Pandiar, DeepakKumar, N. SivaAnand, RahulKamboj, Mala...
4页
查看更多>>摘要：Corona Virus Disease 2019 (COVID 2019)， caused by the severe acute respiratory syndrome coronavirus 2 (SARSCoV-2)， is a dreadful infectious disease which has emerged as one of the most significant medical emergency affecting everyone directly or indirectly。 COVID 2019 is a multisystem disease and causes severe immunosuppression。 Initially thought to affect mainly the respiratory system， it strikes all vital organ systems and cause defects in cardio-circulatory， respiratory system and gastrointestinal systems to name a few leading to copious biochemical alterations。 Reports show there is thromoembolism， raised ferritin levels， lymphocytopenia， thrombocytopenia， lactic acidosis， acute diabetes like state and cytokine storm。 Data regarding levels of neutrophils is equivocal。 Further there is increased incidence regarding high incidents of mucormycosis in COVID 2019 positive subjects。 In the present paper， we identified and correlated the virus mediated biochemical alterations as the potential ideal environment for propagation of mucorales; and thus concentrate on early diagnosis and treatment of mucormycosis in COVID 2019 cases。
查看更多>>摘要：Preexisting hypertension is a known risk factor for severe COVID-19。 Abnormal activation of RAS upregulates angiotensin II (Ang-II) and contributes to severe manifestations of COVID-19。 Although RAS inhibitors (RASi) are a mainstay of antihypertensive therapy， they have been associated (in some animal studies) with an increase in angiotensin converting enzyme 2 (ACE2) receptors that facilitate cellular entry of the SARS-CoV-2 virus。 Nonetheless， current medical practice does not recommend curtailing RASi to protect hypertensive patients from COVID。 On the contrary， there is clinical evidence to support a beneficial effect of RASi for hypertensive patients in the midst of a COVID-19 pandemic， although the precise mechanism for this is unclear。 In this paper， we hypothesize that RASi reduces the severity of COVID-19 by promoting ACE2-AT1R complex formation at the cell surface， where AT1R mediates the major vasopressor effects of Ang-II。 Furthermore， we propose that the interaction between ACE2 and AT1R impedes binding of SARS-CoV-2 to ACE2， thereby allowing ACE2 to convert Ang-II to the more beneficial Ang(1-7)， that has vasodilator and anti-inflammatory activity。 Evidence for ACE2AT1R complex formation during reduced Ang-II comes from receptor colocalization studies in isolated HEK293 cells， but this has not been confirmed in cells having endogenous expression of ACE2 and AT1R。 Since the SARSCoV-2 virus attacks the kidney， as well as the heart and lung， our hypothesis for the effect of RASi on COVID-19 could be tested in vitro using human proximal tubule cells (HK-2)， having ACE2 and AT1 receptors。 Specifically， colocalization of fluorescent labelled: SARS-CoV-2 spike protein， ACE2， and AT1R in HK-2 cells can be used to clarify the mechanism of RASi action in renal and lung epithelia， which could lead to protocols for reducing the severity of COVID-19 in both hypertensive and normotensive patients。
da Silva, Rosangela Lagode Oliveira, Felipe AndradeMedeiros, Rebeca GaldinoCunha, Samira Veras...
4页
查看更多>>摘要：The skin is the largest organ in the human body and has a variable structure。 It is divided into three layers: epidermis， dermis and hypodermis。 Amid aesthetics， this structure works as a systemic administration port or as a route to administration of active principles。 Invasive procedures， however， non-surgical， have been standing out and gaining space globally， as these are techniques that do not bring a significant risk of life or prolonged rest after treatment。 The aim of this work is to raise the hypothesis of the effect of pressurized mesotherapy in relation to injectable mesotherapy。 The method does not use needles; just pressurization to spread the product's principles in the skin tissue。 Assets applied under pressure associated with the minimization of mechanical resistance by distending the elastic components of the skin with the use of skin folds have a better effect on aesthetic dysfunctions。
查看更多>>摘要：Ultrasound (US) is recognized as a useful tool for detecting lung physiology and pathology。 Lung US is compared with standard techniques for evaluating lung structure and function such as computed tomography and pulmonary function tests。 At present， markers of normal physiology and pathology are detected using expected image patterns。 Detecting the latter depends on the experience of the operator。 Diaphragmatic dysfunction is a particularly frequent problem in intensive care。 Diaphragmatic dysfunction is easily assessed using lung US。 Speckle tracking analysis， a known method for assessing tissue displacement and deformation in cardiology， is proposed to be utilized in lung US for detecting and quantifying lung sliding。 Using speckle tracking analysis to diaphragmatic deformation quantification could be an informative and new tool for weaning from mechanical ventilation。
