 participants in the control group experienced a renal or CV event, respectively. Thus,
during the initial and long-term follow-up (median, 84 months), 9 patients in the allopurinol group had a
renal event compared with 24 patients in the control group (HR, 0.32; 95% CI, 0.15-0.69; P50.004;
adjusted for age, sex, baseline kidney function, uric acid level, and renin-angiotensin-aldosterone system
blockers). Overall, 16 patients treated with allopurinol experienced CV events compared with 23 in the
control group (HR, 0.43; 95% CI, 0.21-0.88;P50.02; adjusted for age, sex, and baseline kidney function).
Limitations:Small sample size, single center, not double blind, post hoc follow-up and analysis.
Conclusions: Long-term treatment with allopurinol may slow the rate of progression of kidney disease and
reduce CV risk.
Association and prevalence of different comorbidities in hypertension and management with focus guidelines with benefits & choice of different antihypertensives in different comorbidities.
Drs. Lena, Avery, and Davis’s CMC Abdominal Imaging Mastery Project: August C...Sean M. Fox
Dr. Kelsey Lena is an Emergency Medicine Resident and Drs. Michael Avery and Joshua Davis are Surgery Residents at Carolinas Medical Center in Charlotte, NC. They are interested in medical education. With the guidance of Drs. Kyle Cunningham and Michael Gibbs, they aim to help augment our understanding of emergent abdominal imaging. Follow along with the EMGuideWire.com team as they post these monthly educational, self-guided radiology slides. This month’s topics include:
• Splenic Rupture
• Obstructive jaundice
• Ovarian Torsion
Webinar Series on COVID-19 vaccine: Jointly organized by Malaysian Society of Infection Control and Infectious Diseases (MyICID) & Institute for Clinical Research (ICR), NIH
Speaker: Dr. Richard Lim Boon Leong is a Consultant Palliative Medicine Physician and Head of Palliative Care Unit, Selayang Hospital, Ministry of Health Malaysia.
Similar to CIRCULAT in Chronic Ischemic Heart Disease - 20 Pat, Diabetic Foot and Gene Expression (20)
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
6. Evaluation of the changes in the genetic expression after CIRCULAT Objective: To reveal the underlying molecular mechanisms to the biological activity of the Circulat .
51. GSPECT Cardio-Diagnostic Imaging (Source: www.yale.edu/imaging/) Annualized Cardiac Events Risk Treatment Implications (majority of patients) <1% risk of cardiac death and MI Risk factor modification (RFM) in addition to current regimen Low risk of cardiac death; Intermediate risk of MI Aggressive RFM/medical treatment Intermediate-to-high risk of both cardiac death/MI Catheterization (possible revascularization)/RFM Normal Mildly Normal Moderately / Severely Abnormal anterior inferior septal lat anterior inferior base apex apex lat septal base
52. Chronic Ischemic Heart Disease treatment with complex herbal formulation Study Roberto Guzmán, José Olalde, Francis Amendola, Oswaldo del Castillo Results: Good response (17 out of 20 initial patients) to therapy was observed in 85% of the patients ( p ≤ 6.104e-05; %=99.9999) as determined by Wilcoxon. No patient suffered adverse events or died during the studied period. *Results r anging between six months and one year; in first 20 out of 30 total Patients under study + + = = = One Patient Diffuse Captation Lateral Wall Qualitative 20 Patients * 3 Patients Same Perfusion Defect Quantitative One Patient Diffuse Captation Inferior Wall Qualitative 15 Patients Perfusion Defect Quantitative 3 Patients Same Captation Lateral / Inferior Wall Qualitative 17 Patients Improvement 15 Quant + 2 Qual 3 Patients No Improvement
55. PD%: 40 29 APR 2009 16 SEP 2009 PD%: Post–Effort Perfusion Damage Percentage GSPECT Image PD%: 35 Control 6 months Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 452 post-treatment 386 Time (sec) pre-treatment 66 Increase (sec) 6 month treatment Patient 1
56. PD%: 45 13 MAY 2009 28 OCT 2009 GSPECT Image PD%: 30 Control 6 months PD%: Post–Effort Perfusion Damage Percentage 7 JUL 2010 PD%: 15 One year Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Patient unable to carry out the test due physical limitations Patient 2
57. GSPECT Image PD%: 20 20 MAY 2009 28 OCT 2009 PD%: 10 Control 6 months PD%: Post–Effort Perfusion Damage Percentage 16 JUN 2010 PD%: 10 One year Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Total 442 post-treatment 366 Time (sec) pre-treatment 76 Increase (sec) 6 month treatment Patient 3
58. GSPECT Image PD%: 70 03 JUN 2009 11 NOV 2009 PD%: 60 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 200 post-treatment 155 Time (sec) pre-treatment 45 Increase (sec) 6 month treatment Patient 4
59. GSPECT Image PD%: 30 06 MAY 2009 07 OCT 2009 PD%: 25 Control 6 months 09 JUL 2010 PD%: 0 One year PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Total 615 post-treatment 486 Time (sec) pre-treatment 81 Increase (sec) 6 month treatment 48 Increase (sec) 1 year treatment Patient 5
60. GSPECT Image PD%: 30 06 MAY 2009 07 OCT 2009 PD%: 20 Control 6 months 09 JUN 2010 PD%: 20 One year PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Total 662 post-treatment 553 Time (sec) pre-treatment 88 Increase (sec) 6 month treatment 14 Increase (sec) 1 year treatment Patient 6
