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July 2016 - February 2017
ilanajwriter.com, Rochester, NY, United States
- Freelance Writer and Scientific Editor
April 2015 - July 2015
Harvard School of Public Health
- Visiting Scientist
Conversion from asexual proliferation to sexual differentiation initiates the production of the gametocyte, which is the malaria parasite stage required for human-to-mosquito transmission. This protocol describes an assay designed to probe the effect of drugs or other perturbations on asexual replication, sexual conversion and early gametocyte deve...
The asexual forms of the malaria parasite Plasmodium falciparum are adapted for chronic persistence in human red blood cells, continuously evading host immunity using epigenetically regulated antigenic variation of virulence-associated genes. Parasite survival on a population level also requires differentiation into sexual forms, an obligatory step...
One of the critical gaps in malaria transmission biology and surveillance is our lack of knowledge about Plasmodium falciparum gametocyte biology, especially sexual dimorphic development and how sex ratios that may influence transmission from the human to the mosquito. Dissecting this process has been hampered by the lack of sex-specific protein ma...
The mechanisms underlying sexual stage switching in Plasmodium spp. have hitherto remained a mystery. However, two recent studies have revealed that an apicomplexan-specific DNA-binding protein is essential for the initiation of this cell fate decision, ultimately providing the malaria community with a novel and important tool in the battle to prev...
Humans and mice infected with different Plasmodium strains are known to produce microvesicles derived from the infected red blood cells (RBCs), denoted RMVs. Studies in mice have shown that RMVs are elevated during infection and have proinflammatory activity. Here we present a detailed characterization of RMV composition and function in the human m...
The availability of a large number of expressed sequence tags (ESTs) has facilitated the development of molecular markers in members of the grass family. As these markers are derived from coding sequences, cross-species amplification and transferability is higher than for markers designed from genomic DNA sequences. In this study, 919 EST-based pri...
Lead contamination in the urban environment is a continuing serious public health concern. Historically lead entered the urban residential area though paint pigment and gasoline additives. This legacy persists as the two most important lead sources that affect children in the urban environment: contaminated paint residue and contaminated soil. One...
The respiratory problems that COVID-19 causes have some unusual characteristics. Here's a quote from https://www.hippoed.com/em/ercast/episode/tbd3/covid19weingart:
"One of the most astounding things about treating COVID-19 patients is how well they can look with extreme hypoxia. Patients with saturations of 50% (and consistent ABGs) can be talking, mentating normally, and have otherwise normal vital signs. Thus, this term: “the happy hypoxemic”. It is not well understood why these patients are able to tolerate such low sats without having compensatory measures, such as tachycardia." Clinicians are increasingly talking about these "happy hypoxemics" or "silent hypoxemics" with COVID-19. Not all patients, but a significant proportion fall into this category, at least temporarily. Here are my questions, for discussion:
Why can these patients tolerate such low oxygen saturations? Or can't they- are they on the edge of a crash, but don't know it? There are many stories of patients who thought they were doing ok at home, and sometimes even thought they were getting better, then declined suddenly and died at home or in the ambulance. The same thing is reported with people in the hospital who appear to be doing ok on just oxygen, but then they suddenly decline.
Why don't these patients have compensatory mechanisms, such as tachycardia, faster breathing, etc? Is it because they often have normal CO2 levels, or because of some other dysfunction in triggering compensatory mechanisms?
How can these patients have normal mental state with such low oxygen saturations? Or are their oxygen saturation readings not representative of their true condition, for some reason?
Does this mean no one with COVID-19 should be sent home without at least a pulse oximeter and instructions on when to seek help? Sending people home if they have less severe symptoms is standard in the US today. But people may not be able to tell when they need medical attention, especially if they can have very low oxygen levels without significant distress.
The following is a helpful discussion of the likely respiratory physiology going on with COVID patients. It proposes that natural variation among humans may be responsible for differences in responses to COVID-19- see the chart near the bottom:
I would think the "happy hypoxemics" are actually the worst off in that chart, and that they would be likely to decline. And it might imply that if you could induce either better HPV, stronger ventilatory drive, or both, you could help these patients move into one of the other categories.
Would it be helpful to induce compensatory measures? During pregnancy, the body adapts to take in 40% more oxygen by changing the set point for CO2 and other changes. The body also adapts to handle the lower oxygen conditions at high altitude. For people who don't adapt well on their own, there are ways to speed acclimation by inducing compensatory measures (acetazolamide, for example). Could we mimic this for COVID-19?