bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasminogen activators in oesophageal carcinoma
Authors: Hewin D F , Savage P B , Alderson D , Vipond M N 
Published: March 2007

Abstract
The expression of components of the plasminogen activator system was investigated in patients with oesophageal carcinoma. Tumour and normal mucosa were obtained from resected oesophageal carcinomas and antigens were measured by enzyme-linked immunosorbent assay. Median levels of urokinase plasminogen activator (uPA) and the uPA receptor were higher in carcinoma than in matched normal mucosa (squamous cell carcinoma: uPA 4·05 versus 0·66 ng antigen per mg protein, uPA receptor 1·95 versus 0·50 ng/mg, n = 10, P &lt; 0·05; adenocarcinoma: uPA 2·16 versus 0·61 ng/mg, uPA receptor 2·01 versus 0·49 ng/mg, n = 8, P &lt; 0·05). Tissue plasminogen activator (tPA) level was lower than control values in squamous cell carcinoma but not in adenocarcinoma (1·97 versus 4·70 ng/mg, P &lt; 0·05). There was no difference in plasminogen activator inhibitor (PAI) 1 level between carcinoma and normal mucosa. The PAI-2 level was lower than that in normals in adenocarcinoma only (6·0 versus 64·77 ng/mg, P &lt; 0·05). These data support the hypothesis that membrane-bound uPA has a role in the breakdown of extracellular matrix in invasive oesophageal carcinoma.
Randomized trial of blunt-tipped versus cutting needles to reduce glove puncture during mass closure of the abdomen
Authors: Hartley J E , Ahmed S , Milkins R , Naylor G , Monson J R T , Lee P W R 
Published: March 2007

Abstract
Eighty-five consecutive patients were randomized to undergo mass closure of the abdomen with no. 1 polydioxanone mounted on either a blunt-tipped (n = 46) or cutting (n = 39) needle. Gloves were changed before closure and tested for perforation afterwards using standard air or water techniques. Fourteen pairs of gloves were punctured when using a cutting needle, and three pairs when a blunt-tipped needle was used. The majority of punctures were to the non-dominant glove. The surgeon was aware of the puncture in eight of the 14 instances involving a sharp needle and in one of the three involving a blunt-tipped needle. Blunt-tipped needles, while not eliminating the risk, significantly reduced the incidence of surgical glove puncture (P &lt; 0·001, Fisher's exact test). The use of cutting needles for abdominal closure should be abandoned.
Localization of the transcriptional coactivator PGC‐1α to GABAergic neurons during maturation of the rat brain
Authors: Cowell Rita Marie , Blake Kathryn Rose , Russell James W. 
Published: March 2007

AbstractThe transcriptional coactivator peroxisome proliferator activated receptor γ coactivator 1α (PGC‐1α) can activate a number of transcription factors to regulate mitochondrial biogenesis and cell‐specific responses to cold, fasting, and exercise. Recent studies indicate that PGC‐1α knockout mice exhibit behavioral abnormalities and progressive vacuolization in various brain regions. To investigate the roles for PGC‐1α in the nervous system, we evaluated the temporal and cell‐specific expression of PGC‐1α in the normal developing rat brain. Western blot of whole brain homogenates with a PGC‐1α‐specific antibody revealed that PGC‐1α protein was most abundant in the embryonic and early postnatal forebrain and cerebellum. Using quantitative reverse‐transcriptase polymerase chain reaction (RT‐PCR), we determined that PGC‐1α mRNA expression increased most markedly between postnatal days 3 (P3) and 14 in the cortex, striatum, and hippocampus. Immunohistochemical and immunofluorescence analyses of brain tissue indicated that while PGC‐1α was found in most neuronal populations from embryonic day 15 to P3, it was specifically concentrated in GABAergic populations from P3 to adulthood. Interestingly, PGC‐1α colocalized with the developmentally regulated chemoattractant reelin in the cortex and hippocampus, and the survival‐promoting transcription factor myocyte enhancing factor 2 was highly concentrated in GABAergic populations in the striatum and cerebellum at times of PGC‐1α expression. These results implicate PGC‐1α as a regulator of metabolism and/or survival in GABAergic neurons during a phase of mitochondrial and synaptic changes in the developing brain and suggest that PGC‐1α may be a good target for increasing metabolism in GABAergic populations in neurodevelopmental and neurodegenerative disorders. J. Comp. Neurol. 502:1–18, 2007. © 2007 Wiley‐Liss, Inc.
Combining visual information from the two eyes: The relationship between isthmotectal cells that project to ipsilateral and to contralateral optic tectum using fluorescent retrograde labels in the frog, Rana pipiens
Authors: Dudkin Elizabeth A. , Sheffield Joel B. , Gruberg Edward R. 
Published: March 2007

