High frequency oscillation in newborn infants with respiratory failure

Objective: To report ventilation strategies, survival and complications in 39 outborn infants treated with high frequency oscillatory ventilation (HFOV).
Methodology Data were collected prospectively between 1 May 1992 and 31 December 1993 on all infants treated with HFOV who had severe respiratory failure despite optimal conventional ventilation.
Results Twenty-eight out of 39 (72%) survived. Of the 15 infants with birthweights <1500g, eight survived. Best survival rates were for infants with pulmonary interstitial emphysema with air leak (4/5) and for infants of birthweight >1500g with hyaline membrane disease (8/8), and meconium aspiration syndrome (7/7). Three infants deteriorated while on HFOV and required extracorporeal membrane oxygenation. Complications were: (i) development of pulmonary interstitial emphysema (1); (ii) recurrence of pneumothorax (3); (iii) hypotension (2); and (iv) bronchopulmonary dysplasia (9). One of the eight infants weighing <1500g who received HFOV in the first week of life developed periventricular haemorrhage.
Conclusion The initial results of HFOV for severe respiratory failure were encouraging although a learning curve was encountered with its introduction.     

Control of Bcl-2 expression by reactive oxygen species

Reactive oxygen species (ROS) mediate apoptosis in many different cell types. We have previously shown that the antioxidant Mn(III) tetrakis(5,10,15,20-benzoic acid)porphyrin (MnTBAP) decreased intracellular ROS and prevented the apoptosis of activated T cells in vitro. To determine the mechanism(s) by which MnTBAP afforded such protection, we used Affymetrix (Santa Clara, CA) gene arrays to compare gene expression in T cells activated with staphylococcal enterotoxin B in vivo then cultured with or without MnTBAP. This analysis showed that the antioxidant increased the expression of Bcl-2, an antiapoptotic molecule whose levels are normally decreased by T cell activation. Culture with MnTBAP revealed a tight inverse correlation between the levels of Bcl-2 and ROS within T cells. In vivo, production of ROS in activated T cells occurred before Bcl-2 down-regulation. Furthermore, MnTBAP's ability to prevent death required the expression of Bcl-2 in most T cells. Finally, neither ROS production nor the effects on Bcl-2 expression required Bim, the Bcl-2 antagonist that mediates the death of activated T cells in vivo. Taken together, our results suggest that ROS sensitize T cells to apoptosis by decreasing expression of Bcl-2.     

Nicotine gum-induced atrial fibrillation

A 39-year-old man with no prior history of atrial fibrillation was hospitalized with atrial fibrillation and a rapid ventricular rate. For the 7 months before presentation, he had been chewing nicotine polacrilex gum on his own. The week he first developed palpitations, he was chewing more than 1 piece of nicotine Polacrilex gum per hour during work. His diagnostic work-up during hospitalization found no cause for atrial fibrillation. He was cardioverted to sinus rhythm. At 6-month follow-up, he had not renewed chewing nicotine polacrilex gum, was in sinus rhythm, and had no history of palpitations. The temporal relation between more frequent gum usage and the excessive consumption of nicotine polacrilex chewing gum with a probable high serum nicotine level at the time the patient developed his first episode of atrial fibrillation suggests a causal relationship.     

A descriptive study of youth risk behavior in urban and rural secondary school students in El Salvador

Background  

Adolescence is an important stage of life for establishing healthy behaviors, attitudes, and lifestyles that contribute to current and future health. Health risk behavior is one indicator of health of young people that may serve both as a measure of health over time as well as a target for health policies and programs. This study examined the prevalence and distribution of youth health risk behaviors from five risk behavior domains–aggression, victimization, depression and suicidal ideation, substance use, and sexual behaviors–among public secondary school students in central El Salvador.     

Chemoprevention of spontaneous tumorigenesis in nullizygous p53- deficient mice by dehydroepiandrosterone and its analog 16alpha-fluoro- 5-androsten-17-one

Transgenic mice with both alleles of the p53 tumor suppressor gene product 'knocked out' by gene targeting are susceptible to early development of tumors, chiefly lymphomas and sarcomas. Compared with the control group, administration of dehydroepiandrosterone (DHEA) at 0.3% of the diet to male p53-deficient mice extended their lifespan by delaying death due to neoplasms (from 105 to 166 days on study, P = 0.002), primarily by suppressing lymphoblastic lymphoma (from 45 to 6% of neoplastic deaths, P = 0.010). Treatment with a synthetic DHEA analog, 16alpha-fluoro-5-androsten-17-one (compound 8354), at 0.15% of the diet also increased lifespan, to 140 days for mice that developed tumors (P = 0.037). The effects of these steroids on lifespan and tumor development did not appear to be strongly related to inhibition of food consumption and weight gain, in that a group pair-fed with control diet to the reduced food consumption of the DHEA-treated group developed and died of the same types of neoplasms at the same rate as the controls fed ad libitum. The chemopreventive effect of these steroids has been proposed to be due to suppression of DNA synthesis by inhibition of glucose 6-phosphate dehydrogenase, the rate-limiting enzyme of the pentose phosphate pathway. Although DHEA and its analog are strong non- competitive inhibitors of this enzyme in vitro, treatment with DHEA did not deplete cellular nucleotide pools in the liver, as would have been predicted. The chemopreventive effect of DHEA in this model may be due to steroid-induced thymic atrophy and suppression of T cell lymphoma, permitting these mice to survive long enough to develop tumors with longer latency.