Search PubMed⌕ Search

Biomedical subjects

S Karlsson

Publications and source records attributed to S Karlsson.

At least 181 records · Page 10Linked to original sources
PubMed1992

Functional adaptation to full-arch fixed prosthesis supported by osseointegrated implants in the edentulous mandible.

The objective of the present study was to assess possible adaptive functional changes in the masticatory system after insertion of fixed prostheses supported by osseointegrated implants in the edentulous mandible. Registrations of mandibular movement characteristics and maximal biteforce were performed at insertion and after 1 week, 3 months and 1 year after connection. The duration of the opening and closing phase decreased and maximal biteforce increased significantly (p < or = 0.05-0.001) from connection of the prostheses to the annual check-up. However, the process of functional adaptation implied 2 identified stages. An immediate phase that occurred within the 1st week, probably due to altered impact from mechano-sensitive receptors and a later more time-dependent phase, based on learning and new cortical engrams. Accordingly, the process of adaptation will continue over a long period of time.

Adaptation, Physiological↗
PubMed1992

Influence of lower lip support on recording of vertical dimension in edentulous patients.

The purpose of this investigation was to assess the influence of differences in design of the occlusion rim on recorded vertical dimension in complete denture therapy. Edentulous patients were studied with an opto-electronic method when the vertical dimension of rest was established with and without labial support of the occlusion rim. As no significant differences were found, the results did not support the hypothesis that the contour of the lip support will influence the recorded physiological rest position. However, a significant difference between intra and extraoral placement of the point of measurement was found.

Aged↗
PubMed1992

Levodopa induced ON-OFF motor fluctuations in Parkinson's disease related to rhythmical masticatory jaw movements.

The motor disturbance in Parkinson's disease affects all voluntary movement, including innate rhythmical processes such as gait, breathing, and chewing. While there are good descriptions and pathophysiological hypotheses of the changes in gait less is known about the way masticatory movements are affected. By means of a three-dimensional optoelectronic recording technique the differences were investigated in mandibular movement displacement, velocity, and masticatory cycle duration during levodopa induced OFF and ON states. Recordings were made before ordinary morning medication and one hour after medication with 200 mg levodopa and a decarboxylase inhibitor (madopar). There were no differences before and after medication in the opening and closing duration of the masticatory cycle, but a significantly decreased occlusal level phase duration in the ON state was seen. Mandibular velocity and mandibular movement amplitude were significantly greater after medication. Thus the changes in dopamine transmission selectively influenced parts of the masticatory cycle but not the fundamental rhythmical pattern.

Administration, Oral↗
PubMed1992

Influence of Parkinson's disease on oral health.

Thirty patients with Parkinson's disease were investigated with regard to their oral health. They had significantly more teeth and less caries than a control group of corresponding age. However, the salivary secretion rate was significantly lower with advancing parkinsonian symptoms. It is concluded that not only motor impairment but also autonomic dysfunction, as an expression of a more advanced neuron degeneration, could be of importance when the possibility of maintaining a good oral health in parkinsonian patients is considered.

Activities of Daily Living↗
PubMed1992

A clinical evaluation of the Optec inlay system.

To evaluate the clinical quality of ceramic (Optec) inlays, the inlay production of 10 dentists, served by 3 dental laboratories, was examined independently by 2 calibrated examiners. A total of 57 patients with 205 inlays (mean age, 8.1 months) were examined 1 to 32 months after placement by means of using a slightly modified form of the California Dental Association criteria. Periodontal variables such as plaque index, gingival index, and margin index were also recorded. Eight patients reported postoperative but not persistent hypersensitivity in relation to the Optec therapy. No differences between Optec proximal surfaces and homologous control surfaces were seen with regard to plaque or bleeding on probing. The examination using the CDA criteria showed that 59% of the inlays had a slight color mismatch. Slightly roughened surfaces were most common (86%). As to anatomic form and margin integrity, 24% and 67%, respectively, of the inlays were rated excellent. A difference between the dentist with regard to the clinical quality of the inlay treatment procedure was seen. The present results cannot allow a definitive judgement with regard to the long-term clinical quality of the Optec inlay system but will serve as a base for further studies.

Adolescent↗
PubMed1992

Effects of tacrine on insulin secretion and 86Rb+ and 45Ca++ efflux from rat pancreatic islets.

