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#familial hypercholesterolaemia
cardiologybd · 9 months
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Homozygous Familial Hypercholesterolaemia with Valvular Aortic Stenosis and Significant Coronary Artery Disease: A Case Report
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sustainable-sian · 11 months
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Inherited Heart Conditions
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Inherited heart conditions are passed on through families. They’re sometimes called genetic heart conditions or inherited cardiac conditions. They can affect people of any age. If left untreated, some inherited heart conditions can be life-threatening.
What are the symptoms of an inherited heart condition?
Some people with an inherited heart condition have no symptoms, while other people develop symptoms such as:
Dizzy spells
Palpitations
Blackouts
Shortness of breath
For many families, the first sign there’s something wrong is when someone dies suddenly, with no obvious cause. This is known as sudden arrhythmic death syndrome (SADS).
What are the different types of inherited heart condition?
The most common inherited heart conditions are cardiomyopathies and channelopathies.
Inherited cardiomyopathies:
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Channelopathies (which can cause abnormal heart rhythms):
Long QT syndrome (LQTS)
Brugada syndrome
Catecholaminergic polymorphic ventricular tachycardia (CPVT)
Progressive cardiac conduction defect (PCCD)
Inherited conditions which increase your risk of heart disease:
Familial hypercholesterolaemia (FH) - very high cholesterol levels
What causes an inherited heart condition?
Your body is made up of trillions of cells. Each cell has a nucleus, containing information that makes you unique. This information is called your genes. We all have between 20,000 and 25,000 different genes each.
Genes affect how we look and how our bodies work, and we inherit them from our parents. Inherited heart conditions are caused by a fault (or mutation) in one or more of our genes. If one of your parents has a faulty gene, there’s a 50:50 chance you could have it too. If you do, then there’s also a 50:50 chance you could pass it on to your children.
It’s possible to have a faulty gene that can lead to a heart condition, but you may never develop any signs or symptoms of the condition itself. If this happens, you can still pass the faulty gene onto your child and there’s no way of knowing how it may affect them.
Testing for an inherited heart condition
A member of your family has an inherited heart condition
There’s a history of cardiac arrests or premature deaths in your family
A death in the family is hard to explain or thought to be caused by a faulty gene
You’ve been diagnosed with angina or had a heart attack at a young age, in which case your doctor may suspect you have FH
Treatment for an inherited heart condition
Treatment for an IHC includes:
Changes to your lifestyle
Medication
Implantable cardioverter defibrillators (ICDs)
Harvard Referencing:
BRITISHHEARTFOUNDATION. (N/A) Inherited heart conditions. [Online] Available from: https://www.bhf.org.uk/informationsupport/conditions/inherited-heart-conditions [Accessed: 12th November 2023]
www.youtube.com. (2018). Inherited Heart Conditions. [online] Available at: https://youtu.be/wsLCILJQ18w [Accessed 12 Nov. 2023].
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mikyit · 11 months
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https://lnkd.in/dChxaebB Successful approaches for #Personalised #Medicine 👩‍⚕️👦 are becoming a reality. ---- The best practice examples cover different aspects of the #ValueChain ⛓️‍, in particular, two different types: - - 💥 1. Successful translation of #Personalised #Medicine #research 🔬 into an added value for the #patient 😷. - - 💥 2. #Policy making and impact #analysis 📊 for #Personalised #Medicine #research.
_-_-_ Here are the selected examples, click here (https://lnkd.in/dChxaebB) from more :
🚀 - Mosaic Initiative: a Launchpad for Personalised Medicine - Israel
🚀 - Implementation of Personalised Medicine - Estonia
🚀 - The Ubiquitous Pharmacogenomics (U-PGx) Education Programme - EU
🚀 - Centers for Personalized Medicine (ZPM) - Germany
🚀 - Swiss Personalized Health Network (SPHN) - Switzerland
🚀 - Translational medicine in Familial hypercholesterolaemia - Portugal
🚀 - The “HAZLO” project - Spain
🚀 - MedeA – Pharmacogenetics Personlised Prescription - Spain
🚀 - Strimvelis® Gene Therapy - Italy
🚀 - PERSEPHONE project - Italy
🚀 - MASTER – Innovation Driver for Personalised Oncology - Germany
🚀 - Electronic medical records (EMR) for personalised treatment - Italy
🚀 - 2025 France Genomic Medicine Initiative - France
🚀 - Genomic Medicine Sweden - Sweden
🚀 - Pharmacogenetic Recommendations for PM - Estonia
🚀 - Navarra 1,000 Genomes Project - Spain
🚀 - Network Genomic Medicine (NGM) Lung Cancer - Germany
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bouffees · 2 years
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Are you on Repatha injections? If so, what has been your experience with side effects?
My cardiologist feels that Repatha as well as atozet for my familial hypercholesterolaemia is the best way to elongate my life and reduce the rate of decline in my heart. I have 50% blockage in my right coronary artery and some atherosclerosis development in the left coronary artery and my carotid arteries. I am 33 years old. Despite having several needles all the time, I’ve never had to inject myself. I am hesitant and have since read about people with awful side effects. If you currently take or have taken this, can you please tell me if the injection hurts and what your side effects are/have been?
submitted by /u/User14needsavoice [link] [comments] from For issues related to heart disease, cardiac health and cholesterol control https://ift.tt/OZkI2ou
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a4medicineuk · 3 years
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Familial hypercholesterolaemia ( FH ) is a genetic disorder affecting the metabolism of low density lipoprotein ( LDL ) particles leading to high LDL cholesterol levels maintained over time and higher risk of 
cardiovascular disease early in life ( Atherosclerosis-journal.com )
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southeastgenomics · 4 years
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Heart UK Virtual Lipid Update 2020 (Online Event)
Heart UK are pleased to introduce this for nothing out of pocket, CPD certify occasion for medical services experts both in the UK and globally on November 24. 
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Reserve your seat from Heart UK page!
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lifeguides · 2 years
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FH Australasia Network - familial hypercholesterolaemia
FH Australasia Network – familial hypercholesterolaemia
Familial hypercholesterolaemia (FH) is a dominantly inherited disorder present from birth that markedly elevates plasma low-density lipoprotein (LDL) cholesterol and causes premature coronary heart disease. There are at least 20 million people with FH worldwide, but the majority remain undetected and current treatment is often suboptimal. Source
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leyhejuhyunghan · 2 years
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nature “CRISPR ‘cousin’ put to the test in landmark heart-disease trial, Gene therapy test launches pivotal year for precise genome-editing technique known as base editing.”, The Cas9 directs the base-editing enzyme to the right location in the genome, reduce PCSK9 activity, Religious & Biblical Studies - Brill Publishing The Tree of Life, Pippa Salonius, Chapter 12 The Tree of Life in Medieval Iconography, George Dunlop Leslie (English, 1835-1921), Matilda - Dante, Purgatorio, Canto 28, 1859, Wadsworth Atheneum Museum of Art James Abbott McNeill Whistler (American, 1834 -British, 1903), Coast of Brittany (Alone with the Tide), 1861, Female Artists in History Gabriele Münter (German, 1877-1962), Interieur mit Weinachtsbaum (Interior with Christmas Tree), ca. 1912-14, Christie’s., Staffelsee, 1932, Schloss Elmau im Winter, 1933, Staffelsee, 1934, Straßendurchstich im Winter (Naturstudie. Station Berggeist Schnee), 1935, Ketterer Kunst.
nature “CRISPR ‘cousin’ put to the test in landmark heart-disease trial, Gene therapy test launches pivotal year for precise genome-editing technique known as base editing.”, The Cas9 directs the base-editing enzyme to the right location in the genome, reduce PCSK9 activity, Religious & Biblical Studies - Brill Publishing The Tree of Life, Pippa Salonius, Chapter 12 The Tree of Life in Medieval Iconography, George Dunlop Leslie (English, 1835-1921), Matilda - Dante, Purgatorio, Canto 28, 1859, Wadsworth Atheneum Museum of Art James Abbott McNeill Whistler (American, 1834 -British, 1903), Coast of Brittany (Alone with the Tide), 1861, Female Artists in History Gabriele Münter (German, 1877-1962), Interieur mit Weinachtsbaum (Interior with Christmas Tree), ca. 1912-14, Christie’s., Staffelsee, 1932, Schloss Elmau im Winter, 1933, Staffelsee, 1934, Straßendurchstich im Winter (Naturstudie. Station Berggeist Schnee), 1935, Ketterer Kunst. https://blog.naver.com/artnouveau19/222820741393
https://www.nature.com/articles/d41586-022-01951-1?utm_term=Autofeed&utm_campaign=nature&utm_medium=Social&utm_source=Facebook&fbclid=IwAR19if0Lw95-fmOUpShQi2bDonT5OS1or_WlUAGuwUKTVczRN4VDOCGwgKk#Echobox=1657906344 https://brill.com/view/book/edcoll/9789004423756/BP000013.xml https://www.facebook.com/photo/?fbid=10150948780782151&set=a.10150724112537151 https://www.facebook.com/photo/?fbid=407819374713153&set=a.334687465359678 https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/3125262201091981/
https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/3056631941288341/ https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/1714278678857014/ https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/1714289802189235/ https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/1827048414246706/
NEWS
15 July 2022
CRISPR ‘cousin’ put to the test in landmark heart-disease trial
Gene therapy test launches pivotal year for precise genome-editing technique known as base editing.
