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B F King

Publications and source records attributed to B F King.

At least 91 records · Page 5Linked to original sources
PubMed1996

A novel G protein-coupled P2 purinoceptor (P2Y3) activated preferentially by nucleoside diphosphates.

A partial cDNA was isolated by hybridization screening of an embryonic chick brain library for P2Y purinoceptors. After extension to full length, it revealed an open reading frame that encoded a protein, P2Y3, of 328 amino acids that is nearest in sequence identity to the G protein-coupled P2 purinoceptors obtained by DNA cloning. Expression of P2Y3 in cRNA-injected Xenopus oocytes confirmed that this cDNA encodes a member of the metabotropic purinoceptor family, with a novel order for the relative activities of nucleotides. At 100 microM concentrations, ADP gave the highest activity, and UTP and UDP were also strongly active. When expressed in the human T cell line Jurkat, P2Y3 mediated transient increases in intracellular Ca2+ in response to various nucleotides. Again, an unusual agonist rank order was revealed, with uridine nucleotides being more potent than adenosine nucleotides and UDP being the most potent agonist tested (half-maximal concentration, 0.13 microM) and 10-fold more potent than UTP. 2-Methylthlo-ATP was of relatively low activity in both systems. The receptor transcript is expressed in brain, spinal cord, kidney, and lung and is highly abundant in the spleen but not in other peripheral tissues that we tested. The results indicated that P2Y3 is a previously unknown P2 purinoceptor subtype with a preference for nucleoside diphosphates.

Adenosine Diphosphate↗
PubMed1995

Characterisation of a recombinant P2Y purinoceptor.

We have previously cloned a cDNA encoding a G-protein-coupled P2 purinoceptor from chick brain and designated this as a P2Y1 purinoceptor (Webb, T.E., J. Simon, B.J. Krishek, A.N. Bateson, T.G. Smart, B.J. King, G. Bumstock and E.A. Barnard, 1993, FEBS Lett. 324, 219). Here, we describe the further characterisation of this recombinant receptor expressed in both simian kidney endothelial (COS-7) cells and Xenopus oocytes. In transfected COS-7 cell membranes, the recombinant receptor showed a high level of expression (Bmax = 7.9 +/- 2.2. pmol [35S]dATP alpha S bound/mg protein) and affinity (Kd = 6.6 +/- 0.3 nM). In these COS-7 cells, the activation of the implanted purinoceptor induced a suramin-sensitive formation of inositol 1,4,5-triphosphatic (1,4,5InsP3). Upon expression in Xenopus oocytes, ATP was the only natural nucleoside triphosphate to elicit a Ca(2+)-activated chloride current. The P2 purinoceptor antagonists suramin and Reactive Blue-2 were both able to inhibit this evoked current. Utilizing both expression systems, the binding affinity profile and the functional pharmacological profile of the agonists, the common series found was: 2-methylthioATP (2-MeSATP) > or = ATP > ADP beta S > ADP. These two agonist series and the lack of activity of adenosine, alpha, beta-methyleneATP (alpha, beta-meATP), 3'-O-(4-benzoyl) benzoyl-ATP (Bz-ATP) and UTP, together confirmed that this receptor is a specific subtype of the P2Y purinoceptors.

Adenosine↗
PubMed1995

Cyclohexylamine inhibits the adhesion of lymphocytic cells to human syncytiotrophoblast.

We have previously shown that lymphocytic cells adhere to cultured syncytiotrophoblast and that this may be important in the lymphocyte-mediated infection of trophoblast with the human immunodeficiency virus (HIV). During the course of studies aimed at investigating the role of cell surface carbohydrates in adhesion, it was discovered that a contaminant of commercial fucose-1-phosphate, dicyclohexylamine, inhibited MOLT-trophoblast adhesion. Dicyclohexylamine and the related compounds, cyclohexylamine and hexylamine, inhibited adhesion in a dose-responsive manner with half-maximal inhibition seen at about 4 mM. While the pressor effects of cyclohexylamine, the principal metabolite of cyclamate, are well known, this is the first report of an effect of this and related compounds on cell adhesion activity. The inhibitory effect was reversible and, at concentrations less than 25 mM, did not result in loss of cell viability. Several possible mechanisms of action of cyclohexylamine were examined in an attempt to explain the effect on adhesion. No evidence was found to suggest that the effects of cyclohexylamine were due to inhibition of polyamine synthesis, increase in intracellular Ca2+ concentration or to a lysosomotropic effect. The concentrations of cyclohexylamine used are within the range of plasma concentrations attainable in humans, raising the possibility that the in vitro effects described here may also occur in vivo. The results also suggest that caution should be used in the interpretation of results obtained from experiments where cell adhesion is blocked using exogenous monosaccharides that are in the form of dicyclohexylammonium salts. Appropriate controls must be included or, if possible, sodium, potassium or barium salts should be chosen.

