Acute promyelocytic leukemia(APL),a specific characteristic of t(15;17) chromosomal translocation,molecular gene analyses are conclusive in vivo evidence that oncogenic pml/RARa fusion plays a crucial role in APL leukemogenesis [1-3]. Since the introduction of initial 13-cis retinoic acid(13-cis RA)[4],and currently all-trans RA(ATRA) [5] and tamibarotene [6],RA plus chemotherapy or RA plus As2O3 regimen is currently the standard of care
Slides were presented via a poster board in a class symposium of cancer genes. I reviewed primary literature to present the structure and function of cancer gene Retinoic Acid Receptor Alpha and its implications in Acute Promyelocytic Leukemia.
Austin Journal of Reproductive Medicine & Infertility is an international scholarly, peer review, Open Access journal, aims to promote the research in Reproductive Medicine that compact with prevention, analysis & management of reproductive problems.
Austin Journal of Reproductive Medicine & Infertility is a comprehensive Open Access peer reviewed scientific journal that covers multidisciplinary fields. We provide limitless access towards accessing our literature hub with colossal range of articles. The journal aims to publish high quality varied article types such as Research, Review, Short Communications, Case Reports, Perspectives (Editorials), Clinical Images.
Austin Journal of Reproductive Medicine & Infertility supports the scientific modernization and enrichment in Reproductive Medicine research community by magnifying access to peer reviewed scientific literary works. Austin Publishing Group also brings universally peer reviewed member journals under one roof thereby promoting knowledge sharing, collaborative and promotion of multidisciplinary science.
Slides were presented via a poster board in a class symposium of cancer genes. I reviewed primary literature to present the structure and function of cancer gene Retinoic Acid Receptor Alpha and its implications in Acute Promyelocytic Leukemia.
Austin Journal of Reproductive Medicine & Infertility is an international scholarly, peer review, Open Access journal, aims to promote the research in Reproductive Medicine that compact with prevention, analysis & management of reproductive problems.
Austin Journal of Reproductive Medicine & Infertility is a comprehensive Open Access peer reviewed scientific journal that covers multidisciplinary fields. We provide limitless access towards accessing our literature hub with colossal range of articles. The journal aims to publish high quality varied article types such as Research, Review, Short Communications, Case Reports, Perspectives (Editorials), Clinical Images.
Austin Journal of Reproductive Medicine & Infertility supports the scientific modernization and enrichment in Reproductive Medicine research community by magnifying access to peer reviewed scientific literary works. Austin Publishing Group also brings universally peer reviewed member journals under one roof thereby promoting knowledge sharing, collaborative and promotion of multidisciplinary science.
Naval Daver, MD, and Joseph D. Khoury, MD, FCAP, prepared useful practice aids pertaining to acute myeloid leukemia for this CME/MOC/CC activity titled "The Pathology–Oncology Partnership in AML: Identifying and Treating the Diversity of Disease Subtypes." For the full presentation, complete CME/MOC/CC information, and to apply for credit, please visit us at https://bit.ly/32hvh7Z. CME/MOC/CC credit will be available until October 14, 2022.
Her2Neu positive breast cancer is comprises of about 15-20% of all breast cancer. Among them quite a few number of patients present as de novo metastasis . In this presentation you ll find a guide how to manage it with relevant evidences. Presentation is meant for Oncology trainees.
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Clinic Correlation and Prognostic Value of P4HB and GRP78 Expression in Gastr...eshaasini
Prolyl 4-hydroxylase, beta polypeptide (P4HB) and Glucose‑regulated protein 78 (GRP78) represent for poor prognosis of various cancers, while rare research investigate correlation of them. This study aimed to explore correlation and prognostic value of them in gastric cancer
Clinic Correlation and Prognostic Value of P4HB and GRP78 Expression in Gastr...semualkaira
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Clinic Correlation and Prognostic Value of P4HB and GRP78 Expression in Gastr...semualkaira
: Prolyl 4-hydroxylase, beta polypeptide (P4HB)
and Glucose‑regulated protein 78 (GRP78) represent for poor
prognosis of various cancers, while rare research investigate correlation of them. This study aimed to explore correlation and prognostic value of them in gastric cancer
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Cavernous Sinus Metastasis of Leiomyosarcoma with Orbital Extension along the...ClinicsofOncology
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