61. PD%: 15 29 APR 2009 16 SEP 2009 PD%: Post–Effort Perfusion Damage Percentage GSPECT Image PD%: 15 Control 6 months Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 609 post-treatment 555 Time (sec) pre-treatment 54 Increase (sec) 6 month treatment Patient 7
62. PD%: 10 14 JUL 2009 11 NOV 2009 GSPECT Image PD%: 5 Control 6 months 28 JUL 2010 PD%: 5 One year PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Total 491 post-treatment 433 Time (sec) pre-treatment 68 Increase (sec) 6 month treatment -10 Decrease (sec) 1 year treatment Patient 8
63. PD%: 20 14 JUL 2009 11 NOV 2009 PD%: 20 Control 6 months 04 AGO 2010 PD%: 20 One year PD%: Post–Effort Perfusion Damage Percentage GSPECT Image Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Total 676 post-treatment 516 Time (sec) pre-treatment 132 Increase (sec) 6 month treatment 28 Increase (sec) 1 year treatment Patient 9
64. PD%: 60 13 MAY 2009 07 OCT 2009 GSPECT Image PD%: 35 Control 6 months 02 JUN 2010 PD%: 20 One year PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Total 428 post-treatment 339 Time (sec) pre-treatment 89 Increase (sec) 6 month treatment Patient 10
65. PD%: 25 12 AGO 2009 08 DEC 2009 PD%: Post–Effort Perfusion Damage Percentage GSPECT Image PD%: 15 Control 6 months Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 373 post-treatment 323 Time (sec) pre-treatment 50 Increase (sec) 6 month treatment Patient 11
66. PD%: 15 14 JUL 2009 02 DEC 2009 GSPECT Image PD%: 0 Control 6 months 04 AGO 2010 PD%: 0 One year PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease One year treatment study Funtional Capacity Time (sec) Total 570 post-treatment 432 Time (sec) pre-treatment 83 Increase (sec) 6 month treatment 55 Increase (sec) 1 year treatment Patient 12
67. PD%: 25 23 JUL 2009 02 DEC 2009 PD%: Post–Effort Perfusion Damage Percentage GSPECT Image PD%: 20 Control 6 months Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Patient unable to carry out the test due physical limitations Patient 13
68. GSPECT Image PD%: 70 11 MAR 2010 15 SEP 2010 PD%: 55 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 235 post-treatment 209 Time (sec) pre-treatment 26 Increase (sec) 6 month treatment Patient 14
69. GSPECT Image PD%: 95 04 MAR 2010 15 SEP 2010 PD%: 90 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Patient unable to carry out the test due physical limitations Patient 15
70. GSPECT Image PD%: 35 10 MAR 2010 1 SEP 2010 PD%: 35 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Patient unable to carry out the test due physical limitations Patient 16 * * Slight Qualitative Perfusion Improvement determined by diffuse radioisotope captation in lateral wall
71. GSPECT Image PD%: 50 17 MAR 2010 15 SEP 2010 PD%: 35 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 254 post-treatment 333 Time (sec) pre-treatment -79 Decrease (sec) 6 month treatment Patient 17
72. GSPECT Image PD%: 50 17 MAR 2010 06 SEP 2010 PD%: 35 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 549 post-treatment 479 Time (sec) pre-treatment 70 Increase (sec) 6 month treatment Patient 18
73. GSPECT Image PD%: 45 03 MAR 2010 01 SEP 2010 PD%: 45 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Total 620 post-treatment 610 Time (sec) pre-treatment 10 Increase (sec) 6 month treatment Patient 19 * * Important Qualitative Perfusion Improvement determined by diffuse radioisotope captation in inferior wall
74. GSPECT Image PD%: 15 10 MAR 2010 15 SEP 2010 PD%: 15 Control 6 months PD%: Post–Effort Perfusion Damage Percentage Chronic Ischemic Heart Disease Six month treatment study Funtional Capacity Time (sec) Patient unable to carry out the test due physical limitations Patient 20
77. CIRCULAT IP Protection USA Patent: Circulatory Disorders and Diabetes Russian Patent: Method of elaboration; Circulatory Disorders and Diabetes Mexican Patent: Circulatory Disorders and Diabetes 17 International patents (12/USA; 4/Russia; 1/Mexico)
78. Early results in the administration of CIRCULAT have shown it to be therapeutically efficacious, accessible and safe in the treatment of chronic ischemic heart disease. Evidence of CIRCULAT’s efficacy was determined by state-of-the-art Gamma Single Photon Emission Computerized Tomography (GSPECT) images. CIRCULAT is the only known orally administered treatment capable of obtaining myocardial reperfusion in chronic ischemic heart disease. Conclusions
82. Potential Synergetic Contribution Potential Synergetic Contribution (SC) Number of active principles (n) The synergetic potential of a complex herbal formulation -such as CIRCULAT- is provided by the interactions of the active principles present in each phytoceutical and can be mathematically expressed by SC value below.
94. Circulat 187 genes I 52 E 44 O 14 45 Organization Fraction Intelligence Fraction Common to 2 or 3 Fractions Energy Fraction CIRCULAT’s Synergistic -Gene Modulating- Capacity The formulation modulates 32 additional genes than the sum of formulas’ individual fractions + + + = modulates 155 genes ∑ = modulates 187 genes; while ( )
95. International Publications e CAM: Part I, II and III. Systemic Theory & Systemic Medicine (2005). e CAM: Part IV. The Praxis (2005). Investigación Clínica Sept. 2005 (vol. 46, sup. 2). Phytotherapy Research: Gene Expression (2 007). Phytotherapy Research: Diabetic Foot (2008). Phytopharm 2010 (Abstracts Book) Ischemic Cardiopathy.
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