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Biomedical subjects

J M Roberts

Publications and source records attributed to J M Roberts.

At least 235 records · Page 13Linked to original sources
PubMed1991

Survey of veterinarians' recommendations for treatment and control of intestinal parasites in dogs: public health implications.

A systematic, random sample of 450 small and mixed-animal practitioners was selected from the client list of a prominent veterinary pharmaceutical and animal health company. A telephone survey was conducted, using a standard questionnaire, to assess whether current veterinary practices concerning prophylaxis and treatment of canine roundworm (Toxocara canis) and hookworm (Ancylostoma spp) infections are adequate to prevent transmission to human beings. Analysis of results focused on 3 questions related to prevention: practitioner's frequency of client education regarding zoonotic potential of roundworms and hookworms, pup age at which veterinarian recommends first anthelmintic treatments, and proportion of veterinarians recommending prophylactic drug administration for pups and nursing bitches. Despite the proven association of household pet dogs and human toxocariasis, only a third (148/450) of veterinarian respondents routinely discussed the potential zoonotic hazards of canine roundworms with their clients. A total of 29% (130/450) of veterinarians surveyed either never discussed these potential hazards or discussed them only when asked by their clients. With regard to anthelmintic treatment practices, 31% (140/450) of veterinarians surveyed recommended that pups first be examined and treated for intestinal parasites within 4 weeks of age. Thirty-three percent (163/450) recommended first examination and deworming at 5 to 6 weeks of age, and 36% (163/450) suggested that it be done at or after 7 weeks of age. Less than half (208/450) of veterinarians administered anthelmintics prophylactically to at least some pups and dogs. Sixty-four percent (287/450) of respondents recommended routine testing and treatment of nursing bitches.(ABSTRACT TRUNCATED AT 250 WORDS)

Ancylostomiasis↗
PubMed1991

Selective effects of preeclamptic sera on human endothelial cell procoagulant protein expression.

Current concepts of preeclampsia suggest that dysfunction of maternal vascular endothelium in vivo is a central pathogenetic feature of this syndrome. This hypothesis is suggested by the activation of the coagulation cascade associated with preeclampsia and evidence for a role of endothelium in maintaining thromboresistance. Previous in vitro studies with monolayers of human umbilical vein endothelial cells demonstrated direct cytotoxic effects of sera from preeclamptic parturients. In the current studies, we have examined the in vitro expression of three procoagulant protein activities regulated by endothelial cells: cellular fibronectin, an important mediator of platelet aggregation known to be elevated in preeclamptic women in vivo; tissue factor, the most potent endogenous procoagulant activity; and von Willebrand factor, a major component of coagulation factor VIII. Monolayer cultures of human umbilical vein endothelial cells were incubated with pregnancy sera for 24 hours before these proteins and activities were quantified. Exposure of identical endothelial cell cultures to predelivery preeclamptic sera caused significantly greater release of cellular fibronectin than postdelivery preeclamptic or predelivery or postdelivery normal pregnancy sera (p less than 0.05). However, neither tissue factor activity nor von Willebrand factor expression appeared to be increased preferentially by preeclamptic sera. The data indicate that sera from women with preeclampsia induce a selective, but not a generalized, activation of endothelial cell procoagulant protein production.

Adult↗
PubMed1991

High plasma cellular fibronectin levels correlate with biochemical and clinical features of preeclampsia but cannot be attributed to hypertension alone.

Current concepts of the pathogenesis of preeclampsia involve the generalized dysfunction of maternal vascular endothelial cells. We measured the endothelial isoform of fibronectin as a marker of endothelial cell injury throughout pregnancy in a prospective, case-control study. Nineteen women met strict criteria for the diagnosis of preeclampsia. Nineteen normal pregnant women, and 19 women with gestational hypertension but without other stigmata of preeclampsia (transient hypertension) were selected from the same cohort and matched according to race, age, nulliparity, and gestational age at delivery. Plasma levels of cellular fibronectin were significantly elevated in women meeting strict clinical and biochemical criteria for preeclampsia but not in women with normal pregnancies or transient hypertension. Moderate but significant elevations in mean levels were found in the second trimester in women destined to have preeclampsia, as compared with matched normal and transient hypertension groups (p less than 0.05). The results indicate that elevated plasma levels of cellular fibronectin are not simply the result of increased blood pressure but reflect a maternal insult specific to the syndrome of preeclampsia. Elevation of the mean concentration during the midtrimester is consistent with the hypothesis that endothelial cell injury is a specific lesion that occurs early in the course of preeclampsia, before clinical signs and symptoms.

