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E Carlsson

Publications and source records attributed to E Carlsson.

At least 37 records · Page 2Linked to original sources
PubMed1997

Audiovestibular and neuropsychological outcome of adults who had recovered from childhood bacterial meningitis.

A sample of 22 subjects was studied from a population of adults who had suffered from bacterial meningitis in childhood. Audiovestibular, oculomotor and neuropsychological investigations were performed and quality of life was assessed. An age-matched control group of 20 subjects was recruited. In the meningitis group, nine subjects had abnormal pure tone audiograms. One was previously undiagnosed and a progression was found in four. There was an overrepresentation of subclinical vestibular pathology (6 out of 9 (67%)) in this group. Audiovestibular test results showed a peripheral pattern and oculomotor tests were normal. The quality of life scores of those with hearing loss were significantly higher than those in the control group. Neuropsychological tests of brain dysfunction were abnormal in six out of 22 (27%) who had recovered from meningitis. The prevalence of such dysfunctions was not related to audiovestibular disorder. The quality of life scores of those with brain dysfunctions were similar to those of the control group. The findings of reduced auditory memory and tone level perception in four out of 22 (18%), suggest that lesions of central auditory pathways may follow from bacterial meningitis. The results support the idea that inner ear damage is the major cause of hearing loss after bacterial meningitis. Despite the absence of brainstem involvement, central nervous system lesions with disturbed auditory processing and language functions can be of significance. The high frequency of discrete brain dysfunctions indicate that a thorough neuropsychological investigation is required after bacterial meningitis.

Adult↗
PubMed1995

Effects of hypochlorhydria and hypergastrinemia on structure and function of gastrointestinal cells. A review and analysis.

Since hypochlorhydria can induce hypergastrinemia, and gastrin has a trophic effect on some gastrointestinal cells, states that cause elevated plasma gastrin levels are of interest in terms of effects on cell growth and function. This article reviews the relationship between gastric mucosal cells during periods of acid stimulation and inhibition and analyses the effects of hypochlorhydria and hypergastrinemia on gastric and colonic cells and tumors. Hypochlorhydria releases the inhibitory effect of antral gastrin cells, inducing them to release gastrin in the presence of peptides or amino acids in the gastric lumen or in response to antral distension. Gastrin stimulates the oxyntic mucosa, which may lead to hyperplasia of enterochromaffin-like cells, resulting in enterochromaffin-like carcinoid tumors in aged rats and, rarely, in patients with chronic atrophic gastritis or gastrinomas. In addition to hypergastrinemia, other factors appear to be required for the progression of enterochromaffin-like hyperplasia to carcinoids; genetic factors may be involved. Gastrin elevations due to antisecretory drug therapy are indirectly proportional to the degree of acid inhibition and are reversible upon cessation of therapy. The gastrin levels during omeprazole therapy are similar to those caused by gastric vagotomy. Available evidence does not support a relationship between hypergastrinemia and the occurrence or growth of gastric carcinoma or colonic tumors.

Achlorhydria↗
PubMed1993

Calcitonin gene-related peptide expression at endplates of different fibre types in muscles in rat hind limbs.

Calcitonin gene-related peptide (CGRP) occurs only in some motoneurons. In this study, the presence of CGRP in motor endplates in relation to muscle fibre types was examined in slow (soleus muscle) and fast [tibialis anterior (TA) and extensor digitorum longus (EDL)] leg muscles of the rat. CGRP was detected by use of immunohistochemical methods, and staining for the mitochondrial-bound enzyme NADH-TR was used for demonstration of fibre types. The fibres showing low NADH-TR activity were interpreted as representing IIB fibres. All such fibres located in the superficial portion of TA were innervated by endplates displaying CGRP-like immunoreactivity (LI), whereas in the deep portion of TA some of these fibres lacked CGRP-LI at their endplates. Thirty per cent of the IIB fibres in EDL showed CGRP-LI at the endplates. All fibres in TA and EDL displaying high NADH-TR activity and interpreted as type-IIA fibres, lacked CGRP-LI in their motor innervation. One third of the fibres with intermediate NADH-TR activity in TA exhibited CGRP-LI at their endplates, whereas in EDL only few such fibres displayed CGRP-LI in the endplate formation. These fibres are likely to belong to type-IIX or type-I motor units. CGRP-LI was very rarely detected at the endplates in the soleus muscle. These observations show that distinct differences exist between the slow muscle, soleus, and the fast muscles, TA and EDL, but that there are also differences between the different types of fibres in TA and EDL with respect to presence of CGRP-LI at the endplates.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1993

Backscatter radiation at tissue-titanium interfaces. Biological effects from diagnostic 65 kVp x-rays.