Heidi Ledford
https://www.nature.com/articles/d41586-022-01951-1?utm_term=Autofeed&utm_campaign=nature&utm_medium=Social&utm_source=Facebook&fbclid=IwAR19if0Lw95-fmOUpShQi2bDonT5OS1or_WlUAGuwUKTVczRN4VDOCGwgKk#Echobox=1657906344 A clinical trial that recently treated its first participant will test whether base-editing — a genome-editing method related to the CRISPR–Cas9 system — can safely be used to make precise, single-letter changes to a DNA sequence in a cholesterol-regulating gene without breaking both strands of DNA first, as CRISPR–Cas9 would do.
This study will be followed by another base-editing trial, slated to treat its first participant later this year, that will aim to treat sickle-cell disease, a genetic blood disorder.
In CRISPR–Cas9 genome editing, the Cas9 enzyme breaks both strands of DNA at the site that is to be edited. The cell’s DNA-repair processes stitch the strands back together, but sometimes make mistakes. This means that a range of DNA sequence changes are possible with each edit.
Base editing, by contrast, avoids cutting both strands of the DNA by coupling a Cas9 protein that cuts only one strand of DNA, rather than both, to another enzyme that chemically converts one DNA letter to another. The Cas9 directs the base-editing enzyme to the right location in the genome; the other enzyme then acts on that site, ideally producing only one edit.
Lower cholesterol
The trial announced this week will use a base editor to convert an adenine base (A) to a guanine one (G) in the DNA encoding a protein called PCSK9, a key regulator of blood cholesterol levels. The approach, developed by Verve Therapeutics in Cambridge, Massachusetts, aims to reduce the amount of functional PCSK9 in people with a condition called heterozygous familial hypercholesterolaemia, which causes high cholesterol and can lead to heart disease. Disabling PCSK9 has been shown to reduce cholesterol levels and cut the risk of heart disease, and several therapies already on the market reduce PCSK9 activity.
“It could be very promising,” says Piter Bosma, who studies liver diseases at the Amsterdam University Medical Centers. Bosma points to preclinical results in macaques (Macaca fascicularis) published last year, which showed that the treatment reduced blood levels of PCSK9 by 81% and lowered blood cholesterol levels with no apparent harmful side effects1. Another study in macaques by Schwank and his colleagues also found that the treatment was safe2.
In and out
The Verve trial aims to edit cells directly in the body. The team has encased the base-editing components — messenger RNA encoding the enzyme needed to alter DNA, and an extra snippet of RNA that will direct the enzymes to the correct location — in lipid nanoparticles, similar to those used in the formulation of mRNA COVID-19 vaccines. The nanoparticles will be concentrated in the liver, a key site of PCSK9 production.
By contrast, the upcoming sickle-cell trial will use base editing to alter DNA in blood stem cells that have been removed from the body. The edited cells will then be reinfused into participants. The trial will be conducted by Beam Therapeutics, also based in Cambridge, which collaborated with Verve to develop the cholesterol base-editing therapy. Other base-editing therapies are being developed to treat conditions such as leukaemia; a rare metabolic condition called glycogen storage disease; and Stargardt’s disease, which can cause blindness. And other CRISPR-derived approaches are being readied for their own foray into the clinic. Alternative Cas enzymes have been discovered that can edit RNA rather than DNA. Schwank says that his lab has mostly moved on from base editing, to a technique called prime editing, which offers more precision: “It’s all moving fast.”
doi: https://doi.org/10.1038/d41586-022-01951-1
Religious & Biblical Studies - Brill Publishing
* Prize Winner *
Dr Pippa Salonius, Adjunct Professor at Monash University, Australia, has won the 2022 Constant Mews Early Career Publication Prize for her chapter The Tree of Life in Medieval Iconography, as published in The Tree of Life (Ed. Douglas Estes).  Congratulations!
The prize is awarded biennially by the Australia and New Zealand Association for Medieval and Early Modern Studies for "the best article-length scholarly work in Constant’s broad areas of scholarly interest: the medieval history of religions, intellectual history, and textual editing and translation." 
The chapter is now freely accessible until 31 July 2022: http://ow.ly/U5Ym50JGvKf
The Tree of Life
Series: Themes in Biblical Narrative, Volume: 27
E-Book ISBN: 9789004423756
Publisher: Brill
Print Publication Date: 05 Mar 2020
Chapter 12 The Tree of Life in Medieval Iconography
In: The Tree of Life
Author: Pippa Salonius
Type: Chapter
Pages: 280–343
DOI: https://doi.org/10.1163/9789004423756_014
https://brill.com/view/book/edcoll/9789004423756/BP000013.xml Restricted Access Introduction 
Restricted Access Chapter 1 The Tree of Life in Ancient Near Eastern Literature
Restricted Access Chapter 2 The Tree of Life in Ancient Near Eastern Iconography
Restricted Access Chapter 3 The Tree of Life in Genesis
Restricted Access Chapter 4 The Tree of Life in Proverbs and Psalms
Restricted Access Chapter 5 The Tree of Life in Jewish-Christian Legendary Texts
Restricted Access Chapter 6 The Tree of Life in Ancient Apocalypse
Restricted Access Chapter 7 The Tree of Life in Enochic Literature
Restricted Access Chapter 8 The Tree of Life in the Apocalypse of John
Restricted Access Chapter 9 The Tree of Life in Early Christian Literature
Restricted Access Chapter 10 The Tree of Life in Philo
Restricted Access Chapter 11 The Tree of Life in Gnostic Literature
Full Access Chapter 12 The Tree of Life in Medieval Iconography
Restricted Access Chapter 13 The Tree of Life in the North
Restricted Access Chapter 14 The Tree of Life in Modern Theological Thought
Restricted Access Conclusion Chapter 12 The Tree of Life in Medieval Iconography
In: The Tree of Life
Author: Pippa Salonius
Type: Chapter
Pages: 280–343
DOI: https://doi.org/10.1163/9789004423756_014 Abstract
Throughout Europe and Byzantium, from North Africa and the Holy Land to the British Isles and Scandinavia, the tree of life flourished in the imagery of the medieval Church, where visual metaphors of vegetation and growth conveyed such complex notions as the duel nature of Christ and his role in human salvation. Building on Mesopotamian tradition the tree united human and divine realms as axis mundi. At the center of Paradise in the Hebrew Bible, the Christian tree was associated with the wood of the cross as an image of renewal, which, located in Jerusalem, stood at the center of the Christian world. Using a broad selection of images, this survey explores the tree of life and its symbolism across medieval Christendom. https://brill.com/view/book/edcoll/9789004423756/BP000013.xml?body=contentsummary-43177
At the center of the plate the stylized budding cross is rooted in a mound of earth, from where it stretches upwards to touch the dove of the Holy Spirit hovering above.13 Four rivers flowing from its base confirm that it is the tree of life in the garden of Eden (Genesis 2:9–10).14 The center of the cross is inscribed with the words ‘ZΩH’ (Life) and ‘ΦΩC’ (Light) that intersect at the letter Ω. Both the image and the words at its center reference John 8:12, “Again Jesus spoke to them, saying, ‘I am the light of the world: whoever follows me will not walk in darkness, but will have the light of life.’ ”
The Christian tree of life in the midst of the garden is inextricably linked with the Jewish tradition, with its roots buried deep in Jewish Scripture and legend on the one hand and the Mesopotamian cosmic tree with its fruits of immortality on the other.15 Conceived as a mystical path to God, the tree of life is central to the Kabbalah, a form of Jewish mysticism and theosophy that can be traced to thirteenth-century texts.16 It was associated with judgement, life after death, the Messiah and the new Jerusalem in the early prophetic writings in the books of Ezekiel, Zechariah, in the Psalms and the Proverbs.17 Images of it can be found decorating many of the terracotta lamps found in Palestinian and Roman graves and on stone slabs in the Jewish catacombs from the first centuries AD.18 The earliest image of a tree in a Jewish context appeared in the third-century wall painting above the Holy Ark in the synagogue in Dura Europos. In this position the tree emphasizes the rabbinical view of the Torah as the tree of life.19 It was a path to righteousness and its ascending vegetative growth suggests the Midrash; “And by the tree of life the souls of the righteous are going up and down to heaven and from heaven to the garden of Eden, like a man going up and down a ladder.”20 Use of arboreal motifs on early Christian sarcophagi suggests their dependence on eastern Jewish funerary art (fig. 12.5).21
Associating the cross with the tree of life attests to the crucifixion as an act of victory.37 An idea exquisitely rendered by the literary image of the cross blossoming after Christ’s death in a twelfth-century version of the legend of the Holy Rood (Oxford, Bodleian Library, MS Bodley 343).38 Jacobus de Voragine disseminates the story of the cross and lends support to the idea of it flowering in his extremely popular medieval sourcebook the Legenda aurea (c. 1260), where he explains that the name of Christ’s birthplace ‘Nazareth’ means ‘flower.’39 The idea that wood of some form was taken from paradise is rooted in Jewish tradition. In close proximity and affinity with Jewish culture, the Syrian church began using crosses with vegetative designs drawn from nature as early as the mid-fourth century.40 In fact the tale of Adam and Eve leaving paradise with seeds or a twig from the tree of life, which Seth then planted at Adam’s grave and grew into the tree of the cross may have originated in Syria.41 The legend is still alive in the oral tradition of the Ethiopian Church, where foliate crosses transmit a lifegiving image of Christian salvation. The story was known in Europe by the twelfth-century, together with other more obscure versions, such as the story of Moses, who cut his staff from the tree of life in paradise.42
With its roots buried deep in the authority of the Hebrew Bible, the Christian image of the tree of life springs from Genesis 2:9, where together with the tree of knowledge of good and evil, it is located at the center of the garden of Eden.43 It appears regularly in illustrations of the Fall of Man, as seen on the San Isidoro Reliquary in the Museo de la Basilica de San Isidoro de León (c. 1063) (fig. 12.9).44
As one of the earliest surviving manuscript illuminations of Bonaventure’s Lignum vitae, the Durham example suggests that illustrated models of the text had reached as far as the British Isles by the last quarter of the thirteenth century.
