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Biomedical subjects

S Karlsson

Publications and source records attributed to S Karlsson.

At least 145 records · Page 8Linked to original sources
PubMed1995

Knee extensor performance of dominant and non-dominant limb throughout repeated isokinetic contractions, with special reference to peak torque and mean frequency of the EMG.

The aim of this study was to investigate whether significant differences in peak torque (PT), mean power frequency of EMG (fmean) and perceived fatigue exist between the dominant and non-dominant knee extensors throughout repeated contractions. The present study forms part of a research project aimed at developing tests for the determination of the degree of motor control in patients with sequelae after CNS injury. A total of 22 clinically healthy subjects (14 males and eight females) took part in the investigation. The subjects performed endurance tests of the lower limbs, consisting of 100 repeated knee extensions using a Cybex dynamometer at 1.57 rad s-1. The patterns of PT, fmean and perception of fatigue throughout the endurance test were investigated. The endurance curves of PT and fmean showed, in common with other studies, an initial steep decrease followed by a stable phase. No significant differences existed between dominant and non-dominant knee extensors with regard to PT, fmean or perception of fatigue. The results indicate that it may be possible to use the contralateral knee extensors as an indicator of motor recovery in hemiplegia in patients with a high degree of recovery.

Adult↗
PubMed1995

Effect of masticatory muscle fatigue on cranio-vertical head posture and rest position of the mandible.

The aim of this study was to investigate whether induced fatigue of the masticatory muscles had any influence on the head posture, and whether this influence is related to the rest position and the movement characteristics of the mandible. The sample consisted of 13 female individuals, aged 23-34 yr. For the evaluation of possible changes in the natural cranio-vertical head posture, standardized facial profile photographs were used. Photographs were also used for the study of the facial characteristics. The freeway space and the opening and closing velocity of the mandibular displacement, as well as the duration of the masticatory cycles, were monitored with an optoelectronic method. A controlled dynamic fatigue was induced by a specially constructed spring-loaded device placed in the premolar region. No significant changes in the mean cranio-vertical postural position of the head were found during the various recording stages, while the freeway space was found to increase significantly after the fatigue test. No significant differences were observed concerning the average values of the mandibular movement characteristics. The analysis of the association between the individual changes showed an increase in the freeway space after the fatigue test in the subjects which exhibited an increase in the duration of the masticatory cycle in that period. No significant associations could be found between the changes in the head posture and the mandibular movement characteristics. Also, no significant correlation could be found between the facial type of the subjects and the variables studied.

Adult↗
PubMed1995

Defective haematopoiesis and vasculogenesis in transforming growth factor-beta 1 knock out mice.

Transforming growth factor beta 1 (TGF beta 1) is shown here to be required for yolk sac haematopoiesis and endothelial differentiation. Mice with a targeted mutation in the TGF beta 1 gene were examined to determine the cause of prenatal lethality, which occurs in 50% of homozygous TGF beta 1 null (TGF beta 1-/-) conceptions. 50% of TGF beta 1-/- and 25% of TGF beta 1-+-) conceptions. 50% of TGF beta 1-/- and 25% of TGF beta 1+/- conceptuses were found to die at around 10.5 dpc. The primary defects were restricted to extraembryonic tissues, namely the yolk sac vasculature and haematopoietic system. The embryos per se showed developmental retardation, oedema and necrosis, which were probably secondary to the extraembryonic lesions. The defect in vasculogenesis appeared to affect endothelial differentiation, rather than the initial appearance and outgrowth of endothelial cells. Initial differentiation of yolk sac mesoderm to endothelial cells occurred, but defective differentiation resulted in inadequate capillary tube formation, and weak vessels with reduced cellular adhesiveness. Defective haematopoiesis resulted in a reduced erythroid cell number within the yolk sac. Defective yolk sac vasculogenesis and haematopoiesis were present either together, or in isolation of each other. The phenotypes are consistent with the observation of abundant TGF beta 1 gene expression in both endothelial and haematopoietic precursors. The data indicate that the primary effect of loss of TGF beta 1 function in vivo is not increased haematopoietic or endothelial cell proliferation, which might have been expected by deletion of a negative growth regulator, but defective haematopoiesis and endothelial differentiation.

