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Biomedical subjects

J Fox

Publications and source records attributed to J Fox.

At least 199 records · Page 11Linked to original sources
PubMed1989

Antigenic conservation of the ureases of spiral- and helical-shaped bacteria colonising the stomachs of man and animals.

A monoclonal antibody, CP11, has been produced which is directed against the ureas of Campylobacter pylori. This antibody has been used to look for antigenic cross-reactivity, in other ureolytic and non-ureolytic campylobacters, by immunohistological techniques. It has also been used to investigate the helical-shaped organisms found in the stomach of the human, monkey and cat (CS1) and the ileum of the rat (ST1). Interestingly the antibody cross-reacted with the gastric helical organisms from the human, monkey and cat but not with the rat helical organism. No cross-reactivity was observed with C. mustelae or the other ureolytic campylobacters, C. nitrofigilis and the urease positive thermophilic campylobacters. These results are discussed in relation to the phylotaxonomy of these organisms.

Animals↗
PubMed1989

Luteal phase deficiency after completely normal follicular and periovulatory phases.

Luteal phase defect (LPD) accounts for a significant proportion of reproductive disorders, however its etiology is still debated. A prospective study was performed on 37 ovulatory women to determine whether LPD can occur in cycles characterized by completely normal folliculogenesis. Criteria for normal folliculogenesis included: a gradual rise of serum estradiol, a luteinizing hormone (LH) surge, the presence of a dominant follicle that disappeared, an increase of serum progesterone, and normal serum levels of prolactin, testosterone, dehydroepiandrosterone sulfate, follicle-stimulating hormone, and LH. Thirty of 37 women fulfilled the above mentioned strict criteria and underwent endometrial biopsy in the late luteal phase. Seven of 30 (23%) demonstrated a delay in endometrial development and all had normal hormonal and ultrasonographic parameters of folliculogenesis and ovulation. Women with delayed endometrial development demonstrated slightly longer follicular phases (17.0 +/- 1.1 versus 14.5 +/- 0.3 days). Perfectly normal follicular and periovulatory events may be followed by deficient luteal phases.

Adult↗
PubMed1989

Molecular cloning of rat type 2C (IA) protein phosphatase mRNA.

A full-length cDNA encoding rat type 2C (IA) protein phosphatase was isolated from a kidney cDNA library. The cDNA was identified by screening the library with oligonucleotides based on a partial amino acid sequence determined from purified rat liver phosphatase. This clone is 2.35 kilobase pairs long and has a single extended translation reading frame that predicts a 382-amino acid protein of 42,416 daltons. The deduced amino acid sequence contains segments corresponding to three peptides from rat liver type 2C protein phosphatase and two peptides from rabbit skeletal muscle type 2C phosphatase. Rat kidney type 2C protein phosphatase is distantly related to yeast adenylate cyclase but is not related to the catalytic subunits of two other protein phosphatases (types 1 and 2A).

Adenylyl Cyclases↗
PubMed1989

Cross-reaction of immune sera from patients with rickettsial diseases.

Rickettsia rickettsii and Rickettsia conorii are the causative agents of two common and serious diseases, Rocky Mountain spotted fever and Mediterranean spotted fever, respectively. In patients naturally infected with either of these organisms, antibodies are produced which cross-react with antigens of the other so extensively that diagnostic tests usually cannot identify the causative agents. The results of this study indicate that serodiagnostic tests with antigen from one of these two organisms could be used to detect antibodies in patients with either of the two rickettsial diseases.

Antibodies, Bacterial↗
PubMed1989

Experimental Campylobacter jejuni infection in Macaca nemestrina.

Experimental infection of four specific-pathogen-free Macaca nemestrina monkeys (aged 3.5 and 4.5 months) with Campylobacter jejuni 81-176 caused acute diarrheal illness, characterized by fluid diarrhea, bloody stools, and fecal leukocytes, which lasted for approximately 7 to 11 days. Histologic examination of intestinal biopsies showed acute colitis characterized by infiltration of the mucosa with neutrophils and lymphocytes, and cryptitis. There were no histologic changes in the small intestine. Excretion of C. jejuni was demonstrated for 2 to 4 weeks postchallenge. Plasma antibodies to C. jejuni group antigen were elevated after challenge. Only mild diarrhea occurred after rechallenge with the same strain or with a heterologous C. jejuni strain (79-168) followed by further elevation in specific immunoglobulins A, M, and G. Four 1-year-old juvenile M. nemestrina monkeys which had experienced multiple infections with Campylobacter spp. did not exhibit illness when challenged with C. jejuni 81-176. All had elevated immunoglobulin A, M, and G plasma antibodies prior to challenge, and these humoral antibody levels were indicative of the immunity to challenge. The results demonstrate that C. jejuni infection in M. nemestrina caused colitis with clinical and pathologic results similar to those found in humans and indicate that prior infection protects against subsequent challenge.

