Predicting neurodevelopmental outcomes for at-risk infants: reliability and predictive validity using a Chinese version of the INFANIB at 3, 7 and 10 months.

BACKGROUND: Chinese primary care settings have a heavy patient load, shortage of physicians, limited medical resources and low medical literacy, making it difficult to screen for developmental disorders in infants. The Infant Neurological International Battery (INFANIB) for the assessment of neuromotor developmental disorders in infants aged 0 ~ 18 months is widely applied in community health service centers because of its simplicity, time-saving advantages and short learning curve. We aimed to develop and assess a Chinese version of the INFANIB. METHODS: A Chinese version of the INFANIB was developed. Fifty-five preterm and 49 full-term infants with high risk of neurodevelopmental delays were assessed using the Chinese version of the INFANIB at 3, 7 and 10 months after birth. The Peabody Developmental Motor Scale (PDMS) was simultaneously used to assess the children with abnormalities and diagnose cerebral palsy. The sensitivity, specificity, positive predictive value and negative predictive value of the scale were calculated. RESULTS: At birth, a higher proportion of full-term infants had asphyxia (p < 0.001), brain damage ( p = 0.003) and hyperbilirubinemia ( p = 0.022). The interclass correlation coefficient and intraclass correlation coefficient values for the INFANIB at 3, 7 and 10 months were >0.8, indicating excellent reliability with regard to inter- and intraobserver differences. The specificity, sensitivity, positive predictive value and negative predictive value were high for both high-risk premature infants and full-term infants at the age of 10 months. For premature infants at the age of 7 months or below, INFANIB had low validity for detecting abnormalities. CONCLUSIONS: The Chinese version of the INFANIB can be useful for screening infants with high-risk for neuromotor abnormality in Chinese primary care settings.

Vitamin A deficiency impairs postnatal cognitive function via inhibition of neuronal calcium excitability in hippocampus.

Vitamin A (VA) is important for postnatal brain development, and VA deficiency (VAD) can cause learning and spatial memory deficits in rats. Most of the biological functions of VA are mediated by retinoic acid (RA). To investigate the mechanisms underlying VA deficits, mother rats were fed elemental diets to achieve blood VA levels classified as normal, deficient or severely deficient. Shuttle box and Morris water maze tests revealed impairments in learning ability and spatial memory, respectively, in adolescent VAD rats (p 30-35). Electrophysiology showed weaker long-term potentiation in VAD rats compared to VA normal rats. Examination of NMDA-induced calcium (Ca(2+) ) excitability revealed decreased excitability in hippocampal slices from VAD rats during postnatal development. Relative to VA normal rats, VAD rats also had decreased NMDA receptor NR1 mRNA and protein expression in later stages of postnatal development (p 10-30), as well as differences in retinoic acid receptor (RARα) mRNA and protein expression. Furthermore, primary hippocampal neurons in culture showed increased neuronal Ca(2+) excitability in response to all-trans-RA or 9-cis-RA, coupled with increases in RARα and NR1 expression similar to those observed in vivo. We also found weaker calcium excitability and lower expression of NR1 mRNA and protein after specific silencing of RARα. Finally, we found that RA signals affected the expression of NR1 do not directly through transcriptional regulation. These data support the new idea that continuous postnatal VAD inhibits RARα expression, which decreases NR1 expression via no direct transcriptional regulation and then inhibits hippocampal neuronal Ca(2+) excitability which affects long-term potentiation, finally producing deficits in active learning and spatial memory in adolescence.

The pattern of retinoic acid receptor expression and subcellular, anatomic and functional area translocation during the postnatal development of the rat cerebral cortex and white matter.

Retinoic acid (RA), which is an important modulator of brain development, neural cell proliferation, neurite outgrowth, and synaptic plasticity, is regulated via changes in RA receptors. The pattern of RA receptor changes in the rat cerebral cortex and white matter during postnatal development has not been extensively studied. Therefore, we studied the mRNA expression patterns of 6 RA receptors in the postnatal rat cerebral cortex and white matter at 1, 3, 7, 10, 14, 21, 28, and 35days. We found that RARß, RXRα and RXRß mRNA levels gradually increased during postnatal development. RARα presented a nearly unimodal trend, but RARγ and RXRγ were generally bimodal. RARα, RARγ, and RXRγ mRNA levels peaked at postnatal day 21 (P21). The pattern of RARα expression was consistent with that of its mRNA levels. RARα and RXRγ mRNA levels were the highest among those of all RA receptors during postnatal development. Interestingly, RARα expression was mainly located in the cytoplasm in the postnatal development apart from P3d. We further showed that RARα is expressed mainly in layers 2 and 3, partly in layers 1 and 4, and in a limited manner in layers 5 and 6 in the parietal cortex. Most RARα expression occurs in layers 2, 3, and 4 in the temporal lobe cortex. We realized that the M1 S2 region of RARα is highly expressed and that the position of RARα changes dynamically to meet the needs of different regions during development. These results support the idea that the RA receptor plays an important role in the cerebrum during postnatal development and implementation of these functions may be mainly dependent on the non-transcriptional or post- transcriptional regulation.

[Sequence-dependent cleavage of HBV DNA by combining with triple helix-forming oligodeoxyribonucleotides modified with manganese porphyrin in vitro].

OBJECTIVE: To observe the ability of triple helix-forming oligonucleotides (TFO) modified with manganese porphyrin to combine with and cleave HBV DNA fractions. METHODS: The ends of TFO were modified with manganese porphyrin and acridine; At 37 degrees C and pH 7.4 condition in vitro, TFO modified with manganese porphyrin and acridine were bound with 32P labeled HBV DNA fragments, the affinity and specificity binding to target sequence were tested by electrophoretic mobility shift and DNase 1 footprinting assays, the ability to cleave HBV DNA fractions was observed with cleavage experiments. RESULTS: TFO modified with manganese porphyrin and acridine could bind to target sequence in a sequence-dependent manner with Kd values of 3.5 x 10(-7) mol/L and a relative affinity of 0.008. In the presence of KHSO5, TFO modified with manganese porphyrin and acridine could cleave target sequence in the region forming triple DNA. CONCLUSION: In the presence of KHSO5, TFO modified with manganese porphyrin and acridine could cleave target HBV-DNA in sequence-dependent manner.