Abstract
T11TS is a novel bimolecular therapeutic probe, the disease relevance of which has been worked out for the first time in our laboratory. Recently a patent has been granted on this score.
Main bulk of the work has been done on experimental glioblastoma, the most fatal of all brain tumors despite therapeutic advances. T11TS was isolated, characterised and proved to ameliorate experimental glioma by multimodal mechanistic activities. Usually a specific molecular therapy acts in a specific pathway, but contrary to this T11TS acts as a multi-edged sword intervening each of the pathways like Immune Potentiation, Alteration of Cytokine Levels, Specific Apoptotic Induction, Cell Cycle Modulation, Anti-Angiogenesis.
T11TS immunotherapy in glioma reverses immunosuppression and causes profound immunepotentiation both at the peripheral and intracranial levels. Complete downregulation of T-cell signaling in glioma was reversed by T11TS. T11TS also modulated cytokine levels favoring specific apoptotic killing of glioma cells. T11TS intervention was also studied molecularly at hematopoietic stem cell (HSC) level.
As an Immunotherapeutic agent T11TS was effective against other cancers like Arsenic induced cancer in mouse model, canine pyoderma and canine demidocosis. Our recent studies have proved that T11TS was very effective in complete destruction of Cryptococcus neoformans in rat model, exciting both the Innate and Adoptive Immune system.
Toxicity studies with T11TS revealed that it is totally nontoxic. T11TS acting as an ideal Immunotherapeutic agent act not only as an Anti-neoplastic agent, but also against other diseases. The above studies pave the way for translational research with T11TS.
Biography
Presently working as Emeritus Medical Scientist, ICMR, Prof Swapna Chaudhuri was the former Professor and Head, Department of Laboratory Medicine, Calcutta School of Tropical Medicine. Worked as a Scientist at the Royal Institute of Cancer Research, Surrey, UK. Her research area is in the field of Immunology and Immunotherapy of Cancer; Pollen induced allergy and asthma; Fungal Infection and Hematopoietic Stem cell. Taught at both Postgraduate and Undergraduate levels. Published seventy five papers in peer reviewed journals and also reviews, monograms, book chapters. Has won many Academic laurels and Fellowships, affiliated to twelve Academic Societies, Associate Editor of International journals, Reviewer of 68 high impact factor journals, Principal Investigator of twenty one projects, Supervised 25 PhD, MD and DM students.
Abstract
Rheumatoid arthritis (RA) is characterized, in part, by destruction of articular cartilage by matrix metalloproteinases (MMPs) in response to pro-inflammatory cytokines, such as interleukin-6 (IL-6), a potent activator of JAK-STAT signaling. Tofacitinib a pan-Janus kinase inhibitor,and USFDA-approved for treating RA was employed to determine the extent to which inhibition of STAT protein phosphorylation was accompanied by suppression of matrix metalloproteinase (MMP) gene expression. C28/I2 chondrocytes, used as a surrogate for normal chondrocytes, or normal human chondrocytes (NHC) were grown to high-density confluencyand treated with recombinant human interleukin-6 (rhIL-6) (20ng/mL) for up to 60 min. Activation of STAT proteins was determined by quantifying anti-STAT1, -3, or -5AB immunoblots. C28/I2 chondrocytes produced STAT1, STAT3 and STAT5AB whereas NHC produced only STAT1 and STAT3. Unexpectedly treatment of NHC with rhIL-6 increased the content of total STAT1, STAT3 and, in several cases total STAT content was reduced by tofacitinib. STAT1 and STAT3 were phosphorylated following incubation of NHC with rhIL-6 after 30 min as was STAT1, STAT3 and STAT5AB by rhIL-6-treated C28/I2 chondrocytes. Pre-incubation of C28/I2 chondrocytes or NHC with tofacitinib (2.5nM-100nM) for 30 min followed by rhIL-6 andtofacitinib for an additional 30 min caused a statistically significant decrease in p-STAT1 and p-STAT3. Moreover, tofacitinib reduced MMP-3 and MMP-13gene expression, but not MMP-1, -2 or -9gene expression. These results may have relevance in the context of correcting the altered integrity of articular cartilage associated with chronic synovial joint inflammation and the elevated level of IL-6 characteristic of RA.
