Bone Mineral Density,Body Composition,and Metabolic Health of Very Low Birth Weight Infants Fed in Hospital Following Current Macronutrient Recommendations during the First 3 Years of Life

The present study longitudinally evaluated growth, bone mineral density, body composition, and metabolic health outcome in very low birth weight (VLBW) infants whose in-hospital target nutrient intake was within recent recommendations. From six months to three years, bone mineral density (dual-energy X-ray absorptiometry, DXA), body composition, and metabolic health outcome were compared with a reference group of term infants. The aim was to test whether in-hospital achieved weight gain until 36 weeks of gestation (light or appropriate for term equivalent age; LTEA or ATEA) predicts later growth, bone mineral density (BMD), abdominal obesity, or metabolic health outcomes such as insulin resistance, relative to term infants, during the first three years of life. Target in-hospital energy and protein intake was not achieved. Growth in weight, length and head circumference, mid arm circumference, adiposity, fat free mass (FFM), and bone mineralization in VLBW infants was less than those in term infants and influenced by nutritional status at discharge. Preterm infants had poorer motor and cognitive outcomes. Post-discharge body composition patterns indicate FFM proportional to height but lower fat mass index in LTEA preterm infants than term infants, with no evidence of increased truncal fat in preterm infants. The hypothesis of early BMD catch-up in VLBW infants after discharge was not supported by the present data. The clinical significance of these findings is unclear. The data may suggest a reduced obesity risk but an increased osteoporosis risk. Since postnatal growth restriction may have permanent negative health effects, LTEA VLBW infants would especially appear to benefit from targeted preventive interventions. Further follow-up of the infants is required.     

Congenitally corrected transposition with mirror-image atrial arrangement

Congenitally corrected transposition (discordant atrioventricular and ventriculoarterial connexions) with mirror-image atrial arrangement is much less frequent than the same chamber combinations in the setting of usual atrial arrangement. This scarcity of cases has made their analysis difficult. In this study we have compared the anomalies found in 19 patients with congenitally corrected transposition in mirror-image arrangement with those in 39 patients having usual atrial arrangement. Absolute, relative and attributable risks were calculated for the presence of subvalvar pulmonary stenosis, ventricular septal defect, tricuspid regurgitation, atrioventricular block or the absence of these anomalies for each of the two groups. A greater absolute risk was found for both subvalvar pulmonary stenosis (68.4 vs. 43.6%, respectively) and ventricular septal defect (63.2 vs. 58.9%, respectively). The absolute risk for tricuspid regurgitation was 25.6% in those with usual arrangement as against 21.1% in those with mirror-image arrangement. Atrioventricular block was also more frequent in those with usual arrangement (25.6 vs. 10.5%) as was absence of associated cardiac defects (17.9 vs. 10.5%, respectively). The relative risks were greater for subvalvar pulmonary stenosis and ventricular septal defect in the patients with mirror-image as opposed to usual atrial arrangement (1.57: 1.00 and 1.07: 1.00, respectively), contrasting with greater relative risk for tricuspid regurgitation (1.26: 1.00), atrioventricular block (2.43: 1.00) and absence of associated anomalies (1.70: 1.00) in the patients with usual arrangement. The attributable risk for subvalvar pulmonary stenosis was estimated to be 24.8% and ventricular septal defect 4.3% for those having mirror-image atrial arrangement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Deletion of the cannabinoid CB1 receptor impacts on the ultrastructure of the cerebellar parallel fiber-Purkinje cell synapses