The first images of Bonaventure’s Lignum vitae may well have drawn on the visual tradition of the Tree of Jesse and in some illustrations the two iconographic models are fused (fig. 12.14).110 An image of natural continuity, every single element can be seen as parts relating to a whole, with reference to Christ.111 The Franciscan Life of Christ, which quickly established Christ on the cross as the focal figure in its branches, exploits the same arboreal referencing system that expressed both ‘continuity of line and the community of lineage’ so effectively.112 In fact, later in the fourteenth century the mendicant orders privileged the tree of life as a metaphor of community and belonging in the images of their orders known as ordensstammbäume. The earliest surviving example of this development was painted by the Master of the Dominican Effigies in the Dominican Convent of Santa Maria Novella in Florence (fig. 12.24).113 George Dunlop Leslie (English, 1835-1921), Matilda - Dante, Purgatorio, Canto 28, 1859, Wadsworth Atheneum Museum of Art James Abbott McNeill Whistler (American, 1834 -British, 1903), Coast of Brittany (Alone with the Tide), 1861, Female Artists in History Gabriele Münter (German, 1877-1962), Interieur mit Weinachtsbaum (Interior with Christmas Tree), ca. 1912-14, Christie’s., Staffelsee, 1932, Ketterer Kunst.,  Schloss Elmau im Winter, 1933, Staffelsee, 1934, Ketterer Kunst., Straßendurchstich im Winter (Naturstudie. Station Berggeist Schnee), 1935, Ketterer Kunst. Christa Zaat
July 12, 2012
 George Dunlop Leslie (English genre painter) 1835 - 1921
Matilda - Dante, Purgatorio, Canto 28, 1859
oil on canvas 
20¼ x 36½ in. (51.4 x 92.7 cm.)
signed with monogram and dated 1859 (lower right), and further signed and inscribed 'G D Leslie. 2 Abercorn Place St Johns wood No 2' (on the reverse)
private collection https://www.facebook.com/photo/?fbid=10150948780782151&set=a.10150724112537151
'For thou, Lord, hast made me glad through thy work; I will triumph in the works of thy hands' - Psalm XCII, 4
Lot Notes
The painting illustrates Dante's Purgatorio, Canto 28, in which the poet, accompanied by Virgil and Statius, penetrates the Garden of Eden and encounters
A lady, wandering through the wood alone,
Singing and culling flower after flower,
Wherewith her pathway was all painted o'er.
In Canto 33 the lady is given the name of Matelda (sic), and she is usually identified as Matilda, Countess of Tuscany (1046-1115), a great heiress of the house of Canossa who was renowned for her fortitude in the face of many adversities. In Dante's poem she represents the Active and Beatrice the Contemplative Life.
G.D. Leslie was the son of C.R. Leslie, R.A. (1794-1859), the Anglo-American painter who specialised in literary genre and was the biographer of John Constable. Born in 1835, G.D. Leslie studied under his father before entering the Royal Academy Schools. He began to exhibit at the R.A. in 1857, and for a few years was profoundly influenced by the Pre-Raphaelites. Matilda, which was exhibited in 1860, when the artist was twenty-five, is an outstanding example. Rich in meticulously-handled naturalistic detail inspired by Dante's graphic account of the Garden of Eden, it is almost a textbook illustration of Pre-Raphaelite and Ruskinian principles. Cosmo Monkhouse, publishing the picture in 1883, described it as coming 'nearer to what the public reckons as Pre-Raphaelite than any other of the works we print: for (it is) "purist" in feeling and filled with almost infinite detail of grass and leaf and flower'. Sixteen years later Percy Bate included it in The English Pre-Raphaelite Painters, his pioneering study of the movement.
Although the Pre-Raphaelites' earliest works, exhibited within a year or two of the Brotherhood's foundation in 1848, had provoked a bitterly hostile reaction from the critics, it was not long before taste began to change. This was partly due to the sheer appeal of the pictures themselves, especially those of Millais, and partly to the advocacy of John Ruskin, who came to the Brothers' defence in two letters to the Times in May 1851 and went on to champion them in a pamphlet (1851), in the Edinburgh Lectures (1853), and in the third volume of Modern Painters (1854). Leslie was one of many young artists who succumbed to these influences and experienced a brief Pre-Raphaelite phase before moving on to develop a less demanding style, whether this was more classical, more Aesthetic, or simply more conventional. His later speciality was domestic genre in the Aesthetic mode. Pot Pourri, a fine example exhibited at the R.A. in 1874, in which two young women in 'Queen Anne' dress make the eponymous mixture in oriental bowls within a tightly-structured and delicately-toned composition, was sold in these Rooms on 27 November 2002 , lot 13, (£446,650). By the time he painted Matilda in 1859, Leslie was already living in St John's Wood, and he was to become a prominent member of the St John's Wood Clique, a group of artists, also including Philip Calderon, W.F. Yeames, Henry Stacy Marks and others, who all favoured genre subjects, whether of a pathetic or frivolous kind. However in 1884 he left the area, settling at Wallingford in Berkshire, where he found many subjects for landscapes. 
Dante's Vision of Matilda gathering Flowers had also been the subject of a watercolour by D.G. Rossetti, executed for Ruskin in 1855. The watercolour itself is lost, but a related pen-and-ink drawing exists in the Ashmolean Museum (fig. 1). This was the moment when Ruskin was still a passionate admirer of Rossetti's work, and was encouraging him to illustrate the poet whom he regarded as 'the great prophetic exponent of the heart of the Middle Ages'. Matilda gathering Flowers was one of seven watercolours based on the Purgatorio that he commissioned from Rossetti, and was a pair to a subject from Canto 27, Dante's Vision of Rachel and Leah, now in the Tate Gallery.
It would be interesting to know if Leslie was aware of these watercolours, and if they inspired him to tackle the Matilda subject himself. It seems highly likely since Ruskin was on close terms with the Leslie family, and had already praised earlier works by George in Academy Notes. Moreover, although the composition of Leslie's picture has little in common with Rossetti's corresponding design (fig. 1), Leslie shows Dante, Virgil and Statius standing in the distance contemplating Matilda in much the same way that Rossetti had shown Dante watching the two girls in his Rachel and Leah. It may also be noted, for what it is worth, that Leslie's picture was entitled Dante's Leah when it was published in the Magazine of Art in 1883 and again when Percy Bate reproduced it in 1899.
The picture was one of two, both rather similar in conception, that Leslie exhibited at the R.A. in 1860. The other (no. 588) was entitled Meditation, and, like Matilda, was accompanied in the catalogue by a quotation from one of the Psalms (no. XCIV). The pictures were commended by Tom Taylor writing in his capacity as art critic on the Times. 'Two figures by Mr G.D. Leslie - one called 'Matilda' from Dante's Purgatorio, a lady reclining (sic) in a green garden on the edge of a pool starred with water lillies; the other a meditative figure in a similar landscape - without the water - show at once a power of faithful landcape painting and a thoughtful and graceful feeling for female form and character, which promise well for this young painter's future. The fault of both pictures is a want of keeping between landscape and figures, and a certain rawness and over-emphasis, the result of honest painstaking not yet matured by study and practice'.
