Search PubMed⌕ Search

Biomedical subjects

J A Thompson

Publications and source records attributed to J A Thompson.

At least 145 records · Page 8Linked to original sources
PubMed1995

Use of performance ratios to calculate the economic impact of thin cows in a beef cattle herd.

OBJECTIVE: To determine gross income lost that was attributable to thin cows in a beef cattle herd, to estimate the cost of added nutrition necessary to prevent thin cows in the herd, and to determine the financial outcome of the improved nutritional practices. DESIGN: Prospective, observational study. ANIMALS: Four hundred and twenty-two Santa Gertrudis cows and their calves. PROCEDURE: At pregnancy examination in the fall of 1992, cows were assigned a body condition score (BCS), using a scale of 1 (emaciated) to 9 (obese), and the ratio of the productivity of BCS-3 and BCS-4 cow groups (thin cows), compared with the mean productivity of BCS-5 and BCS-6 cows (cows in good condition), was determined. Measures of productivity evaluated included pregnancy rates, weaning weights, and prices per hundredweight of calves. The performance ratios of BCS-3 and BCS-4 cows were multiplied by the mean gross income of BCS-5 and BCS-6 cows to calculate their gross income. This was then subtracted from the mean income of BCS-5 and BCS-6 cows to estimate the amount of lost gross income per thin cow. The cost of a nutritional program that would prevent thin cows in the herd was subtracted from the lost gross income of the thin cows to yield the amount of increased net income that could be generated from a nutritional program that would maintain cows in the herd at a BCS of 5 or 6. RESULTS: Cows with a BCS of 3 were 0.48 as productive, and cows with a BCS of 4 were 0.74 as productive as the average of the BCS-5 and BCS-6 cows combined. Each BCS-3 cow generated $215.06 less, and each BCS-4 cow generated $107.53 less gross income than the average gross income of BCS-5 and BCS-6 cows. The added cost of nutrition that would have reconditioned BCS-3 and BCS-4 cows to a BCS of 5.5 was $91.48/BCS-3 cow and $43.67/BCS-4 cow. Implementation of the reconditioning nutrition program the previous fall would have resulted in an extra net income of $123.58/BCS-3 cow and $63.86/BCS-4 cow, received over a 2-year period. The 262 thin cows in the herd accounted for a total net income loss of $19,897. CLINICAL IMPLICATIONS: The time of pregnancy examination is a strategic intervention point to estimate the past negative economic impact of thin cows and to implement a plan to prevent these losses in the future. Pregnancy examinations should be performed at least 100 days before the beginning of the calving season, and thin pregnant cows should be sorted into a special group and fed a reconditioning diet that will improve their body condition to an average BCS of 5.5 by the onset of the calving season.

Animal Husbandry↗
PubMed1995

Role of cytochrome P450 in the metabolism and toxicity of hydroperoxides in isolated rat hepatocytes.

The contributions of cytochromes P450 (P450) to the metabolism and toxicity of hydroperoxides in freshly isolated rat hepatocytes were investigated utilizing 2,6-di-tert-butyl-4-hydroperoxy-4-methyl-2,5-cyclohexadienone (BHTOOH). This hydroperoxide was rapidly degraded in cell suspensions, and the products were identical to those determined previously with subcellular preparations of ferric P450. With 250 microM BHTOOH, the ratio of glutathione peroxidase-mediated:P450-mediated metabolism was estimated to be about 3:1. Surprisingly, BHTOOH was found to be a more potent cytotoxin than cumyl hydroperoxide (CuOOH), despite the fact that it caused substantially less lipid peroxidation than the latter. P450 inhibition enhanced the toxicity of BHTOOH, but lowered the toxicity of CuOOH. These data demonstrate that intracellular ferric P450 can compete with glutathione peroxidase to reduce hydroperoxides by 1- and 2-electron processes. If the alkoxy radical from homolytic cleavage of the O-O bond can undergo facile intramolecular reactions to nontoxic products, as with BHTOOH, the role of P450 is detoxification. On the other hand, if the alkoxy radical preferentially attacks membrane lipids, as with CuOOH, P450 contributes to lipid peroxidation and toxicity. It was determined that the levels of glutathione, protein thiols, and ATP decreased in parallel with BHTOOH-induced cell death, but no conclusions are possible concerning mechanisms underlying the relatively potent toxicity of BHTOOH. Toxicity may be related to the high lipophilicity of this hydroperoxide which, presumably, facilitates its passage into cells and distribution to various intracellular sites. BHTOOH appears to be an excellent model compound for investigating mechanisms of hydroperoxide-mediated cytotoxicity which do not involve lipid peroxidation.