AbstractThe frog nucleus isthmi (homolog of the mammalian parabigeminal nucleus) is a visually responsive tegmental structure that is reciprocally connected with the ipsilateral optic tectum; cells in nucleus isthmi also project to the contralateral optic tectum. We investigated the location of the isthmotectal cells that project ipsilaterally and contralaterally using three retrograde fluorescent label solutions: Alexa Fluor 488 10,000 mw dextran conjugate; Rhodamine B isothiocyanate; and Nuclear Yellow. Dye solutions were pressure‐injected into separate sites in the superficial optic tectum. Following a 6‐day survival, brains were fixed, sectioned, and then photographed. Injection of the different labels at separate, discrete locations in the optic tectum result in retrograde filling of singly labeled clusters of cells in both the ipsilateral and contralateral nucleus isthmi. Generally, ipsilaterally projecting cells are dorsal to the contralaterally projecting cells, but there is a slight overlap between the two sets of cells. Nonetheless, when different retrograde labels are injected into opposite tecta, there is no indication that individual cells project to both tecta. The set of cells that project to the ipsilateral tectum and the set of cells that project to the contralateral tectum form a visuotopic map in a roughly vertical, transverse slab. Our results suggest that nucleus isthmi can be separated into two regions with cells in the dorsolateral portion projecting primarily to the ipsilateral optic tectum and cells in the ventrolateral nucleus isthmi projecting primarily to the contralateral optic tectum. J. Comp. Neurol. 502:38–54, 2007. © 2007 Wiley‐Liss, Inc.
Pathology of cytoskeleton of liver cells: Demonstration of mallory bodies (alcoholic hyalin) in murine and human hepatocytes by immunofluorescence microscopy using antibodies to cytokeratin polypeptides from hepatocytes
Authors: Denk Helmut , Franke Werner W. , Dragosics Brigitte , Zeiler Ingrid 
Published: March 2007

A cytoskeleton fraction enriched in intermediate-sized filaments and resistant to high and low salt buffer containing Triton X-100 was prepared from dissociated mouse liver cells and mouse liver homogenates. One-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed a family of polypeptides in the relative molecular weight (Mr) range from 41,000 to 55,000, with two polypeptides (component A, Mr 55,000; component D, Mr 48,000) as major constituents. Antibodies to isolated cytokeratin components of lower molecular weights (48,000 and 45,000 to 41,000) decorated, in indirect immunofluorescence microscopy, a distinct cytoplasmic filament meshwork in hepatocytes of various species whereas antibodies to higher molecular weight components were less or even not effective. The antibodies also reacted with cytokeratin filaments present in epithelial cells of various other organs and species, confirming the widespread occurrence of immunologically related cytokeratin filaments in epithelial tissues. The antibodies to higher molecular weight components showed a higher affinity to cytokeratin filaments of epidermis, stratified epithelia, and myoepithelial cells compared to epithelial cells of other organs, including small intestinal crypt epithelium and secretory cells of the submandibular gland. These observations further support the biochemical and immunologic heterogeneity in the cytokeratin family.
Mallory bodies (MBs) present in murine and human livers specifically reacted not only with antibodies to lower molecular weight polypeptides, but also even more so with antibodies to higher molecular weight components, indicating (i) the relatedness of MB material to hepatocyte cytokeratin, and (ii) differences of exposed antigenic determinants of cytokeratin(s) during MB development. In polypeptide composition, MB material differed from hepatocyte cytokeratin by polypeptides of molecular weights in the range of 55,000 to 66,000, which is more reminiscent of the pattern of epidermal cytokeratin. The development of MBs was associated with severe derangement of the cytokeratin filament meshwork in the affected hepatocytes, as revealed by immunofluorescence microscopy, indicating that cytoskeletal material progressively coalesced and was incorporated into MBs. The results present the first demonstration of the hepatocyte cytokeratin meshwork and an example of a pathologic change of this structure. The observations suggest that liver disorders associated with MB development can be regarded as cytoskeleton diseases.
Transferrin receptors and the uptake and release of iron by isolated hepatocytes
Authors: Young Stephen P. , Aisen Philip 
Published: March 2007

