Exercise-induced left ventricular dilatation.
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Biomedical subjects
Publications and source records attributed to W C Reeves.
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To determine the influence of tobacco abuse on thallium 201 lung uptake during exercise, we examined 185 consecutive subjects with normal myocardial perfusion scans and without electrocardiographic evidence of left ventricular hypertrophy. The subjects were divided into two groups: group 1 subjects (n = 60) had histories of smoking and group 2 subjects (n = 125) were nonsmokers. Eighty-eight percent of group 1 subjects and 92% of group 2 subjects were examined using single-photon emission computed tomography and the remaining patients underwent planar imaging. 201Tl lung and heart activities were quantified from the immediate anterior planar images that were obtained in all subjects and reported as lung to heart ratio (L/H). 201Tl L/H in smokers (0.39 +/- 0.11) was significantly higher (P < 0.05) than in nonsmokers (0.34 +/- 0.06) when subjects who achieved 85% of the target heart rate were compared. In conclusion, 201Tl L/H was higher in smokers than in nonsmokers when subjects who achieved 85% of the target heart rate and had no myocardial perfusion defects were compared.
This investigation was performed to determine whether diabetes mellitus has an additive effect on diminishing coronary perfusion reserve index in hypertensive patients. Coronary perfusion reserve index, thallium lung uptake, the electrocardiogram and haemodynamic parameters were evaluated by exercise thallium myocardial perfusion scintigraphy. In 18% of hypertensive and 13% of diabetic-hypertensive patients there was evidence of left ventricular hypertrophy on electrocardiogram. The maximum heart rate achieved in hypertensive, diabetic and diabetic-hypertensive patients was significantly lower (P < 0.05) than in control patients. The maximum SBP achieved in hypertensive (210 +/- 40 mmHg) and diabetic-hypertensive patients (216 +/- 36 mmHg) was higher (P < 0.05) than in control patients (186 +/- 32 mmHg). A significantly higher number of diabetic patients (53%) did not achieve the exercise rate pressure product of > 26,000 when compared with control (27%), hypertensive (24%) and diabetic-hypertensive (30%) patients. Coronary perfusion reserve index in hypertensive patients decreased significantly (P < 0.05) when compared with control (no hypertension, no diabetes) patients (1.67 +/- .14 vs. 1.79 +/- .17). Coronary vasodilatory reserve index was also reduced significantly (P < 0.05) in diabetic patients in comparison with controls (1.66 +/- .17 vs. 1.79 +/- .17), and was further reduced in diabetic-hypertensive patients when compared with control patients (1.63 +/- .13 vs. 1.79 +/- .17). Thallium uptake in the lung quantified as thallium lung to heart ratio were comparable in all four groups. The results suggest that diabetes mellitus diminishes the coronary perfusion reserve index in patients with hypertension and therefore many account for the increased cardiovascular morbidity in these patients.
Increasing evidence indicates that infection with genital types of human papillomavirus (HPV) can occur prior to the onset of sexual activity, possibly by perinatal transmission. Evidence is also accumulating that women infected with the human immunodeficiency virus (HIV) more frequently express HPV. We conducted this study to measure HPV prevalence in HIV-seropositive and -seronegative women in Kinshasa, Zaire and in their children. We collected cervico-vaginal lavage specimens from 80 mothers (52 HIV-seropositive and 28 HIV-seronegative at the time of delivery) and oropharyngeal and perineal specimens from their 81 3-year old children (21 HIV-seropositive and 60-seronegative). We used the ViraPap and ViraType assay to test specimens for HPV DNA by the dot-blot technique. Detection of HPV in the mother was highly associated with HIV: 20 HIV-seropositive women and one seronegative woman had HPV DNA. Ten children had HPV DNA. However, detection of HPV in the children was not associated with the mothers' HPV or HIV status or with the child's own HIV status. These findings document a substantial prevalence in young children of HPV DNA types that are linked to genital-tract neoplasia in adults, but do not specifically support a hypothesis of mother-to-child transmission of genital HPV types.
We report 4 cases of deep venous thrombosis and/or pulmonary embolism after diagnostic cardiac catheterization. Two of these cases followed left heart catheterization alone.