Biography
Charles J. Malemud received the Ph.D. from George Washington University and did his post-doc at the State University of New York (Stony Brook, NY). He is on the faculty at Case Western Reserve University School of Medicine where he is Professor of Medicine & Anatomy in the Division of Rheumatology and Chair of the Fellowship Research Committee. He has published over 275 papers, book chapters, commentaries and, reviews primarily in the field of chondrocyte biology. Dr. Malemud is on the editorial board of several journals and is Editor-in-Chief of the Journal of Clinical and Cellular Immunology, and Current Rheumatology Reviews.
Abstract
Cancer cells can evade immune recognition by losing major histocompatibility complex (MHC) class I. Hence, MHC class I-negative cancers represent the most challenging cancers to be treated. Chemotherapeutic drugs not only directly kill tumors but also modulate tumor immune microenvironment. However, it remains unknown whether chemo-treated cancer cells can activate CD8 T cells independent of tumor-derived MHC class I and whether such MHC class I-independent CD8 T cell activation can be exploited for cancer immunotherapy. Here, we showed that chemo-treated cancer cells directly activated CD8 T cells in an MHC class I-independent manner and that these activated CD8 T cells exhibit virtual memory (VM) phenotypes. Consistently, in vivo chemotherapeutic treatment preferentially increased tumor infiltrating VM CD8 T cells. Mechanistically, MHC class-I-independent activation of CD8 T cells requires cell-cell contact and the activation of PI3K pathway. VM CD8 T cells contribute to a better therapeutic effect on MHC class I-deficient tumors. Using humanized mouse models or primary human CD8 T cells, we also demonstrated that chemo-treated human lymphomas activated VM CD8 T cells independent of tumor-derived MHC class I. In conclusion, CD8 T cells can be directly activated in an MHC class-I-independent manner by chemo-treated cancers, and these activated CD8 T cells may be exploited for developing new strategies to treat MHC class I-deficient cancers.
Biography
Dr. Jing Hong Wang, M.D., Ph.D., is an Associate Professor in the Department of Immunology and Microbiology at the University of Colorado School of Medicine at Anschutz Medical Campus (https://medschool.cuanschutz.edu/immunology-and-microbiology/faculty/wang). Dr. Wang graduated from Beijing Medical University (now known as Peking University Health Science Center) with a M.D., Ohio State University with a M.S. and University of Chicago with a Ph.D. Dr. Wang completed postdoctoral fellowship at Children’s Hospital in Boston. Dr. Wang joined her department in 2011 as an Assistant Professor and was promoted to Associate Professor in 2016. Her research program is currently supported by multiple NIH grants.
Abstract
COVID-19 has left mankind desperately seeking how to manage dramatically rising infection rates associated with severe disease progressions. COVID-19 courses range from mild symptoms up to multiple organ failure and death, triggered by excessively high serum cytokine levels (IL 1β, IL6, TNF α, IL8). The vagally driven cholinergic anti-inflammatory pathway (CAP) stops the action of nuclear factor κB (NF-κB), the transcriptional factor of pro-inflammatory cytokines. Thus, well-balanced cytokine release depends on adequate vagal signaling. Coronaviruses replicate using NF-κB transcriptional factor as well. By degrading the cytoplasmatic inhibitor of NF-κBsubunits (IκB), coronaviruses induce unrestricted NF-κB expression accelerating both, virus replication and cytokine transcription.
We hypothesize that CAP detriment due to depressed vagal tone critically determines the severity of COVID-19.
Biography
Abstract
The coronavirus disease 2019 (COVID-19) pandemic, since its first emergence in China in December 2019from SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection, caused more than103 million people sick with2,237,636 deaths globally, as of February3, 2021. The highly infectiousBetacoronavirus, SARS-CoV-2,replicates inthe upper respiratory system at the disease initial stage (causing mild or asymptomatic COVID-19 in most cases), followed by immunopathological stage of inflammatory response to SARS-CoV-2 infection causing severe/criticalCOVID-19 with cytokine storm (a stage with substantial elevation of serum pro-inflammatory cytokines levels) and ARDS(acute respiratory distress syndrome) and multiple organ failure (majorly lungs, as well as heart, liver and kidney). However, no specific drug or vaccine is available to effectively combat theCOVID-19 pandemicthat devastated the most vulnerable (people of old age, or with medical conditions). Vaccine is therefore urgently required to prevent SARS-CoV-2 transmission, and deaths due to COVID-19. This communication thus stands for analysis (based on the available published information) withanupdateof the vaccinesthat are in the pipeline of rapid pace of COVID-19vaccine development.