Cell Adhesion↗
PubMed1995

Kinetics of HIV infection of human placental syncytiotrophoblast cultures: an ultrastructural and immunocytochemical study.

We previously demonstrated that syncytiotrophoblast (ST) cells from term human placentas could be infected when cocultured with HIV-infected lymphocytic cells. Here, we have used fluorescence microscopy and transmission electron microscopy to examine the kinetics of this infection process. Molt-4 clone 8 cells infected with HIV-1Lai or filtered supernatant from these cultures were incubated with ST cells for different times. In cell-associated infection, immunofluorescence microscopy revealed that some ST colonies were positive for HIV core proteins (p24,p55) after 1 hr. The number of positive colonies and the intensity of the ST-associated fluorescence increased with time. Transmission electron microscopy showed viral particles with HIV morphology associated with the ST cell surface at 1 hr. Immature virions with budding morphology were observed at 2 hr. In cell-free infection, positive p24,p55 staining was first detected in a few ST colonies at 4 hr. The number of positive colonies increased with time. At 24 hr, the fluorescence pattern and intensity resembled that seen with cell-mediated infection at 4 hr. Transmission electron microscopy revealed an increasing number of viral particles associated with the ST cell plasma membrane with respect to time, and budding virions first appeared at 8 hr. These results demonstrate that HIV infection of placental ST cells proceeds very rapidly in culture and that, furthermore, cell-associated infection of ST is much more efficient than the infection with cell-free virus.

Clone Cells↗
PubMed1995

Antagonism by SB 204070 of 5-HT-evoked contractions in the dog stomach: an in-vivo model of 5-HT4 receptor function.

The ability of 5-hydroxytryptamine (5-HT) to evoke contractile activity in the gastric Heidenhain pouch was measured in conscious dogs using a method in which 5-HT4 receptor-antagonist activity can be measured in-vivo. At doses of 5-HT which evoked short-lived measurable responses (5 or 10 micrograms kg-1, i.v.), it was found that this activity was greatly reduced by atropine (100 micrograms kg-1, i.v.), but was unaffected by methysergide, methiothepin, ketanserin (each at 100 micrograms kg-1, i.v.) or granisetron (10 or 100 micrograms kg-1, i.v.). At best SDZ 205-557 2-diethylaminoethyl-[2-methoxy-4-amino-5-chloro] benzoate; 100 micrograms kg-1, i.v.) reduced the action of 5-HT in 4/5 animals and increased it in the other but its effects were variable in magnitude and not consistently maintained. However, the more potent and selective 5-HT4-receptor antagonist SB 204070 (1-butyl-4-piperidinylmethyl 8-amino-7-chloro-1, 4-benzodioxan-5-carboxylate hydrochloride) dose-dependently antagonized the 5-HT-evoked contractions in all dogs tested. This action was reversible, but long-lasting with an effective half-life of 18.0h when administered at 1 microgram kg-1. The estimated ID50 value was 0.55 microgram kg-1.

4-Aminobenzoic Acid↗
PubMed1995

Evidence for a local role of inhibin or inhibin alpha subunits in compensatory ovarian hypertrophy.

