PubMed Health⌕ Search

Biomedical subjects

J R Wood

Publications and source records attributed to J R Wood.

At least 19 recordsLinked to original sources
PubMed1992

Functional homologs of the Arabidopsis RPM1 disease resistance gene in bean and pea.

We showed that a bacterial avirulence (avr) gene function, avrPpiA1, from the pea pathogen Pseudomonas syringae pv pisi, is recognized by some, but not all, genotypes of Arabidopsis. Thus, an avr gene functionally defined on a crop species is also an avr gene on Arabidopsis. The activity of avrPpiA1 on a series of Arabidopsis genotypes is identical to that of the avrRpm1 gene from P.s. pv maculicola previously defined using Arabidopsis. The two avr genes are homologous and encode nearly identical predicted products. Moreover, this conserved avr function is also recognized by some bean and pea cultivars in what has been shown to be a gene-for-gene manner. We further demonstrated that the Arabidopsis disease resistance locus, RPM1, conditioning resistance to avrRpm1, also conditions resistance to bacterial strains carrying avrPpiA1. Therefore, bean, pea, and conceivably other crop species contain functional and potentially molecular homologs of RPM1.

Amino Acid Sequence↗
PubMed1992

The effect of combined therapy with ranitidine and pirenzepine in the treatment of reflux oesophagitis.

The combination of a histamine H2-receptor antagonist and a muscarinic receptor antagonist has been reported to result in greater suppression of intragastric acidity than either agent alone. The present randomized, double-blind, multicentre trial compared the effects of the oral combination of 150 mg ranitidine b.d. plus 50 mg pirenzepine b.d. with 150 mg ranitidine b.d. plus placebo pirenzepine b.d. in the treatment of patients with reflux oesophagitis. All 157 patients had symptoms of gastro-oesophageal reflux with endoscopically confirmed oesophageal erosions (Savary and Miller grades I-III). After four weeks of treatment, healing rates were 32/75 (43%) in the combined treatment group and 34/76 (45%) in the group receiving ranitidine alone. After eight weeks, the cumulative healing rates had increased to 48/72 (67%) and 51/75 (68%), respectively. More patients receiving ranitidine plus pirenzepine had complete relief of day- and night-time heartburn after four weeks compared with those receiving ranitidine alone (day: 59% vs. 38%, P = 0.02; night: 69% vs. 52%, P = 0.04). After eight weeks, symptom relief was comparable in both groups. Clinical adverse effects were reported by nine patients receiving ranitidine and by 19 patients receiving the combination. It is concluded that combining ranitidine with pirenzepine does not aid the healing of reflux oesophagitis but does improve symptom relief at four weeks.

Administration, Oral↗
PubMed1991

Interactive effects of 1-octen-3-ol and carbon dioxide on mosquito (Diptera: Culicidae) surveillance and control.

Responses of natural populations of biting Diptera were studied at Everglades National Park, Fla., to three levels (0, 3.0, and 41.1 mg/h) of 1-octen-3-ol (octenol), four levels (0, 20, 200, and 2,000 ml/min) of carbon dioxide (CO2), and their combinations. Catches of mosquitoes (Aedes taeniorhynchus (Wiedemann), Culex [Melanoconion]) spp., Cx. nigripalpus Theobald, and Wyeomyia spp.) and one tabanid (Diachlorus ferrugatus (F.)) were affected significantly by CO2 and octenol. Significantly greater numbers of all taxa were collected as the level of CO2 was increased. The 3.0-mg/h release rate of octenol alone resulted in increased trap catches relative to no bait for all taxa except Cx. (Melanoconion) spp., whereas the 41.1-mg/h release rate alone generally reduced trap catches relative to either no bait or 3.0 mg/h octenol. The effect of CO2 and octenol was additive for Cx. (Melanoconion) spp. and D. ferrugatus and synergistic for Ae. taeniorhynchus. Six octenol-supplemented CO2 treatments produced mixed results for Cx. nigripalpus.