查看更多>>摘要：Primary Hypothesis: In cancer therapy， normalization of the vasculature， and not disruption， to facilitate the reversal of the immuno-phenotypic changes， is the sine-qua-non for cancer elimination。 The triad of normalization of the vasculature， leading to the improved immunological tumour microenvironment and increased susceptibility of resistant phenotypic cancer cells (VIP model)， forms the basis of this hypothesis。 This article hypothesizes the absolute need for vascular normalization for the eradication of cancer。 Locally advanced and oligometastatic cancers have the potential to be cured with aggressive therapy。 The focus on vascular normalization its clinical relevance in this situation is essential。 Most traditional approaches have focused on the elimination of cancer by targeting and disrupting vasculature。 Initially， antiangiogenic drugs showed significant promise in animal experiments。 However， this vascular disruption approach has not paid the expected long-term dividends in the clinical setup。 However， antiangiogenics are playing a significant role when used concurrently with chemotherapy/immunotherapy。 Antiangiogenics have dual temporal actions - an initial normalization effect with improved oxygenation followed by pruning of blood vessels， resulting in exaggerated hypoxia along with a rebound progression。 The literature is replete with phenomena of initial vascular normalization with a paradigm shift in the immuno-phenotypic milieu of cancer as part of vascular targeting approaches。 The hypothesis in this article stresses the need to have strategies to extend this normalization window or to have preclinical trials to optimize the dose scheduling of antiangiogenics cyclically along with chemo/targeted/immune therapy and other combination therapies。 We can implement this hypothesis by a combinatorial harmonization of present-day cancer therapies in the setting of tumor vasculature integrity。 In addition， based on the proposed hypothesis， the current normalization effect of antiangiogenics and newer therapy development should focus primarily on normalization of the vasculature as well as targeting hypoxia-Inducible-factor-1 alpha (HIF-1 alpha) in the presence of differential genetic modulation of vascular endothelial cell resistance enhancement along with cancer cell sensitization。 Also， the article enumerates six supporting hypotheses supplementing the primary hypothesis。
查看更多>>摘要：Since Nixon famously declared war on cancer in 1971， trillions of dollars have been spent on cancer research but the life expectancy for most forms of cancer is still poor。 There are many reasons for the partial success of cancer translational research。 One of these can be the predominance of certain paradigms that potentially narrowed the vision in interpreting cancer。 The main paradigm to explain carcinogenesis is based on DNA mutations， which is well interpreted by the somatic mutation theory (SMT)。 However， a different theory claims that cancer is instead a tissue disease as proposed by the Tissue Organization Field Theory (TOFT)。 Here， we propose new hypotheses to explain the origin and pathogenesis of cancer。 In this perspective， the systemic-evolutionary theory of cancer (SETOC) is discussed as well as how the microenvironment affects the adaptation of transformed cells and the reversion to a unicellular-like or embryo-like phenotype。
查看更多>>摘要：Coronavirus pandemic has emerged as an extraordinary healthcare crisis in modern times。 The SARS-CoV-2 novel coronavirus has high transmission rate， is more aggressive and virulent in comparison to previously known coronaviruses。 It primarily attacks the respiratory system by inducing cytokine storm that causes systemic inflammation and pulmonary fibrosis。 Decorin is a pluripotent molecule belonging to a leucine rich proteoglycan group that exerts critical role in extracellular matrix (ECM) assembly and regulates cell growth， adhesion， proliferation， inflammation， and fibrogenesis。 Interestingly， decorin has potent anti-inflammatory， cytokine inhibitory， and anti-fibrillogenesis effects which make it a potential drug candidate against the COVID-19 related complications especially in the context of lung fibrosis。 Herein， we postulate that owing to its distinctive pharmacological actions and immunomodulatory effect， decorin can be a promising preclinical therapeutic agent for the therapy of COVID-19。
查看更多>>摘要：Sars Cov-2， the pathogen which belongs to the beta coronavirus family that is responsible for COVID-19， uses Angiotensin Converting Enzyme 2 (ACE2) as a receptor， which is responsible for controlling the actions of reninangiotensin system (RAS)。 Sars Cov-2 - ACE2 binding leads to a RAS mediated immune response， which targets especially lungs to form ARDS， which in turn， is the most important cause of mortality in COVID-19。 CD8+ T cell response dominates over CD4+ T cell response and natural killer cell dysfunction also leads to CD4+ cell dysfunction in COVID-19; this immune dysregulation leads to inappropriate (ARDS) and inadequate (low or quickly waning antibodies) responses to the disease and unfortunately， prepares the patients for re-infections。 The peripheral anergy seen in chronic sarcoidosis has much resemblance to COVID-19; CD8+ T cell accumulation is also responsible for inadequate reaction to tuberculin and antigenic stimulus。 This article， based on the similarity of COVID-19 and sarcoidosis， discusses a combination of the therapeutic strategy of the tetanusdiphtheria vaccine and dual RAS inhibition， alongside with hydroxychloroquine and antiviral agents， as a solution to overcome the problems described above。
查看更多>>摘要：The pathogenesis of Adolescent Idiopathic Scoliosis (AIS) remains unclear。 Previous research proposed that ligament laxity is a clinical feature that can be easily overlooked in patients with AIS。 We speculated a new hypothesis which is an improvement of our three-dimensional spring model hypothesis of AIS pathogenesis。 The tethered string in the spring model stimulates the spinal ligament instead of spinal cord。 Spinal overgrowth in the adolescent age leads to higher tension of posterior spinal ligament。 And the ligament laxity leads to lower tension of anterior spinal ligament。 This uncoupled anterior and posterior spinal ligament tension maybe the key cause of AIS。
NSTL
Elsevier