The pictures were hung in the North Room, not far from Whistler's At the Piano (Taft Museum, Cincinnatti), a revolutionary work in this context which inevitably excited much comment.
Matilda was bought direct from the artist by John Hamilton Trist (1811-1891), a Brighton wine-merchant who formed a large collection of works by the Pre-Raphaelites and their contemporaries. The collection was considered worthy of an article in the Magazine of Art in 1883, and by the time Trist died it consisted of well over a hundred items. The artists represented included Rossetti, Burne-Jones, Madox Brown, Leighton, Alma-Tadema, Albert Moore, Legros, George Heming Mason and many others, but Trist's favourite artist was Arthur Hughes, by whom he owned some twenty examples. One of the most important, Silver and Gold, was sold in these Rooms on 25 October 1991 (lot 50). There were two works by George Dunlop Leslie in the collection, the other being Marguerite, a work of 1866.
At Trist's sale in 1892, Matilda was one of a number of pictures that were bought in by the family (Silver and Gold was another). In 1899 it was published by Bate, and in 1905 it was lent to an exhibition at the Whitechapel Art Gallery. When J.H. Trist's son, Herbert Hardwick Trist, died in 1935, the picture passed to his widow, who sold it at Christie's two years later. At this date it was still accompanied by the original receipt, but this has since been lost.
* * *
George Dunlop Leslie was an English genre painter, author and illustrator. Leslie was born in London, the son of notable genre painter Charles Robert Leslie. Leslie lived early on in St John's Wood (London), and was part of the St John's Wood Clique, a group of artists who favoured light-hearted genre subjects. His early works, such as "Mathilda" (1860) showed the strong influence of the Pre-Raphaelites, but he settled into a more academic, aesthetic, style of painting with the aim of showing "pictures from the sunny side of English domestic life". He often used children as subjects and his work was praised by John Ruskin for its portrayal of the "sweet quality of English girlhood”.
Wadsworth Atheneum Museum of Art 
July 12 at 9:42 AM
 “Alone with the Tide”, James Abbott McNeill Whistler’s first ever seascape, is the subject of our next Spotlight exhibition, opening August 4.⁣
In 1861 Whistler spent three months on the coast of Brittany in northern France to recover from rheumatic fever, and while there he painted “Alone with the Tide.” This painting and related letters by the artist will be brought together to tell the story of Whistler’s early masterpiece.⁣
(#Whistler was born in Lowell, MA #onthisday in 1834.⁣)
Image: “Coast of Brittany” (Alone with the Tide), 1861. Oil on canvas. In memory of Willian Arnold Healy, given by his daughter, Susie Healy Camp https://www.facebook.com/photo/?fbid=407819374713153&set=a.334687465359678 https://en.wikipedia.org/wiki/James_Abbott_McNeill_Whistler
Female Artists in History
December 11, 2021
Gabriele Münter (German painter) 1877 - 1962 
Interieur mit Weinachtsbaum (Interior with Christmas Tree), ca. 1912-14
oil on canvas
88.3 x 72.7 cm. (34.75 x 28.63 in.)
with Nachlass stamp (on the reverse)
private collection
© photo Christie's
Catalogue Note Christie's
Peter Walter and Dr. Isabelle Jansen will include this work in their forthcoming Gabriele Münter catalogue raisonné. https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/3125262201091981/
Female Artists in History
September 21, 2021
Gabriele Münter (German painter) 1877 - 1962 
Staffelsee, 1932
oil on board
33.1 x 44.5 cm. (13 x 17.5 in.)
signed and dated in lower left, rear of board once more signed in blue chalk and inscribed "96/4 XII.31" in pencil
private collection https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/3056631941288341/
© photo Ketterer Kunst
Catalogue Note Ketterer Kunst
Spirited Murnau landscape with a view of Staffelsee.
Clearly contoured forms in bright colors.
Continuation of the characteruistc "Blaue Reiter" style.
After longer stays in Berlin and Paris Gabriele Münter returned to Murnau in 1931 and planned to stay for good. In context of this decision she planned to rebuild the "Russen-Haus". After the completion of the conversion she rewarded the architect with this painting of her much beloved Staffelsee. The relationship with the art historian Johannes Eichner helped her to regain inner peace which gave her a chance to develop her art. Münter stated she wanted to see the landscape "large and simple" and thus she attained a very mature conception. This work offered here is typical of her style that began to form in Murnau and its surroundings as early as in the 1910s. Forms are connected by broken colors and become part of a larger master plan and the previously favored strong contours make way for a barely perceptible accentuation. Münter’s clear form language must be seen as the result of a longer readjustment process that kept the artist from walking into the trap of too great a love for details for all her life. Female Artists in History
May 23, 2016
Gabriele Münter (German painter) 1877 - 1962 
Schloss Elmau im Winter, 1933
oil on panel
32.9 x 41 cm. (12.9 x 16.1 in)
with estate stamp "Gabriele Münter Nachlass" on verso as well as inscribed (by artist?) "7/33 16. I. 33 n. Zch [nach Zeichnung]". 
with two small labels, numbered "L 285" and "1050" respectively.
private collection https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/1714278678857014/
Catalogue Note Ketterer Kunst Sale: 380 Modern Art, June 04. 2011 in Munich Lot 47
Gabriele Münter received her first art lessons at the 'Damen-Kunstschule' (Ladies Art School) in Düsseldorf and then attended the Society of Woman Artists as M. Dasio's and A. Jank's pupil. Then she went to Munich where she visited the private art school 'Phalanx' which was run by Wassily Kandinsky. In 1904 Münter and Kandinsky began travelling together: to Holland, Italy, France - where they met Rousseau and Matisse - and elsewhere. Stylistically she now distanced herself from Impressionism and her works began showing Fauve and Expressionist influences. In 1908 she and Kandinsky began leading a calmer life in their apartment in Munich. They often met with Klee, Marc, Macke, Jawlensky and Marianne von Werefkin. The country house Münter bought in Murnau provided an ideal working environment. In 1909 the artist began painting glass, a medium which would later also be adopted by Kandinsky, Marc, Macke and Campendonk. Münter was a member of the 'Neue Künstlervereinigung München' for two years and in 1911 she joined the 'Blaue Reiter', the artist group founded by Kandinsky and Marc. She was interested in Kandinsky's development towards abstract art, but her own works continued to be figurative. Her landscapes, figurative scenes and portraits show a reduction to the essential with an inclination towards humorous characterization. When war broke out, Münter and Kandinsky at first moved to Switzerland. Münter, however, decided a year later to go to Stockholm, where she separated from Kandinsky. In late autumn 1917 she moved to Copenhagen. She traveled a lot during the 1920s and spent some time in Munich, Murnau, Cologne and Berlin. After 1931 she spent most of her time in Murnau and Munich.
In the reclusiveness of Murnau, far away from the Munich and Berlin art scenes, Gabriele Münter developed a painting style that, based on her own experience and taken to calmer paths, never denied her artistic roots. Gabriele Münters later partner Dr. Johannes Eichner described this process as follows: "The art of Gabriele Münter does not reflect anything of the jaggedness of the outward existence. Neither the maladies nor the disasters of our century tempted her or incited her views. [..] Deeply rooted in nature, in comparison with which personal fates, contemporary events and mankinds lapses are mere ripples on the surface, Gabriele Münters painting has an air of the eternal. Fundamental changes, stages of development and revolutions cannot be found in her oeuvre since 1908 " (Gabriele Münter, Werke aus 5 Jahrzehnten, ex. cat. Braunschweiger Kunstverein 1950, no page).