Aedes↗
PubMed1991

Ranitidine in the treatment of duodenal ulcer disease: relationship between antisecretory effect and ulcer healing rate.

The relationship between drug-induced suppression of intragastric acidity and the rate of duodenal ulcer healing was examined using data for a single drug, ranitidine, from 156 clinical trials involving 16,362 patients together with data on acid suppression from 37 studies of intragastric acidity in 630 subjects. In these studies ranitidine was given in doses ranging from 150 mg to 1200 mg per day administered in 9 different dosage regimens. The overall percentage of patients whose duodenal ulcers healed at 2 and 4 weeks on the different regimens was highly correlated with the percentage suppression of 24-hour intragastric acidity induced by different regimens. Thus the therapeutic benefit of a given ranitidine dosage regimen in healing duodenal ulcers relates directly to its antisecretory effect.

Drug Administration Schedule↗
PubMed1990

Long-term versus short-term treatment with recombinant interferon alfa-2a in patients with chronic hepatitis B: a prospective, randomized treatment trial.

We conducted a prospective, randomized trial to study the efficacy and tolerance of long-term versus short-term treatment with recombinant interferon alfa-2a in patients with chronic hepatitis B. Ten patients were randomly assigned to a 6-month interferon regimen, and 10 patients were assigned to a 3-week interferon trial. Eleven patients (five assigned to long-term treatment and six to short-term treatment) did not complete interferon therapy: eight had either severe thrombocytopenia or neutropenia; one had pronounced fatigue in relationship to administration of interferon; one had spontaneous bacterial peritonitis and sepsis and died; and one had a massive fatal variceal hemorrhage during interferon therapy. Most of the serious hematologic complications occurred in patients with cirrhosis and hypersplenism. In one patient, seroconversion to hepatitis B virus DNA negativity occurred before the onset of treatment. Four of the five patients able to complete the 6-month interferon regimen and only one of four patients able to complete the 3-week trial had seroconversion to hepatitis B virus DNA negativity. Thus, we conclude that the therapeutic response was better among patients who were able to complete a 6-month interferon trial. In patients with cirrhosis and hypersplenism, development of either severe thrombocytopenia or leukopenia associated with interferon therapy precluded completion of treatment.

Adult↗
PubMed1990

The timing of the evening meal affects the pattern of 24-hour intragastric acidity.

The object of the study was to examine the effect of varying the time of the evening meal on the pattern of 24-h intragastric acidity. Ten healthy subjects were studied; they ate regular meals throughout the day, but between 17.00 and 21.35 hours were separated into three groups. On three different days each group was fed the same dinner at either 17.15, 19.15, or 21.15 hours (early, standard or late). Variation in the evening meal's time caused significant changes in the pattern of acidity in the afternoon and evening, but did not affect 24-h intragastric acidity or nocturnal acidity. Integrated afternoon acidity (14.00 hours to dinner) was 69, 169 and 324 mmol.h/L when the subjects ate early, standard and late meals, respectively; evening acidity (dinner to midnight) was 235, 43 and 1 mmol.h/L with the three meals, respectively. The results suggest that, to control intragastric acidity, when the evening meal is eaten early (17.15 hours) dosing with an H2-antagonist should be after that meal, when eaten at the standard time (19.15 hours) dosing should be at bedtime, but when dinner is late (21.15 hours) the optimal regimen may involve dosing after lunch and also at bedtime.

Adult↗
PubMed1990

Field studies on the potential of butanone, carbon dioxide, honey extract, 1-octen-3-ol, L-lactic acid and phenols as attractants for mosquitoes.

