COVID-19 is a new strain of Coronaviruses virus declared by the World Health Organization (WHO) as a pandemic on March 11th, 2020. While the majority of patients with COVID-19 typically have characteristic respiratory presentations subsequently
Corona viruses are a group of RNA viruses. In late December 2019, Patients with pneumonia with unknown etiology was get admitted in health care facilities in Wuhan, China, and resulted in a pandemic disease which affected more than 200 countries and responsible for 182,989 deaths world wide. The disease is officially named as Coronavirus Disease 2019 COVID 19, by WHO on February 11, 2020 . COVID 19 is a potential zoonotic disease with low to moderate estimated 2 -5 mortality rate. Currently, there is no definite treatment for COVID 19 although some trials are under investigation. Hence, appropriate use of PPE, regular hand hygiene, Respiratory and cough etiquettes, social distancing are some key elements to prevent the spread of disease. Ms. Pabalpreet Kaur | Ms. Eenu | Ms. Pooja Jaswal | Dr. (Mrs.) Jyoti Sarin "The Outbreak of COVID-19: An Overview" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-4 | Issue-4 , June 2020, URL: https://www.ijtsrd.com/papers/ijtsrd30859.pdf Paper Url :https://www.ijtsrd.com/medicine/nursing/30859/the-outbreak-of-covid19-an-overview/ms-pabalpreet-kaur
Coronavirus Disease-19 and Reinfections: A Review of Casesasclepiuspdfs
Since first surfacing in Wuhan, China, in December 2019, the novel coronavirus disease-2019 (COVID-19) has led to a global pandemic with confirmed cases and death bells tolling in the millions with new cases still emerging daily. Despite sharing genetic similarities to the severe acute respiratory syndrome (SARS) virus, the specific viral proteins found on the novel SARS coronavirus 2 and its structure seems to make this strain much more elusive and destructive. Based on peer-reviewed cases, there seems to be an increase in patient reinfection, but due to current testing and treatment limitations, it is yet to be determined if the new trend of reinfection is due to a persistent COVID-19 infection that involves a latent period, a recurrent infection due to the same strain of COVID-19, or a mutated strain of COVID-19. The purpose of this study is to discuss the recent reports of the development of reinfection in previously confirmed COVID-19 cases in an attempt to gain a further understanding of the mechanisms of virulence, the effects on the human immune system, and how current testing and treatment modalities are faring. While the virus seems to have a penchant for patients with existing comorbidities, newer data indicate that everyone may be susceptible to possible infection and that not all patients will present with typical respiratory symptoms, making it imperative to examine established cases of reinfection in an attempt to further help with developing drugs for treatment, vaccines, and protocols for prevention.
A review of literature covering current knowledge areas about pathophysiology and progression of CoVid-19 in humans. I gave a day to day disease account along with serum markers and clinical condition of patients. My objectives are: Appreciate the background knowledge about CoVid-19 in most recent literature.
Explain the progression of CoVid-19 disease in a human body based on current literature.
Correlate the known risk factors for adverse outcomes with pathogenesis of CoVid-19.
Describe the pharmacologic mechanisms being used to halt disease progression and prevent adverse outcomes.
Corona viruses are a group of RNA viruses. In late December 2019, Patients with pneumonia with unknown etiology was get admitted in health care facilities in Wuhan, China, and resulted in a pandemic disease which affected more than 200 countries and responsible for 182,989 deaths world wide. The disease is officially named as Coronavirus Disease 2019 COVID 19, by WHO on February 11, 2020 . COVID 19 is a potential zoonotic disease with low to moderate estimated 2 -5 mortality rate. Currently, there is no definite treatment for COVID 19 although some trials are under investigation. Hence, appropriate use of PPE, regular hand hygiene, Respiratory and cough etiquettes, social distancing are some key elements to prevent the spread of disease. Ms. Pabalpreet Kaur | Ms. Eenu | Ms. Pooja Jaswal | Dr. (Mrs.) Jyoti Sarin "The Outbreak of COVID-19: An Overview" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-4 | Issue-4 , June 2020, URL: https://www.ijtsrd.com/papers/ijtsrd30859.pdf Paper Url :https://www.ijtsrd.com/medicine/nursing/30859/the-outbreak-of-covid19-an-overview/ms-pabalpreet-kaur
Coronavirus Disease-19 and Reinfections: A Review of Casesasclepiuspdfs
Since first surfacing in Wuhan, China, in December 2019, the novel coronavirus disease-2019 (COVID-19) has led to a global pandemic with confirmed cases and death bells tolling in the millions with new cases still emerging daily. Despite sharing genetic similarities to the severe acute respiratory syndrome (SARS) virus, the specific viral proteins found on the novel SARS coronavirus 2 and its structure seems to make this strain much more elusive and destructive. Based on peer-reviewed cases, there seems to be an increase in patient reinfection, but due to current testing and treatment limitations, it is yet to be determined if the new trend of reinfection is due to a persistent COVID-19 infection that involves a latent period, a recurrent infection due to the same strain of COVID-19, or a mutated strain of COVID-19. The purpose of this study is to discuss the recent reports of the development of reinfection in previously confirmed COVID-19 cases in an attempt to gain a further understanding of the mechanisms of virulence, the effects on the human immune system, and how current testing and treatment modalities are faring. While the virus seems to have a penchant for patients with existing comorbidities, newer data indicate that everyone may be susceptible to possible infection and that not all patients will present with typical respiratory symptoms, making it imperative to examine established cases of reinfection in an attempt to further help with developing drugs for treatment, vaccines, and protocols for prevention.
A review of literature covering current knowledge areas about pathophysiology and progression of CoVid-19 in humans. I gave a day to day disease account along with serum markers and clinical condition of patients. My objectives are: Appreciate the background knowledge about CoVid-19 in most recent literature.
Explain the progression of CoVid-19 disease in a human body based on current literature.
Correlate the known risk factors for adverse outcomes with pathogenesis of CoVid-19.
Describe the pharmacologic mechanisms being used to halt disease progression and prevent adverse outcomes.