Adult↗
PubMed1991

Cocaine directly augments the alpha-adrenergic contractile response of the pregnant rabbit uterus.

Cocaine use in pregnancy is associated with a premature labor rate as high as 50%, but little is known about its effect on uterine contractility. To determine whether cocaine directly augments pregnant uterus contractility, uterine strips from 27-day pregnant New Zealand White rabbits (term, 31 days) were exposed to cocaine alone (30 mumol/L) or cocaine plus epinephrine (10(-9) to 10(-5) mol/L) or oxytocin (10(-10) to 10(-6) mol/L). Cocaine alone produced no contractions, but increased the epinephrine sensitivity by 51% and the maximal response by 33%. When beta-adrenoceptors were blocked with DL-propranolol (2 mumol/L), the contractile response to epinephrine was increased, and cocaine's effect was blocked. In the presence of the stereoisomer D-propranolol (2 mumol/L) with no beta-adrenergic antagonist activity, the contractile response to epinephrine was unchanged, but the effect of cocaine was still blocked. We conclude that cocaine directly augments the alpha-adrenergic contractile response of the pregnant rabbit uterus by a mechanism that is blocked by the non-beta-adrenergic effects of propranolol.

Adrenergic beta-Antagonists↗
PubMed1991

Functional antagonism in rabbit pulmonary veins contracted by endothelin.

An endothelium-derived 21-residue peptide, endothelin, has been shown to be a constrictor of arteriolar smooth muscle. This study investigated the effect of endothelin on isolated pulmonary veins and arteries using tissue bath techniques. Endothelin elicited concentration-dependent contractions and maximal responses were equal in magnitude to those of phenylephrine (PE) or norepinephrine (NE). Responses to endothelin were long lasting and persisted despite repeated washing. The following agents had no significant effect on endothelin-induced contractions: FPL 55712 (1 microM), indomethacin (10 microM), methysergide (3 microM), phentolamine (3 microM), pyrilamine (3 microM) and the putative thromboxane A2 receptor antagonist SQ 29,548 (3 microM). Moreover, removal of the endothelium did not alter responses to endothelin. Isoproterenol, forskolin, and 8-bromo-cAMP had a differential inhibitory effect on matched contractions induced by endothelin and the putative thromboxane A2 receptor agonist U-46619. Isoproterenol (0.1 microM) relaxed endothelin and U-46619 contractions by 2 +/- 1% and 74 +/- 5%, respectively; forskolin (3 microM) by 12 +/- 3% and 84 +/- 9%, respectively and 8-bromo-cAMP (10 mM) by 23 +/- 8% and 82 +/- 9%, respectively. Likewise, 10 microM sodium nitroprusside relaxed endothelin contractions by 32 +/- 4% and PE contractions by 80 +/- 9%. Endothelin is a very potent pulmonary vasoconstrictor that appears to have a direct effect on vascular smooth muscle. Compared to U-46619 or PE, endothelin-induced contractions are highly resistant to relaxing agents that increase either cAMP or cGMP. Moreover, resistance to cAMP does not appear to involve inhibition of adenylate cyclase.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Clinical and biochemical evidence of endothelial cell dysfunction in the pregnancy syndrome preeclampsia.

The pregnancy disorder preeclampsia continues as a major cause of maternal and infant mortality and morbidity. Despite intensive research since its recognition 100 years ago, our lack of understanding is evidenced by therapy which remains empiric, early delivery. Part of our failure to more completely understand the syndrome is due to excessive attention to the blood pressure elevation which accompanies the disorder, to the exclusion of a panoply of other physiologic aberrations. Although hypertension, if markedly elevated, can lead to maternal morbidity, it is not usually an important contributor to the pathophysiology of preeclampsia. It is primarily important as a marker for vasoconstriction, which in association with activation of coagulation reduces perfusion to many organs, including the fetal-placental unit. The earliest and likely most important pathophysiologic change is reduced placental perfusion secondary to abnormal implantation and/or a relative increase in placental mass. We propose that reduced placental perfusion results in the production of agent(s) by this organ, which injures or activates endothelial cells. The resulting endothelial cell dysfunction increases sensitivity to normal endogenous pressors, activates the coagulation cascade, and increases vascular permeability. These changes produce the characteristic pathophysiologic changes of the disorder. Evidence supporting this hypothesis includes abnormal endothelial morphology long recognized in glomerular capillaries, increased circulating fibronectin, and increased plasma mitogenic activity that long antedates the clinical disorder. In addition, an agent(s) is present in the blood of these women which activates endothelial cells in vitro as evidenced by increased release of [51Cr] chromium and increased production of PDGF. Preeclampsia is clearly more than "pregnancy induced hypertension."

