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Biomedical subjects

S Sell

Publications and source records attributed to S Sell.

At least 55 records · Page 3Linked to original sources
PubMed1998

Aflatoxin exposure produces serum alphafetoprotein elevations and marked oval cell proliferation in young male Pekin ducklings.

Feeding of aflatoxin to ducks produces extensive oval cell proliferation in the liver associated with a prolonged elevation of serum alphafetoprotein (AFP). Short term feeding of 0.075-0.6 microgram/g of aflatoxin to young male Pekin ducks results in rapid and massive dose-related proliferation of "oval" cells, which extend from the portal zone across the hepatic lobule within three to five weeks. Longer term feeding of 0.15 microgram/g and 0.3 microgram/g results in prolonged elevations of serum AFP. Prolonged elevation of serum AFP serves as a marker of oval cell proliferation preceding hepatocellular carcinoma (HCC) development. These results confirm that ducks are sensitive to low amounts of aflatoxin and develop early lesions that have been shown in other studies to be associated with hepatocarcinogenesis. These findings in ducks support the likelihood that aflatoxin exposure contributes to the risk for development of HCC in humans.

Administration, Oral↗
PubMed1998

Immunolocalization of putative human liver progenitor cells in livers from patients with end-stage primary biliary cirrhosis and sclerosing cholangitis using the monoclonal antibody OV-6.

The term oval cell describes small cells with oval nuclei that arise in the periphery of the portal tracts in rat models of hepatocarcinogenesis and injury and can differentiate into either hepatocytes or bile duct cells, ie, are bipotential. The presence of such cells in human liver is controversial. Here, immunolocalization of OV-6 and two biliary markers, cytokeratin 19 (CK-19) and human epithelial antigen 125 (HEA-125) is compared in normal adult human livers and in primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) liver sections. CK-19 and HEA-125 stained bile ducts and ductules in normal liver as well as proliferating ductular structures in diseased livers. OV-6 did not label ducts or ductules in normal liver, but in PBC and PSC stained numerous proliferating ductular and periductular cells and lobular hepatocytes. In PBC, discrete OV-6-positive cells with a mature biliary-cell-like morphology were seen integrated into some intact bile ducts as well as occasional small immature oval-like cells. In addition, in PSC, hepatocytes in regenerating lobules were also strongly stained with OV-6, and on close inspection, in both PBC and PSC, oval cells and small hepatocytes at the margins of the lobules were strongly labeled. In contrast to the rat liver, OV-6 and CK-19 staining did not always co-localize. It is proposed that the small OV-6-positive oval cells are analogous to those seen in rat models and may represent human liver progenitor cells that may differentiate into OV-6-positive ductal cells or lobular hepatocytes.

Adolescent↗
PubMed1997

Electron microscopic identification of putative liver stem cells and intermediate hepatocytes following periportal necrosis induced in rats by allyl alcohol.

The ultrastructural characteristics of the putative liver stem cells that repopulate the necrotic periportal zones after allyl alcohol induced liver injury are described. Periportal liver cell necrosis was induced in adult female Sprague-Dawley rats by i.p. injection with 0.62 mmol/kg of allyl alcohol. Electron microscopic examination of the livers was carried out at 33, 57, 81 and 129 h after injection. After periportal necrosis small nondescript intraportal cells (putative liver stem cells) as well as three type of "progenitor" cells are seen: type I, immature "precursor" cells; type II, bile duct-like; and type III, hepatocyte-like, with numerous cells of intermediate type between type I and type III. The periportal necrotic zone (zone I) is reconstituted largely by an increase in hepatocyte-like cells containing mitochondria, lysosomes, lipid-filled vacuoles, rare peroxisomes, prominent endoplasmic reticulum and lateral microvilli (type III cells) with a relatively small number of type I (immature) cells participating. The type III cells display different degrees of differentiation; the less mature are termed "restitutive" and the more mature "transitional" hepatocytes to emphasize the probable relationship between these cell types. Immature ductular cells (type II cells) are seen located basally within hyperplastic ducts in the periportal zone. It is postulated that hepatocyte restitution after periportal necrosis is accomplished by proliferation and differentiation of stem cells with both biliary and hepatic potential that specifically differentiate into hepatic cells through "restitutive" and "transitional" intermediates. These postulated liver stem cells may be intraportal cells seen 33-57 h after injury that precede the type I and type III hepatic precursors seen later.

