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Biomedical subjects

J J Welch

Publications and source records attributed to J J Welch.

17 recordsLinked to original sources
PubMed2000

Tumour volume estimated by computed tomography as a predictive factor in carcinoma of the tongue.

This retrospective study evaluated tumour volume, estimated by computed tomography (CT), as a predictive factor in carcinoma of the tongue. Tumour volume was measured from pretreatment CT scans of 20 consecutive patients, followed up for at least 3 years, and this measurement was compared with tumour volume estimated from pathological specimens. T-stage and CT-derived tumour volume were compared with the clinical and pathological status of the nodes, and with the outcome of treatment. The measurement of tumour volume derived from CT correlated well with measurements derived from pathological examination, and tumour volume also predicted overall treatment failure. The disease-specific survival rate was 100% for patients with low-volume tumours (<13 cc) compared with 79% for those with stage T1 and T2 tumours.CT is a reliable way of measuring the volume of tumours in carcinoma of the tongue, and tumour volume is useful adjunct to the clinical tumour-node-metastases staging system.

Adult↗
PubMed1998

Managed care: the dominant paradigm in US healthcare.

What does "managed care" really represent--and what effect has managed care had on the healthcare market? The author describes how managed care came to be a critical market force, offers a snapshot of its proliferation, and examines its effects on the traditional payment system.

Cost Control↗
PubMed1996

Effect of DNA-binding drugs on early growth response factor-1 and TATA box-binding protein complex formation with the herpes simplex virus latency promoter.

Adjacent binding sites for early growth response factor-1 (EGR1) and TATA box-binding protein (TBP) were identified on the herpes simplex virus latency promoter in previous work. The binding of EGR1 to the GC-rich region prevented TBP binding to the AT-rich region. With the simultaneous addition of both EGR1 and TBP, the intercalator nogalamycin prevented EGR1 complex formation, resulting in a dose-dependent increase of the TBP.DNA complex. The minor groove binder chromomycin A3 inhibited EGR1 complex formation but resulted in a smaller increase of the TBP complex. In contrast, an alkylating intercalator hedamycin strongly inhibited binding of both proteins. The ability of these GC-binding drugs to prevent EGR1.DNA complex formation was in the following order: hedamycin > nogalamycin > chromomycin A3, and the specificity was nogalamycin > chromomycin A3 > hedamycin. With transcription factor IIA (TFIIA) in the assay, TBP was able to bind the promoter whereas formation of the EGR1.DNA complex was reduced. An AT minor groove-binding drug, distamycin A, disrupted the TBP.TFIIA.DNA complex and restored the EGR1.DNA complex. We conclude that the binding motif and sequence preference of DNA-interactive drugs are manifested in their ability to inhibit the transcription factor-DNA complexes.

Alkylating Agents↗
PubMed1994

Targeting DNA-binding drugs to sequence-specific transcription factor.DNA complexes. Differential effects of intercalating and minor groove binding drugs.

Intercalating, minor groove binding, and covalently bonding drugs were evaluated by mobility shift assays for their ability to interfere with transcription factors binding to their respective DNA recognition sequences. The Cys2His2 zinc finger proteins EGR1, WT1, and NIL2A, the basic leucine-zipper protein wbJun/wbFos, and the minor groove binding protein hTBP were chosen as representative transcription factors. Their DNA recognition sites include G/C-rich, mixed, and A/T-rich sequences. The intercalators nogalamycin and hedamycin, and the G/C-specific minor groove binding drug chromomycin A3 were the most potent drugs, preventing transcription factor.DNA complex formation at concentrations less than 1 microM. Similar concentrations of chromomycin A3 disrupted preformed complexes while nogalamycin and hedamycin were 50-fold less potent if proteins were allowed to bind DNA prior to drug treatment. Echinomycin inhibited EGR1.DNA complex formation 50% at 5 microM but had little effect on the formation of NIL2A.DNA complexes. Conversely, doxorubicin was found to inhibit NIL2A complex formation 50% at less than 1 microM, but did not achieve this level of inhibition of EGR1/DNA complex formation even at 50 microM. The A/T-directed minor groove binding drugs, while inhibiting hTBP at submicromolar concentrations, had no effect on either EGR1 or NIL2A.