Endothelium, Vascular↗
PubMed1991

Evidence of nonsusceptibility to diethylcarbamazine in Wuchereria bancrofti.

This study assessed Wuchereria bancrofti-infected patients who received diethylcarbamazine (DEC) to determined if drug levels were comparable between individuals who continued to harbor circulating microfilariae and those whose blood became clear of parasites, between those with high and low microfilaria counts, and between infected and noninfected persons. Haitian volunteers undergoing treatment for W. bancrofti and two nonendemic controls were enrolled. DEC levels in serum and urine samples were determined using a gas chromatographic method. No correlation was found between pre- and posttreatment microfilarial levels and drug levels. Drug levels were comparable in persons with or without residual microfilaria and in infected and uninfected persons. These results indicate that incomplete drug regimens, differences in serum drug levels, and inadequate drug dosage are not the primary causes of treatment failure and suggest there is a degree of parasite tolerance for DEC.

Animals↗
PubMed1991

Preeclamptic sera stimulate increased platelet-derived growth factor mRNA and protein expression by cultured human endothelial cells.

Monolayer cultures of human endothelial cells were incubated with pre- and postdelivery sera from five women with preeclampsia and four matched, normal pregnancies. Conditioned media collected from endothelial cells pretreated in vitro with prepartum sera from preeclamptic women contained greater mitogenic activity and elevated levels of platelet-derived growth factor (PDGF)-like peptides than cells exposed to normal pregnancy sera or postpartum preeclamptic sera. Under the same experimental conditions, predelivery preeclamptic sera stimulated greater expression of endothelial cell PDGF-B-chain mRNA than that accumulated in the presence of matched postdelivery sera. By contrast, no differences in endothelial cell PDGF-B mRNA levels were noted when pre- and postdelivery sera from normal parturients were tested. The results suggest that a factor(s) in the blood of preeclamptic women can stimulate the synthesis and release of a potent growth factor and vasoconstrictor from human endothelial cells.

Cells, Cultured↗
PubMed1991

Differentiation of type II cells during explant culture of human fetal lung is accelerated by endogenous prostanoids and adenosine 3',5'-monophosphate.

Explant culture of the fetal lung, in the absence of serum or hormones, results in precocious biochemical and morphological differentiation of alveolar epithelial cells. In this study we tested the hypothesis that these maturational events are induced by endogenous cAMP. During culture of human fetal lung the content of tissue cAMP increased 140% from days 3-6. Treatment with isobutylmethylxanthine caused a further doubling of cAMP content, and indomethacin blocked most of the increase in cAMP. Isobutylmethylxanthine accelerated and indomethacin inhibited the increases during culture in surfactant protein-A (SP-A), SP-A mRNA, SP-B mRNA, phosphatidylcholine content, and activity of fatty acid synthetase. There was no effect of these treatments on the content of SP-C mRNA, which did not increase during culture. Increasing concentrations of prostaglandins E1 and E2 in the presence of indomethacin produced a parallel stimulation of cAMP content, SP-A, and fatty acid synthetase activity. The temporal increase in SP-A was also blocked by inhibitors of protein kinase-A. In morphological studies, indomethacin-treated explants appeared less mature, with decreased intralumenal volume and more columnar epithelial cells. We conclude that increased tissue cAMP levels, stimulated by endogenous prostaglandins, accelerate differentiation of alveolar epithelial cells during explant culture.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Prostaglandins modulate hormonal effects on rabbit myometrial alpha 1-adrenergic responses.

