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Biomedical subjects

J B Jensen

Publications and source records attributed to J B Jensen.

At least 73 records · Page 4Linked to original sources
PubMed1990

Specificity and sensitivity of sexually anatomically correct dolls in substantiating abuse: a pilot study.

Sexually anatomically correct dolls are often used to verify or refute allegations of sexual abuse in young children. As a test of their effectiveness in facilitating decisions about the abuse status of young children, the authors conducted blind interviews with six abused subjects, five nonclinic controls and four psychiatric controls. The child psychiatrist interviewer followed a standardized protocol and was able to correctly categorize 33% of the abused and 67% of the nonabused children. Proper classification was 53% for the sample using this protocol. The authors' preliminary conclusion is that, without other information available to the interviewer, sexually anatomically correct dolls are a poor source of information to decide the abuse status of a young child. The authors recommend that professionals should be cautious when basing decisions on a single instrument, such as sexually anatomically correct dolls. Mental health professionals are encouraged to maintain quality standards in evaluation of children by conducting a comprehensive examination in child sexual abuse cases.

Child↗
PubMed1990

Cell-mediated immune responses to soluble Plasmodium falciparum antigens in residents from an area of unstable malaria transmission in the Sudan.

This paper describes immune responses to P. falciparum infection in individuals living in an area of highly seasonal, unstable malaria transmission. The in vitro cellular immune responses of peripheral blood mononuclear cells (PBMC) from 36 Sudanese donors to a complex of affinity purified soluble P. falciparum antigens (SPag) and two components thereof (Ag1 and Ag7) were examined and compared to humoral immune parameters. In 29/36 Sudanese donors, SPag induced a significant lymphoproliferative response in vitro. In contrast only 3/27 Danish donors never exposed to malaria responded to SPag. Ag1 and Ag7 induced significant lymphoproliferation in 9/34 and 13/36 Sudanese donors respectively, whereas no Danish donors responded. Significant interferon-gamma production was observed in 16/27, 1/5 and 3/12 Sudanese donors when stimulated by SPag, Ag1 and Ag7 respectively. Lymphoproliferative responses to SPag correlated with proliferative responses to Ag1 and Ag7, and with Spag-induced interferon-gamma production. These results indicate that T-cell clones recognizing epitopes on Ag1 and Ag7 have been expanded in the studied population as a result of exposure to P. falciparum infection. The T-cell parameters did not correlate with the presence of antibodies to SPag, Pf155/RESA or a crude parasite sonicate or with the schizont IFA titers of the plasma. This indicates that parameters outside the degree of exposure to P. falciparum influence the cellular immune responses to malaria.

Adult↗
PubMed1990

Cerebral blood flow and end-tidal PCO2 during prolonged acetazolamide treatment in humans.

One oral dose of 1,000 mg of acetazolamide caused an acute 38% increase in cerebral blood flow (CBF) in eight healthy volunteers. During the following 10 days the subjects took 1,000 mg acetazolamide daily. CBF normalized within the first 2 days. The drug induced mild hyperventilation, gradually decreasing alveolar PCO2 to 70% of the control value at the end of the treatment period. In healthy humans the hyperventilation will not increase brain oxygenation significantly at sea level. But at high altitudes the enhanced ventilatory drive will improve oxygenation of the brain, and this may account for the beneficial effects of the drug on the symptoms of acute mountain sickness. During the treatment there was a significant 10% decrease of the hematocrit but an unaltered hemoglobin concentration. In combination with data in the literature our studies suggest that the initial CBF increase is a consequence of a transient extracellular acidosis dilating brain arterioles, whereas increased ventilatory drive results from a gradually increasing mild intracellular acidosis in the brain.

Acetazolamide↗
PubMed1990

Cerebral blood flow in acute mountain sickness.