Animals↗
PubMed1995

An electropalatographic and optoelectronic analysis of Swedish [s] production.

The objective of this study was to evaluate the usefulness of electropalatography (EPG) as a method for diagnostic analysis of the [s] sound and also to make a multiple analysis of the production of the normal Swedish [s] sound in various contexts. Eleven dental students participated. EPG registration, optoelectronic recording of jaw movements, and acoustic registration of a test phrase were made simultaneously. A speech perceptual test was also made. There were four separate recording sessions. Except for at session I, subjects wore an EPG palate. At session II they were not adapted to it, in contrast to the later occasions. The EPG appeared to be a valid method for investigating the [s] sound. In general, EPG and mandibular movement patterns were similar between sessions, and the sound quality normal throughout. At session II, however, the tongue groove was wider, the mandibular movements smaller, and the [s] quality somewhat deteriorated. [s] in various contexts had different tongue groove widths but similar high average mandibular position. To prevent speech and especially [s] sound problems when constructing prosthetic devices, it is important to advance our knowledge of [s] sound production.

Adult↗
PubMed1995

Characteristics of masticatory movements and velocity in children with juvenile chronic arthritis.

Oral motor function (mandibular displacement and velocity) in individuals with juvenile chronic arthritis was studied by using an optoelectronic method. The children were compared with two asymptomatic groups: one group with Class I occlusion and the other with Class II malocclusion. The results showed that children with juvenile chronic arthritis and condylar lesions had reduced lateral mandibular masticatory movements. In children with Class II malocclusion, a longer three-dimensional closing distance and a slower closing velocity were found. In children with both juvenile chronic arthritis and Class II malocclusion, an interaction between juvenile chronic arthritis and malocclusion resulted in a longer occlusal time, a shorter amplitude, and a slower velocity. It can be concluded that juvenile chronic arthritis and Class II malocclusion, per se, might have minor influences on the chewing characteristics, but the two factors seem to interact, resulting in an altered masticatory pattern. A possible explanation is that children with juvenile chronic arthritis have an increased risk of developing a Class II malocclusion because of the growth disturbances sequelae of condylar lesions. The alteration in occlusion, together with restricted movements in the arthritic condyle, may be the underlying reasons for the findings.

Adolescent↗
PubMed1995

Transforming growth factor-beta 1 null mice. An animal model for inflammatory disorders.

Approximately 40% of transforming growth factor-beta 1 null (knockout) mice generated in our laboratory develop normally to term, but 60% die in utero. The animals appear normal during the first 2 weeks of life but develop a rapid wasting syndrome and die by 3 to 4 weeks of age. All of the knockout mice have a multifocal inflammatory disease in many tissues. The heart and lungs are most severely affected. Increased adhesion of leukocytes to the endothelium of pulmonary veins is the initial lesion seen at day 8 postnatally and is soon followed by perivascular cuffing as well as inflammatory infiltrates in lung parenchyma. The lesions in the heart begin as endocarditis and then progress to myocarditis and pericarditis. Within the lung, chronic inflammatory infiltrates consist of T and B lymphocytes, including plasma cells, whereas macrophages are the primary inflammatory cell type in the heart. Increased expression of major histocompatibility complex class I and II proteins is seen in pulmonary vascular endothelium as early as day 8. An immunoblastic response in mediastinal and mandibular lymph nodes and spleen is also seen. In the absence of any pathogens, this massive inflammatory disease, together with overexpression of major histocompatibility complex class I and II proteins and overproduction of immunoglobulins by lymphocytes, offers circumstantial evidence for an autoimmune etiology.

Animals↗
PubMed1994

Targeted deletion of the TGF-beta 1 gene causes rapid progression to squamous cell carcinoma.