Biography
Dr. Shyamapada Mandal, Professor, Department of Zoology, University of Gour Banga, India, is interested re-PhD, PhD, and post-PhD research under the guidance of Professor Nishith Kumar Pal at Calcutta School of Tropical Medicine, India. He has published 115 articles with seven book chapters. He is life member of IAMM and IASR, India, and fellow member of SASS, India. Eight national academic and research awards have been conferred to him. He has guided 52 post graduate students; supervised three MPhil and three PhD students, and supervising 6 PhD students. Professor Mandal is among the world’s top 2% scientists as per the survey of the Stanford University, published in PLOS (Public Library of Science) Biology (October, 2020).
Abstract
Background: Inflammation is a response of the immune system, guarding the individual against infection. It is a major burning problem worldwide and billions of individuals are affected. Some of the spices used daily in Algerian cuisine have been known to possess major anti-inflammatory effects. Turmeric, red pepper, ginger, cinnamon and cumin etc. are a few of the wide spectrum of spices used in Algeria.
The aim of the study was to investigate the antiinflammatory effect and anti actvity of some dietary spices in carrageenan induced models of inflammation on Wistar rats.
Methods: Albino wistar rats were divided into four groups. Inflammation was induced on the animal by injecting the right hand paw with carrageenan (0.1 ml of 1%). Group 1 was fed with food and water and treated with carrageenan (control) whereas group 2 and 3 treated with different doses (100 and 200 mg/kg/bw) of aqueous extract of some dietary spices with carrageenan, respectively. Group 4 treated with standard drug diclofenac sodium (10 mg/kg b.w., reference drug for inflammation), once for 24 hrs.
Results:
The content of total phenolic was 137.2±21.6 mg/g and flavonoids 122.3±5.8 mg/g. After 60, 120, 180, 240 and 300 min, the data indicate that some dietary spices 100 and 200 mg/kg was significantly effective reducing paw edema volumes induced by carrageenan compared to control (p <0.01). The levels of serum pro-inflammatory white blood cells, neutrophile, lymphocyte, monocyte, eosinophile, total protein and protein c reactive and total cephalin KADIN and platelts in the control group were significantly increased by carrageenan injection compared with the normal group. The rats pretreated with some spices 100 and 200 mg/kg had significantly lower levels of pro-inflammatory to compare control group.
The paw edema in carrageenan-induced rats was considerably reduced by treating with 100 and 200 mg/kg aqueous extract of some dietary spices when compared to the untreated rats (p<0.001).
Conclusion : The present results clearly demonstarted that carrageenan significantly increased paw edema whereas some dietary treated rats significantly decreased the paw edema. The study underlines the importance of some of the frequently used spices (Turmeric, red pepper, ginger, cinnamon and cumin) in the treatment of inflammation.
Biography
Abstract
Introduction: Neurological manifestations associated to dengue virus are being reported more frequently.
Objective: To identify the neuroimmune response evaluated by Reibergram in patients with neurological manifestations because of dengue virus.
Material and methods: The highest levels of immunoglobulin and albumin were quantified in serum and the cerebrospinal fluid in six adult patients with neurological manifestations of dengue. Q function was calculated with the concentration values in serum and cerebrospinal fluid of these analytes. Values of immunoglobulin Q vs Q albumin were introduced in the specific Reibergrams for each immunoglobulin. Albumin was used as a marker for the evaluation of Blood-Cerebrospinal Fluid barrier.
Results: Reibergram allowed to establish the incidence of intrathecal synthesis of higher immunoglobulins (three types of patterns) in both the postinfectious and parainfectious neurological manifestations, except a patient who developed Guillain-Barre Syndrome. It also allowed to evaluate the blood-cerebrospinal fluid barrier in each patient.
Conclusions: The use of Reibergram is important in the assessment of the immune response in patients with neurological manifestations of dengue virus.
Biography
Abstract
Ion exchange chromatography and chromatofoccusing serve as two important techniques used to isolate proteins based on the PH. RNaseA has an isoelectric PH of 9.6 where as testicular characterisation of RNase By HPLC and chromatofocussing proved to contain two RNases in which one of the RNase has similar structure and isoelectric PH similar to standard RNaseA. The molwt. of the RNase A in rat testes was found to be about 24kd determined by MALDI- TOF.Long term treatment of rats with metosartan does not shown effect on histology of rat testes but elevated apoptosis in rat testes and epididymal sperms. Affect of metosartan on weight of testes was not satisfactory but some what significant.
