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Biomedical subjects

S Sell

Publications and source records attributed to S Sell.

At least 37 records · Page 2Linked to original sources
PubMed2000

Precision of the measurements of periprosthetic bone mineral density in hips with a custom-made femoral stem.

Our aim was to determine the precision of the measurements of bone mineral density (BMD) by dual-energy x-ray absorptiometry in the proximal femur before and after implantation of an uncemented implant, with particular regard to the significance of retro- and prospective studies. We examined 60 patients to determine the difference in preoperative BMD between osteoarthritic and healthy hips. The results showed a preoperative BMD of the affected hip which was lower by a mean of 4% and by a maximum of 9% compared with the opposite side. In addition, measurements were made in the operated hip before and at ten days after operation to determine the effect of the implantation of an uncemented custom-made femoral stem. The mean increase in the BMD was 8% and the maximum was 24%. Previous retrospective studies have reported a marked loss of BMD on the operated side. The precision of double measurements using a special foot jig showed a modified coefficient of variation of 0.6% for the non-operated side in 15 patients and of 0.6% for the operated femur in 20 patients. The effect of rotation on the precision of the measurements after implantation of an uncemented femoral stem was determined in ten explanted femora and for the operated side in ten patients at 10 degrees rotation and in 20 patients at 30 degrees rotation. Rotation within 30 degrees influenced the precision in studies in vivo and in vitro by a mean of 3% and in single cases in up to 60%. Precise prediction of the degree of loss of BMD is thus only possible in prospective cross-sectional measurements, since the effect of the difference in preoperative BMD, as well as the apparent increase in BMD after implantation of an uncemented stem, is not known from retrospective studies. The DEXA method is a reliable procedure for determining periprosthetic BMD when positioning and rotation are strictly controlled.

Absorptiometry, Photon↗
PubMed1999

Synovial Epstein-Barr virus infection increases the risk of rheumatoid arthritis in individuals with the shared HLA-DR4 epitope.

OBJECTIVE: To investigate the presence of the Epstein-Barr virus (EBV) in rheumatoid arthritis (RA) synovium and its correlation with the HLA genotype in an attempt to elucidate the role of EBV in the pathogenesis of RA. METHODS: EBV DNA/RNA was investigated by polymerase chain reaction (PCR) analysis of synovial tissue from 84 patients with RA and from 81 patients with non-RA arthritis (controls) and was correlated with the patients' HLA genotype. RESULTS: EBV DNA and EBV-encoded RNA 1 transcripts were significantly more frequently present in synovial tissue from the RA patients (29 of 84) than in that from the non-RA patient controls (8 of 81). EBV DNA-positive individuals had a 5.47 times higher risk of presenting with RA than did EBV DNA-negative individuals. In HLA-DRB1*0401,0404,0405,0408-positive or shared epitope-positive patients, the risk was further increased (odds ratio for EBV and HLA-DR4 approximately 41, for EBV and the shared epitope approximately 15) compared with those who lacked both EBV DNA and RA-linked HLA genotypes. CONCLUSION: EBV seems to function as an environmental risk factor for RA, particularly in patients with the RA-linked HLA-DRB1 alleles.

Adult↗
PubMed1999

Bone mineral density of the proximal femur after unilateral cementless total hip replacement.

It was the aim of this study to examine bone mineral density changes in the non-operated contralateral femur of patients undergoing total hip replacement. Bone density in the contralateral femur of 45 patients with an average age of 54 years was measured with the aid of the DEXA technique at one week, 3 and 6 months after total hip replacement. Within the first 3 months there was an average reduction of bone density of 3.9% (3.0%-5.9%). After a further 3 months the average difference was 2.5%.

Absorptiometry, Photon↗
PubMed1999

[Effect of diclofenac on human osteoblasts and their stromal precursors in vitro in relation to arthroplasty].