In 1956 she received the Culture Prize of the City of Munich. The year 1960 saw the first exhibition of Münter's work in the US, followed in 1961 by a large show in the Mannheim Kunsthalle. The artist died in her house at Murnau on 19 May 1962. [KD]
Female Artists in History
October 5, 2016
Gabriele Münter (German painter) 1877 - 1962 
Staffelsee, 1934
oil on cardboard
33.1 x 40.7 cm. (13 x 16 in.)
signed and dated lower left. With a monogrammed dedication by Gabriele Münter on verso
additionaly inscribed "Staffelsee" on verso presumably by a hand other than that of the artist on verso and dated as well as with an inscription regarding the work's origin by the previous owner 
private collection
Catalogue Note Ketterer Kunst Sale: 368 Modern Art, June 12. 2010 in Munich Lot 59
https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/1714289802189235/
Female Artists in History
December 26, 2016
Gabriele Münter (German painter) 1877 - 1962 
Straßendurchstich im Winter (Naturstudie. Station Berggeist Schnee), 1935
oil on cardboard
33 x 41 cm. (12.9 x 16.1 in.) 
signed and dated lower right. Verso inscribed in circle with work number "17/35" and dated "1. III.", as well as with a label with the stamped number "592"
private collection
Catalogue Note Ketterer Kunst Sale: 428 Modern Art, Dec. 03./05. 2015 in Munich Lot 277
The landscape of the Ammergau mountains, which Gabriele Münter found right in front of her doorstep, inspired her to ever new atmospheric landscapes. Bold and experimental in design and coloring during her early period and with a stronger feel for reality later on as a result of her new concept of interpretation. Münter's depictions are statements of her love for the landscape: She avoids any kind of heroic notion as it is often ascribed to mountain landscapes. She sort of rounds the mountains and thus allows a peaceful atmosphere. In large and swiftly painted color fields, preferrably in Münter's beloved blue, she renders her view of a calm lower Alps landscape, in which a small wooden house makes for the focal point. https://www.facebook.com/female.artists.in.history/photos/a.1456056671345884/1827048414246706/
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agappediagnostics · 3 years
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LIPOPROTEIN (a) or Lp(a) – IS’T THE MOST IMPORTANT CARDIAC MARKER IN EARLY HEART ATTACKS? 
Lipoprotein (a), or LP(a), is a large lipoprotein particle made by the liver. It includes particle similar to LDL & two proteins known as Apo B & Apo A. The Apo A particle is a very sticky protein particle, considered to be involved in the clotting system & it’s addition can be likened to adding a patch of Velcro on to a normal LDL particle. Lp(a) is a highly heritable biomarker independently associated with atherosclerotic cardiovascular disease especially at younger age.
LP(a) is not routinely measured in general practice earlier, but family screening for high levels is very important as its concentration is genetically determined or it’s hereditary & difficult to control with drugs. A Lp(a) test is used to check for risk of stroke, heart attack, or other heart diseases. It’s usually tested in people who have certain risk factors, such as a family history of heart disease.
Current recommendations from the European Atherosclerosis Society are to screen people who are at intermediate, moderate or high risk of developing cardiovascular system disorders (CVS), like premature CVS, family history of premature CVS, family history of elevated LP(a), familial hypercholesterolaemia, those with recurrent CVS, despite optimum medical treatment.
People with high Lp(a) levels are much more prone to accumulating fatty deposits in the arteries, known as atherosclerosis, making them at very higher risk for blockages in the leg arteries & narrowing of the heart's aortic valve (aortic stenosis) & heart attacks.
Normal values of Lp(a) are below 30 mg/dL. As per US guidelines, elevated Lp(a) is defined as ≥ 50 mg/dL is considered a “risk-enhancing” factor that can be used to determine proper lifestyle changes or treatment.
Lp(a) concentrations predict incident atherosclerotic cardiovascular disease-among middle-aged adults within primary & secondary prevention contexts, with a linear risk gradient across the distribution. Concentrations are slightly variable across racial subgroups, but the associated risk appears to be very similar.
TAILPIECE: If Lp(a) is higher, you should immediately change your lifestyle accordingly without fail, to be in safer side, so that all other lipid parameters like Cholesterol, LDL, TGL are well controlled. Agappe, your best partner in diagnostics, serves you with Lp(a) & other lipid profile reagents in Fully automatic clinical chemistry analysers & Nephelometry platforms like Mispa i2 & Mispa i3 protein analyzers.
https://www.agappe.com/in/blog-details/260
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ffrepos · 6 years
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PATH3305 - UWA
Medical Genetics (2018, Sem 1)
Unit coordinator: Dr Clayton Fragall
L1-7 (Mid Sem 1): pp. 4-5 (Organisation of Human Genome) 14 & 17 (Human Genetic Variation) 20-21, 31-32 (Mechanisms of Mutation) 35-36 (Cytogenomics) 37-42** (Population Genetics)
L9-16 (Mid Sem 2): pp. 3-4, 9-10: Interpret thermal curve (Detection of Genetic Variation) 16: No. of exomes sequenced (Overview of NGS) 19-20, 23-25, 27, 29-30 (Phenotypic consequences of genetic variants) 36, 47: Understand all the detection methods & in which situations should each method be used; pros & cons (DNA CNVs: Methods of Detection & Disease)
CNV Detection summary table
48, 50-54: Prevalence of CML & ALL, special cases (Cancer cytogenomics) 55, 57-58 (Pharmacogenetics) 65 (Genetic diagnostic strategies)
L17-22: pp. 1-3: Risk factors (Familial Hypercholesterolaemia) 5-6: Inheritance pattern of hypoalphalipoproteinemia & FHBL (Rare lipid disorders) 11-13, 16: Diseases screened and screening methods (Newborn screening) 17-25: Understand mutational hotspots, causative genes & upregulation treatment (Finding disease genes & Genetic muscle diseases) 26: Introduces many concepts for PATH3308 (Investigating Therapies for NMD)
L23-24: pp. 1-3: Starred items (Mitochondrial Genetics) 4-7: Just appreciate that these are very complicated (Mitochondrial Diseases)
L25-26: See starred items in summary slides (Psychiatric Genetics)
L27: p.1 (Epigenetic Variation)
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pharmaphorumuk · 4 years
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Regeneron’s cholesterol drug evinacumab claims February FDA date
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The FDA has started a speedy review of Regeneron’s ANGPTL3-targeting antibody evinacumab for a rare, inherited disorder that dramatically raises the risk of heart disease.
The cholesterol-lowering drug has been classed as a breakthrough therapy for homozygous familial hypercholesterolaemia (HoFH) by the FDA, which is due to deliver a decision on the marketing application by 11 February after a truncated six-month review.
HoFH affects around 1,300 people in the US, says the biotech, and raises cholesterol levels in the blood to very high levels. As a consequence, people with the condition can develop cardiovascular disease very early, even in childhood in some cases, despite aggressive treatment with cholesterol-lowering drugs like statins and PCSK9 inhibitors.
Evinacumab (formerly REGN1500) was developed after scientists discovered that people with genetic profiles that reduced ANGPTL3 gene activity had significant lower levels of LDL cholesterol, and a decrease in the risk of developing heart disease,
If approved, it will sit alongside Sanofi-partnered PCSK9 inhibitor Praluent (alirocumab) – which has underperformed since its launch in 2015 – in Regeneron’s emerging cardiovascular franchise.
The ANGPTL3 antibody has been filed for approval in the US and Europe on the back of the phase 3 ELIPSE trial, which tested the antibody in 65 HoFH patients already being treated with statins, PCSK9 inhibitors and other drugs like ezetimibe.
Adding in Regeneron’s antibody resulted in a 49% drop in cholesterol levels from the start of the study compared to patients sticking with their current therapy alone, according to results presented earlier this year at the American College of Cardiology’ congress in March.
The FDA awarded evinacumab breakthrough status in 2017 on the strength of phase 2 data which also showed that the antibody could achieve impressive 50% reductions in LDL cholesterol, as well as cutting blood lipids like triglycerides, in HoFH patients.
There’s no data showing that the drug can reduce progression to heart disease yet, but it’s widely believed that cutting blood lipids can reduce that risk.
Not all patients with HoFH are the same however as there are multiple genes involved in the disease, including those for LDL receptors, apolipoprotein B and PCSK9.
Crucially, Regeneron’s drug seems to work even in so-called ‘null-null’ patients, which have very low levels of receptors that remove LDL cholesterol from the blood and so progress to cardiovascular complications very quickly.
Evinacumab may not be so significant commercially however, at least in the near term, although it will likely be able to command higher pricing than Praluent due to the rarity of HoFH. Analysts put peak US sales in the region of $200 million to $400 million.
Once tipped as blockbusters, Praluent and a rival PCSK9 drug from Amgen – Repatha (evolocumab) – have struggled to gain sales momentum in the much larger population of people with other forms of high cholesterol, and have yet to crack the $1 billion sales threshold, even when their sales are combined.
They now also face the threat of competition from Novartis PCSK9 rival inclisiran, which offers much less frequent dosing.
Evinacumab is expected to be a smaller product, thanks to the tiny population affected by the ultra-rare indication, although Regeneron will be able to detail using the same salesforce that sells Praluent, reducing the cost of rollout if approved.
The biotech is also running trials that could end up expanding its use into patients with heterozygous familial hypercholesterolaemia (HeFH) – a less severe inherited disorder – as well as for patients with non-inherited forms of high cholesterol who can’t meet treatment targets with a statin and PCSK9 inhibitor.
The post Regeneron’s cholesterol drug evinacumab claims February FDA date appeared first on .
from https://pharmaphorum.com/news/regenerons-cholesterol-drug-evinacumab-claims-february-fda-date/
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lapakhobi · 5 years
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Mengetahui penyebab masalah kolesterol dan tekanan darah tinggi
PENYEBAB TEKANAN DARAH & KOLESTEROL
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1.  Faktor Genetik
​Familial hypercholesterolaemia merupakan kolesterol tinggi yang dialami secara turun temurun dalam keluarga. Lakukan pengecekan kadar kolesterol sejak usia anak-anak.