The induced secondary electrons from a metal surface by diagnostic x-rays are thought to contribute to cell damage near the tissue-metal boundaries of metal implants. Titanium implants are becoming increasingly more popular for tissue reconstructions and it is rather often desirable to take radiographs of the operated area. In this study we compared the biological effects of radiation on cultured mammalian test cells grown on titanium plates with the radiation effects on cells that were grown on plastic control plates. In order to study the acute radiation effects on cell growth it was necessary to work with rather high radiation doses (0.7-5 Gy). Photon energies, suitable for diagnostic radiography in odontology, 65 kV, were applied. We found that the cells grown on titanium plates were, in terms of the applied dose in the surrounding culture medium, more sensitive to the irradiations than the cells growing on plastic plates. The survival curve for the cells on titanium had a steeper slope, showed no shoulder in the low-dose region and looked like curves normally obtained for high LET radiation. It was not possible to resolve to what degree the titanium-dependent changes were due to an increased dose near the titanium surface or to a change in the radiobiological effectiveness. Although there was a significant decrease in cellular survival near the metal, postoperative intraoral radiography after titanium implantations need not be excluded. The maximal doses given in odontological x-ray examinations are less than 1 mGy and, if the results in this study are applied, the biological effects near the titanium implant will correspond to biological effects in soft tissue of doses less than 20 mGy which is lower than the doses that give acute effects. The risk of acute healing disturbances are significant only at much higher radiation doses.

Animals↗
PubMed1992

Studies on the distribution of calcitonin gene-related peptide-like and substance P-like immunoreactivities in rat hind limb muscles.

The tibialis anterior, extensor digitorum longus and soleus muscles in the rat were examined with respect to the presence of calcitonin gene-related peptide-like as well as substance P-like immunoreactivity. In some of the motor endplates in these muscles, identified by staining for acetylcholinesterase activity, calcitonin gene-related peptide-like immunoreactivity was detected, but in others it was not. Calcitonin gene-related peptide-like immunoreactivity was found to coexist with substance-P-like immunoreactivity in nerve fibres located outside and inside the capsule of the muscle spindles, as well as in nerve fibres located in nerve fascicles. These fibres presumably represent sensory nerve fibres. Calcitonin gene-related peptide-like immunoreactivity, but not substance P-like immunoreactivity, was also detected in cap-like structures located on the surface of the intrafusal muscle fibres in the polar regions of the spindles, structures which are likely to correspond to motor plate endings. The observations suggest that calcitonin gene-related peptide is heterogeneously present in the endplates of rat hind limb muscles, and gives for the first time immunohistochemical evidence for the presence of calcitonin gene-related peptide and substance P in the innervation of muscle spindles.

Animals↗
PubMed1991

Partial gastric corpectomy results in hypergastrinemia and development of gastric enterochromaffinlike-cell carcinoids in the rat.

Studies in the rat have shown that partial gastric corpectomy, in which about 75% of the acid-producing oxyntic mucosa was removed, leads to markedly reduced acid secretion and a feedback increase in the plasma gastrin levels. Ten weeks after operation, the gastric enterochromaffin (ECL)-like cell density in the remaining part of the oxyntic mucosa had increased significantly. In the present study, the effects on the gastric ECL cells of lifelong persistent hypergastrinemia induced by partial (75%) corpectomy have been investigated. Seventy-five partially corpectomized rats and 40 control rats were investigated for plasma gastrin and oxyntic mucosal changes in a 124-week study. The partially corpectomized rats showed increased plasma gastrin levels after the operation; the mean increase compared with the controls was almost 10-fold during the entire study. The remaining oxyntic mucosa of the partially corpectomized rats differed from that of control rats in two respects, showing first general hypertrophy and second a marked hyperplasia of argyrophil ECL cells. The degree and incidence of these changes increased towards the end of the study, i.e., in the aging rats. An age-related increase in ECL-cell density occurred spontaneously also in the control rats but to a lesser extent than in the partially corpectomized group. ECL-cell carcinoids were found in the oxyntic mucosa of 26 of the 75 partially corpectomized rats. The first carcinoid was found 78 weeks after the beginning of the study. Six rats with carcinoids (23%) were found before week 104 (2 years) and the remainder, 20 (77%), were discovered later. No carcinoid tumor was found in the control rats. It is concluded that lifelong hypergastrinemia induced by partial corpectomy leads to the development of ECL-cell carcinoids in the oxyntic mucosa of some rats towards the end of their life span. This observation strongly supports the hypothesis that the gastric ECL-cell carcinoids found in rats treated with antisecretory drugs are caused by long-standing hypergastrinemia developing secondary to inhibition of gastric acid secretion.