INTRODUCTION: Results of animal experiments have demonstrated that the osseous integration of non-cemented prostheses can, at the very least temporarily, be impaired by the application of non-steroidal antiphlogistic agents (such as diclofenac). It is the objective of this study to examine whether there is a direct influence of diclofenac used in usual clinical dosages (3 times 50 mg daily) on bone cells and their progenitor cells which would explain the observed slow integration of the prostheses. METHODS: To investigate this, cultivated human in vitro osteoblasts and stromal bone marrow cells were incubated with increasing doses of the medications. Our study focused on the effect of diclofenac application on proliferation and functional metabolism in both cell lines. The measurable maximal plasma concentration 2 h after the application of one tablet Voltaren 50 reached 1.6 micrograms/ml. This correlated with diclofenac concentrations between 1 and 10 ml found in our experiments. The detected values were correlated to the control group (0 microgram/ml diclofenac). RESULTS: The drug effect upon osteoblasts was higher than on progenitor cells. The proliferation of in vitro stromal bone marrow cells, compared to untreated cells, was found to be decreased. We observed a decrease to 82% at a diclofenac concentration of 1 microgram/ml, Osteoblasts exhibited a decrease to 97.5% at the same concentration. The DNA synthesis increased to 118% in stromal bone marrow cells, in osteoblasts to 144%. In contrast, we detected a neglectible decrease to 92% in the collagen synthesis of osteoblasts compared to untreated cells. The synthesis of osteocalcin by osteoblasts increased to 119%. The alkaline phosphatase activity was found to be decreased to 88% in stromal bone marrow cells and increased in osteoblasts to 111%. CONCLUSION: Temporary inhibiting effects on osseous integration in non-cemented prosthesis by diclofenac could be caused by a disturbance in the anabolic bone metabolism, exhibited by an increase of osteoblastic osteocalcin expression. Osteocalcin as a known negative regulator of the osteoneogenesis is most likely inhibiting the collagen matrix deposition.

Aged↗
PubMed1999

[Influence of osteoarthrosis, osteoporosis, and rheumatoid arthritis at precision of osteodensitometry of lumbar spine and proximal femur].

UNLABELLED: Precision of osteodensitometric measurements using dual energy X-ray absorptiometry (DEXA) depends on various known factors, such as positioning, aortic calcification or vertebral fractures. The purpose of this study was to investigate the influence of various diseases or bone density on the reproducibility of measurements in the lumbar spine and the proximal femur. Measurements in the LWS p.a. , LWS lat. and at Ward's triangle were made in a total of 100 patients. The subjects were repositioned between measurements. In order to be able to determine the influence of various diseases, four groups of 25 patients each were formed: three with the diagnosis osteoarthrosis, osteoporosis and rheumatoid arthritis and one control group. The mean percentual difference and coefficient of variation were calculated as the measure for reproducibility. Mean percentual differences of 0.18 to 2.6% were found in the four groups at the three measurements sites. After calculation of coefficient of variation, a value between 1.2 and 2.7% was found for LWS p.a., between 7.1 and 15.7% for LWS lat. and between 4.1 and 9.9% at Ward's triangle. It was also conspicuous that the difference in coefficient of variation in osteoporosis patients was nearly double that in the control group in all measured areas. CONCLUSION: Lateral lumbar spinal measurements using DEXA cannot presently be recommended. LWS p.a. measurements and, with limitations, measurements at Ward's triangle have good precision and could be used for course documentation of bone density.

Absorptiometry, Photon↗
PubMed1999

High tibial osteotomy: factors influencing the duration of satisfactory function.

In 94 patients 112 knees were examined after high tibial osteotomy for varus and valgus gonarthrosis. Preoperatively, there were 71 varus and 23 valgus deformities. The mean follow-up period was 9.0 years (range 2-21 years). Concerning the pain on walking and the pain at rest, we noted good and excellent results in 73% and 65%, respectively. The radiological evaluation showed an improvement or a persistence of the stage of arthrosis in 69.5% of the reviewed cases. The results according to the HSS score as an objective parameter showed in over 50% an improvement of the patients' situation. The data were subjected to multivariate statistical analysis in which three of four evaluated risk factors were found to be associated with the duration of pain-free survival: certain preoperative injuries, preoperative meniscopathies and a deterioration of the stage of arthrosis (P < 0.05). There was no significance for weight in excess of 10% above the normal body mass index (BMI) limits. However, in a Kaplan-Meier survival analysis this parameter could be determined as a significant factor for a reduced pain-free survival interval (P < 0.05): patients with a BMI of more than 10% above normal limits had a pain-free period of 5.07 years, whereas those with a BMI of less than 10% had a pain-free period of 7.80 years.

