Posted in HTN, Pharmacotherapy of Cardiovascular Disease on October 9, 2015| Leave a Comment »
Low dose beta-blockers as effective as high dose after a heart attack
Reporter: Aviva Lev-Ari, PhD, RN
In a surprising new finding, heart attack patients treated with a substantially lower dosage of beta-blockers than used in earlier clinical trials showing their effectiveness survived at the same rate, or even better, than …
Sourced through Scoop.it from: medicalxpress.com
See on Scoop.it – Cardiovascular Disease: PHARMACO-THERAPY
Posted in Frontiers in Cardiology and Cardiovascular Disorders, Pharmacotherapy of Cardiovascular Disease on September 26, 2015| Leave a Comment »
Reporters: Aviva Lev-Ari, PhD, RN and Gerard Loiseau, ESQ
VIEW VIDEO
Basel, September 25, 2015 – Novartis announced today that the Committee for Medicinal Products for Human Use (CHMP) has adopted a positive opinion for Entresto™ (sacubitril/valsartan), marking an important milestone towards becoming available in the EU. Pending final approval by the European Commission (EC) Entresto, previously known as LCZ696, will be available for the treatment of adult patients with symptomatic chronic heart failure and reduced ejection fraction (HFrEF).
“The striking results in the PARADIGM-HF trial led me to believe that once approved LCZ696 could quickly replace what has been the bedrock treatment for more than 20 years, ACE-inhibitors” said Professor John McMurray of the University of Glasgow and one of two Principal Investigators. “Thousands of lives could be extended and hospital admissions prevented with LCZ696’s unique ability to boost natriuretic peptides, heart-helpful hormones, while simultaneously inhibiting the RAAS system.”
SOURCE
ENTRESTOTM is indicated to reduce the risk of cardiovascular death and hospitalization for heart failure in patients with chronic heart failure (NYHA Class II–IV) and reduced ejection fraction.
ENTRESTO is usually administered in conjunction with other heart failure therapies, in place of an ACE inhibitor or other ARB.
Entresto exhibits the mechanism of action of an Angiotensin Receptor Neprilysin Inhibitor that reduces the strain on the failing heart. A twice-a-day tablet, it acts to enhance the protective neurohormonal systems of the heart (NP system) while simultaneously suppressing the harmful system (the RAAS)4.
ENTRESTO is contraindicated with concomitant use of an angiotensin-converting enzyme (ACE) inhibitor. If switching from an ACE inhibitor to ENTRESTO, allow a washout period of 36 hours between administration of the two drugs.The recommended starting dose of ENTRESTO is 49/51 mg twice-daily.
Double the dose of ENTRESTO after 2 to 4 weeks to the target maintenance dose of 97/103 mg twice daily, as tolerated by the patient.
A starting dose of 24/26 mg twice daily is recommended for patients with severe renal impairment (eGFR <30 mL/min/1.73 m2). Double the dose of ENTRESTO every 2 to 4 weeks to the target maintenance dose of 97/103 mg twice daily, as tolerated by the patient.No starting dose adjustment is needed for mild or moderate renal impairment.
A starting dose of 24/26 mg twice daily is recommended for patients with moderate hepatic impairment (Child-Pugh B classification). Double the dose of ENTRESTO every 2 to 4 weeks to the target maintenance dose of 97/103 mg twice daily, as tolerated by the patient.No starting dose adjustment is needed for mild hepatic impairment.
Use in patients with severe hepatic impairment is not recommended.
SOURCE
HIGHLIGHTS OF PRESCRIBING INFORMATION
These highlights do not include all the information needed to use ENTRESTO safely and effectively. See full prescribing information for ENTRESTO. ENTRESTO™ (sacubitril and valsartan) tablets, for oral use Initial U.S. Approval: 2015 WARNING: FETAL TOXICITY See full prescribing information for complete boxed warning.
When pregnancy is detected, discontinue ENTRESTO as soon as possible. (5.1) Drugs that act directly on the renin-angiotensin system can cause injury and death to the developing fetus. (5.1)
INDICATIONS AND USAGE
ENTRESTO is a combination of sacubitril, a neprilysin inhibitor, and valsartan, an angiotensin II receptor blocker, indicated to reduce the risk of cardiovascular death and hospitalization for heart failure in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction. (1.1) ENTRESTO is usually administered in conjunction with other heart failure therapies, in place of an ACE inhibitor or other ARB. (1.1)
DOSAGE AND ADMINISTRATION
The recommended starting dose of ENTRESTO is 49/51 mg (sacubitril/valsartan) twice-daily. Double the dose of ENTRESTO after 2 to 4 weeks to the target maintenance dose of 97/103 mg (sacubitril/valsartan) twice-daily, as tolerated by the patient. (2.1)
Reduce the starting dose to 24/26 mg (sacubitril/valsartan) twice-daily for: – patients not currently taking an angiotensin-converting enzyme inhibitor (ACEi) or an angiotensin II receptor blocker (ARB) or previously taking a low dose of these agents (2.2) – patients with severe renal impairment (2.3) – patients with moderate hepatic impairment (2.4) Double the dose of ENTRESTO every 2 to 4 weeks to the target maintenance dose of 97/103 mg (sacubitril/valsartan) twice-daily, as tolerated by the patient. (2.2, 2.3, 2.4)
SOURCE
http://www.pharma.us.novartis.com/product/pi/pdf/entresto.pdf
Publications on Heart Failure by Prof. William Gregory Stevenson, M.D., BWH
Reporter: Aviva Lev-Ari, PhD, RN
Is there a role for Galectin-3 in the management of heart failure?
