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Biomedical subjects

J A Yates

Publications and source records attributed to J A Yates.

At least 19 recordsLinked to original sources
PubMed1997

Congenital esophageal webs.

Congenital esophageal webs are rare entities. These lesions generally occur in the upper one third of the esophagus and present symptomatically in early childhood. Dysphagia and 'feeding' difficulties are characteristic presenting symptoms. Radiographic studies generally reveal a normal appearing esophageal lumen with the exception of a single thin indentation of the esophageal lumen that is located either anteriorly or circumferential in nature. We describe two children with congenital esophageal webs and review the pathophysiology, diagnosis and management of these unusual lesions.

Adolescent↗
PubMed1997

Isolated congenital internal auditory canal atresia with normal facial nerve function.

The internal auditory canal forms as a result of mesoderm enveloping the eighth cranial nerve in the developing embryo. The mesoderm eventually transforms into cartilage and ultimately ossifies around the nerve, forming the internal auditory canal. It is theorized that atresia or stenosis of the internal auditory canal results from altered cochleovestibular nerve development secondary to faulty chemotactic mechanisms or a lack of end organ targets. Unilateral internal auditory canal anomalies are frequently seen in conjunction with other inner ear anomalies and occasionally with middle or external ear anomalies. Infrequently, it will occur as either an isolated or bilateral finding, but rarely simultaneously. The few citations of isolated, unilateral or bilateral internal auditory canal anomalies that are reported in the literature are usually associated with other systemic developmental anomalies, such as, cardiac septal defects, polycystic kidney disease, skeletal deformities and duodenal atresia. We present a case report of a patient with bilateral, congenital, internal auditory canal atresia and cochleovestibular deficits but, normal facial nerve function. A review of the literature is discussed as well as diagnostic considerations and treatment options including audiologic and communication rehabilitation.

Child, Preschool↗
PubMed1996

Role of nitric oxide in host defense against an extracellular, metazoan parasite, Brugia malayi.

The mechanisms by which mammalian hosts eliminate microparasites such as bacteria and viruses are well established. In viral infections, these mechanisms include the interferons, neutralizing and opsonizing antibodies, and cytotoxic T lymphocytes. In bacterial infections, polymorphonuclear leukocytes and macrophages, often facilitated by opsonizing antibodies, ingest the infectious agent and mediate host defense. In addition, complement, in the presence of specific antibodies directed against surface antigens, can lyse certain bacterial pathogens. In contrast, our understanding of the host defenses against metazoan, extracellular parasites is less well grounded. We obtained data by two different approaches to document the role of nitric oxide (NO) as a mediator of host defense against a human nematode parasite. First, treatment of immunocompetent, nonpermissive mice with an inhibitor of NO synthase abrogated resistance to Brugia malayi, one of the causative agents of human lymphatic filariasis. Second, treatment of permissive, immunodeficient mice with a compound that releases NO conferred resistance to infection. These data reinforce studies by James and her coworkers (I. P. Oswald, T. A. Wynn, A. Sher, and S. L. James, Comp. Biochem. Physiol. Pharmacol. Toxicol. Endocrinol. 108:11-18, 1994) on the role of NO in defense against trematode parasites and of Kanazawa et al. (T. Kanazawa, H. Asahi, H. Hata; K. Machida, N. Kagei, and M. J. Stadecker, Parasite Immunol. 15: 619-623, 1993) on cestode parasites.

Aedes↗
PubMed1996

Localization of paramyosin, myosin, and a heat shock protein 70 in larval and adult Brugia malayi.