Animals↗
PubMed1995

Genetic services for familial cancer patients: a survey of National Cancer Institute cancer centers.

In the past decade, significant progress has been made in understanding the genetic component of familial cancers. Genes associated with familial colon and breast cancers have recently been isolated and molecular diagnostic tests are expected to become available in the near future. Clinicians now have the opportunity to recognize and counsel individuals with elevated risk of cancer by identifying risk factors and genes associated with cancer predisposition. The rapid advances in molecular technology are a direct challenge to the medical community and cancer centers to supply specialized clinical services for familial cancers. We sought to ascertain the activities of cancer centers in the development of programs and the provision of genetic services for familial cancer. We surveyed 41 centers with National Cancer Institute (NCI) cancer center support grants. One half of the centers responding (17 of 34) reported that they provide some genetic services for familial cancer. About one half of these 17 centers (eight [57%] of 14; the three remaining clinics that responded had incomplete information on this indicator) see a variety of patient types on a small scale (fewer than 100 patients per year), and most provide four basic clinical evaluations: medical evaluation, cancer risk assessment, genetic counseling, and pedigree analysis. Staffing of each center varied widely, as did the types of screening services offered (including molecular diagnostic testing). Several centers (six [35%] of 17) indicated that they were in the developmental stages for serving familial cancer patients, and many seem to be increasing their activities in this area. The remaining 17 NCI-supported centers that responded, however, currently provide no genetic services for familial cancers. The results of this survey suggest that there is interest in developing clinical programs for familial cancers by NCI-supported cancer centers, but most of these programs are in developmental stages. A base line has been established to monitor future progress for the provision of cancer genetic services.

Cancer Care Facilities↗
PubMed1995

Outcome of scrotal hydrocele in 26 bulls.

Changes in scrotal sonograms and semen quality were monitored in 26 bulls with idiopathic scrotal hydrocele over a 4-month period. After 120 days, scrotal hydrocele had resolved (ultrasonographically, fluid was not detectable within the vaginal process) in 85% (22/26) of the bulls. Percentage of bulls with unilateral scrotal hydrocele that resolved was higher than that for bulls with bilateral hydrocele (94 vs 62.5% or 17/18 bulls vs 5/8 bulls, respectively). After 120 days, 77% (20/26) of the bulls passed a breeding soundness evaluation. At 90 days, semen quality was satisfactory in more of the bulls with unilateral disease (9/18) than with bilateral disease (1/8). The finding of multifocal echodensities in the testicular parenchyma was not correlated with a poor breeding soundness score or with a high number of spermatozoal abnormalities. The prognosis for full recovery in bulls with scrotal hydrocele likely depends on the severity and duration of the condition.

Animals↗
PubMed1995

The HIV-1 TAT protein induces the expression and extracellular appearance of acidic fibroblast growth factor.

Mounting experimental evidence suggests that the TAT protein, released from human immunodeficiency virus-1 (HIV-1)-infected inflammatory cells, may genetically reprogram targeted cells within a localized environment to develop highly vascularized tumors of mesenchymal origin. The fibroblast growth factor (FGF) family of polypeptides has gained general acceptance as initiators of angiogenesis and functions as potent mitogens for mesoderm-derived cells. To evaluate a potential biological relationship between TAT and acidic FGF (FGF-1), primary murine embryonic fibroblasts either were transfected with the viral transactivator or were transduced (retrovirally mediated) with a secreted, chimeric form of the human polypeptide growth factor, human stomach tumor/Kaposi's sarcoma (hst/KS)FGF-1. Reverse transcriptase-polymerase chain reaction, Western blotting, in situ immunohistochemical, heparin affinity, DNA synthesis, and transient transfection techniques were used to confirm expression, localization, and functionality of the transgenes. Both transfected and transduced cells constitutively expressing either TAT or (hst/KS)FGF-1 adopted a transformed phenotype, maintained aggressive growth behavior, and demonstrated both induction of FGF-specific phosphotyrosyl proteins and nuclear association of FGF-1 and FGF-1 receptor. Increased levels of endogenous, murine FGF-1 mRNA (reverse transcriptase-polymerase chain reaction) and protein (immunoblot analysis) were apparent in both (hst/KS)FGF-1- and TAT-transformed cells. Medium conditioned by (hst/KS)FGF-1-transduced cells contained steady-state levels of biologically active FGF-1 which exhibited a representative molecular weight. Limited sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis of the conditioned medium from TAT-transformed cells demonstrated the appearance of FGF-1 as latent, high molecular weight complexes requiring reducing agents to activate full biological activity. Collectively, these results suggest that TAT induces the expression and secretion of FGF-1, which may be potentially relevant to the pathophysiological development of AIDS-Kaposi's sarcoma.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Identification of the domain within fibroblast growth factor-1 responsible for heparin-dependence.