Isolated rat hepatocytes accumulate iron from iron-transferrin by a process which is dependent on the temperature and on the transferrin concentration, and which is diminished by treatment of the cells with a proteolytic enzyme. These observations are consistent with a mechanism for iron uptake into hepatocytes involving the binding of iron-transferrin to a specific cell-surface receptor.
Apotransferrin is also able to bind to the hepatocyte but the apparent binding constant is about 35 times lower than that observed for the binding of iron-transferrin. The binding of apotransferrin to the cells is completely abolished by a low concentration of iron-transferrin. This suggests that the apotransferrin is binding weakly to the same receptor to which iron-transferrin binds and that there are no receptors on the surface of the hepatocyte specific for apotransferrin. In the absence of such specific-binding sites, apotransferrin may act as a passive acceptor of iron released from the hepatocyte.
Presence and meaning of anti-HBc IgM as determined by ELISA in patients with acute type B hepatitis and healthy HBsAg carriers
Authors: Kryger Peter , Mathiesen Lars R. , Aldershvile Jan , Nielsen Jens O. 
Published: March 2007

To evaluate the clinical implication of IgM antibody against hepatitis B core antigen (anti-HBc IgM), a consecutive series of 87 patients with acute type B hepatitis and 16 healthy carriers of hepatitis B surface antigen (HBsAg) were studied by a newly developed reverse ELISA technique.
Anti-HBc IgM was present for at least 2 months in 81 of the 82 patients with HBsAg at the time of admission. Seroconversion from HBsAg to anti-HBs was observed in 38 patients during the time of observation, and in all patients, anti-HBc IgM was present until clearance of HBsAg. Thirty-three of the 38 patients remained anti-HBc IgM positive, at least until the appearance of anti-HBs. Quantitation of anti-HBc IgM by ratio unit (RU) values revealed that 3 of 8 patients with RU values ≧5 for more than 6 months subsequently developed chronic liver disease, as compared to 1 of 72 patients with anti-HBc IgM above this level for less than 6 months.
Anti-HBc IgM was demonstrated in 3 of 5 patients with total anti-HBc titer above 1:100 despite the presence of anti-HBs. In these patients, anti-HBc IgM steadily decreased after the onset of illness indicating a recent acute hepatitis B infection.
Anti-HBc IgM was present in 12 of 16 healthy HBsAg carriers (75%). However, these 12 carriers had RU values between 2.5 to 5.5, compared with RU values above 5 (mean RU value 11.3) at the onset of illness in 80 of 82 HBsAg-positive patients with acute hepatitis.
Anti-HBc IgM seems to be a specific serological marker for recent or ongoing hepatitis B infection which may be useful in differentiation between hepatitis B infection with or without HBsAg and acute non-A, non-B hepatitis.
δ antigen in hepatitis B: Immunohistology of frozen and paraffin-embedded liver biopsies and relation to HBV infection
Authors: St. Öcklin Elisabeth , Gudat Fred , Krey Gunthild , Dürmüller Ursula , Gasser Markus , Schmid Martin , Stalder Georg , Bianchi Leonardo 
Published: March 2007

The finding that the recently described hepatitis B (HB)-associated delta antigen (δ Ag) is preserved in pronase-treated, formalin-fixed paraffin sections allowed a combined prospective and retrospective immunohistological study of its occurrence in 571 liver biopsies.
Among 116 frozen biopsies (69 HBAg seropositive, 47 HBAg seronegative) and 455 paraffin-embedded biopsies (296 HBAg seropositive, 159 HBAg-negative), δ Ag was found in 10 HBAg seropositive patients. With the exception of 1 patient with chronic persistent HB, all had chronic-active HB and none had acute HB; 5 patients were i.v. drug abusers. In follow-up biopsies, the δ Agpersisted with HBsAg for as long as 6 years. The expression of δ Ag showed similarities to the HBcAg system including nuclear localization, mixed nuclear cytoplasmic expression, and coexistence with anti-δ in blood.
The findings are compatible with the hypothesis that δ Ag represents a transmissible, defective viral agent which requires HBV as a helper and may modulate, but not terminate, ongoing HBV infection.
Hepatic lysosomal copper protein in dogs with an inherited copper toxicosis
Authors: Johnson Gerald F. , Morell Anatol G. , Stockert Richard J. , Sternlieb Irmin 
Published: March 2007