The cannabinoid CB₁ receptor localizes to the glutamatergic parallel fiber (PF) terminals of the cerebellar granule cells and participates in synaptic plasticity, motor control and learning that are impaired in CB₁ receptor knockout (CB ₁-KO) mice. However, whether ultrastructural changes at the PF-Purkinje cell (PC) synapses occur in CB ₁-KO remains unknown. We studied this in the vermis of the spinocerebellar lobule V and the vestibulocerebellar lobule X of CB ₁-KO and wild-type (CB ₁-WT) mice by electron microscopy. Lobule V, but not lobule X, of CB ₁-KO had significantly less and longer synapses than in CB ₁-WT. PF terminals were significantly larger in both lobules of CB ₁-KO with no changes in PC dendritic spines. The PF terminals in lobule V of CB ₁-KO contained less synaptic vesicles and lower vesicle density; by contrast, vesicle density in lobule X of CB ₁-KO remained unchangeable relative to CB ₁-WT. There were as many vesicles in lobule V of CB ₁-KO as in CB ₁-WT, but their distribution decreased drastically at 300 nm of the active zone. In lobule X of CB ₁-KO, less vesicles were found within 150 nm from the presynaptic membrane; however, no vesicles were at 450–600 nm of the active zone. A significant higher amount of synaptic vesicles close to the active zone in lobule V and X of CB ₁-KO was observed. In conclusion, the absence of CB₁ receptors strikingly and distinctively impacts on the ultrastructural architecture of the PF-PC synapses located in cerebellar lobules that differ in vulnerability to damage and motor functions.     

Neuroprotective effect of melatonin against ischemia is partially mediated by alpha‐7 nicotinic receptor modulation and HO‐1 overexpression

Melatonin has been widely studied as a protective agent against oxidative stress. However, the molecular mechanisms underlying neuroprotection in neurodegeneration and ischemic stroke are not yet well understood. In this study, we evaluated the neuroprotective/antioxidant mechanism of action of melatonin in organotypic hippocampal cultures (OHCs) as well as in photothrombotic stroke model in vivo. Melatonin (0.1, 1, and 10 μm ) incubated postoxygen and glucose deprivation (OGD) showed a concentration‐dependent protection; maximum protection was achieved at 10 μm (90% protection). Next, OHCs were exposed to 10 μm melatonin at different post‐OGD times; the protective effect of melatonin was maintained at 0, 1, and 2 hr post‐OGD treatment, but it was lost at 6 hr post‐OGD. The protective effect of melatonin and the reduction in OGD‐induced ROS were prevented by luzindole (melatonin antagonist) and α‐bungarotoxin (α‐Bgt, a selective α7 nAChR antagonist). In Nrf2 knockout mice, the protective effect of melatonin was reduced by 40% compared with controls. Melatonin, incubated 0, 1, and 2 hr post‐OGD, increased the expression of heme oxygenase‐1 (HO‐1), and this overexpression was prevented by luzindole and α‐bungarotoxin. Finally, administration of 15 mg/kg melatonin following the induction of photothrombotic stroke in vivo, reduced infarct size (50%), and improved motor skills; this effect was partially lost in 0.1 mg/kg methyllycaconitine (MLA, selective α7 nAChR antagonist)‐treated mice. Taken together, these results demonstrate that postincubation of melatonin provides a protective effect that, at least in part, depends on nicotinic receptor activation and overexpression of HO‐1.     

Brooding rumination as a mediator in the relation between early maladaptive schemas and symptoms of depression and social anxiety in adolescents

Theory states that different cognitive constructs can be included in an integrated sequential model. This 3-wave longitudinal study assessed whether schema domains predict brooding rumination and brooding in turn predict depression and social anxiety symptoms among adolescents. A total of 1170 adolescents (M_age = 13.44 years old, SD_age = 1.30) completed measures of schema domains, brooding rumination, depression and social anxiety symptoms at baseline, 6- and 12-month follow-up (T1, T2, T3, respectively). Results revealed that the Disconnection and Rejection schema domain at T1 predicted prospective depression symptoms at T3 directly but not through brooding rumination. However, this schema domain did not predict social anxiety symptoms. The Other-Directedness schema domain at T1 predicted social anxiety symptoms at T3 both directly and through brooding at T2. Furthermore, this schema domain also predicted depression symptoms at T3 through brooding at T2. Identifying specific schema domains and the mechanisms through which these domains predict psychological symptoms has implications for interventions with adolescents.