Biography
Eswari beeram is currently working as a Assistant Professor in Sree Vidyanikethan Degree College and she is engaged mainly in research on drug metosartan.
Abstract
Background
Systemic lupus erythematosus (SLE) isan autoimmune disease with a multiple organsinvolvement. SLE pathogenesisissustained by innate and adaptive immune systemdisregulation, complementactivation, immune complexes, and tissueinflammation. The pattern of clinicalmanifestationsisheterogenous and changes over time.
Hydroxychloroquine (HCQ)isprimarydrug in the treatment of SLE. Itmodulates the immune response by inhibiting B cellreceptor and TLR signaling and activation (1).
Clinical Case
Thisis a case report of a 61 yearsoldfemaleaffected by SLE with recurrentoralaftosis, Lupus anticoagulantantibodies and previouspleuritis in remission.
The patienthad a long course treatment with low dose oralcorticosteroids (5 mg prednisone) and HCQ from three weeks.
After 20 days of treatment with HCQ shedeveloped an abruptcutaneousmanifestationconsisting in painful and infiltratingpapulesraised over the uppertrunk and limbs, rednessscaleslesions to palm and soles, lipswelling,painfulconjunctivitis and milddisphagia.
Slowly progressive improvement of cutaneous and mucosalsignswasobservedafterdrugdiscontinuation,twodaysafterappearance of clinicalmanifestations, andintroducing medium-high dose oforalcorticosteroidstherapy.
Results
Clinicalexams, performed in acute phasehighlighted a markedlymphocytopenia and raised of Reactive C Protein (RCP).Nicolskysignwasslightly positive.
Afterdiscontinuation of HCQ the patientdidnot show cutaneous or infectivesequelae due to promptidentification of Steven-Johnson Syndrome (SJS).
The patientreplaced HCQ with increasing of mainteinance dose of oralcorticosteroids.
Skintestswerenotperfomedfor therisk of SJS exacerbation and concomitantcorticosteroidstherapy.
Conclusions
Like allmedications, HCQ has side effects and mayoccur in autoimmune diseasepatients. The mainundesirableeffectsobserved are digestive disorders and skinmanifestations.
Althoughskindisease are common side effects of HCQ severe toxidermiais a rare conditiondescribed in few case reports of DRESS and SJS (2-4).
Despite the rare occurrence of thesereactions, weobservedothercases of toxidermiaduring the pandemicbreakthrough in Italywhen HCQ waswidelyused for teratment of COVID-19.
Biography
Abstract
Last decade, local allergic rhinitis (LAR) is recognized as a separate endotype of allergic rhinitis compared to the disease's conventional endotype. LAR is attributed to the negative allergic skin prick tests, the normal value of serum total IgE, and positive allergen-specific (Der p 1) nasal provocation tests. So far, it is known that patients with LAR have the same classic symptoms as those with conventional allergic rhinitis. Still, the accurate pathogenesis of allergen tolerance breakdown, structure of comorbidity and complications, peculiarity of course, and approaches to the proper therapy for LAR remains unclear. Our study made use of interviews, ENT diagnostic procedures, allergic skin tests, determination of the serum total IgE and allergen (Der p 1) nasal provocation test in 20 persons with conventional allergic rhinitis and 21 patients with LAR. We found the comparable frequency of allergic asthma, rhinosinusitis, polyps, mucosal edema, mucosal cyanosis, nasal obstruction revealed by rhinometry in two groups. However, there has been a 4-folded increase in LAR anxiety disorders compared to conventional allergic rhinitis. Accordingly, we studied the serum concentration of critical pro-tolerogenic neurotransmitter serotonin, which proved to be significantly lower in LAR than in conventional allergic rhinitis. Thus, serotonin and other pro-tolerogenic synaptic neuro molecules may be a fertile field to study the neuroimmune-pathogenesis of LAR.
Biography
Andrew Klimov has completed his MD and PhD from the Immunology and Allergy Department, Siberian State Medical University, Russia. He has been working as a Associate Professor of the Immunology and Allergy Department and ENT Department, Siberian State Medical University, Russia since 2013. He has published about 30 papers in reputed journals and has been serving as the director of the Immunopathology Center LLC in Tomsk, Russia.