Curator: Larry H Bernstein, MD, FCAP
ESC: Novel Heart Failure Drug a Game-Changer
Reporter: Aviva Lev-Ari, PhD, RN
http://pharmaceuticalintelligence.com/2014/09/02/esc-novel-heart-failure-drug-a-game-changer/
Of the Cardiac-specific Deaths, Deaths from Heart Attack and Sudden Heart Rhythm Disturbances declined steeply, no decline in deaths from Heart Failure in a 20,000 PCI patients Study @ Mayo Clinic
Reporter: Aviva Lev-Ari, PhD, RN
Posted in Chemical Biology and its relations to Metabolic Disease, Clinical & Translational, Curation, Discovery process, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Gastroenterology, Genetics & Innovations in Treatment, Genome Biology, HTN, Pharmacotherapy of Cardiovascular Disease, tagged colonic epithelial cells, platelets, stem cells on September 8, 2015| Leave a Comment »
Mature cells can be reprogrammed to become pluripotent – John Gurdon and Shinya Yamanaka
Larry H. Bernstein, MD, FCAP, Curator
Leaders in Pharmaceutical Innovation
Series E: 2; 7.1
In 1962, John B. Gurdon successfully cloned frogs. He took the nucleus of an adult frog cell – the part of the cell that holds the DNA – and put it into a frog egg cell. The egg was able to develop into a normal tadpole. These experiments showed that an adult, specialised cell still had the information needed to form a new tadpole. The same technique was later used to produce the famous cloned sheep, Dolly.
In 2006, Shinya Yamanaka’s work again took the scientific community by surprise and changed the way researchers think about how cells develop.Yamanaka showed that adult, fully specialised mouse cells could be reprogrammed to become cells that behave like embryonic stem cells – so-called induced pluripotent stem cells, which can develop into all types of cells in the body.
Gurdon and Yamanaka’s work is celebrated and explained in the award-winning documentary, Stem Cell Revolutions, by Clare Blackburn and Amy Hardie. The short clip above is taken from the film and links Gurdon and Yamanaka’s work (click the red button on the image above to watch the clip). Amy Hardie, who directed the film, commented: “So many scientists have said that Shinya Yamanaka has overturned our understanding of basic developmental biology. And he has – with the discovery of iPS cells. What Shinya Yamanaka himself points out and we were able to show in our film, Stem Cell Revolutions, is the lineage from John Gurdon who cloned frogs in Cambridge. Shinya’s groundbreaking discovery would not have been possible without Gurdon’s pioneering work.
Proc Natl Acad Sci U S A. 2013 Apr 9; 110(15): 5740–5741.
Published online 2013 Mar 28. doi: 10.1073/pnas.1221823110
Sir John Bertrand Gurdon, FRS, FMedSci (born 2 October 1933), is an English developmental biologist. He is best known for his pioneering research in nuclear transplantation[2][3][4] and cloning.[1][5][6][7] He was awarded the Lasker Award in 2009. In 2012, he and Shinya Yamanaka were awarded the Nobel Prize for Physiology or Medicine for the discovery that mature cells can be converted to stem cells.[8]
The Nobel Prize in Physiology or Medicine 2012
Sir John B. Gurdon, Shinya Yamanaka
ohn Bertrand Gurdon (JBG), born 2 October 1933, was brought up in a comfortable home by his parents (fig.1) on the Surrey/Hampshire border in a village, Frensham in South England, endowed with a large amount of National Trust heathland and ponds. His mother, Marjorie Byass, was from an East Yorkshire farming family. Brought up on a farm, and educated in that region, she became a physical training teacher working for some time in an American private school. When her son and daughter (Caroline, who trained as a nurse) had been raised, she gave much time to the regional administration of the “Women’s Institute,” a voluntary organisation for educating women.
His father, William Gurdon, was from a longstanding Suffolk family whose ancestors go back to 1199 (fig. 2; Muskett, 1900; Cunnington, 2008); with the family motto “virtus viget in arduis” [virtue flourishes in adversity].
Figure 2. Paternal lineage of JBG.