Various combinations of six candidate attractants--butanone, carbon dioxide (CO2), honey, octenol, lactic acid and mixed phenols--were tested against natural populations of mosquitoes in Everglades National Park, Florida, U.S.A., using unlighted CDC-baited traps. With few exceptions, the attractancy of these candidate compounds to mosquitoes, when used alone, was less than that of CO2 alone. The exceptions were that octenol and honey extract alone attracted larger numbers of Coquillettidia perturbans (Walker). Addition of lactic acid and/or octenol to CO2 increased trap collections of Aedes taeniorhynchus (Wiedemann), Anopheles atropos D. & K., and An. crucians Wiedemann by 1.4-13.8 times. Culex nigripalpus Theobald collections were increased 2.7 times by the addition of lactic acid, while the addition of octenol produced mixed results. Whereas the addition of lactic acid reduced collections of Cx (Melanoconion) spp., the addition of octenol generally increased collections. The opposite happened for Wyeomyia mitchellii (Theobald). For the biting midge, Culicoides furens (poey), octenol (1.6-23.4 x ) and phenol (2.7 x ) alone attracted larger numbers, and lactic acid alone attracted approximately the same numbers as CO2 alone. The combinations octenol + phenol and octenol + 200 ml/min CO2 increased C. furens collections c. 100 times over CO2 alone. The combination of octenol + CO2 increased (1.6 x ) collections of the tabanid Diachlorus ferrugatus (Fabricius). Butanone appeared to decrease the trap collections of all species when combined with CO2 or octenol + CO2.

Animals↗
PubMed1990

Evaluation of 1-octen-3-ol as an attractant for Coquillettidia perturbans, Mansonia spp. and Culex spp. associated with phosphate mining operations.

Field studies were conducted in phosphate mined areas of Polk County, FL, to determine the responses of mosquitoes produced as a result of mining operations to octenol and carbon dioxide. There was a highly significant response of all species except Culex erraticus and Anopheles quadrimaculatus to CO2. Also, a significant negative octenol response was shown for An. quadrimaculatus. Coquillettidia perturbans, Mansonia titillans and Cx. salinarius had an increased response to octenol relative to no attractant. There was a slightly negative interactive effect between octenol and 500 cc/min CO2 for Anopheles spp. and Culex (Melanoconion) spp. Both Cq. perturbans and Ma. titillans showed a significant synergistic enhancement in catch with octenol supplemented CO2 when compared with CO2 alone. However, their response to CO2 was not significantly different at 2 release rates (200 and 500 cc/min). There was a slightly greater than additive effect for the combination of octenol and CO2 for Cx. nigripalpus.

Animals↗
PubMed1989

Acute treatment of reflux oesophagitis: a multicentre study to compare 150 mg ranitidine twice daily with 300 mg ranitidine at bedtime.

A randomized, double-blind, clinical trial was undertaken to compare 150 mg ranitidine b.d. with 300 mg ranitidine nocte in the treatment of reflux oesophagitis. Endoscopy data were evaluable for 336 patients after 8 weeks of treatment. At this time 75% of patients who received 150 mg ranitidine b.d., and 73% of those who received 300 mg nocte, had healed or showed endoscopic improvement to grade I oesophagitis. At 12 weeks these rates had increased to 89 and 88%, respectively. Oesophageal biopsies from 258 patients at 8 weeks showed histological improvement in 44 and 47% of those treated with 150 mg ranitidine b.d. and 300 mg ranitidine nocte, respectively. After 12 weeks histological improvement was apparent in 57 and 54% of biopsies from each group, respectively. Symptom severity and frequency was reduced to a similar extent by both treatments. Adverse events were reported by 15 patients. A 300-mg bedtime dose of ranitidine was found to be a well-tolerated, effective alternative to twice daily treatment in reflux oesophagitis.

Adult↗
PubMed1989

Acute treatment of reflux oesophagitis: a multicentre trial to compare 150 mg ranitidine b.d. with 300 mg ranitidine q.d.s.