Abstract
Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized clinically by recurrent venous or arterial thrombosis and/or fetal loss and biologically by the presence of persistently elevated levels of antiphospholipid (aPL) antibodies.
Definite APS, fulfilling at least one clinical and one laboratory criteria of the updated Sapporo classification criteria, can primary (primary APS) or can occur in association with other autoimmune diseases, mainly systemic lupus erythematosus (SLE). APS is a complex disease and remains a challenge in terms of both diagnostic issues and clinical praxis. Its management often involves collaboration among several medical specialties (internal medicine, immunology, obstetrics/gynaecology, neurology…). This conference provides a brief overview with an update on primary APS (epidemiology, etiopathogenesis, clinical manifestations, classification criteria, testing for antiphospholipid antibodies and management guidelines).
Clinical symptoms comprise vascular thrombosis, which can affect any vascular bed, including venous, microvascular and arterial vessels. Obstetric manifestations include recurrent early and late pregnancy loss, pre-eclampsia, eclampsia and intrauterine growth restriction.
According to current laboratory criteria for APS, aPL antibodies can be one of three types: lupus anticoagulant (LA), anticardiolipin antibodies (ACL) or antibeta2 glycoprotein I antibodies which should be present in moderate-to-high titre on two occasions at least 12 weeks apart. Progress has been made on the standardization of tests as guidelines on LA testing and immunological assays for aCL and aβ2GPI are published. Moreover, laboratory criteria are very important since the type and level of aPL determine the risk in APS patients. Recent studies demonstrate that aPL may be more common in the general population. More reliable techniques are now available to measure aPL antibodies on a large scale.Future studies should address their role as cardiovascular risk factors.
Based on extensive literature review the European League Against Rheumatism (EULAR) recently published EULAR recommendations for the management of antiphospholipid syndrome in adults. Anticoagulant therapy with VKA remains the conventional therapy in patients with thrombotic APS, whereas in obstetric APS the first line treatment is low-molecular-weight heparin in combination with low-dose aspirin. The 13th International Congress on Antiphospholipid Antibodies task force, as well as current EULAR guidance recommend that patients with definite APS and a first venous event receive lifelong oral anticoagulation to a target INR of 2.0–3.0. EULAR also distinguishes those patients with unprovoked first venous thrombosis and recommend that anticoagulation in this group be continued for a duration for patients without APS, unless a high-risk aPL profile or other risk factors for recurrence are present. Direct oral anticoagulant drugs represent an attractive alternative to conventional vitamin K antagonist drugs but emerging evidence suggests these may not be suitable for high-risk patients with thrombotic APS.
Biography
Abstract
Background
EBV establishes a lifelong infection in B lymphocytes achieved through a highly regulated viral gene expression program. Like all herpesviruses, EBV can choose between two alternative lifestyles: latent or lytic replication. EBV lytic replication, which is required for horizontal spread of the virus from cell to cell, and from host to host, occurs in both epithelial cells and B cells.
Numerous studies have been focused on the contributions of EBV latent infection in the pathogenesis of EBV-induced malignancies. In immune-competent hosts, the outgrowth of EBV-immortalized B cells is prevented through a robust expansion of EBV-specific memory T cells directed toward both lytic and latent antigens. In recent years, the viral lytic cycle was shown to play an essential role in carcinogenesis through several potential mechanisms. EBV lytic infection may increase the total number of latently infected cells by enhancing transmission of the virus from cell to cell and thus constitutes an essential aspect of viral pathogenesis.In some recent reviews, the role of the lytic EBV proteins in tumor progression was highlighted in tumor development (1, 2). Overall, it was clearly demonstrated that these EBV proteins (although very immunogenic) played a critical role in tumorigenesis. They also showed that EBV reactivation may aid virus transmission within the tumor microenvironment to establish latency and drive cellular proliferation. Having said that, the likely predominant role of the EBV lytic cycle is likely to provide the necessary paracrine, anti-apoptotic, and immunomodulatory signals required for tumorigenesis.
Aims
We have focused on the critical role of the IE ZEBRA trans-activator (Zta), because this protein has a key role in the balance between the EBV latent and lytic cycles. The switch from latent to lytic infection is mediated by the IE protein ZEBRA (Orf BZLF1) and R (Orf BRLF1). More recently we reported that the replicative form of EBV, as investigated using anti-ZEBRA IgG titers, correlates with the severity of EBV-associated tumors and with poorer outcomes, especially in women with breast cancer. All in all, these studies investigating serological lytic EBV markers have emphasized the prominent role importance of the lytic infection in EBV malignancies.