The aim of this study was to determine whether immunoneutralization of inhibin altered compensatory ovarian hypertrophy. Crossbred postpubertal gilts actively immunized with a synthetic bovine inhibin peptide fragment (bINH) conjugated to human alpha globulins (HAG, n = 4 gilts) or HAG alone (control; n = 5) were unilaterally ovariectomized at mid-cycle. After unilateral ovariectomy, the remaining ovary was removed between day 8 and day 12 of the subsequent oestrous cycle. The number of corpora lutea per ovary was determined at each ovariectomy. Blood samples were collected at frequent intervals beginning 1 h before and continuing until the first oestrus after unilateral ovariectomy, and serum concentrations of FSH, LH, progesterone and oestradiol were determined. Inhibin antibody titres were estimated from the percentage of 125I-labelled bINH bound to serum diluted 1:4000. At unilateral ovariectomy, the number of corpora lutea per ovary was similar for bINH:HAG-immunized and control gilts (8.6 +/- 0.7 versus 7.6 +/- 0.6). During the next oestrous cycle after unilateral ovariectomy, the number of corpora lutea on each remaining ovary had doubled (P < 0.05) in controls compared with the number of corpora lutea per ovary in the previous cycle. In contrast, the number of corpora lutea remained unchanged in bINH:HAG-immunized gilts. Titre of anti-inhibin antibodies in bINH:HAG-immunized gilts was 9 +/- 1% at unilateral ovariectomy compared with 0% for controls. Alterations in serum concentrations of hormones after unilateral ovariectomy did not differ between treatment groups. Compensatory ovarian hypertrophy was blocked after unilateral ovariectomy in immunized gilts independent of alterations in serum hormones, duration of oestrous cycle, or normal ovulation rate per ovary.(ABSTRACT TRUNCATED AT 250 WORDS)

Alpha-Globulins↗
PubMed1995

Extrapulmonary lymphangioleiomyomatosis and lymphangiomatous cysts in tuberous sclerosis complex.

OBJECTIVE: To describe the clinical manifestations, imaging findings, and histologic features of extrapulmonary lymphangioleiomyomatosis (LAM) in the tuberous sclerosis complex (TSC). DESIGN: We retrospectively reviewed institutional medical records since 1940 to identify patients with TSC and extrapulmonary LAM. MATERIAL AND METHODS: Of 403 patients with TSC, 3 had pulmonary and extrapulmonary LAM and retroperitoneal lymphangiomatous cysts. The clinical, imaging, and histologic features of these three patients were summarized, including analysis of biopsy specimens by conventional histology, immunohistology, radiolabeled ligand-binding assays, and tissue culture. RESULTS: The three young women had characteristic dermatologic findings of TSC and pulmonary LAM. Two patients were of normal intelligence, and one had a recent history of contraceptive use. All three patients had intra-abdominal lymphangiomatous cysts, uterine LAM, and renal angiomyolipomas. Renal and uterine biopsy specimens demonstrated positive immunostaining for melanoma-related antigens and expression of estrogen and progesterone receptors by ligand-binding assay and immunohistology. Cells cultured from LAM tissue of one of the patients exhibited a mitogenic response to estradiol. CONCLUSION: Clinically significant extrapulmonary LAM is a rare manifestation of TSC and may occur in women with this disease who also have pulmonary LAM. The clinical features of these patients confirm the importance of sex steroids in the development of these lesions. Immunohistochemical findings suggest that LAM and angiomyolipomas have a neuroectodermal origin. The development of lymphangiomatous cysts in these patients is probably due to smooth muscle proliferation in lymph vessels, which can result in lymphatic obstruction.

Abdominal Neoplasms↗
PubMed1994

Developmental expression of Ki-67 antigen and proliferating cell nuclear antigen in macaque placentas.

