Ascospore Release and Infection of Apple Leaves by Conidia and Ascospores of Venturia inaequalis at Low Temperatures.

ABSTRACT Mills' infection period table describes the number of hours of continuous leaf wetness required at temperatures from 6 to 25 degrees C for infection of apple leaves by ascospores of Venturia inaequalis and reports that conidia require approximately two-thirds the duration of leaf wetness required by ascospores at any given temperature. Mills' table also provides a general guideline that more than 2 days of wetting is required for leaf infection by ascospores below 6 degrees C. Although the table is widely used, infection times shorter than those in the table have been reported in lab and field studies. In 1989 a published revision of the table eliminated a potential source of error, the delay of ascospore release until dawn when rain begins at night, and shortened the times reported by Mills for ascospore infection by 3 h at all temperatures. Data to support the infection times below 6 degrees C were lacking, however. Our objective was to quantify the effects of low temperatures on ascospore discharge, ascospore infection, and infection by conidia. In two of three experiments at 1 degrees C, the initial release of ascospores occurred after 131 and 153 min. In the third experiment at 1 degrees C, no ascospores were detected during the first 6 h. The mean time required to exceed a cumulative catch of 1% was 143 min at 2 degrees C, 67 min at 4 degrees C, 56 min at 6 degrees C, and 40 min at 8 degrees C. At 4, 6, and 8 degrees C, the mean times required to exceed a cumulative catch of 5% were 103, 84, and 53 min, respectively. Infection of potted apple trees by ascospores at 2, 4, 6, and 8 degrees C required 35, 28, 18, and 13 h, respectively; substantially shorter times than previously were reported. In parallel inoculations of potted apple trees, conidia required approximately the same periods of leaf wetness as ascospores at temperatures from 2 to 8 degrees C, rather than the shorter times reported by Mills or the longer times reported in the revision of the Mills table. We propose the following revisions to infection period tables: (i) shorter minimum infection times for ascospores and conidia at or below 8 degrees C, and (ii) because both ascospores and conidia are often present simultaneously during the season of ascospore production and the required minimum infection times appear to be similar for both spore types, the adoption of a uniform set of criteria for ascosporic and conidial infection based on times required for infection by ascospores to be applied during the period prior to the exhaustion of the ascospore supply. Further revisions of infection times for ascospores may be warranted in view of the delay of ascospore discharge and the reduction of airborne ascospore doses at temperatures at or below 2 degrees C.

Tinidazole and doxycycline compared to doxycycline alone as prophylactic antimicrobial agents in elective colorectal surgery.

Forty-two patients admitted for elective colorectal surgery were given tinidazole and doxycycline or doxycycline alone as prophylactic antimicrobials in a double-blind study. There was altogether one abdominal wound infection (2.4%), and one patient developed a perineal fistula three months after the operation. No significant difference in postoperative infections between the two groups could be demonstrated. It is concluded that doxycycline seems effective in reducing wound sepsis after operations on the large intestine and that additional administration of tinidazole will yield little in prophylaxis.

Prognostic value of the pentagastrin and insulin tests after proximal gastric vagotomy.

A review was made of 72 patients 3--6 years after proximal gastric vagotomy without drainage operation for duodenal ulcer. To assess the prognostic value of gastric acid secretory analyses, the correlation between the clinical results and the pentagastrin and insulin tests made preoperatively and 2 months postoperatively was determined. The preoperative secretory analyses showed no such correlation. Comparing recurrences and non-recurrences, only the basal acid output 2 months postoperatively showed any discriminatory ability, 2 mmol/h representing the critical level. When clinically satisfactory and clinically unsatisfactory patients were compared, the insulin-stimulated acid output and peak acid concentration 0--45 min after stimulation, in addition to the basal acid concentration and output, had statistically significant discriminatory levels. There was no correlation between the clinical results and seven different criteria for positive insulin response.

Maintenance treatment of duodenal ulcer patients with a single bedtime dose of cimetidine.