H2-receptor antagonists administered in conventional dosage regimens fail to heal a significant proportion of patients with moderate or severe reflux oesophagitis. We have compared the effects of a higher dose of ranitidine (300 mg q.d.s.) with the currently recommended dosage regimen (150 mg b.d.) in 138 patients suffering from reflux oesophagitis. After 4 weeks of treatment 29% of patients who received 150 mg ranitidine b.d., and 63% of patients who received 300 mg ranitidine q.d.s. had complete endoscopic healing of their lesions (P less than 0.0001). After 8 weeks these proportions had increased to 54% and 75%, respectively (P less than 0.01). After 4 weeks of treatment, compete symptomatic relief had been achieved in 46% of patients who received 150 mg ranitidine b.d. and in 67% of patients who received 300 mg ranitidine q.d.s. (P less than 0.05). After 8 weeks these proportions were 64% and 84%, respectively (P less than 0.05). Both dosage schedules were well-tolerated. We conclude that more rapid symptom relief and healing in reflux oesophagitis can be achieved with 300 mg ranitidine q.d.s. than with 150 mg ranitidine b.d.

Acute Disease↗
PubMed1989

Geographical differences of gastric ulcer healing rate in patients treated with ranitidine or placebo.

The literature was searched for clinical trials evaluating the use of 300 mg ranitidine daily in the acute treatment of gastric ulcer. All available trials were examined, and the results compared between countries to determine the extent of any geographical variation in ulcer healing rates. Published placebo studies in gastric ulcer were also reviewed for comparison. Sixty-six publications were inspected to determine the trial design, country of origin, gastric ulcer healing rates, determined endoscopically, and details of patient demography. Overall worldwide healing rates for ranitidine treatment were 63% at week 4 and 86% at week 8 (n = 2349 and 2256 respectively), compared with 34% at week 4 and 52% at week 8 for placebo (n = 790 and 231 respectively). Statistically significant differences were found between the healing rates for individual countries at week 4 (P less than 0.001) and week 8 (P less than 0.001). However, after exclusion of the results from Japan (35%, n = 278) and Yugoslavia (97%, n = 32) at week 4, and from Japan (80%, n = 467) and France (65%, n = 52) at week 8, the healing rates from the remaining countries were not statistically different from one another. The limited data available in relation to age, sex and smoking habits, or placebo healing rates contributed little to explaining these aberrant results. It is concluded that there is variation in gastric ulcer healing rates between countries, but only results from Japan seem to be out of line with the rest of the world.

Cimetidine↗
PubMed1989

Can higher doses of an H2-receptor antagonist accelerate duodenal ulcer healing?

Drugs that inhibit gastric acid secretion heal duodenal ulcers at a rate that correlates with the ability of individual treatment regimens to decrease 24-h intragastric acidity. As current therapeutic regimens of ranitidine decrease 24-h intragastric acidity submaximally, higher dosages may expedite duodenal ulcer healing. To test this hypothesis a randomized, double-blind clinical trial was conducted in 245 patients with duodenal ulcer to compare the effects of standard dose (300 mg nocte) and high-dose (300 mg q.d.s.) ranitidine. Patients were assessed after 2 weeks of treatment and, if unhealed, after a further 2 weeks of therapy. The therapeutic gain in ulcer healing at the 2-week endoscopy of the higher dose over the lower dose of ranitidine was 22% (68% vs 46%, P less than 0.001). The cumulative ulcer healing rates at the 4-week endoscopy were 88% and 92% for the standard and high-dose ranitidine groups, respectively (N.S.). By 2 weeks, 61% of patients treated with standard ranitidine therapy and 79% of those receiving 300 mg ranitidine q.d.s. were pain-free (P less than 0.01). A further 2 weeks of therapy enabled 88% and 97% of patients (N.S.) to become pain-free on these two regimens, respectively. The drug regimens were equally well tolerated. Thus higher-dose ranitidine can significantly accelerate the healing of duodenal ulcer with improvement in pain relief.

Adult↗
PubMed1989

The pharmacology of histamine H2-receptor antagonists.