A case-control study in four Latin American countries enabled assessment of risk factors for different histologic types of invasive cervical cancers, with the main analyses focusing on 667 patients with squamous cell cancers and 43 with adenocarcinomas. The epidemiology of the squamous cell tumors resembled that found in other studies, namely a high risk associated with multiple sexual partners (RR = 1.5 for > or = 2 vs 1), early ages at first intercourse (RR = 2.3 for < 16 vs > or = 20), history of a sexually transmitted disease (RR = 1.8), multiple births (RR = 2.2 for > or = 7 vs 1-3), absence of prior Pap smear screening (RR = 3.0 vs Pap within 24 months), detection of HPV DNA (RR = 3.6), and limited years of schooling (RR = 1.9 for < 4 vs > or = 7). The adenocarcinomas appeared less affected by sexual, reproductive, or socioeconomic factors. There was no relationship with age at first intercourse, history of a sexually transmitted disease or education, and only marginal associations with number of sexual partners or parity. Absence of prior Pap smear screening as well as detection of HPV DNA, however, were associated with relationships equally strong as those for the squamous cell tumors. Oral contraceptive use distinctly affected risk of the adenocarcinomas, increasing risk by approximately two-fold. Analyses of the 18 subjects with adenosquamous cancer suggested some resemblance to the squamous cell tumors, especially with respect to the role of sexual and sociodemographic variables. These findings support the need for detailed studies of etiologic differences between the different histologic types of cervical cancers, with an emphasis on careful pathologic review and precise measurement of HPV.
Compared with other laboratory techniques, the polymerase chain reaction (PCR) is a simple, rapid, sensitive method for detecting human papillomavirus (HPV) DNA in cervical samples. However, since many cervical samples contain multiple HPV types, we decided to investigate whether PCR results from such samples accurately reflected the relative amounts of each HPV type present. Theoretical calculations of product accumulation when multiple DNAs with different amplification efficiencies are present in the same sample were done. In addition a set of samples in which cloned HPV DNAs were mixed in varying proportions prior to PCR was tested. Finally, four clinical samples containing multiple HPV types by hybridization assays were subjected to PCR, using two different primer sets. Each of these lines of investigation showed that selective amplification of one HPV DNA over another can occur when mixed HPV types are present. This effect may lead to inaccurate information regarding both types and relative amounts of HPV DNAs in samples containing multiple HPV types. A protocol to avoid this problem is described.
Epidemiologic studies show an association between infection with human immunodeficiency virus type 1 (HIV-1) and human papillomavirus (HPV) associated anogenital disease. To investigate possible molecular mechanisms of HIV-1 modulation of HPV expression, we studied the effect of an HIV-1 regulatory protein, tat1, on gene expression directed by the upstream regulatory region (URR) of HPV type 16 (HPV 16). HPV 16 URR-directed chloramphenicol acetyltransferase (CAT) expression driven by the native HPV 16 promoter (P97) was increased in the presence of tat1 alone. Tat1 also reversed E2-mediated repression of P97-directed CAT expression. E2 mediated CAT expression with URR constructs containing the SV40 promoter was enhanced when tat1 and E2 were cotransfected. Using a cervical carcinoma cell line (SiHa), E2 enhancement of URR-directed gene expression was elevated in the presence of extracellular tat1 or during cocultivation with HIV-1-infected cells. These results show HIV can modulate HPV gene expression in cell culture and that the increased rate of HPV-associated cervical disease in asymptomatic HIV-seropositive women may result from HPV-HIV molecular interactions.
Mosquitoes collected from alpine, Central Valley, and coastal habitats in California were evaluated for their vector competence for four strains of Jamestown Canyon (JC) virus. Three of the viral strains examined were isolated from alpine Aedes species collected in California, and one, the prototype JC virus, was isolated from Culiseta inornata (Williston) collected in Colorado. Alpine Aedes tahoensis Dyar, Ae. cataphylla Dyar, Ae. hexodontus Dyar, Ae. increpitus Dyar, Ae. clivis Lanzaro and Eldridge, and coastal Aedes washinoi Lanzaro and Eldridge were variably susceptible to alpine strains of JC virus. Infection rates ranged from 22 to 77%, and peroral transmission rates of the infected females ranged from 0 to 26%. The differences were related to both mosquito species and viral strain. Coastal populations of Cs. inornata, Ae. washinoi, and Ae. sierrensis (Ludlow) were incompetent vectors when fed an alpine strain of JC virus, whereas Ae. squamiger (Coquillet) and Ae. dorsalis (Meigen) were competent vectors. Peroral transmission rates following parenteral infection of females of most species were about twofold higher than those for perorally infected females. A population of Cs. inornata from the Central Valley was highly susceptible when fed an alpine strain of JCV and transmitted virus both horizontally and vertically. Alpine strains of JC virus also were transmitted vertically by Ae. tahoensis, Ae. washinoi, and Ae. squamiger following parenteral infection of females.