corona is a pandemic disease in the world so many people are died because of this disease, it's not coming in a particular structure. it's having a different type of structure . how to prevent this disease maintain social distance, maintain hand hygiene, wear masks .nowady vaccines are available covishield ,covaxin, Pfizer, sputnik vaccine etc...this mainly helpful to prevent the corona
Coronaviruses are important human and animal pathogens. At the end of 2019, a novel coronavirus was identified as the cause of a cluster of pneumonia cases in Wuhan, in the Hubei Province of China. It is rapidly spreading, resulting in an epidemic throughout china, followed by an increasing number of cases in other countries throughout the world. In February 2020, the WHO designated the disease COVID 19, which stands for corona viruses 2019. The virus that causes COVID 19 is designated severe acute respiratory syndrome coronavirus 2 SARS COV 2 previously, it was referred to as 2019 nCoV. Anushka Bharti | Dr. Gaurav Kumar Sharma | Dr. Kaushal Kishore Chandul "COVID-19" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-5 | Issue-6 , October 2021, URL: https://www.ijtsrd.com/papers/ijtsrd46439.pdf Paper URL : https://www.ijtsrd.com/pharmacy/pharmaceutics/46439/covid19/anushka-bharti
Covid-19: Summary Recommendations - Brazilian Medical Association (AMB)
Authors: S. E. TANNI, H.A. BACHA, C. E. FERNANDES, J. E. L. DOLCI, A.N. BARBOSA, W. BERNARDO
Publication date: 2021
Journal: World Medical Journal
ISSN: 2256-0580
Volume: 2
Pages: 37-52
Publisher
World Medical Association
Advanced age, having comorbidities, and vitamin D deficiency are three most important reasons for increased vulnerability to COVID-19 and also worsen complications and increase the risk of death. Despite the vast amount of information available and lessons learned, many countries are still not fully utilizing these to manage secondary peaks of COVID-19 infection. Factors associated with worse COVID-19 prognosis include, older age, ethnicity, male sex, having comorbidities, obesity, diabetes, hypertension, and smoking; all these are associate with vitamin D deficiency. COVID-19 symptomatology varies from mostly asymptomatic, to, up to 2% fatality.
Advanced age, having comorbidities, and vitamin D deficiency are three most important reasons for increased vulnerability to COVID-19 and also worsen complications and increase the risk of death.
Despite the vast amount of information available and lessons learned, many countries are still not fully utilizing these to manage secondary peaks of COVID-19 infection. Factors associated with worse COVID-19 prognosis include, older age, ethnicity, male sex, having comorbidities, obesity, diabetes, hypertension, and smoking; all these are associate with vitamin D deficiency. COVID-19 symptomatology varies from
mostly asymptomatic, to, up to 2% fatality. The latter is characterized by cytokine storm, an immune reaction, diffuse arterial thromboembolism, acute respiratory distress syndrome, pulmonary oedema,and death.
Review on strategies to counteract sars cov-2 by anti-inflammatory and anti-o...sagapolarajini
Therefore, exploring the repurposing of natural compounds may provide alternatives against COVID19. Several nutraceuticals have a proven ability of immune- boosting, antiviral, antioxidant, anti-inflammatory effects. These include Zn, vitamin D, vitamin C, curcumin, cinnamaldehyde, probiotics,
selenium, lactoferrin, quercetin, etc. Grouping some of these phytonutrients in the right combination
in the form of a food supplement may help to boost the immune system, prevent virus spread, preclude the disease progression to severe stage, and further suppress the hyperinflammation providing both
prophylactic and therapeutic support against COVID-19
Human Coronaviruses (HCoV) exhibit positive single stranded RNA genome with enveloped nucleocapsid. Coronavirus belongs to the family Coronaviridae, originated from avian and mammalian species causes upper respiratory tract infection in humans by novel HCoVs viruses named as HCoV-HKU1, HCoV-NL63 but predominant species is Middle East respiratory syndrome (MERS-CoV) across the world. HCoV-HKU1 sp. is associated with chronic pulmonary disease, while HCoV-NL63 causes upper and lower respiratory tract disease in both children and adults, but most recent one was MERS-CoV, which caused acute pneumonia and occasional renal failure. The novel coronavirus SARS-CoV-2 is a new strain that causes the Coronavirus Disease 2019 (COVID-19) as named by the World Health Organization. According to the recent world statistics report about the COVID-19 cases approx. 101,500 confirmed cases and 3,500 death cases appeared. And mostly, a case of infection with CoV was identified in Wuhan, China. Structurally viral genome constitutes of 2/3rd of replicase gene encoding ORFs regions and rest of the 1/3rd region of genome form the structural proteins. The aim of the study was to understand the viral genetic systems in order to facilitate the genetic manipulation of the viral genome and to know the fundamental mechanism during the viral replication, facilitating the development of antidotes against the virus.
Corona virus was first identified as a cause of the common cold in 1960. Until 2002, the virus was considered a relatively simple, nonfatal virus.Over the last three decades there have been three attacks of three different coronaviruses, SARS-CoV, MERS CoV and the recent one 2019 novel coronavirus (2019-nCoV).
Deadenylase Expression in Small Cell Lung Cancer Related To Clinical Characte...daranisaha
Lung cancer is the second common malignancy and the most aggressive cancer worldwide with late diagnosis and poor prognosis. The search for biomarkers that promote early diagnosis and improve therapeutic strategies focuses to the understanding of the mechanisms underlying cancer development and progression. The deregulation of gene expression is one of the cancer hallmarks reflected to the stability...
A 43-Year-Old Male with PCM1-JAK2 Gene Fusion Experienced T-Lymphoblastic Lym...daranisaha
Myeloid/lymphoid neoplasms associated with eosinophilia and PCM1-JAK2 is a provisional entity in WHO 2016. Prior case reports have shown quite a few clinical presentations in different patients with this chromosome translocation,characterized by eosinophilia in combination with myelodysplastic/ myeloproliferative neoplasms, acute myeloid leukemia(AML) and rarely,
corona is a pandemic disease in the world so many people are died because of this disease, it's not coming in a particular structure. it's having a different type of structure . how to prevent this disease maintain social distance, maintain hand hygiene, wear masks .nowady vaccines are available covishield ,covaxin, Pfizer, sputnik vaccine etc...this mainly helpful to prevent the corona
Coronaviruses are important human and animal pathogens. At the end of 2019, a novel coronavirus was identified as the cause of a cluster of pneumonia cases in Wuhan, in the Hubei Province of China. It is rapidly spreading, resulting in an epidemic throughout china, followed by an increasing number of cases in other countries throughout the world. In February 2020, the WHO designated the disease COVID 19, which stands for corona viruses 2019. The virus that causes COVID 19 is designated severe acute respiratory syndrome coronavirus 2 SARS COV 2 previously, it was referred to as 2019 nCoV. Anushka Bharti | Dr. Gaurav Kumar Sharma | Dr. Kaushal Kishore Chandul "COVID-19" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-5 | Issue-6 , October 2021, URL: https://www.ijtsrd.com/papers/ijtsrd46439.pdf Paper URL : https://www.ijtsrd.com/pharmacy/pharmaceutics/46439/covid19/anushka-bharti
Covid-19: Summary Recommendations - Brazilian Medical Association (AMB)
Authors: S. E. TANNI, H.A. BACHA, C. E. FERNANDES, J. E. L. DOLCI, A.N. BARBOSA, W. BERNARDO
Publication date: 2021
Journal: World Medical Journal
ISSN: 2256-0580
Volume: 2
Pages: 37-52
Publisher
World Medical Association
Advanced age, having comorbidities, and vitamin D deficiency are three most important reasons for increased vulnerability to COVID-19 and also worsen complications and increase the risk of death. Despite the vast amount of information available and lessons learned, many countries are still not fully utilizing these to manage secondary peaks of COVID-19 infection. Factors associated with worse COVID-19 prognosis include, older age, ethnicity, male sex, having comorbidities, obesity, diabetes, hypertension, and smoking; all these are associate with vitamin D deficiency. COVID-19 symptomatology varies from mostly asymptomatic, to, up to 2% fatality.