Many of them had distinguished careers in government and as regional administrators, including Sir Adam Gurdon [Muskett, 1900]. JBG’s ancestors lived in a stately home, Assington Hall, in West Suffolk (fig. 3).
Figure 3. Assington Hall, Suffolk. Burnt down in 1957.
His grandfather had to leave the family home through lack of money to maintain it, due to repeal of the Corn Laws (1846) so that tenant farmers could no longer pay their rent, because of foreign imports. Assington Hall was requisitioned by the army during World War II, and was burnt down in a supposedly accidental fire in 1957. The remaining part of the house was partly restored and part of the original home, including its minarets, is still present in Assington. One of JBG’s ancestors married again after his first wife died and the outcome of a second marriage yielded a distinguished lawyer who accepted the hereditary title of Baron Cranworth. JBG’s father left school at the age of 16 and took a position in a rice broking firm in Burma. He was an early volunteer in the First World War and was decorated with the Distinguished Conduct Medal (DCM) before being commissioned to an officer rank. After that he led a career in banking in Assam and East India. He retired, in his forties, and in retirement, he gave much time to the transcribing of professional textbooks (especially legal) into Braille for the blind as voluntary work.
World War II started in 1939 when JBG was aged six. It was a time of austerity. Limited rations of food were managed by his mother, and the garden was used to raise chickens. He did not see luxuries like a banana or an orange until well after the end of the war. At the age of eight he was sent to a local private school, Frensham Heights. In an intelligence test at that age, he was asked to draw an orange. He started drawing the stalk by which the orange would hang from a tree, reasoning that an orange would not exist in space. The teacher tore up the piece of paper and reported to his parents that he was mentally subnormal and would need special teaching. The teacher meant to say, draw a circle. He was moved to another private school in the village, namely Edgeborough, where he thrived. At that age he had an intense interest in plants and insects. In most of his spare time he collected butterflies and moths and raised their caterpillars.
At the age of 13, he started school at Eton as a boarder. He found life there intensely uncomfortable, because senior boys acted as despots, administering punishments for trivial misdemeanours. As a means of survival, he took up squash, and as a result of hard work rather than ability, he became eventually the school captain in this sport. While at school he continued his interest in Lepidoptera, raising large numbers of moths from their larval stage.
Gurdon attended Edgeborough and then Eton College, where he ranked last out of the 250 boys in his year group at biology, and was in the bottom set in every other science subject. A schoolmaster wrote a report stating “I believe he has ideas about becoming a scientist; on his present showing this is quite ridiculous.”[9] Gurdon explains it is the only document he ever framed; Gurdon also told a reporter “When you have problems like an experiment doesn’t work, which often happens, it’s nice to remind yourself that perhaps after all you are not so good at this job and the schoolmaster may have been right.”[10]
It was during his first term of being taught Science at the school, at the age of 15, that he received a totally damning report from the Biology master (fig. 4). This report resulted from JBG being placed in the bottom position of the lowest form in a group of 250 students of the same age. The report, sent to his housemaster, resulted in him being taken off any further study of Science of any kind at the school. For the rest of his school days, for the next three years, he was given no Science teaching and was placed in a class which studied Ancient Greek, Latin and a modern language, a course intended for those judged to be unsuited for studying any subject in depth.
Entrance to University was a problem: having sat the Entrance examination in Latin and Greek, the Admissions tutor at Christ Church Oxford University told JBG that he would be accepted for Entrance on condition that he did not plan to study the subject in which he took the Entrance (Classics). Later the Admissions tutor admitted that he had under-filled the college and had his mind on other things; he was Hugh Trevor-Roper, later Lord Dacre, and author of The Last Days of Hitler. In due course it emerged that JBG’s acceptance for Christ Church involved a complicated arrangement between JBG’s uncle, at that time a Fellow of Christ Church, JBG’s school housemaster and a friend of his uncle, Sir John Masterman, who was Master of Worcester College, Oxford and in charge of the wartime Enigma operation at Bletchley, agreeing to accept the housemaster’s son. Such a manoeuvre, and admission to Oxford on those terms, could never happen now. At that time, 1952, it was not very easy to fill a college with paying students. Before entering University, JBG had to take a year off to learn elementary Biology with a private tutor, generously funded by his parents who had already paid several years of Eton fees. He was told that he could formally enter the Department of Zoology course at Oxford if he passed the elementary exams in Physics, Chemistry and Biology in a preliminary year. He survived this and started the course in Zoology at Oxford in 1953. The course was extremely oldfashioned, by today’s standards. A major part of the teaching involved learning Palaeontology, and the names of skeletal parts of dinosaurs. JBG later became a personal friend of Sir Alister Hardy, the Head of that department, through his Oxford aunt (see later).
