Is there a role for Notch signalling in human breast cancer?

Aberrant Notch signalling has been observed in several human cancers, including acute T-cell lymphoblastic leukaemia and cervical cancer, and is strongly implicated in tumourigenesis. Unregulated Notch signalling in the mouse mammary gland leads to tumour formation. These results raise the possibility that Notch signalling might play a role in human breast cancer. There are currently few reports that address this question directly and this appears to be an area worthy of further investigation.     

Italian multicentre study on very low-birth-weight babies. Neonatal mortality and two-year outcome

The Italian multicentre study on very low-birth-weight babies is the first collaborative project in Italy on the health status of newborns weighing 500–1499 g at birth: 634 such babies were admitted in 1987–88 to eight Italian NICUs; 424 infants survived and were followed until two years of age, corrected for prematurity. Logistic regression analysis of pre-admission risk factors of in-hospital mortality identified eight statistically significant variables: birth weight, gestational age, sex, antepartum steroids, I-min Apgar score and, on admission to the NICU, body temperature, pH and absence of spontaneous respiration. Using the equation derived from the logistic model, a theoretical mortality rate was calculated for each centre, predicted on the basis of the local incidence of preadmission risk factors. In no case was the predicted mortality significantly different from the observed one. At two years of age, 8 children were blind and 48 had motor disability. Of these, 46 had cerebral palsy: based on a functional evaluation score 14 had severe (degree 4), 20 intermediate (degree 3) and 12 mild cerebral palsy (degree 2). Among 25 variables entered in a logistic regression as risk factors for cerebral palsy, only periventricular leucomalacia and acidosis were significantly associated with the outcome.     

Barriers to working with impaired trainees: A resident's viewpoint

Psychiatric trainees and educators alike know that significant impairment may occur during training. Although psychiatry programs can do much to identify, treat, and prevent trainee impairment, barriers that may hinder programs from adequately addressing the problems of the impaired trainee continue to exist. These barriers include stigmatization and rejection of the impaired trainee, lack of focus on primary prevention, problematic supervisor-resident relationships, and trainee resistance to intervention. An atmosphere of candor and support, impairment-related seminars, and informed and alert supervisors can be helpful in easing the stress of training and reducing trainee impairment.     

Morbid Obesity and Gastric Bypass Surgery: Biochemical Profile

Background: Morbid obesity (MO) and the pathologies associated with it constitute an important public health problem, accounting for 7% of the health expenditure in industrialized countries. An important percentage of this expense is attributed to the different biochemical tests performed in these patients, who suffer from several metabolic derangements. We evaluated the basic biochemical abnormalities in MO patients and their reversibility by weight loss after gastric bypass, to standardize the surveillance of the different metabolic abnormalities in obese patients. Methods: By a retrospective analysis on 125 patients operated in our hospital, we evaluated anthropometric and biochemical data before and 1, 3, 6, 12 and 24 months after gastric bypass. Results: Preoperatively hyperinsulinemia, hyperglycemia, dyslipidemia and hypertensive disease were present, and began to improve 1 and 3 months after surgery (although not significantly) and significantly at 6, 12 and 24 months after it. We also observed deficient protein nutrition and a deficiency of micronutrients both before bypass and during the follow-up. Conclusion: After gastric bypass, a marked decrease in insulin occurred, with normalization of blood pressure and the biochemical parameters associated with the metabolic syndrome. We propose a biochemical follow-up protocol for MO patients.