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J Lawlor

Publications and source records attributed to J Lawlor.

6 recordsLinked to original sources

Modification of syphilitic genital ulcer manifestations by coexistent HIV infection.

BACKGROUND: Conflicting data exist regarding whether HIV infection leads to changes in the clinical manifestations and severity of genital ulcer disease (GUD). GOAL: To determine the impact of HIV on the etiology and clinical severity of GUD. STUDY DESIGN: From July 1990 to July 1992, consecutive patients presenting to the two Baltimore City Health Department (BCHD) Sexually Transmitted Diseases clinics were approached as candidates for enrollment in a prospective study to determine factors associated with the transmission and acquisition of sexually transmitted diseases (STDs). RESULTS: Of the 1368 patients who presented to the BCHD, 214 (16%) had genital ulcerations: 160 (21%) of 757 men and 54 (9%) of 611 women. Among the patients with GUD who had undergone HIV testing, 28 (14%) of 204 were infected with HIV: 25 (17%) of 151 men and 3 (6%) of 53 women. Although both groups-those infected with HIV and those not infected with HIV--presented with GUD of similar duration (10 versus 11 days; P = 0.17), multiple lesions were found more frequently in men with HIV infection than in uninfected men: 87% versus 62% (P = 0.02). Although not statistically significant, GUD in men with HIV infection more often were deep (64% versus 44%, respectively) rather than superficial (36% versus 57%, respectively; P = 0.08), and larger (505 mm(2) versus 109 mm 2; P = 0.06). Primary syphilis caused more GUD among men with HIV infection than among uninfected men: 9 (36%) of 25 versus 24 (19%) of 126, respectively (P < 0.01). Secondary syphilis was diagnosed with concomitant GUD more frequently among men with HIV infection than among uninfected men: 3 (13%) of 25 versus 3 (2%) of 123, respectively (P < 0.01). CONCLUSIONS: In this study, patients who presented with GUD were more likely to be infected with HIV. A higher proportion of men with HIV infection had multiple lesions, and the lesions were more likely to be caused by syphilis.

Adolescent↗

Comment on TMD.

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Bruxism↗

Voluntary testing for human immunodeficiency virus (HIV) in a prison population with a high prevalence of HIV.

This study evaluated voluntary testing for human immunodeficiency virus (HIV) in a prison population with a high HIV seroprevalence. Data on demographic variables and participation in voluntary testing were linked to a blinded HIV serosurvey of consecutive Maryland prison entrants (April-July 1991). Among 2,842 entrants, HIV seroprevalence was 8.5% (men, 7.9%; women, 15.3%). Voluntary testing was accepted by 47% of the entrants, and it identified 34% of the HIV-seropositive inmates detected by serosurvey. Refusers of testing were more likely to test HIV-seropositive than were accepters (adjusted odds ratio (OR) = 1.84, 95% confidence interval (CI) 1.58-2.16). Refusers and accepters of testing had similar risk factors for HIV infection, chiefly current syphilis infection (adjusted OR = 5.96, 95% CI 3.15-10.27) and prior injected drug use (adjusted OR = 4.26, 95% CI 3.15-5.76). Among 100 entrants asked why they refused testing, primary reasons given included low risk of HIV, fear of testing HIV-seropositive, and lack of interest. Voluntary testing appears only moderately successful in identifying HIV-seropositive inmates in a high-seroprevalence prison population. However, the alternative, mandatory HIV testing of prisoners, can be construed as discriminatory and unethical when similar screening is not imposed on the population at large. Data presented here suggest strategies to improve acceptance of voluntary testing, especially by high risk inmates.

Adult↗

A point mutation in transthyretin increases affinity for thyroxine and produces euthyroid hyperthyroxinemia.

In a family expressing euthyroid hyperthyroxinemia, an increased association of plasma thyroxine (T4) with transthyretin (TTR) is transmitted by autosomal dominant inheritance and is secondary to a mutant TTR molecule with increased affinity for T4. Eight individuals spanning three generations exhibited the abnormality. Although five of eight individuals had elevated total T4 concentrations, all affected individuals were clinically euthyroid and all had normal free T4 levels. Purified TTR from the propositus had an affinity for 125I-T4 three times that of control TTR. Exons 2, 3, and 4 (representing greater than 97% of the coding sequence) of the TTR gene of DNA prepared from the propositus' peripheral blood leukocytes were amplified using the polymerase chain reaction (PCR) and were sequenced after subcloning. Exons 2 and 3 were indistinguishable from normal. In 50% of clones amplified from exon 4, a substitution of adenine (ACC) for guanine (GCC) in codon 109 resulted in the replacement of threonine-for-alanine, a mutation confirmed by amino acid sequencing of tryptic peptides derived from purified plasma TTR. The adenine-for-guanine substitution abolishes one of two Fnu 4H I restriction sites in exon 4. PCR amplification of exon 4 of TTR and restriction digestion with Fnu 4H I confirmed that five affected family members with increased binding of 125I-T4 to TTR are heterozygous for the threonine 109 substitution that increases the affinity of this abnormal TTR for T4.

Amino Acid Sequence↗