Placental growth is largely determined by the proliferation of cytotrophoblast cells. However, the distribution of cytotrophoblast cells engaged in the cell cycle during placental development is poorly understood. Recently, antibodies have been developed that identify two proteins directly involved with DNA synthesis: Ki-67 protein and proliferating cell nuclear antigen (PCNA). Immunolocalization of Ki-67 and PCNA provides a measure of the proliferating cells in tissues. We examined, in macaque placentas, the spatiotemporal pattern of expression of these proteins during gestation. Tissues from 24 macaque placentas collected from 22-153 days of pregnancy were prepared for paraffin sections. Standard immunoperoxidase techniques were used to identify Ki-67 and PCNA. The proteins generally co-localized, although PCNA was usually represented in more cells than Ki-67. Early in gestation the cell columns contained many labeled cells. The cytotrophoblastic shell was occupied by numerous cells with PCNA positive nuclei, but few were reactive for Ki-67. By 45 days of pregnancy the immunolabeled cells in the cell columns were concentrated in the proximal regions, adjacent to the anchoring villus tips. The number of positive cells decreased by 100 days when the cell columns were diminished, leaving the anchoring villus tips buried in the shell. Labeled cells were rarely present in the shell at late pregnancy. The single layer of cytotrophoblast cells in the chorionic plate contained numerous reactive cells throughout early and mid-gestation. After approximately 100 days the cytotrophoblast layer of the chorionic plate was stratified over large areas. Soon thereafter few cells of the chorionic plate were labeled. The chorionic villi contained reactive cytotrophoblastic cells throughout gestation. Extravillous cytotrophoblast cells invading spiral arteries were sometimes labeled for PCNA but not Ki-67. We conclude that compartments of the placenta are distinguished by specific patterns of cytotrophoblast cell proliferation. Moreover, these patterns correspond to macroscopic growth parameters of the placenta. Evidence suggests that the macaque placenta slows its rate of diametrical growth at approximately 100 days of gestation. It is at about this time that the cell columns are absorbed into the trophoblastic shell and this pool of proliferating cells is diminished. The growth in diameter of the chorionic plate matches that of the shell. In this compartment also the architecture changes at about 100 days as the cytotrophoblast layer stratifies. This stratification may result from continued proliferation of cytotrophoblast cells when the diametrical rate of growth is decreasing. Soon thereafter, proliferation decreases in this compartment also. By contrast, labeled cells were found in chorionic villi throughout gestation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Ultrastructure and development of a thick basement membrane-like layer in the anchoring villi of macaque placentas.

BACKGROUND: Anchoring villi and cytotrophoblastic cell columns are important structural components involved in placental morphogenesis. We have previously described the presence of an unusual basement membrane-like layer (BMLL) that separates these placental compartments. The purpose of the present study was to identify developmental changes in the ultrastructure of the BMLL and to assess its changes in extracellular matrix composition over the course of gestation. METHODS: Conventional techniques were used to examine macaque placental tissue by transmission electron microscopy. Standard immunoperoxidase methods were used to identify type IV collagen, laminin and fibronectin in paraffin sections. RESULTS: Until day 35 of gestation the BMLL was 70-100 nm thick and appeared similar to basement membranes seen in other regions of the villus, although it usually lacked a lamina lucida along the surface adjacent to the cytotrophoblast cells. Immunohistochemistry revealed the presence of laminin and type IV collagen in the BMLL. By 53 days of gestation the BMLL had hypertrophied at the junction of the anchoring villus and cell column, measuring 2,000-5,000 nm in thickness. The BMLL retained immunoreactivity for laminin and type IV collagen. Ultrastructural examination revealed the presence of a new component in the form of 10 nm microfibrils. By 89 days of gestation the BMLL was not reactive for laminin or type IV collagen but otherwise maintained the structural organization seen at 53 days. No additional changes were observed in the BMLL during late pregnancy. CONCLUSIONS: The BMLL is a distinct extracellular matrix region that separates the distal aspect of the anchoring villus from the proximal portion of the cell columns. Evidence indicates that adjacent cytotrophoblast plays a prominent role in the production of the BMLL. The BMLL may serve to organize this complex tissue by separating fetal mesenchyme from cytotrophoblast cells that are proliferating, differentiating, and migrating. Modifications to the composition of the BMLL may indicate changes in the role this matrix plays in the development of the placenta.

Animals↗
PubMed1994

Differentiation of the chorionic plate of the placenta: cellular and extracellular matrix changes during development in the macaque.

BACKGROUND: The chorionic plate forms the fetal side of the placental disc, and its proper growth and development is important to the formation of a normal placenta. The development and structure of the chorionic plate has received little attention. Therefore, we have conducted a developmental and immunohistochemical study of the chorionic plate of the macaque placenta. METHODS: Conventional light and transmission electron microscopy techniques were used to study macaque placental tissues collected from 22 days of gestation to near term. Standard immunoperoxidase methods were used to identify type IV collagen, laminin, and fibronectin in paraffin sections. RESULTS: Early in gestation the chorionic plate trophoblast consisted of an outer layer of syncytiotrophoblast and a single underlying layer of cytotrophoblast. Beginning at about 100 days of gestation, the cytotrophoblast layer became stratified. The cytotrophoblast cells also became surrounded by variable amounts of extracellular matrix containing type IV collagen, laminin, and fibronectin. Ultrastructurally, the matrix contained abundant 10-12 nm diameter microfibrils. During later gestation the syncytiotrophoblast had a tendency to separate from the cytotrophoblast. CONCLUSIONS: The chorionic plate of the macaque placenta undergoes several distinctive morphological changes over the course of gestation. During the period of rapid diametrical growth of the disc, the chorionic plate trophoblast consists of a layer of syncytiotrophoblast and a single layer of cytotrophoblast. During later gestation the cytotrophoblast layer stratifies at a time coincident with that at which diametrical growth of the disc slows. The cytotrophoblast cells of later gestation appear synthetically active and at least some of their products are extracellular matrix components that encapsulate many of these cells. These components include type IV collagen, laminin, fibronectin, and microfibrils.