Fifty-eight patients with endoscopically verified duodenal ulcers were treated with cimetidine, 1 g/day, for 6--10 weeks. The ulcers healed in 52 out of the 54 patients completing the treatment (96.3%). Forty-seven of the patients with healed ulcer were randomly allocated to 1 year of maintenance treatment, 23 patients with cimetidine, 400 mg at night, and 24 patients with placebo tablets. In the cimetidine-treated group 2 out of the 20 patients (10%) completing the trial had recurrence of ulceration, whereas 16 out of the 23 patients (70%) completing the placebo treatment had ulcer recurrence (p less than 0.001). The drug was well tolerated and, except for a marked increase in serum transaminases in three patients, no serious side effects were seen.

Comparison of gastric secretory response in man to duodenal and jejunal liver extract perfusion.

The stomachs of six healthy volunteers were intubated with a Levine tube. In addition, a thin polyethylene tube was placed in the proximal jejunum or in the proximal duodenum. After a 1-h period with no perfusion the intestine was perfused for 2 h with 7% liver extract (LE) (pH 5.5; 380 MOsm/kg water) at a rate of 100 ml/h. In control tests 200 ml of 0.9% physiologic saline solution were used as perfusate. Reflux to the stomach was determined by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin levels were measured in 15-min periods. During perfusion of the proximal jejunum only pepsin outputs were increased significantly. During duodenal perfusion of LE, gastric acid and pepsin outputs were increased to 31% and 73% of maximal pentagastrin stimulation, respectively. Controls showed no changes in gastric secretion. Plasma gastrin levels were not elevated after jejunal or duodenal perfusion. These results confirm that the intestinal phase of gastric secretory stimulation does exist in humans. Furthermore, it appears that the major portion of this stimulation originates from the duodenum and is not gastrin-dependent.

Effect of cimetidine on pentagastrin-stimulated gastric secretion before and after proximal gastric vagotomy for duodenal ulcer.

Nine patients with duodenal ulcer were studied before and 2--3 months after proximal gastric vagotomy (PGV). Infustion or cimetidine, 1.2 mg.kg-1h-1, reduced mean gastric acid output, in response to infusion of 1.5 microgram.kg-1h-1 of pentagastrin, by, on an average, 79.4% before and 79.1% after vagotomy. The corresponding values for pepsin output were 66.5% before and 77.0% after the operation. The values were not statistically different. Thus, in terms of per cent inhibition, cimetidine was similarly effective before and after PGV. No correlation was found between per cent reduction of acic output by vagotomy and by cimetidine. The effect of the drug was added to that of the vagotomy. Patients with relapse ulcer after vagotomy are therefore interesting candidates for cimetidine treatment.

Effect of cimetidine on pentagastrin-stimulated gastric secretion in healthy man.

Two series of experiments were carried out in three healthy volunteers. In one series increasing doses of cimetidine were tested on a constant background stimulation with 0.15 microgram-kg-1h-1 of pentagastrin. In the other series of experiments increasing doses of pentagastrin were given either alone or in combination with a fixed dose of cimetidine (1.2 mg-kg-1h-1). Pentagastrin and cimetidine were given as continuous intravenous infusions, the various doses tested on separate days. The inhibition of acid output in response to pentagastrin stimulation increased almost linearly with the log dose of cimetidine. Fifty per cent inhibition of the response to 0.15 microgram-kg-1h-1 of pentagastrin was achieved by about 0.6 mg-kg-1h-1 of cimetidine. 2.4 mg-kg-1h-1 of cimetidine gave on average 90% inhibition. The inhibition caused by cimetidine decreased to a minimum of 57% and could not be overcome by increasing the doses of pentagastrin. The results suggest a mixture of competitive and noncompetitive interaction. The effect of cimetidine on pepsin secretion was less regular. Generally, pepsin output was less inhibited than acid output.

Plasma gastrin and gastric secretory response to duodenal perfusion with liver extract in healthy human subjects.