Animals↗
PubMed1991

Backscatter radiation at tissue-titanium interfaces. Analyses of biological effects from 60Co and protons.

It has been claimed that implanted metals can cause backscatter radiation in radiation therapy with a dose enhancement at the bone-metal and tissue-metal interfaces on the beam entrance side. Theoretical calculations and experimental measurements with ionization chambers have indicated that such effects might be significant. Titanium implants are increasingly used in oral and maxillo-facial surgery for reconstruction purposes. A more detailed knowledge of backscatter-induced effects is therefore desired when head and neck cancers in patients with implants are treated with radiotherapy. We have made comparisons of cell survival after irradiation of two types of cultured cells grown directly on titanium metal and on plastic control supports. The cell cultures were irradiated with either 60Co photons or range modulated protons. No significant differences in the colony-forming capacity were found between the irradiated cells grown on titanium and those grown on plastic control supports. This was the case for both radiation types and the results were also observed to be dose-independent. The only observed phenomena were that the two cell-lines differed in radiosensitivity and that protons gave higher biological effects than gamma radiation. The results show that there were no significant changes in cell survival at the interface between the tissue equivalent medium and titanium support indicating that a dose increase induced by backscatter radiation, which possibly could demolish the osseointegration or induce osteoradionecrosis, are minimal when high energy photons or range modulated protons are applied.

Animals↗
PubMed1991

P450/losec.

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Acetaminophen↗
PubMed1990

Myofibrillar M-band proteins in rat skeletal muscles during development.

The distribution of three myofibrillar M-band proteins, myomesin, M-protein and the muscle isoform of creatine kinase, was investigated with immunocytochemical techniques in skeletal muscles of embryonic, fetal, newborn and four-week-old rats. Furthermore, muscles of newborn rats were denervated and examined at four weeks of age. In embryos, myomesin was present in all myotome muscle fibres of the somites, whereas M-protein was detected only in a small proportion of the myotome muscle fibres and muscle creatine kinase was not detected at all. In fetal and newborn muscles, all fibres contained all three M-band proteins. At four weeks of age, when fibre types (type 1 or slow twitch fibres and type 2 or fast twitch fibres) were clearly discernable, the pattern was changed. Myomesin and muscle creatine kinase were still observed in all fibres, whereas M-protein was present only in type 2 fibres. On the other hand, in muscle fibres denervated at birth all three M-band proteins were still detected. Our results suggest 1) that during the initial stages of myofibrillogenesis expression and incorporation of myomesin into the M-band precede that of M-protein and muscle creatine kinase; 2) that expression and incorporation of all three M-band proteins during fetal development is nerve independent and non coordinated to the expression of different forms of myosin heavy chains, and 3) that the suppression of M-protein synthesis during postnatal development is nerve dependent and reflects the maturation of slow twitch motor units.

Adenosine Triphosphatases↗
PubMed1990

Gastrin stimulates the self-replication rate of enterochromaffinlike cells in the rat stomach. Effects of omeprazole, ranitidine, and gastrin-17 in intact and antrectomized rats.

The enterochromaffinlike cells in the rat stomach are rich in histamine and are thought to be under the influence of gastrin. The effect of sustained endogenous and exogenous hypergastrinemia on the activity and proliferation rate of the enterochromaffinlike cells was studied by determining the histidine decarboxylase activity and histamine concentration and by combining histamine immunocytochemistry and autoradiography after in vivo labeling with [3H]thymidine. The proliferation rate of the stem cells in the oxyntic mucosal progenitor zone was also studied. Exogenous hypergastrinemia was induced by infusion of rat gastrin-17 (60 nmol.kg-1.day-1). Endogenous hypergastrinemia was induced by inhibition of gastric acid secretion with omeprazole (80 mumol.kg-1.day-1) or ranitidine (1200 mumol.kg-1.day-1). The effect of omeprazole was also studied in antrectomized rats. In intact rats, all treatments resulted in elevated plasma gastrin levels and were accompanied by an increase in the histidine decarboxylase activity and the histamine content of the oxyntic mucosa. This resulted in an increase in the enterochromaffinlike cell proliferation rate, leading to enterochromaffinlike cell hyperplasia. The number of labeled stem cells was increased, but this effect was not as pronounced as in the enterochromaffinlike cells. In antrectomized rats, the inhibition of acid secretion by omeprazole did not result in elevated plasma gastrin or in an increase in the activity or number of enterochromaffinlike cells, indicating that omeprazole per se had no effect on these cells. These data support the view that gastrin stimulates the proliferation rate of both enterochromaffinlike cells and stem cells. Gastrin also stimulates the activity of the enterochromaffinlike cells.