Animals↗
PubMed1994

Effect of cytokines and anti-adhesion molecule antibodies on the adhesion of lymphocytic cells to human syncytiotrophoblast.

We have previously shown that lymphocytic cells bind to cultured syncytiotrophoblast and that this may be important in the lymphocyte-mediated infection of trophoblast with the human immunodeficiency virus (HIV). Leukocyte-trophoblast adhesion may also have implications for normal trophoblast function. The following experiments were designed to characterize the adhesion systems that mediate the attachment of lymphocytic cells to trophoblast. Adhesion was assayed by labelling lymphocytic MOLT-4, clone 8 cells with the fluorescent marker, calcein-AM, and then incubating them with primary cultures of human syncytiotrophoblast. Adhesion was stimulated by pretreatment of the trophoblast cultures with several cytokines either alone or together. These included tumor necrosis factor-alpha (TNF-alpha), granulocyte/macrophage-colony stimulating factor (GM-CSF), interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma). Stimulation was time- and dose-dependent. In contrast, preincubation of trophoblast cultures with anti-TNF-alpha antibodies for 2 days reduced MOLT adhesion by almost 50%. Preincubation with other anti-cytokine antibodies had no significant effect on adhesion. In other experiments, adhesion was measured in the presence of antibodies to known adhesion molecules. Adhesion was reduced by 50% in the presence of antibodies to alpha 4 integrin or beta 1 integrin. When present together, these antibodies reduced adhesion by almost 85%. Incubation in the presence of antibodies to the very late activation antigen-4 (VLA-4; alpha 4 beta 1 integrin) counter-receptors, VCAM-1 and CS-1, was without effect. Adhesion was also unaffected by antibodies to LFA-1, ICAM-1, ICAM-2, LFA-2, or LFA-3. These results suggest that adhesion is mediated by an adhesion system consisting of lymphocyte VLA-4 (alpha 4 beta 1) and an as yet unidentified counter receptor on trophoblast.

Antibodies↗
PubMed1994

Prejunctional autoinhibition of purinergic transmission in circular muscle of guinea-pig ileum; a mechanism distinct from P1-purinoceptor activation.

The role of prejunctional purinoceptors (P1-subtype) in the control of ATP-release from inhibitory motoneurons was investigated electrophysiologically, by studying fast purinergic inhibitory junction potentials (IJPs) in guinea-pig ileal circular muscle. Pressure ejections of adenosine and ATP (but not of alpha,beta-methylene ATP) onto circular muscle depressed the amplitude of fast IJPs, indicating the presence of prejunctional P1-purinoceptors. An adenosine (A1/2)-receptor antagonist, theophylline (10(-8)-10(-4) M), increased the amplitude of fast IJPs in a dose-related manner (EC50 = 17.5 microM), suggesting the existence of a basal 'adenosine tone' that regulated ATP-release from ileal motoneurons. However, three methylxanthine derivatives, caffeine (10(-8)-10(-4) M), 3-isobutyl-1-methylxanthine (IBMX; 10(-8)-10(-4) M) and the potent A1-receptor antagonist 1,3-dipropyl-8-(2-amino-4-chlorophenyl)-xanthine (DPCPX; 10(-8)-10(-4) M), failed to potentiate fast IJPs and placed in doubt the existence of this inhibitory adenosine tone. Caffeine and IBMX, but not DCPCX, hyperpolarised ileal circular muscle in a dose-related manner and reduced IJP-amplitude; DPCPX did not alter the amplitude of IJPs. The non-specific inhibitor of phosphodiesterases, Ro-20-1724 (5 x 10(-7)-5 x 10(-5) M), increased the amplitude of fast IJPs, mimicking the actions of theophylline. To this extent, facilitation of inhibitory transmission appeared to involve phosphodiesterase inhibition and modification of intra-axonal cAMP levels and phosphorylation of intra-axonal protein kinases. The phenomenon of IJP rundown, presumed to be a manifestation of prejunctional autoinhibition, was studied using theophylline and DPCPX as A1-receptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Testicular microlithiasis: imaging appearances and pathologic correlation.