Animals↗
PubMed1997

Evaluation of synovial cytokine patterns in rheumatoid arthritis and osteoarthritis by quantitative reverse transcription polymerase chain reaction.

To compare the cytokine profile with the degree and composition of cellular infiltration in rheumatoid arthritis (RA) and osteoarthritis (OA) synovium, synovial membranes from patients with RA (n = 14) and OA (n = 5) were examined, employing immunohistochemistry and competitive reverse-transcriptase polymerase chain reaction (RT-PCR), for interleukin (IL)-I beta, IL-2, IL-4, IL-5, IL-6, and IL-10, and tumour necrosis factor-alpha (TNF-alpha) gene expression. It was found that the strength of cytokine gene expression within the synovial membranes of patients with RA was not significantly correlated with the degree of synovial infiltration of T-cells, B-cells, or macrophages. No IL-2, IL-4, or IL-5 RNA was detected in the synovium of either RA or OA. Quantitative cytokine determination showed a similar pattern in RA and OA, although the two diseases differed in total synovial infiltration and the composition of infiltrating cellular elements. Thus the number of cell types known to produce certain cytokines does not appear to determine the strength of synovial cytokine expression measured by quantitative RT-PCR. Furthermore, the pattern of T-cell specific cytokines found in RA synovium does not accord with the concept of the TH0, TH1, and TH2.

Arthritis, Rheumatoid↗
PubMed1997

Heterogeneity of the "oval-cell" response in the hamster liver during cholangiocarcinogenesis following Clonorchis sinensis infection and dimethylnitrosamine treatment.

BACKGROUND: Small intraportal "oval" cells which appear in the livers of humans and experimental animals after liver injury, are suspected to be early progenitor cells for both hepatocytes and bile duct cells, as well as cells of origin of hepatocellular and cholangiocellular carcinomas. METHODS: The origin and fate of small "oval" cells expressing different immunohistologic phenotypes and ultrastructural appearance were examined in livers of Syrian hamsters during cholangiocarcinogenesis induced by dimethylnitrosamine and promoted by Clonorchis sinensis infection. RESULTS: Three different "oval" cell types are identified in portal and/or periportal areas: 1) Small periductal cells with abundant heterochromatin and scant cytoplasm that are negative for AFP, CK19, OV-6 and GST-p (primitive oval cells); 2) Glycogen-rich cells, positive for AFP, but negative for CK19, OV-6 and GST-p mainly adjacent to ductal plates (hepatocyte-like oval cells); and 3) small cells with desmosomes and basement membrane, containing GST-p CK19 and OV-6 but negative for AFP, present in ducts (ductular-like oval cells). It appears that C. sinensis infection stimulates proliferation and differentiation of small ductular or periductal cells (primitive oval cells) into either hepatocyte-like oval cells, which mature into hepatocytes without malignant transformation, or into ductular-like oval cells. CONCLUSIONS: We propose that the ductular-like oval cells are precursors of dysplastic ductular cells that give rise to cholangiocarcinomas after dimethylnitrosamine treatment and conclude that primitive oval cells are bipolar progenitor cells for hepatocytes and biliary cells, and that activation (initiation) of these cells by carcinogen (dimethylnitrosamine), followed by stimulation of proliferation of biliary cells by C. sinensis, promotes primitive oval cells or their progeny (ductular-like oval cells) to transform into cholangiocarcinomas.

Animals↗
PubMed1997

[Ultrasonography of Achilles tendon lesions--an experimental study].