While the prototype members of the fibroblast growth factor (FGF) family, FGF-1 and FGF-2 are structurally related, the structural differences between these polypeptides predict that they will ultimately exhibit different biological roles. Indeed, a significant difference between these proteins is the dependence of FGF-1 on heparin for the generation of maximal mitogenic activity. In order to gain structural insight into the issue of FGF-1 heparin-dependence, a synthetic gene encoding FGF-2 was constructed with oligonucleotides in a four-cassette format similar to a synthetic gene previously constructed for FGF-1 (Forough et al. 1992, Biochem. Biophys. Acta 1090 293-298). This strategy permitted the molecular shuffling of corresponding cassette(s) between FGF-1 and FGF-2 to yield FGF-1:FGF-2 chimeras. Three amino acid changes (Lys86-->Glu, Tyr120-->His, and Thr121-->Ala) were introduced into the synthetic FGF-2 gene by the cassette format to generate convenient FGF-1 restriction sites, but these alterations did not significantly affect the mitogenic activity or the heparin-binding affinity of the recombinant FGF-2 protein when compared with native FGF-2. Among the various FGF-1:FGF-2 chimeric constructs, one designated FGF-C(1(1/2)1 1), which represents FGF-1 containing FGF-2 amino acid residues 65 to 81, displayed FGF-1-like heparin-binding affinity but it did not require the addition of exogenous heparin to manifest its mitogenic activity. These data suggest that the sequence within residues 65 and 81 from FGF-2 significantly contributes to the heparin-dependent character of FGF-1.

Amino Acid Sequence↗
PubMed1995

Interactions of peroxyquinols with cytochromes P450 2B1, 3A1, and 3A5: influence of the apoprotein on heterolytic versus homolytic O-O bond cleavage.

In studies of the mechanisms involved in oxygen activation by cytochromes P450 (P450s), organic hydroperoxides are frequently used to model the putative peroxyferrous complex formed immediately prior to oxygen-oxygen bond cleavage during the reaction cycle of this monooxygenase. Heterolysis of the O-O bond by ferric P450 generates the catalytically competent oxo-ferryl intermediate analogous to peroxidase Compound I, and homolysis produces the Compound II analog capable only of one-electron oxidations. As P450s have been shown to catalyze both modes of O-O bond scission, the present investigation was focused on the influence of the apoprotein on the relative contributions of these competing processes. Liver microsomes from rats treated with the P450-inducing agents phenobarbital, beta-naphthoflavone, and dexamethasone, as well as purified P450s 2B1, 3A1, and 3A5 were incubated with 2,6-di-tert-butyl-4-hydroperoxy-4-methyl-2, 5-cyclohexadienone (BHTOOH). Ratios of heterolysis to homolysis were determined by analyzing the products derived from this hydroperoxide. The data demonstrate that BHTOOH is cleaved with a ratio of approximately 1.0 with all of the liver microsomal or purified P450s investigated, except with liver microsomes from dexamethasone-treated rats or with P450s 3A1 and 3A5. In these cases, heterolysis predominated over homolysis by factors of 2.5 to 4.0. On the other hand, microsomes rich in P450 2B1 catalyzed predominantly heterolysis with analogs of BHTOOH containing smaller alkyl substituents. The data are consistent with a requirement for solvent access to the peroxyferrous complex and general acid catalysis of heterolytic O-O bond cleavage by water.

