Talk:2009 Lecture 22

<Flowplayer height="400" width="380" autoplay="true">fetal growth.flv</Flowplayer>

Fetal Growth 3.0 Freeware for MacOS X 10.3 or later. Graphs of biparietal diameter, head circumference, abdominal circumference and femur length are plotted against gestation. These graphs are then available for importing into the medical record. Fetal Growth is useful for obstetricians, radiologists, midwives, general practitioners and any health professional involved in pregnancy care. It may also be of interest to prospective parents.

Developmental weeks (clinical, LMP) - crown to rump (CR) measurements in millimeters 9 - 50mm, 12 - 95mm 16 -140mm 20 - 190mm 24 - 230mm 28 - 270mm 32 - 300mm 36 - 340mm 40 - 380mm

Neural Background Reading

Different timings of dicer deletion affect neurogenesis and gliogenesis in the developing mouse central nervous system http://www3.interscience.wiley.com/journal/122616509/abstract?CRETRY=1&SRETRY=0

"MicroRNAs, processed by the RNAase III enzyme Dicer, are 22 nucleotide endogenous noncoding small RNAs. The function of Dicer in the mouse central nervous system (CNS) development is not well understood. Here, we show that specifically deleting Dicer expression in the CNS and in the cerebral cortex using two Cre lines results in reduced progenitor numbers, abnormal neuronal differentiation, and thinner cortical wall. Incomplete Dicer deletion during early embryonic stages contributes to normal development of early-born neurons in the cortex and motor neurons in the spinal cord. However, at late embryonic stages when Dicer is completely ablated in the CNS, the migration of late-born neurons in the cortex and oligodendrocyte precursor expansion and differentiation in the spinal cord are greatly affected. Our studies of different timings of Dicer deletion demonstrate the importance of the Dicer-mediated microRNA pathway in regulating distinct phases of neurogenesis and gliogenesis during the CNS development. "

Early fetal brain growth. Burn J, Birkbeck JA, Roberts DF. Hum Biol. 1975 Dec;47(4):511-22. No abstract available PMID: 1193577

Quantitative growth and development of human brain. Dobbing J, Sands J. Arch Dis Child. 1973 Oct;48(10):757-67. No abstract available. PMID: 4796010 Excellent early paper showing graphically growth in weight, cellularity and myelination.

Perinatal ontogeny of brain growth in the domestic pig. Pond WG, Boleman SL, Fiorotto ML, Ho H, Knabe DA, Mersmann HJ, Savell JW, Su DR. Proc Soc Exp Biol Med. 2000 Jan;223(1):102-8. PMID: 10632968 "velocity of human brain growth is greatest from a few weeks before to a few weeks after birth"

http://www.abbs.info/fulltxt/41-08/41080677.htm Lissencephaly is a severe disease characterized by brain malformation. The main causative gene of lissencephaly is LIS1. Classical lissencephaly has two major types: Miller–Dieker syndrome (MDS) and isolated lissencephaly sequence (ILS). All MDS and some cases of ILS have haploinsufficiency at human chromosome 17p13.3, from where LIS1 (Lissencephaly-1) gene was isolated [2]. Mutation or deletion of LIS1 leads to proliferation and migration deficiency of neurons in brain development [3]. Thus, LIS1 is the main causative gene responsible for classical lissencephaly.