AIM: In an experimental study the accuracy of ultrasound in the detection of lesions of the achilles tendon was examined. METHODS: 60 Achilles tendons were examined post mortem macroscopically, histologically and by means of ultrascan. RESULTS: All macroscopical changes were found in the sonograms. Especially changes of the form proved to be good diagnostic patterns for degenerative lesions of the tendon. At a distance of 2 cm proximal to the calcaneus histological changes could be detected with an accuracy of 73.3%. At 4 and 6 cm to the calcaneus we found similar results. CONCLUSION: A differentiation of the histological diagnosis by means of the sonographic behaviour was not possible. As a reproducible, effective and inexpensive method ultrasound examination has proved very useful in the detection of degenerative lesions of the Achilles tendon.

Achilles Tendon↗
PubMed1996

Lesions of the Achilles tendon. A sonographic, biomechanical and histological study.

Thirty-four Achilles tendons were explanted post-mortem. The explanation took place less than 24 h after death. The tendons were examined by means of ultrasonography and after explanation assessed histologically and biomechanically. In the sonograms 19 changes in echogenicity were noted. Changes in form with an increase in the diameter of the tendon of up to 10 mm (compared with the contralateral side) were found in 6 tendons. The changes in echogenicity and form were found most frequently 2-4 cm from the insertion of the tendon at the os calcis. At a speed of 5 mm/min, the average force needed until rupture occurred was calculated as 27.6 N/mm2. The tear was located on average 29.7 mm from the bony insertion of the tendon at the calcaneus. Histologically, necroses could be found most frequently in all regions of the tendon, followed by scars and fissures. When there were differences of more than 25% in tensile strength between the right and left sides, there was a histological change in the weaker tendon at the site of the tear. Sonographic changes in form pointed to histological lesions in this region. Changes in the echogenicity led to the detection of degenerative changes of the tendon, but they have to be analysed carefully, as they are prone to artefacts. There was not statistically relevant correlation either with regard to tensile strength or to the site of the rupture for sonographically proven changes in the area of the rupture. However, when there was a sonographically abnormal finding in the course of a tendon, the tendon tore at an earlier point than those exhibiting no abnormality. Sonography proved to be a useful method in the detection of degenerative lesions of tendons. A direct influence on the biomechanics of the tendon could not be found.

Achilles Tendon↗
PubMed1996

Determination of periprosthetic bone density with the DEXA method after implantation of custom-made uncemented femoral stems.

Implantation of a total hip replacement leads to resorption of bone, especially in the upper femoral shaft and this depends mainly on the design of the stem, and also on the survival time of the implant. Density of the periprosthetic bone was examined with the DEXA method in both femurs in 27 patients at a mean of 21 months after implantation of uncemented custom-made femoral stems. A loss of bone density between 5% and 21% was found which was independent of the survival time of the implant. The maximum decrease was at the upper medial part of the calcar. The negligible loss of bone density, compared to other reports, favours the use of a computer tomography assisted custom-made femoral stem.

Absorptiometry, Photon↗
PubMed1996

Cell kinetics of repair after allyl alcohol-induced liver necrosis in mice.

The cellular kinetics of repair and scarring which occurs after induction of periportal necrosis in mice by allyl alcohol were examined by histology and immunohistochemistry. Thirty-six six-week-old female C57BI/6J mice were injected intraperitoneally with two doses of allyl alcohol on day 0 and tissue sections were taken at various times and stained by haematoxylin and eosin or immunostained for proliferating cell nuclear antigen (PCNA), bile duct/oval cell marker A-6, and DNA fragments (apoptosis). Within 6 hours, periportal necrosis was seen extending to produce large zones of confluent, pan-acinar irregular necrosis, predominantly in the right and medial lobes with sparing of the left and caudate lobes. Restoration of liver mass was accomplished mainly by proliferation of mature hepatocytes in the surviving lobes of the liver (hyperplasia). In the right and medial lobes where necrosis was limited to the periportal zone, there was some, but much less, proliferation of small, oval periportal cells. The large necrotic zones in the right and median lobes shrank and were replaced by granulomatous inflammation. This cellular contribution of liver regeneration in the mouse was different from that previously reported in the rat and provides a means of inducing only a small proliferation of oval cells.

