Organic matter balance in ECF kraft mill fiberline.

Organic matter balances of an ECF kraft mill fiberline were studied in three different operational conditions of the oxygen delignification stage by implementing mill measurements, collecting routine mill data and combining them in a modified PROCELL steady state model. Dissolved volatile solids was the basic measurement for organic matter in liquid streams. Normal operation of the O2D0E(O)D1E(OP)D2 fiberline was described successfully. It was also possible to describe exceptional operating situations in the oxygen delignification stage and their effects on other parts of the production process reasonably well in order to focus studies on aspects requiring further attention. The existence of organic matter lost through complete degradation and volatile organic compounds in unit processes as well as its sensitivity to yield and operational situations is shown. The different perspectives of pulp production and wastewater treatment can be brought closer to each other using the approach in this study. The variation in the fractions discharged to wastewater treatment, although a relatively small share of the overall organic matter balance, will continue to become more important also for pulp production when effluent streams are increasingly turned back to the production line through further closure. Studies like the one presented here, can contribute to the evaluation of this development.

Degradation of EDTA and DTPA in chlorine dioxide bleaching conditions.

The decomposition of EDTA and DTPA was studied in simulated chlorine dioxide bleaching conditions. Under the investigated conditions EDTA and DTPA decomposed readily. Accordingly, feeding the chelating agents to the first chlorine dioxide stages (D0) should be reconsidered, when successful metal removal is desired. On the other hand, chlorine dioxide water may be utilized to degrade the chelating agents.

The role of organic matter lost in kraft pulping material balances .

Efficiency improvement in a pulp mill includes minimisation of environmental discharges simultaneously with the development of pulp quality and production economy. Material balances in production processes, including fate of sidestreams, are key in proceeding these matters. Different approaches of determining the material balances increase understanding of process behaviour. We have focused on measuring sidestream (carryovers, washing water, filtrate) dissolved organic matter (DOM) in fibreline unit process blocks of softwood ECF bleached kraft production. The DOM was analysed by traditional wastewater methods (volatile solids, organic carbon, chemical oxygen demand). The measured data was combined with primarily simulated water balances and routine operational mill data in a simulation model. From this balance, yield estimate included, lost organic matter through complete degradation (CD) and volatile organic compounds (VOC) can be calculated throughout the fibreline. The sensitivity of this considerable amount (23-35 kgDVS/adt in total) to various factors is discussed in this paper.

Insulin sensitivity in a long-term crossover trial with celiprolol and other antihypertensive agents.

The effects of a vasodilating beta-blocker, celiprolol, on insulin sensitivity and cardiovascular risk factors were compared with those of another beta1-selective adrenoceptor blocker, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors. A randomized 21-month crossover trial was carried out with 25 patients with dyslipidemia receiving antihypertensive monotherapy. The study consisted of a 3-month active run-in period and two treatment periods, during which the patients received celiprolol (200-400 mg daily) or the control drug for 12 and 6 months in a crossover manner. A hyperinsulinemic euglycemic clamp and an oral glucose tolerance test (OGTT) were performed every 6 months. According to the clamp tests, the insulin-sensitivity index increased on average by 32% (p < 0.0001) during celiprolol treatment compared with that with the other antihypertensive agents, including ACE inhibitors. In OGTT, area under the incremental glucose curve decreased by 36% (p = 0.002) during celiprolol treatment, whereas insulin secretion diminished on average by 26% (p = 0.006). The mean decrease in fasting serum triglycerides was 11% (NS), whereas the high-density lipoprotein to low-density lipoprotein (HDL/LDL) ratio increased by 15% (p = 0.012). The results suggest that celiprolol improves insulin sensitivity of hypertensive patients with dyslipidemia in long-term therapy.

Enterochromaffin cell density in the gastric mucosa of patients with chronic renal failure.

Thirty patients with chronic renal failure (CRF) and 30 age- and sex-matched controls were assessed for gastrointestinal diseases by gastroscopy, serum gastrin determination, and routine clinical and laboratory evaluation. Biopsy specimens from their gastric oxyntic mucosa were immunohistochemically stained with monoclonal antibodies against serotonin (5-hydroxytryptamine) and chromogranin A, the latter staining all gastric endocrine cells, the former disclosing serotonin-containing enterochromaffin (EC) cells only. The average EC cell density (cells/mm2) in the CRF patients was significantly lower than in the controls: 2.6 vs 12.9 (p = 0.0005). The EC cell counts also correlated negatively with serum gastrin values (p = 0.0031). The densities of the chromogranin-positive cells did not differ between CRF patients (74 cells/mm2) and controls (76 cells/mm2) (p = 0.7559). We conclude that, in addition to the previously known findings of hypoacidity, persistent hypergastrinaemia, and G and parietal cell hyperplasia, CRF also reduces the number of oxyntic EC cells. The negative correlation between EC cell density and serum gastrin levels reflects the complex interplay between different endocrinological activities in the gastrointestinal tract.