To study the contribution of autocrine and paracrine TGF-beta 1 to tumor progression in a well-defined system of multistage carcinogenesis, keratinocytes with a targeted deletion of the TGF-beta 1 gene were initiated in vitro with the v-rasHa oncogene and their in vivo tumorigenic properties were determined by skin grafting initiated cells onto athymic mice in combination with either wild-type or null dermal fibroblasts. Grafts of v-rasHa-initiated null keratinocytes progressed rapidly to multifocal squamous cell carcinomas within dysplastic papillomas irrespective of the fibroblast genotype, whereas the initiated control genotypes formed well-differentiated papillomas. Malignant progression was not associated with mutations in the c-rasHa gene, alterations in p53 protein, or loss of responsiveness to TGF-beta 1. The tumor cell labeling index was elevated in grafts of initiated null keratinocytes with wild-type fibroblasts compared to tumors of other genotypes. However, labeling index in all tumors was reduced when TGF-beta 1 null fibroblasts formed the stroma. The null tumor cells could not accumulate TGF-beta 1 from the host, but grafts of uninitiated null keratinocytes, which formed a normal epidermis, became TGF-beta 1 positive even though they did not express TGF-beta 1 mRNA. These results demonstrate that autocrine TGF-beta 1 suppresses the frequency and rate of malignant progression, and that autocrine and paracrine TGF-beta 1 can have opposing effects on tumor cell proliferation. The lack of paracrine inhibition of tumor cell progression appears to result from the inability of tumor cells to localize host-derived TGF-beta 1 by a mechanism that operates in normal cells.

Animals↗
PubMed1994

Retroviral vector design for long-term expression in murine hematopoietic cells in vivo.

A series of retroviral vectors containing the human glucocerebrosidase (GC) cDNA driven by various promoters have been constructed in an attempt to discover which vector design can most efficiently transduce murine hematopoietic stem cells (HSCs) and drive expression of the transferred gene in hematopoietic cells of mice reconstituted with the transduced stem cells. The simplest vector, LG, in which the GC gene is driven by the viral LTR, was the most efficient vector at infecting HSCs, with an average viral copy number in hematopoietic tissues of 3 copies/cell in recipient mice. In general, the viral vectors that contained any additional promoters or enhancers to drive expression of either the GC gene or a selectable marker gene (Neo) had lower titers and/or transduced HSCs at a lower efficiency. This was seen most markedly when the human phosphoglycerate (PGK) promoter was used to drive the human GC cDNA. Despite repeated attempts to obtain a high titer producer clone, this virus consistently produced low titers and subsequently resulted in the lowest proviral copy numbers in long-term reconstituted mice. Only the viral LTR and PGK promoter were capable of driving significant levels of human GC RNA in hematopoietic cells of long-term reconstituted mice, with a much lower level of RNA generated by an internal herpes TK or SV40 immediate early promoter. Insertion of the internal transcription unit in the opposite orientation relative to the viral LTRs had a detrimental effect on gene expression. The levels of RNA generated by a hybrid LTR containing the myeloproliferative sarcoma virus enhancer were higher in bone marrow-derived macrophages than in nonadherent cells of the bone marrow when compared with the LG vector. The presence of an internal promoter to drive expression of the human GC cDNA did not seem to have a detrimental effect on expression levels from the viral LTR. In fact, in the presence of an internal TK or PGK promoter expression from the LTR was increased despite the presence of lower proviral copy numbers. Insertion of a second gene (Neo) into the vector had a negative impact on long-term expression in hematopoietic cells in vivo; however, this seems to be due solely to the lower transduction efficiency of this vector. Overall, the highest levels of GC activity in macrophages of long-term reconstituted mice were generated by the LG vector; however, these levels were variable.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Immune dysregulation in TGF-beta 1-deficient mice.

