Therapeutics

LITERATURE

코로나 치료 시리즈

Jong Hoon, LEE. 코로나 사망자수를 줄여주는 아스피린: 코로나 치료제 시리즈 1. 2022. https://books.google.co.kr/books?id=E2ViEAAAQBAJ.

JONG Hoon, LEE. 코로나 호흡기질환을 예방치료하는 답손: 코로나 치료제 시리즈 2. 2022. https://books.google.co.kr/books?id=JOBiEAAAQBAJ.

Lee, J.H. 잠자는 나라 시리즈 3. 코비드-19 호흡부전 치료법: 천치와 수재가 코로나 바이러스를 만났을 때. 2021. https://books.google.co.kr/books?id=ESs_EAAAQBAJ.

Jong Hoon, L. E. (2022). 코로나 호흡기바이러스 2형 질병 (COVID-19) 치료 기전, infomedpress. https://books.google.co.kr/books?id=1E96EAAAQBAJ

Jong Hoon, LEE. 코로나 호흡기바이러스 2형 질병 (Covid-19) 병리 기전: 코로나 병리를 알면 쉽게 예방 및 치료된다. infomedpress, 2022. https://books.google.co.kr/books?id=Hn13EAAAQBAJ.

발표 논문

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.

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.

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.

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.

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…

백신 부작용과 코비드-19 치료법은 증상은 달라도 근본 발병 기전을 공유하기 때문에 치료법이 거의 같습니다. 이를 설명하는 논문입니다.

우리가 사용하는 백신에 대한 안정성에 대한 평가는 아직도 신뢰성 면에서 여전히 부족한 상태입니다. 관련 연구도 여전히 미진한 상태이고 너무 짧은 기간 빠른 개발에 따라서 발생한 문제점 이었습니다.

백신 저항성이 높아져서 논문에 발표하는 것조차 금기시 되었으나 이제 발표하게 되었습니다.

Nguyen NH, Tran KM, Jong LH, Le STD, Nguyen AQ, Duong DM, Nguyen TD, Nguyen LNT, Dam LTP, Nguyen TNM. Clinical characteristics of COVID-19 patients treated in emergency COVID-19 hospitals in Vietnam: Experience from Phutho province, Vietnam. Int J Med Sci 2024; 21(6):1072-1078. doi:10.7150/ijms.94461. https://www.medsci.org/v21p1072.htm

Study Cohort

Critical Care Results of SARS-CoV-2 ARDS by Dapsone and Standard COVID-19 Treatment - Full Text View - ClinicalTrials.govCritical Care Results of SARS-CoV-2 ARDS by Dapsone and Standard COVID-19 Treatment - Full Text View.

Dapsone Coronavirus SARS-CoV-2 Trial (DAP-CORONA) COVID-19 - Full Text View - ClinicalTrials.govDapsone Coronavirus SARS-CoV-2 Trial (DAP-CORONA) COVID-19 - Full Text View.

Article for COVID-19, Long Covid Treatment

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…

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.

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