Animals↗
PubMed1990

Effects of partial resection of acid-secreting mucosa on plasma gastrin and enterochromaffin-like cells in the rat stomach.

Female rats were subjected to various degrees (50, 75, 90 and 100%) of fundectomy, i.e. resection of the acid-producing part of the stomach, to compare the effects of different degrees of reduction of the amount of acid reaching the antrum. Plasma gastrin was monitored for 10 weeks after the operation. Histidine decarboxylase (HDC) activity, histamine concentration and density of enterochromaffin-like (ECL) cells in the remaining oxyntic mucosa were determined in the rats subjected to 50 or 75% fundectomy. There was a close correlation between the amount of acid-producing mucosa removed and the plasma gastrin levels, the highest gastrin level being observed in the rats subjected to 100% fundectomy. HDC activity, histamine concentration and ECL cell density seemed to reflect plasma gastrin concentration. These findings indicate that hypergastrinemia induced by surgical removal of acid-producing mucosa in the rat has the same effects on oxyntical mucosal HDC activity, histamine concentration and ECL cell density as hypergastrinemia induced by continuous gastrin infusion or by long-term treatment with effective antisecretagogues.

Animals↗
PubMed1990

Effect of 20 weeks' ranitidine treatment on plasma gastrin levels and gastric enterochromaffin-like cell density in the rat.

In this study, the effect of ranitidine treatment on the activation and proliferation of rat gastric enterochromaffin-like (ECL) cells was investigated. The drug was given in a high dose in the food (1.7-1.8 g/kg/day) for 20 weeks. This dose corresponds to the high dose given in the ranitidine oncogenicity study performed by Glaxo. With this dose regimen ranitidine induced hypergastrinaemia for 10 h of the day. The duration and the extent of the hypergastrinaemia closely followed the occurrence of ranitidine in plasma, strongly suggesting that the hypergastrinaemia was secondary to inhibition of acid secretion. Following 20 weeks treatment with ranitidine, both the relative weight of the stomach and that of the oxyntic mucosa were increased. The oxyntic histamine concentration and ECL-cell density were also increased significantly. These results show that when ranitidine is given in the diet the resulting hypergastrinaemia, which had a duration of 10 h each day, leads to a general increase in the oxyntic mucosal weight and a proliferation and activation of the ECL cells, indicating that sustained hypergastrinaemia is not a necessary requirement for development of ECL-cell hyperplasia.

Animals↗
PubMed1990

Enterochromaffin-like cell carcinoids in the rat gastric mucosa following long-term administration of ranitidine.

Long-term administration of some long-acting inhibitors of gastric acid secretion has been associated with the development of gastric enterochromaffin-like (ECL)-cell carcinoids in the rat. It has been argued that short-acting, surmountable histamine H2-receptor blockers such as ranitidine do not cause carcinoids. In this study, female rats (n = 100) were treated for 2 years with the histamine H2-receptor blocker ranitidine, 2 g/kg/day in the diet. Specimens from the stomachs of all rats, including 50 controls, were stained for argyrophil cells. Plasma gastrin and ranitidine levels were measured in separate groups of rats at different times during the study. The mean plasma level of ranitidine was 37.5 mumol/l, measured at midnight when the maximal level after food intake was expected. The resulting acid inhibition was associated with an approximately 3-fold increase in plasma gastrin which persisted throughout the whole period of the study. The ranitidine treatment resulted in a pronounced hyperplasia of gastric ECL cells. In 19 rats carcinoids were found, 4 of which were micro-invasive. No carcinoids were found in the control animals. The results provide further support for the gastrin mechanism, i.e. that the development of ECL-cell carcinoids in the rat gastric mucosa is a consequence of prolonged hypergastrinaemia and is not a unique effect of any individual acid-inhibiting drug.

