Search PubMed⌕ Search

Biomedical subjects

J M Allen

Publications and source records attributed to J M Allen.

At least 127 records · Page 7Linked to original sources
PubMed1993

Incidence and simple management of priapism following dynamic infusion cavernosometry-cavernosography.

Of 239 patients with erectile dysfunction (aged 36 to 70 years) who were evaluated with dynamic infusion cavernosometry-cavernosography, 32 (13.4%) developed priapism after the procedure and were successfully managed with immediate intracorporal injection of phenylephrine. No single risk factor for the development of priapism was identified in this group. Early pharmacologic intervention for priapism induced by dynamic infusion cavernosometry-cavernosography is a simple, safe, and time-saving measure to achieve detumescence and prevent potential sequelae such as corporal ischemia or fibrosis.

Adult↗
PubMed1993

Neural modulation of bovine mesenteric lymph node contraction.

Spontaneous isometric contractions and field-evoked responses were recorded in vitro from strips of bovine mesenteric lymph node capsule. Field stimulation (0.3 ms pulses, 60 V nominal, 2 min trains) at frequencies > or = 2 Hz evoked a frequency-dependent increase in baseline tension which was maximum at frequencies > or = 16 Hz. Evoked contractions were significantly reduced (P = 0.02) by the neurotoxin tetrodotoxin (10(-6) M) although they were unaffected by the alpha-adrenoceptor antagonists phentolamine, rauwolscine and prazosin (3 x 10(-6) M). Similarly, responses were unaffected by the beta-adrenoceptor antagonist propranolol (10(-6) M), the cholinergic antagonist atropine (10(-6) M) or the uptake blocker cocaine (10(-6) M). Field-evoked contraction was also unaffected by a 30 min exposure to alpha,beta-methylene ATP (10(-6) M). The results suggest that bovine lymph node capsular smooth muscle is innervated by excitatory nerves which are non-adrenergic, non-cholinergic and non-purinergic in nature.

Adenosine Triphosphate↗
PubMed1993

Depressive symptoms and family history in seasonal and nonseasonal mood disorders.

OBJECTIVE: The authors' goal was to compare the symptoms and family history of seasonal affective disorder with those of nonseasonal mood disorders. METHOD: From a subspecialty mood disorders clinic, 34 patients with major depression, seasonal pattern (seasonal affective disorder), diagnosed with DSM-III-R criteria, were matched in age, sex, and diagnostic subtype (recurrent unipolar, bipolar I, or bipolar II) to 34 patients with nonseasonal mood disorders. Data on symptoms during the most recent depressive episode were obtained by chart review and compared by using chi-square tests. Family history data for first-degree relatives of patients with seasonal and nonseasonal mood disorders were gathered by using the family history method, and diagnoses were based on Family History Research Diagnostic Criteria. RESULTS: Patients with seasonal affective disorder reported significantly more hypersomnia, hyperphagia, and weight gain and reported less suicidal ideation and morning worsening of mood than the patients with nonseasonal mood disorders. No differences were found in family histories of mood disorders, other psychiatric disorders, and any psychiatric disorder between the groups with seasonal versus nonseasonal mood disorders. Alcoholism was found more frequently in the relatives of the patients with seasonal affective disorder. CONCLUSIONS: Differences in symptoms between seasonal and nonseasonal mood disorders provide some support for seasonal affective disorder as a diagnostic subtype of mood disorders. However, the genetic loading for mood disorders (of unspecified seasonality), as determined by the family history method, is similar for seasonal and nonseasonal mood disorders.

Adult↗
PubMed1993

A novel expression system for Gs-coupled receptors.

Renal epithelial cells LLC-PK1 secrete high amounts of urokinase-type plasminogen activator (uPA) when stimulated through the cAMP-signaling pathway. Here we show that this characteristic can be used to identify rapidly LLC-PK1-derived cell lines expressing heterologous receptors that couple to Gs-proteins. A genomic clone encoding the mouse beta 2 adrenergic receptor (beta 2AR) was transfected stably into LLC-PK1 cells. Drug-resistant colonies were subsequently stimulated with isoproterenol and screened for the secretion uPA activity. Positive clones displayed dose-dependent uPA activity in response to isoproterenol, specifically bound the beta 2AR-agonist iodocyanopindolol and expressed beta 2AR-mRNA. The functional coupling of beta 2AR expression to the inducible uPA gene establishes that LLC-PK1 cells can be used to assay for beta 2AR (and beta 2AR-agonist) function. Our data suggest that this system can be used for functional expression of other heterologous receptors that couple to Gs-proteins.

Animals↗
PubMed1992

Functional dissection of the lck proximal promoter.