2. Malas berolahraga/bergerak.
​kurang aktif bergerak dan malas berolahraga bisa meningkatkan risiko Anda mengalami kondisi ini. Apalagi jika hal ini didukung…
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siva3155 · 5 years
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300+ TOP DOCTOR Interview Questions and Answers
DOCTOR Interview Questions for freshers experienced :-
1) Explain who is Doctor? A physician is someone who practices medicine to treat illnesses and injuries. Physicians go to medical school to be trained. They typically hold a college degree in medicine. Physicians once made house calls to treat patients at home, but now mostly see patients in their offices or in hospitals. Physicians may also work for schools, companies, sports teams, or the military. Physicians are often assisted by nurses or other staff. 2) How doctor treat patients? Physicians treat patients by diagnosing them, or figuring out what is wrong. When Physicians diagnose a patient, they begin by asking questions about the patient's symptoms such as fever, headache, or stomach ache. They may ask other questions about things like past illnesses or family members who have been sick. They will then examine the patient, often looking at different parts of the body and listening to the heart and lungs with a stethoscope. Sometimes they may need to collect blood, use an x-ray machine, or use other tools to look for things they cannot see when examining the patient. Usually, when they have gathered enough information, a doctor can make a diagnosis and then prescribe a treatment. Often they prescribe . 3) Who is a specialists doctor? Some doctors specialise in a certain kind of medicine. These physicians are called specialists. They may only treat injuries to a certain part of the body, or only treat patients who have certain diseases. For example, there are physicians who specialise in diseases of the stomach or intestines. Other physicians are "general practitioners" or "family practitioners". This means that they do a little bit of everything. They try to deal with as much of a patient's health problems as they can without sending them to a specialist. A doctor who performs surgery is called a surgeon. 4) How communication skills help patient? Once a patient begins developing trust in a doctor, the chances of him/her recovering increases as his/her confidence in the doctor goes up and s/he begins to believe that s/he can recover. 5) Why doctors should learn communication skills? Communication skills play a major role in developing patient-doctor relationship. And miscommunication could lead to clashes with relatives/friends of patients over care given to the latter. 6) What is Venous thrombosis? There are numerous extra-gastrointestinal manifestations of inflammatory bowel disease that occur in both ulcerative colitis and Crohn's disease, such as uveitis, conjunctivitis, arthritis, pyoderma gangrenosum and erythema nodosum. Some occur primarily in Crohn's, such as gallstones and renal stones due to the area of bowel affected, while patients with ulcerative colitis are more likely to develop primary sclerosing cholangitis and venous thromboses. 7) What is Azathioprine? Azathioprine takes a number of months to exert its anti-inflammatory effect and therefore has a limited role in the acute management of Crohn's disease, though it can be started at the time of an acute flare of Crohn's. 8) What is Bendroflumethiazide? Treatment of hypercalcaemia can include fluid rehydration, loop diuretics, bisphosphonates, steroids, salmon calcitonin and chemotherapy. In clinical practice intravenous fluids are the first-line agent used to treat hypercalcaemia, both rehydrating the patient and helping to lower the calcium levels. This is combined with the co-administration of bisphosphonates such as pamidronate, which exert their maximal effect 5-7 days after administration. 9) What is Ceftriaxone? A cephalosporin such as ceftriaxone is first-line treatment in patients with streptococcal meningitis. Benzylpenicillin would be more appropriate if Neisseria meningitidis was suspected. 10) What is Anti-Histone antibody? In induced SLE anti-histone antibody is present in 90% of patients, although this is not specific for the condition. Anti-nuclear antibody is positive in 50% of patients as opposed to 95% of patients with idiopathic SLE.
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DOCTOR Interview Questions 11) What is C-reactive protein? In SLE the erythrocyte sedimentation rate is classically raised while C-reactive protein levels can stay normal and therefore CRP is also not as useful as the other investigations to monitor disease activity and progression. 12) What are the parameters of life-threatening asthma? Peak expiratory flow rate of Tachycardia: heart rate > 100 beats per minute Inability to complete sentences with one breath 14) What is terbutaline 10 mg nebulised In the management of asthma, patients should be sitting upright in bed and receiving 100% oxygen. Salbutamol is given at a dose of 5 mg nebulised, not 500 micrograms. Ipratropium bromide and steroids should then be considered. 15) Medical Abbreviations part 19: TFTs - thyroid function tests U - units UC - ulcerative colitis V/Q - ventilation/perfusion WCC - white cell count 16) Medical Abbreviations part 18: RBBB - right bundle branch block SIADH - syndrome of inappropriate ADH secretion SLE - systemic lupus erythematosus STEMI - ST-elevation myocardial infarction STD 17) Medical Abbreviations part 17: p.r.n. - pro re nata PSA - prostate-specific antigen PSC - primary sclerosing cholangitis PSGN - post-streptococcal glomerulonephritis RAS - renal artery stenosis 18) Medical Abbreviations part 16: PaO2 - partial pressure of oxygen PCA - patient-controlled analgesia PCI - primary coronary intervention PCP - Pneumocystis carinii pneumonia PCR - polymerase chain reaction 19) Medical Abbreviations part 15: --> NICE 1) Formerly: National Institute for Clinical Excellence 2) Currently: National Institute for Health and Clinical Excellence --> NMDA - N-methyl-D-aspartate --> NSAIDs - non-steroidal anti-inflammatory --> NSTEMI - non-ST-elevation myocardial infarction --> PaCO2 - partial pressure of carbon dioxide 20) Medical Abbreviations part 14: MRI - magnetic resonance imaging MRSA - methicillin-resistant Staphylococcus aureus MSH - melanocyte-stimulating hormone NAC - N-acetylcysteine NG - nasogastric 21) Medical Abbreviations part 13: LFT - liver function test LTOT - long-term oxygen therapy MCV - mean cell volume MHC - major histocompatibility complex MMSE - mini mental state examination 22) Medical Abbreviations part 12: J - joules JVP - jugular venous pressure LBBB - left bundle branch block LDH - lactate dehydrogenase LDL - low-density lipoprotein 23) Medical Abbreviations part 11: HONKC - hyper-osmolar non-ketotic coma HSP - Henoch-Schnlein purpura HUS - haemolytic uraemic syndrome IV - intravenous IVDU - intravenous user 24) Medical Abbreviations part 10: HAART - highly active antiretroviral treatment hCG - human chorionic gonadotrophin HDL - high-density lipoprotein HDU - High-Dependency Unit HLA - human leukocyte antigen 25) Medical Abbreviations part 9: G6PD - glucose-6-phosphate dehydrogenase GCS - Glasgow coma scale GFR - glomerular filtration rate GORD - gastro-oesophageal reflux disease GTN - glyceryl trinitrate 26) Medical Abbreviations part 8: FEV1 - forced expiratory volume in 1 second FFP - fresh frozen plasma FH - familial hypercholesterolaemia Fi(O)2 - fraction of inspired oxygen FVC - forced vital capacity 27) Medical Abbreviations part 7: DVT - deep vein thrombosis ERCP - endoscopic retrograde cholangiopancreatography ESR - erythrocyte sedimentation rate F1 - Foundation year 1 doctor F2 - Foundation year 2 doctor 28) Medical Abbreviations part 6: CPAP - continuous positive airway pressure (ventilation) CPR - cardiopulmonary resuscitation CRP - C-reactive protein CSF - cerebrospinal fluid dsDNA - double-stranded DNA 29) Medical Abbreviations part 5: CDT - Clostridium difficile toxin CIN - cervical intraepithelial neoplasia CLL - chronic lymphocytic leukaemia COMT - catechol-O-methyltransferase COPD - chronic obstructive pulmonary disease 30) Medical Abbreviations part 4: BCG - bacille Calmette-Guerin BHL - bilateral hilar lymphadenopathy BMI - body mass index BNP - B-type natriuretic peptide CEA - carcinoembryonic antigen 31) Medical Abbreviations part 3: AMT - abbreviated mental test ANA - antinuclear antibody ANCA - anti-neutrophil cytoplasmic antibody APACHE - acute physiology and chronic health evaluation AST - aspartate aminotransferase 32) Medical Abbreviations part 2: ADH - antidiuretic hormone AFB - acid-fast bacilli AIDS - acquired immunodeficiency syndrome ALP - alkaline phosphatase ALT - alanine aminotransferase 33) Medical Abbreviations part 1: AF - atrial fibrillation aFP - alpha-fetoprotein ABG - arterial blood gas ACE - angiotensin-converting enzyme ACTH - adrenocorticotrophic hormone 34) How many childrens affected with asthma in UK? Asthma affects over 5 million individuals in the UK. Approximately 1 million children are affected. 35) Can medication is known to cause hypokalaemia? The medication is most likely to be a selective 2-agonist such as salbutamol, which leads to a tremor, palpitations, headaches and hypokalaemia at high doses. Washing the mouth after administration of inhaled steroids is recommended, no matter what dose is given. Atrovent is the trade name for ipratropium bromide, which is more useful in chronic obstructive pulmonary disease than in asthma, although it can be used in an acute asthma attack. 