Advanced age, having comorbidities, and vitamin D deficiency are three most important reasons for increased vulnerability to COVID-19 and also worsen complications and increase the risk of death.
Despite the vast amount of information available and lessons learned, many countries are still not fully utilizing these to manage secondary peaks of COVID-19 infection. Factors associated with worse COVID-19 prognosis include, older age, ethnicity, male sex, having comorbidities, obesity, diabetes, hypertension, and smoking; all these are associate with vitamin D deficiency. COVID-19 symptomatology varies from
mostly asymptomatic, to, up to 2% fatality. The latter is characterized by cytokine storm, an immune reaction, diffuse arterial thromboembolism, acute respiratory distress syndrome, pulmonary oedema,and death.
Review on strategies to counteract sars cov-2 by anti-inflammatory and anti-o...sagapolarajini
Therefore, exploring the repurposing of natural compounds may provide alternatives against COVID19. Several nutraceuticals have a proven ability of immune- boosting, antiviral, antioxidant, anti-inflammatory effects. These include Zn, vitamin D, vitamin C, curcumin, cinnamaldehyde, probiotics,
selenium, lactoferrin, quercetin, etc. Grouping some of these phytonutrients in the right combination
in the form of a food supplement may help to boost the immune system, prevent virus spread, preclude the disease progression to severe stage, and further suppress the hyperinflammation providing both
prophylactic and therapeutic support against COVID-19
Human Coronaviruses (HCoV) exhibit positive single stranded RNA genome with enveloped nucleocapsid. Coronavirus belongs to the family Coronaviridae, originated from avian and mammalian species causes upper respiratory tract infection in humans by novel HCoVs viruses named as HCoV-HKU1, HCoV-NL63 but predominant species is Middle East respiratory syndrome (MERS-CoV) across the world. HCoV-HKU1 sp. is associated with chronic pulmonary disease, while HCoV-NL63 causes upper and lower respiratory tract disease in both children and adults, but most recent one was MERS-CoV, which caused acute pneumonia and occasional renal failure. The novel coronavirus SARS-CoV-2 is a new strain that causes the Coronavirus Disease 2019 (COVID-19) as named by the World Health Organization. According to the recent world statistics report about the COVID-19 cases approx. 101,500 confirmed cases and 3,500 death cases appeared. And mostly, a case of infection with CoV was identified in Wuhan, China. Structurally viral genome constitutes of 2/3rd of replicase gene encoding ORFs regions and rest of the 1/3rd region of genome form the structural proteins. The aim of the study was to understand the viral genetic systems in order to facilitate the genetic manipulation of the viral genome and to know the fundamental mechanism during the viral replication, facilitating the development of antidotes against the virus.
Corona virus was first identified as a cause of the common cold in 1960. Until 2002, the virus was considered a relatively simple, nonfatal virus.Over the last three decades there have been three attacks of three different coronaviruses, SARS-CoV, MERS CoV and the recent one 2019 novel coronavirus (2019-nCoV).
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Lung cancer is the second common malignancy and the most aggressive cancer worldwide with late diagnosis and poor prognosis. The search for biomarkers that promote early diagnosis and improve therapeutic strategies focuses to the understanding of the mechanisms underlying cancer development and progression. The deregulation of gene expression is one of the cancer hallmarks reflected to the stability...
A 43-Year-Old Male with PCM1-JAK2 Gene Fusion Experienced T-Lymphoblastic Lym...daranisaha
Myeloid/lymphoid neoplasms associated with eosinophilia and PCM1-JAK2 is a provisional entity in WHO 2016. Prior case reports have shown quite a few clinical presentations in different patients with this chromosome translocation,characterized by eosinophilia in combination with myelodysplastic/ myeloproliferative neoplasms, acute myeloid leukemia(AML) and rarely,
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. species including, birds, livestock various mammals such as cats,
mice, and dogs [9].
While pathogenic CoV subtypes that affect humans generally
cause mild clinical features, severe respiratory manifestations are
the hallmark of two CoV exceptions, namely Middle East respira-
tory syndrome coronavirus (MERS-CoV) and severe acute respira-
tory syndrome-related coronavirus (SARS-CoV). MERS-CoV was
first identified in the Arabian Peninsula in 2012 with 2,494 infect-
ed cases and 858 fatalities, while earlier in 2002, what began as an
outbreak of the βCoV subtype in Guangdong province in China
ultimately resulted in just over 8,000 confirmed infections with 774
fatalities across 37 countries [9]. The more recently described out-
break in Wuhan, China, in 2020 presented a type of pneumonia of
unknown origin that was later identified by deep sequencing stud-
ies to be a novel strain of CoV [10]. Originally designated as 2019-
nCoV, the virus was renamed SARS-CoV-2 by the International
Committee on Taxonomy of Viruses [11], and the resultant disease
subsequently labeled coronavirus disease-2019 (COVID-19) by the
WHO on February 11, 2020.
2.1. Modes of Transmission of the COVID-19 Virus
While animal-to-human transmission by direct contact with in-
fected animals at the Wuhan seafood market in China probably
accounts for the first cases of COVID-19, the appearance of clinical
cases with a variable history of virus introduction has increased,
so much so that the primary type of transmission is currently hu-
man-to-human transmission, even from asymptomatic patients.11
Respiratory droplets and contact routes are currently evidenced
as the principle methods of transmission of COVID-19 infection
[12,13,14].
Close contact of less than 1m between an individual and a patient
with respiratory symptoms, such as coughing or sneezing, subjects
that individual to risk of exposure to COVID-19 infection through
potentially infectious respiratory droplets. Similarly, fomites with-
in the direct vicinity of an infected patient also have the potential to
act as a source of infection [15]. Therefore, COVID-19 virus trans-
mission is possible either by direct contact with an infected patient
or by contact with objects contaminated by that patient, such as
with stethoscopes or thermometers.
While some evidence supports the occurrence of COVID-19 in-
testinal infection with the presence of the virus in feces [16], fe-
co-oral route has not been reported as means of transmission of
COVID-19 virus.
2.2. Clinical Features
The wide range of clinical findings presenting with COVID-19
extends from simple asymptomatic infection to multiorgan fail-
ure with septic shock, forming the basis for characterization of
COVID-19 based on the severity of manifestations into mild, mod-
erate, severe, and critical. Typically, 98.6% of patients exhibit symp-
toms of fever and 69.6% have fatigue, while dry cough and diarrhea
are also commonly presented [11,17].
2.3. Extra-Pulmonary Symptoms
2.3.1. 1-Gastrointestinal Symptoms of COVID-19
A-Enteric Manifestations of SAR-CoV2
Gastrointestinal symptoms have been reported in 2-40% of patients
in case series [18, 19], but meta-analysis studies approximate the
prevalence of GI manifestations at 17.6%, with anorexia being the
most common complaint described by 26.8% of patients. Diarrhea
presented in 12.5% of cases, followed by nausea and vomiting in
10.2% and abdominal pain in 9.2% of patients. Severe disease was
characterized by 17.1% prevalence of GI symptoms whereas pa-
tients with the non-severe disease had GI symptoms in only 11.8%.