Antibody-secreting cells in acute urinary tract infection as indicators of local immune response.

Mucosal immune mechanisms are believed to be important in host defense against urinary tract infection. To study the human immune response in the urinary tract, peripheral blood antibody-secreting cells (ASC), believed to originate from the mucosal surfaces, were investigated with the enzyme-linked immunospot assay. Pathogen-specific ASC were found in 17 (89%) of 19 patients with pyelonephritis and in 12 (70%) of 17 with LUTI (lower urinary tract infection); for infections caused by Escherichia coli, the respective figures were 17 (100%) and 10 (71%). The responses in pyelonephritis were stronger (P < .001) and lasted longer than those in LUTI: 15 patients with pyelonephritis (74%) but only 1 with LUTI (6%) had > 100 ASC/10(6) cells. A similar difference was seen in the number of all immunoglobulin-secreting cells. The ASC assay offers a new means for assessing the human immune response in urinary tract infection and may be useful in localizing the infection. It might prove valuable in predicting harmful postinfection processes.

Gastric Helicobacter and upper gastrointestinal symptoms in chronic renal failure.

We studied histologically antral biopsies from 89 consecutive patients with chronic renal failure for Helicobacter pylori (previously Campylobacter pylori). A dose-response gastric secretion test was also performed. The frequency of Helicobacter-positive subjects was low (15/89, 17%), corresponding to figures reported in the literature for young symptomless volunteers. Helicobacter-positive patients had significantly more frequently upper gastrointestinal symptoms than Helicobacter-negative individuals (P less than 0.05). Antral gastritis was more common in the Helicobacter-positive than in the Helicobacter-negative renal patients (P less than 0.01), but the incidence of body gastritis did not differ between them. The Helicobacter-positive patients had lower serum urea levels (P less than 0.01) and higher acid outputs (P less than 0.001) than Helicobacter-negative subjects. All patients had raised fasting serum gastrin levels, which possibly obscured the difference between Helicobacter-positive (283 pg/ml) and -negative (331 pg/ml) patients. We conclude that in chronic renal failure gastric colonization of Helicobacter pylori is not more frequent than usual. It correlates positively with antral gastritis, gastric acid output and upper gastrointestinal symptoms, but negatively with serum urea levels.

Gastric parietal, chief, and G-cell densities in chronic renal failure.

We calculated morphometrically the amount of antral gastrin-producing (G) cells and body parietal and chief cells in gastric biopsy specimens from 30 undialysed patients with chronic renal failure (CRF) and from sex- and age-matched controls. The CRF patients had raised fasting serum gastrin levels, whereas these were normal in the controls (mean, 290 +/- 283 (+/- SD) ng/l (n = 27) versus 33 +/- 36 (n = 30)). Serum gastrin values of the patients and controls correlated positively with G-cell density (r = 0.501, n = 36, p = 0.002), as did the maximal acid output of the CRF patients with parietal cell density (r = 0.617, n = 14, p = 0.019). In CRF patients the densities of G, parietal, and chief cells were higher than those in the controls (G cells, 351 +/- 151 (+/- SD) cells/mm2, n = 21 versus 211 +/- 90, n = 16, p = 0.002; parietal cells, 299 +/- 94, n = 15 versus 224 +/- 72, n = 14, p = 0.025; chief cells, 886 +/- 346, n = 15 versus 743 +/- 182, n = 14, p = 0.181). The results agree with previous findings indicating that hyposecretion of gastric acid in CRF does not derive from decreased capacity for acid secretion but rather from the inhibition of acid output. Increased parietal cell density in CRF patients gives cause to suspect that the maximum acid output might even in raised, possibly depending on the permanent hypergastrinaemic state with its trophic influence on the gastric body mucosa.

Serum gastrin in chronic renal failure: its relation to acid secretion, G-cell density, and upper gastrointestinal findings.