36) Patient feeling randomly sick with headaches. What could it be? Persistent headaches are not something that can be ignored, as this could be your body trying to send you a signal that there is something wrong. Often, the history and description of the headache can be quite helpful as you attempt to determine what is the cause of your headaches so that you can know how to get better. If your headaches are associated with certain movements, activities, foods, or other triggers, than this can serve as a clue to you and your doctor to help you feel better. If, on the other hand, your symptoms are somewhat predictable and come on in the same way, then it is also possible to use this information to diagnose the type of headache, which then gets you closer to getting some help with your pain and other symptoms. Migraines are classically associated with light sensitivity, nausea and vomiting, and intractable and incapacitating pain. People with migraines may have a family history of them, and they may have an aura, or symptoms that routinely come before the headache and let them know it is coming. 37) Why should be pain in neck? There are times that infections can happen in the neck, and these infections can be very serious because of the number of important structures that run through the neck. Some of these include nerves that are relevant to moving some of the muscles of your upper extremities, and others are the very important arteries and veins that run through your neck to and from your head. Often, if people have an infection, they will also have symptoms of an infection, such as a high fever, swelling, redness, etc. These can be more common in those with a history of injecting, as this allows serious and dangerous bacteria direct access to the rest of the body through the arteries and veins. If it has been a while since your last injection, then it may make an infection less likely. Swelling and pain can also happen from muscle spasms that come with poor posture or increased exertion out of the norm. There are also some other possible explanations. 38) Why do in some cases patients feel chest, neck and hands flush? Certainly the thought of carcinoid syndrome is something that crosses the mind in hearing about your symptoms. That is, however, a rather rare process that would be unusual for most people to have. In such a situation, it is good to describe your symptoms and your concerns to your doctor so that he or she can test for the possibility of something as serious or as rare as that condition. There are many other possible explanations, however, many of which are much more common. It is not unusual for some people to have changes of flushing and some of the other feelings that you describe when they are in stressful or unusual situations. Some of this can sometimes be understood in context of the response that some people have to loud noises or fright, ie, they can faint. This reaction is one extreme on the spectrum of a vagal reaction that can occur in some. On a less extreme note, other can have some of the same symptoms you describe without having something as notable as a syncopal episode. There are often things that can be done to help. 39) Suppose if a patient have abnormal blood on his underwear how you deal? Abnormal bleeding can have many different causes, but you have provided some valuable information. First, we have to clarify where exactly the bleeding is coming from. While vaginal bleeding is perhaps the most likely, both the urinary tract and the GI tract can also be a source of bleeding. Either of those would have different causes and explanations, with infections and small sources of bleeding such as hemorrhoids being among the most common reasons for abnormal or untimely bleeding. With regards to vaginal bleeding, there is a clue that is suggested by the fact that the blood is bright red in color. In general, this can reflect fresher blood that has not started to be broken down. It may also suggest blood that is coming from a source further down the vaginal tract, although that is not necessarily true. There are different conditions that can affect the vaginal or uterine lining and are common explanations for symptoms such as you describe. There are also tumors that can result in abnormal bleeding, and these tumors can be both benign and malignant. 40) Suppose if patient have unbearable neck to shoulder pain only while on his period. What could it be? This is a somewhat interesting phenomenon that will take more visits to your doctor to help explain. Your OB/GYN is likely a good place to start, as he or she will be best positioned to help sort out the hormonal element to your symptoms. Another option might be a neurologist or spine surgeon, either of which may be able to help with your symptoms at the level of your neck. An ear nose and throat surgeon may offer some other insight that could be helpful. Whichever you choose, the approach to your problem will likely be different. Primary care and medical doctors are more likely to use lab work and your symptoms to help arrive at an answer, and may use medications empirically to see what helps to make you better. A surgeon, on the other hand, is more likely to listen to your symptoms, complete an exam, and recommend imaging and other anatomic studies that can help to determine what is causing your symptoms. The pain may have a component of something that changes on a monthly basis with your menstrual cycle. This could be a swelling, or even something as simple as a change in the blood flow. 41) Suppose if patient having chronic neck pain for 4 days. Medication and RMT massage have done nothing, pain is 10/10 now. What could it be? It is not normal for pain to become so severe and fail to respond in any way to conservative therapy, and so your doctor should discuss this with you in more detail to make sure that there is nothing serious that is causing your symptoms. Neck and muscle spasms can be common in some people with a history of c spine injury or trauma, and can be severe and debilitating. They should not be a new onset symptom for most people, however, unless you have had some precipitating event. Massage and things to help the muscles relax is often a great idea to help with some of the mild aches and pains that we can have from time to time, and the fact that you had no improvement is worrisome. Your doctor may entertain other possible explanations for this pain in addition to trauma and misuse injuries. He or she may decide it is important to get some imaging and complete a physical exam looking for things that might be amiss. Shooting pain can be a concern for nerve injury. 42) Suppose if I am patient of acid reflux, how can I get rid off? Fortunately, there are things that can be done to help with reflux. The most obvious answer is some of the many medications that are available to help reduce stomach acid. Some of the least expensive and most effective are even available over the counter, but should be used after discussing your symptoms with your doctor. There are some medications, such as ranitidine and other anti histamine medications (H2 blockers as they are sometimes called), that can be very effective for many people and have a very mild side effect profile. They are most effective when taken as directed, and the efficacy does tend to decrease if they are not timed appropriately with regards to the meals. Other excellent medications are those that are known as proton pump inhibitors, or PPIs, which can be even more effective. The over the counter doses are effective for most people, but in severe cases prescription strength doses can also be used. These medications also have relatively mild side effects, but should be discussed with your doctor. In addition to these medications, lifestyle changes should be tried before any medications. These can be found suggested in many places. Please speak with your doctor. DOCTOR Questions and Answers pdf Download Read the full article
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queenketouk · 5 years
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56 today 🎉... Time to celebrate!!! Not because it's my birthday, but because it was 18 years ago that I ditched statins despite a grim prognosis due to FH (Familial Hypercholesterolaemia). Doctors insisted that the neuro-muscular debility I suffered from day 1 of statination was not a side effect of the drugs (liars), that I'd lost my mind, and that with a sky-high cholesterol like mine I wouldn't reach my 40s. Scary stuff, considering I was 38 then... only 2 years 😱 left! But I decided to do it my way. No statins ❇️, fewer carbs ❇️, then keto♥️♥️♥️. Hippocrates would have been proud that I chose food as my medicine 😁. Today, 18 years later, my TC, HDL and LDL are high, but trygs are low, and so is CrP. Even my GP (reluctantly and with great reservations about keto... lol) had to admit that I'm as fit as a fiddle, and NOT at metabolic risk, despite FH. I weigh 52 kg (115 lb) and take ZERO meds - not even occasional pain killers or anti-inflammatories, as I never get aches & pains, colds or headaches. Do I care or worry about my TC (10.3 mmol/L, or 400 mg/dL) being mind-blowingly high? Nope 😁. My body clearly needs it. I WILL FOREVER BE INDEBTED to the few intelligent and unbiased doctors who opened my eyes by disclosing the cholesterol myth, the true cause of CVD and the statins damage crisis. THANK YOU♥️. THANK YOU♥️. THANK YOU♥️. https://www.instagram.com/p/B1vrw7bo1Dq/?igshid=1b7nznok2cv8j
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chimeperson23-blog · 5 years
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Very high LDL and no cardiovascular disease – at all!
12th May 2018
[A classic black swan]
If your hypothesis is that all swans are white, the discovery of one black swan refutes your hypothesis. That is how science works. Or at least that is how science should work. In the real world, scientists are highly adept at explaining away contradictions to their favoured hypotheses. They will use phrases such as, it’s a paradox. Or, inform you that you didn’t measure the correct things, or there are many other confounding factors – and suchlike.
Anyway, accepting that the finding of someone with a very high LDL level, and no detectable atherosclerosis, will always be dismissed – in one way or another – I am still going to introduce you to a ‘case history’ of a seventy-two-year-old man with familial hypercholesterolaemia, who has been studied for many, many, years. Try as they might, the researchers have been unable to discover any evidence for cardiovascular disease (CVD) – of any sort.