Adolescent↗
PubMed1999

C-reactive protein as an early indicator of the formation of heterotopic ossifications after total hip replacement.

The formation of heterotopic ossifications after total hip endoprosthesis implantation is a well-known complication. During the postoperative course laboratory parameters are subject to partial change due to the development of heterotopic ossifications. However, these changes occur relatively late at a time when the application of prophylactic precautions is usually already decided. Any meaningful prophylactic treatment, however, has to be initiated immediately after surgery. In a prospective study we assessed the postoperative C-reactive protein (CRP) levels in 95 patients twice after total hip replacement surgery. The initial assessment took place on the 1st day following surgery and again between the 5th and 7th day. All patients received three doses of 50 mg diclofenac daily for 7 days starting on the 1st postoperative day. Average CRP values on the 1st postoperative day were 6.33 +/- 2.28 mg/dl for ossification grade Brooker 0, 7.04 +/- 1.8 mg/l for Brooker 1 and 7.65 +/- 3.7 mg/dl for Brooker grades 2-4. At the time of the second CRP assessment (postoperative day 5-7), CRP values in the groups of patients showing ossifications were higher. Whereas patients without ossifications (A) exhibited an average level of 4.22 +/- 3.13 mg/dl, in patients with ossification grade 1 (B) CRP was 5.57 +/- 2.78 mg/dl and in the group with ossification grades 2-4 (C) was 6.38 +/- 4.48 mg/dl. The differences between group A on the one hand and the combined groups B and C values on the other were significant (P = 0.036). We are able to assert that after total hip replacement, significantly higher CRP levels can be recorded immediately after surgery in those patients who will eventually develop heterotopic ossifications, as compared with those who do not. Hence, the postoperative rise of CRP levels should be introduced as a further risk factor for the formation of heterotopic ossifications since its recording at such an early stage still allows for the timely initiation of prophylactic treatment.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Participation of different cell types in the restitutive response of the rat liver to periportal injury induced by allyl alcohol.

BACKGROUND/AIM: Restitution of periportal liver necrosis induced by allyl alcohol involves proliferation and differentiation of putative liver stem cells. The participation of different non-epithelial cell types required to restore the liver cord structure in this process has not been well documented. The aim of the study was to determine the anatomic relationships among cells of liver lineage, extracellular matrix, and non-parenchymal cells during repair of periportal liver injury. METHODS: Periportal liver injury in rats was induced by intraperitoneal injection of allyl alcohol. Cells of the liver lineage, as well as Kupffer cells, hepatic stellate cells, macrophages, and the extracellular matrix components fibronectin and laminin were localized using immunohistologic methods for 7 days after injury. RESULTS: During the first day there was loss of periportal hepatocytes, as well as sinusoidal nonparenchymal cells, including macrophages, Kupffer cells and hepatic stellate cells. After day 1 macrophages appeared within the necrotic zone, increased until days 3-4, and then decreased to a few cells within reappearing sinusoids. At days 2-5 there was first proliferation of small "null" intraportal cells, which later acquired markers of ductular (OV-6, CKPan ) and liver cell differentiation (alphafetoprotein, carbamoylphosphate synthetase-I), eventually assuming mature hepatocyte morphology. There was also moderate bile duct hyperplasia with extension of small newly-formed ducts from the intraportal zone into the immediate periportal zone. Kupffer cells and hepatic stellate cells became enlarged at the borders of the necrotic and non-necrotic central zone and then appeared to migrate into the oval cell population expanding across the periportal zone. During the restitution phase, hepatic stellate cells were closely associated with the proliferating oval cells, surrounding small aggregates of oval cells which appeared to be forming liver cords. Kupffer cells also stained for fibronectin, and fibronectin was seen at the intersection of the injured portal and uninjured central zones and around the expanding oval cells. In some intraportal zones, the laminin surrounding the bile ducts was lost. It was speculated that this may permit proliferating ductular cells to migrate out of the bile ducts into the periportal zone. By days 6 and 7 most of the injured liver was restored to normal, with a few foci of chronic inflammation remaining. CONCLUSIONS: There is a close anatomic relationship between immature liver lineage cells (oval/duct cells) and non-parenchymal cells during the restitutive repair of periportal injury. The nature of this relationship to the possible production of growth factors and expression of growth factor receptors by the cells involved during the restitution process is discussed.