Selected mosquito species from Central Valley, coastal, and alpine habitats of California were evaluated for their vector competence for Northway (NOR) virus. Culiseta incidens Thomson, Culiseta inornata (Williston), and Anopheles freeborni Aitken were the only competent vectors when fed virus. Aedes sierrensis (Ludlow), as well as alpine snow pool Aedes (i.e., Ae. cataphylla Dyar, Ae. hexodontus Dyar, Ae. increpitus Dyar and Ae. tahoensis Dyar), Ae. melanimon Dyar, Ae. washinoi Lanzaro & Eldridge, Culex erythrothorax Dyar, and Cx. tarsalis Coquillett were highly refractory to peroral infection. Alpine snow pool species were poor vectors even following parenteral infection, but 21-35% of intrathoracically inoculated Ae. sierrensis from several lower elevation localities and 39-46% of parenterally infected Cx. tarsalis were able to transmit NOR virus per os. Perorally infected Cs. inornata transmitted NOR virus vertically to their F1 adult progeny at a low rate (minimal filial infection rate, 1:248).
Nearly 80,000 immature and adult mosquitoes in three genera were collected in high-elevation (> 1,000 m) areas of California (68,229), Nevada (3,721), Oregon (5,918), and Washington (1,629) during 1990-1992 and tested for virus as adult males or females in 1,799 pools. Collections comprised primarily alpine Aedes in the Aedes communis (De Geer) group of the subgenus Ochlerotatus. Thirteen strains of Jamestown Canyon (JC) virus were recovered by plaque assay in Vero cell culture from three members of the Ae. communis group: 10 from Aedes tahoensis Dyar, 2 from Aedes cataphylla Dyar, and 1 from Aedes hexodontus Dyar. All isolates came from collections made in Alpine, Sierra, Tulare, or Tuolumne counties in the Sierra Nevada of California. Vertical transmission of JC virus in all three mosquito species was demonstrated by the isolation of virus from adult males or females reared from field-collected larvae or pupae. The prevalence of infected Ae. tahoensis was significantly higher in field-collected adult females than in reared adult males and females in Alpine County, which indicated that JC virus was being amplified by horizontal transmission. This study further incriminated Ae. tahoensis, Ae. cataphylla, and Ae. hexodontus as natural vectors of JC virus in California and greatly extended the known geographical range of this virus in the Sierra Nevada.
Verapamil can produce depression of left ventricular function, delayed atrioventricular conduction, and hypotension, which can be potentiated by hyperkalemia. We sought to investigate a direct cardiac interaction between verapamil and hyperkalemia. Studies utilized isolated guinea pig hearts (Langendorff) paced at 250 beats/min. Hearts were randomly assigned to perfusion (Krebs-Henseleit buffer) with potassium concentrations ([K]+) of 1.5, 3, 6 and 9 mmol/l. Infusion of verapamil at rates of 0.2 to 60 micrograms/min (approximately 3 x 10(-8) to 10(-5) mol/l) produced concentration-dependent reduction of isovolumic left ventricular developed pressure. As [K]+ increased, concentration response curves showed parallel shifts to the left. The ED50 for reduction of left ventricular developed pressure significantly decreased: 8.2 +/- 3.7, 2.9 +/- 1.4, 1.2 +/- 0.7, 0.6 +/- 0.2 micrograms/min (mean +/- SD), respectively. Nifedipine and diltiazem were also studied in hearts perfused with 3 and 9 nmol/l [K]+. Infusion of nifedipine 0.003-1 microgram/min (approximately 10(-9) to 3 x 10(-7) mol/l) produced concentration-dependent reduction of left ventricular developed pressure but the ED50 was not affected by [K]+: 0.06 +/- 0.03 and 0.05 +/- 0.04 microgram/min, respectively. Nifedipine vehicle was without effect at the infusion rates tested. Infusion of diltiazem 2-200 micrograms/min (approximately 3 x 10(-7) to 3 x 10(-5) mol/l) also produced concentration-dependent reduction of left ventricular developed pressure. The ED50 for diltiazem-induced reduction of left ventricular developed pressure was significantly reduced by elevated [K]+: 20.1 +/- 6.7 and 3.5 +/- 0.9 micrograms/min with 3 and 9 mmol/l [K]+, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
We conducted a study to look for a simian counterpart of human T-lymphotropic virus (HTLV) in wild-caught monkeys in the Republic of Panama. Serum specimens were obtained from 102 monkeys (Ateles fusciceps, n = 75; Alouatta villosa, n = 18; and Cebus capucinus, n = 9) captured in Panama's Darien rain forest in 1979-1980. Specimens were screened for HTLV antibody by enzyme-linked immunosorbent assay, and reactive specimens were further tested by Western blot. None of the 102 specimens were seropositive for HTLV. Our findings provide no evidence for an HTLV-like virus in New World primates from Panama, but the sample size was small, and further studies are warranted.
