Information of Universe

Commentary for the Elderly in the Pandemic Era

JL recommends it to the elderly living in this pandemic era. However, we must consult our doctor before taking it.

https://www.karger.com/Article/Abstract/515926

코비드-19의 병리 기전 설명 논문.

본 논문의 연구 방법은 팬데믹 초기 500여 SCI 저널을 분석하여 SARS-CoV-2 바이러스의 스파이크 프로테인에 의하여 질병이 유발되는 경로를 분석한 후에 인체의 다양한 수용체가 어떻게 이용되어 병리 증상을 유발하는 가를 설명하고 있다. 분석을 위하여 저자는 비트겐슈타인의 '논리-철학 논고'에 사용된 분석 기법을 활용하였다. 또한 정보검색엔진을 개발한 경험을 살려서 의미있는 데이터를 활용하여 분석하였고 2년이 지나서 실험 결과가 발표되는 것을 역시 모니터링하여 정확한 분석 이었음을 실험데이터로 다시 입증하였다. 이는 철학 방법론을 바이러스 질환 분석에 사용한 세계 최초의 방법론을 적용한 논문이다.

2024년 COVID-19 악화 이유에 대한 병리 논문 (1)

Basic implications on three pathways associated with SARS-CoV-2Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) interacts between the host and virus and govern induction, resulting in multiorgan impact…

2024년 COVID-19 악화 이유에 대한 병리 논문 (2)

Aggravating mechanisms from COVID-19 - Virology JournalSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated diseases. The pathophysiology of COVID-19 uses the following three mechanisms: (1) inflammasome activation mechanism; (2) cGAS–STING signaling mechanism; and (3) SAMHD1 tetramerization mechanism, which leads to IFN-I production. Interactions between the host and virus govern induction, resulting in multiorgan impacts. The NLRP3 with cGAS–STING constitutes the primary immune response. The expression of SARS-CoV-2 ORF3a, NSP6, NSP7, and NSP8 blocks innate immune activation and facilitates virus replication by targeting the RIG-I/MDA5, TRIF, and cGAS–STING signaling. SAMHD1 has a target motif for CDK1 to protect virion assembly, threonine 592 to modulate a catalytically active tetramer, and antiviral IFN responses to block retroviral infection. Plastic and allosteric nucleic acid binding of SAMHD1 modulates the antiretroviral activity of SAMHD1. Therefore, inflammasome activation, cGAS–STING signaling, and SAMHD1 tetramerization explain acute kidney injury, hepatic, cardiac, neurological, and gastrointestinal injury of COVID-19. It might be necessary to effectively block the pathological courses of diverse diseases.

Nguyen, N.H., Tran, K.M., Jong, L.H., Le, S.T.D., Nguyen, A.Q., Duong, D.M., Nguyen, T.D., Nguyen, L.N.T., Dam, L.T.P., Nguyen, T.N.M. (2024). Clinical characteristics of COVID-19 patients treated in emergency COVID-19 hospitals in Vietnam: Experience from Phutho province, Vietnam. International Journal of Medical Sciences, 21(6), 1072-1078. https://doi.org/10.7150/ijms.94461

2023. Immune Triad for treatment, COVID-19 치료에 대한 논문

시중에서 의사 처방을 받아서 구하실 수 있는 의약품 아스피린 답손도 코로나19 치료제라는 것을 설명한 논문입니다.

백신은 국가와 기업들이 정성스럽게 준비하고 있으므로 별 이상 반응이 없으시다면 맞으십시오. 그리고 코로나19에 걸렸을 때 치료제로 사용하여 중증화와 후유증을 예방합니다.

Treatment mechanism of immune triad from the repurposing drug against COVID-19COVID-19 is an immune-mediated disease whose pathophysiology uses SAMHD1 tetramerization and cGAS–STING signaling, toll-like receptor 4 (TLR4) cascade…

COVID-19 Molecular Pathophysiology: Acetylation of Repurposing DrugsSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces immune-mediated type 1 interferon (IFN-1) production, the pathophysiology of which involves sterile alpha motif and histidine-aspartate domain-containing protein 1 (SAMHD1) tetramerization and the cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)–stimulator of interferon genes (STING) signaling pathway. As a result, type I interferonopathies are exacerbated. Aspirin inhibits cGAS-mediated signaling through cGAS acetylation. Acetylation contributes to cGAS activity control and activates IFN-1 production and nuclear factor-κB (NF-κB) signaling via STING. Aspirin and dapsone inhibit the activation of both IFN-1 and NF-κB by targeting cGAS. We define these as anticatalytic mechanisms. It is necessary to alleviate the pathologic course and take the lag time of the odds of achieving viral clearance by day 7 to coordinate innate or adaptive immune cell reactions.

2005-2020 장기 코호트 엔데믹 연구

바이러스 감염에 대응하는 인체의 면역 반응은 아세틸콜린 리셉터를 통해서 인터페론을 생성하여 바이러스를 퇴치합니다. 치매약물은 아세틸콜린 농도를 인체에서 높여줍니다. 기능이 억제되는 아세틸콜린 리셉터의 작용으로 노인들은 바이러스성 감염에 취약해지며 기관지염과 COPD가 증가하게 됩니다.