Furthermore, adults, children, and pregnant women exhibited a
similar prevalence of this clinical picture. Viral RNA was detect-
able in stool and respiratory samples at a rate of 48%, but studies
on serial testing reported stool RNA positivity in 70% of patients,
even after negativity of respiratory results [20].
Pathogenesis of SARS-CoV-2 infection of the gastrointestinal tract
remains unknown, but it has been suggested that the virus may
cause a functional disturbance in cell receptors of angiotensin-con-
verting enzyme 2 (ACE2) present in large numbers in enterocytes
of the proximal and distal small intestine, consequently resulting
in diarrhea.
In SARS-CoV-2 infection, a metallopeptidase, ACE II (ACE2) has
been proven to be the cell receptor [21,22,23].
This role of ACE2 receptors as the point of entry of SARS-CoV-2
virus into the GIT is evidenced by staining of viral nucleocapsid
protein and ACE2 protein expression inside epithelial cells of the
stomach, duodenum, and rectum [24,25].
B- Hepato-Biliary Manifestations
Liver comorbidities manifest in 2-11% of infected COVID-19 pa-
tients, of whom 14-53% demonstrate abnormally elevated levels
of alanine aminotransferase (ALT) and aspartate aminotransfer-
ase (AST) during the progressive course of the disease [26,27,28].
However, a number of factors regarding the liver remain unclear,
including whether pre- and post-transplant patients undergoing
immunosuppressive therapy and those with autoimmune hepatitis
are more susceptible for severe COVID-19 infection [29], whether
patients suffering from chronic hepatic diseases including infec-
tions with viral hepatitis C and B have increased risk of develop-
ing liver damage with COVID-19 [30], and whether COVID-19
infection in patients with underlying cirrhosis or cholestatic liver
disease experience exacerbation of the cholestasis condition [31].
AST elevation was a characteristic finding in 62% of intensive care
clinicsofoncology.com 2
Volume 3 Issue 3 -2020 Review Article
3. patients compared to only 25% of non-ICU patients in a study
by Huang et al., while a large cohort comprising cases from 552
hospitals showed that patients with more severe disease had more
disturbance of aminotransferase levels when compared to patients
with milder forms of the disease. [26] Furthermore, patients with
CT-confirmed diagnosis of COVID-19 before the presentation of
symptoms exhibited much lower AST irregularities than those di-
agnosed after becoming symptomatic. These observations indicate
more apparent liver injury with increasing severity of COVID-19
disease [28].
Hospitalized COVID-19 patients also present with other hepat-
ic enzymes abnormalities such as Gamma-Glutamyl Transferase
(GGT), a biomarker indicative of cholangiocyte injury, that was
found to be elevated in 54%of patients, and alkaline phosphatase
that was increased in one in every 54 patients. [32] However, de-
spite these enzymatic level disturbances, post-mortem liver tissue
specimens taken from a patient with fatal COVID-19 infections
did not demonstrate viral inclusions on pathological examination
[33].
The liver is potentially a target for COVID-19 infection due to the
presence of ACE2 receptors in hepatic and biliary epithelial cells
that may provide a possible pathogenic mechanism for the liver
damage occurring with this infection.32 In addition, elevated liver
enzymes seen in these patients may be indicative of a direct cy-
topathic effect by the virus and/or immune damage induced by
the host inflammatory response to the virus [34]. Therefore, he-
patic dysfunction may be due to direct binding of SARS-CoV-2 to
ACE2-positive cholangiocytes propagated by inflammation which
is mediated by an immune reaction in the form of cytokine storm
leading to possible progression to hepatic failure in critically ill
COVID-19 patients. This is in contrast to transient liver damage
associated with milder COVID-19 infection where liver affection
is typically normalized without therapy.
3. Myocarditis in COVID-19
Cardiac injury in patients with COVID-19 infection was associ-
ated with increased development of ARDS and a higher mortality
rate when compared to non-cardiac patients. Interstitial mononu-
clear inflammatory cell infiltration of the myocardium has been
suggested from sporadic autopsy findings [33], while severe myo-
carditis with diminished systolic function has been described as a
post-COVID-19 infection [35,36]. Increased incidence of cardiac
injury has been detected in cardiac biomarker studies conducted
on hospitalized COVID-19 patients [37,38], most likely due to
infection-associated myocarditis and/or ischemia, the latter be-
ing a powerful determinant of prognosis in COVID-19 infection.
The importance of cardiac affection on mortality of hospitalized
COVID-19 patients was demonstrated by the death of 57 of 416 pa-
tients who had either coronary heart disease (10.6%), heart failure
(4.1%), or cerebrovascular disease (5.3%).
Cardiac injury in about 20% of patients was characterized by the
presence of increased blood levels of the cardiac biomarker hs-TnI
(high-sensitivity troponin I) irrespective of electrocardiography
(ECG) and echocardiography (ECHO) detection of recent anom-
alies. These patients were typically older with more comorbidi-
ties, and exhibited increased leukocyte but decreased lymphocyte
counts, and higher levels of N-terminal pro-brain natriuretic pep-
tides, C-reactive protein, and procalcitonin [37].
Utilization of medications such as ACE inhibitors and angiotensin
II receptor blockers are more regularly being used by patients with
elevated TnT, but have no effect on the mortality rate of these pa-
tients [38].
4. Nervous System Involvement in COVID-19
The neurotropic features of SARS-CoV-2 account for the detrimen-
tal effects of this virus on the Central Nervous System (CNS). This
wasinitiallyevidencedbyreportsfromBeijingDitanHospitalofthe
first case of viral encephalitis due to a new coronavirus on March 4,
2020, subsequently confirming the causative pathogen to be SARS-
CoV-2 via genome sequencing of cerebrospinal fluid [39]. Further
support was provided by another published article also regarding
cases of acute viral necrotizing encephalitis related to SARS-CoV-2
infection. The patient verified hemorrhagic rim-enhancing lesions
within the bilateral thalami, medial temporal lobes, and subinsular
regions on brain MRI. Noncontrast CT images demonstrated sym-
metric hypoattenuation within the bilateral medial thalami with a
normal CT angiogram and CT venogram. [40] In addition, a study
by Mao et al found that neurological symptoms such as headache,
altered conscious state, and paresthesia developed in 36.4% of
COVID-19 infected patients, these symptoms being more mani-
fest in critically ill patients compared to those with milder forms of
the disease [41]. Moreover, Guillain Barre syndrome was reported
in an infected patient with COVID-19. The patient presented with
acute progressive symmetric ascending quadriparesis. The electro-
diagnostic test revealed that, the patient is an AMSAN variant of
GBS [42].