Animals↗
PubMed1998

Control of mouse hepatocyte proliferation and ploidy by p53 and p53ser246 mutation in vivo.

The effect of expression of the p53 gene, in the presence or absence of the p53ser246 mutation (p53*), on ploidization (image cytometry), proliferation (expression of proliferating cell nuclear antigen and radioactive thymidine histoautoradiography), and apoptosis (in situ detection of DNA fragments) is determined in hepatocytes of p53-null and p53*-transgenic mice. The mouse p53ser246 mutation is equivalent to the p53ser249 mutation found in human hepatomas associated with hepatitis B virus infection and aflatoxin exposure. The hepatocytes of heterozygous or homozygous p53-knockout mice (p53+/-; p53-/-), as well as knockout mice expressing one allele of p53ser246 (p53+/-, p53*; p53-/-, p53*), do not undergo normal polyploidization with aging and show an increase in the number of cycling (G1-, S-, and M-phase) cells. In addition, p53ser246-transgenic mice (p53+/+, p53*; p53+/-, p53*; and p53-/-, p53*) have a greatly increased number of hepatocytes in the G1 phase. No differences in rates of apoptotic hepatocytes are found among any of the mouse groups studied, so the increased proliferation results in a hyperplasia manifested by a increased number of small periportal cells. We conclude that loss of p53 removes blocks in the cell cycle, leading to increased proliferation, whereas expression of the p53ser246 mutation stimulates G0 to G1 and/or M to G1 transition of hepatocytes. Increased proliferation of hepatocytes, combined with no concomitant increase in apoptosis, may in part explain the enhanced development of hepatocellular carcinomas in p53-knockout and p53*-transgenic mice exposed to aflatoxin.

Amino Acid Sequence↗
PubMed1998

Comparison of liver progenitor cells in human atypical ductular reactions with those seen in experimental models of liver injury.

The ultrastructural characteristics of liver progenitor cell types of human atypical ductular reactions seen in chronic cholestasis, in regenerating human liver after submassive necrosis, in alcoholic liver disease, and in focal nodular hyperplasia are compared with liver progenitor cell types seen during experimental cholangiocarcinogenesis in hamsters; during hepatocarcinogenesis in rats; and in response to periportal liver injury induced by allyl alcohol in rats. Three types of progenitor cells have been identified in human atypical ductular reactions: type I: primitive, has an oval shape, marginal chromatin, few cellular organelles, rare tonofilaments, and forms desmosomal junctions with adjacent liver cells; type II: bile duct-like, is located within ducts, has few organelles, and forms lateral membrane interdigitations with other duct-like cells; and type III: hepatocyte-like, is located in hepatic cords, forms a bile canaliculus, has tight junctions with other hepatocyte-like cells, prominent mitochondria and rough endoplasmic reticulum, and some have lysosomes and a poorly developed Golgi apparatus. Each type is seen during cholangiocarcinogenesis in hamsters, but the most prominent cell type is type II, duct-like. A more primitive cell type ("type 0 cell"), as well as type I cells, are seen in the intraportal zone of the liver within 1 to 2 days after carcinogen exposure or periportal injury in the rat, but both type II and type III are seen later as the progenitor cells expand into the liver lobule. After allyl alcohol injury, type 0 cells precede the appearance of type I and type III cells, but most of the cells that span the periportal necrotic zone are type III hepatocyte-like cells showing different degrees of hepatocytic differentiation. Some type II cells are also seen, but these are essentially limited to ducts. It is concluded that there is a primitive stem cell type in the liver (type 0) that may differentiate directly into type I and then into type II, duct-like or or type III hepatocyte-like cells. The terms oval cell, transitional hepatocyte, biliary hepatocyte, hepatocyte-like cell, atypical ductular cell, neocholangiole, etc., are used to describe these cells. Although these terms are useful as general descriptive terms for liver precursor cells at the light microscopic level, the cells included in these descriptive categories may be very different from one another biologically and ultrastructurally.