Animals↗
PubMed1995

A phase II trial of piroxantrone in disseminated malignant melanoma. A Southwest Oncology Group study.

Piroxantrone is one of the anthrapyrazoles developed in an effort to combine the broad antitumor activity of the anthracyclines with decreased myocardial toxicity. It has shown activity in metastatic melanoma during phase I trials. The Southwest Oncology Group (SWOG) conducted a phase II trial in disseminated malignant melanoma with piroxantrone administered at 150 mg/m2 intravenously over 1 h every 21 days, based upon the phase I experience. Forty-six eligible patients were registered to the trial and 44 were evaluable for response. Two partial responses, Wayne of 6 and 9 months duration were observed for an overall response rate of 5% (95% confidence interval 1%-15%). Thirty-six of 46 eligible patients have died with an estimated median survival of 5 months (95% confidence interval 3-8 months). Toxicities were tolerable with granulocytopenia being the predominant toxicity. Based upon the observed response rate, it is concluded that piroxantrone administered at this dose and schedule has detectable but minimal activity, and does not warrant further investigation in this disease.

Adult↗
PubMed1995

Scrotal size of yearling sires and early calving in beef herds: epidemiological investigation of possible causal pathways.

Scrotal circumference has been recommended as a clinical test for predicting the fertility potential of yearling bulls. The objectives of this study were to determine if scrotal size of yearling bulls influences herd fertility and to investigate specific causal pathways. Calving records from 44 herds enrolled in the Beef Herd Improvement Plan were selected from the data base for 1984 to 1989. Logistic regression was used to model the event of calving within the first 3 wk of the calving season as a function of scrotal circumference, herd size, age and the interactions of scrotal circumference with age, scrotal circumference with herd size, and herd size with age and the random effects of herd. The odds of cows calving in the first 3 weeks of the calving season were lower in large herds (>30 vs 20 to 30 calves born per season) and with younger yearling bulls (12 to 15 vs. 16 to 18 months of age). Early calving was not associated with scrotal circumference, or the interactions scrotal circumference with herd size and scrotal circumference with age (p > 0.15). It was concluded that the female:male ratio and age of bull both affected the odds of a cow calving early, but neither of the associations was altered by selection for bulls with a larger scrotal circumference, and therefore scrotal circumference is not included in either of the 2 causal pathways.

Journal Article↗
PubMed1995

The determination and correlation of reproductive parameters of performance-tested Hereford and Simmental bulls.

Purebred Hereford and Simmental bulls (n = 120), managed similarly to bulls in the Ontario Bull Evaluation Program, were evaluated for reproductive parameters. Four diets, equivalent except for the form of dietary fiber, were fed in a growth performance trial. Diet had no direct effect (P > 0.10) on any of the reproductive variables examined. Of the 117 bulls that had complete breeding soundness evaluations, 75% were classified as satisfactory potential breeders, 24% as questionable potential breeders and 1% as unsatisfactory potential breeders. The 2 breeds were significantly different (P < 0.05) for several end of test parameters. When controlling for age and weight differences, Herefords had a higher backfat thickness, smaller scrotal circumference, lower paired testicular weight and lower epididymal weight. Semen morphology and motility did not differ (P > 0.10) between the breeds. When examining simple correlations, scrotal circumference was highly correlated with paired testicular weight, moderately correlated with epididymal weight, daily sperm production and extragonadal sperm reserves, and negatively correlated with backfat thickness. Scrotal circumference was not related to backfat thickness when controlling for breed effects. The degree of germinal epithelium loss was moderately and negatively correlated with the percentage of spermatozoa with normal morphology and progressive motility, epididymal sperm reserves and epididymal weight, but was not correlated with scrotal circumference.

Journal Article↗
PubMed1995

Peroxynitrite-induced cytotoxicity in PC12 cells: evidence for an apoptotic mechanism differentially modulated by neurotrophic factors.

