Is Rett syndrome a subtype of pervasive developmental disorders?

The author reviews the issue on whether Rett syndrome (RS) is a subtype of pervasive developmental disorders (PDDs). More than 200 articles of RS have been published in the last 10 years. Internal and external validities of RS have been established by several independent studies. There remains the question whether RS presents clinical features that meet the total criteria for PDDs. The available data seem to support the idea of classifying RS as a subtype of PDDs in the DSM-IV.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44607/1/10803_2005_Article_BF01046327.pd

Book reviews

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44602/1/10803_2005_Article_BF02216065.pd

Brief report: Violence in asperger syndrome, a critique

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44604/1/10803_2005_Article_BF02207331.pd

Brief report: Haloperidol treatment of trichotillomania in a boy with autism and mental retardation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44605/1/10803_2005_Article_BF02207333.pd

Brief report: A comparison of the diagnostic criteria for Asperger syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44608/1/10803_2005_Article_BF01046332.pd

Brief report: Search for DNA markers in two autistic males with the fragile X syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44601/1/10803_2005_Article_BF02211885.pd

Brief Report: Brief Syntactic Analysis in Asperger Syndrome: A Preliminary Study

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44618/1/10803_2004_Article_221279.pd

CP violating polarizations in semileptonic heavy meson decays

We study the $T$-violating lepton transverse polarization ($P^\perp_l$) in three body semileptonic heavy meson decays to pseudoscalar mesons and to vector mesons. We calculate these polarizations in the heavy quark effective limit, which simplifies the expressions considerably. After examining constraints from $CP$ conserving (including $b \rightarrow s \gamma$) and $CP$ violating processes, we find that in $B$ decays, $P^\perp$ of the muon in multi-Higgs doublet models can be of order $10\%$, while $P^\perp$ of the $\tau$ can even approach unity. In contrast, $P^\perp_\mu$ in $D$ decays is at most 1.5\%. We discuss possibilities for detection of $P^\perp_l$ at current and future $B$ factories. We also show that $P^\perp_l$ in decays to vector mesons, unlike in decays to pseudoscalars, can get contributions from left-right models. Unfortunately, $P^\perp_l$ in that case is proportional to $W_L$-$W_R$ mixing, and is thus small.Comment: 32pp plain LATEX, 3 figs (by EMAIL request), TRI-PP-94-1

Brief report: Autism and herpes simplex encephalitis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44606/1/10803_2005_Article_BF01046406.pd

A Pro-Cathepsin L Mutant Is a Luminal Substrate for Endoplasmic-Reticulum-Associated Degradation in C. elegans

Endoplasmic-reticulum associated degradation (ERAD) is a major cellular misfolded protein disposal pathway that is well conserved from yeast to mammals. In yeast, a mutant of carboxypeptidase Y (CPY*) was found to be a luminal ER substrate and has served as a useful marker to help identify modifiers of the ERAD pathway. Due to its ease of genetic manipulation and the ability to conduct a genome wide screen for modifiers of molecular pathways, C. elegans has become one of the preferred metazoans for studying cell biological processes, such as ERAD. However, a marker of ERAD activity comparable to CPY* has not been developed for this model system. We describe a mutant of pro-cathepsin L fused to YFP that no longer targets to the lysosome, but is efficiently eliminated by the ERAD pathway. Using this mutant pro-cathepsin L, we found that components of the mammalian ERAD system that participate in the degradation of ER luminal substrates were conserved in C. elegans. This transgenic line will facilitate high-throughput genetic or pharmacological screens for ERAD modifiers using widefield epifluorescence microscopy