Tacrine (1,2,3,4-tetrahydro-9-aminoacridine), a drug that has attained interest because of its ability to alleviate symptoms in Alzheimer's type of dementia, was found to stimulate insulin secretion from isolated rat pancreatic islets. The insulinotropic effect of the drug was observed at 8.3 mM but not at 3.3 mM glucose and was dependent on extracellular Ca++. From perifused 86Rb(+)-prelabeled islets, tacrine inhibited the fractional efflux of 86Rb+ at 3.3 mM glucose, but stimulated 86Rb+ efflux at 8.3 mM glucose. These effects persisted in the absence of extracellular Ca++. Tacrine also stimulated 45Ca++ efflux from perifused 45Ca(++)-prelabeled islets at 8.3 mM but had no effect on 45Ca++ efflux at 3.3 mM glucose or in the absence of extracellular Ca++. It is concluded that tacrine potentiates glucose-stimulated insulin secretion by a mechanism that is dependent on extracellular Ca++ and involves an increased Ca++ influx. The increased Ca++ influx is either secondary to a decreased K+ permeability induced by an inhibition of ATP-dependent K+ channels and/or due to a direct effect of tacrine on glucose-activated Ca++ channels.

Animals↗
PubMed1992

Changes in mandibular masticatory movements after insertion of nonworking-side interference.

To investigate the influence of nonworking-side interferences on mandibular masticatory movements and signs and symptoms of dysfunction of the masticatory system, an experimental balancing-side interference was introduced in 12 healthy subjects for 1 week. The individual response to the interference varied substantially. However, some of the movement variables were significantly changed immediately after insertion, but an adaptation of the neuromuscular system to the interference was evident at the end of the experimental period.

Adult↗
PubMed1991

CCKA receptor antagonism inhibits mechanisms underlying CCK-8-stimulated insulin release in isolated rat islets.

The influence of the cholecystokinin (CCK)A receptor antagonist, L-364,718, on beta-cell activation was examined in isolated perifused prelabelled rat islets. Insulin secretion and 3H efflux from myo-[2-3H]inositol-prelabelled islets (reflecting phosphoinositide hydrolysis) stimulated by CCK-8 (100 nM) were both inhibited by L-364,718, partially at 1 nM and totally at 10 nM. 45Ca2+ efflux from prelabelled islets was markedly stimulated by CCK-8. This stimulation was inhibited equally by 1 and 10 nM L-364,718. CCK-8 stimulated the 86Rb+ efflux (reflecting K+ movements) from prelabelled islets, which probably reflects an indirect effect of CCK-8 due to opening of Ca(2+)-activated K+ channels. This 86Rb+ efflux was inhibited by L-364,718 at 10 nM but not affected by L-364,718 at 1 nM. It is concluded that insulin secretion, phosphoinositide hydrolysis, Ca2+ and K+ movements stimulated by CCK-8 in isolated islets are all events mediated by CCKA receptors. The L-364,718-induced inhibition of phosphoinositide hydrolysis was most closely correlated to the inhibition of insulin secretion. This suggests that induction of cellular events activated through stimulation of phosphoinositide hydrolysis is a major mechanism underlying CCK-8-stimulated insulin secretion.

Animals↗
PubMed1991

Insulin and glucagon secretion in swimming mice: effects of adrenalectomy and chemical sympathectomy.

Swimming-stress is known to inhibit glucose-stimulated insulin secretion and stimulate glucagon secretion. In the present study, in mice, we investigated the relative contribution of sympathetic nerves and the adrenals to these effects. Mice were pretreated either with adrenalectomy or chemical sympathectomy induced by i.v. injection of 6-hydroxydopamine (6-OHDA), which destroys sympathetic nerve terminals. Two days later, the mice were injected i.v. with either glucose (5.6 mmol/kg) or saline, immediately before being subjected to 2 min swimming-stress or 2 min resting. Directly thereafter, blood was sampled. In normal controls, swimming inhibited glucose-stimulated insulin secretion and elevated plasma glucagon levels (P less than 0.01). Both these responses were absent both in adrenalectomized and in chemically sympathectomized mice. We also found that in resting animals, adrenalectomy reduced plasma levels of glucagon (P less than 0.05) and glucose (P less than 0.01), and that in adrenalectomized mice, swimming lowered basal plasma insulin levels (P less than 0.05). Furthermore, 6-OHDA-treatment elevated basal plasma glucagon levels (P less than 0.01). Thus, we show that, in the mouse, the inhibition of glucose-stimulated insulin secretion and the stimulation of glucagon secretion that occur during swimming-stress are both dependent on mechanisms requiring both the adrenals and intact sympathetic nerve terminals.

Adrenalectomy↗
PubMed1991

Diazepam binding inhibitor and the endocrine pancreas.

Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the endocrine pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or endocrine pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10(-8)-10(-7) M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused pancreas of the rat. Furthermore, secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro. Long-term exposure of cultured fetal rat islets to pDBI (10(-8) M) significantly decreased the synthesis of DNA in islet cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Pancreatic procolipase activation peptide-enterostatin-inhibits pancreatic enzyme secretion in the pig.