Results
Soluble ZEBRA concentrations of>100 ng/mL detected by an enzyme-linked immunosorbentassay (ELISA) in serum of patients after solid organ or hematopoietic stem cell transplant were predictive of PTLD in 80% of the cases within three weeks. Interestingly, the circulating ZEBRA could be detected during periods in which the viral DNA was not detectable by qPCR (3). Thus, ZEBRA testing in serum could help identify patients likely todevelop severe outcomes during the critical posttransplant period and serve as a potential diagnosticmarker for EBV follow-up in immunocompromised patients. All in all, we hypothesize that early abortive infection associated with fully lytic cycles may occur in the tumor or its environment, eventually releasing ZEBRA in the bloodstream. At the end, this phenomenon could stimulate the secretion of cytokines and factors promoting angiogenesis, B-cell proliferation, thereby further aggravating the immunosuppressive environment, as we frequently detected sZEBRA associated with high serum IL-10 levels (3).
Discussion
The relevance of EBV lytic cycle to human pathology prompted researchers to target certainlytic proteins with therapeutic aims. Adenovirus vectors expressing BZLF1 or BRLF1 were used totreat EBV-positive tumors [182]. On the other hand, Food and Drug Administration (FDA)-approvedleflunomide, which targets EBV replication, was shown to inhibit the earliest step of lytic EBV reactivation (BZLF1andBMRF1expression) and prevented the development of EBV-inducedlymphomas in both a humanized mouse model and a xenograft model. More recently, duvelisib(a molecule inhibiting the PI3K/AKT signaling pathway, and B cell receptor (BCR) signaling) wasshown to reduce cell growth and expression of EBV lytic genesBZLF1andgp350/220in EBV-positivecell lines. The histone deacetylase (HDAC) and DNA methyltransferase inhibitors are alsopossible avenues to suppress the ZEBRA expression and the entire lytic cascade.Immunotherapeutic approaches, such as vaccination against IE proteins or IE-specific therapeuticmonoclonal antibodies also represent a promising approach.
All of these results show that the lytic cycle of EBV could be targeted for prognostic and therapeutic purposes. The ZEBRA protein although immunogenic behaves like a toxoid protein capable of disrupting the homeostatic balance of this double-facetted persisting virus
Biography
Abstract
Colorectal cancer (CRC) is the second major cause of cancer-related deaths. Notably, immune checkpoint blockade therapy has become a promising treatment for many cancer patients. However, the majority of CRC patients do not respond to this therapy due to poor Tcell infiltration and downregulated immune checkpoint genes. Elucidating tumor-cell intrinsic mechanisms that inhibit antitumor Tcell responses and developing strategies to boost T cell infiltration is critical to improving immune checkpoint blockade therapy in CRC patients. Tumors use a variety of mechanisms to evade, deceive and suppress the host immune system. This presentation will cover, the role of tumor secreted exosomes in the regulation of tumor immune response. The novel discoveries in this area of investigation will provide insights in stimulating tumor-specific T cell response and form the foundation for a novel anticancer therapeutic strategy.
Biography
Abstract
When the disease made by virus becomes a threat to life or organs blood circulation decreases, Temperature of fever will emerge to increase prevailing blood circulation. And it acts as a protective covering of the body to sustain life.
When blood flow decreases to the brain, the patient becomes fainted-delirious. If we try to decreases the temperature of fever, the blood circulation will further be reduced. Blood circulation never increases without temperature increase. Delirious can never be cured without an increase in blood circulation.
The temperature of fever is not a surplus temperature or it is not to be eliminated from the body. During fever, our body temperature increases like a brooding hen`s increased body temperature.
The actual treatment to fever is to increase blood circulation. Two ways to increase blood circulation. 1. Never allow body temperature to lose 2. Apply heat from outside to the body. When the temperature produced by the body due to fever and heat which we applied on the body combines together, the blood circulation increases.
Then the body will stop to produce heat to increase blood circulation. And the body will get extra heat from outside without any usage of energy.
How can we prove that the temperature of fever in Covid -19 is to increase blood circulation?