OBJECTIVE: To determine the influence on survival from cervical cancer of human papillomaviruses (HPVs) and other factors including age, herpes simplex virus type 2 (HSV-2) antibody status, and number of pregnancies. METHODS: We followed 196 women diagnosed with invasive cervical cancer in Panama for an average of 32 months. Clinical and risk-factor information was obtained from these women through an interview and review of medical records. We assessed HPV DNA status by testing tumor specimens using polymerase chain reaction, Southern blot, and slot blot techniques. Kaplan-Meier survival curves and Cox proportional hazards model were used to assess the risk of mortality associated with selected variables. RESULTS: Eighty-one percent (N = 144) of the women tested for HPV were positive. Absence of HPV DNA was associated with a 1.9-fold excess risk of mortality (95% confidence interval [CI] 1.1-3.3) after controlling for age, clinical stage at diagnosis, number of pregnancies, and HSV-2 seropositivity. Women diagnosed with cervical cancer before the age of 30 had a ninefold excess risk of dying compared with those diagnosed at age 50 or older (relative risk [RR] 9.3, 95% CI 3.4-25.5). Parity was also an independent prognostic factor. Women with six or more pregnancies had a 2.5-fold excess risk of dying compared with women with three or fewer (95% CI 1.2-5.3). Years of education, presence of HSV-2 antibodies, age at first intercourse, number of sexual partners, oral contraceptive use, and cigarette smoking were not significantly associated with prognosis. CONCLUSION: These findings suggest that women negative for HPV DNA, those who are diagnosed at an early age, and those who have multiple pregnancies might have more aggressive tumors.
This study shows that 10% of Panamanian women are infected with VPH. This incidence of premalign and malign infection is one of the highest in the world. It is necessary that panamanian women be educated to participate in the program of the early detection of the disease to control the incidence of cancer in the uterine cervix.
The incidence of cervical cancer in Costa Rica is about twice as high in the coastal regions as in the interior. To study these regional variations, we used data from a 1986-1987 case-control study of 192 Costa Rican women with invasive cervical cancer and 372 controls. Risk factors identified included the following: The study participant's (1) number of sexual partners, (2) age at first sexual intercourse, (3) number of live births, (4) presence of type 16/18 human papillomavirus (HPV) DNA, (5) venereal disease (VD) history, (6) Pap smear history, and (7) socioeconomic status. The adjusted relative risks (RR) and 95% confidence intervals (CI) for each of these risk factors were as follows: (1) > or = 4 vs. 1 sexual partner: RR = 2.0, 95% CI = 1.1-3.5; (2) age of initiation < or = 15 vs. > or = 18 years: RR = 1.5, 95% CI = 0.9-2.5; (3) > or = 6 vs. < or = 1 live birth: RR = 1.7, 95% CI = 0.7-3.9; (4) HPV 16/18 DNA in cervix: RR = 2.8, 95% CI = 1.9-4.2; (5) VD history: RR = 2.2, 95% CI = 1.2-4.0; (6) no Pap smear: RR = 2.4, 95% CI = 1.5-3.8; and (7) low socioeconomic status: RR = 2.0, 95% CI = 1.2-3.2. The population-attributable risks related to HPV detection, four or more sexual partners, six or more live births, no prior Pap smear, and low socioeconomic status were 39%, 38%, 29%, 23%, and 22%, respectively. Several of the sexual and reproductive risk factors were relatively more prevalent in the high-risk region, but Pap screening and detection of HPV were equally prevalent in the high-risk and low-risk regions. Though differences in screening quality (laboratory and follow-up) may have been involved, we conclude that the observed regional differences reflect behavioral more than screening differences. This suggests that screening programs should be more aggressive in the high-risk area, given the more frequent occurrence of the disease there. Failure to detect a higher prevalence of HPV in the high-risk region could reflect weaknesses in the in situ hybridization test employed. Alternatively, cofactors may have to be present in order for HPV to exert its role in cervical carcinogenesis.
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