As the Zoology course came to an end, JBG enquired about the possibility of doing a PhD in Entomology, in accord with his continuing interest in insects. While still a student, he had got permission to go to Oxford University’s nature reserve, namely Wytham Woods, with his butterfly net. No butterflies were to be seen, but he caught the only moving thing, which was a kind of fly. He used the taxonomic reference works to try to identify this “fly.” Having realised that the fly was a Hymenopteron, he was still unable to identify it. He therefore went to the Natural History Museum in London for help. They pronounced that it was in fact a species of sawfly new to Britain. This must have been intensely irritating to the Professor of Entomology, whose main research project was to identify animals and plants in Wytham Woods. JBG was later rejected for PhD work in Entomology. This was a great blessing because the work he would have done in Entomology was not well regarded and had very little, if any, analytical component to it. By his immense good fortune, he was invited to do a PhD with the Oxford University lecturer who taught Developmental Biology, Dr Michael Fischberg.
Fischberg was born in St Petersburg, Russia, in 1919. He was educated in Switzerland and was a PhD student of E. Hadorn. Hadorn in turn was a student of F. Baltzer, who was a student of H. Spemann, himself a student of T. Boveri. This German-Swiss lineage of eminent Developmental Biologists turns out to be the background of a great many of the successful Developmental Biologists of the mid-1950s. Most of those that did not have this background can trace their own training back to R. G. Harrison (1870–1959) of the USA, who pioneered cell culture. Having finished his PhD with Hadorn, Fischberg took a position in the Institute of Animal Genetics under Waddington in Edinburgh, from where he accepted his appointment in the Oxford Zoology department, headed by Professor Sir Alister Hardy, an eminent marine biologist [Royal Society memoirs].
Starting his PhD work in 1956, Fischberg suggested to JBG that he should try to carry out somatic cell nuclear transfer in Xenopus, a procedure for this having been recently published by Briggs and King (1952). The advisability and technical problems that arose at this point are described in the accompanying papers (Gurdon 2013 a,b). Once these technical obstacles had been overcome, largely as a result of good luck, JBG’s work proceeded extraordinarily fast; strongly motivated by early success, he became an intensely hard worker. By the end of his PhD he had succeeded in obtaining normal development of intestinal epithelium cell nuclei transplanted to enucleated eggs of Xenopus. When these tadpoles had eventually reached sexual maturity, he was able to publish a paper entitled “Fertile intestine nuclei.”This was the first decisive evidence that all cells of the body contain the same complete set of genes. This answered a long-standing and important question in the field of Developmental Biology. However it also showed very clearly, as was commented on in JBG’s papers at the time, the remarkable ability of eggs to reprogram somatic cell nuclei back to an embryonic state. Eventually this phenomenon attracted increasingly large interest, and led to the idea of cell replacement using accessible adult cells, such as skin. A key future discovery was that of Martin Evans (Nobel Prize, 2006) that a permanently proliferating embryonic stem cell line could be established from mouse embryos. Under appropriate conditions these cells could be caused to differentiate into all different cell types. The combination of somatic cell nuclear transfer and the derivation of embryonic stem cells in mammals made it realistic to think of cell replacement for human diseases. A huge boost for this idea was later provided by Takahashi and Yamanaka (2006), with their discovery that the overexpression of certain transcription factors can also yield embryonic stem cells from adult somatic tissue. The accompanying Nobel lecture provides more detail of the later scientific part of JBG’s career.
A visit by the Nobel Laureate George Beadle to the Fischberg Group in the Oxford Zoology department in 1960 led to an offer from the California Institute of Technology (CalTech) (previous chairman George Beadle) for JBG to do postdoctoral work there. Fischberg very wisely advised JBG to accept the CalTech offer of postdoctoral work rather than offers from other nuclear transplant labs. Stimulated by his mother’s adventurous spirit, JBG decided to buy a secondhand Chevrolet in New York and drive across the USA to California, using the famous Route 66 (now replaced). He gave lectures as he travelled across the USA and stopped at laboratories of Briggs and King, Alexander Brink (paramutation) etc. He had hoped to become a post-doctoral student of R. Dulbecco at CalTech (Nobel Prize), but the chairman of that department advised against this because JBG had no training in virology. Therefore JBG did his postdoctoral work with Robert Edgar on Bacteriophage Genetics. JBG found he had no aptitude at all for Phage Genetics and decided to return to Britain after one year at CalTech. Nevertheless, that year at CalTech was extremely formative because it provided some acquaintance with Molecular Biology, which had so far entirely escaped his training. During that year he met Sturtevant, a student of Morgan, who pioneered the whole field of Drosophila Genetics. He also got to know Ed Lewis (future Nobel Laureate). Thanks to James Ebert (director of the Department of Embryology, Carnegie Institute of Washington, in Baltimore) JBG visited various labs in the USA at the end of his post-doctoral period and met Donald Brown in Baltimore on that visit. Meantime, the success of the nuclear transfer work in Oxford had led to Michael Fischberg being offered a head of department professorship in Geneva, Switzerland. JBG was offered the teaching position in Oxford vacated by M. Fischberg. JBG returned from California to England via Japan and many other countries over a two-month period. One month of that time he spent in Japan and met Tokindo Okada and made other friends in Japan, including M. Furusawa and subsequently Koichiro Shiokawa.