Approximately 2 wk after birth, mice having a TGF-beta 1 null mutation (TGF-beta 1(-/-)) exhibit a progressive wasting syndrome and death. Associated with this phenotype is a multifocal infiltration of lymphocytes and macrophages into target organs, especially the heart, lungs, and salivary glands. To explore the consequences of TGF-beta 1 deficiency on the immune system, lymphocyte phenotype and function were analyzed. Initially, lymphoid organ architecture seemed to be normal and, as symptoms developed, the thymus decreased in size, whereas lymph nodes were enlarged. Phenotypically, the TGF-beta 1(-/-) lymphoid cells seemed to be more differentiated in the thymus and activated in the lymph nodes, but remarkably unaffected in the spleen. Moreover, TGF-beta 1(-/-) spleen and lymph nodes displayed enhanced numbers of proliferating cells, as measured by proliferating cell nuclear Ag and/or cyclin-dependent kinase levels. Consistent with this hyperproliferative response, constitutive levels of IL-2 mRNA were elevated in the thymus and both IL-2 and IL-2R mRNA were increased in the lymph nodes. In contrast with the activation profile of TGF-beta 1(-/-) lymphoid cells in vivo, mitogen challenge of these cells in vitro revealed suppressed proliferation that was associated with a defect in inducible IL-2 mRNA expression and IL-2 secretion. Moreover, the addition of rIL-2 restored the deficient mitogen-induced proliferation. The mechanism leading to T cell anergy remains unclear; however, these data confirm the essential role for TGF-beta 1 in maintaining normal immune function.

Animals↗
PubMed1994

Synthetic fibronectin peptides interrupt inflammatory cell infiltration in transforming growth factor beta 1 knockout mice.

Pronounced mononuclear leukocyte (MNL) infiltration occurs in multiple organs of mice homozygous for a transforming growth factor beta 1 (TGF-beta 1) loss-of-function gene mutation [TGF-beta 1 (-/-)], followed by cachexia and eventually death. Consistent with the increased leukocyte adhesion and tissue infiltration, MNLs isolated from spleen, thymus, and peripheral blood of symptomatic TGF-beta 1 (-/-) mice, as compared to littermate controls, exhibited increased adhesion to extracellular matrix proteins and to endothelial cells in vitro. Incubation of TGF-beta 1 (-/-) MNLs with selected synthetic peptides corresponding to cell- and heparin-binding sequences of fibronectin (FN) significantly attenuated adhesion of these cells not only to FN but also to endothelial cells in vitro. Based on these observations, mice were treated with the FN peptides in an attempt to rescue them from tissue inflammation and cardiopulmonary failure. Daily injections of a combination of four synthetic FN peptides that interact with beta 1-integrins and/or cell surface proteoglycans blocked the massive infiltration of MNLs into the heart and lungs of TGF-beta 1 (-/-) mice. Peptide treatment initiated on day 8, coincident with the first evidence of increased leukocyte-endothelial cell interactions, not only blocked tissue infiltration but also moderated the lethal wasting syndrome.

Amino Acid Sequence↗
PubMed1994

Mechanisms underlying the insulinostatic effect of peptide YY in mouse pancreatic islets.

Peptide YY is an insulinostatic peptide which is released into the circulation from the intestinal mucosa upon food intake. Peptide YY is also co-stored with glucagon in the secretory granules of the pancreatic alpha cells. We examined the mechanisms underlying the insulinostatic effect of peptide YY in isolated mouse pancreatic islets. We found that peptide YY (0.1 nmol/l-1 mumol/l) inhibited glucose (11.1 mmol/l)-stimulated insulin secretion from incubated isolated islets, with a maximal inhibition of approximately 70% observed at a dose of 1 nmol/l (p < 0.001). Also in perifused islets the peptide (1 nmol/l) inhibited insulin secretion in response to 11.1 mmol/l glucose (p < 0.001). Furthermore, peptide YY inhibited glucose-stimulated cyclic AMP formation (by 67%, p < 0.05), and insulin secretion stimulated by dibutyryl cyclic AMP (p < 0.01). In contrast, the peptide was without effect both on the cytoplasmic Ca2+ concentration in dispersed mouse islet-cell suspensions as measured by the FURA 2-AM technique, and on insulin release in isolated islets, when stimulated by the protein kinase C-activator 12-O-tetradecanoyl phorbol 13-acetate. Finally, in pre-labelled perifused islets, peptide YY caused a small and transient increase in the 86Rb+ efflux (p < 0.001), but only in the absence of extracellular Ca2+. We conclude that peptide YY inhibits glucose-stimulated insulin secretion from isolated mouse islets by inhibiting two different steps in the cyclic AMP cascade, that is, both the accumulation and the action of the cyclic nucleotide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The mean frequency of the EMG of the knee extensors is torque dependent both in the unfatigued and the fatigued states.