If we ask any type of question-related to fever by assuming that the temperature of fever is to increase blood circulation we will get a clear answer. If avoid or evade from this definition we will never get a proper answer to even a single question
If we do any type of treatment by assuming that the temperature of fever is to increase blood circulation, the body will accept, at the same time body will resist whatever treatment to decrease blood circulation.
If we measure the heat energy used for which activities in fever, we will know the purpose of the temperature of fever.
No further evidence is required to prove the temperature of fever in Covid -19 is to increase blood circulation.
Biography
A practicing physician in the field of healthcare in the state of Kerala in India for the last 30 years and very much interested in basic research. My interest is spread across the fever, inflammation and back pain. I am a writer. I already printed and published nine books on these subjects. I wrote hundreds of articles in various magazines. After scientific studies, we have developed 8000 affirmative cross checking questions. It can explain all queries related to fever.
Abstract
We have been hearing for centuries that ‘fever is not a disease but a symptom’. Physicians say that fever is a symptom of diseases like flu to cancer.
The conservative fever definition, diagnosis, and treatments are based on fever as a symptom.
All the studies related to fever as a symptom of a disease have been done without knowing the Purpose of the temperature of fever is.
Without knowing the Purpose of the temperature of fever, how can fever included in the symptom definition?
Temperature between 38o to 41o centigrade can be symptom of a disease?
Most of the diseases may not have a fever. Sometimes it disappears. Then, is fever a symptom of which disease?
Symptom Definition is the only parameter necessary for a Symptom. As with any or all other definitions, symptom definition should describe the symptom scientifically. If it cannot describe clearly, there is no use of a symptom definition. A symptom is a departure from normal function or feeling which is noticed only by a patient, indicating the presence of disease or abnormality. One cannot be understood directly the temperature is elevated in the hypothalamus. A mechanical device is necessary to measure elevated temperature in the hypothalamus. In symptom definition, fever definition can’t be found. The elevation of body temperature is not included in symptom definition.
Different cause of diseases never shows the same symptoms.
Different causes of diseases like virus, bacteria, fungi, venom, horror scene, horror dream,... never shows the same symptoms. Its actions are different and sometimes opposite. No similarities can be seen between their actions.
Elevated temperature or increased temperature never make fever or symptoms of fever. It may create hyperthermia.
None of the diseases or causes of diseases require fever as its symptom.
If the mosquito bites its virus, bacteria, venom gets deposited in the body as a result according to nature and strength of Viruses, bacteria, venom symptoms like itching, pain, and signals like colour change, inflammation may occur.
we can see the symptoms, Signals, and indications of the virus, bacteria, the venom which multiple or spreading or damages(disease) the body before fever emerge. Patients who have flu to cancer may not have a fever.
How can we separate symptoms of the disease and symptoms of fever and symptoms of rising temperatures?
In fever, both symptoms of disease and symptoms of Fever are included. Deduct symptom of disease from total symptoms, we will get symptoms of fever.
(Disease +Fever)- Disease =Fever.
(Symptoms of disease +Symptoms of Fever)- Symptoms of disease =Symptoms of Fever (bitter taste, body pain, fatigue to mind and body, reduced appetite, reduced motion and indigestion, internal and external discomfort,…)
Like that we can separate signs, signals, and actions of both fever and disease.
(Signals of disease +Signals of Fever) - Signals of disease =Signals of Fever(high temperature, shivering, unconscious,....)
(Signs of disease +Signs of Fever) - Signs of disease =Signs of Fever.
(Actions of disease +Actions of Fever) - Actions of disease =Actions of Fever. In fever does not show any actions of temperature rise.
How can we prove the fever is not a symptom.
The fever is not symptom when examined in various directions. In fever, both symptoms of disease and symptoms of fever are included. Deduct symptom of disease from total symptoms, we will get symptoms of fever. we can separate signs, signals, and actions of both fever and disease and rising temperature.
Temperature between 38 degrees and 41 degrees cannot be a symptom of any of the diseases.
A different cause of diseases like virus, bacteria, fungi, venom, horror scene, and horror dream never shows the same symptoms.
Fever has never been scientifically proved as a symptom of a disease. Fever has the properties of adaptation.
If we ask any type of question-related to fever by assuming that the fever is not a symptom we will get a clear answer. If we avoid or evade from this we will never get a proper answer to even a single question.