Animals↗
PubMed1990

Gastrin and gastric enterochromaffin-like cell carcinoids in the rat.

Life-long administration (greater than or equal to 2 years) of a number of long-acting gastric acid inhibitors (including H2-receptor antagonists, omeprazole and ciprofibrate) has been associated with the development of gastric enterochromaffin-like cell (ECL cell) carcinoids in rats. It has been postulated that they are a consequence of some unique property of the longer-acting acid inhibitors. There is, however, a great deal of evidence to support the hypothesis that these gastric ECL cell carcinoids develop as a result of life-long hypergastrinaemia in rats. Several lines of investigation reported here show that gastric ECL cell hyperplasia occurs when gastrin levels are increased without the use of acid-inhibiting drugs. In rats, hypergastrinaemia developed after 4 weeks' administration of exogenous gastrin (4 micrograms/kg/h). The number of gastric ECL cells per visual field had increased to 250 compared with 180 in the controls. Long-term hypergastrinaemia, induced by partial gastric corpectomy, increased plasma gastrin levels from 200 to 800 pg/ml and the density of gastric ECL cells increased from 190 to 310 cells/visual field 10 weeks after the operation. Importantly, gastric ECL cell hyperplasia, which was produced in rats by administration of omeprazole, 14 mg/kg/day for 1 year, was fully reversible following normalization of gastrin levels. Until now, gastric ECL cell carcinoids have not been reported in studies of shorter-acting, reversible H2-receptor antagonists such as ranitidine, perhaps because the correct staining techniques (i.e. Grimelius and Sevier-Munger silver stains) have not been used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Omeprazole and ranitidine, antisecretagogues with different modes of action, are equally effective in causing hyperplasia of enterochromaffin-like cells in rat stomach.

Female rats were treated for 28 days with high doses of the gastric acid secretion inhibitors omeprazole and ranitidine. Omeprazole, which is long-acting, was given orally once daily. Ranitidine, which is short-acting, was given by continuous infusion (via osmotic minipumps, implanted subcutaneously). The aim was to produce a similar degree of acid inhibition with the two drugs. The inhibition of acid secretion over the day and night was more pronounced in the omeprazole-treated rats (maximal inhibition 100%, minimum 85%) than in those receiving ranitidine (mean 70%). In both groups, there was a great increase in plasma gastrin, somewhat greater after omeprazole than after ranitidine. The gastrin concentration in the antrum was almost doubled by both treatments and there was a moderate increase in the number of antral gastrin cells in the omeprazole-treated rats. The number of enterochromaffin-like (ECL) cells (per visual field) increased in the oxyntic mucosa to the same extent (greater than 100%) in the ranitidine- and omeprazole-treated rats. Apart from the gastrin cells in the antrum and the ECL cells in the corpus no other gastric endocrine cell type seemed to respond to treatments with antisecretagogues. We conclude that, regardless of the type of antisecretagogue used, effective and long-term suppression of gastric acid secretion results in sustained hypergastrinemia and increased number of ECL cells. Conceivably therefore, the ECL cell hyperplasia reflects the trophic effect of gastrin.

Animals↗
PubMed1989

Omeprazole and cimetidine versus pentagastrin in canine ex vivo gastric chamber.

The effects of acid inhibitory doses of omeprazole were compared with equieffective doses of cimetidine in the canine ex vivo stomach model (n = 30). Systemic blood pressure, temperature, stomach fluid and ion fluxes, potential difference, blood flow rates, and arterial and venous blood gases were monitored during each of nine 30-min periods. Two resting periods preceded seven periods of pentagastrin stimulation. During the last four of these, the drug effect was recorded (cimetidine 1.2 or 4.8 mumol.kg-1.h-1; omeprazole 0.3, 0.6, or 1.2 mumol/kg). Omeprazole (1.2 mumol/kg) produced 100% inhibition of stimulated acid efflux, no significant decrease in total gastric blood flow (venous outflow), 90% return of potential difference (PD) toward resting values, and a 55% reduction in stimulated oxygen consumption. Omeprazole also showed a dose-dependent K+ efflux at the two lower doses. Cimetidine (4.8 mumol.kg-1.h-1) given during pentagastrin stimulation showed a 70% decrease in total gastric blood flow, a 40% return of PD toward resting, and a 77% reduction in stimulated oxygen consumption. Neither drug showed significant changes in mucosal blood flow from resting values, thus supporting the principle that changes in gastric acid secretion and changes in blood flow are not necessarily correlated.

Animals↗