Changes in cerebral blood flow (CBF) were measured using the radioactive xenon technique and were related to the development of acute mountain sickness (AMS). In 12 subjects, ascending from 150 to 3,475 m, CBF was 24% increased at 24 h [45.1 to 55.9 initial slope index (ISI) units] and 4% increased at 6 days (47.1 ISI units). Four subjects had similar increases of CBF when ascending to 3,200 m 3 mo later, indicating the reproducibility of the measurements. In nine subjects, ascending from 3,200 to 4,785-5,430 m, CBF increased to 76.4 ISI units, 53% above estimated sea-level values. CBF and increases in CBF were similar in subjects with or without AMS. In six subjects, CBF was measured before and after therapeutic intervention. At 2 h CBF increased 22% (71.3 to 87.3 ISI units) above pretreatment values in three subjects given 1.5 g acetazolamide, while three subjects given placebo showed no change. Symptoms remained unaltered in all subjects during the 2 h of the study. Overall, the results indicated that increases in CBF were similar in subjects with or without AMS while acetazolamide-provoked increases of CBF in AMS subjects caused no acute change in symptoms. Alterations in CBF cannot be directly implicated in the pathogenesis of AMS.

Acetazolamide↗
PubMed1990

Epirubicin cardiotoxicity: a study of 135 patients with advanced breast cancer.

The cardiotoxicity of epirubicin (EPI) was evaluated clinically, radiologically, with ECG, and with multiple ECG-gated radionuclide determination of the left ventricular ejection fraction (LVEF) during rest in 135 patients with advanced breast cancer. The EPI doses were 60 mg/m2 on days 1 and 8 every 4 weeks or 45 mg/m2 plus vindesine 3 mg/m2 on the same schedule. The median cumulative dose of EPI was 500 mg/m2 (range, 47 to 1,563). Eight of the 135 patients developed congestive heart failure (CHF). Of 67 patients treated with EPI less than 500 mg/m2, none developed CHF. Among 48 patients treated with doses between 500 and 1,000 mg/m2, one had CHF (2%; 95% confidence limits, 0.1 to 11.1). Among 20 patients who received EPI from 1,000 to 1,563 mg/m2, seven developed CHF (35%; 95% confidence limits, 15.4 to 59.2). Four patients died due to cardiotoxicity. The risk of EPI cardiotoxicity at the present schedule is considerable at doses above 1,000 mg/m2. At doses between 500 and 1,000 mg/m2 the risk of CHF decreases, and at doses below 500 mg/m2, it is negligible. For all patients, the prevalence of CHF was 6% and the sensitivity of LVEF high (95%), mainly due to the low incidence of CHF. Among the 20 patients who received EPI at more than 1,000 mg/m2, the prevalence of CHF was 35% and the sensitivity only 64%. The specificity was maximally 62%. Our results suggest that LVEF is of no value as a predictor for CHF.

Adult↗
PubMed1989

HLA genotypes and variant alleles in Sudanese families of Arab-Negroid tribal origin.

The indigenous population of the Blue Nile Province, Sudan, is an Arab-Negroid admixture, although some isolates of west African origin (Fallata) have begun to intermix with the indigenous population. Consanguineous marriages are common in these Muslim families. Members of 22 nuclear families were typed for HLA class I and II antigens using complement-dependent microcytotoxicity with Ninth International Workshop (9th WS) and local reagents. Considerable polymorphism was observed at each locus with a majority of the World Health Organization (WHO)-recognized alleles represented in the parental sample, albeit at low frequency. Seven parental haplotypes carried A locus alleles which were not identical to WHO-recognized specificities. All appeared to be Aw19-related specificities. Five B locus serologic variants were observed; all appeared distinct from WHO-recognized specificities. In one family we observed a new DR-DQ association; DR4 segregated with DQw2, rather than with DQw3. As has been observed for several other genetic systems in these tribes, considerable polymorphism was found for all class I and class II gene products in spite of a high level of consanguinity. Tribal admixture and/or a selective advantage in protecting the population against disease may account for this unexpectedly high level of heterozygosity.

Black People↗
PubMed1989

Stage specific actions of antimalarial drugs on Plasmodium falciparum in culture.

Chemicals with antimalarial effects show different patterns against ring stages, trophozoites, and schizonts of Plasmodium falciparum in culture. Amodiaquine, mefloquine, quinine, quinacrine, primaquine, qinghaosu, halofantrine, rifampin, antimycin A1, cycloheximide, and actinomycin D were preferentially toxic to the mature stages. Ammonium chloride killed ring stages faster than mature forms, while tetracycline, clindamycin, and halofuginone acted with equal speed on all 3 stages.