Neurotropism of SARS-CoV-2 in the current COVID-19 pandemic
is suggested to be attributed to its furin-like cleavage site. Furin and
furin-like proteases resulted in cleavage of viral S protein, thereby
influencing invasion and virulence properties as well as determin-
ing host specificity and tissue tropism of SARS-CoV and MERS-
CoV [43]. These features may support membrane fusion, possibly
enabling nervous system infection by the coronavirus. However, it
is not yet clear whether the furin-like cleavage site on SARS-CoV-2
spike protein functions in any specific capacity towards nervous
system invasion, an issue requiring further studies. Nevertheless,
the lack of pathological evidence supporting viral infection of ner-
vous tissue despite the presence of these isolated cases necessitates
clinicsofoncology.com 3
Volume 3 Issue 3 -2020 Review Article
4. clinical consideration of brain affection by SARS-CoV-2.
5. Cutaneous Manifestations in COVID-19.
Approximately 20% of COVID-19 patients (18 of 88 patients) at
the Alessandro Manzoni Hospital in the northern Italian city of
Lecco developed skin manifestations, of whom 44% (8 patients)
had skin lesions at the onset of symptoms before admission while
the remaining patients developed skin eruptions after hospitaliza-
tion. A red rash developed in fourteen patients (78%), widespread
urticaria was present in three cases, and chickenpox-like vesicles
appeared in one patient, all most commonly affecting the trunk.
Not correlating with disease severity, lesions typically subsided af-
ter a few days of mild or absent itching [44].
Moreover, skin lesions may be categorized as acral areas of erythe-
ma with vesicles or pustules (19%), other vesicular eruptions (9%),
urticarial lesions (19%), maculopapular eruptions (47%) and live-
do or necrosis (6%) [45]. Many reports from Italy of acrocyanotic
lesions earlier than skin rash onset had been reported in some pa-
tients. These patients have lesions on their feet and hands. The foot
lesions mainly affect the toes and plantar aspect, however, may not
affect all the toes. The lesions may appear red to blue, may become
bullous or develop blackish crusts, be, but finally resolved [46]. The
appearance of skin lesions before fever or respiratory symptoms
suggests that, skin eruptions may be of COVID-19 origin [47].
One suggestion is that these skin manifestations may be due to
the development of venous or arterial thrombosis occurring with
COVID-19 infection.
6. Coagulopathy and Vascular Endothelial Dysfunction
It has been suggested that COVID-19 infection may be complicat-
ed by vascular endothelial dysfunction and coagulopathy [48]. Af-
fection of the endothelium, leads to vasodilation, anti-aggregation
abilities and fibrinolysis may lead to a systemic state of endothelial
dysfunction [49].
The common respiratory symptoms associated with COVID-19
infection can be explained by the same pathophysiologic mech-
anisms of viral access of host cell-mediated by angiotensin-con-
verting enzyme 2 (ACE2) was found extensively in the lungs [28].
Expression of ACE2 by endothelial cells (ECs) [50,51], along with
clinical observations of thrombosis and occurrence of pulmonary
embolism in COVID-19 patients [52,53], may suggest affection of
the endothelium by SARS-CoV-2 [54].
Coagulopathy associated with organ dysfunction accounts for the
higher mechanical ventilation requirement, ICU admission, and
mortality rate evidenced in patients with COVID-19 infection
[55,56]. Abnormalities in hemostasis most commonly include mild
thrombocytopenia [57], elevated levels of D-dimer,58 and devel-
opment of disseminated intravascular coagulation (DIC) in late in
the course of disease [56].
7. Oral Cavity and COVID-19
Expression of ACE2 has been demonstrated in the mouth, partic-
ularly in epithelial cells of the tongue, thus explaining the funda-
mental part played by the oral cavity in allowing viral entry, there-
by acting as a site for potentially increased host susceptibility to
infectious SARS-CoV-2 [59].
Dentistry is considered one of the most hazardous profession re-
garding COVID-19 infection [60]. This increased risk arises from
the close face-to-face contact with patients [61], with studies
showing that infection with COVID-19 may be acquired directly
through airborne dissemination of aerosols created during med-
ical procedures or indirectly through saliva [62,63]. SARS-CoV-2
might be present in saliva from the upper or lower respiratory tract
after gaining entry along with liquid droplets through the oral
cavity [64,65]. Another route is via an exudate specific to the oral
cavity called crevicular fluid containing regional proteins originat-
ing from extracellular matrix and serum [66]. In addition, salivary
gland infection may result in subsequent release through salivary
ducts of viral particles into saliva. SARS-CoV can infect salivary
gland epithelial cells in rhesus macaques, so these glands might be
a source of virus in saliva [67]. Moreover, studies have shown that
SARS-CoV-specific secretory immunoglobulin. A (sIgA) was pro-
duced in saliva of immunized animal models [68], leading to the
assumption that COVID-19 infection diagnosed by saliva can be
achieved using antibodies specific to viral proteins.
8. Possible Links Between Diabetes and COVID-19 Infec-
tion
Diabetes, occurring in an estimated 20% of patients, acts as a risk
factor for the occurrence of extreme pneumonia [69]. The Centers
for Disease Control (CDC), reported that COVID-19 infection is
associated with a higher risk of fatality in up to 50% of diabetic pa-
tients compared with non-diabetics [70]. Another study included
a cohort of 339 patients with COVID-19 suggested that diabetes
was associated with about 4-fold increased risk of having severe
COVID-19 illness [71]. While defective innate immunity, mani-
fested by altered phagocytic and neutrophil chemotactic functions,
and cell-mediated immunity account for the increased risk of in-
fection in all types of diabetic patients, the presence of increased
incidence of type 2 diabetes in older patients may explain the high-
er frequency of diabetes with severe COVID-19 infections. In ad-
dition, the presence of cardiovascular disease in association with
diabetes in older aged individuals may account for the increased
death rate characteristic of COVID-19 [72]. Entry into the host
of SARS-Cov-2 results in reduced expression of ACE2 leading to
hyper inflammation, cellular damage, and respiratory failure asso-
ciated with COVID-19 infection [73]. Upregulation of cell ACE2
expression with acute hyperglycemia might promote entry of the
virus into the host, but downregulation of ACE2 expression in
clinicsofoncology.com 4
Volume 3 Issue 3 -2020 Review Article
5. chronic hyperglycemia subjects host cells to inflammatory and
damaging consequences of viral effect. In addition, ACE2 expres-
sion on β cells of the pancreas can directly affect the function of
these cells. These observations, not only suggest that diabetes may
increase the risk to severe COVID-19 infection but may also be
induced by infection [74,75,76].
Potential insulin deficiency resulting from β cell injury induced by
viral infection is supported by Italian reports of frequent incidenc-
es of severe diabetic ketoacidosis (DKA) during hospitalization
of COVID-19 patients and increased insulin demand by patients
with severeCOVID-19 infection. However, the exact role played
by SARS-CoV-2 in promoting this enhanced insulin resistance re-
mains unknown [72].