While doing graduate and postdoctoral work in Oxford, JBG made other contacts and friendships. His mother’s sister lived in Oxford, and he spent much time at her house and visiting famous gardens, fostering a lifelong interest in plants. Through that connection he met Miriam Rothschild, and became a lifelong friend of hers (Van Emden and Gurdon, 2006). This friendship contained, through Miriam Rothschild’s generosity, ski mountaineering holidays based in her house in Wengen. JBG had achieved the British ski club’s Gold standard ski medal, again through relentless practice rather than any natural ability. Also, in accord with his interest in the open air and dogged determination, he became a reasonably accomplished ice figure skater.
Nobel Lecture by Sir John B. Gurdon (42 minutes)
Sir John B. Gurdon delivered his Nobel Lecture on 7 December 2012 at Karolinska Institutet in Stockholm. He was introduced by Professor Urban Lendahl, Chairman of the Nobel Committee for Physiology or Medicine.
Credits: Sveriges Television AB (production)
Copyright © Nobel Media AB 2012
The Nobel Prize in Physiology or Medicine 2012 Lecture (pdf)
Nuclear transfer
In 1958, Gurdon, then at the University of Oxford, successfully cloned a frog using intact nuclei from the somatic cells of a Xenopus tadpole.[14][15] This work was an important extension of work of Briggs and King in 1952 on transplanting nuclei from embryonic blastula cells[16] and the successful induction of polyploidy in fish Stickleback, Gasterosteus aculatus, in 1956 by Har Swarup reported in Nature.[17] However, he could not yet conclusively show that the transplanted nuclei derived from a fully differentiated cell. This was finally shown in 1975 by a group working at the Basel Institute for Immunology in Switzerland.[18] They transplanted a nucleus from an antibody-producing lymphocyte (proof that it was fully differentiated) into an enucleated egg and obtained living tadpoles.
Gurdon’s experiments captured the attention of the scientific community and the tools and techniques he developed for nuclear transfer are still used today. The term clone[19] (from the ancient Greek word κλών (klōn, “twig”)) had already been in use since the beginning of the 20th century in reference to plants. In 1963 the British biologist J. B. S. Haldane, in describing Gurdon’s results, became one of the first to use the word “clone” in reference to animals.
Messenger RNA expression
Gurdon and colleagues also pioneered the use of Xenopus (genus of highly aquatic frog) eggs and oocytes to translate microinjected messenger RNA molecules,[20] a technique which has been widely used to identify the proteins encoded and to study their function.
Recent research
Gurdon’s recent research has focused on analysing intercellular signalling factors involved in cell differentiation, and on elucidating the mechanisms involved in reprogramming the nucleus in transplantation experiments, including the role of histone variants,[21][22] and demethylation of the transplanted DNA.[23]
Reprogramming of Mature Cells
Our lives begin when a fertilized egg divides and forms new cells that, in turn, also divide. These cells are identical in the beginning, but become increasingly varied over time. As a result of this process, our cells become specialized for their location in the body – perhaps in a nerve, a muscle, or a kidney. It was long thought that a mature or specialized cell could not return to an immature state, but this has been proven incorrect.
In 1962, John Gurdon removed the nucleus of a fertilized egg cell from a frog and replaced it with the nucleus of a mature cell taken from a tadpole’s intestine. This modified egg cell grew into a new frog, proving that the mature cell still contained the genetic information needed to form all types of cells. In 2006, Shinya Yamanaka succeeded in identifying a small number of genes within the genome of mice that proved decisive in this process. When activated, skin cells from mice could be reprogrammed to immature stem cells, which, in turn, can grow into all types of cells within the body. In the long-term, these discoveries may lead to new medical treatments.
Shinya Yamanaka
A winding road to pluripotency
http://www.nobelprize.org/nobel_prizes/medicine/laureates/2012/yamanaka-lecture.pdf
http://www.nobelprize.org/nobel_prizes/medicine/laureates/2012/ypdfamanaka-lecture_slides.
Nobel Lecture
In 1989, however, my life took a new turn from clinical medicine in orthopedic surgery to basic science research for two reasons. First, I found that I was not a very talented surgeon. Second, I saw many patients suffering from intractable diseases and injuries, which even highly talented surgeons and physicians were not able to cure. For example, I had encountered patients suffering from spinal cord injuries, amyotrophic lateral sclerosis and osteosarcomas. Furthermore, I lost my father due to liver cirrhosis during my residency. Basic medical research is the only way to find cures for these patients. For these reasons, I decided to go back to school. I became a Ph.D. student at Osaka City University Medical School in April of 1989.