Peroxynitrite is a powerful oxidant formed by the near-diffusion-limited reaction of nitric oxide with superoxide. Large doses of peroxynitrite (> 2 mM) resulted in rapid cell swelling and necrosis of undifferentiated PC12 cells. However, brief exposure to lower concentrations of peroxynitrite (EC50 = 850 microM) intially (3-4 h) caused minimal damage to low-density cultures. By 8 h, cytoplasmic shrinkage with nuclear condensation and fragmentation became increasingly evident. After 24 h, 36% of peroxynitrite-treated cells demonstrated these features associated with apoptosis. In addition, 46% of peroxynitrite-treated cells demonstrated DNA fragmentation (by terminal-deoxynucleotide transferase-mediated dUTP-digoxigenin nick end-labeling) after 7 h, which was inhibited by posttreatment with the endonuclease inhibitor aurintricarboxylic acid. Serum starvation also resulted in apoptosis in control cells (23%), the percentage of which was not altered significantly by peroxynitrite treatment. Although peroxynitrite is known to be toxic to cells, the present study provides a first indication that peroxynitrite induces apoptosis. Furthermore, pretreatment of cells with nerve growth factor or insulin, but not epidermal growth factor, was protective against peroxynitrite-induced apoptosis. However, both acidic and basic fibroblast growth factors greatly increased peroxynitrite-initiated apoptosis, to 63 and 70%, respectively. Thus, specific trophic factors demonstrate differential regulation of peroxynitrite-induced apoptosis in vitro.

Animals↗
PubMed1995

An open trial of exposure therapy based on deconditioning for post-traumatic stress disorder.

Twenty-three patients who had experienced a major stressful event were given a debriefing session followed by eight weekly sessions of imaginal exposure and in vivo exposure. Patients recounted their traumatic experiences aloud, using the first person and the present tense, and included as much detail as possible. This account was audiotaped and patients were asked to listen to the tape between treatment sessions. There were reductions of 42 percent in the Impact of Events Scale (IES), of 61 percent in the General Health Questionnaire (GHQ), of 38 percent in the Symptom Checklist-90 (SCL-90) questionnaire, and of 35 percent in the Clinician Administered Post-Traumatic Stress scale (CAPS), all of which were statistically significant. The number of patients who satisfied the diagnostic criteria for post-traumatic stress disorder was halved.

Adult↗
PubMed1995

Molecular cloning and expression of carcinoembryonic antigen gene family members.

The carcinoembryonic antigen (CEA) gene family consists of approximately 30 genes, of which 17 are transcriptionally active. These genes are tightly clustered on the long arm of chromosome 19. Two main subgroups are distinguishable, one encoding CEA and its classical non-specific cross-reacting antigens (NCAs) and the second encoding the pregnancy-specific glycoproteins (PSGs). The CEA family belongs to the immunoglobulin superfamily. CEA subgroup members are either membrane bound through a glycosyl phosphatidylinositol anchor, or are integral membrane proteins, whereas PSG molecules are secreted from the cell. Despite high sequence similarity, CEA family members reveal variable expression patterns, indicating different functions. Apart from its high expression in various adenocarcinomas, CEA is found in epithelia lining the gastrointestinal tract, in eccrine sweat glands, lung epithelia and testes. The NCAs are often coexpressed with CEA, but are also found in granulocytes. PSGs are coexpressed in syncytiotrophoblast cells of the placenta, submandibular salivary glands and fetal liver, as well as in choriocarcinomas and breast tumours.

Biomarkers, Tumor↗
PubMed1995

Expression of a truncated FGF receptor results in defective lens development in transgenic mice.

Members of the fibroblast growth factor (FGF) family are thought to initiate biological responses through the activation of cell surface receptors which must dimerize to transmit an intracellular signal. Mammalian lens epithelial cells respond to exogenous extracellular FGF, either in tissue culture or in transgenic mice, by initiating fiber cell differentiation. The role of FGF signalling in normal lens development was evaluated by lens-specific synthesis of a kinase-deficient FGF receptor type I (FGFR1) in transgenic mice. This truncated FGF receptor is thought to act as a dominant negative protein by heterodimerization with endogenous FGF receptors. The presence of transgenic mRNA in the lens was confirmed by in situ hybridization and by polymerase chain reaction amplification of reverse transcribed lens RNA (RT-PCR). The presence of transgenic protein was determined by Western blotting with antibodies to an extracellular domain of FGFR1. Three of four transgenic families expressing the truncated FGF receptor exhibited lens defects ranging from cataracts to severe microphthalmia. While the microphthalmic lenses displayed a normal pattern of differentiation-specific crystallin expression, the lens epithelial cells were reduced in number and the lens fiber cells displayed characteristics consistent with the induction of apoptosis. Our results support the view that FGF receptor signalling plays an essential role in normal lens biology.