Anthraquinones↗
PubMed1993

Endemic giardiasis in New Hampshire: a case-control study of environmental risks.

Giardiasis is the most frequently reported diarrheal disease in northern New England. A case-control study of endemic giardiasis and environmental risk factors among residents of New Hampshire involved 273 cases from the state's 1984 disease registry and 375 controls. Giardiasis was associated with a shallow dug well as a residential water source (odds ratio [OR] = 2.4; 95% confidence interval [CI], 1.3-47.0), a recent history of drinking untreated surface water (OR = 3.4; CI, 2.1-5.5), a history of swimming in a lake or pond (OR = 4.6; CI, 2.4-86.0) or swimming in any natural body of fresh water (OR = 4.0; CI, 2.3-70.0), contact with a person thought to have giardiasis (OR = 2.3; CI, 1.4-36.0), and recent contact with a child in day care (OR = 1.5; CI, 1.0-2.1). Multivariate modeling supported these associations. Shallow wells, relatively common in New Hampshire, have not previously been established as important sources of giardiasis.

Adolescent↗
PubMed1986

CGS 10746B: an atypical antipsychotic candidate that selectively decreases dopamine release at behaviorally effective doses.

CGS 10746B, a benzothiadiazepine, has a behavioral profile in mice and monkeys similar to the atypical antipsychotic clozapine. Unlike clozapine, CGS 10746B suppresses dopamine neuron firing rates and, when administered at behaviorally effective doses by the oral or intraperitoneal route, decreases neostriatal dopamine release without changing dopamine metabolism or occupying D2 receptors. CGS 10746B is the first atypical antipsychotic candidate that selectively decreases dopamine release.

Action Potentials↗
PubMed1986

Isolation of malignant cells from human bone marrow using a discontinuous Percoll gradient.

A technique for examining relatively large volumes of bone marrow for involvement by malignancy is described. The use of discontinuous Percoll gradients offers no advantage over conventional methods in the diagnosis of hematological malignancy. Its usefulness in detecting infiltration by solid tumor is uncertain. Complete exclusion of malignancy from the fraction containing hematologic stem cells in three patients raises the possibility that this technique is a useful adjunct to other methods of marrow purging before autologous marrow rescue in malignant disease.

Biopsy, Needle↗
PubMed1983

Postsynaptic dopamine agonist properties of TL-99 are revealed by yohimbine co-treatment.

The claim that TL-99 (6,7-dihydroxy-2-dimethylaminotetralin hydrobromide) is a selective dopamine autoreceptor agonist relies partly upon indirect behavioral evidence, particularly the absence of stereotyped behavior in treated rats. The possibility was examined that concurrent alpha 2-adrenoceptor agonist properties of TL-99 could have masked postsynaptic dopamine agonist activity. Co-administration of yohimbine or piperoxan with a high dose of TL-99 (30 mg/kg) dramatically increased motor activity in reserpinized rats, whereas each drug by itself had no effect. Contralateral rotational behavior in 6-hydroxydopamine-lesioned rats resulted from combined treatment with yohimbine and a high dose of TL-99 (30 mg/kg) but appeared to be suppressed by concurrent flaccidity if TL-99 was given by itself. Yohimbine failed to alter the effects of 3-PPP (N-n-propyl-3-(3-hydroxyphenyl)-piperidine), another putative dopamine autoreceptor agonist, in either model of postsynaptic dopamine agonism. It is concluded that a concurrent behaviorally depressant action of TL-99, possibly alpha 2-agonism, masks the stimulation of postsynaptic dopamine receptors by high doses of TL-99.

Animals↗