Animals↗
PubMed1998

Hepatitis B injury, male gender, aflatoxin, and p53 expression each contribute to hepatocarcinogenesis in transgenic mice.

The major risk factors for human liver cancer: hepatitis B virus (HBV) related liver injury, male gender, aflatoxin exposure, and p53 expression, are evaluated and compared in experimental transgenic mouse models. Transgenic mice that express hepatitis B surface antigen (HBsAg) in their liver and develop liver tumors at 18 months of age (HBV+ mice) were bred to p53 null mice (p53-/-) to produce mice p53+/-, HBV+ mice. These mice and control littermates ([p53+/+, HBV+], [p53+/-, HBV-], and [p53+/+, HBV-) were divided into groups that did or did not receive an injection of aflatoxin at 1 week of age. At sacrifice at 13 months of age, 100% (7/7) of male mice with each of the three risk factors (p53+/-, HBV+, AFB1+) developed high-grade hepatocellular carcinomas (HCC). If any one of the risk factors was absent, the incidence drops: if both p53 alleles are present, 62% (10/16); if HBsAg is not expressed, 14% (1/7); if AFB1 is not given, 25% (2/8). If only one of the risk factors is present no tumors above grade I are found. Similar results were observed in female mice except that HCC incidence in each group is less than in male mice. Some of the tumors in mice with more than one risk factor are of unusual histological types, such as hepatocholangio-carcinomas, adenocarcinomas and undifferentiated carcinomas that are not usually seen in HBV transgenic C57BL/6 mice. No loss or mutation of the p53 gene is detected in any of the tumors. Possibilities of how the four major risk factors for HCC interact to produce malignant liver tumors in these transgenic mouse models of hepatocarcinogenesis are discussed.

Aflatoxins↗
PubMed1998

The mouse equivalent of the human p53ser249 mutation p53ser246 enhances aflatoxin hepatocarcinogenesis in hepatitis B surface antigen transgenic and p53 heterozygous null mice.

The relative contribution to development of hepatocellular carcinoma of the mouse equivalent to the human p53ser249 mutation, found in human hepatocellular carcinoma associated with aflatoxin (AFB1) exposure, is compared with other major risk factors in a transgenic mouse model. Transgenic p53ser246 mice, expressing the mutant protein gene under the control of a truncated albumin promoter, were bred to mice lacking p53 (p53-/-) and to transgenic mice expressing hepatitis B surface antigen (HBsAg). AFB1 hepatocarcinogenesis was then determined in offspring with single or multiple risk factors by determination of the numbers of high-grade hepatic tumors at 13 months of age. In AFB1-treated male mice, expression of the p53ser246 mutation increases the incidence of high-grade tumors from 0% to 14% in HBsAg-negative, p53+/+ (wild-type homozygous) control mice; from 14% to 71% in HBsAg-negative, p53+/- (wild-type heterozygous) mice; and from 62% to 100% in HBsAg-positive, p53+/+ mice. Thus, whereas HBsAg expression and AFB1 together are strongly cocarcinogenic, the presence of the p53ser246 mutant not only significantly enhances this cocarcinogenic effect, it also increases tumorigenesis in AFB1-treated p53 heterozygous and homozygous mice not expressing HBsAg. The possibility that the p53ser246 mutant protein may act as a promoting agent for AFB1 hepatocarcinogenesis is discussed.