The lck gene encodes a protein tyrosine kinase that participates in lymphocyte-specific signal transduction pathways. Previous studies have established that lck transcription is regulated by two distinct promoter elements termed proximal (or 3') and distal (or 5'). The proximal promoter is active almost exclusively in thymocytes and becomes inactive later during T-cell maturation. To dissect the mechanisms responsible for lck gene regulation, we generated transgenic animals bearing 5' truncations in the proximal promoter element. Sequences between -584 and +37 with respect to the proximal promoter transcription start site act to direct tissue-specific and temporally correct transcription of either a tagged version of the lck gene itself or a heterologous reporter sequence (lacZ). This region contains binding sites for at least five distinct nuclear proteins, of which one is found only in cells that support proximal lck promoter activity and a second appears only in nonexpressing cells. Interestingly, the transcribed region of the lck gene contains positive control elements that can substantially boost expression from minimal (-130 bp) proximal promoter constructs. These results provide a basis for the biochemical dissection of transcriptional regulators that act at defined points during T-cell development.

Animals↗
PubMed1991

Developmental regulation of lck gene expression in T lymphocytes.

In the mouse and human, mRNA transcripts encoding the lymphocyte-specific protein tyrosine kinase p56lck are derived from two separate promoters resulting in heterogeneity in the 5' untranslated region sequence. The proximal promoter lies just 5' to the coding region for the gene and is active only in thymocytes. In contrast, the distal promoter lies 34 kilobases (kb) 5' in the human, and is active both in thymocytes and mature peripheral T cells. As previously reported, transgenic mice bearing functional proximal promoter sequence juxtaposed with the SV40 large T antigen gene invariably develop lymphoid tumors confined to the thymus. In the current work, transgenic mice bearing a 2.6-kb fragment of the human distal promoter fused to the SV40 large T antigen gene express large T antigen in thymocytes and in peripheral lymphoid cells, and develop tumors of both the thymus and the peripheral lymphoid organs. The ability of the human distal promoter to function appropriately in transgenic mice is consistent with the strong similarity observed between the mouse and human distal promoter sequences. With the exception of a single short interval that serves as a target for binding of nuclear factors, significant sequence similarity is not seen when the distal and proximal promoter sequences are compared. Hence, developmentally regulated, lineage-specific transcription of the lck gene is mediated by distinct promoter sequences that appear to be capable of functioning independently.

Animals↗
PubMed1991

Decreased beta 2-adrenergic receptor mRNA expression in receptor-deficient S49 lymphoma cells.

Many variants of the S49 mouse lymphoma cell have been isolated along the pathway of cyclic AMP generation and response. Two such variants, beta p and beta d, were isolated by Johnson and colleagues and described in 1979 [Mol. Pharmacol. 15:16-27 (1979)]. The beta p and beta d variants express one half and one quarter, respectively, of the wild-type number of beta 2-adrenergic receptors. This observation has now been extended through the use of DNA-excess solution hybridization. Using this exquisitely sensitive technique for quantitation of gene and mRNA, we have been able to demonstrate that the beta 2-adrenergic receptor-deficient variant cells contain the same quantity of the beta 2-adrenergic receptor gene as the wild-type cells. In contrast, the beta 2-adrenergic receptor-deficient variant cells express reduced quantities of beta 2-adrenergic receptor-specific mRNA. The amount of beta 2-adrenergic receptor-specific mRNA correlates very well with the reduction in receptor expression in these cells. Both gene and mRNA in the wild-type and variant cells appear to be the same size, as judged by Southern and Northern analysis. Thus, the diminution of beta 2-adrenergic receptors in the beta p and beta d variants appears to reflect primarily the relative paucity of gene transcripts in the variant cells. These data imply that variations in cellular content of beta 2-adrenergic receptor mRNA, which may occur among closely related cells, is one explanation for differences in receptor number.

Animals↗
PubMed1990

Neuropeptide Y (NPY)-containing nerves in mammalian ureter.

The distribution of neuropeptide Y in the ureter of the rat, rabbit, and man has been determined by radioimmunoassay and chromatographic analysis of the tissue extract. The localization of neuropeptide Y-immunoreactivity has been identified by immunocytochemistry. A regional distribution of neuropeptide Y was found; highest concentrations being present in the ureterovesical junction. Throughout the ureter, neuropeptide Y-immunoreactive nerve fibers were identified to surround the blood vessels and a few plexuses of neuropeptide Y-containing nerves were present within the muscle layers. Neuropeptide Y was not present within ganglion cells. Treatment of rats with 6-hydroxydopamine resulted in a significant reduction of neuropeptide Y concentrations in the upper, middle, and lower thirds of the ureter. This depletion in extractable neuropeptide Y was associated with morphologic changes typical of axonal degeneration of the neuropeptide Y-containing nerve fibers.

Animals↗