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“Purpose of review
Type 1 diabetes (T1D) is an autoimmune disorder which affects millions around the world. The incidence of T1D in children is increasing worldwide at a rate that cannot be explained by genetics alone. This review explores the recent research regarding possible causes of this epidemic.
Recent selleck products findings
Investigation into T1D epidemiology has recently focused on several hypotheses. These theories include the role of infections, early childhood diet, vitamin D exposure, environmental pollutants, increased height
velocity, obesity, and insulin resistance in the risk for T1D. Over the past year, the evidence has strengthened for early childhood infections, dietary proteins, and insulin resistance as risk factors
for T1D, but not for vitamin D exposure or environmental pollutants.
Summary
Investigation into the source of the current epidemic of T1D has shed light on several possible causes, but has not provided definitive answers, yet.”
“Background and objective:
The expression of Fc receptors for IgG (Fc gamma Rs) on neutrophils, including CD16, CD32 and CD64, may be modulated in response to sepsis. We investigated the expression of Fc gamma Rs on neutrophils and procalcitonin (PCT) find more as biomarkers of sepsis among critically ill patients.
Methods:
This prospective study was conducted in a 24-bed respiratory intensive care unit between July 2007 and June 2008. Critically ill patients requiring mechanical ventilation were enrolled and categorized into three groups: those with systemic inflammatory response syndrome (SIRS), those with severe sepsis and those with septic shock. Expression of Fc gamma hypoxia-inducible factor pathway Rs on neutrophils was quantitatively measured by flow cytometry immediately after enrolment of the patient. Serum PCT levels were also measured. Receiver
operating characteristic (ROC) curves were used to evaluate the performance of Fc gamma R expression and PCT as biomarkers of sepsis.
Results:
Sixty-six patients were enrolled, including 11 with SIRS, 31 with severe sepsis and 24 with septic shock. Nineteen healthy volunteers served as normal controls. CD64 was upregulated, CD16 was downregulated and CD32 remained unchanged during sepsis. CD64 expression and the ratio of CD64/CD16 increased significantly with the severity of sepsis. However, serum PCT levels were not significantly different between SIRS and severe sepsis patients. CD64, CD64/CD16 and PCT all significantly predicted sepsis, septic shock and bacteraemia. As assessed using ROC curves, CD64 was better than PCT for differentiating SIRS from severe sepsis and septic shock. CD64 and CD64/CD16 were associated with mortality.
Conclusions:
CD64 and CD16 were differentially modulated by sepsis. CD64, CD64/CD16 and PCT may be biomarkers of sepsis. CD64 was better than PCT for identifying patients who required treatment with antibiotics.