Aflatoxin B1↗
PubMed1998

Different behavior of human osteoblast-like cells isolated from normal and heterotopic bone In vitro.

In this study, a characterization of human bone-forming cells responsible for heterotopic ossification was carried out in vitro. The biological and biochemical cell characteristics of the heterotopic osteoblast-like (HOB) cells were compared with those of orthotopic osteoblast-like (OB) cells from normal bone and stromal bone marrow cells believed to contain a subpopulation of osteogenic precursor cells. We found that HOB's from the spongiosa of heterotopic ossification required less time until the beginning of migration and the achievement of confluence in vitro compared with OBs from femoral shaft spongiosa. The fraction of mitotically active cells assessed by a clonogenic assay was higher as well in HOB cells. The in vitro studies of mitogenesis and the efficiency of colony formation of osteogenic cells indicate that with increasing differentiation and relative age they become more dependent on growth factors in the medium, otherwise the morphology of osteoblast-like cells changes and they pass irreversibly into the postmitotic stage of the cell cycle. The activity of the alkaline phosphatase is distinctly higher in the HOB than in the OB cells, HOB cells exhibit a lower level of osteocalcin expression compared with OB cells. No significant difference was found between OB and HOB cells in the amount of procollagen of type I sequestered by the cells. After 30 days, HOB and OB cells formed a mineralized matrix on exposure to 2 mM beta-glycerophosphate. Since HOBs were isolated from heterotopic bone that had developed within 3-6 months after hip surgery, the differences in cellular behavior compared with OBs may be attributed to the relatively young age of HOB cells.

Alkaline Phosphatase↗
PubMed1998

Prevention of periarticular heterotopic ossification after endoprosthetic hip joint replacement by means of diclofenac.

This prospective study involves 644 patients who received ossification prophylaxis by means of the drug diclofenac after implantation (87.5%) or revision (12.5%) of a total hip endoprosthesis between August 1992 and June 1994. One hundred patients (15.5%) stopped the treatment because of side-effects of the drug, and medication was stopped when gastrointestinal troubles occurred. The follow-up examination after 6 months revealed ossification of HO degree 1 according to Brooker in 13.8% of cases, of degree 2 in 4.8%, and of degree 3 in 1.4% of cases. Severe HO of degree 4 was not observed at all, and 80% of the patients exhibited no ossification what ever. Thus, in comparison to our own studies and to the literature, diclofenac must be regarded as an extremely effective drug for the prevention of ossification.

Administration, Oral↗
PubMed1998

The suppression of heterotopic ossifications: radiation versus NSAID therapy--a prospective study.

This prospective, randomized study compares the effect of postoperative irradiation and nonsteroidal anti-inflammatory drug (NSAID) therapy on the prevention of heterotopic ossifications after the implantation of a total hip endoprosthesis. A total of 154 operations were performed; one group of patients underwent radiation treatment of 3 x 3.3 Gy, and the other group took 3 x 50 mg of diclofenac per day over a period of 3 weeks. Average age, sex, preoperative diagnosis, and risk factors were similar in both groups. Postoperative radiation began on average 2.9 days after operation, and the radiation therapy was finished on average within 3.8 days. NSAID prophylaxis was begun on the first postoperative day. Heterotopic ossifications occurred in two of the patients who had undergone postoperative prophylaxis by radiation. In both cases, the ossification was Brooker I, and there was no functional impairment. There were no ossifications of Brooker II-IV in this group. One patient had a Staphylococcus epidermidis infection, and fistula revision had to be carried out; the prosthesis could be left in place. In the group treated with NSAID, 16 heterotopic ossifications stage Brooker I and 2 stage Brooker II could be detected. Eleven patients stopped the treatment because of gastrointestinal problems. Both postoperative radiation and NSAID therapy have proved to be effective prophylactic methods. In direct comparison, radiation prophylaxis by 3 x 3.3 Gy proved to be slightly more successful than NSAID prophylaxis.

Anti-Inflammatory Agents, Non-Steroidal↗