Fungal infections are a cause of morbidity in humans, and despite the availability of a range of antifungal treatments, the mortality rate remains unacceptably high. Although our knowledge of the interactions between pathogenic fungi and the host continues to grow, further research is still required to fully understand the mechanism underpinning fungal pathogenicity, which may provide new insights for the treatment of fungal disease. There is great interest regarding how microbes induce programmed cell death and what this means in terms of the immune response and resolution of infection as well as microbe-specific mechanisms that influence cell death pathways to aid in their survival and continued infection. Here, we discuss how programmed cell death is induced by fungi that commonly cause opportunistic infections, including Candida albicans, Aspergillus fumigatus, and Cryptococcus neoformans, the role of programmed cell death in fungal immunity, and how fungi manipulate these pathways.

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During the management of a 3 kg term black female infant whose chylothorax was diagnosed at 7 days of age, a total of 450 ml of chyle was removed by repeated thoracentesis before spontaneous heal ing occured. The total n mber of lymphocytes removed Y during 18 days was greater than 10 . Monoclonal antibody studies showed 95% of these cells were T-lymphocytes which were functionally immature as evidenced by their non-responsiveness to mitogen. There was no associated peripheral blood lymphopenia. Nevertheless, peripheral T-cells were abnormal as shown by lack of sheep RBC rosette formation and lack of response to mitogens. The thymus which was absent during the 18 days of therapy, reappeared 2 weeks after disappearance of the chylothorax accompanied by normalization of peripheral T-lymphocyte functions.Loss Detroit.Intravenous administration of ritodrine has been shown to prolong pregnancy in selected patients. However the drug has been associated with maternal cardiovascular and mLtabolic derangements. If tocolytic therapy fails and the neonate delivers soon after ritodrine is discontinued significant drug levels could increase neonatal morbidity.he DurDose of this studv was to examine the following neonatal out'combs: Apgar score min. and 5 min., neonatal pH, plasma bicarbonate,hypotension, hypoglycemia, respiratory distress syndrome & neonatal mortality in infants exposed to IV ritodrine within 12 hours of delivery. Fifty-eight neonates delivered within 12 hours of discontinuing intravenous maternal ritodrine were matched for birthweight and gestational age with 58 control infants without ritodrine exposure. The study infants had a mean G+ of 32.8 + 2.8 wks & a mean BW of 1744 + 512 gm. The potentlal effect-of the total ritodrine dose used and the drug discontinuance to delivery intervals (DDDI) on the 8 neonatal outcomes were evaluated The frequencies of maternal medical and obstetric complications were similar in both groups PROM ar4 prolon ed rupt re of membranes >12 hours were moye.co&non, in t JnfroK