A scandal involving Japanese stem-cell research took a surprising turn Monday when the nation’s most revered researcher in the field, Nobel Prize laureate Shinya Yamanaka, apologized for what he described as poor record-keeping.
The apology came after months of soul-searching in Japan over research ethics. A researcher at the prestigious Riken institute, Haruko Obokata, apologized earlier this month after admitting errors in a paper in the journal Nature that described a possible new method of creating stem cells.
Last week, the head of the Riken panel investigating Dr. Obokata had to resign from the panel after admitting that a paper he co-authored used some of the same improper methods of cutting and pasting images that he had criticized in Dr. Obokata’s work.
On Monday evening, Dr. Yamanaka, a professor at Kyoto University, spoke at a news conference after questions arose about an image in a 2000 paper on which he was the lead author. In the paper, Dr. Yamanaka, then at Nara University, described a protein that played a role in turning embryo cells into cells specific to a part of the body.
The university said it conducted an investigation after Dr. Yamanaka informed administrators about allegations he discovered online that an image in the paper was doctored.
Posted in Academic Publishing, Bone Disease and Musculoskeletal Disease, Cancer and Current Therapeutics, Cardiac and Cardiovascular Surgical Procedures, Cardiovascular Pharmacogenomics, Curation, Disease Biology, Frontiers in Cardiology and Cardiovascular Disorders, Myocardial Ischemia, Nephrology, Nitric Oxide in Health and Disease, Origins of Cardiovascular Disease, Pharmacotherapy of Cardiovascular Disease, tagged Alzheimers Disease, Aviva Lev-Ari, Cardiovascular Disorders, Cell Biology, Conditions and Diseases, Content Curation, Curation methodology, health, Heart disease, Larry H. Bernstein, medical ebook, myocardial infarction, nitric oxide, Nitric oxide synthase, research, science on August 17, 2015| Leave a Comment »
Leaders in Pharmaceutical Business Intelligence would like to announce their First Volume of their BioMedical E-Book Series A: eBooks on Cardiovascular Diseases
Perspectives on Nitric Oxide in Disease Mechanisms
which is now available on Amazon Kindle at
http://www.amazon.com/dp/B00DINFFYC
This book is a comprehensive review of Nitric Oxide, its discovery, function, and related opportunities for Targeted Therapy written by Experts, Authors, Writers. This book is a series of articles delineating the basic functioning of the NOS isoforms, their production widely by endothelial cells, and the effect of NITRIC OXIDE production by endothelial cells, by neutrophils and macrophages, the effect on intercellular adhesion, and the effect of circulatory shear and turbulence on NITRIC OXIDE production. The e-Book’s articles have been published on the Open Access Online Scientific Journal, since April 2012. All new articles on this subject, will continue to be incorporated, as published, in real time in the e-Book which is a live book.
We invite e-Readers to write an Article Reviews on Amazon for this e-Book.
All forthcoming BioMed e-Book Titles can be viewed at:
http://pharmaceuticalintelligence.com/biomed-e-books/
Leaders in Pharmaceutical Business Intelligence, launched in April 2012 an Open Access Online Scientific Journal is a scientific, medical and business multi expert authoring environment in several domains of life sciences, pharmaceutical, healthcare & medicine industries. The venture operates as an online scientific intellectual exchange at their website http://pharmaceuticalintelligence.com and for curation and reporting on frontiers in biomedical, biological sciences, healthcare economics, pharmacology, pharmaceuticals & medicine. In addition the venture publishes a Medical E-book Series available on Amazon’s Kindle platform.
Analyzing and sharing the vast and rapidly expanding volume of scientific knowledge has never been so crucial to innovation in the medical field. WE are addressing need of overcoming this scientific information overload by:
This curation offers better organization and visibility to the critical information useful for the next innovations in academic, clinical, and industrial research by providing these hybrid networks.
Table of Contents for Perspectives on Nitric Oxide in Disease Mechanisms
Chapter 1: Nitric Oxide Basic Research
Chapter 2: Nitric Oxide and Circulatory Diseases
Chapter 3: Therapeutic Cardiovascular Targets
Chapter 4: Nitric Oxide and Neurodegenerative Diseases
Chapter 5: Bone Metabolism
Chapter 6: Nitric Oxide and Systemic Inflammatory Disease
Chapter 7: Nitric Oxide: Lung and Alveolar Gas Exchange
Chapter 8. Nitric Oxide and Kidney Dysfunction
Chapter 9: Nitric Oxide and Cancer
Posted in Electrophysiology, Frontiers in Cardiology and Cardiovascular Disorders, Heart Failure (HF), HTN, Pharmacotherapy of Cardiovascular Disease on August 9, 2015| Leave a Comment »
Reporter: Aviva Lev-Ari, PhD, RN
Monday, 06 April 2015 11:59 AM EDT
According to Patient, beta-blockers are drugs prescribed to many patients to lower blood pressure, treat angina, control abnormal heart rhythms and prevent heart attack. The medication is effective and powerful but there are still beta-blocker risks you should discuss with your doctor.Beta-blockers slow the heart by blocking adrenaline your body produces naturally. According to WebMD, although many people who take beta-blockers will not have side effects, others may experience fatigue, dizziness or shortness of breath, as well as headache, upset stomach, constipation or diarrhea, or other minor discomforts.