9. Kidney Involvement in COVID-19 Infection
Increased incidence of renal affection has been reported with
COVID-19 infection, as evidenced by the development of albu-
minuria in 34% of 59 studied patients on initial hospital admission,
with 63% subsequently developing proteinuria later during hospi-
talization. Two-thirds of fatalities demonstrated elevated blood
urea nitrogen, as did 27% of overall patients, with signs suggestive
of kidney inflammation and edema present on CT scan [77]. A re-
cent study by Cheng et al also reported that 44% of 710 consecutive
hospitalized COVID-19 patients had proteinuria and hematuria on
admission while 26.7% had only hematuria, with increased serum
creatinine and blood urea nitrogen found in 15.5% and 14.1% of
patients, respectively. Prognosis of this infection was found to be
dependent on the presence of acute kidney injury (AKI), protein-
uria, hematuria, and elevated blood creatinine and urea nitrogen
[78].
Studies reported SARS-CoV-2 viral entry via ACE2 receptors
abundantly present in renal tissue, indicating effective targeting of
renal cells in COVID-19 infection [78,79,80,81]. This is supported
by the identification of viral RNA from tissue in infections of both
the kidney and urinary tract [81,82], as well as by successful isola-
tion of the virus from a urine sample of an infected individual in
Guangzhou [83].
Moreover, quantification of the SARS-CoV-2 viral load in autop-
sy tissue samples obtained from 22 patients who had died from
Covid-19 demonstrated that seventeen patients had more than two
coexisting conditions, and the commonest coexisting conditions
were associated with SARS-CoV-2 tropism for the kidneys, even in
patients without a history of chronic kidney disease [84]. Depend-
ing on these findings, renal tropism is a potential explanation of
frequently reported new clinical signs of kidney injury in patients
with COVID-19 [85], even in patients with SARS-CoV-2 infection
who are not critically ill.
10. Obesity & COVID-19
In COVID-19 the main risk factors are cardiovascular disease,
diabetes mellitus, chronic respiratory diseases, hypertension, and
cancer. Obesity is the main risk factor for these comorbidities. In
the UK, a report suggested that, 2/3 of people presented by criti-
cally ill coronavirus infection were overweight or had obesity [86].
Meanwhile, a report from Italy suggests 99% of deaths have been
in patients with pre-existing conditions, including those which are
commonly seen in people with obesity such as hypertension, can-
cer, diabetes, and heart diseases [87].
Among 383 patients from Shenzhen with COVID-19, overweight
was associated with an 86% higher, and obesity with 2.42-fold
higher odds, risk of developing severe pneumonia compared with
patients of normal weight in statistical models that controlled for
potential confounders [88]. Moreover, among 4,103 patients with
COVID-19 at an academic health system in New York City, BMI
>40 kg/m2 was the second strongest independent predictor of hos-
pitalization, after old age [89]. Furthermore, in a study from France
included 124 patients with COVID-19, the need for invasive me-
chanical ventilation was associated with a BMI of ≥35kg/m2, inde-
pendently of other comorbidities [90]. So, obesity can shift the risk
of COVID-19 to younger age raising the importance of obesity as a
risk factor in patients with COVID-19.
The presence of metabolic Associated Fatty Liver Disease (MA-
FLD) was associated with a 4-fold increase in risk of severe
COVID-19, independent of other metabolic risk factors [91].
Notably, MAFLD was also associated with increased risk among
younger [92]. Furthermore, patients with MAFLD with increased
fibrosis scores, such as FIB-4 or NFS were at higher risk of having
severe COVID-19 illness, regardless of other metabolic comorbid-
ities [93].
References
1. World Health Organization. Novel coronavirus (2019-nCoV). Situa-
tion report-1. 2020 Jan 21 [cited 2020 Feb 20].
2. Lu H, Stratton CW, Tang YW. Outbreak of pneumonia of unknown
etiology in Wuhan, China. The mystery and the miracle. J Med Virol.
2020; 92(4): 401-2.
3. Rehman SU, Shafique L, Ihsan A, et al. Evolutionary trajectory for the
emergence of a Novel Coronavirus SARS-CoV-2. Pathogens. 2020;
9(3).
4. Lupia T, Scabini S. Mornese Pinna S, et al. 2019 novel coronavirus
(2019-nCoV) outbreak: a new challenge. J Glob Antimicrob Resist
2020; 21: 22-7.
5. Centers for Disease Control and Prevention (CDC) Update. Novelin-
fluenza A (H1N1) virus infections – worldwide, May 6, 2009. MMWR
Morb Mortal Wkly Rep. 2009; 58; 453-8.
6. Zhang S-F, Tuo J-L, Huang X-B, et al. Epidemiology characteristics
of human coronaviruses in patients with respiratory infection symp-
toms and phylogenetic analysis of HCoV-OC43 during 2010-2015 in
Guangzhou. PLoS One. 2018; 13(1): e0191789-e0191789.
clinicsofoncology.com 5
Volume 3 Issue 3 -2020 Review Article
6. 7. Cheng VCC, Lau SKP, Woo PCY, et al. Severe acute respiratory syn-
drome coronavirus as an agent of emerging and reemerging infec-
tion. Clin Microbiol Rev. 2007; 20(4): 660-94.
8. Fehr AR, Perlma S. Coronaviruses: an overview of their replication
and pathogenesis. Methods Mol Biol. 2015; 1282: 1-23.
9. Lu R, Zhao X, Li J, et al. Genomic characterisation and epidemiology
of 2019 novel coronavirus: implications for virus origins and recep-
tor binding. Lancet. 2020; 395: 565-74.
10. Chen Y, Liu Q, Guo D. Emerging coronaviruses: genome structure,
replication, and pathogenesis. J Med Virol. 2020; 92: 418-23.
11. Cascella M, Rajnik M, Cuomo A, et al. Features, Evaluation and
Treatment Coronavirus (COVID-19). StatPearls Publishing, Trea-
sure Island, FL. 2020.
12. Liu J, Liao X, Qian S, et al. Community transmission of severe acute
respiratory syndrome coronavirus 2, Shenzhen, China, 2020. Emerg
Infect Dis. 2020; 17; 26(6).
13. Chan J, Yuan S, Kok K, et al. A familial cluster of pneumonia asso-
ciated with the 2019 novel coronavirus indicating person-to-person
transmission: a study of a family cluster. Lancet. 2020; 395(10223):
514-23.
14. Li Q, Guan X, Wu P, et al. Early transmission dynamics in Wuhan,
China, of novel coronavirus-infected pneumonia. N Engl J Med.
2020.
15. Ong SW, Tan YK, Chia PY, et al. Air, surface environmental, and
personal protective equipment contamination by severe acute respi-
ratory syndrome coronavirus 2 (SARS-CoV-2) from a symptomatic
patient. JAMA. 2020.
16. Zhang Y, Chen C, Zhu S, et al. Isolation of 2019-nCoV from a stool
specimen of a laboratory-confirmed case of the coronavirus disease
2019 (COVID-19). China CDC Weekly. 2020; 2(8):123-4.
17. Wang Y, Wang Y, Chen Y, et al. Unique epidemiological and clin-
ical features of the emerging 2019 novel coronavirus pneumonia
(COVID-19) implicate special control measures. J Med Virol 2020;
J Med Virol. 2020.
18. Guan WJ, Ni ZY, Hu Y, et al. Clinical Characteristics of Coronavirus
Disease 2019 in China. N Engl J Med. 2020.