Animals↗
PubMed1989

Production of antibody to and cellular localization of erythrocyte-sensitizing substance from Rickettsia rickettsii.

Antibodies to Rickettsia rickettsii erythrocyte-sensitizing substance (ESS) were raised in rabbits by using a derivatized ESS. The resulting antibodies reacted with R. rickettsii and cross-reacted with Rickettsia conorii, a member of the spotted fever group rickettsiae, but did not react with Rickettsia typhi, a member of the typhus group rickettsiae, Legionella bozemanii, or Proteus vulgaris OX19 or OX2. Immunoblot analysis indicated that ESS was present in more than one fraction and that the major haptenic fraction was proteinase resistant. Immunoelectron microscopy indicated that the antibodies to R. rickettsii were specific to components located on the cell surface and intracellularly to components between the cell wall and cytoplasmic membrane.

Animals↗
PubMed1989

Oral verapamil and calcium and vitamin D metabolism in rats: effect of dietary calcium.

Prior studies showed that chronic oral verapamil administration increased plasma immunoreactive parathyroid hormone (irPTH) but decreased 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels in rats fed a high (1.2%)-Ca diet. These and other findings suggested that verapamil may induce target-organ PTH resistance. This study determined the effects of verapamil (4, 20, or 100 mumol.kg-1.day-1 for 2 wk) in rats fed high (1.2%)-, low-normal (0.47%)-, and low (0.02%)-Ca diets (higher irPTH levels). With 1.2 and 0.47% Ca diets, verapamil administration was associated with increases in irPTH (92 and 44%, respectively) and decreases in 1,25(OH)2D3 levels (22 and 21%, respectively), increases in duodenal Ca transport (13 and 8%, respectively), and increases in tibia mineral content (1.3 and 2.8%, respectively). The decrease in 1,25(OH)2D3 levels was caused by decreased production, not by increased clearance. In contrast, verapamil was without effect in rats fed the 0.02% Ca diet. Thus severe dietary Ca deficiency abolished the stimulatory effects of verapamil on irPTH levels, Ca absorption, and tibia mineral content. Importantly, these results indicate that verapamil, in contrast to nifedipine, appears not to have adverse effects on Ca homeostasis in rats, irrespective of dietary Ca intake.

Administration, Oral↗
PubMed1989

Interventional dysrhythmia management and the role of laser.

Drug-resistant dysrhythmias may require interventional management. Laser energy can be used for interruption or destruction of dysrhythmia-generating foci or conductive pathways. Lasers may, therefore, be useful tools for interventional management of supraventricular or ventricular dysrhythmias and preexcitation syndromes. Although the role of lasers in interventional dysrhythmia management is not clearly defined, the advantages may be substantial.

Arrhythmias, Cardiac↗
PubMed1988

Sequencing and synthesis of pardaxin, a polypeptide from the Red Sea Moses sole with ionophore activity.

Pardaxin, an amphipathic polypeptide secreted by the Red Sea flatfish Pardachirus marmoratus whose sequence is NH2-G-F-F-A-L-I-P-K-I-I-S-S-P-L-F-K-T-L-L-S-A-V-G-S-A-L-S-S-S-G-G-Q-E, was synthesized by the solid-phase method. The structure was verified by sequencing. The synthetic polypeptide changed the resistance of lipid bilayers by forming pores. At 10(-7)-10(-8) M, the synthetic pardaxin increased the frequency of the spontaneous release of quanta of acetylcholine at the neuromuscular junction by up to 100-fold, resembling the native product. Synthetic pardaxin seems to be a suitable tool for investigating the molecular structures underlying channel selectivity.

Acetylcholine↗
PubMed1988

Alterations in the binding site of the cyclic AMP receptor protein at the Escherichia coli galactose operon regulatory region.

