A novel concept in DNA vaccine design is the creation of an inhaled DNA plasmid construct containing a portion of the coronavirus spike protein for treatment and vaccination. The secretion of a spike protein portion will function
One approach to understanding the physiologically relevant events during the induction of an immune response is to identify genes that are expressed when the immune system first encounters antigen. Such an investigation requires a naive but fully functional immune system, and the fetal lamb provides these conditions during the last trimester of gestation. 'Intestinal segments,' containing a jejunal Peyer's patch, were surgically prepared in fetal lambs (>120 days gestation) and individual 'intestinal segments' were injected with either culture medium or infectious bovine rotavirus. Peyer's patch tissue was collected 18 h postinfection. Histology and virus culture confirmed that bovine rotavirus had infected the mucosal epithelium. RNA was extracted from jejunal Peyer's patch tissue and mRNA differential display was used to identify genes expressed following rotavirus infection. Ten cDNAs were identified by differential display and these cDNAs were isolated, cloned, and sequenced. One of the cDNAs sequenced, displayed homology to the gene encoding the sperm surface protein Sp17. Differential expression of this gene in antigen-exposed jejunal Peyer's patches was confirmed by Northern blot and RT-PCR. The complete sequence for sheep Sp17 mRNA was obtained from a lambda cDNA library, prepared from the jejunal Peyer's patch of a young lamb. Sp17 expression was detected by RT-PCR in a variety of mucosa-associated lymphoid tissues but not in primary or other secondary lymphoid tissues. Thus, the fetal lamb model may be appropriate for identifying genes relevant to mucosal immunity.
Drug toxicity is traditionally treated by reducing the amount of the drug absorbed, enhancing elimination, and providing supportive care. Once the drug has been absorbed, there are few methods that help decrease morbidity and mortality caused by a toxic drug level. Albumin infusion is a new approach that changes that, as it can rapidly reverse a toxic drug level back to a therapeutic level. It is believed with most drugs that the toxic effects are related to the total amount of the free drug. In this method, albumin binds to the free drug and acts as a reservoir or depot from which the drug is slowly released to the free form, thereby limiting the effects of drug toxicity. In this case report, an elderly female patient who experienced phenytoin toxicity was treated with albumin infusion, after which her phenytoin level returned to a therapeutic level with corresponding improvements in her symptoms. Based on our calculations, it was predicted that a small amount of albumin would reverse the patient's toxic symptoms. With this approach, the patient's toxic symptoms improved when free phenytoin levels dropped from 15 to 8 μmol/L. Albumin infusion is a promising new therapy that can rapidly reverse a toxic drug level back to a therapeutic level by binding the free drug to albumin.
Currently chemotherapy dosing is determined by a patient's weight, height and renal function. Dosing chemotherapy based on these parameters is generally effective, assuming all other physiological conditions are normal. In hypoalbuminaemia patients a decrease in albumin often results in more severe side-effects, since this may lead to higher chemotherapy free drug levels. A new method to dose chemotherapy based on a patients albumin will maintain the same effective free drug levels as in patients with normal albumin. This can reduce the severity of chemotherapy side-effects and may: ensure better outcomes for patients since it allows them to complete their course of chemotherapy without interruption, decrease the cost and complications associated with severe side-effects, and will allow for enhanced treatment options.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) undergoes blood type specific glycosylation which has implications for infection susceptibility and replication without detection from the immune system. SARS-CoV-2 hijacks the host cell glycotransferase resulting in spike protein glycosylation resembling blood type antigens. Infection risk correlates to blood types that do not have anti-A and/or anti-B antibodies similar to that seen for ABO blood type recipients. The universal recipient AB is highly susceptible to infection lacking both anti-A and B antibodies, whereas blood type O has both antibodies resulting in less risk of infection. Once infected, SARS-CoV-2 obtains the blood type specific glycosylation of the host resulting in an effective camouflage against immune system recognition. Decoding the link between blood type and coronavirus disease 2019 (COVID-19) susceptibility exposes a role for miglustat a glycosyltransferase inhibitor in treatment. Use of the FDA-approved glycosyltransferase inhibitor miglustat can inhibit spike protein glycosylation revealing the SARS-CoV-2 virus for immune system recognition.
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