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S A Svensson

Publications and source records attributed to S A Svensson.

15 recordsLinked to original sources
PubMed1996

On the influence of superstructure connection on implant preload: a methodological and clinical study.

In a combined in vitro and in vivo study strain gauges were used to register the deformation in two terminal implant abutment cylinders, when connecting three different prosthetic appliances. The prosthetic constructions were placed on the abutments and fastened in vitro and in vivo by using different torque sequences. Furthermore, in the in vitro situation the three medial abutments were replaced by abutments which were 100 microns shorter. The results show that even if the prosthetic constructions were judged to have a good clinical fit, relatively large External Preloads were registered both in vitro and in vivo. No significant differences in axial force or in bending movement were found between the torque sequences in vivo. There were, however, significant differences in axial force as well as in bending moment in the in vitro experiment. When the shorter medial abutments were used in vitro, a change in the axial force of approximately 200 N was registered. The results confirm that the methodological approach used in this study is valid when evaluating preloads.

Analysis of Variance↗
PubMed1989

MR imaging of the temporomandibular joint: comparison of images of autopsy specimens made at 0.3 T and 1.5 T with anatomic cryosections.

We made MR images of 39 autopsy specimens of the temporomandibular joint at 0.3 and 1.5 T and compared the images with anatomic cryosections. Imaging time and slice thickness were the same on scans made at each field strength. The purpose was to determine which field strength provides the best scans for imaging of the joint. Additionally, we used imaging times two and four times longer on the 0.3-T scanner to assess to what extent image quality and diagnostic accuracy could be improved. The cryosections showed that 27 of the joints were normal. Twelve had disk displacements. Ten of the joints with disk displacement also had disk deformities, and seven had bony abnormalities. Investigators who analyzed the MR images had no knowledge of the findings on the cryosections. The disk position, disk configuration, and bony abnormalities were correctly diagnosed in 85%, 77%, and 100%, respectively, on 1.5-T MR images compared with 46%, 41%, and 85%, respectively, on the 0.3-T images. When the imaging time was increased by a factor of four, the accuracy rate on the 0.3-T system became comparable to that of the 1.5-T MR scanner: 73% for disk position, 67% for disk configuration. The results suggest that the diagnostic quality of MR images of the temporomandibular joint is better on scans made at 1.5 T than on those done at 0.3 T when comparable imaging times are used.

Aged↗
PubMed1988

Correlation between cytosolic Ca2+ concentration and cytotoxicity in hepatocytes exposed to oxidative stress.

To investigate the relationship between alterations of cytosolic Ca2+ concentration and development of cytotoxicity, isolated rat hepatocytes were loaded with the fluorescent indicator Quin-2 AM and then incubated with non-toxic or toxic levels of menadione (2-methyl-1,4-naphthoquinone) or tert-butyl hydroperoxide (t-BH). The resulting changes in cytosolic Ca2+ concentration were compared to those seen upon exposure of the hepatocytes to an alpha 1-adrenergic agonist, phenylephrine, as well as to those induced by menadione and t-BH in hepatocytes pretreated with agents that modify their toxicity. Exposure of hepatocytes to phenylephrine or non-toxic levels of menadione caused a moderate and transient increase in cytosolic Ca2+ (less than or equal to 0.7 microM), whereas a toxic concentration of menadione produced a marked, sustained increase in Ca2+ which fully saturated the binding capacity of Quin-2 (greater than 1.5 microM). Treatment of the hepatocytes with the protective agent, dithiothreitol, prevented both the increase in cytosolic Ca2+ and the cytotoxicity induced by menadione. On the other hand, pretreatment of cells with diethylmaleate to deplete intracellular glutathione made otherwise non-toxic concentrations of menadione cause both a sustained increase in cytosolic Ca2+ and cytotoxicity. Similarly, toxic concentrations of t-BH also caused a sustained increase in cytosolic Ca2+. The iron chelator, desferrioxamine, and dithiothreitol (DTT), which protected the cells from t-BH toxicity, also prevented the sustained elevation of cytosolic Ca2+. Our findings provide further support for the hypothesis that a perturbation of intracellular Ca2+ homeostasis is an early and critical event in the development of toxicity in hepatocytes exposed to oxidative stress.

Animals↗
PubMed1987

Temporomandibular joint: comparison of MR images with cryosectional anatomy.

The accuracy of magnetic resonance (MR) imaging in the assessment of internal derangements of the temporomandibular joint (TMJ) has not been systematically evaluated. We obtained multiple 3-mm-thick sagittal and coronal MR images of 15 fresh TMJ autopsy specimens and compared the MR imaging findings with observations in corresponding sagittal cryosections. MR imaging correctly delineated the position of the disk in 11 (73%) joints and incorrectly delineated it in four (27%) joints. Disk configuration was depicted accurately in nine (60%) joints, inaccurately in five (33%), and was not visible in one (7%). Errors observed with sagittal MR images were correlated with mediolateral alterations of disk position. These abnormalities were depicted in coronal images, however. Osseous anatomy was correctly assessed in nine joints (60%). MR imaging demonstrated the margin between the disk and its attachments, which is not possible by arthrography. MR imaging is an acceptable alternative to other imaging modalities for assessing soft and hard tissues of the TMJ.

