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Biomedical subjects

S Karlsson

Publications and source records attributed to S Karlsson.

At least 19 recordsLinked to original sources
PubMed1992

High levels of human glucocerebrosidase activity in macrophages of long-term reconstituted mice after retroviral infection of hematopoietic stem cells.

Gaucher disease is a leading candidate for somatic gene therapy using bone marrow (BM) cells as target tissue. Towards this end, we have constructed a retroviral vector (LG) in which the human glucocerebrosidase (GC) cDNA is driven by the Moloney murine leukemia virus (MoMLV) long terminal repeat (LTR). Day 12 to 14 colony-forming unit-spleen progenitor cells were infected by the LG virus with a 100% efficiency, and GC messenger RNA (mRNA) and protein were detected in the progeny of these cells. Tissues from long-term reconstituted mice analyzed 8 months posttransplantation with LG-infected BM contained the intact provirus at greater than 1 copy per cell, indicating effective infection of hematopoietic stem cells. Human GC mRNA generated by the viral LTR was detected in macrophages as well as other hematopoietic cells. Enzyme activity was increased fivefold and twofold in macrophages from BM and spleen, respectively, and could be precipitated with an antibody specific for human GC. Immunohistochemical analysis detected the human GC protein in 81% of the macrophages from five recipient mice. These data indicate that, after transduction of hematopoietic stem cells, the LG vector is capable of directing expression of human GC in the majority of macrophages from long-term reconstituted mice and producing enzyme levels comparable with endogenous mouse activity, suggesting that this virus may be useful in the treatment of Gaucher disease.

3T3 Cells↗
PubMed1992

Neonatal capsaicin-treatment in mice: effects on pancreatic peptidergic nerves and 2-deoxy-D-glucose-induced insulin and glucagon secretion.

It is not known whether sensory nerves are involved in the insulin, glucagon or glucose responses to autonomic nerve activation induced by 2-deoxy-D-glucose (2-DG). We therefore treated mice neonatally with capsaicin which permanently destroys sensory afferent nerve fibers. Immunohistochemistry of the pancreas at 13-14 weeks of age revealed a substantial reduction of calcitonin gene-related peptide (CGRP)-immunoreactive nerves and a partial reduction of substance P-immunoreactive nerves. In contrast, no effect was observed on galanin-immunoreactive nerves. At age 10-12 weeks, the mice were injected intravenously with 2-DG (500 mg/kg). In controls, 2-DG stimulated insulin and glucagon secretion and induced hyperglycemia (P less than 0.01). Capsaicin treatment partially reduced the glucose and glucagon responses to 2-DG (P less than 0.01). In contrast, the insulin response to 2-DG was not affected by capsaicin. It is concluded that the mouse pancreas contains capsaicin-sensitive sensory CGRP- and substance P-immunoreactive nerve fibers, whereas the galanin-immunoreactive nerve fibers are not sensitive to capsaicin. Furthermore, capsaicin-sensitive sensory nerve fibers are partially involved in 2-DG-induced glucagon secretion and hyperglycemia, whereas sensory nerves are not involved in 2-DG-induced insulin secretion.

Animals↗
PubMed1992

Effects of CCK-8 on the cytoplasmic free calcium concentration in isolated rat islet cells.

The C-terminal octapeptide of cholecystokinin (CCK-8) is known to stimulate insulin secretion. We examined its effects on the cytoplasmic free calcium concentration ([Ca2+]IC) in isolated rat pancreatic islet cells. At 8.3 mM glucose and 1.28 mM Ca2+, CCK-8 (100 nM) rapidly increased [Ca2+]IC to a short-lived peak, whereafter the [Ca2+]IC, within 1.5 minutes, fell to values below baseline. CCK-8 also rapidly increased the [Ca2+]IC at 3.3 mM glucose and in a calcium deficient medium. However, either at low glucose or in the absence of extracellular Ca2+, the post-peak [Ca2+]IC did not fall below baseline levels. The CCKA receptor antagonist, L-364,718 (20 nM), inhibited the effects of CCK-8 on [Ca2+]IC. The results suggest that CCK-8 in islet cells liberates calcium from intracellular stores by activating CCKA receptors.

Animals↗
PubMed1992

CCK-8-stimulated insulin secretion in vivo is mediated by CCKA receptors.

The effects of the cholecystokinin A (CCKA) receptor antagonist, L-364,718, and the CCKB receptor antagonist, L-365,260, on CCK-8-stimulated insulin secretion were studied in vivo in the mouse. It was found that CCK-8-stimulated insulin secretion was suppressed by L-364,718 at a low dose level (0.078 mumol/kg). In contrast, L-365,260 caused a partial inhibition of CCK-8-stimulated insulin release only at the high dose level (24 mumol/kg). It is concluded that the CCK-8-stimulated insulin release in vivo is mediated by CCK receptors of the CCKA subtype.

Animals↗
PubMed1992

Effects of intense chewing on some parameters of masticatory function.

This study recorded the influence of 30 minutes of intense chewing on the masticatory function in 17 healthy subjects. Functional recordings of mandibular movements and velocity, measurements of masticatory efficiency, maximal occlusal force, and occlusal force endurance time were performed before and after functional stimulation and finally in a 2- to 5-day follow-up registration. After intense chewing, a substantially decreased masticatory cycle and occlusal level phase duration were recorded. No major mandibular displacements or changes in velocity were recorded. Masticatory efficiency and maximal occlusal force in the incisal region diminished after 30 minutes of intense chewing. Occlusal force endurance time was also lowered after intense chewing. The measurements were close to their original values at the follow-up. Intense chewing had various short-term effects on masticatory function, including a significant reduction of masticatory efficiency, maximal occlusal force, occlusal force endurance, and masticatory cycle duration.

Adult↗
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↗