The interrelations among fasting serum gastrin, serum creatinine, gastric acid secretion variables, and G-cell densities were analyzed in 47 patients with chronic renal failure (CRF). The patients also underwent gastroscopy and radiologic upper gastrointestinal barium examination. It is suggested that the hypergastrinemia seen in CRF is related to several factors: gastric acidity, grade of renal failure, G-cell density, and basal gastrin secretion rate. With regard to serum gastrin two different populations can be found, the cutting-off point being 300 ng/l. Although the group with high gastrin levels included significantly more patients with gastric body atrophy than the other group (4 of 11 versus of 1 of 36), most of them had no atrophy, which indicates that (an)other mechanism(s) is responsible for the hypergastrinemia. In the relation between serum gastrin and gastric acidity also, two differently behaving subgroups emerged. In the first, strong acidity change corresponded to minor gastrin change, whereas in the other, minor acidity change corresponded to marked gastrin change. The correlation coefficients between gastrin and acidity were high within both subgroups. During regular dialysis patients preserve the characteristics delineated from non-dialyzed values. Patients with signs of duodenal ulcer disease had high maximal acid output and low serum gastrin. Otherwise no associations were found between GI findings and the variables studied.

Reduced thickness of gastric mucosa and retarded progression of chronic gastritis in patients with renal failure.

Conflicting results are reported in the literature on the structure and function of gastric mucosa in patients with chronic renal failure (CRF). In the present endoscopic study of 68 CRF patients on conservative treatment (regular dialyses or transplantations had not yet been undertaken), we sought to clarify whether CRF leads to hypertrophic or hypotrophic phenomena in gastric mucosa, as interpreted by the presence and grade of gastritis and by the thickness of the gastric mucosa. We found that the mean progression of gastritis in both antrum and body was significantly slower than expected in CFR patients, and that the thickness of both antral and body mucosa was significantly lower in CFR patients than in non-CRF controls. Furthermore, although the thickness of the oxyntic body mucosa in CRF showed a positive correlation to serum gastrin (SeGa) levels and even though 12 of the patients showed high SeGa levels corresponding to those seen in the Zollinger-Ellison synbdrome (300-1500 ng/l), the thickness of the oxyntic body mucosa in CRF patients did not exceed that seen in control subjects with normal SeGa. We conclude that CRF exerts inhibitory effects on the gastric mucosa resulting in retardation in the progression of chronic gastritis and hypotrophy of the gastric mucous membrane.

Increased incidence of duodenitis in chronic renal failure.

Forty-six consecutive patients with chronic renal failure (CRF) were assessed radiographically, endoscopically and histologically for duodenal inflammation. Their gastric secretion was also examined. Thirty-eight patients with non-ulcer dyspepsia served as controls. Histologically established duodenitis was more common in CRF patients than in controls. Among the non-dialyzed patients its prevalence reached 28% (9/32), while in the controls it was 5% (2/38) (p less than 0.05). The CRF patients with duodenitis had upper GI symptoms, hypersecretion of acid (p less than 0.05) and duodenal ulcer disease (p less than 0.05) more frequently compared with the CRF subjects with normal duodenal mucosa. The correlation of radiographically and endoscopically detected duodenitis with that found microscopically was poor.

Gastric secretion kinetics in chronic renal failure.

A dose-response gastric secretion test was performed in 87 nondialyzed patients with chronic renal failure (CRF) and in 87 age- and sex-matched controls without renal disease. Twenty-six of the CRF patients were reexamined, 18 undergoing regular hemodialysis and 8 after successful transplantation. The gastric acidity, acid output, and volume output of the nondialyzed CRF subjects were decreased when compared with those of the controls or of patients in the posttransplant phase. This decrease was more marked with low than with high stimulant doses. The decrease in acid output was significantly greater than that in volume output. Moreover, when compared with the dialysis phase the nondialyzed patients had lowered gastric acidity and acid output, but no decrease in volume output was evident. The results indicate that there is an inhibition of gastric secretion in CRF. This inhibition is dependent on strength of stimulation and is abolished by active treatment of CRF, more clearly by transplantation than by maintenance dialysis. In addition, the inhibition is predominantly on the secretion of acid, the output of gastric juice being less affected.

Sensitivity of gastric acid secretion in patients with chronic renal failure.

By means of a dose-response secretion test the sensitivity of gastric acid secretion was investigated in 85 patients with chronic renal failure and in 85 age- and sex-matched controls. The renal patients were also gastroscoped, with biopsy specimens taken from the gastric body. The examinations were repeated on 18 patients undergoing regular dialysis and 8 patients after successful transplantation. The acid secretion sensitivity of the stomach among the non-dialyzed patients was decreased when compared with the controls (p less than 0.01) but tended to normalize during the intermittent dialysis treatment (p less than 0.05) and particularly after transplantation (p less than 0.01). The low secretion responses were independent of gastric body histology and were also seen in patients with normal body mucosa. The maximum theoretic acid output did not differ significantly from that of the controls. It is concluded that there is an inhibition of gastric acid secretion in chronic renal failure. This inhibition depends on the decreased sensitivity to stimulation and is diminished by treatment of renal failure by dialysis or transplantation.

