They should primarily focus on T-cells (as T-cells is most important in anti-viral and anti-tumor activity), reagents such as IL-2 and T-cell costimulators need to be used, such as 41BB (CD137), CD28, OX40L...Stimulating B-cells will be important as well. I remember when we grow T-cell ex vivo, we always need to coat IL-2 on the tissue culture plate for T-cells to grow. High dosage of Mucinex should also be added to dilute the mucous in the lung.
To summarize (medications that can treat and support): Early Remdesivir treatment Mucinex Vit C IL-2 (such as Aldesleukin) Maybe other T-cell costimulators
This does not make sense if the absolute B and T cells are all decreased. Where the cytokines and chemokines are made from? Has anyone ever tested all of the cytokine and chemokine levels in real patients? Are high levels of cytokines negatively correlate with the prognosis? 炎症风暴 is only an assumption, and I don't think the pathology findings actually support that.
In the autopsy report, the lung has numerous macrophages and giant cells formation. Not sure if lots of lymphocytes are there and being activated. In fact, I suspect there is immune anergy.
In addition, peripheral blood does not harbor lots of lymphocytes, it is the lymphoid organs such as lymph node, spleen, etc that store all of the lymphocytes.
IL-1alpha, IL-6, IL-10 will dramatically increase and other cytokines such as IL-2, IL-3, IL-5, IL-15, IP-10 IFN-gama, G-CSF and GM-CSF, MCP-1 can also upregulated if it is cytokine storm
IL-1alpha, IL-6, IL-10 will dramatically increase and other cytokines such as IL-2, IL-3, IL-5, IL-15, IP-10 IFN-gama, G-CSF and GM-CSF, MCP-1 can also upregulated if it is cytokine storm fish_fish 发表于 2/27/2020 2:00:56 PM
In CAR-T therapy, cytokine storm is common and if the patient survives that, the prognosis is good. The question is how much research has been done to see if cytokine storm in the majority of the coronavirus patients is present, and what is the real effect of the cytokines store? (effective vs ineffective) If it is ineffective, how to re-direct the immune system to mount the right reaction is the real question.
There is no real pathology report in this link. They only did the autopsy, everything is gross (sample collection). It is impossible to draw a conclusion of 过度炎症反应 only upon gross examination.
There is no real pathology report in this link. They only did the autopsy, everything is gross (sample collection). It is impossible to draw a conclusion of 过度炎症反应 only upon gross examination. kamchee 发表于 2/27/2020 2:17:28 PM
I think you are welcome to educate us here, but right now it is urge to feedback to cdc or relevant parties. Perhaps you have done so already, then we salute you!
I think you are welcome to educate us here, but right now it is urge to feedback to cdc or relevant parties. Perhaps you have done so already, then we salute! noshock 发表于 2/27/2020 2:42:42 PM
I am just sharing my thoughts (based on my background and experience) here. I dialed in one of the state department of health meeting regarding the coronavirus, and in the Q&A sections, I raised my concerns of not testing candidates without travel or close contact history, and no one responded to me. Although they responded to people before and after me (it is all typing). I don't really have any channel to voice my suggestions right now. CDC is a department full of politics. If it eventually come to the hospital that I work at, I could provide some suggestions to some of the clinicians who are treating the patients with coronavirus locally. That is all what I could do.
I am just sharing my thoughts (based on my background and experience) here. I dialed in one of the state department of health meeting regarding the coronavirus, and in the Q&A sections, I raised my concerns of not testing candidates without travel or close contact history, and no one responded to me. Although they responded to people before and after me (it is all typing). I don't really have any channel to voice my suggestions right now. CDC is a department full of politics. If it eventually come to the hospital that I work at, I could provide some suggestions to some of the clinicians who are treating the patients with coronavirus locally. That is all what I could do.
kamchee 发表于 2/27/2020 2:50:09 PM
Your post is the most serious discussion here, almost par academic level. I can’t judge the full meaning of it, but will try to get someone’s attention. I am curious, do you see any reference in the literature?
Treatment for SARS There's currently no cure for SARS, but research to find a vaccine is ongoing. A person suspected of having SARS should be admitted to hospital immediately and kept in isolation under close observation. Treatment is mainly supportive, and may include: assisting with breathing using a ventilator to deliver oxygen antibiotics to treat bacteria that cause pneumonia antiviral medicines high doses of steroids to reduce swelling in the lungs There's not much scientific evidence to show that these treatments are effective. The antiviral medicine ribavirin is known to be ineffective at treating SARS. https://www.nhs.uk/conditions/sars/
https://onlinelibrary.wiley.com/doi/full/10.1002/path.4458 In SARS, the development of severe lower respiratory tract disease correlates partly with aberrant immune responses, with unbalanced cytokine and chemokine profiles 39, 50, 89, 90. The levels of both cytokines and chemokines in the blood are elevated: IL‐1, IL‐6, IL‐8, IL‐12, IFNγ, monocyte chemotactic protein (MCP)‐1 (or CC‐motif ligand 2, CCL2), monokine induced by IFNγ (MIG), IFN‐inducible protein (IP‐10, or CXCL10), and transforming growth factor (TGF)β 89-94. Some of these chemokines are important for chemotaxis and activation of neutrophils and monocytes 95-97, which corresponds with the infiltration of these cells in the respiratory tract of human SARS cases 83, 91, 92, 98.