Animals↗
PubMed1988

Epidemiological and immunological aspects of human crisis form factor in falciparum malaria: cell-mediated responses?

Crisis forms in malaria are degenerated intra-erythrocytic asexual parasites which appear at the time of immunologic crisis and thus may be part of the immune response to this disease. The factor(s) involved in this phenomenon are poorly understood, but are believed to be related to products of phagocyte activation. This hypothesis is supported by observations that animals, whose cell-mediated immune responses have been hyperstimulated by BCG, are protected from otherwise lethal malaria infections and their sera induce crisis forms in vitro. Many human serum samples collected from malaria-endemic areas of Sudan induce crisis forms in cultures of Plasmodium falciparum. Two popular models to explain this intra-erythrocytic, anti-parasitic action have been proposed: (i) the presence in the immune serum of a cytotoxic cytokine, crisis form factor, or (ii) that crisis forms result from oxidant stress generated during respiratory bursts associated with phagocyte activation, or indirectly by toxic products of lipid peroxidation produced by reactive oxygen species which appear in the serum during phagocyte respiratory bursts. Experimental evidence has been generated to support both of these hypotheses and both mechanisms may be involved in the induction of crisis forms.

Animals↗
PubMed1988

Affinity-purified antibodies to ring-infected erythrocyte surface antigen do not correlate with merozoite invasion inhibition in Plasmodium falciparum.

We affinity purified, from malaria-immune serum, antibody to the ring-infected erythrocyte surface antigen (RESA), using petri dishes containing a monolayer of Plasmodium falciparum ring-infected erythrocytes. Except for one out of eight samples, the purified antibody positive by RESA-immunofluorescent assay was not inhibitory to the in vitro invasion of merozoites into erythrocytes in three geographically distinct strains of P. falciparum. However, the initial high level of merozoite-inhibiting antibodies of the intact serum samples remained in the immunoglobulin G fraction from which the RESA antibodies had been removed by affinity chromatography. These results suggest that, although in some cases RESA-immunofluorescent assay-positive antibodies may be inhibitory to merozoite invasion, there are more important antibodies capable of merozoite invasion inhibition.

Animals↗
PubMed1988

Uptake of antibiotics by Plasmodium falciparum in culture.

The ability of Plasmodium falciparum to accumulate 3H-clindamycin, 3H-tetracycline, and 3H-dihydrostreptomycin was determined in synchronized trophozoites and schizonts in 87% parasitemia 5% hematocrit cultures. Accumulation was time-dependent and modestly concentration-dependent. At 0.1 mM initial external drug concentration, the ratio of drug concentration in cells:medium after 120 min was 5.5 for 3H-clindamycin, 2.8 for 3H-tetracycline, and 0.95 for 3H-dihydrostreptomycin. Corresponding values for uninfected erythrocytes were 3.2, 2.3, and 0.78, respectively. These data may explain the lack of antimalarial activity of the aminoglycosides and may partially explain the slow onset of therapeutic action of clindamycin and tetracycline. The low intracellular concentrations attained for the latter two drugs have important implications for understanding the kinetics and mechanism of their antiplasmodial effects.

Animals↗
PubMed1988

Neuroendocrine aspects of attention deficit hyperactivity disorder.

This article summarizes the existing neuroendocrine literature and reports the growth hormone response to stimulation with L-dopa and clonidine in male children and adolescents with attention deficit hyperactivity disorder. Because growth hormone secretion is regulated by monoamine neurotransmitters, hyposecretion of growth hormone may reflect generalized changes in the neurochemical substrate of this disorder. With refinement, these neuroendocrine challenge tests may become unique biologic markers in identifying attention deficit hyperactivity disorder in children and adolescents.

Attention Deficit Disorder with Hyperactivity↗
PubMed1988

Inhibition of the intraerythrocytic development of Plasmodium falciparum in glucose-6-phosphate dehydrogenase deficient erythrocytes is enhanced by oxidants and by crisis form factor.