The present study aimed to investigate the shift in the mean frequency (fmean) of the power density spectrum of the electromyogram (EMG) during endurance tests of the knee extensors at three different torque levels (70% MVC, 25% MVC and 10% MVC). Fourteen clinically healthy men performed the three endurance tests until exhaustion. Surface EMG(s) were obtained from the vastus medialis, the vastus lateralis and the rectus femoris muscles and fmean and signal amplitude (RMS) were computed. The subjects rated the perception of fatigue in the knee extensor muscles throughout the three tests using a 10-point graded scale. The endurance time increased with decreasing torque level. A significantly higher perception of fatigue was found at the low torque level (10% MVC) at the end of the endurance time. Individual time series analysis (using linear regression) was performed. It was found that linear models described well the behaviour of fmean throughout the endurance time at the three torque levels. When the endurance times were normalized significant differences in the rate of decrease in fmean were found for vastus lateralis and rectus femoris; the rate decreased with decreasing torque level. For these two muscles significant differences were also found in fmean in the unfatigued state; at 10% MVC significantly lower fmean was found. The present study demonstrated both that the unfatigued fmean and the rate of decrease in fmean (with normalized endurance time) were torque dependent. The latter finding, combined with our result that the subjective fatigue was highest at the lowest torque level, calls into question the use of fmean as a valid indicator of peripheral fatigue.

Adult↗
PubMed1994

Poor transduction efficiency of human hematopoietic progenitor cells by a high-titer amphotropic retrovirus producer cell clone.

The transduction efficiency of human bone marrow CD34+ cells with supernatants from the retrovirus producer cell clone PA317/LGSN 16 was only one-fifth of that with supernatants from GP+ envAm12/LGSN 15, even though both producers had similar infection titers on 3T3 cells. PA317/LGSN 16-conditioned medium inhibited the proliferation of the bone marrow CD34+ cells, and this inhibitory effect was partially blocked by anti-transforming growth factor beta antibodies. These studies suggest that cytokine secretion plays a role in the suppression of retrovirus transduction of human CD34+ cells.

3T3 Cells↗
PubMed1994

Involvement of capsaicin-sensitive nerves in regulation of insulin secretion and glucose tolerance in conscious mice.

The impact of sensory nerves in glucose-stimulated insulin secretion and glucose tolerance was investigated in conscious mice treated neonatally with either capsaicin (Cap) or vehicle (Veh). At 10-12 wk after Cap, both the early (1 min) insulin secretory response to intravenous glucose (2.8 mmol/kg) (by 67%) and glucose elimination were potentiated (P < 0.05). In contrast, basal insulin, glucagon, and glucose were not affected by Cap. Plasma norepinephrine and epinephrine levels did not differ between Cap- and Veh-treated animals, whereas the increase in plasma insulin levels normally induced by alpha-adrenoceptor blockade by phentolamine was absent after Cap treatment. In isolated islets, the insulin secretory response to glucose (20 mmol/l), carbachol (0.1 mmol/l), or phentolamine (0.5 mmol/l) was not affected after Cap. It is concluded that sensory denervation by Cap results in increased glucose tolerance, which is in part because of a potentiated early insulin response to glucose. This potentiation does not seem secondary to altered plasma catecholamine levels or to altered islet secretory capacity. The results suggest rather that Cap-sensitive nerves, by a local effector function and/or as the afferent loop of a neural reflex, exert inhibitory influences on insulin secretion.

Afferent Pathways↗
PubMed1994

Inhibition by rat diazepam-binding inhibitor/acyl-CoA-binding protein of glucose-induced insulin secretion in the rat.