Hepatic copper overload inherited as an autosomal recessive trait in Bedlington Terriers is characterized by the presence of hepatocellular lysosomal granules of unusually high specific gravity and electron density which contain at least two thirds of the total hepatic copper.
Fractionation of homogenates of liver from such affected Bedlington Terriers yielded a low-speed pellet which contained the lysosomal granules. This fraction was used for isolation of a copper-binding protein by alkaline-reduction, solubilization, fractional acetone precipitation, and gel filtration. The purified protein yielded a single band on polyacrylamide gel electrophoresis and resembled other metallothioneins in containing 15 cysteine residues and 7 to 8 atoms of copper (but no zinc) per 54 amino acid residues. No methionine, histidine, or any aromatic amino acid was present. The accumulation of this lysosomal copper protein appears to be related to the primary genetic defect which underlies the hepatic copper toxicosis of the Bedlington Terrier.
Pigment Gallstone Formation in the Cholesterol–Fed Guinea Pig
Authors: Lamorte Wayne W. , Brotschi Erica A. , Scott Thayer E. , Williams Lester F. 
Published: March 2007

Female Hartley guinea pigs fed a 0.5% cholesterol–supplemented diet were found to form pigmented gallstones after 6 weeks (17/23) and 12 weeks (11/11), while only 2 of 44 animals fed a trace cholesterol diet formed gallstones over a comparable period. The light brown stones consisted primarily of aggregates of fine granular crystals, morphologically similar to calcium bilirubinate crystals. The stones were soluble in 0.1 N sodium hydroxide and were found to contain a substance which co–migrated with unconjugated bilirubin during thin–layer chromatography.
Despite hypercholesterolemia (202 ± 34 vs. 59 ± 22 mg per dl in controls, p < 0.05) and fatty infiltration of the liver, cholesterol–fed animals had a lithogenic index of only 0.22 ± 0.04 in gallbladder bile as compared to a lithogenic index of 0.02 ± 0.01 in animals fed the trace cholesterol diet. Accordingly, no cholesterol monohydrate crystals were found in any animals. Hematocrits among cholesterol–fed animals (47.6 ± 1.2%) were lower than those of controls (54.8 ± 1.3%, p < 0.05) probably as a result of the cholesterol–induced hemolytic anemia which has been reported by others in this species.
Fasting gallbladder volume was greater in cholesterol–fed animals (2.4 ± 0.18 ml) than in controls (1.7 ± 0.11, p < 0.0025), and a comparable increase in gallbladder dry tissue mass was found. There was no evidence of biliary obstruction, however, and the gallbladder contractile response to octapeptide cholecystokinin was comparable in both groups. The increase in gallbladder volume appeared to result from: (a) an increase in hepatic bile salt secretion with an associated increase in bile flow and (b) a decrease in the capacity of the gallbladder to absorb fluid from hepatic bile (6.0 ± 1.4 mg fluid per hr per mg tissue with cholesterol diet vs. 12.9 ± 0.9 in controls, p < 0.0005). Total bile salt concentration was also decreased in gallbladder bile of cholesterol–fed animals (13.79 ± 0.51 vs. 18.56 ± 2.19 mmoles per liter in controls, p < 0.05), probably as a result of increased hepatic bile flow and decreased gallbladder absorption. The absence of cholesterol gallstones in this model is consistent with the failure to supersaturate bile with cholesterol. The reasons for pigment gallstone formation are less clear but their occurrence may be the result of a cholesterol–induced hemolytic anemia.
T Lymphocyte Sensitization to Hbcag and T Cell–Mediated Unresponsiveness to Hbsag in Hepatitis B Virus–Related Chronic Liver Disease
Authors: Vento Sandro , Hegarty John E. , Alberti Alfredo , O'brien Charles J. , Alexander Graeme J.M. , Eddleston Adrian L.W.F. , Williams Roger 
Published: March 2007