The structure of the first histamine H2-receptor antagonist, burimamide was described in 1972. Since then, numerous compounds with diverse chemical structures have been shown to possess H2-receptor antagonist activity. Most of these compounds comprise an aromatic ring and polar group linked by a flexible chemical chain. Currently five H2-receptor antagonists are available for therapeutic use. In vitro studies have confirmed the competitive nature of the interaction between agonist and antagonist for these compounds and a comparison of the pA2 values generated shows a rank order of potency cimetidine less than nizatidine = ranitidine less than or equal to roxatidine less than famotidine. The duration of action of these agents is largely dependent upon their pharmacokinetic properties; with the possible exception of roxatidine, all have plasma elimination half-lives in the range 2-4 hours. Competitive antagonists with a high degree of selectivity for the H2-receptor and with a longer duration of action are currently being investigated, e.g., sufotidine. In addition to competitive agents, several non-competitive H2-antagonists, e.g., loxtidine, have been described. These have a prolonged duration of action. Relative potency varies between animal species and pharmacological models studied but the results of animal pharmacological studies have generally provided a good indication of the likely effects in man. Studies of 24-hour intragastric acidity represent the most physiological model available in man for evaluating the effects of different antisecretory drug regimens. Comparative studies with ranitidine 150 mg b.i.d. and cimetidine 400 mg b.i.d. have shown a reduction in 24-hour acidity of 65% and 30%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Prevention of gastroduodenal damage induced by non-steroidal anti-inflammatory drugs: controlled trial of ranitidine.

OBJECTIVE: To evaluate the prophylactic effect of ranitidine 150 mg twice daily in patients requiring one of the following non-steroidal anti-inflammatory drugs: naproxen, piroxicam, diclofenac, and indomethacin. In addition, risk factors were studied in order to help in targeting of such treatment to specific groups of patients. DESIGN: Double blind, placebo controlled, randomised, parallel group with endoscopic assessments at 0, 4, and 8 weeks. SETTING: Multicentre outpatient study at secondary referral centres in five European countries. PATIENTS--297 patients with rheumatoid arthritis or osteoarthritis over the age of 18 without lesions in the stomach and duodenum at baseline endoscopy (after one week without taking non-steroidal anti-inflammatory drugs). Those taking other antirheumatic agents, concomitant ulcerogenic drugs, or treatment for peptic ulcers within the previous 30 days were excluded. Age, sex, arthritic disease, and type of non-steroidal anti-inflammatory drug used were comparable in the two treatment groups. In all, 263 patients completed the trial. INTERVENTIONS: Ranitidine 150 mg twice daily or placebo (plus the selected non-steroidal anti-inflammatory drug) was prescribed within five days after the baseline endoscopy for two consecutive periods of four weeks. Paracetamol was permitted during the study, but not antacids. Patients were withdrawn if the most severe grade of damage (including ulceration) was found at the four week endoscopy or when indicated, or with lesser damage at the investigator's discretion. END POINT: Frequency of gastric and duodenal ulceration or lesions, or both. MEASUREMENTS AND MAIN RESULTS: The cumulative incidence of peptic ulceration by eight weeks was 10.3% (27/263); 2 out of 135 (1.5%) developed duodenal ulceration in the ranitidine group, compared with 10 out of 126 (8%) taking placebo. The frequency of gastric ulceration was the same (6%) for the two groups at eight weeks. Though significantly fewer gastric lesions developed in the ranitidine group by eight weeks. The frequency of non-ulcerative lesions in the duodenum did not differ greatly for the two groups at either time point. Twelve out of 75 (16%) patients taking piroxicam developed peptic ulceration, of whom two thirds had duodenal ulceration. Patients with a history of peptic ulcer were particularly susceptible to recurrent ulceration, against which ranitidine offered some protection. CONCLUSIONS: Ranitidine 150 mg twice daily significantly reduced the incidence of duodenal ulceration but not gastric ulceration when prescribed concomitantly with one of four commonly used non-steroidal anti-inflammatory drugs.

Adult↗
PubMed1988

Pattern and duration of HBV DNA seropositivity in acute hepatitis B.

