Daris I. González Hernández, Xiomara Herrera Argüelles
Celiac disease (CD) is a chronic disease causing inflammation of the proximal small intestine that occurs in genetically predisposed individuals when they eat gluten which is a binding protein common in grains wheat, barley, and rye. The disease injury usually resolves when gluten is excluded from the diet. Although the injury will heal, the reaction to gluten is permanent and will recur with the reintroduction of gluten. The condition is surprisingly common, affecting as many as 1% of white populations. The consequences of the disease are predominantly those of malnutrition due to maldigestion and malabsorption, such as diarrhea, weight loss, and anemia. Symptoms caused by inflammation of the small intestine are also common. CD, although it is common and its pathology is well understood, frequently goes undiagnosed, probably because of the nonspecific or vague nature of many of the symptoms that occur. The cornerstone of treatment for CD is elimination of gluten from the diet. In most patients diagnosed with CD, a strict gluten‐free diet (GFD) alone should result in complete symptomatic and histologic resolution of the disease and reduce risk of complications. Noncompliance with diet is the leading cause of failure to respond in patients with CD. For these reasons, thorough assessment and counseling and management at the time of diagnosis and ongoing care are crucial. This article addresses the overview and diagnosis of CD and addresses its nutritional management in detail.
{"title":"Nutritional Management of Celiac Disease","authors":"Daris I. González Hernández, Xiomara Herrera Argüelles","doi":"10.33140/jcei.08.02.03","DOIUrl":"https://doi.org/10.33140/jcei.08.02.03","url":null,"abstract":"Celiac disease (CD) is a chronic disease causing inflammation of the proximal small intestine that occurs in genetically predisposed individuals when they eat gluten which is a binding protein common in grains wheat, barley, and rye. The disease injury usually resolves when gluten is excluded from the diet. Although the injury will heal, the reaction to gluten is permanent and will recur with the reintroduction of gluten. The condition is surprisingly common, affecting as many as 1% of white populations. The consequences of the disease are predominantly those of malnutrition due to maldigestion and malabsorption, such as diarrhea, weight loss, and anemia. Symptoms caused by inflammation of the small intestine are also common. CD, although it is common and its pathology is well understood, frequently goes undiagnosed, probably because of the nonspecific or vague nature of many of the symptoms that occur. The cornerstone of treatment for CD is elimination of gluten from the diet. In most patients diagnosed with CD, a strict gluten‐free diet (GFD) alone should result in complete symptomatic and histologic resolution of the disease and reduce risk of complications. Noncompliance with diet is the leading cause of failure to respond in patients with CD. For these reasons, thorough assessment and counseling and management at the time of diagnosis and ongoing care are crucial. This article addresses the overview and diagnosis of CD and addresses its nutritional management in detail.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136185946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The plasmid vector pET-28b(+) named “Young” was produced according a work of 2014 [1]. This construct is designed to allow the expression of a 13.6 kDA protein with a C-terminal 6histag. It is supposed to be an anti-HRP (Horse-radish peroxydase protein). This protein was not expressed in first E.coli: we attempt to explain this phenomenon.
{"title":"Other Sea Star Igkappa Gene Cloning Assay in E.Coli with New Parameters","authors":"","doi":"10.33140/jcei.08.02.02","DOIUrl":"https://doi.org/10.33140/jcei.08.02.02","url":null,"abstract":"The plasmid vector pET-28b(+) named “Young” was produced according a work of 2014 [1]. This construct is designed to allow the expression of a 13.6 kDA protein with a C-terminal 6histag. It is supposed to be an anti-HRP (Horse-radish peroxydase protein). This protein was not expressed in first E.coli: we attempt to explain this phenomenon.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"112 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135778009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Australian official mortality data show no clear evidence of significant excess deaths in 2020, implying from an older WHO definition that there was no COVID-19 pandemic. A seasonality analysis suggests that COVID-19 deaths in 2020 were likely misclassifications of influenza and pneumonia deaths. Australian excess mortality became significant only since 2021 when the level was high enough to justify calling a pandemic. Significant excess mortality was strongly correlated (+74%) with COVID-19 mass injections five months earlier. Strength of correlation, consistency, specificity, temporality, and dose-response relationship are foremost Bradford Hill criteria which are satisfied by the data to suggest the iatrogenesis of the Australian pandemic, where excess deaths were largely caused by COVID-19 injections. Therefore, a strong case has been presented for the iatrogenic origins of the Australian COVID-19 pandemic and therefore, the associated mortality risk/benefit ratio for COVID injections is very high.
