PubMed · 3500884
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M Gaglio, O Mazzone, V Crisafulli. [Low-grade fevers].. https://pubmed.ncbi.nlm.nih.gov/3500884/
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The body's ability to regulate core temperature depends on both host (internal) and environmental (external) factors. Although athletes are commonly thought to be most at risk for heat illnesses, children and the elderly are particularly vulnerable. Heat cramps, which are caused by fluid and electrolyte imbalances, are treated with massage, and fluid and electrolyte replacement. Heat exhaustion occurs both as water- and sodium-depleted types, with associated symptoms such as malaise, vomiting, and confusion. Treatment involves taking the affected person to a cool environment and replacing fluids and electrolytes if needed. In more serious cases, intravenous hydration may be necessary, although monitoring of serum sodium levels is important to prevent cerebral edema. If not treated promptly, heat exhaustion may evolve into heatstroke, a deadly form of heat illness. Heatstroke occurs in classic and exertional forms and is present when the core body temperature exceeds 40 degrees C (104 degrees F). The patient may experience cardiac arrhythmias, rhabdomyolysis, serum chemistry abnormalities, disseminated intravascular coagulation, and death. Heatstroke is a medical emergency that should be treated immediately with temperature-lowering techniques such as immersion in an ice bath or evaporative cooling. Fluid resuscitation is important but should be closely monitored, and renal function may need to be protected with mannitol and diuretics. It is important to be vigilant for heat illnesses because they occur insidiously but progress rapidly.
Heat shock (HS) induces a wide variety of biological processes, including inhibition of protein synthesis, elevated expression of heat shock proteins, induction of thermotolerance, and apoptotic cell death in a dose-dependent manner. We compared phosphorylated proteins in heat-shocked and thermotolerant cells using proteome analysis. After HS treatment of control RIF-1 and their thermotolerant derivatives, TR-RIF-1 cells, cellular proteins were separated by two-dimensional gel electrophoresis and the phosphorylated proteins were detected with the anti-phosphotyrosine antibodies. We found that 93 proteins showed significant changes in phosphorylation between control and thermotolerant cells as a function of recovery time after HS; we identified 81 of these proteins with peptide mass fingerprinting using MALDI-TOF MS after in-gel trypsin digestion. These phosphorylated proteins exhibit various cellular functions, including chaperones, ion channels, signaling molecules, in transcription and translation processes, in amino acid biosynthesis, oxidoreduction, energy metabolism, and cell motility or structure, suggesting that HS turns on the various signaling pathways by activating protein-tyrosine kinases (PTKs). Of these, 20 proteins were previously identified phosphorylated proteins and 64 were newly identified. These proteins can be grouped into three families: 1) proteins highly phosphorylated in TR-RIF-1 cells at basal level and phosphorylated more significantly by HS in RIF-1 than TR-RIF-1; 2) proteins highly phosphorylated in control RIF-1 cells at basal level and phosphorylated more easily by HS in TR-RIF-1 than in RIF-1 cells; and 3) proteins with a similar basal phosphorylation level in both RIF-1 and TR-RIF-1 cells and responding to HS similarly in both cells. Most of the phosphorylated proteins are presumably involved in HS signaling in different ways, with the first and second families of proteins influencing thermotolerance. The possible tyrosine phosphorylation sites, the possible PTKs phosphorylating these proteins, and the proteins binding to these phosphorylated sites were predicted by the Netphos, ScanProsite, and Scansite programs. These results suggest that HS can activate various PTKs and HS responses can be regulated by phosphorylations of proteins having various functions.
Thermo-neutrality is one of the major environmental factors affecting a premature or low-birth-weight neonate inside an incubator. Severe temperature differences inside an incubator lead to neonate heat loss, hypothermia and apnoea, which are closely related to air flow and air velocity. In the study, flow visualisations, hot-wire velocity measurements and computational fluid dynamics simulate the airflow inside a neonatal incubator. An anatomically correct neonate model is designed using a three-dimensional laser scanner system and a rapid prototyping machine. Flow visualisations demonstrate that large-scale rotating airflow is produced inside the chamber, and a number of small, stationary eddies are found in regions between the air inlet and the neonate. Hot-wire measurements show that air velocities along the long inlets are not uniform. Computational fluid dynamics show relatively uniform temperatures of about 34 degrees C on the neonate's anterior aspect and the highest temperature of 36.1 degrees C at the right armpit and the crotch. Flow fields from airflow visualisations, hot-wire measurements and computational fluid dynamics are very similar, both qualitatively and quantitatively. The small eddies produced between the neonate and the mattress could interfere with convective and evaporative heat transfers from the neonate. Therefore it is important to eliminate eddies around the neonate in future designs of neonatal incubators.