Survival and developmental disability in infants with birth weights of 501 to 800 grams, born between 1979 and 1994

OBJECTIVE: Because the survival rate has increased for extremely low birth weight neonates, many have raised the concern that the rate of developmental disability among survivors will also increase. To address this concern, we analyzed changes over time in survival and major neurosensory impairment in a sample of extremely low birth weight infants born between July 1, 1979, and June 30, 1994. METHODS: The study sample included 513 infants with birth weights of 501 to 800 g who were cared for in either of the two neonatal intensive care units that serve a 17-county region in northwest North Carolina and who were born to mothers residing in that region. At 1 year of age (corrected for gestation), survivors were examined by a pediatrician and were tested using the Bayley Scales of Infant Development. Major neurosensory impairment was defined as cerebral palsy, a Bayley Mental Developmental Index <68, or blindness. A total of 209/216 (97%) of survivors were examined at 1 year of age. Epoch of birth was defined as follows: epoch 1, July 1, 1979 to June 30, 1984; epoch 2, July 1, 1984 to June 30, 1989; and epoch 3, July 1, 1989 to June 30, 1994. RESULTS: Survival rates for epochs 1, 2, and 3 were, respectively, 24/120 (20%), 63/175 (36%), and 129/218 (59%). In contrast, the proportions with a major neurosensory impairment did not increase over time; rates for successive epochs were 6/24 (25%), 17/61 (28%), and 26/124 (21%). Rates of cerebral palsy were 3/24 (13%), 12/61 (20%), and 9/124 (7%); rates of delayed mental development were 4/24 (17%), 12/61 (20%), and 17/124 (14%); and rates of blindness were 2/24 (8%), 0/62, and 5/124 (4%), respectively. CONCLUSIONS: This analysis suggests that the increasing survival of extremely low birth weight neonates since the late 1970s has not resulted in an increased rate of major developmental problems identifiable at 1 year of age.     

Amphetamine-induced anorexia: analysis with hypothalamic lesions and knife cuts

The present study examined the hypotheses that the midlateral perifornical region of the hypothalamus (PFH), at the level of the ventromedial nucleus, plays a crucial role in amphetamine (AMPH)-induced anorexia and that mediating fibers ascending to this brain region follow a midlateral course through the caudal hypothalamus. Electrolytic lesions that destroyed the PFH region attenuated the feeding suppression induced by intraperitoneal administration of AMPH. Lesions placed anterior, dorsal, or medial to this region, in contrast, did not decrease AMPH's effect. The medially-placed paraventricular nucleus lesion, in fact, enhanced drug response. Midlateral coronal wire-knife cuts in the caudal hypothalamus also attenuated AMPH anorexia. The crucial midlateral caudal hypothalamic cut also disrupted anorexia induced by direct injection of AMPH into the PFH area. The results obtained from the lesion data support the hypothesis that the PFH region is essential to AMPH's suppressive effect upon feeding, and the KC data suggest that crucial catecholamine fibers mediating this drug response ascend specifically through the midlateral portion of the hypothalamus.     

Amikacin-resistant gram-negative bacilli: correlation of occurrence with amikacin use

The incidence of amikacin resistance among gram-negative bacilli isolated at the New York V.A. Medical Center increased from 2.0% to greater than 7% during an 18-month period from January 1980 to July 1981. This increase coincided with a threefold increase in amikacin use at this institution. The amikacin-resistant (AKR) isolates most frequently recovered in 1981 were species of Klebsiella, Serratia, and Pseudomonas. These organisms were recovered from multiple sites, including urine, sputum, wounds, blood, peritoneal fluid, and pleural fluid. The amikacin-modifying enzyme 6'-N-acetyltransferase was detected in 27 (67.5%) of 40 randomly selected AKR isolates. These data indicate that resistance to amikacin in this hospital is enzymatically mediated in most strains of AKR Klebsiella and Serratia and in about one-third of AKR strains of P. aeruginosa. This finding supports the conclusion that amikacin resistance is enhanced by the pressure of increased amikacin use.     

Changing epidemiology of gastroesophageal reflux disease in the Asian–Pacific region: An overview

Abstract   Gastroesophageal reflux disease (GERD) is a common disease in the West, which now appears to be also increasing in prevalence in the Asian Pacific region. The reasons for this changing epidemiology are two-fold: an increased awareness among doctors and patients, and/or a true increase in the prevalence of the disease. Prevalence rates of reflux esophagitis (RE) of up to 16% and prevalence of GERD symptoms of up to 9% have been reported in the Asian population. However, the frequency of strictures and Barrett's esophagus remain very low. Non-erosive reflux disease (NERD) appears to be the most common form of GERD among Asian patients accounting for 50–70% of cases with GERD. Among Asian patients differences can also be discerned among different ethnic groups. For example, in Malaysia where a multiracial society exists, RE is significantly more common among Indians compared to Chinese and Malays whereas NERD is more frequently seen in the Indian and Malays compared to the Chinese. The reasons for these differences are not known but may indicate both genetic factors and environmental factors peculiar to the particular racial group. GERD has also been increasing in the region demonstrating a time-lag phenomenon compared to the West. Differing predisposition to GERD among different ethnic groups would mean that such an increase would be more prominent among certain racial groups.     

Peroxisome proliferator-activated receptor (PPAR) gamma: a new target for the treatment of inflammatory bowel disease

The peroxisome proliferator-activated receptor (PPAR) gamma is highly expressed in the colon mucosa. In vitro, it regulates inflammation. AIM: To evaluate the anti-inflammatory functions of PPARgamma agonist during a trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. METHODS: Colitis was induced in Balb/c mice after intra-rectal administration of TNBS. The intensity of inflammation was assessed 2 and 5 days after colitis induction by macroscopic and histologic scores and by the quantification of colon myeloperoxidase (MPO), IL-1B and TNFalpha mRNA concentrations. The therapeutic role of PPARgamma agonist given by oral gavage was assessed in preventive and treatment modes. RESULTS: TNBS induced severe macroscopic and histologic lesions, with high mucosal MPO, IL-1B and TNFalpha mRNA concentrations. PPARgamma agonist given preventively or in treatment mode allowed a significant decrease of macroscopic and histologic scores through a normalization of MPO, IL-1B and TNFalpha mRNA concentrations. CONCLUSION: PPARgamma agonist decreases the intensity of TNBS induced colitis through normalization of IL-1B and TNFalpha expression. PPARgamma agonists may be proposed as new therapeutic agents in inflammatory bowel diseases.