Biography
A practicing physician in the field of healthcare in the state of Kerala in India for the last 30 years and very much interested in basic research. My interest is spread across the fever, inflammation and back pain. I am a writer. I already printed and published nine books on these subjects. I wrote hundreds of articles in various magazines. After scientific studies, we have developed 8000 affirmative cross checking questions. It can explain all queries related to fever.
Abstract
The nonspecific innate immune mechanism is essential for the initial response against any type of injury -physical, chemical or microbial. This type of immunity screens 24*7 for any type of foreign invasion and protects the host from both external and internal danger associated molecular patterns. The innate immune mechanism is not only essential for the initial response of the host but also plays a major role in the regulation of the specific secondary response or adaptive immunity. The innate immune regulators includes various surface receptors, intracellular receptors and molecular factors …
Periodontitis is an inflammatory disease and it shares similar pathogenic mechanism like other inflammatory diseases like arthiritis, atherosclerosis… The innate immune factors like Toll like receptors (TLRs), nod like receptors (NLRs), various signalling molecules like cytokines, antimicrobial peptides plays an essential role in the initiation and progression of the disease. This presentation will briefly elaborate the recent advances in the molecular mechanisms of the pathogenesis of the inflammatory diseases like periodontitis.
Biography
Abstract
Many epidemic outbreaks of Chikungunya fever (CHIKF) has been reported throughout the world including India after its reemergence in 2005. The protective role of envelope proteins during Chikungunya Virus (CHIKV) infection has been reported. With the aim to identify immunodominant epitopes within the envelope protein we investigated the detailed analysis of fine specificity of antibody response in different individuals with CHIKV infection. The peptides corresponding to the full length of E1, E2 and E3 proteins of S27 strain of Chikungunya virus were synthesized and their seroreactivity with CHIKV positive patient’s sera collected from different epidemic regions of India was determined. The data analysis reveals many potent epitopes throughout the length of envelope E2 protein thus displaying it as the most promising antigen for diagnostic purpose. We found that the main IgG isotype response to envelope proteins was predominantly of subclass IgG3. Interestingly most of the epitopes were found to be conserved for inducing IgM, IgG and IgG3 antibody response. In conclusion Peptides E2P3, E2P7, E2P16 and E2P17 were revealed as most immunodominant peptides. When all the peptides were designed as multiple antigen peptide approach by connecting all the peptides through lysine residue and while studying the diagnosis, this approach showed 100% sensitivity and specificity. The study clearly reveals MAP could be a alternate approach for accurate diagnosis of CHIKV infection. This study provides new and important insight into the humoral response generated by CHIKV S27 strain in the early phase of infection. This approach is an important area of diagnosis. Initially, I am giving a talk on different immulologicaltechiniques and later how these techniques has been used for immunodiagnosis of chikungunya.
Biography
Abstract
Role of Gadd45b in Hepatocellular Carcinoma DevelopmentUmberto Rosato, Nicoas De Migueland Jesus Maria Salvador, National Center for Biotechnology, Madrid, SpainThe Gadd45 family proteins play a central role as stress sensors that modulate the response of mammalian cells to stress inflicted by physiological and environmental factors. Gadd45b behaveseither as oncogeneor as tumor suppressor genein a cell-type dependent manner. Despite itsrole has been extensively studied in various cancers, the functions played by thisproteinin hepatocellular carcinoma development remains unknown. We addressed this issue by studying HCC development in a cohort of wild-typesand Gadd45b null mice injected with diethylnitrosamine (DEN),anhepatocarcinogenic agent. We show that loss ofGadd45b strongly inhibits DEN-induced hepatocarcinogenesis. The lack Gadd45bin mice decreased hepatocyte death and compensatory proliferation, after DEN treatment. IL-6 is required for proliferation upon DEN-injection and the decrease of IL-6 production in Gadd45b null mice was linked to a decrease in JNK activation. Furthermore, we show that ablation of Gadd45b in Kupffer cells, but not in hepatocytes, is sufficient to recapitulate the decrease in proliferation and IL-6 production observed in whole body Gadd45b null mice. Altogether, these results provide a novel role forGadd45bduring DEN-induced HCC, and establish Gadd45b as critical player in regulating IL-6 production during liver injury.
Biography
UmbertoRosatohas completed his PhD from the Department ofOncology, University Autonoma of Madrid, Spain and postdoctoral studies from the National Institutes of Health and Weill Cornell Medicine College, USA. He has published various papersin high impact factor journalsfocusing on Hepatocellular Carcinoma and Immunotherapy.
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