19. Zhang JJ, Dong X, Cao YY, et al. Clinical characteristics of 140 pa-
tients infected with SARS-CoV-2 in Wuhan. Allergy 2020.
20. Cheung KS, Hung IF, Chan PP, et al. Gastrointestinal manifestations
of SARS-CoV-2 infection and virus load in fecal samples from the
Hong Kong cohort and systematic review and meta-analysis. Gastro-
enterology. 2020.
21. Gui M, Song W, Zhou H, et al. Cryo-Electron microscopy structures
of the SARS-CoV spike glycoprotein reveal a prerequisite conforma-
tional state for receptor binding. Cell Res 2017; 27: 119–29.
22. Zhou P, Yang X-L, Wang X-G, et al. A pneumonia outbreak associat-
ed with a new coronavirus of probable bat origin. Nature 2020; 579:
270–3.
23. Xu X, Chen P, Wang J, et al. Evolution of the novel coronavirus from
the ongoing Wuhan outbreak and modeling of its spike protein for
risk of human transmission. Sci China Life Sci 2020; 63: 457–60.
24. Wan Y, Shang J, Graham R, et al. Receptor recognition by novel coro-
navirus from Wuhan: An analysis based on decade-long structural
studies of SARS. J Virol 2020; 94: e00127-20.
25. Xiao F, Tang M, Zheng X, et al. Evidence for gastrointestinal infec-
tion of SARSCoV-2. Gastroenterology. 2020.
26. Huang C, Wang Y, Li X, et al. Clinical features of patients infected
with 2019 novel coronavirus in Wuhan, China. Lancet 2020; 395:
497–506.
27. Chen N, Zhou M, Dong X, et al. Epidemiological and clinical charac-
teristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan,
China: a descriptive study. Lancet. 2020; 395: 507–13.
28. Shi H, Han X, Jiang N, et al. Radiological findings from 81 patients
with COVID-19 pneumonia in Wuhan, China: a descriptive study
Lancet Infect Dis. 2020; 20 (4): 425-434.
29. AASLD. Clinical insights for hepatology and liver transplant provid-
ers during the covid-19 pandemi. 2020.
30. Xu L, Liu J, Lu M, Yang D, Zheng X. Liver injury during highly patho-
genic human coronavirus infections. Liver Int 2020.
31. Zhang C, Shi L, Wang F-S. Liver injury in COVID-19: Management
and challenges. Lancet Gastroenterol Hepatol.
32. Chai X, Hu L, Zhang Y, et al. Specific ACE2 expression in cholan-
giocytes may cause liver damage after 2019-nCoV infection. bioRxiv
2020.
33. Xu Z, Shi L, Wang Y, et al. Pathological findings of COVID-19 asso-
ciated with acute respiratory distress syndrome. Lancet Respir Med.
2020; 8 (4): 420-422.
34. Fan Z, Chen L, Li J, Tian C, Zhang Y, Huang S, et al. Clinical features
of COVID-19 related liver damage. MedRxiv 2020.
35. Inciardi RM, Lupi L, Zaccone G, et al. Cardiac Involvement in a Pa-
tient With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol.
2020.
36. Hu H, Ma F, Wei X, Fang Y. Coronavirus fulminant myocarditis
saved with glucocorticoid and human immunoglobulin. Eur Heart
J. 2020.
37. Shi S, Qin M, Shen B, et al. Cardiac injury in patients with corona
virus disease 2019. JAMA Cardiol. 2020.
38. Guo T, Fan Y, Chen M, et al. Association of cardiovascular disease
and myocardial injury with outcomes of patients hospitalized with
2019-coronavirus disease (COVID-19). JAMA Cardiol. 2020.
39. Xiang P, Xu XM, Gao LL, et al. First case of 2019 novel coronavirus
disease with Encephalitis. ChinaXiv. 2020; T202003: 00015.
40. Ye M, Ren Y, Lv T. Encephalitis as a clinical manifestation of
COVID-19 Brain Behav. Brain Behav Immun. 2020.
41. Mao L, Jin H, Wang M, et al. Neurological manifestations of hospital-
ized patients with COVID-19 in Wuhan, China. JAMA Neurol. 2020.
clinicsofoncology.com 6
Volume 3 Issue 3 -2020 Review Article
7. 42. Sedaghat Z, Karimi N. Guillain Barre syndrome associated with
COVID-19 infection: a case report. J. Clin. Neurosci. 2020.
43. Millet JK, Whittaker GR. Host cell proteases: critical determinants
of coronavirus tropism and pathogenesis. Virus Res. 2015; 202: 120–
134.
44. Recalcati S. Cutaneous manifestations in COVID-19: a first perspec-
tive. JEADV. 2020.
45. Galván Casas C, Català A, Carretero Hernández G. Classification
of the cutaneous manifestations of COVID-19: a rapid prospective
nationwide consensus study in Spain with 375 cases. Br J Dermatol.
2020.
46. Mazzotta F, Troccoli T. Acute acroischemia in the child at the time of
COVID-19. International Federation of Podiatrists. 2020.
47. Henry D, Ackerman M, Sancelme E, et al. Urticarial eruption in
COVID-48. 19 infection.J Eur Acad Dermatol Venereol. 2020.
48. Zhou F, Yu T, Du R. Clinical course and risk factors for mortality of
adult inpatients with COVID-19 in Wuhan, China: a retrospective
cohort study. Lancet. 2020; 395(10229): 1054-62.
49. Avogaro A, Albiero M, Menegazzo L, et al. Endothelial dysfunction
in diabetes: the role of reparatory mechanisms. Diabetes Care. 2011;
34 Suppl 2: S285-90.
50. Lovren F, Pan Y, Quan A, et al. Angiotensin converting enzyme-2
confers endothelial protection and attenuates atherosclerosis. Am J
Physiol Heart Circ Physiol. 2008; 295: H1377-84.
51. Sluimer JC, Gasc JM, Hamming I, et al. Angiotensin-converting en-
zyme 2 (ACE2) expression and activity in human carotid atheroscle-
rotic lesions. J Pathol. 2008; 215: 273-9.
52. Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortali-
ty of adult inpatients with COVID-19 in Wuhan, China: a retrospec-
tive cohort study. Lancet. 2020; 395: 1054-1062.
53. Chen J, Wang X, Zhang S, et al. Findings of Acute Pulmonary Embo-
lism in COVID-19 Patients. Lancet. 2020.
54. Cooke JP. The endothelium: a new target for therapy. Vasc Med.
2000; 5: 49-53.
55. Zhang MD, Xiao M, Zhang S, et al. Coagulopathy and Antiphospho-
lipid Antibodies in Patients with Covid-19. NEJM. 2020.
56. Lin L, Lu L, Cao W, et al. Hypothesis for potential pathogenesis of
SARS-CoV-2 infection-a review of immune changes in patients with
viral pneumonia. Emerg Microbes Infect. 2020; 9: 727-732.
57. Lippi G, Plebani M, Michael Henry B. Thrombocytopenia is associ-
ated with severecoronavirus disease 2019 (COVID-19) infections: A
meta-analysis. Clin Chim Acta 2020.