{"title":"Australian COVID-19 pandemic: A Bradford Hill Analysis of Iatrogenic Excess Mortality","authors":"","doi":"10.33140/jcei.08.02.01","DOIUrl":"https://doi.org/10.33140/jcei.08.02.01","url":null,"abstract":"Australian official mortality data show no clear evidence of significant excess deaths in 2020, implying from an older WHO definition that there was no COVID-19 pandemic. A seasonality analysis suggests that COVID-19 deaths in 2020 were likely misclassifications of influenza and pneumonia deaths. Australian excess mortality became significant only since 2021 when the level was high enough to justify calling a pandemic. Significant excess mortality was strongly correlated (+74%) with COVID-19 mass injections five months earlier. Strength of correlation, consistency, specificity, temporality, and dose-response relationship are foremost Bradford Hill criteria which are satisfied by the data to suggest the iatrogenesis of the Australian pandemic, where excess deaths were largely caused by COVID-19 injections. Therefore, a strong case has been presented for the iatrogenic origins of the Australian COVID-19 pandemic and therefore, the associated mortality risk/benefit ratio for COVID injections is very high.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"36 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135778010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Swarupa Pahan, Sumita Raha, Sridevi Dasarathi, Kalipada Pahan
Chronic inflammation driven by proinflammatory cytokines (TNFα, IL-1β, IL-6, etc.), and nitric oxide (NO) plays an important role in the pathogenesis of several autoimmune, inflammatory as well as neurodegenerative disorders like rheumatoid arthritis, multiple sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, etc. Therefore, identification of nontoxic anti-inflammatory drugs may be beneficial for these autoimmune, inflammatory and neurodegenerative disorders. Cinnamein, an ester derivative of cinnamic acid and benzyl alcohol, is used as a flavoring agent and for its antifungal and antibacterial properties. This study underlines the importance of cinnamein in inhibiting the induction of proinflammatory molecules in RAW 264.7 macrophages and primary mouse microglia and astrocytes. Stimulation of RAW 264.7 macrophages with lipopolysaccharide (LPS) and interferon γ (IFNγ) led to marked production of NO. However, cinnamein pretreatment significantly inhibited LPS- and IFNγ-induced production of NO in RAW 264.7 macrophages. Cinnamein also reduced the mRNA expression of inducible nitric oxide synthase (iNOS) and TNFα in RAW cells. Accordingly, LPS and viral double-stranded RNA mimic polyinosinic: polycytidylic acid (polyIC) stimulated the production of TNFα, IL-1β and IL-6 in primary mouse microglia, which was inhibited by cinnamein pretreatment. Similarly, cinnamein also inhibited polyIC-induced production of TNFα and IL-6 in primary mouse astrocytes. These results suggest that cinnamein may be used to control inflammation in different autoimmune, inflammatory and neurodegenerative disorders.