PURPOSE: To determine the spectrum of sonographic findings, clinical implications, and pathologic correlation in patients with testicular microlithiasis (TM). MATERIALS AND METHODS: The cases of 42 patients with the characteristic appearance of TM on sonograms were retrospectively evaluated for the number, pattern, and distribution of echogenic foci and for associated intratesticular abnormalities. Medical records and pathologic reports were reviewed. RESULTS: Considerable variation was found in the number and distribution of occurrences of TM (five to 60 echogenic foci per transducer field). In some patients, peripheral clustering was seen. Most patients demonstrated side-to-side symmetry, but asymmetric distribution was seen in eight patients and unilateral foci were seen in one patient. In 17 patients, a germ cell neoplasm was seen. One additional patient had a focal lesion that was proved to be an infarct. CONCLUSION: TM has a characteristic sonographic appearance. Because of the 40% occurrence of primary testicular neoplasm in association with it, TM cannot continue to be considered a benign finding.

Adolescent↗
PubMed1994

Renal cell carcinoma in autosomal dominant polycystic kidney disease.

To provide information on the clinical presentation, diagnosis, pathology, and biologic behavior of renal cell carcinoma in patients with autosomal dominant polycystic kidney disease (ADPKD), three cases seen at this institution between 1955 and 1992, as well as the cases reported in the literature, were reviewed in detail. No male predominance was observed (12 men, 13 women) in the 25 patients who met the inclusion criteria. The age of presentation was earlier than that seen in the general population (45 versus 61 yr). Fever, night sweats, and weight loss were prominent at presentation. Fever is a more common presenting symptom of renal cell carcinoma in ADPKD (32%) than in the general population (7%). Twenty percent of the patients had metastatic disease at presentation. Even with computed tomography and magnetic resonance, the diagnosis was difficult and often delayed, and the accumulation of 111In-labeled white blood cells can wrongly suggest a cyst infection. Renal cell carcinoma in ADPKD is more often concurrently bilateral (12 versus 1 to 5%), multicentric (28 versus 6%), and sarcomatoid in type (33 versus 1 to 5%) than in the general population. Because previous studies have failed to demonstrate a higher prevalence of renal cell carcinoma in ADPKD, this information suggests either a malignant potential restricted to a small subset of patients with this disease or an alteration in the biologic behavior of renal cell carcinoma when it develops in the setting of ADPKD.

Adult↗
PubMed1994

Hepatic venous outflow obstruction in autosomal dominant polycystic kidney disease.

To discuss the clinical presentation, diagnosis, and treatment of hepatic venous outflow obstruction as a complication of polycystic liver disease, four cases diagnosed and treated at our institution have been reviewed and the information from six previously published case reports has been summarized. Eight of the 10 patients were women. All presented with severe ascites. Nine had polycystic kidneys. Three had moderate-to-advanced renal insufficiency, four were on hemodialysis, and one had a renal allograft. Possible predisposing factors were identified in seven patients; the most common was recent abdominal surgery, which, in three cases, was a bilateral nephrectomy. All patients had extrinsic compression of the hepatic veins and the inferior vena cava by hepatic cysts, and four had proven superimposed thrombosis of the inferior vena cava and/or hepatic veins. In the patients seen in this institution, magnetic resonance imaging was helpful in determining the level of obstruction in the inferior vena cava and the patency of the hepatic and portal veins. The outcome was worse in the patients with thrombosis; one recovered after a portocaval shunt, and the remaining three patients died. On the other hand, five of the six patients without thrombosis recovered after alcohol sclerosis of a large dominant cyst (one patient) or after hepatic resection and cyst fenestration (four patients). Hepatic venous outflow obstruction probably has been underrecognized as a cause of portal hypertension, ascites, and liver dysfunction in polycystic liver disease. The diagnosis can be reliably established with current imaging techniques, especially magnetic resonance imaging.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