Recombinant filarial proteins are of interest as potentially protective immunogens for lymphatic filariasis. We have previously identified paramyosin, myosin, and a heat shock protein 70 (HSP) 70 as prominent immunogens in individuals residing in an area endemic for lymphatic filariasis. Our goal in the present work was to identify the Brugia malayi tissues that contain these proteins. Polyclonal rabbit antisera with high levels of immunoglobulins to each of these proteins were prepared for use in indirect immunofluorescence microscopy studies of third-and fourth-stage larvae (L3's and L4's) and adult worms. Myosin and paramyosin were found within the longitudinal somatic musculature in all of these life stages. In L4's and adult worms, myosin and paramyosin were also detected within the walls of the reproductive and alimentary tracts of male and female worms. HSP 70 was evident within the somatic musculature, hypodermis, lateral chords, alimentary tract, and reproductive structures in L4's and adult worms. HSP 70 was not detected in sections of freshly obtained L3's. However, L3's cultured at 37 C for 24 hr before fixation demonstrated a classic heat shock response. In these larvae, intracellular HSP 70 was observed in all tissues. None of the antigens studied appeared to be located on cuticular surfaces.

Animals↗
PubMed1994

CD4+ T-lymphocytes are not required for murine resistance to the human filarial parasite, Brugia malayi.

Immunocompetent mice are nonpermissive for the development and maturation of the human filarial parasite, Brugia malayi. We and others have shown that the absence of T-lymphocytes, alone or in combination with B-lymphocytes, renders mice permissive to infection. In a previous study, we showed that mice lacking CD8+ T-lymphocytes are also completely nonpermissive for B. malayi, indicating that CD8+ T-lymphocytes are not an obligate requirement for resistance. In the present study, we have examined the role of CD4+ T-lymphocytes in resistance to filarial infection using two experimental systems. In the first, we used an anti-CD4 monoclonal antibody to deplete CD4+ T-cells in vivo in immunocompetent BALB/c mice. In the second system, we used mutant mice in which the gene encoding the CD4 antigen had been disrupted by homologous recombination, resulting in a lack of CD4+ T-cells. Challenge of either the anti-CD4 antibody depleted BALB/c mice or CD4 knockout mice with B. malayi infective-stage larvae demonstrated that mice lacking CD4+ T-lymphocytes were resistant to infection. These data indicate that CD4+ T-cells are not an obligate requirement for murine resistance to B. malayi.

Animals↗
PubMed1994

Maternal influence on susceptibility of offspring to Brugia malayi infection in a murine model of filariasis.

We have used the severe combined immunodeficient C.B-17-scid/scid mouse to investigate the influences of maternal immune status and parasite burden on the susceptibility (or resistance) of offspring to infection with the human filarial parasite, Brugia malayi. C.B-17-scid/scid mice are permissive for infection while immunocompetent C.B-17(-)+/+ mice are uniformly resistant. Reciprocal matings of C.B-17-scid/scid and C.B-17(-)+/+ mice were performed. The C.B-17-scid/scid females were either naive or infected with Brugia malayi. The resulting immunocompetent C.B-17-scid/+ and C.B-17(-)+/scid progeny were challenged at weaning with an intraperitoneal injection of Brugia malayi third stage larvae known to produce patent infection in > 95% of C.B-17-scid/scid mice. We observed that 40.0%l (34/85) of the immunocompetent offspring of C.B-17-scid/scid females x C.B-17(-)+/+ males were permissive for the growth and development of Brugia malayi larvae to adults. No difference was observed in susceptibility to infection between the progeny of infected or uninfected C.B-17-scid/scid mothers mated with C.B-17(-)+/+ fathers, arguing against acquired immunological tolerance to the parasite in the former. In marked contrast, only 4.8% (2/42) of the heterozygous progeny of wild type C.B-17(-)+/+ females mated with C.B-17-scid/scid males were permissive. These observations document conversion of a 'resistant' phenotype to a 'susceptible' phenotype by manipulation of maternal immune status and provide clear evidence of maternal influence on offspring susceptibility to infection with Brugia malayi.

Alleles↗
PubMed1994

Infectivity and normal development of third stage Brugia malayi maintained in vitro.