58. Lippi G, Favaloro EJ. D-dimer is associated with severity of corona-
virus disease 2019(COVID-19): a pooled analysis. Thromb Haemost
In press.
59. Xu H, Zhong L, Deng J, et al. High expression of ACE2 receptor of
2019-nCoV on the epithelial cells of oral mucosa. International Jour-
nal of Oral Science. 2020; 12: 8.
60. The workers who face the greatest coronavirus risk. The New York
Times (New York) 2020.
61. Peng X, Xu X, Li Y, Cheng L, Zhou X, Ren B. Transmission routes of
2019-nCoV and controls in dental practice. Int J Oral Sci 2020; 12: 9.
62. Wax S, Christian M D. Practical recommendations for critical care
and anaesthesiology teams caring for novel coronavirus (2019-
nCoV) patients. Can J Anaesth. 2020.
63. To KK, Tsang OT, Chik-Yan Yip C, et al. Consistent detection of 2019
novel coronavirus in saliva. Clin Infect Dis. 2020.
64. Zhu N, Zhang D, Wang W, et al. (2019) China Novel Coronavirus
Investigating and Research Team. A novel coronavirus from pa-
tientswith pneumonia in China. N Engl J Med: 2020.
65. Zhou P, Yang XL, Wang XG, et al. A pneumonia outbreakassociated
with a new coronavirus of probable bat origin. Nature 2020.
66. Silva-Boghossian CM, Colombo AP, Tanaka M, et al. Quantitative
proteomic analysis of gingival crevicular fluid in different periodon-
tal conditions. PLoS 2013; One 8(10): e75898.
67. Liu L, Wei Q, Alvarez X, et al. Epithelial cells lining salivary gland
ducts are early target cells of severe acute respiratory syndrome coro-
navirus infection in the upper respiratory tracts of rhesus macaques.
J Virol 2011; 85(8): 4025–30.
68. Lu B, Huang Y, Huang L, et al. Effect of mucosal and systemic im-
munization with virus-like particles of severe acute respiratory syn-
drome coronavirus in mice. Immunology 2010; 130(2): 254–61.
69. Hespanhol VP, Barbara C. Pneumonia mortality, comorbidities mat-
ter?. Pulmonology. 2019.
70. Remuzzi A, Remuzzi G. COVID-19 and Italy: what next?. Lancet.
2020; 395: 1225-1228.
71. Targher G, et al. Patients with diabetes are at higher risk for severe
illness from COVID-19. Diabetes Metab. 2020.
72. SR Bornstein, F Rubino, K Khunti, et al. Practical recommendations
for the management of diabetes in patients with COVID-19. Lancet
Diabetes Endocrinol. 2020.
73. Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 cell
entry depends on ACE2 and TMPRSS2 and is blocked by a clinically
proven protease inhibitor. Cell. 2020.
74. Bindom SM, Lazartigues E. The sweeter side of ACE2: physiological
evidence for a role in diabetes. Mol Cell Endocrinol. 2009; 302: 193-
202
75. Roca-Ho H, Riera M, Palau V, et al. Characterization of ACE and
ACE2 expression within different organs of the NOD mouse. Int J
Mol Sci. 2017; 18: e563.
76. Yang JK, Lin SS, Ji XJ, et al. Binding of SARS coronavirus to its re-
ceptor damages islets and causes acute diabetes. Acta Diabetol. 2010;
47: 193-199.
77. Li Z, Wu M., Guo J. Caution on kidney dysfunctions of 2019-nCoV
clinicsofoncology.com 7
Volume 3 Issue 3 -2020 Review Article
8. patients. medRxiv 2020; 02.08.20021212
78. Cheng Y, Luo R, Wang K, et al. Kidney impairment is associated with
in-hospital death of COVID-19 patients. medRxiv. 2020; 20023242.
79. Hamming I, Timens W, Bulthuis M, Lely A, Navis G, van Goor H.
Tissue distribution of ACE2 protein, the functional receptor for
SARS coronavirus. A first step in understanding SARS pathogenesis.
J Pathol. 2004; 203(2): 631–7.
80. Li W, Moore M.J, Vasilieva N. Angiotensin-converting enzyme 2 is
a functional receptor for the SARS coronavirus. Nature. 2003; 426:
450–454.
81. Peiri J.S.M., Chu C.M., Cheng V.C.C. Clinical progression and vi-
ral load in a community outbreak of coronavirus-associated SARS
pneumonia: a prospective study. Lancet. 2003; 361: 1767–1772.
82. Ding Y., He L., Zhang Q. Organ distribution of severe acute respi-
ratory syndrome (SARS) associated coronavirus (SARS-CoV) in
SARS patients: implications for pathogenesis and virus transmission
pathways. J Pathol. 2004; 203: 622–630.
83. The team of Zhong Nanshan responded that the isolation of SARS-
CoV-2 from urine remind us to pay more attention to the cleaning
of individuals and families. Guangzhou Daily. 2020.
84. Puelles VG, Lütgehetmann M, Lindenmeyer MT, et al. Multiorgan
and Renal Tropism of SARS-CoV-2. N Engl J Med. 2020.
85. Pei G, Zhang Z, Peng J, et al. Renal involvement and early prognosis
in patients with COVID-19 pneumonia. J Am Soc Nephrol. 2020.
86. https://www.icnarc.org/About/Latest-News/2020/03/22/Report-
On-196-Patients-Critically-Ill-With-Covid-19.
87. https://www.epicentro.iss.it/coronavirus/bollettino/Re-
port-COVID-2019_20_marzo_eng.pdf.
88. Qingxian C, Chen F, Fang L, et al. Obesity and COVID-19 Severity
in a Designated Hospital in Shenzhen, China. 2020.
89. Petrilli CM, Jones SA, Yang J, et al. Factors associated with hospi-
talization and critical illness among 4,103 patients with COVID-19
disease in New York City. Preprint at medRxiv 2020; 20057794.
90. Simonnet A, Chetboun M, Poissy J, et al. High prevalence of obesity
in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2)
requiring invasive mechanical ventilation. 2020.
91. Feng Gao, Kenneth Zheng, Xiao‐Bo Wang, Hua‐Dong Yan, Qing‐
Feng Sun, Ke‐Hua Pan, et al. Metabolic associated fatty liver dis-
ease increases COVID-19 disease severity in non-diabetic patients. J
Gastroenterol & Hepatol. 2020.
92. Ji D, Qin E, Lau G. Reply to: ‘Younger patients with MAFLD are at
increased risk of severe COVID-19 illness: A multicenter prelim-
inary analysis’ [published online ahead of print, 2020 May 10]. J
Hepatol. 2020; S0168-8278(20)30297.
93. Targher G, Mantovani A, Byrne CD, et al. Risk of severe illness from
COVID-19 in patients with metabolic dysfunction-associated fatty
liver disease and increased fibrosis scores [published online ahead of
print, 2020 May 15]. Gut. 2020; gutjnl-2020-321611.
clinicsofoncology.com 8
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