Aged↗
PubMed1987

CT and MR of the temporomandibular joint: comparison with autopsy specimens.

CT and MR imaging have been advocated for use in the diagnosis of disorders of the temporomandibular joint. A systematic comparison of these imaging techniques has not been made. We performed direct sagittal CT and sagittal MR on 15 fresh temporomandibular joint autopsy specimens and compared our diagnoses with cryosectional findings in a blinded fashion. We found no statistically significant differences between these procedures in detecting bony abnormalities or disk position. However, a side-by-side comparison between the CT and MR images demonstrated that MR depicted the soft-tissue anatomy of the joint with greater detail than did CT. Thus, MR clearly displayed the disk when it was positioned either superiorly or anteriorly, whereas CT only showed the disk adequately when it was positioned anteriorly. MR further showed the configuration of the disk and the borderlines between the disk and its attachments; these relationships could not be assessed from CT images. This experimental study indicates that MR is superior to CT for depiction of soft-tissue changes, whereas CT is superior in showing osseous abnormalities. Clinical confirmation of these results is necessary before one method can be definitively recommended over the other for clinical studies.

Aged↗
PubMed1986

Cystamine induces toxicity in hepatocytes through the elevation of cytosolic Ca2+ and the stimulation of a nonlysosomal proteolytic system.

Infusion of cystamine into the isolated, perfused rat liver resulted in tissue damage preceded by the formation of cystamine-protein mixed disulfides which were mainly detected in the plasma membrane fraction. Hepatotoxicity was prevented when dithiothreitol was infused after cystamine or when the calcium antagonist, verapamil, was co-infused with the disulfide. In isolated hepatocytes, the formation of cystamine-protein mixed disulfides was associated with an inhibition of plasma membrane Ca2+-ATPase activity and a decreased rate of Ca2+ efflux from the cells. This resulted in intracellular Ca2+ accumulation which was followed by a stimulation of both phospholipid hydrolysis and proteolysis, as indicated by enhanced rates of release of radioactivity from hepatocytes prelabeled with [14C]arachidonate and [14C]valine, respectively. Preincubation of hepatocytes with the calmodulin inhibitor, calmidazolium, or with the phospholipase inhibitors, chlorpromazine and dibucaine, inhibited the stimulation of [14C]arachidonate release by cystamine. However, none of these agents prevented the onset of cystamine toxicity in hepatocytes. In contrast, pretreatment of the cells with antipain or leupeptin, two inhibitors of Ca2+-activated proteases, abolished the stimulation of proteolysis by cystamine and also protected the cells from cystamine toxicity. Our results suggest that the perturbation of intracellular Ca2+ homeostasis by cystamine is caused by the inhibition of Ca2+ efflux associated with the formation of cystamine-protein mixed disulfides in the plasma membrane and that subsequent cytotoxicity results from Ca2+-activation of a nonlysosomal proteolytic system.

Animals↗
PubMed1985

On the role of thiol groups in the inhibition of liver microsomal Ca2+ sequestration by toxic agents.

ATP-dependent Ca2+ sequestration by rat liver microsomes was assayed using three different methods, and characterized with regard to the effect of various inhibitors. When glucose and hexokinase were added in combination to deplete ATP in the incubation, Ca2+ uptake was followed by rapid release of Ca2+ from the microsomes. Ca2+ sequestration was inhibited by reagents that cause alkylation (e.g. p-chloromercuribenzoate) or oxidation (e.g. diamide) of protein sulfhydryl groups. Moreover, pretreatment of the microsomes with cystamine, which causes formation of mixed disulfides with protein thiols, also resulted in the inhibition of Ca2+ sequestration. It is concluded that microsomal Ca2+ sequestration is critically dependent on protein sulfhydryl groups, and that modification of protein thiols may be an important mechanism for the inhibition of microsomal Ca2+ sequestration by a variety of toxic agents.

Adenosine Triphosphate↗
PubMed1985

Glutathione S-conjugates stimulate ATP hydrolysis in the plasma membrane fraction of rat hepatocytes.

Incubation of a rat hepatocyte plasma membrane fraction with micromolar concentrations of either glutathione disulfide or various glutathione S-conjugates resulted in a several-fold increase in the rate of ATP hydrolysis. This stimulation was further enhanced when the plasma membrane fraction had been pretreated with agents that arylate or oxidize sulfhydryl groups, suggesting that this ATPase activity is modulated by the protein thiol status of the plasma membrane. It is proposed that this newly discovered ATPase may function in the cellular extrusion of both glutathione disulfide and glutathione S-conjugates.

Adenosine Triphosphatases↗
PubMed1985

Accumulation of Ca2+ induced by cytotoxic levels of menadione in the isolated, perfused rat liver.