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Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Pharynx and Clinical Correlations BY Dr.Rabia Inam Gandapore.pptx
APL:Retinoic Acid and Retinoid Pharmacology, a Breakthrough Today
1. APL:RetinoicAcidandRetinoidPharmacology,aBreakthrough
Today
Zhu G*
The Institute of Oncology,Tehran University of Medical Sciences,Tehran
Volume 1 Issue 1- 2019
Received Date: 23 Apr 2019
Accepted Date: 15 May 2019
Published Date: 22 May 2019
1. Clinical Image
Acute promyelocytic leukemia(APL),a specific characteristic of t(15;17) chromosomal
translocation,molecular gene analyses are conclusive in vivo evidence that oncogenic pml/RARa
fusion plays a crucial role in APL leukemogenesis [1-3]. Since the introduction of initial 13-cis
retinoic acid(13-cis RA)[4],and currently all-trans RA(ATRA) [5] and tamibarotene [6],RA plus
chemotherapy or RA plus As2O3 regimen is currently the standard of care [7]. APL has a very
good prognosis,with long-term survival rates up to near 70%-90%.The elucidation of the molecu-
lar basis of retinoic acid and retinoid pharmacology in APL has been illustrated in several pub-
lications [8-11],the detail molecular model of gene regulation had also been proposed by Zhu in
1990s [12-14]. From the following figure clear shown,oncogenic pml/RARa is a constitutive tran-
scriptional repressor to differentiation block at the promyelocyte stage whereas retinoic acid over-
come the transcriptional repressor activity of pml/RARa,including the dissociation of repressor
complexes N-CoR,SMAT and HDACs from oncogenic pml/RARa. Consequentially,pml/RARa
chimera converted receptor from a repressor to a RA-dependent activator of transcription.This
transcriptional depression occurs at RARE on pml/RARa DNA binding. The resulting pml/RARa
oncoprotein proteolytic degradation occurs through autophagy or the proteasome system(UPS)
or caspase 3 or/and E1-like ubiquitin-activating enzyme(UBE1L) induction. An effect is to relieve
the blockade of pml/RARa-mediated RA dependent promyelocyte differentiation,and induce
promyelocyte maturation. This earliest proposal has now been demonstrated by structure and
functional analysis of oncogenic pml/RARa chimera protein in vitro and in vivo studies [15-27].
This is first described in eukaryotes.
Moreover,this oncogenic receptor pml/RARa is locked in its “off” regular mode thereby constitu-
tively repressing transcription of genes or key enzymes(for examples AP-1,PTEN,DAPK2,PU.1)
that are critical for differentiation of hematopoietic cells[28-31]. Whether silencing of these RA-
RE-responsive target genes such as myeloid transcription factors such as C/EBPa,PU.1 or other
unknown key enzymes that are really critical for neutrophil differentiation needs to be further
identification and under investigation.
Clinics of Oncology
Citation: Zhu G, APL:Retinoic Acid and Retinoid Pharmacology, a Breakthrough Today Clinics of Oncol-
ogy. 2019; 1(1): 1-3.
clinicsofoncology.com
*Corresponding Author (s): George Zhu, The Institute of Oncology,Tehran University of
Medical Sciences,Tehran, E-mail:sansan4240732@163.com
Clinical Image
ISSN: 2640-1037
3. forms in acute promyelocytic leukemia. Leukemia. 2007; 21:647-50
23. Raelson JV, Nervi C, Rosenauer A, Benedetti L, Monczak Y, et al. The
PML/RAR alpha oncoprotein is a direct molecular target of retinoic acid
in acute promyelocytic leukemia cells. Blood. 1996;88:2826-32.
24. Yoshida H, Kitamura K, Tanaka K, et al. Accelerated degradation of
PML-RARA oncoprotein by ATRA in APL: possible role of the protea-
some pathway. Cancer Res. 1996; 56(13):2945-48.
25. Isakson P, Bjoras M,Boe SO, Simonsen A. Autophagy contributes to
therapy-induced degradation of the PML/RARA oncoprotein. Blood.
2010; 116:2324-31.
26. Nervi C, Ferrara FF, Fanelli M, Rippo RM, Tomassini B. Caspases
mediate retinoic acid-induced degradation of the acute promyelocytic
leukemia PML/RARa fusion protein. Blood. 1998;92(7):2244-51.
27. Kitareewan S, Pitha-Rowe I,Sekula D, Lowrey CH, Nemeth MJ.
UBE1L is a retinoid target that triggers PML/RAR alpha degradation
and apoptosis in acute promyelocytic leukemia. ProcNatlAcadSci USA.
2002; 99(6):3806-11.
28. Doucar V, Brockes JP, Yaniv M, de The H, Dejean A. The PML-reti-
noic acid alpha translocation converts the receptor from an inhibitor to
a retinoic acid-dependent activator of transcription factor AP-1. Proc-
NatlAcadSci USA. 1993; 90:9345-9.
29. Humbert M, Federzoni EA, Britschgi A. The tumor suppressor gene
DAPK2 is induced by the myeloid transcript factors PU.1 and C/EBPa
during granulocytic differentiation but repressed by PML-RARa in APL.
J Leuk Biol. 2014; 95:83-93.
30. Noguera NI, Piredda ML, Taulli R, Catalano G, Angelini G. PML/
RARa inhibits PTEN expression in hematopoietic cells by competing
with PU.1 transcriptional activity. Oncotarget. 2016;7(41):66386-397.
31. Zhu G, Ahmed Al-kaf AG. Vitamin A, retinoic acid and tamibaro-
tene, a front toward its advances: a review. Universal Journal of Pharma-
ceutical Research. 2018; 3(6): 38-48.
Volume 1 Issue 1 -2019 Clinical Image
clinicsofoncology.com 3