Here are seven risks of beta-blockers your doctor doesn’t tell you:
1. People with asthma or COPD should not take beta-blockers, which may trigger severe asthma attacks or otherwise worsen symptoms, according to the Mayo Clinic. Doctors don’t normally prescribe them for those conditions.
2. If you have diabetes, beta-blockers could prevent warning signs of low blood sugar like a rapid heartbeat. Be sure to monitor your blood sugar as directed if you take beta-blockers, reports the Mayo Clinic.
3. Beta-blockers may trigger a modest increase in triglycerides, fats in the blood, while slightly decreasing high-density lipoprotein, the “good” cholesterol that cleans the arteries of unhealthy cholesterol, according to the Mayo Clinic. Although these effects are generally temporary, be sure you have regular cholesterol checks.
4 Hidden Symptoms Could Cause a Heart Attack; Take This Test to Reveal Them — Click Here Now
4. Beta blockers are occasionally prescribed for other conditions not related to blood pressure. Doctors don’t usually prescribe them for low blood pressure or a slow pulse, which can lower the heart rate, causing dizziness and lightheadedness, according to WebMD. Patients should record their pulse regularly and contact their doctor if the pulse is slower than normal.
5. Beta blockers stimulate the muscles that surround the air passages so they contract and lead to difficulty in breathing, according to MedicineNet.com.
6. Talk to your doctor about all other medications you take, including those sold over the counter. Aspirin, for example, may interact with your prescribed beta-blockers and reduce the effects.
7. Suddenly stopping the medication could increase beta-blocker risks such as heart troubles or even a heart attack. A doctor will advise you on stopping the medication by slowly decreasing the dosage.
SOURCE
https://www.newsmax.com/FastFeatures/beta-blocker-risks/2015/04/06/id/636670/
Sourced through Scoop.it from: www.newsmax.com
Posted in Frontiers in Cardiology and Cardiovascular Disorders, HTN, Pharmacotherapy of Cardiovascular Disease on August 9, 2015| Leave a Comment »
Use of Beta and Alpha blockers in treatment of Hypertension | Medicine made Easy
Reporter: Aviva Lev-Ari, PhD, RN
This article is to discuss the use of Alpha and Beta blockers in the management of cases of hypertension regarding types,mechanism of action,pharmacological action, indications and side effects of the drugs .
Sourced through Scoop.it from: www.med4al.com
Posted in Frontiers in Cardiology and Cardiovascular Disorders, Heart Failure (HF), HTN on August 9, 2015| Leave a Comment »
Beta-blocker withdrawal linked to negative outcomes in patients with acute … – Healio
Reporter: Aviva Lev-Ari, PhD, RN
Patients with acute decompensated HF who discontinue beta-blockers may have an increased risk for mortality and rehospitalization, according to results of a new systematic review and meta-analysis.
Sourced through Scoop.it from: www.healio.com
Posted in Academic Publishing, BioIT: BioInformatics, Biomarkers & Medical Diagnostics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cardiac and Cardiovascular Surgical Procedures, Cell Biology, Chemical Genetics, Clinical Diagnostics, CRISPR/Cas9 & Gene Editing, Disease Biology, Frontiers in Cardiology and Cardiovascular Disorders, Genetics & Innovations in Treatment, Genetics & Pharmaceutical, Genome Biology, Genomic Testing: Methodology for Diagnosis, Personalized and Precision Medicine & Genomic Research, Pharmacotherapy of Cardiovascular Disease on July 31, 2015| Leave a Comment »
Curators:
Adam Sonnenberg, BSc, Content Digitization
and
Stephen J Williams, PhD, Senior Editor – Series A: Volume 1, Series B, Volume 1, Series C, Volumes 1 & 2
The Journal Articles are written by Experts, Authors, Writers. The results of Original Research are gaining value added for the e-Reader by the Methodology of Curation. The e-Book’s articles have been published on the Open Access Online Scientific Journal, since April 2012. All new articles on this subject, will continue to be incorporated, as published with periodical updates.