Diazepam-binding inhibitor (DBI) has been localized immunohistochemically in many organs. In porcine and rat pancreas, DBI is present in non-B-cells of the pancreatic islets. Porcine peptide also has been shown to suppress insulin secretion from rat pancreas in vitro. Recently, acyl-CoA-binding protein (ACBP) was isolated from rat liver and shown to be identical structurally to DBI isolated from rat brain. Using this rat DBI/ACBP, we have studied its effects on glucose-stimulated insulin secretion in the rat, both in vivo and in isolated pancreatic islets. Infusion iv of rDBI/ACBP (25 pmol/min) during glucose stimulation induced a moderate and transient reduction of plasma insulin levels. Moreover, rDBI/ACBP suppressed insulin release from batch-incubated isolated islets, stimulated by 16.7 mmol/l glucose, by 24% at 10 nmol/l (p < 0.05) and by 40% at 100 nmol/l (p < 0.01). The peptide (100 nmol/l) also inhibited the insulin response to glucose (16.7 mmol/l) from perifused rat islets by 31% (p < 0.05), mainly by affecting the acute-phase response. Finally, incubation of isolated islets in the presence of rDBI/ACBP antiserum (diluted 1:100 and 1:300) augmented the insulin response to 16.7 mmol/l glucose (p < 0.05 or even less). We conclude that rDBI/ACBP, administered iv or added to the incubation media, suppresses insulin secretion in the rat but that the effect is moderate despite the high concentration used. It is therefore unlikely that the peptide modulates islet hormone release, acting as a classical hormone via the circulation. However, the occurrence of DBI/ACBP in the islets and the enhancing effect by the rDBI/ACBP antibodies on glucose-stimulated insulin release suggest that the peptide is a local modulator of insulin secretion.

Animals↗
PubMed1994

Flexural strength of two electro-plated dental ceramics.

This study aimed to investigate the influence on flexural strength of electro-plating two dental porcelains, Vita Omega and Vita Omega 800. The porcelains were treated in accordance with the manufacturer's instructions, and the specimens were produced following the ISO 6872 standard for rectangular bars. Specimens were divided into three groups, of which none, one, or three of the surfaces were plated with a thin layer of gold. Flexural strength was tested with a three-point bending test. Ten specimens were tested for each combination of porcelain and plating, for a total of 60 test pieces. For both porcelains, a significantly higher flexural strength was found for the specimens furnished with a gold layer. The number of covered surfaces did not significantly influence the tested strength. This increase in strength is most likely due to decreased crack initiation and fracture propagation after the covering of random defects in the porcelain. A better stress distribution might also be anticipated and partly explain the results.

Aluminum Silicates↗
PubMed1994

Expression of human glucocerebrosidase in murine macrophages: identification of efficient retroviral vectors.

Gaucher's disease is an autosomal recessive disorder characterized by a functional deficiency in beta-glucocerebrosidase enzymatic activity and the resultant accumulation of the glycolipid glucocerebroside in macrophages. Due to the nature of the affected cells, Gaucher's disease is an excellent candidate for gene therapy of hematopoietic stem cells and autologous bone marrow transplantation of transduced cells using retroviral vectors containing the glucocerebrosidase (GC) gene. In order to identify a retroviral vector capable of high levels of expression of the GC gene in macrophages, we have used the murine myeloid leukemia cell line, M1, a cell line that can be differentiated with interleukin-6 (IL-6) from blasts to macrophages. Two vectors use the Moloney murine leukemia virus (MoMLV) enhancer/promoter (LG vector) or the myeloproliferative sarcoma virus (MPSV) enhancer/MoMLV promoter (MG vector), both located in the viral long-terminal repeat (LTR); the third vector uses the phosphoglycerate kinase (PGK) promoter located internally in the vector (PG vector). The amphotropic PA317 and GP+am12 packaging cell lines were used as virus producer cells, and the GP+am12 cell line demonstrated higher titers, higher levels of GC protein expression, and specific GC enzymatic activity as well as higher transduction efficiencies for all three vectors. The LG retroviral vector was the most efficient in transducing the M1 cells. On average, higher levels of RNA and protein expression were seen in the M1 clones transduced with the LG vector, and these levels increased after differentiation. Thus, the LG retroviral vector in which the expression of the GC gene is driven by the MoMLV LTR enhancer/promoter is the best vector of the three studied for future studies for gene therapy of Gaucher's disease and other hematopoietic disorders that involve macrophages.

Animals↗