{"title":"Cinnamein Inhibits the Induction of Nitric Oxide and Proinflammatory Cytokines in Macrophages, Microglia and Astrocytes.","authors":"Swarupa Pahan, Sumita Raha, Sridevi Dasarathi, Kalipada Pahan","doi":"10.33140/jcei.08.01.01","DOIUrl":"https://doi.org/10.33140/jcei.08.01.01","url":null,"abstract":"<p><p>Chronic inflammation driven by proinflammatory cytokines (TNFα, IL-1β, IL-6, etc.), and nitric oxide (NO) plays an important role in the pathogenesis of several autoimmune, inflammatory as well as neurodegenerative disorders like rheumatoid arthritis, multiple sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, etc. Therefore, identification of nontoxic anti-inflammatory drugs may be beneficial for these autoimmune, inflammatory and neurodegenerative disorders. Cinnamein, an ester derivative of cinnamic acid and benzyl alcohol, is used as a flavoring agent and for its antifungal and antibacterial properties. This study underlines the importance of cinnamein in inhibiting the induction of proinflammatory molecules in RAW 264.7 macrophages and primary mouse microglia and astrocytes. Stimulation of RAW 264.7 macrophages with lipopolysaccharide (LPS) and interferon γ (IFNγ) led to marked production of NO. However, cinnamein pretreatment significantly inhibited LPS- and IFNγ-induced production of NO in RAW 264.7 macrophages. Cinnamein also reduced the mRNA expression of inducible nitric oxide synthase (iNOS) and TNFα in RAW cells. Accordingly, LPS and viral double-stranded RNA mimic polyinosinic: polycytidylic acid (polyIC) stimulated the production of TNFα, IL-1β and IL-6 in primary mouse microglia, which was inhibited by cinnamein pretreatment. Similarly, cinnamein also inhibited polyIC-induced production of TNFα and IL-6 in primary mouse astrocytes. These results suggest that cinnamein may be used to control inflammation in different autoimmune, inflammatory and neurodegenerative disorders.</p>","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"8 1","pages":"520-529"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9949320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9423908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Compared with the annual record high, 17 therapeutic monoclonal antibodies (mAb) approved in 2017, this year total 16 therapeutic mAb were approved by FDA, interestingly 4 of them targeted at VEGF (Vascular Endothelial Growth Factor), two indicated for solid tumor, two for Neovascular (Wet) Age-Related Macular Degeneration [1]. Monoclonal antibody technique was created by Georges Köhler, César Milstein, and Niels Kaj Jerne in 1975 by using a mouse x mouse hybridoma. In 1984 they were awarded the Nobel Prize in Medicine for the discovery. Eight years later, in 1992 US FDA approved the first therapeutic mAb muromonab
与2017年批准的17种治疗性单克隆抗体(mAb)的年度最高纪录相比，今年FDA共批准了16种治疗性mAb，有趣的是，其中4种针对VEGF(血管内皮生长因子)，2种用于实体瘤，2种用于新血管(湿)年龄相关性黄斑变性[1]。单克隆抗体技术是由Georges Köhler、csamar Milstein和Niels Kaj Jerne于1975年利用小鼠x小鼠杂交瘤发明的。1984年，他们因这一发现获得了诺贝尔医学奖。8年后的1992年，美国FDA批准了首个治疗性单抗
{"title":"Therapeutic Monoclonal Antibodies Approved by FDA in 2022","authors":"","doi":"10.33140/jcei.08.01.03","DOIUrl":"https://doi.org/10.33140/jcei.08.01.03","url":null,"abstract":"Compared with the annual record high, 17 therapeutic monoclonal antibodies (mAb) approved in 2017, this year total 16 therapeutic mAb were approved by FDA, interestingly 4 of them targeted at VEGF (Vascular Endothelial Growth Factor), two indicated for solid tumor, two for Neovascular (Wet) Age-Related Macular Degeneration [1]. Monoclonal antibody technique was created by Georges Köhler, César Milstein, and Niels Kaj Jerne in 1975 by using a mouse x mouse hybridoma. In 1984 they were awarded the Nobel Prize in Medicine for the discovery. Eight years later, in 1992 US FDA approved the first therapeutic mAb muromonab","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"134 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135585513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Imagine how to start a new research department and you will find many suggestions: how to find the right expertise, how to find investment, how to organise an effective research system. When you have the right contacts, you will surely get the opportunity to build up a constructive beginning. A new idea might be in bringing existing research laboratories together facing the same goal and subject looking for ways to ameliorate the working conditions and results. Organizing a new company formed by complementary laboratories and co-operative agents with different disciplines would be an exciting challenge.