Animals↗
PubMed1995

Multiple superinfections fail to activate defective human immunodeficiency virus-1 (HIV-1) infection of rabbits.

Superinfection of human immunodeficiency virus (HIV)-1-infected rabbits with Treponema pallidum, Mycobacterium avium, herpes simplex, Candida albicans, Mycoplama incognitus, and malignant catarrhal fever virus, as well as irradiation or cortisone treatment, fails to activate production of infectious virus. For up to 6 months after infection of rabbits with HIV-infected cells or free virus, there are neither clinical symptoms nor positive laboratory tests for detection of HIV. However, after superinfection with other agents, HIV sequences may be transiently found in peripheral blood mononuclear cells by polymerase chain reaction (PCR), and multiple antibodies to HIV antigens may be detected by Western blotting. Both the PCR positivity and Western blot reactivity become negative with time after superinfection. Other than delayed healing of the skin lesions produced by T. pallidum and vaccinia in HIV-infected rabbits, there is no evidence of any immune abnormality. After death, gag sequences are detectable in the splenocytes of essentially every HIV-infected rabbit, and the splenocytes of eight of 25 infected rabbits responded by proliferation to HIV peptides. In addition, gag sequences are detectable in rabbits that are injected with lymphoid cells from HIV-infected rabbits. However, after multiple testing of both peripheral blood of living rabbits and organs of rabbits that died or were killed (spleen, brain, lymph nodes, liver, and gastrointestinal tract), no viable virus has ever been convincingly detected by in vitro cultivation with indicator cells. In contrast to some other published reports, these data indicate that HIV-1 infection of rabbits does not provide a model for AIDS pathogenesis therapy or prevention, but it may be useful as a model to study the relative resistance of a small fraction of the human population to development of AIDS after HIV infection.

Animals↗
PubMed1995

Characterization of a murine p53ser246 mutant equivalent to the human p53ser249 associated with hepatocellular carcinoma and aflatoxin exposure.

A mutation in the tumor suppressor p53 gene resulting in an Arg-->Ser substitution in position 249 is found frequently in human hepatocellular carcinomas associated with hepatitis B infection and with aflatoxin exposure. To determine the significance of this mutation in an in vivo experimental model using transgenic mice, we introduced a two-nucleotide change in the mouse p53 gene at amino-acid position 246, which is equivalent to position 249 in human p53, by the recombinant polymerase chain reaction mismatched primer method. This p53 mutation resulted in the same change, an Arg-->Ser substitution, as in the human p53 gene at position 249. We now report that the protein product of this mutant mouse p53ser246 had properties similar to those of the wild-type protein when tested by binding to (i) monoclonal antibodies PAb246 and PAb240, ii) simian virus 40 large T antigen, and (iii) heat-shock protein. However, it had mutant-type transforming properties when tested for colony formation with an osteosarcoma cell line. It was not active, as is wild-type p53, in transcription activation of the muscle creatine kinase promoter. These properties are the same as those found in the p53trp248 product of the p53 mutation associated with the Li-Fraumeni syndrome. Although less is known about the human p53ser249 product associated with hepatocellular carcinoma, the mutant murine p53ser246 protein shares the known properties of the human gene product.

Aflatoxin B1↗
PubMed1995

Developmental control of transcription of the CAT reporter gene by a truncated mouse alphafetoprotein gene regulatory region in transgenic mice.

A truncated mouse alphafetoprotein (AFP) gene promoter/enhancer region was tested for its ability to regulate the expression of the Escherichia coli chloramphenicol acetyltransferase (CAT) reporter gene in the livers of transgenic mice. The AFP regulatory region lacked any AFP gene structural DNA, included one enhancer sequence together with the proximal promoter sequence, and an element believed to be responsible for the postnatal repression of AFP gene transcription. The neonatal livers of AFP/CAT transgenic mice showed a high level of CAT enzyme expression, which was dramatically reduced between 7 and 14 days after birth. The staining of liver sections with anti-CAT antibodies showed that this expression was limited to hepatocytes. In one lineage, reexpression of CAT in the adult liver could be achieved by restitutive proliferation of hepatocytes following partial hepatectomy or CCl4-induced necrosis; reexpression in young animals (3-4 weeks of age) was even greater. These studies show that a truncated AFP promoter/enhancer region functions in a tissue-specific and developmental stage-specific fashion, and may be used to control the expression of other genes in the livers of transgenic mice.