Shipment of infective-stage filarial larvae (L3s) usually has been accomplished by transporting living infected vectors or L3s cryopreserved in liquid nitrogen. Our objective was to find culture conditions for transporting L3s that would promote survival of Brugia malayi larvae without altering their capacity to infect susceptible animals. In preliminary studies we observed that Ham's nutrient mixture F-12, with antibiotics and 1% fetal calf serum, could support L3s without apparent development for at least 10 days. In order to evaluate the effect of culture temperatures on infectivity, fresh L3s were divided into groups that were either immediately injected into jirds (infectivity control) or incubated for 24, 48, or 120 hr in tightly sealed tubes maintained horizontally at either 0 C, 20 C, or 37 C, before they were injected into jirds. Necropsies were performed on the jirds 120-130 days after injection to recover and count adult worms. Levels of microfilaremia were also determined. We found that L3s held overnight at 0 C, although apparently viable, were unable to survive in jirds. However, larvae kept at 20 C and 37 C produced patent infections with adult worms in normal locations even after 120 hr of in vitro cultivation. There was no statistical difference in mean worm recovery or size of worms from jirds infected with freshly harvested L3s and jirds injected with larvae that were maintained overnight at 20 C or 37 C. When cultured L3s were shipped from Michigan to Connecticut by overnight air courier, along with infected living mosquitos, the L3s appeared to be 99% viable upon arrival. L3s shipped in F-12 produced patent infections in C.B.-17 scid/scid mice with worm recoveries comparable to those observed in mice injected with L3s freshly obtained from shipped mosquitos.

Animals↗
PubMed1994

Microscopic visualization of Wuchereria and Brugia larval stages in intact cleared mosquitoes.

Over the past several decades, epidemiologic data from filarial vectors typically has been obtained by mass dissection or by dissection of individual specimens. The former is quick and easy to do on large numbers of insects but provides no information on the frequency distribution of infection, presence of early developmental stages, or larval location; the latter is labor-intensive and tedious. We describe a new technique that can provide data comparable to those obtained by individual dissection, including calculation of infection and infective rates, and this technique is easy enough to accommodate large numbers of insects. Brief treatment of ethanol-fixed, intact mosquitoes in sodium hypochlorite, followed by treatments in increasing concentrations of ethanol and an organic solvent allowed microscopic visualization of filarial larvae within the abdomen, thorax, head, and proboscis of Brugia malayi-infected Aedes aegypti and Wuchereria bancrofti-infected Anopheles punctulatus. We compared the classic techniques to our technique using Ae. aegypti infected by feeding on jirds with B. malayi microfilaremias. Comparisons of the infective rate, total number of infective stage larvae (L3s) observed, and locations of L3s showed that this new technique was comparable to the established methods, while being faster and more precise in determining the location of larvae.

Aedes↗
PubMed1992

Root fractures in permanent teeth: a clinical review.

A retrospective study of 22 root fractures in 21 patients was performed. Ten patients were less than 11 years of age, and boys were involved more often than girls. Ten patients had more than one injured tooth, but there was no case of alveolar fracture. Twenty-one of the teeth were upper central incisors. Only 11 teeth were seen within the first week, so that not all teeth were splinted and not all displaced teeth were repositioned. Long-term clinical and radiographic review showed that loss of vitality of the coronal pulp could not be reliably detected for at least 1 year. No tooth became abscessed or developed a sinus tract, and resorption of bone at the fracture line was observed in only one out of five non-vital teeth. Lack of displacement and placing of a splint increased the chances of the pulp remaining vital and healing of the fracture occurring with hard tissue. Sclerosis of the coronal pulp occurred mainly when healing was by connective tissue. The apical pulp always remained vital, and there was sclerosis of the apical pulp in almost every case.

Adolescent↗
PubMed1991

Vaccine induced immunity to Schistosoma mansoni: spleen cell proliferative responses before and after challenge in BALB/c mice given irradiated or normal schistosomula.