{"title":"Factors, Contributing to Set up Effective Experimental Research","authors":"","doi":"10.33140/jcei.07.01.02","DOIUrl":"https://doi.org/10.33140/jcei.07.01.02","url":null,"abstract":"Imagine how to start a new research department and you will find many suggestions: how to find the right expertise, how to find investment, how to organise an effective research system. When you have the right contacts, you will surely get the opportunity to build up a constructive beginning. A new idea might be in bringing existing research laboratories together facing the same goal and subject looking for ways to ameliorate the working conditions and results. Organizing a new company formed by complementary laboratories and co-operative agents with different disciplines would be an exciting challenge.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"69 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77509041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The variants of SARS-CoV-2 have been affecting people globally since 2020. The Delta variant, mainly in India and the omicron variant in multiple countries since Nov 2021, has infected millions of people; many died out of them. Amongst all factors, food allergy is one factor that also accelerates many infected people’s comorbidities and overall health status during the pandemic. Aims: The study aimed to assess the role of some common food allergies in Delta and Omicron infected people in the Indian population. Methods: The study was designed with 50 covid positive home-isolated patients (out of 62) infected by both the mentioned variants from April 2021 until 15th January 2022. However, they were not severely ill but had comorbidities such as diabetes, obesity, hepatomegaly, etc. After the negative test result, each participant was requested to attend a telephonic interview for 15 minutes. Further, they were offered free online diet consultation considering the fatigue and some allergic symptoms. ATLAS-Ti-9 software was used for the fundamental analysis. Results: Based on their self-referred serological allergy test (SAT), we found that 23 samples of milk (46%), 14 (28%) samples of citrus fruits, 12 (24%) patients were allergic due to mustard oil and other detections too based on the positive interpretation (+ to +++) of specific IgE (IU/ml). The patients were facing type-1 hypersensitivity but no other severe allergic issues. Conclusions: Food allergy accelerated respiratory syndromes and comorbidities, mainly among the infected (Delta and Omicron) patients who could also have a high chance of hypersensitivity due to some common ingesting allergens.
{"title":"Effect of Food Allergy among Patients Affected by Delta and Omicron Variants-A Case Study","authors":"","doi":"10.33140/jcei.07.01.04","DOIUrl":"https://doi.org/10.33140/jcei.07.01.04","url":null,"abstract":"Background: The variants of SARS-CoV-2 have been affecting people globally since 2020. The Delta variant, mainly in India and the omicron variant in multiple countries since Nov 2021, has infected millions of people; many died out of them. Amongst all factors, food allergy is one factor that also accelerates many infected people’s comorbidities and overall health status during the pandemic. Aims: The study aimed to assess the role of some common food allergies in Delta and Omicron infected people in the Indian population. Methods: The study was designed with 50 covid positive home-isolated patients (out of 62) infected by both the mentioned variants from April 2021 until 15th January 2022. However, they were not severely ill but had comorbidities such as diabetes, obesity, hepatomegaly, etc. After the negative test result, each participant was requested to attend a telephonic interview for 15 minutes. Further, they were offered free online diet consultation considering the fatigue and some allergic symptoms. ATLAS-Ti-9 software was used for the fundamental analysis. Results: Based on their self-referred serological allergy test (SAT), we found that 23 samples of milk (46%), 14 (28%) samples of citrus fruits, 12 (24%) patients were allergic due to mustard oil and other detections too based on the positive interpretation (+ to +++) of specific IgE (IU/ml). The patients were facing type-1 hypersensitivity but no other severe allergic issues. Conclusions: Food allergy accelerated respiratory syndromes and comorbidities, mainly among the infected (Delta and Omicron) patients who could also have a high chance of hypersensitivity due to some common ingesting allergens.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77394248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lord please save us from the poor choices of food we pile on our plates. We are often unaware of how it determines our fate. With all the meat, fish, and eggs prepped with butter. Is it the saturated fat on our brains that blinds us to the fact that millions of animals suffer? We’re anxious, we’re angry, we have such low mood. Is it possible it’s because of our unhealthy food? “Oh no don’t take away my cheese, I’ll risk it all.” Those are the words from a victim of high cholesterol.