Pancreatic procolipase, a protein cofactor for lipase, is activated by trypsin, with a simultaneous formation of colipase and a pentapeptide with the sequence Val-Pro-Asp-Pro-Arg (VPDPR). This peptide was found to significantly inhibit pancreatic protein secretion after intraduodenal infusion in pigs (2 mg/kg/h). The inhibition, amounting to 60%, occurred under base-line conditions as well as after stimulation with cholecystokinin (CCK)/secretin (1 U of each peptide/h/kg body wt). In contrast, intravenous infusion of VPDPR (0.2 mg/h/kg) did not affect pancreatic secretion. There was no significant change in the plasma levels of pancreatic polypeptide, insulin, glucagon, or glucose following intraduodenal infusion of VPDPR. It is concluded that the procolipase activation peptide might have an inhibitory function in pancreatic enzyme secretion mediated indirectly through a gut action. Therefore, the lipolytic enzymes of pancreas may also take part in the feed-back regulation of the pancreatic function. We suggest the name enterostatin for this novel regulatory peptide.

Amino Acid Sequence↗
PubMed1991

Mandibular movement and velocity in relation to state of dentition and age.

Parameters of mastication, such as mandibular displacement, velocity and chewing cycle duration, were investigated in relation to age and rehabilitation with complete dentures. Two groups of elderly subjects (mean age 80 years), one with natural dentition and the other with complete dentures, and one group of young dentate adults (mean age 26 years) participated. Three-dimensional records of masticatory mandibular movements were obtained using the Selspot movement analysis system. There were no differences in the duration of the total or individual components of a chewing cycle, except for the closing phase, which was significantly longer in the complete denture group. Mandibular closing velocity was significantly lower in the two groups of elderly subjects than in the group of young adults. There was a high degree of inter-individual variation in mandibular displacement in all groups, but the mean vertical amplitude was smaller in the elderly groups compared to the group of young adults. For many of the parameters the variation was significantly greater in the groups of elderly subjects than in the younger group. Ageing thus appeared to have a more important effect than the state of the dentition on the parameters studied.

Adult↗
PubMed1991

Orofacial functions in patients with congenital and acquired maxillary defects: a fluoroscopic study.

By means of videofluoroscopic recordings, chewing, swallowing and speech were monitored in nine patients with congenital and acquired maxillary defects. All of them were rehabilitated with a maxillary obturator prosthesis. The defective region was seldom used for chewing. No leakage between the obturator and surrounding tissue was observed, either for solids or for liquids. All of the prosthetic reconstructions were surprisingly stable during function. In the phonetic analysis, speech production was judged to be restored almost to normal. Videofluoroscopy may be valuable as a complement to other functional diagnostic procedures, and for the evaluation and improvement of rehabilitation with an obturator prosthesis.

Adult↗
PubMed1991

Cholecystokinin-stimulated insulin secretion and protein kinase C in rat pancreatic islets.

In isolated rat pancreatic islets, the possible involvement of protein kinase C in cholecystokinin-8-stimulated insulin secretion was investigated. In islets exposed for 24 hours to the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (500 nmol l-1), a procedure known to down-regulate islet protein kinase C-activity, the insulinotropic effect of cholecystokinin-8 (10(-7) mol l-1) was partially reduced (by 34 +/- 8%, P less than 0.001). In contrast the insulinotropic response to acute exposure to 12-O-tetradecanoyl phorbol 13-acetate (10(-6) mol l-1) was totally abolished (P less than 0.001), whereas the insulin response to glucose (8.3 mmol l-1) was not affected. In normal islets, the protein kinase C-inhibitor, staurosporine, inhibited 12-O-tetradecanoyl phorbol 13-acetate- and glucose-stimulated insulin secretion (P less than 0.01), but was without effect on cholecystokinin-8-stimulated insulin release. Furthermore, in normal islets, cholecystokinin-8 had no effect on insulin release at a low glucose level (3.3 mmol l-1). However, at this low glucose level, cholecystokinin-8 clearly potentiated insulin release induced by acute exposure to 12-O-tetradecanoyl phorbol 13-acetate (10(-8) -10(-6) mol l-1, P less than 0.001). This potentiating effect was abolished by the removal of extracellular Ca2+. It is concluded that the insulinotropic effect of cholecystokinin-8 in rat islets is partially mediated by the protein kinase C pathway. Furthermore, the lack of effect of cholecystokinin-8 on insulin secretion at a low glucose level might be explained by an insufficient activation of protein kinase C under these conditions.

Alkaloids↗