Animals↗
PubMed1995

Extracellular FGF-1 acts as a lens differentiation factor in transgenic mice.

The vertebrate ocular lens undergoes a spatially defined pattern of differentiation which may be regulated by the ocular distribution of proteins from the fibroblast growth factor (FGF) family. The ability of altered FGF-1 (acidic FGF) distribution to disrupt the normal pattern of lens differentiation was evaluated by the production of transgenic mice which express FGF-1 under the control of the lens-specific alpha A-crystallin promoter. Since FGF-1 lacks a classical signal peptide consensus sequence, transgenic mice were also produced with a chimeric construct containing the signal peptide sequence of the FGF-4 gene fused in frame to the coding sequences of the FGF-1 cDNA in order to obtain extracellular expression of the transgene. The presence of transgenic mRNA and protein was confirmed by in situ hybridization, Western analysis and immunohistochemistry. The ocular histology of newborn and young adult transgenic mice expressing FGF-1 without a signal peptide appeared normal. In contrast, mice expressing secreted FGF-1 exhibited lens abnormalities including the elongation of anterior epithelial cells. Epithelial cell elongation was accompanied by expression of the fiber cell differentiation marker, beta-crystallin. These observations provide an in vivo demonstration that FGF-1 can induce anterior lens epithelial cells to express characteristics consistent with the onset of fiber cell differentiation. The transgenic induction of differentiation confirms that normal lens morphology reflects an asymmetric distribution of inductive factors within the eye.

Animals↗
PubMed1995

Behavioral effects of felbamate in childhood epileptic encephalopathy (Lennox-Gastaut syndrome).

The behavioral effects of felbamate were assessed in 20 persons, (ages 2 to 19 years) who were participating in a compassionate plea protocol for children with Lennox-Gastaut syndrome. Parents completed a questionnaire concerning aspects of behavioral change once all medications were in a constant regimen. Significant improvements were suggested in social functioning, intellectual functioning, motor functioning, attention and concentration, alertness, initiative, variability in performance, and memory. There was a tendency for these effects to reverse when the drug was discontinued.

Adolescent↗
PubMed1995

Immunotherapy with interleukin 2 with or without lymphokine-activated killer cells after autologous bone marrow transplantation for malignant lymphoma: a feasibility trial.

Early relapse remains a major challenge after autologous bone marrow transplant for malignant lymphoma (ML). It is postulated that consolidative immunotherapy with interleukin 2 (IL-2) with or without lymphokine-activated killer (LAK) cells administered after autologous bone marrow (ABMT) or peripheral blood stem cell transplantation (PBSCT) for ML might eradicate residual disease and reduce relapse rates. A previous trial identified an IL-2 regimen that could be administered early after ABMT. This paper presents the clinical results of 16 patients with ML, who participated in a study to determine whether LAK cells could be administered after ABMT with this IL-2 regimen, as well as 6 patients who received IL-2 alone after ABMT or PBSCT. Seventeen patients with non-Hodgkin's lymphoma (NHL), and 5 with Hodgkin's disease (HD), underwent ABMT (20 patients) or PBSCT (2 patients). At the time of transplantation, 7 patients were in untreated or chemotherapy-sensitive first relapse, 3 were in CR2, and 12 were beyond CR2. Beginning 22-85 days (median 43) after ABMT/PBSCT, patients received IL-2 at 3.0 x 10(6) U/m2/day by continuous infusion days 1-5 of the IL-2 protocol. On protocol days 7-9 the first 16 patients underwent apheresis for LAK cell generation. The cells were cultured in IL-2 for 5 days and were infused on days 12-14. Low-dose IL-2 (0.9 x 10(6) IU/m2/day) was administered on days 12-21 in the outpatient department. Patients received a median of 148 (62-279) x 10(9) LAK cells. LAK cell infusions were associated with transient fevers, chills and dyspnea in most patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