The stomachs of 8 healthy volunteers were intubated with a Levine tube under radiological control. In addition, a thin polyethylene tube was placed in the proximal duodenum. After a 1-hour period with no perfusion, the duodenum was perfused for two hours with 15% liver extract (LE) (pH 4.5--5.5; 1027 mosm/kg water) at a rate of 100 ml/hour either alone or in combination with intravenous infusion of different doses of exogenous pentagastrin. All subjects were also tested with the tubes in place for 3 hours, but with no perfusion or pentagastrin. Reflux to the stomach was monitored by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin were measured in 15-minute periods. During perfusion of the proximal duodenum, where reflux of the perfusates was less than 4%, only a slight and inconstant change in plasma gastrin was seen. Gastric acid and pepsin outputs were increased to approx. 18% and 25% of the maximal pentagastrin stimulation respectively. Whereas 15% LE was shown to release gastrin by antral perfusion however, such release was not found by duodenal perfusion, except where reflux to the antrum was seen. The results suggest that intestinal stimulation of gastric secretion exists, but has not been found to be gastrin dependent in the present investigation.

Emepronium bromide (Cetiprin) as a postoperative spasmolytic agent in transvesical prostatectomy.

To find out whether Cetiprin reduces the vesical spasms seen after cystotomias, a double-blind investigation including 22 men was carried out. Eleven of the men were given 25 mg Cetiprin i.m. twice a day for 2 days after transvesical prostatectomy, then 200 mg orally 3 times a day the following 12 days. The rest of the men, 11 patients, received placebo. In the Cetiprin group 9 patients had no vesical spasm postoperatively, whereas 1 had moderate and 1 had severe spasms. Only 4 patients were without spasms in the control group, whereas 5 had moderate and 2 severe spasms. The postoperative reduction of the bladder volume were counteracted by Cetiprin. No significant influence on liver- or kidney function was seen with the dosages mentioned.

The intestinal phase of gastric secretion. Response to liver extract infusion into the proximal jejunum of healthy human subjects.

A Levine tube was placed under radiological control in the stomach, and a thin polyethylene tube in the proximal jejunum of 6 healthy volunteers. The stomach and proximal part of jejunum were perfused for 2 hours with 1% acetylcholine, 20% meat extract (Bovril), and 15% liver extract (LE) alone and in combination with simultaneous infusion of different doses of exogenous pentagastrin intravenously. A significant increase in serum gastrin concentration was found with antral perfusion of LE only, whereas perfusion of the proximal jejunum did not change the basal level of the serum gastrin concentration. No change from control values was observed in gastric acid, and pepsin output on perfusing proximal jejunum with LE alone, or in combination with pentagastrin. Reflux to the stomach varied between 0-1.4%, as determined by addition of radioactive B12 to the perfusates. The experiments showed that gastrin was released from the antrum of the stomach by perfusion with 15 per cent LE, but not from the jejunum under the present experimental conditions. In the present experiments Bovril and acetylcholine perfusions did not cause significant responses from the antrum or from the proximal jejunum.

The effect of atropine and vagotomy on the secretion of gastric intrinsic factor (IF) in man.

The gastric secretion of IF, acid, and pepsin during basal conditions and stimulation by pentagastrin decreased significantly in 8 unoperated duodenal ulcer patients following administration of atropine. The basal concentrations of acid and pepsin decreased, whereas that of IF remained unchanged. An increase of plasma gastrin concentration from the basal value was observed after injection of atropine alone. The secretions of IF and acid decreased significantly from the pre-operative values after proximal gastric vagotomy in 7 duodenal ulcer patients. The basal IF output decreased by 19.8 per cent and the stimulated output by 41.4 per cent. The basal and stimulated secretions of acid decreased by 50.0 and 44.1 per cent, respectively. It is suggested that the smaller reduction of IF than of acid may be of importance for the vitamin B12 absorption after vagotomy. The decreased secretion of IF was secondary to the reduction of volume both after'medical' and surgical vagotomy.