Open Access Online Journal
The Journal is a scientific, medical and business, multi-expert authoring environment for information syndication in several domains of
Scientific critical interpretations and original articles are written by PhDs, MDs, MD/PhDs, PharmDs, Technical MBAs as Experts, Authors, Writers (EAWs) on an Equity Sharing basis.
|
Author Name |
Author NameTotal Views 4/2012 to 7/2015 |
# of Articles |
| Aviva Lev-Ari, PhD, RN | 207,592 | 2,004 |
| Larry H Bernstein, MD, FCAP | 114,265 | 620 |
| Tilda Barliya, PhD | 32,651 | 46 |
| Stephen J Williams, PhD | 20,508 | 77 |
| Dror Nir, PhD | 17,372 | 53 |
| Sudipta Saha, PhD | 16,301 | 58 |
| Ritu Saxena, PhD | 12,664 | 40 |
| Demet Sag, PhD | 7,160 | 24 |
| Aviral Vatsa, PhD | 6,922 | 20 |
| Ziv Raviv | 4,905 | 9 |
| Anamika Sarhar, PhD | 2,901 | 7 |
| Prabod Kandala, PhD | 1,998 | 43 |
| Alan F Kaul, PharmD, FCCP | 1,730 | 4 |
| Asshir Awan, PhD | 1,366 | 4 |
| Meg Baker, PhD | 1,266 | 4 |
| Justin D Pearlman, MD, PhD, FACC | 773 | 3 |
2013 e-Book on Amazon.com
2015 e-Books on Amazon.com
1. Metabolomics, on Amazon since 7/21/2015
2. Cancer Volume One
3. Genomics Volume One
4. Physiology, Genomics and Pharmaceutical
5. Cardiovascular, Volume Two: Co-Curation, Methodology
6. Cardiovascular Diseases, Volume Three: Etiology, Genetics and Genomics
7. Cardiovascular Diseases, Volume Four: Regenerative and Translational Medicine
8. Cancer Volume Two: Immunotherapy, Nanotechnology in drug delivery
2016 we need to FIND Editors for Two e-Books
– Genomics Volume Two on NGS – Dr. Williams and another Editor
– Patient Voice on Invasive Procedures – New Editor
2016, We will continue with
– Aviva will work with Larry on CVD 5: Pharmacology-Therapy,
– With Adam and Dr. Pearlman, on CVD 6: Cardiac Surgery and Interventional
– With Adam and Dr. Pearlman, on CVD 7: CV Imaging
– Dr. Pearlman alone:
Three CVD Hardcopy Volumes, 1-Etiology, 2-Diagnostics, 3-Therapies
Posted in Atherogenic Processes & Pathology, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Origins of Cardiovascular Disease, Pharmacotherapy of Cardiovascular Disease on July 27, 2015| Leave a Comment »
Reporter: Aviva Lev-Ari, PhD, RN
The first of a powerful new class of cholesterol-lowering medicines won approval from U.S. regulators Friday—a highly anticipated medical advance that nevertheless promises to escalate the growing clamor over drug costs.
The drug, called Praluent and developed by Regeneron Pharmaceuticals Inc. and SanofiSA, provides a new and in some cases desperately needed option for several million high-risk heart patients who can’t get their cholesterol to desirable levels with the blockbuster group of medicines known as statins.
But the companies are pricing the drug at $14,600 a year, an especially high amount for a medicine aimed at a common condition like heart disease. By contrast, statins, which are available in generic versions and remain the mainstay drug option for cholesterol reduction, can be purchased for just a few dollars a month.
Regeneron and Sanofi defended Praluent’s price. An antibody that patients inject themselves, it will cost substantially less than similarly administered drugs such as Humira and Enbrel for rheumatoid arthritis and other autoimmune diseases, which are prescribed for thousands of patients and which they said list for more than $38,000 a year.
The toll in the U.S. for cardiovascular disease amounts to more than $300 billion a year, according to estimates, while treating an individual heart attack can range from $60,000 to $120,000, said Leonard Schleifer, Regeneron’s chief executive officer. Expectations—not yet proven—are that the marked cholesterol reductions seen with Praluent will translate into fewer deaths and costly events.
The company believes “we’ve come up with a price that provides value to the health-care system,” Dr. Schleifer said.
SOURCE
http://www.wsj.com/articles/fda-approves-cholesterol-drug-from-regeneron-sanofi-1437762374
Posted in Frontiers in Cardiology and Cardiovascular Disorders, Pharmacotherapy of Cardiovascular Disease on May 15, 2015| Leave a Comment »
Reporter: Larry H. Bernstein, MD, FCAP
Angiogenesis related drug
Motesanib (AMG 706) is an experimental drug candidate originally developed by Amgen[1] but is now being investigated by theTakeda Pharmaceutical Company. It is an orally administered small molecule belonging to angiokinase inhibitor class which acts as an antagonist of VEGF receptors, platelet-derived growth factor receptors, and stem cell factor receptors.[2] It is used as thephosphatesalt motesanib diphosphate.
2012pharmaceutical
sjwilliamspa