Bronchitis, COPD, and pneumonia after viral endemic of patients with leprosy on Sorok Island in South Korea - Naunyn-Schmiedeberg's Archives of PharmacologyViral respiratory diseases (VRDs) cause lung inflammation and inflammatory cytokine production. We study whether dapsone is responsible for its observed preventive treatment effects of the sustained viral RNA interferon response. Around 2008 and 2012, Korea’s Dementia Management Act stipulated drastic changes in the administration of dementia medication by medical staff. Participants were randomized and we compared leprosy patients with VRDs after prescribing dapsone as a standard treatment from 2005 to 2019. Significance was evaluated based on the dapsone-prescribed (+) subgroup and the dapsone-unprescribed (−) subgroup of the VRD diagnosed (+) and VRD undiagnosed (−) subgroup. We analyzed VRD ( +)/(− with dapsone (+)/(−) group and used a T-test, and designed the equation of acetylation with dapsone and acetylcholine (AA) equation. The 6394 VRD participants who received the dapsone intervention compared to the 3255 VRD participants in the control group demonstrated at T2 VRD (+) dapsone (−) (mean (M) = 224.80, SD = 97.50): T3 VRD (−) dapsone (+) (M = 110.87, SD = 103.80), proving that VRD is low when dapsone is taken and high when it is not taken. The t value is 3.10, and the p value is 0.004395 (significant at p < 0.05). After an increase in VRDs peaked in 2009, bronchitis, COPD, and pneumonia surged in 2013. The AA equation was strongly negatively correlated with the prevalence of bronchitis and chronic obstructive pulmonary disease (COPD): with bronchitis, r(15) = −0.823189, p = 0.005519, and with COPD, r(15) = −0.8161, p = 0.000207 (significant at p < 0.05). Dapsone treated both bronchitis and COPD. This study provides theoretical clinical data to limit acetylcholine excess during the VRD pandemic for bronchitis, COPD, and pneumonia.

미국립도서관 등록 코호트

https://clinicaltrials.gov/ct2/show/NCT04935476

https://clinicaltrials.gov/ct2/show/NCT04918914

Benefits of Using Dapsone in Patients Hospitalized with COVID-19Since the start of the SARS-CoV-2 pandemic, refractory and relentless hypoxia as a consequence of exuberant lung inflammation and parenchymal damage remains the main cause of death. We have earlier reported results of the addition of dapsone in this population to the standard of care. We now report a further chart review of discharge outcomes among patients hospitalized for COVID-19. The 2 × 2 table analysis showed a lower risk of death or discharge to LTAC (Long term acute care) (RR = 0.52, 95% CI: 0.32 to 0.84) and a higher chance of discharge home (RR = 2.7, 95% CI: 1.2 to 5.9) among patients receiving dapsone compared to those receiving the usual standard of care. A larger, blinded randomized trial should be carried out urgently to determine if dapsone indeed improves outcomes in COVID-19.

Specific Treatment Exists for SARS-CoV-2 ARDSThe COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), seems to be difficult to overcome. A pandemic of such a scale has not been seen since the 1918 influenza pandemic. Although the predominant clinical presentation is respiratory disease, neurological manifestations and sequelae are increasingly being recognized. We observed a case series of rapid recovery of ARDS within 24 h in the preliminary clinical features of COVID-19 ARDS-associated neurological disease. It was also noted that by 15 April, 2021, there was no SARS-CoV-2 ARDS on Sorok Island in South Korea, where lepers had been living together. We compared each of dapsone’s effects on humans and considered those of SARS-CoV-2. Dapsone showed different effects in the brain. The Sorokdo National Hospital reported a relationship between dapsone and the neuroinflammasome of Alzheimer’s disease (AD) in Sorok Island from January 2005 to June 2020. AD prevalence was low in the leprosy patient group who took dapsone regularly. The preliminary cross-sectional study of the trial group (22 subjects) and the control group (22 subjects) in the Hunt Regional Hospital reported the following results: The chi-square statistic is 5.1836. The p-value is 0.022801. The result is considered significant at p < 0.05. The results from the medical treatment from 21 December to 29 December 2020 were considered. The mortality rates at the ARDS onset stage were 0% with dapsone administered as a standard COVID-19 treatment and 40% without dapsone administered as a standard COVID-19 treatment, respectively. Based on the respiratory failure and sudden high death rate originating from the involvement of the brainstem, especially the pre-Bötzinger complex, dapsone can be used to significantly reduce the incidence of the cases of acute respiratory distress syndrome and other illnesses caused by SARS-CoV-2.

4,4′-Diaminodiphenyl Sulfone (DDS) as an Inflammasome CompetitorThe aim of this study is to examine the use of an inflammasome competitor as a preventative agent. Coronaviruses have zoonotic potential due to the adaptability of their S protein to bind receptors of other species, most notably demonstrated by SARS-CoV. The binding of SARS-CoV-2 to TLR (Toll-like receptor) causes the release of pro-IL-1β, which is cleaved by caspase-1, followed by the formation and activation of the inflammasome, which is a mediator of lung inflammation, fever, and fibrosis. The NLRP3 (NACHT, LRR and PYD domains-containing protein 3) inflammasome is implicated in a variety of human diseases including Alzheimer’s disease (AD), prion diseases, type 2 diabetes, and numerous infectious diseases. By examining the use of 4,4′-diaminodiphenyl sulfone (DDS) in the treatment of patients with Hansen’s disease, also diagnosed as Alzheimer’s disease, this study demonstrates the diverse mechanisms involved in the activation of inflammasomes. TLRs, due to genetic polymorphisms, can alter the immune response to a wide variety of microbial ligands, including viruses. In particular, TLR2Arg677Trp was reported to be exclusively present in Korean patients with lepromatous leprosy (LL). Previously, mutation of the intracellular domain of TLR2 has demonstrated its role in determining the susceptibility to LL, though LL was successfully treated using a combination of DDS with rifampicin and clofazimine. Of the three tested antibiotics, DDS was effective in the molecular regulation of NLRP3 inflammasome activators that are important in mild cognitive impairment (MCI), Parkinson’s disease (PD), and AD. The specific targeting of NLRP3 itself or up-/downstream factors of the NLRP3 inflammasome by DDS may be responsible for its observed preventive effects, functioning as a competitor.

Page updated

Report abuse