In the past, I have spoken to many people with very high LDL and/or total cholesterol levels who are CVD free, even in very old age. The mother of a friend of mine has a total cholesterol of level of 12.5mmol/l (483mg/dl). She is eighty-five, continues to play golf and has not suffered from any cardiovascular problems.
However, none of these people had been studied in any detail. Which means that they can, and are, dismissed as irrelevant ‘anecdotes’. Yes, the widely used and highly exasperating phrase that I often encounter is that ‘the plural of anecdote is not data’. This, of course, is completely untrue, or at least it is untrue if you start dismissing detailed individual cases as anecdote.
Whilst an anecdote may simply be a story, often second hand, a case history represents a painstaking medical history, including biochemical and physiological data. In reality, the plural of case histories is data. That is how medicine began, and how most medical breakthroughs have been made. We look at what happens to real people, over time, we study them, and from this we can create our hypotheses as to how diseases may be caused and may then be cured.
So, a single case is NOT an anecdote, and cannot be lightly dismissed with a wave of the hand and a supercilious smirk.
In fact, the man who is the subject of this case history has written to me on a few occasions, to tell me his story. I have not written anything about him before, as I knew his case was going to be published, and I did not want to stand on anyone’s toes. With that in mind, here we go.
The paper was called ‘A 72-Year-Old Patient with Longstanding, Untreated Familial Hypercholesterolemia but no Coronary Artery Calcification: A Case Report.’ 1
The subject has a longstanding history of hypercholesterolemia. He was initially diagnosed while in his first or second year as a college student after presenting with corneal arcus and LDL-C levels above 300 mg/dL [7.7mmol/l]
He reports that pharmacologic therapy with statins was largely ineffective at reducing his LDL-C levels, with the majority of lab results reporting results above 300 mg/dL and a single lowest value of 260 mg/dL while on combination atorvastatin and niacin. In addition to FH-directed therapy, our subject reports occasionally using baby aspirin (81 mg) and over-the-counter Vitamin D supplements and multivitamins.
In the early 1990s, our patient underwent electron beam computed tomography (EBCT) imaging for CAC following a series of elevated lipid panels. Presence of CAC (coronary artery calcification) was assessed in the left main, left anterior descending, left circumflex, and right coronary arteries and scored using the Agatston score.
His initial score was 0.0, implying a greater than 95% chance of absence of coronary artery disease. Because of this surprising finding, he subsequently undertook four additional EBCT tests from 2006 to 2014 resulting in Agatston scores of 1.6, 2.1, 0.0, and 0.0, suggesting a nearly complete absence of any coronary artery calcification. In February of 2018, he underwent multi-slice CT which revealed a complete absence of coronary artery calcification.
So, here we have a man who has an LDL consistently three to four times above ‘average’. He had tried various LDL lowering agents over the years. None of which had done anything much to lower LDL. Therefore, his average LDL level over a twenty-year period has been 486mg/dl (12.6mmol/l.
Despite this he has absolutely no signs of atherosclerotic plaque, in any artery, no symptoms of CVD and is – to all intents and purposes – CVD free. What of his relatives? If he has FH, so will many others in his family.
‘He has one sister three years his senior who also has FH and a history of high lipid levels. She also has no history of myocardial infarction, angina, or other symptoms of coronary artery disease. His mother had FH, although she died of pancreatic cancer at age 77. She and her three siblings were never treated for, and had no history of, cardiovascular disease. The patient reports that his father had one high cholesterol score (290s), but was never diagnosed with FH, had no history of cardiovascular disease and died in his 80s during surgery for hernia repair.’
What to make of this? Well, I know that the ‘experts’ in cardiology will simply ignore this finding. They prefer to use the ‘one swallow does not a summer make’ approach to cases like this. For myself I prefer the black swan approach to science. If your hypothesis is that a raised LDL causes CVD, then finding someone with extremely high LDL, and no CVD, refutes your hypothesis.
Unfortunately, but predictably, the authors of the paper have not questioned the LDL approach. Instead, they fully accept that LDL does cause CVD. So, this this man must represent ‘a paradox’. They have phrased it thus:
‘Further efforts are underway to interrogate why our patient has escaped the damaging consequences of familial hypercholesterolemia and could inform future efforts in drug discovery and therapy development.’
To rephrase their statement. We know that high LDL causes CVD. This man has extremely high LDL, with no CVD, so something must be protecting him. I have an alternative, and much simpler explanation: LDL does not cause CVD. My explanation has the advantage that it fits the facts of this case perfectly, with no need to start looking for any alternative explanation.
And just in case you believe this is a single outlier, something never seen before or since. Let me introduce you to the Simon Broome registry, set up in the UK many years ago to study what happens to individuals diagnosed with familial hypercholesterolaemia (FH). It is the longest, if not the largest, study on FH in the world.
It has mainly been used as one of the pillars in support of the cholesterol hypothesis. However, when you start to look closely at it – fascinating things emerge. One of the most interesting is that people with FH have a lower than expected overall mortality rate – in comparison to the ‘normal’ population. Or, to put this another way. If you have FH, you live longer than the average person.
Even if we look at death from heart disease (those with FH have never been found to have an increased rate of stroke) we find that in the older population, the rate of death from Coronary Heart Disease (CHD) was actually lower than the surrounding population in some age groups.
For instance, in the male population aged 60 – 79 (who were CHD free on entry to the study) the rate of death from heart attacks was lower than the surrounding population. Not significantly, but it certainly was not higher.
In fact, in the total male population aged 20 – 79 with FH, the rate of death from CHD was virtually identical to the surrounding population. Over a period of 13,717 years of observation, the expected number of fatal heart attacks was calculated to be 46. The actual observed number was 50.
In women, the expected number of heart attacks in the population aged 20 – 79 was 40, the actual number of observed fatal heart attacks was 40. Which means that FH was not found to be a risk factor for CHD in those enrolled in the study – who had no diagnosed heart disease prior to enrolment2.
Which represents, I suggest, another fully grown black swan. There you go. Two in one day.
1: https://www.cureus.com/articles/11752-a-72-year-old-patient-with-longstanding-untreated-familial-hypercholesterolemia-but-no-coronary-artery-calcification-a-case-report
2: https://academic.oup.com/eurheartj/article/29/21/2625/530400
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Source: https://drmalcolmkendrick.org/2018/05/12/very-high-ldl-and-no-cardiovascular-disease-at-all/
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aaagurls · 8 years
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hi i was tagged in this & im doing it a day late instead of going to bed 
first of all thank u @brian-mcshook for thinking of me!! and enjoy these boring as heck answers 
nicknames: kal / kalimantan??? smh (my name is kalina.... idk if ive said that before lmao how secretive!!1!) 

star sign:
 pisces & proud 
height: 5′5 and hoping to grow more :-)) but im almost 19 :-)) so :-) 
last thing i googled: familial hypercholesterolaemia..... yeah 
fave music artist: right now i just listen to w/e but i used to be obsessed with vampire weekend & i looove some of the drag music thats out there

song stuck in my head: chicago - sufjan stevens 
last movie i watched: i actually have no clue bc my memory is trash 
last tv show i watched: santa clarita diet (and half an episode of as1 but we dont talk about that) 

when did you create your blog: i think like a year and a half ago maybe>??

what kind of stuff do i post: literally only drag like i will see a nondrag related meme or smth and go “ha ha funny” in my mind but i wont reblog it idk why!!!
do i have any other blogs: i have like 3 abandoned tumblrs that i dont know passwords to .. i get bored easily 
do i get asks regularly: regularly NO it honestly feels like i have like...2 followers but i love asks so :-( 

why did i choose my url: p self explanatory and im not very happy w/ it but i have about 2183 other urls saved that im too lazy to choose from 
gender: im a girl. i will post a selfie soonish 
bc 1. i crave attention 2. i wanna prove i am a Real human Person 
hogwarts house: idk slytherin is such an ~~edgy~~ answer but oh well 
pokemon team: i only played pokemon go for like a week so idk teams or what they mean i think i chose the blue one 

favoUrite coloUr (u nasty americans):
 hi my name is kalina & i am Indecisive so no 
average hours of sleep: if i have a 9am lecture (yuck!) then like 6-7hrs but if u just let me sleep i will never wake up i s2g 
favoUrite characters: anyone from parks n rec honestly. pls. i love that show more than anything ! and also im drawn to any kind of sarcastic and/or troubled character with witty humour
how many blankets do i sleep with: i have like... a duvet ... ? 
one? 
dream job: im in my first year of med school rn so i think......doctor...
following: 363
i usually tag these things with the mutuals i currently reblog the most from (xkit shows tumblr ““crushes”” i think they used to be called that??) so here ya go if u dont wanna do it just think of it as my declaration of my love for u. 
@untuckedqueens @biancadelqueen @alaskashorsemask @vichachk @sharonstone @flvzeda @frank-ieru @adoredelanos 
ur supposed to tag 20 people what kind of bs 
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