Previous studies have indicated that the presence of cytotoxic levels of menadione (2-methyl-1,4-naphthoquinone) causes rapid changes in intracellular thiol and Ca2+ homeostasis in isolated rat hepatocytes. The present investigation was undertaken to examine these effects in the intact liver. Rat livers were therefore perfused with Krebs-Henseleit buffer containing 1.3 mM Ca2+ using a single-pass mode, and the perfusate Ca2+ level was monitored with an on-line Ca2+-selective electrode. Infusion of menadione elicited an increased O2 uptake by the liver, followed by a dose-dependent decrease in the perfusate level of Ca2+. Hepatic accumulation of Ca2+ was accompanied by stimulation of cytosolic phosphorylase a activity. Cessation of menadione infusion resulted in gradual recovery of perfusate Ca2+ to base levels. Ca2+ uptake was not accompanied by decreases in reduced pyridine nucleotide or ATP levels in the liver as evidenced by measurements either during maximal Ca2+ uptake or after recovery. However, Ca2+ uptake was correlated with decreased glutathione and increased glutathione disulfide levels in the liver, both of which reversed during recovery from Ca2+ uptake. Moreover, depletion of hepatic glutathione by pretreatment with diethylmaleate resulted in increased Ca2+ uptake during menadione infusion. The amount of protein-bound mixed disulfides showed a particularly striking relationship to Ca2+ uptake, reaching a maximal level during Ca2+ uptake and reversing toward normal value during recovery from Ca2+ accumulation. The present findings suggest that menadione-induced Ca2+ uptake is due to plasma membrane dysfunction as a result of loss of protein thiol groups critical for maintaining the plasma membrane Ca2+ extrusion mechanism. Our model offers a particularly useful opportunity to study mechanisms underlying toxic disturbances in Ca2+ homeostasis in the intact liver, since Ca2+ fluxes can be monitored under conditions in which cellular control mechanisms are not obliterated by excessive toxicity.

Animals↗
PubMed1984

Metabolism of benzo[a]pyrene-7,8-dihydrodiol and benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide to protein-binding products and glutathione conjugates in isolated rat hepatocytes.

Isolated hepatocytes from 3-methylcholanthrene (MC)-treated rats metabolized trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (BP-7,8-diol) and (+/-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE) to water soluble conjugates including glutathione (GSH) conjugates. Under the conditions employed 35% of total water soluble products derived from BP-7,8-diol could be accounted for by GSH conjugates. The corresponding figure for anti-BPDE was estimated to be greater than or equal to 80%. Isolated hepatocytes metabolized BP-7,8-diol and anti-BPDE to GSH conjugates at maximal rates of 0.5 and 9 nmol per 10(6) cells per min, respectively. Thus, identifying the rate limiting step in the reaction sequence as the metabolism of BP-7,8-diol to the GSH conjugating intermediates. In addition to the direct conjugation of anti-BPDE with GSH, anti-BPDE but not the corresponding BP-tetraols, was further metabolized to reactive intermediates that subsequently bound to cellular proteins or reacted with GSH forming water soluble conjugates. The identity or identities of these novel reactive intermediates is discussed.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1984

On functional strain in fixed mandibular reconstructions. I. An in vitro study.

Six linear strain gauges and one rosette strain gauge were used on three different types of models prepared from one partially dentate subject, to study loading deformation in a six-unit fixed mandibular bridge. The bridge was mounted on each of the models on an adjustable articulator and loaded in a universal testing machine at loading levels ranging from 0 to 491 N. The results showed considerable differences between the three types of model, with regard to both the magnitude of the recorded strains for the individual gauges and the calculated direction of the principal strains under the rosette gauges. The findings indicate that the mechanical properties and the design of the supporting structures have a major influence on the functional deformation of fixed dental appliances.

Adult↗
PubMed1981

Studies on the in vitro transfer of DNA binding benzo[a]pyrene metabolites from rat hepatocytes to human fibroblasts.

The release and reabsorption of benzo[a]pyrene (BP) metabolites were studied in isolated rat hepatocytes incubated with BP. There was a rapid uptake of BP by the hepatocytes which was followed by an excretion of organic as well as water-soluble metabolites. Upon further incubation the BP-dihydrodiols and BP-phenols were reabsorbed by the cells and finally excreted as water-soluble conjugates. The metabolism of BP by the hepatocytes also resulted in the formation and release of reactive intermediates to the incubation medium. The DNA-binding intermediates released from the cells were consistent with trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene-9,10-oxide(s) and 9-hydroxybenzo[1]pyrene-4,5-oxide(s). The BP-metabolites were found to bind to hepatocyte and fibroblast DNA. The degree of DNA binding was estimated as the formation of DNA strand breaks. BP metabolites formed within the hepatocytes and transferred to the fibroblasts were found to induce DNA strand breaks in the latter cells. Addition of DNA to the medium markedly decreased the fraction of single stranded DNA in these cells. Under conditions where the excretion from hepatocytes of BP-phenols and BP-dihydrodiols were increased, the amount of DNA strand breaks in the fibroblasts increased.

Animals↗