{"title":"A Prayer from a Vegan Doctor","authors":"","doi":"10.33140/jcei.07.01.03","DOIUrl":"https://doi.org/10.33140/jcei.07.01.03","url":null,"abstract":"Lord please save us from the poor choices of food we pile on our plates. We are often unaware of how it determines our fate. With all the meat, fish, and eggs prepped with butter. Is it the saturated fat on our brains that blinds us to the fact that millions of animals suffer? We’re anxious, we’re angry, we have such low mood. Is it possible it’s because of our unhealthy food? “Oh no don’t take away my cheese, I’ll risk it all.” Those are the words from a victim of high cholesterol.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78696682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: The propose of study was to determine the viral load of Parvovirus B19 in children with proven acute lymphoblastic leukemia (ALL) Methods: A cross-sectional study designed in pediatric ward of Rasoul-e-Akram Hospital (educational, third referral) in Tehran, Iran (2015 – 2016). Sixty-nine children (mean age: 6.57 ± 4.25 years) in preservative phase of ALL selected. BMA had done, and the viral load for Parvovirus B19 determined by quantitative PCR. Results: Type of ALL was Pre B cell: 76.8%; Pro B cell: 14.5% and T-cell type: 7.8%. Low viral load determined in 18.8% (n=13); intermediate in 39.1% (n=27). High and very high viral load observed in 27.1% 15 (n=15) and 20.3% (n=1) of cases respectively. Viral load was related to Pro B cell type (p = 0.050) and lymphadenopathy (p = 0.040), but not related to gender (p = 0.350) and severity of ALL (p = 0.403); like hepatosplenomegaly, anemia, thrombocytopenia or need to transfusion. Conclusion: Parvovirus B19 is a common viral infection in young Iranian population. Near one-third of childbearing age, women in Iran are at risk for primary Parvovirus B19 infection. Here, to evaluate the possible role of parvovirus B19 Infection in the etiology of ALL, 42 % of ALL cases had high and very high viral load (21.7% and 20.3); the low or intermediate viral load is detectable in all cases. The viral load was related to Pro B cell type of ALL (p = 0.050) and the presence of lymphadenopathy. However, there is no relationship observed between Parvovirus B19 viral load and the severity of ALL and gender. It probably might be due to viral detection in the early stages of the ALL
{"title":"Association between parvovirus B19 virus and childhood acute lymphoblastic leukemia: A cross-sectional study in Tehran; Iran","authors":"","doi":"10.33140/jcei.07.01.01","DOIUrl":"https://doi.org/10.33140/jcei.07.01.01","url":null,"abstract":"Objective: The propose of study was to determine the viral load of Parvovirus B19 in children with proven acute lymphoblastic leukemia (ALL) Methods: A cross-sectional study designed in pediatric ward of Rasoul-e-Akram Hospital (educational, third referral) in Tehran, Iran (2015 – 2016). Sixty-nine children (mean age: 6.57 ± 4.25 years) in preservative phase of ALL selected. BMA had done, and the viral load for Parvovirus B19 determined by quantitative PCR. Results: Type of ALL was Pre B cell: 76.8%; Pro B cell: 14.5% and T-cell type: 7.8%. Low viral load determined in 18.8% (n=13); intermediate in 39.1% (n=27). High and very high viral load observed in 27.1% 15 (n=15) and 20.3% (n=1) of cases respectively. Viral load was related to Pro B cell type (p = 0.050) and lymphadenopathy (p = 0.040), but not related to gender (p = 0.350) and severity of ALL (p = 0.403); like hepatosplenomegaly, anemia, thrombocytopenia or need to transfusion. Conclusion: Parvovirus B19 is a common viral infection in young Iranian population. Near one-third of childbearing age, women in Iran are at risk for primary Parvovirus B19 infection. Here, to evaluate the possible role of parvovirus B19 Infection in the etiology of ALL, 42 % of ALL cases had high and very high viral load (21.7% and 20.3); the low or intermediate viral load is detectable in all cases. The viral load was related to Pro B cell type of ALL (p = 0.050) and the presence of lymphadenopathy. However, there is no relationship observed between Parvovirus B19 viral load and the severity of ALL and gender. It probably might be due to viral detection in the early stages of the ALL","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"13 6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82618451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This 73-year-old female patient has suffered from type 2 diabetes (T2D), hypertension, and hyperlipidemua for over 20 years. She started taking Metformin in 1999 and ceased taking it on 1/7/2019. As of 4/3/2019, her HbA1C level was at 6.6%. Since 4/4/2019, she implemented a lifestyle management program which not only focuses on diet and exercise but also factors in