Spleen cell proliferative responses in BALB/c mice were assessed at varying intervals after vaccination or primary infection and subsequent cercarial challenge. Mice were vaccinated with 500 50-Krad-irradiated Schistosoma mansoni schistosomula or infected with 20 normal schistosomula. Prior to challenge, splenic responses in the two test groups to phytohemagglutinin (PHA) declined progressively while schistosomula (SMA)-driven responses increased. After challenge, PHA responses increased in both groups on day 3 then declined to significantly lower levels compared to normal controls. On day 3 after challenge, SMA responses in vaccinated mice were vigorous, and greater than twice the responses in infected mice. Thereafter, responses in vaccinated mice declined while responses in infected mice increased on days 7 through 25 but dropped markedly by day 39. For the infected group, in vitro depletion of plastic adherent cells or Lyt 2.2+ lymphocytes resulted in augmented SMA responses 3 days post-challenge by greater than 400% and greater than 100%, respectively. Depletion of either cell population in the vaccinated group had no significant effect. Protection assessed by total worm burdens showed a reduction of 62% in vaccinated mice and 43% reduction in infected mice. The post-challenge results indicate that these two models of anti-schistosomula immunity differed in the dynamics of their splenocyte antigen-specific proliferative responses. These findings may contribute to an understanding of the mechanisms by which resistance to S. mansoni is induced.

Animals↗
PubMed1990

Use of parasite antigen detection to monitor macrofilaricidal therapy in Brugia malayi-infected jirds.

Improved methods are needed to evaluate new treatments for filarial infections. We have recently developed a monoclonal antibody-based enzyme immunoassay to detect circulating parasite antigen in sera from Brugia malayi-infected jirds. In the present study, parasite antigen levels were compared to parasitological parameters after treatment of B. malayi-infected jirds with CGP 20376 that has been reported to be active against both microfilariae and adult worms of this parasite. Microfilariae were cleared promptly and permanently after CGP 20376 treatment, and no adult worm was recovered in jirds at necropsy 20 wk after treatment. In contrast, untreated animals had sustained microfilaremia throughout the course of the study, and adult worms were recovered in all control animals (mean worm recovery; 24.3 +/- 7.8 SE). Parasite antigen was present in sera from all infected animals before treatment. Parasite antigen titers in sera were unchanged 5 wk after treatment but fell to undetectable levels in 4 of 6 animals by 20 wk after treatment. Low-level antigenemia was detected in 2 of 6 animals at 20 wk, perhaps suggesting incomplete killing of parasites or incomplete clearance of antigen. Parasite antigen levels were stable throughout the study in control animals. These preliminary results suggest that parasite antigen detection is useful as a means of noninvasively monitoring the efficacy of anti-filarial drug therapy.

Animals↗
PubMed1989

Differential recognition of two cloned Brugia malayi antigens by antibody class.

The humoral and cellular immune response to filarial parasites is complex. Numerous studies have shown that antibodies to a large number of protein and non-protein antigens may be produced over the course of infection and that immune recognition of any given antigen may vary by disease manifestation and by immunoglobulin class. We have used the techniques of molecular cloning to attempt to dissect this complex interaction, and describe here two clones, isolated from an expression library constructed from Brugia malayi genomic DNA, whose products are recognized by distinct immunoglobulin classes. A lambda gt11 fusion protein containing part of the B. malayi myosin tail region is recognized by antibodies of the IgG class from a high percentage of bancroftian filariasis patients. A fusion protein containing a collagen-like sequence is less frequently and weakly recognized under the same experimental conditions, but is almost universally recognized when the developing reagent is specific for IgE. We thus identify specific filarial proteins against which the infected human host responds preferentially with antibodies of a specific immunoglobulin class.

Adolescent↗
PubMed1989

Course of infection and humoral response to Leishmania major in inbred Meriones unguiculatus.

Numerous species of Meriones have been incriminated as natural reservoir hosts of Leishmania major in Mongolia, Soviet Asia, Afghanistan, the Middle East, and North Africa. However, little is known about the immunological response or course of infection in these small rodents. In this study, 40 commercially obtained inbred Meriones unguiculatus were divided into equal groups and injected in the right hind footpad with various doses of L. major promastigotes or with medium only. At regular intervals, blood was collected from the animals for subsequent evaluation of the kinetics of anti-L. major serum antibody production. Footpad lesions were measured periodically for 13 wk, beginning just before infection. The humoral response to infection and the course and severity of disease were dose related. However, metastasis lymph nodes, liver, spleen, and secondary cutaneous sites occurred at each of the doses tested.

