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Biomedical subjects

K A Gwinn

Publications and source records attributed to K A Gwinn.

13 recordsLinked to original sources
PubMed1998

Olfactory function in restless legs syndrome.

Restless leg syndrome (RLS) is usually idiopathic but may occur in patients with Parkinson's disease (PD). Both respond to dopaminergic medications. Whether these disorders share a common pathophysiology is unclear. Because PD is associated with a loss of olfactory function, we compared the olfactory function of patients with RLS with control and PD patients. Using the University of Pennsylvania Smell Identification Test (UPSIT), olfactory function was found to be normal in patients with idiopathic RLS and significantly reduced in patients with PD. This suggests that the pathophysiology of RLS differs from PD, and that RLS likely is not a "forme fruste" or a preclinical sign of PD.

Aged↗
PubMed1998

Effective treatment of orthostatic tremor with gabapentin.

We report seven patients with orthostatic tremor (OT) who were successfully treated with the anticonvulsant gabapentin. Five of the patients had been previously tried on clonazepam, the most commonly used drug for OT, four without any benefit. The degree of improvement perceived by the patients with gabapentin varied from 60-80% (mean 73%). The effective dose of gabapentin ranged from 300-1800 mg/day (mean 1030 mg/day). The side effects were generally mild, transient, and dose-related. Duration of response has so far ranged from 2-22 months (mean 11 months) with all patients still currently benefiting from gabapentin. We conclude that gabapentin may be an effective treatment for OT. Further trials are indicated.

Acetates↗
PubMed1997

Electrophysiological observations in idiopathic opsoclonus-myoclonus syndrome.

To supplement existing knowledge regarding the pathophysiology of the opsoclonus-myoclonus syndrome, electrophysiological findings are reported in three patients with idiopathic opsoclonus-myoclonus. Surface electromyography (EMG) revealed < 100-ms synchronous discharges correlating with the clinical myoclonus. Short duration EMG discharges, with no back-averaged cortical correlate, normal gross electroencephalogram, and no exaggerated responses with either evoked potential testing or long latency EMG responses were observed. The clinical and electrophysiological findings we describe are consistent with a brainstem origin of the myoclonus in this syndrome, with concurrent abnormalities in cerebellar circuits, similar to those described for paraneoplastic cases. The constellation of these electrophysiological findings differentiates the myoclonus in these patients from other clinical myoclonic entities.

Adult↗
PubMed1987

Multiple basal elements of a human hsp70 promoter function differently in human and rodent cell lines.

The human heat shock protein 70 (hsp70) gene is expressed constitutively in a wide variety of cells. Two separate promoter domains determine this basal level of hsp70 expression. The proximal domain is contained within 84 bases of the transcription initiation site and consists of three elements which appear to interact with the TATA factor(s) and CCAAT-box-binding transcription factor and SP1, respectively. The proximal domain is sufficient for near-maximal basal expression to rodent cell lines. The distal promoter domain consists of sequences upstream of -84 and is necessary in conjunction with the proximal domain for full basal expression in human cell lines. Although in BALB/c 3T3 cells the distal promoter domain plays little role in basal expression, it is functional as evidenced by the ability to compensate efficiently for mutations in the proximal CCAATC homology. The distal domain does not compensate as efficiently for proximal-domain mutations in HeLa cells. Basal expression of this human hsp70 promoter is, therefore, determined by multiple elements. Fewer elements are required for basal expression in rodent cell lines than in human cell lines, suggesting that there are significant differences between the rodent and human transcription apparatuses.

Animals↗
PubMed1986

Inducible overproduction of the mouse c-myc protein in mammalian cells.

We have made Chinese hamster ovary (CHO) cell lines that contain up to 2000 copies of the coding region of the mouse c-myc gene fused to the promoter of the Drosophila gene (hsp70) encoding a Mr 70,000 heat shock protein. Incubation of these cells at 43 degrees C results in an estimated 100-fold induction of c-myc mRNA. Translation of this mRNA occurs when the cells are returned to 37 degrees C, and during the first 3 hr of recovery at 37 degrees C, the c-myc protein is one of the most abundantly synthesized proteins in the cells. The products of the induced c-myc gene are phosphoproteins of apparent Mr 64,000, 66,000, and 75,000. Induced cells die, suggesting that elevated levels of c-myc are cytotoxic. Amplification of genes placed under control of the Drosophila hsp70 promoter may provide a general method for inducibly over expressing proteins in mammalian cells.

Animals↗
PubMed1986

Binding of polyomavirus large T antigen to the human hsp70 promoter is not required for trans activation.

Polyomavirus large T antigen binds to two sites located between positions -110 and -170 of a human heat shock protein 70 (hsp70) promoter. Methylation interference studies show that binding for each site is determined by two GPuGGC pentanucleotide sequences. The specificity of this binding interaction is similar to that observed for large T binding to the viral genome. The existence of sequences that bind a viral protein in a cellular promoter raises the possibility that these sequences play a role in gene expression in an uninfected cell. We show that hsp70 large T antigen binding site 1 is capable of functioning as an upstream promoter element in cells that do not contain any viral T antigen. Genetic analysis of this effect suggests that a cellular factor exists that has a binding specificity that overlaps but is not identical to that of polyomavirus large T antigen. To determine whether binding of polyomavirus large T antigen can regulate expression of the intact human hsp70 promoter, we have introduced the promoter into mouse cells with plasmids that express the polyomavirus early proteins. These proteins stimulate the level of correctly initiated hsp70 transcripts, but surprisingly the degree of stimulation remains unchanged for promoter constructs in which the large T antigen binding sites have been deleted. These observations suggest that trans activation of the hsp70 promoter by the polyomavirus early proteins occurs through protein-protein interactions and not through sequence-specific DNA binding.

Acetyltransferases↗