Gene manipulation techniques have been used to alter the binding site for the cyclic AMP-cyclic AMP receptor protein complex (cAMP-CRP) at the regulatory region of the Escherichia coli galactose (gal) operon. The effects of these changes on CRP-dependent stimulation of expression from the galP1 promoter in vivo have been measured, and gel binding assays have been used to measure the affinity of cAMP-CRP for the modified sites. Firstly we have deleted progressively longer sequences from upstream of the gal CRP site in order to locate the functional limit of the site. A deletion to -49, removing the first base that corresponds to the consensus sequence for a CRP binding site, is sufficient to reduce CRP binding and block CRP-dependent stimulation of P1. Secondly, we used synthetic oligonucleotides to invert the asymmetric nucleotide sequence at the gal CRP binding site or to make the sequence symmetric. Inversion of the site has little effect on CRP binding, the architecture of open complexes at P1 revealed by DNAase I footprinting, or the stimulation of transcription from P1. Making the site symmetric increases the affinity for CRP by over 50-fold and leads to increased transcription from P1, whilst hardly altering the DNAase I footprint of open complexes. Our results confirm that the strength of binding of CRP depends on the nature of the site and show that it is this that principally accounts for differences in CRP-dependent stimulation of transcription.

Base Sequence↗
PubMed1988

Calcium phosphate-coated porous titanium implants for enhanced skeletal fixation.

Porous titanium fiber implants for cementless skeletal fixation by bone ingrowth were treated with a calcium phosphate coating applied by a plasma flame-spray technique. In a paired experiment, treated and control implants were inserted in the humeri and olecranons of 36 adult dogs for periods of 1, 2, 4, and 6 weeks. After the animals were sacrificed, a biomechanical evaluation of the strength of skeletal fixation of the implants and a histologic evaluation of bone ingrowth was done. The mean shear strength of skeletal fixation at four weeks for the calcium phosphate-coated implants was 24% greater (P less than .01) than for paired controls. No difference in strength of fixation between treated and control implants was present at other time periods. The osteoconductive properties of the ceramic coating were demonstrated by bone forming in direct contact with the calcium phosphate coating on the metal fibers of the treated implants. No significant increase for the volume of bone ingrowth was established for treated implants compared to paired controls at any time period.

Animals↗
PubMed1988

Verapamil induces PTH resistance but increases duodenal calcium absorption in rats.

In vitro, verapamil inhibits duodenal Ca absorption, parathyroid hormone (PTH) secretion, and PTH-stimulated bone resorption. This study was designed to determine if any effects of chronic oral verapamil treatment on PTH secretion-action are reflected by changes in vitamin D metabolism, duodenal Ca absorption, and bone Ca content. Rats (100 g) received verapamil in the drinking water at doses of 4, 20, or 100 mumol.kg-1.day-1 for 2 wk. Verapamil administration did not significantly affect growth, plasma Ca or phosphate, or bone Ca content. However, verapamil treatment was associated with a dose-dependent 90% increase in plasma PTH levels. The elevated PTH was accompanied by a 22% decrease in 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] levels, such that there was a significant negative correlation (r = -0.52; P less than 0.01) between PTH and 1,25(OH)2D3 levels. Despite the decreased plasma 1,25(OH)2D3 levels, verapamil treatment was associated with a dose-dependent increase in duodenal Ca absorption. The increased Ca absorption did not seem to be caused by a verapamil-induced increased intestinal sensitivity to 1,25(OH)2D3, since verapamil-treated vitamin D-deficient rats showed the same absorptive response to administered 1,25(OH)2D3 as untreated rats. Thus chronic oral verapamil treatment induces an apparent PTH resistance but does not appear to have major effects on overall Ca homeostasis in young male rats.

Absorption↗
PubMed1987

Laser catheter ablation of simulated ventricular tachycardia.

Catheter-directed laser injury of the left ventricular endocardium for ablation of ventricular tachycardia was studied in a canine model of simulated ventricular tachycardia. Bipolar plunge electrodes were placed at thoracotomy into the left ventricular endocardium in nine anesthetized dogs. Ventricular tachycardia was simulated by pacing at 200 beats per minute. After four days of recovery, catheter-directed neodymium:yttrium-aluminum-garnet laser injury was produced at the site of earliest recorded electrical activation during pacing tachycardia as detected by endocardial catheter mapping. Immediately after laser injury and again five days after injury, pacing tachycardia was attempted. Failure to pace after laser injury was defined as successful arrhythmia ablation. In 3/9 (33%) experiments, the laser-injured tissue surrounded the tachycardia source (pacing wires), and pacing-simulated ventricular tachycardia was prevented. When the laser injury did not involve the tachycardia source, 6/9 animals, due to limitations of the mapping system, pacing was not prevented. One animal developed sustained ventricular tachycardia during laser injury, with conversion to sinus rhythm by lidocaine. One animal, without recognized ventricular arrhythmia, died five days after laser injury. No unusual findings were noted at autopsy. These preliminary data suggest that catheter-directed laser-induced injury can ablate arrhythmia sources. Further studies are indicated in a more physiologic model, and the safety and risks of the procedure need further evaluation.

Animals↗