To determine the pattern and duration of HBV DNA seropositivity in acute hepatitis B, six patients were assessed during the incubation, clinical, and convalescent stages of their illness by DNA hybridization using a slot blot technique. Patients were identified by the detection of HBsAg nearly one month before the development of clinical and laboratory features of acute hepatitis (mean 22 +/- 4 days) and they were followed at one- to three-week intervals for 6 +/- 1 months. Each patient lacked antibody to delta virus. During the incubation period, HBV DNA was not detected in serum. At symptomatic onset, all were seropositive for HBV DNA and HBeAg. At peak biochemical disease, three patients had already cleared HBV DNA and five continued to harbor HBeAg. The duration of HBV DNA seropositivity was as short as one week. At the time of biochemical resolution, all patients had cleared HBV DNA, while four of five remained HBeAg-positive. Clearance of HBeAg and HBsAg occurred 4 +/- 2 months after loss of HBV DNA. We conclude that HBV DNA is not detectable in serum during the early incubation period but that it is present at the onset of symptoms. Its duration in serum can be brief and clearance is possible by the peak of aminotransferase activity. HBV DNA usually disappears before HBeAg, and it is invariably lost by the time of biochemical resolution. Its detection in serum coincides with the clinical illness, but it may be missed unless sampling is done early in the clinical course.

Acute Disease↗
PubMed1988

Frequency and significance of immunoglobulin M antibody to hepatitis B core antigen in corticosteroid-treated severe chronic active hepatitis B.

To assess the frequency and significance of immunoglobulin M (IgM) antibody to hepatitis B core antigen (anti-HBc) in corticosteroid-treated severe chronic active hepatitis B, we tested 96 serum samples from 16 patients who were seropositive for hepatitis B surface antigen (HBsAg) (group 1) and 8 HBsAg-negative, anti-HBc-positive patients (group 2) by enzyme-linked immunoassay. Samples obtained in the presence and absence of disease activity before, during, and after long-term corticosteroid therapy (mean duration, 42 +/- 7 months) were evaluated. Seropositivity for IgM antibody was demonstrated in 12 group 1 patients, including 9 tested before corticosteroid therapy; no group 2 patients were seropositive. Seropositivity was more common in serum samples obtained during active than during inactive disease (51% versus 22%; P less than 0.05) and more frequent in serum samples that contained hepatitis B e antigen (46% versus 11%; P less than 0.02) and hepatitis B virus deoxyribonucleic acid (50% versus 24%; P less than 0.05) than in those without these markers. In some patients, seropositivity persisted or recurred intermittently during corticosteroid therapy for up to 57 months. We conclude that seropositivity for IgM antibody can be demonstrated frequently by enzyme-linked immunoassay in corticosteroid-treated patients with severe disease. Seropositivity reflects active virus replication, and it is commonly associated with inflammatory activity. The duration of seropositivity may be protracted during long-term corticosteroid therapy.

Adrenal Cortex Hormones↗
PubMed1988

A comparison of two ranitidine intravenous infusion regimens in critically ill patients.

The effect of two ranitidine intravenous infusion regimens on intragastric pH was studied in 134 critically ill patients admitted to 15 intensive care units. Intragastric pH was determined hourly for 30 hours. Those patients whose intragastric acidity fell below pH 4.0 for 3 or more of the first 6 hours were considered 'at risk' of developing stress-related gastric lesions and randomized to receive a 50 mg bolus of ranitidine together with a continuous intravenous infusion of either 0.125 or 0.25 mg kg-1 h-1 ranitidine for 24 hours. The maximal elevation in intragastric pH was achieved within 12 hours. The median intragastric pH for the last 20 hours of the infusion period was 5.9 for the higher dose group and 5.6 for the lower dose group. The increase in intragastric pH achieved by the two dosage regimens did not differ significantly throughout the 24 hour period. Patients having two or more of five major risk factors (head injury, major trauma, sepsis, respiratory failure/insufficiency and major surgery) had better overall control of intragastric pH on the higher dose of ranitidine than those receiving the lower dose. The majority of intensive care patients are likely to receive satisfactory treatment with the lower dosage regimen that was tested (0.125 mg kg-1 h-1). Those with multiple risk factors may, however, require treatment with higher doses of ranitidine (0.25 mg kg-1 h-1).

Adolescent↗