Animals↗
PubMed1995

Participation of small intraportal stem cells in the restitutive response of the liver to periportal necrosis induced by allyl alcohol.

To determine the involvement of different hepatocyte populations in response to periportal injury, the restitutive response to allyl alcohol (AA) injury was examined. Adult female Sprague-Dawley rats were injected intraperitoneally (IP) with 0.62 mmol/kg AA, killed at 6, 9, 12, 33, 57, 81, and 153 hours after injection, and the livers were examined for injury and for restitutive proliferation by histology, autoradiography, and immunohistochemistry to detect alpha-fetoprotein (AFP), glutathione-s-transferase-p (GST-p), desmin, leukocyte common antigen, albumin, and monoclonal antibodies to liver cells: OV-6, H-4, and T-6. AA produces variable periportal liver necrosis predominantly at 6 to 12 hours. Proliferation of hepatocytes throughout the hepatic cord is seen early after injury in nonnecrotic areas: predominantly in zone II, but also in zones I and III, including some cells adjacent to the central vein. Within 2 to 3 days the necrotic zones are filled with small cells and by 1 week the liver architecture is essentially restored. During the active restitutive reaction from the immediate periportal rim the following cell phenotypes are seen: null cells: -->(AFP+, OV-6-, GST-p-) cells-->(AFP-, OV-6+, GST-p+) cells-->large (AFP-, OV-6-, GST-p-, H-4+) liver cells. Albumin staining was negative. We conclude that restitutive proliferation of periportal necrosis induced by AA appears to be accomplished by proliferation of intraportal (?stem) cells whose progeny differentiate and eventually repopulate the necrotic zone.

1-Propanol↗
PubMed1994

Isokinetic force-velocity curves in patients following implantation of an individual total hip prosthesis.

There are only a few studies which could support conclusions concerning the strength of the muscles surrounding the hip joint and especially concerning the strength relationships following implantation of endoprostheses. The aim of this study was to examine the post-operative course of strength deficits in this musculature compared to clinical parameters. Fifty-eight patients between 30 and 67 years of age, in whom individual total hip prostheses were implanted, were clinically examined prior, 9 weeks and 6 months after surgery. Moreover, the maximum isometric strengths of abductors, flexors, and rotator muscles as well as maximum isokinetic strengths of the extensors and flexor musculature at 60 degrees/s and 120 degrees/s were measured. The flexor and extensor musculature already showed a clear increase in maximum strength after 9 weeks and 6 months. By contrast, the isometric strengths of the rotators increased only slightly, the abductor strength decreased after 9 weeks to below the preoperative baseline level and attained this level again only after 6 months. The clinical parameters Trendelenburg sign, limping, and walking capacity were clearly improved after 6 months, but no correlation to the abductor strength could be demonstrated. It is concluded that limp-free gait can be attained even without maximum strength increase in the abductors, which are important for fluid gait, at least for short distances. The importance of regular training of the rotator and abductor musculature in coxarthrosis is emphasized to delay limitation of movement and decreased strength in the sense of a capsule pattern.

Adult↗
PubMed1994

[The problem of radiation exposure during radiography of the entire spine].

The stimulus for this investigation concerning radiation exposure during radiography of the spine, particularly in children with scoliosis, is the fact that there are no data in the literature. In 16 series of measurements we studied the effect of grids, kilovoltage, focus-film distance and film-screen systems using dosimeters. The use of grids led to a 5-7 times increase in radiation dose compared with exposures without grids. For this reason grids are not recommended for serial examinations in cases of scoliosis. It is easier to evaluate the spine on a single large film than on several small films and radiation dose is also halved. Therefore, the use of large single films is recommended, particularly for children and adolescents.

Adolescent↗