2019‐nCoV Initial plasma IL‐1β, IL‐1Rα, IL‐7, IL‐8, IL‐9, IL‐10, basic FGF, GCSF, GMCSF, IFNγ, IP10, MCP1, MIP1A, MIP1B, PDGF, TNF‐α, and vascular endothelial growth factor concentrations were higher in 2019‐nCoV‐infected patients as compared to healthy controls. Moreover, ICU patients showed higher plasma levels of IL‐2, IL‐7, IL‐10, GSCF, IP10, MCP1, MIP1A, and TNF‐α than non‐ICU patients.38 These results suggest that immunopathology may also play a relevant role in the development of disease severity. https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.25709
I remember when we grow T-cell ex vivo, we always need to coat IL-2 on the tissue culture plate for T-cells to grow.
High dosage of Mucinex should also be added to dilute the mucous in the lung.
To summarize (medications that can treat and support):
Early Remdesivir treatment
Mucinex
Vit C
IL-2 (such as Aldesleukin)
Maybe other T-cell costimulators
The recent pathology finding supported viral effect as the cause of death, not cytokine storm.
哪里看到的病理分析？我看到的文章说王福生发表的第一篇病理文章中提到TH17和CD8过度活化，提示过度炎症反应。
There are viral-associated change and macrophage reactions including giant cell formation. B and T lymphocytes are suppressed by number.
准备去囤点
这个是OTC药吗，有哪些作用？
It is an OCT, it reduces the viscosity of secretions in the respiratory tract.
This does not make sense if the absolute B and T cells are all decreased. Where the cytokines and chemokines are made from? Has anyone ever tested all of the cytokine and chemokine levels in real patients? Are high levels of cytokines negatively correlate with the prognosis?
炎症风暴 is only an assumption, and I don't think the pathology findings actually support that.
In the autopsy report, the lung has numerous macrophages and giant cells formation. Not sure if lots of lymphocytes are there and being activated.
In fact, I suspect there is immune anergy.
Thanks
In addition, peripheral blood does not harbor lots of lymphocytes, it is the lymphoid organs such as lymph node, spleen, etc that store all of the lymphocytes.
In CAR-T therapy, cytokine storm is common and if the patient survives that, the prognosis is good. The question is how much research has been done to see if cytokine storm in the majority of the coronavirus patients is present, and what is the real effect of the cytokines store? (effective vs ineffective) If it is ineffective, how to re-direct the immune system to mount the right reaction is the real question.
研究团队在论文中写道： “ 2019冠状病毒病 病理特征与严重急性呼吸综合征（SARS）、中东呼吸综合征（MERS）的冠状病毒感染非常相似。 ”具体而言，研究人员认为 X 线片显示患者肺炎进展迅速，左肺和右肺之间存在一些差异。此外，肝组织显示中度微血管脂肪变性和轻度小叶活动，但没有确凿的证据支持新冠病毒感染或药物性肝损伤是病因。心脏组织未见明显组织学改变，提示新冠病毒感染可能不会直接损害心脏。虽然不推荐常规使用皮质类固醇治疗新冠肺炎，但研究组根据对肺水肿和肺透明膜形成的病理诊断，重症患者应考虑及时、适当地使用皮质类固醇和呼吸机支持，以防止 ARDS 的发生。 同时，淋巴细胞减少是 COVID-19 患者的常见特征，这很可能与疾病严重程度和死亡率有关。
There is no real pathology report in this link. They only did the autopsy, everything is gross (sample collection). It is impossible to draw a conclusion of 过度炎症反应 only upon gross examination.
上压制免疫系统的药，象以前sars 那样，但很多后遗症，极大降低生活质量。
所以要搞清这个是不是炎症风暴致死的很重要。
Where is your link?
是上激素不是抗生素吧？
激素作用就是抑制免疫细胞产生细胞因子，如果激素有作用，能救活重症病人，就说明抑制免疫是对的。如果激活免疫，就会产生更多细胞因子，加重cytokine storm
I saw it in wechat
Mucinex是化痰吗？另外EmergenC VC tablet 有用吗？多吃水果蔬菜补充VC不行吗？
Mucinex是化痰吗 (yes) ？另外EmergenC VC tablet 有用吗 (yes)？多吃水果蔬菜补充VC不行吗 (probably not enough)？
I am just sharing my thoughts (based on my background and experience) here. I dialed in one of the state department of health meeting regarding the coronavirus, and in the Q&A sections, I raised my concerns of not testing candidates without travel or close contact history, and no one responded to me. Although they responded to people before and after me (it is all typing). I don't really have any channel to voice my suggestions right now. CDC is a department full of politics. If it eventually come to the hospital that I work at, I could provide some suggestions to some of the clinicians who are treating the patients with coronavirus locally. That is all what I could do.
Your post is the most serious discussion here, almost par academic level. I can’t judge the full meaning of it, but will try to get someone’s attention. I am curious, do you see any reference in the literature?