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L Baum

Publications and source records attributed to L Baum.

86 records · Page 5Linked to original sources
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Glycogen synthase kinase 3 alteration in Alzheimer disease is related to neurofibrillary tangle formation.

Highly phosphorylated tau protein is the main component of paired helical filaments (PHF), which comprise the neurofibrillary tangles (NFT) in some neurons of patients with Alzheimer disease (AD). Glycogen synthase kinase 3 (GSK3) phosphorylates tau in vitro at several sites also found to be phosphorylated in PHF-tau; tau is phosphorylated at these sites in both AD and normal control (NC) brains, although the extent of phosphorylation is far greater in tau from AD. If GSK3 levels are increased in AD, then tau phosphorylation and perhaps PHF formation may occur. To quantify GSK3, blots of AD and NC brain supernatant and particulate fractions were probed with antibodies to GSK3. In particulate fractions of AD compared to NC, GSK3 alpha immunoreactivity did not increase, but in fact, decreased 40%, and GSK3 beta immunoreactivity decreased 30%. GSK3 alpha and GSK3 beta levels correlated well with each other. GSK3 levels correlated negatively with numbers of NFT.

Aged↗
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Congenital hypertrophy of the retinal pigment epithelium and APC mutations in Chinese with familial adenomatous polyposis.

Mutations in the adenomatous polyposis coli gene (APC) often cause both congenital hypertrophy of the retinal pigment epithelium (CHRPE) and familial adenomatous polyposis (FAP). To investigate the relationship between APC mutations, CHRPE and FAP, all FAP patients at the Prince of Wales Hospital, Hong Kong, were asked to participate in a study. Ten Chinese patients from 6 kindreds and their family members volunteered, along with 12 healthy control subjects selected among hospital visitors and staff. All were examined for dilated fundus by indirect ophthalmoscopy. Mutations in APC coding exons were detected by sequencing. In one FAP patient, a novel A insertion at codon 1023 was detected. Three previously reported mutations were detected in 6 FAP patients: a deletion of ACAAA at codon 1061, and 2 truncating point substitutions at codons 216 and 283. In 3 FAP patients, no APC mutation was found, suggesting that mutations in APC coding regions are not the sole cause of FAP or CHRPE. A total of 64 CHRPE lesions were found in FAP patients and some relatives with and without APC mutations. Contrary to most reports, APC mutations before exon 9 did cause CHRPE lesions, albeit relatively few.

Adenomatous Polyposis Coli↗
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Award of Excellence.

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Awards and Prizes↗
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[Diagnostic and prognostic value of the brain stem reflexes in severe post-traumatic coma].

Authors study the neurological evolution of 50 cases of traumatic coma and recognize 5 misfunction levels corresponding to five steps of rostrocaudal deterioration. The level 1 (cortico-sub-cortical) is defined by the persistence of the mimic and flexion response to painful stimulation. The level 2 (diencephalic) is characterized by stereotypic responses to pain and lack of mimic. At these two levels, the fronto-orbicular and vertical oculo-vestibular reflexes are persistent. These reflexes disappear when the status impair caudodal to the level 3 (meso-diencephalix junction). The photomotor reflex disappear at the level 4 (mesencephalic), where the motor response to pain may be very poor, or may be a bilateral extension. The horizontal oculo-vestibular reflex is always persistent, except for the level 5 corresponding to a pontine lesion. The meso-diencephalic level 3 appears to be a critical impairment point: as long as the level is not overpassed, the half of the patients do improve and 10% only die. More than 75% of those who improve from this level have an excellent recovery. The restructuration probability is diminished by the half when the level of mesencephalic misfunction is reached.

Brain↗