Using a newly developed indirect T lymphocyte migration inhibition test, cell–mediated immunity to HBsAg and HBcAg was directly and simultaneously examined in a total of 21 patients with HBsAg–positive chronic liver disease (CLD), and in seven subjects whose sera contained anti–HBs (2 previous acute hepatitis B; 4 hepatitis B vaccine recipients and 1 chronic active hepatitis). T cell sensitization to HBcAg was invariably detected in the HBsAg–positive CLD patients tested (12/12), whereas T cell sensitization to HBsAg was not present in any of the patients (0/21). In contrast, T cell sensitization to HBsAg was present in all anti–HBs–positive subjects.
These results support the hypothesis that the cellular immune response to HBcAg, rather than to HBsAg, is implicated in the pathogenesis of HBsAg–positive CLD. Moreover, the observation that the addition of T cells from patients with HBsAg–positive CLD to T cells from anti–HBs positive subjects in a ratio of 1 to 9 reversed their sensitization to HBsAg, suggests that a hyperactivity of HBsAg–specific suppressor T cell population may be responsible for persistent HBs antigenemia.
Endocytosis and Binding of Asialoorosomucoid by Hepatocytes From Rats With Jejunoileal Bypass
Authors: Serbource-Goguel/Seta Nathalie , Borel Béatrice , Dodeur Michèle , Scarmato Pierre , Bourel Benoit , Feger Jeanne , Durand Geneviève 
Published: March 2007

Rats with Jejunoileal bypass were used to study the biological activity of the hepatic binding protein. Hepatocytes were prepared 11 weeks after surgical procedure, and presence of asialoo–rosomucoid in serum has been determined.
Compared to control rat hepatocytes, endocytosis of [3H]asialoorosomucoid by bypassed rat hepatocytes was decreased by about 60%. This was due to a decreased number of total and surface receptors. In most sera, an accumulation of asialoorosomucoid was found. A reduction of protein synthesis or turnover could be considered.
Detection of An Igm Antiidiotype Directed Against Anti–Hbs in Hepatitis B Patients
Authors: Troisi Catherine L. , Hollinger Blaine F. 
Published: March 2007

An IgM–specific anti–[anti–HBs] antibody was detected by radioimmunoassay using anti–IgM–coated beads and 125I–labeled anti–HBs. This antiidiotype was found only in the sera of hepatitis B virus–infected patients, both acute and chronic. However, not all HBsAg–positive patients exhibited this reaction, and activity was correlated with the presence of HBeAg. Approximately 93% of sera that contained antiidiotype activity also contained HBeAg. Conversely, 70% of the sera positive for HBeAg reacted in the IgM assay. No correlation was observed between the presence of antiidiotype and rheumatoid factor or elevated SGPT levels.
Two approaches were used to determine whether the reactive moiety was an IgM anti–[anti–HBs] as postulated or an IgM anti–HBs/HBsAg complex. It was shown that chicken anti–HBs sera, which does not share the common idiotype of human and other mammalian anti–HBs, did not block a positive reaction in this radioimmunoassay even though it specifically bound HBsAg. It was also demonstrated that treatment with polyethylene gylcol, which will precipitate IgM anti–HBs/HBsAg activity, did not precipitate the reactive moiety in 6 of 7 sera tested, lending further evidence to the existence of an IgM antiidiotype in these patients.
It is suggested that this antiidiotype directed against anti–HBs may be involved in a defective feedback mechanism resulting in the suppression of production of anti–HBs and maintenance of the carrier state.
Changes of Laboratory Variables With Time in Cirrhosis: Prognostic and Therapeutic Significance
Authors: Christensen Erik , Schlichting Poul , Fauerholdt Lis , Juhl Erik , Poulsen Hemming , Tygstrup Niels 
Published: March 2007

The time change of laboratory variables in cirrhosis was studied by analysis of data from 488 patients with cirrhosis included in a controlled clinical trial of long–term prednisone vs. placebo.
In the placebo group, a marked regression towards normal was seen within 3 months of entry into the trial (increase in serum albumin, acetylcholinesterase, cholesterol, hemoglobin and decrease in erythrocyte sedimentation rate). The subsequent course did not show a clear pattern, except for a slight increase in serum bilirubin and decrease in albumin. When studied in relation to the time of death in patients dying from a “hepatic” cause, marked increase in bilirubin and decrease in prothrombin index, albumin and cholesterol were seen in the year prior to death with little change before that time.
In the prednisone group, a more marked decrease in bilirubin, SGOT, alkaline phosphatase, γ–globulin, sulfobromophthalein retention, erythrocyte sedimentation rate and increase in leukocytes, prothrombin index and cholesterol were seen during the first 3 months. In relation to time of death from a “hepatic” cause, similar changes were seen as in the placebo group except that alkaline phosphatase increased and cholesterol did not decrease.
A beneficial effect of prednisone on survival, as expressed by a previously developed therapeutic index, was associated with decrease in SGOT, alkaline phosphatase and γ–globulin within the first 3 months. An increase in SGOT during prednisone seemed to be associated with harmful effects of therapy.