Upper gastrointestinal findings in chronic renal failure.

Twenty-nine patients with chronic renal failure were examined both during the predialytic stage and after active treatment (dialysis, transplantation) for upper GI diseases. They underwent a gastric dose-response secretion test, gastroduodenoscopy, radiologic upper GI series, and fasting serum gastrin determination. Upper GI diseases increased in the active treatment stage. At the time of examination, patients with these diseases had a positive ulcer history, duodenitis, duodenogastric reflux, and blood group O more often in the predialytic stage. Their stimulation sensitivity to pentagastrin and their acid secretion capacity were greater, and they were less achlorhydric. Their fasting serum gastrin level was also lower. They had less endoscopically discovered gastritis, but microscopically, with regard to gastritis, they did not differ from those who did not develop upper GI complications. In conclusion, in chronic renal failure upper GI findings increase after the active treatment. Secretion tests and endoscopy performed before active treatment give an indication of those who will develop upper GI complications during active treatment.

The gastric secretion profile of patients with chronic renal failure.

The secretion of gastric juice, HCI, and sialic acid was investigated in 45 patients with chronic renal failure, 13 patients with gastric ulcers, 52 with duodenal ulcers, and 27 control patients during the dose-response pentagastrin test. The renal patients had low gastric juice and HCI secretion both in the basal condition and during pentagastrin stimulation. It was almost of the same magnitude as in patients with gastric ulcers. The basal sialic acid secretion in renal patients did not differ from that of the controls, but in patients with peptic ulcers it was significantly higher. During pentagastrin stimulation the differences decreased. Stimulated maximal HCI output values in relation to sialic acid output were also similar in the gastric ulcer and renal patients. Thus the gastric secretion profiles, excluding the basal sialic acid secretion, were quite alike in patients with chronic renal failure and those with gastric ulcers.

Sialic acid secretion of patients with gastric and duodenal ulcers in the dose-response pentastrin test.

The secretion of HCl and sialic acid into the gastric juice was investigated in 13 patients with gastric, 52 with duodenal ulcers and 27 control patients, during the dose-response pentagastrin test. The basal output of sialic acid was clearly highest in patients with gastric ulcers, and the differences between these and other groups of patients were significant. During pentagastrin stimulation a significant initial decrease was found in patients with gastric ulcers with small doses, and the minimum was reached with a dose of 0.1 micrograms/kg/h. After increasing the dose, an increase in sialic acid output occurred in all groups, reaching its maximum with a pentagastrin infusion rate of 1.0 micrograms/kg/h. The basal concentration of sialic acid was also highest in patients with gastric ulcers. In all groups the concentration decreased during the stimulation, which obviously depended on the sialic output not increasing in the same relationship as the volume of gastric secretion.

Effect of calcium p-chlorphenoxyisobutyrate and calcium carbonate on plasma lipids and lipoproteins of patients with hyperlipoproteinaemia.

Since dietary calcium had been reported to reduce plasma lipids, the effects of calcium carbonate (CaCO3, 2 g/day) and the calcium salt of p-chlorphenozyisobutyrate (Ca-CPIB, 2 g/day), both singly and in combination, were studied in outpatients with primary hyperlipidaemia. Three groups of five patients were followed in a double-blind cross-over study, in which placebo and the drugs were given alternately during four-week periods. The main results were: 1) CaCO3 alone did not produce any significant changes in plasma lipids. 2) Ca-CPIB reduced LDL-cholesterol in patients with type IIa and IIb by an average of 29 and 21%, respectively. It also lowered VLDL-triglyceride by 50% in type IIb and by 48% in four out of five patients with type IV. 3) The combination of CaCO3 and Ca-CPIB reduced LDL-cholesterol by 31 and 25% in types IIa and IIb, respectively. It also lowered VLDL-triglyceride by 48-52% in types IIa and by 46% in four out of five patients with type IIb. 4) Three out of five patients with type IV had a rise of LDL-cholesterol while on Ca-CPIB alone; two of the patients had the rise while on the combination. 5) After treatment with Ca-CPIB, either singly or in combination, there was a statistically significant lowering of ESR and of plasma inorganic phosphate and alkaline phosphatase. No clinical side effects were noted.