sleep, stress, life routines and habits, as well as environmental factors. In this article, the author applies the final conclusions from the American Diabetes Association (ADA) 2021 consensus report regarding “T2D Remission”. For this clinical case, he analyzes the patient’s present conditions to determine if she satisfies the criteria of “T2D remission” or not. The defined criteria of “remission” include timespan of at least one year, HbA1C level less than 6.5%, fasting plasma glucose (FPG) level less than 126 mg/dL, and estimated HbA1C (eA1C) values based on the mean continuous glucose monitoring (CGM) glucose data less than 6.5%. In conclusion, according to the ADA 2021 consensus report, this female patient is in “remission” for T2D. In summary, over the past year from 9/5/2020 to 9/5/2021, her average lab-A1C is 6.3%, mean CGM FPG value is 102 mg/dL, and CGM eAG is 5.7%. First, the selected one year satisfies the timespan requirement cited in the 2021 consensus report. Her set of glucose data has been collected over ~3 years, after post-Metformin (started on 1/7/2019) and her initiation of lifestyle management program that began on 4/4/2019. Second, all of her A1C values, both lab-tested and CGM eA1C, are less than 6.5% and her mean CGM FPG level is less than 126 mg/dL. Finally, she keeps a regular routine with quarterly medical examinations to monitor various diabetes complications, including macrovascular, micro- vascular, neural, and hormonal systems. The author understands and agrees with the consensus report that diabetes is non-curable and at most is “controllable” or “partially reversible”. Nevertheless, this female patient has also adopted a similar lifestyle improvement program as the author in order to deal with the root causes of her multiple metabolic disorders, particularly T2D, instead of suppressing the external symptoms of diabetes through medication intervention.
{"title":"Assessment of a Clinical Case for A Female Patient with Type 2 Diabetes Using the 2021 Consensus Report on Type 2 Diabetes Remission Discussions Sponsored by American Diabetes Association Based on GH-Method: math-physical medicine (No. 506)","authors":"","doi":"10.33140/jcei.06.06.07","DOIUrl":"https://doi.org/10.33140/jcei.06.06.07","url":null,"abstract":"This 73-year-old female patient has suffered from type 2 diabetes (T2D), hypertension, and hyperlipidemua for over 20 years. She started taking Metformin in 1999 and ceased taking it on 1/7/2019. As of 4/3/2019, her HbA1C level was at 6.6%. Since 4/4/2019, she implemented a lifestyle management program which not only focuses on diet and exercise but also factors in sleep, stress, life routines and habits, as well as environmental factors. In this article, the author applies the final conclusions from the American Diabetes Association (ADA) 2021 consensus report regarding “T2D Remission”. For this clinical case, he analyzes the patient’s present conditions to determine if she satisfies the criteria of “T2D remission” or not. The defined criteria of “remission” include timespan of at least one year, HbA1C level less than 6.5%, fasting plasma glucose (FPG) level less than 126 mg/dL, and estimated HbA1C (eA1C) values based on the mean continuous glucose monitoring (CGM) glucose data less than 6.5%. In conclusion, according to the ADA 2021 consensus report, this female patient is in “remission” for T2D. In summary, over the past year from 9/5/2020 to 9/5/2021, her average lab-A1C is 6.3%, mean CGM FPG value is 102 mg/dL, and CGM eAG is 5.7%. First, the selected one year satisfies the timespan requirement cited in the 2021 consensus report. Her set of glucose data has been collected over ~3 years, after post-Metformin (started on 1/7/2019) and her initiation of lifestyle management program that began on 4/4/2019. Second, all of her A1C values, both lab-tested and CGM eA1C, are less than 6.5% and her mean CGM FPG level is less than 126 mg/dL. Finally, she keeps a regular routine with quarterly medical examinations to monitor various diabetes complications, including macrovascular, micro- vascular, neural, and hormonal systems. The author understands and agrees with the consensus report that diabetes is non-curable and at most is “controllable” or “partially reversible”. Nevertheless, this female patient has also adopted a similar lifestyle improvement program as the author in order to deal with the root causes of her multiple metabolic disorders, particularly T2D, instead of suppressing the external symptoms of diabetes through medication intervention.","PeriodicalId":73657,"journal":{"name":"Journal of clinical & experimental immunology","volume":"24 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78238709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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