Animals↗
PubMed1988

Cutaneous leishmaniasis in Jordan: biochemical identification of human and Psammomys obesus isolates as Leishmania major.

As part of a series of epidemiological and ecological studies of leishmaniasis in Jordan, we have made functional studies of four isolates from human lesions and from ear lesions of three field-collected Psammomys obesus. Primary isolates were subcultured, frozen stabilates prepared and BALB/c mouse infectivity experiments initiated. Each mouse was inoculated with 4-8 x 10(4) promastigotes into a hind footpad. Quantitative evaluation of the footpads showed enlargement three to four weeks postinoculation. Amastigotes were readily identified in smears from footpad lesions and promastigotes in culture. At 47 days, liver and spleen samples grew out promastigotes. Biochemical characterization of these seven isolates was made by isozyme analysis using cellulose acetate membrane electrophoresis of fructokinase, phosphoglucose isomerase, phosphoglucomutase, aspartate aminotransferase, malate dehydrogenase, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. Reference isolates used for comparison were Leishmania major, L. tropica minor, L. donovani, L. aethiopica and L. m. mexicana. All seven Jordan isolates showed enzyme electromorphs identical to L. major, confirming our ecological/epidemiological studies that P. obesus is a major reservoir for human cutaneous leishmaniasis in Jordan.

Animals↗
PubMed1987

Effects of feeding sows fat or fructose during late gestation and lactation.

The effects of dietary fat or fructose supplementation during late gestation and lactation on sow milk production and composition and on progeny were examined. On d 88 of gestation, 24 sows were allotted by parity to three dietary treatments (eight sows/treatment). Treatments were 1) a 12.5% crude protein, corn-soybean meal control, 2) the control + 10% added fat or 3) the control + 23% high fructose corn syrup. All treatments were fed to supply 1.82 kg/d of the control diet from d 89 of gestation to parturition with sows in treatments 2 or 3 receiving .18 kg of additional fat or .53 kg of additional high fructose corn syrup, respectively. Feed was gradually increased from d 1 to 7 of lactation to 4.54 kg/d of the control diet (plus .45 kg of added fat and 1.33 kg of added fructose for treatments 2 and 3) and remained at these levels for the remainder of the 21 d lactation period. All treatments were iso-nitrogenous; treatments 2 and 3 were iso-caloric. Litter birth weights, number of pigs born alive, weaning weights and piglet survival rate were not affected by sow treatment. Stillbirths were less (P less than .05) for sows fed fat. Lipid content of milk 24 h post-farrowing was greater (P less than .05) from sows fed fat compared with sows fed fructose. Milk production estimates indicated that multiparous sows fed fat produced more (P less .05) milk than sows fed the control diet. On d 112 of gestation and d 15 of lactation, serial blood samples were drawn to monitor sow response to a glucose challenge (1 g/kg body weight).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effect of dietary fructose on broiler chick performance.

The effect of feeding various levels of dietary fructose, furnished by high fructose corn syrup (HFCS), to broiler-type chicks housed in Petersime batteries was studied in two experiments. In experiment 1, HFCS was added to a corn-soybean meal basal diet at levels of 0, 5, 10, and 15%. In Experiment 2, HFCS was added to the diet at levels of 0, 2, 4, 6, and 15%. In both experiments diets were isocaloric and isonitrogenous. In Experiment 1, chicks fed HFCS consumed more feed (P less than or equal to .05) and grew more rapidly (P less than or equal to .05) than chicks fed the control diet. No differences in the feed to gain ratio were observed among treatments. Feeding HFCS resulted in non-significantly higher liver weight and percent liver lipid. Values for kidney weights and plasma uric acid were higher (P less than or equal to .05) in chicks fed 15% HFCS. In Experiment 2, adding 4, 6, and 15% HFCS resulted in more rapid growth (P less than or equal to .05). No significant differences were observed in feed intake and kidney weights. Chicks fed the 15% HFCS diet had heavier (P less than or equal to .05) livers.

Animal Nutritional Physiological Phenomena↗