Estrogen increases the alpha 1-adrenergic contractile sensitivity of the rabbit uterus. Since estrogen treatment increases prostaglandin (PG) production by the perfused rabbit uterus, and PGs contribute to the alpha 1-adrenergic contractile response, we postulated that estrogen's effects on PG production or response may play a role in the increased alpha 1-adrenergic sensitivity induced by estrogen. We studied the effects of the eicosanoid synthesis inhibitor meclofenamate (60 microM) on the response to epinephrine (10(-9)-10(-5) M) of uterine strips from ovariectomized, mature, and estrogen-treated rabbits in terms of both contractile response and PGE2 and PGF2 alpha production. We also measured the contractile response to PGE2 and PGF2 alpha (both 10(-10)-10(-5) M) and KCl (70 mM) of uterine strips from these groups. We found that in the ovariectomized rabbits, meclofenamate decreased PG production, but did not alter the alpha 1-adrenergic sensitivity. In the mature rabbit uterus, meclofenamate decreased both PGE2 and PGF2 alpha production and reduced the alpha 1-adrenergic sensitivity. In the estrogen-treated rabbit uterus, meclofenamate decreased PGF2 alpha, but not PGE2, production and did not alter the alpha 1-adrenergic sensitivity. Finally, meclofenamate reduced the contractile response to KCl in all three groups, and exposure to PGE2 increased the contractile response to KCl in both the mature and estrogen-treated rabbits. We conclude that PGs play a role in the increase in the alpha 1-adrenergic sensitivity of the uterus in mature rabbits, and that this may be the result of an estrogen-mediated alteration in the postreceptor effects of PGs.

Animals↗
PubMed1991

Pathophysiology of preeclampsia.

Preeclampsia is a complex clinical syndrome, with hypertension representing but one manifestation. Pathogenetically important events in the development of preeclampsia include incomplete trophoblastic invasion of the maternal spiral arteries, poor trophoblastic perfusion, elaboration of a putative endothelial cell toxin, and endothelial cell injury with resulting activation of coagulation, impairment of vasodepressor function, and altered endothelial permeability. These changes lead to the clinical signs and symptoms, which occur relatively late in the course of preeclampsia. The primary immunologic, genetic, and biochemical basis of preeclampsia remains speculative.

Endothelium, Vascular↗
PubMed1991

Results of testing for intestinal parasites by state diagnostic laboratories, United States, 1987.

We analyzed results of 216,275 stool specimens examined by the state diagnostic laboratories in 1987; parasites were found in 20.1%. Percentages were highest for protozoans: Giardia lamblia (7.2%), Entamoeba coli and Endolimax nana (4.2% each), Blastocystis hominis (2.6%), Entamoeba histolytica (0.9%), and Cryptosporidium species (0.2%). Identifications of Giardia lamblia increased broadly from the 4.0% average found in 1979, with 40 states reporting increases and seven decreases. Most states that identified Giardia in more than 9% of specimens were located around the Great Lakes or in the Northwest. Seasonally, Giardia identifications increased in the summer and fall, especially in northern states. The most identified helminths were nematodes: hookworm (1.5%), Trichuris trichiura (1.2%), and Ascaris lumbricoides (0.8%). Other less commonly identified helminths included Clonorchis and Opisthorchis species (0.6%), Strongyloides stercoralis (0.4%), Hymenolepis nana (0.4%), Enterobius vermicularis (0.4%), and Taenia species (0.1%). Tape tests for Enterobius, reported for 35 states, were positive for 11.4% of 9,597 specimens. Nine states (California, Colorado, Hawaii, Idaho, New Jersey, Oregon, Rhode Island, Washington, Wisconsin) reported hookworms in more than 2% of specimens; none were states traditionally associated with indigenous transmission. Cryptosporidium diagnoses, reported by 25 of 49 states, were recorded for the first time in a national survey and showed no marked regional clustering. The Giardia data revealed changes in rates of identification and in geographic patterns compared with state laboratory data collected a decade earlier (1976-1978).

Feces↗
PubMed1991

Anopheles gambiae as a host for geographic isolates of Plasmodium vivax.

The G-3 strain of Anopheles gambiae was compared with 2 other strains of An. gambiae and An. freeborni, An. stephensi, and An. dirus for susceptibility to infection with 7 different geographic strains of Plasmodium vivax. Ratios of infection varied, indicating that certain strains of P. vivax were more infectious to the G-3 strain of An. gambiae than to other anopheline species/strains. Based on the comparative number of oocysts per mosquito, the relationships between the 3 strains of An. gambiae were closer than between the G-3 strain of An. gambiae and the 3 other species of Anopheles. Anopheles gambiae appears to be a very useful host for laboratory studies with P. vivax from different geographic origins.

Animals↗