In this study, we have examined P. falciparum development in untreated normal or G6PD deficient erythrocytes as well as in parasitized cells exposed to isouramil--a fava bean extract known to induce oxidant stress in G6PD deficient erythrocytes (a condition known as favism), to diamide--a thiol oxidizing agent and to crisis form factor (CFF)--a non-immunoglobulin product found in the sera of man immune to malaria. We observed a significant retardation in intraerythrocytic development of parasites cultured in the G6PD deficient cells in comparison with parasites grown in the normal ones. Plasmodia within the G6PD deficient erythrocytes were markedly more sensitive to the inhibitory activity of CFF or the oxidizing agents diamide and isouramil. Mature stages of the parasites in both normal and G6PD deficient erythrocytes were more vulnerable than young ring forms, to oxidizing agents. The overall results show that the genetic trait of the host cell and the degree of maturation of the plasmodia are both crucial factors in determining the sensitivity of the parasite to oxidant stress.

Animals↗
PubMed1988

RESA-IFA assay in Plasmodium falciparum malaria, observations on relationship between serum antibody titers, immunity, and antigenic diversity.

RESA-IFA assays were conducted using 63 adult sera from 7 different malarious areas against 7 different strains of Plasmodium falciparum, and 28 children's sera against 3 different parasite strains. Generally, where immunity to malaria was high, there was little or no antigenic diversity among the different strains examined. However, where sera were collected from semi-immunes, or from children, some variation in the RESA-IFA endpoint titers was discernible. Correlation between antibody titers determined by RESA-IFA and in vitro parasite invasion inhibition was not complete. Sera having high RESA-IFA titers were predictably inhibitory; however, many sera having low RESA-IFA titers were as inhibitory as sera having high titers, indicating that antibodies with specificities different from the RESA may be as important, or more important, to clinical immunity to blood-stage infections.

Adolescent↗
PubMed1988

Neuroendocrine aspects of attention deficit hyperactivity disorder.

This article summarizes the existing neuroendocrine literature and reports the growth hormone response to stimulation with L-dopa and clonidine in male children and adolescents with attention deficit hyperactivity disorder. Because growth hormone secretion is regulated by monoamine neurotransmitters, hyposecretion of growth hormone may reflect generalized changes in the neurochemical substrate of this disorder. With refinement, these neuroendocrine challenge tests may become unique biologic markers in identifying attention deficit hyperactivity disorder in children and adolescents.

Adolescent↗
PubMed1987

Activity of quinoline-containing antimalarials against chloroquine-sensitive and -resistant strains of Plasmodium falciparum in vitro.

9 quinoline-containing antimalarials and the phenanthrene methanol halofantrine were tested in vitro against 6 strains of Plasmodium falciparum with known sensitivity to chloroquine. Sensitivity to chloroquine was not uniformly associated with sensitivity to mepacrine (quinacrine), halofantrine, SN-12108 or SN-6911 (3-methylchloroquine, sontochin). Amodiaquine was slightly less potent with chloroquine-resistant strains, whereas SN-12309 closely resembled chloroquine in the pattern of sensitivity. (Bis)desethylchloroquine was nearly as potent as chloroquine against chloroquine-sensitive strains but was about 10-fold less potent than the parent drug against chloroquine-resistant strains. 2 8-aminoquinolines, primaquine and pamaquine, were more potent against chloroquine-resistant than chloroquine-sensitive strains. The mutation(s) responsible for chloroquine resistance in P. falciparum greatly reduce(s) the sensitivity to a major metabolite of the drug but also generate(s) parasites which are more susceptible to a different class of drugs, the 8-aminoquinolines.

Animals↗
PubMed1987

Tumor necrosis factor does not induce Plasmodium falciparum crisis forms.

Mouse and rabbit sera from animals treated with Mycobacterium bovis BCG and lipopolysaccharide contained tumor necrosis factor (TNF) and induced malaria parasite crisis forms. However, neither purified mouse- nor recombinant DNA-produced human TNF induced crisis forms in cultured Plasmodium falciparum. Furthermore, rabbit polyclonal and mouse monoclonal antibodies against human TNF did not block the parasite inhibitory activity of human malaria crisis form factor serum from Sudan.

Animals↗