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Biomedical subjects

S Weitz

Publications and source records attributed to S Weitz.

26 records · Page 2Linked to original sources
PubMed1992

Human casein kinase II subunit alpha: sequence of a processed (pseudo)gene and its localization on chromosome 11.

A human 4.3 kb genomic DNA fragment, containing the information of a processed (pseudo)gene of casein kinase II subunit alpha (CKII alpha) was isolated and sequenced. The genomic CKII alpha sequence is 99% homologous to the CKII alpha cDNA, carries several nucleotide exchanges, a poly(A) stretch at its 3' end and is flanked at both ends by a 16 bp repeat. It has a promoter-like region including two TATA boxes and a CAAT box. Although translation of transcripts would be terminated by a stop codon after two third of the coding region, the resulting protein would still contain the catalytic domains. However, so far Northern blots with a 3' specific probe were negative. The 4.3 kb genomic fragment containing the processed CKII alpha (pseudo)gene was mapped by in situ hybridization to chromosome 11p15.

Base Sequence↗
PubMed1992

Human perforin (PRF1) maps to 10q22, a region that is syntenic with mouse chromosome 10.

Perforin (PRF1) is a cytolytic, channel-forming protein of cytolytic T cells, natural killer cells, and granulated metrial gland cells and plays a crucial role in the killer cell-mediated elimination of virally infected host cells, tumor cells, and allotransplants. Two-thirds of the perforin sequence is homologous to the lytic, channel-forming complement proteins C6, C7, C8 alpha, C8 beta, and C9. Using cosmid DNA containing the PRF1 gene as a probe for fluorescence in situ hybridization, we have reevaluated its chromosomal location. Previously assigned to chromosome 17q11-q21, it has now been mapped to 10q22. The human PRF1 locus lies within a conserved synteny segment present on mouse chromosome 10, consistent with the previous chromosomal assignment of mouse perforin. The perforin locus is not linked to any of the genes of the terminal complement system.

Animals↗
PubMed1992

The human APO-1 (APT) antigen maps to 10q23, a region that is syntenic with mouse chromosome 19.

The APO-1 (APT) antigen is a cell surface antigen expressed on a variety of normal and malignant cells. Binding of anti-APO-1 antibody to the APO-1 antigen induces programmed cell death (apoptosis). The APO-1 antigen shows homology to the members of the tumor necrosis factor receptor/nerve growth factor receptor superfamily. Using cosmid DNA containing the APO-1 gene as a probe for fluorescence in situ hybridization, we have mapped the gene to a subregion of chromosomal band 10q23. The human APO-1 locus lies within a conserved synteny segment present on mouse chromosome 19 consistent with the previous chromosomal assignment of the corresponding mouse antigen.

Antigens, Neoplasm↗
PubMed1986

Cerebral granular cell tumor: immunohistochemical and electron microscopic study.

A rare intracerebral granular cell tumor (GCT) was studied by immunocytochemical and ultrastructural methods. The tumor was composed of two cell types--filament-rich and granular cells. Granular cells contained PAS-positive, diastase-resistant granules that ultrastructurally corresponded to autophagic cytosegresomes. Glial fibrillary acidic protein, the intermediate filament protein specific for astrocytes, was demonstrated in the filament-rich and, to a lesser extent, in the granular cells. Unlike noncerebral GCT, neither S-100 protein nor vimentin was detected in the tumor cells. On the other hand, both cerebral and noncerebral GCT were labeled immunocytochemically with peanut lectin (Arachis hypogaea). The results suggest that cerebral GCT share some features with noncerebral GCT, but differ in other respects. They further suggest that GCT may be derived from different cell types depending on the tissue of origin, and that cerebral GCT may be derived from astrocytes.

Adult↗
PubMed1986

Rhinorrhea and pneumocephalus after cerebrospinal fluid shunting. The role of lateral extensions of the sphenoid sinus.

Pneumocephalus is usually seen after trauma or neurologic surgery. A rare presentation is after cerebrospinal fluid (CSF) shunting for rhinorrhea. This may be a manifestation of shunt malfunction or of the failure to close a preexisting fistulous tract. A common site of failure is the sphenoid sinus, where CSF may leak from a dehiscence in the middle cranial fossa floor. These dehiscences often communicate with lateral extensions of the sphenoid. This complication is best managed by craniotomy with direct inspection of the floor of the middle cranial fossa and correction of deranged CSF dynamics.

Brain↗
PubMed1983

Cerebrospinal fluid dynamics and rhinorrhea: the role of shunting in repair.

CSF rhinorrhea can have many causes: traumatic, neoplastic, and iatrogenic origins are common. Most traumatic rhinorrhea ceases after a trial of conservative management. While obvious erosion or traumatic destruction of vital structures may be the underlying cause, other pathophysiologic mechanisms may be working in the formation of CSF rhinorrhea, which may require the combined skills of the otolaryngologist and the neurosurgeon. Leakage of CSF is seen in "high-pressure rhinorrhea," a pathophysiologic state wherein the underlying problem is poor CSF resorption. The result is increased intracranial pressure and eventual rhinorrhea or otorrhea. Areas of CSF leakage correspond to sites of congenital weakness in the cribriform plate region, the parasellar region, or the temporal bone. Weak areas in old base-of-skull fracture sites may leak with increased intracranial pressure. The initial management should stress correction of the deranged pathophysiology, namely shunting. Surgical repair is secondary to controlling the abnormal CSF dynamics.

Adolescent↗
PubMed1981

The acquisition of language skills by autistic children: can parents do the job?

The mothers and fathers of 11 preschool autistic children were taught operant procedures used in teaching speech to nonverbal children. The children's speech skills were assessed twice before and once after their parents were trained. At posttreatment, the children showed significant gains in prespeech and speech skills as measured by a 21-step hierarchy of speech behaviors. Those children who had acquired at least verbal imitative skill after training made greater progress than those who had not. Although children maintained their gains in a 1-year follow-up assessment, there was no evidence of significant improvement beyond that achieved at the end of training. The importance of support for parents in continuing to do formal "teaching" after the training program ends was stressed.

Adult↗