NADPH oxidase Covid-19 Oxygen treatment?

Severe COVID-19 infection leads to respiratory complications, which may adversely affect the supply of oxygen to the brain. Due to insufficient supply of oxygen, the central nervous system may get adversely affected resulting in various degree of neural damage. Thus, the damage to the brain due to respiratory complications may lead to adverse neuroendocrinological change.

Respected sir/madam

In our covid facility when patient admitted we do d-dimer, LDH and s. Ferritin along with chest x ray and other investigations

Usually elderly people with comorbid conditions we found high d dimer, LDH and s. Ferritin. Very few young patients had it compared to elderly.

We assumed that high LDH and ferritin is due to inflammation and started them on injection dexamethasone 6mg IV OD and patients with high d dimer started on injection clexane/heparin s/c.

patient whos initially d dimer, LDH and serum ferritin were high had more sever symptoms, required oxygen and high flow oxygen, nebulisation and other respiratory support medications. They were hospitalised more than patients with normal initial values.

Share you opinions about this please..Thank you

I am stimulating mouse bone marrow PMN with PMA in a luminol ROS detection system, and reading the luminescence with a luminometer for 1 hour. I always get two peaks in my curve (an sharp, immediate peak and a broad sustained peak), but I'm not sure why. All the literature I read only has one, sharp peak followed by a steady decline back to zero. Can anyone tell me why this is happening, or suggest ways to get more consistent results?

Do you know if (anonymised) clinical high-frequency datasets of COVID-19 patients, such as pulmonary function, blood oxygen level, blood pressure, cardiac interbeat interval etc., are available anywhere for download and analysis?

I've seen many links to GitHub repositories, but they only contain daily statistics of confirmed/recovered/death cases for various regions worldwide, not the clinical high-frequency time series.

In pulmonary failure especially due to thrombosis in complicated corona infection when there is no or very little gaseous exchange through lung, in spite of huge oxygen supply by ventilator, only way to remove carbon dioxide from blood and oxygenation it is by using an extra corporeal method like hemo-dialyser will be effective. Another weaker method will be by infusing oxygenated iv fluid.

I'm using the probes DCFDA to measure ROS production in hippocampal slices 200 um thik, treated with OGD (oxygen and glucose deprivation), I'm using DCFDA 30 uM and TMRE 100 nM. The point is that often the DCFDA signal is stronger in the control than in the OGD slices. What could be wrong? Do you have any protocol?

Many theories are proposed for the spreading of 'Mucormycosis' or 'Black Fungus'. Although, hot and humid weather is considered as one of the reasons to develop this infection which has been declared as Epidemic in India.

I am curious to know the followings:

1) Whether oxygen, humidifiers and oxygen delivery masks are the contributing factors if they are not properly sterilized or changed frequently as per the protocol ?

2) Are there any research evidence that 'Mucormycosis' may occur due to the use of Industrial Grade Oxygen instead of Medical Grade Oxygen?

..

I am currently testing certain compounds' effects on neutrophil activation and ROS generation (i.e. luminol-based chemiluminescence) is one of my readouts. Both PMA and LPS are included as positive controls. However, donor-dependent variable response to LPS has been observed. Is there a way for me to minimise or eliminate this problem?

Separately, my compound-of-interest reduced ROS generation by neutrophils when compared to no treatment control (spontaneous ROS observed). It has been reproduced several times regardless of response to LPS. Is there a good biological negative control I could use to verify this, instead of DPI or TEMPOL?