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C T Chiu

Publications and source records attributed to C T Chiu.

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

Uncoupling of bradykinin-induced phosphoinositide hydrolysis and Ca2+ mobilization by phorbol ester in canine cultured tracheal epithelial cells.

1. Regulation of the increase in inositol phosphates (IPs) production and intracellular Ca2+ concentration ([Ca2+]i by protein kinase C (PKC) was investigated in canine cultured tracheal epithelial cells (TECs). Stimulation of TECs by bradykinin (BK) led to IPs formation and caused an initial transient [Ca2+]i peak in a concentration-dependent manner. 2. Pretreatment of TECs with phorbol 12-myristate 13-acetate (PMA, 1 microM) for 30 min attenuated the BK-induced IPs formation and Ca2+ mobilization. The maximal inhibition occurred after incubating the cells with PMA for 2 h. 3. The concentrations of PMA that gave half-maximal (pEC50) inhibition of BK-induced IPs accumulation and an increase in [Ca2+]i were 7.07 M and 7.11 M, respectively. Inactive phorbol ester, 4alpha-phorbol 12,13-didecanoate at 1 microM, did not inhibit these responses. Prior treatment of TECs with staurosporine (1 microM), a PKC inhibitor, inhibited the ability of PMA to attenuate BK-induced responses, suggesting that the inhibitory effect of PMA is mediated through the activation of PKC. 4. In parallel with the effect of PMA on the BK-induced IPs formation and Ca2+ mobilization, the translocation and down-regulation of PKC isozymes were determined. Analysis of cell extracts by Western blotting with antibodies against different PKC isozymes revealed that TECs expressed PKC-alpha, betaI, betaII, gamma, delta, epsilon, theta and zeta. With PMA treatment of the cells for various times, translocation of PKC-alpha, betaI, betaII, gamma, delta, epsilon and theta from cytosol to the membrane was seen after 5 min, 30 min, 2 h, and 4 h treatment. However, 6 h treatment caused a partial down-regulation of these PKC isozymes. PKC-zeta was not significantly translocated and down-regulated at any of the times tested. 5. Treatment of TECs with 1 microM PMA for either 30 min or 6 h did not significantly change the KD, and Bmax receptor for BK binding (control: KD=1.7+/-0.3 nM; Bmax=50.5+/-4.9 fmol/mg protein), indicating that BK receptors are not a site for the inhibitory effect of PMA on BK-induced responses. 6. In conclusion, these results suggest that activation of PKC may inhibit the phosphoinositide hydrolysis and consequently attenuate the [Ca2+]i increase or inhibit independently both responses to BK. The translocation of pKC-alpha, betaI, betaII, delta, epsilon, gamma, and theta induced by PMA caused an attenuation of BK-induced IPs accumulation and Ca2+ mobilization in TECs.

Animals↗
PubMed1998

Effect of forskolin on endothelin-induced phosphoinositide hydrolysis and calcium mobilization in cultured canine tracheal smooth muscle cells.

1. The effects of increase in intracellular adenosine 3':5'-cyclic monophosphate (cAMP) on endothelin-1 (ET-1)-induced generation of inositol phosphates (IPs) and increase in intracellular Ca2+ ([Ca2+]i) were investigated in canine cultured tracheal smooth muscle cells (TSMCs). 2. Pretreatment of TSMCs with either cholera toxin (CTX; 10 microg ml(-1), 4 h), forskolin (10 microM, 30 min), or dibutyryl cAMP (1 mM, 30 min) inhibited ET-1-stimulated Ca2+ mobilization (by 23 +/- 5%, n = 8) and IPs accumulation (by 32 +/- 6%, n = 4). While after treatment with forskolin for 24 h, the cells retained the ability to respond to ET-1-induced Ca2+ mobilization to the same extent as the control group. 3. Forskolin (1-100 microM) inhibited the ET-1-induced increase in [Ca2+]i, but the lower concentrations had little effect on this response. The inhibitory effects of these agents produced both depression of the maximal response and a shift to the right of the concentration-response curve of ET-1 without changing the -logEC50 values. 4. The water-soluble forskolin analogue L-858051, 7-deacetyl-7beta-(gamma-N-methylpiperazino)-butyryl forskolin, significantly inhibited ET-1-stimulated IPs accumulation. In contrast, the addition of 1,9-dideoxy forskolin, an inactive analogue of forskolin, had little effect on stimulated responses. Moreover, SQ-22536, 9-(tetrahydro-2-furanyl)-9H-purin-6-amine, an inhibitor of adenylate cyclase, and both H-89, N-(2-aminoethyl)-5-isoquinolinesulfonamide, and HA-1004, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide, inhibitors of cAMP-dependent protein kinase (PKA), attenuated the ability of forskolin to inhibit ET-1-induced IPs accumulation. These results suggest that activation of cAMP/PKA was involved in these inhibitory effects of forskolin. 5. The locus of this inhibition of forskolin treatment on AlF4(-)-stimulated IPs accumulation was investigated in canine TSMCs. The AlF4(-)-induced IPs accumulation was inhibited by forskolin, supporting that G protein(s) are directly activated by AlF4- and uncoupled to phospholipase C by forskolin treatment. 6. We conclude that cAMP elevating agents inhibit ET-1-stimulated generation of IPs and Ca2+ mobilization in canine cultured TSMCs. Since generation of IPs and increases in [Ca2+]i are very early events in the activation of ET-1 receptors, attenuation of these events by cAMP elevating agents might well contribute to the inhibitory effect of cAMP on tracheal smooth muscle function.

Animals↗
PubMed1997

Purinoceptor-stimulated phosphoinositide hydrolysis in Madin-Darby canine kidney (MDCK) cells.

Extracellular nucleotides, acting through P2-purinoceptors, have been implicated in the regulation of ion transport in epithelia, including Madin-Darby canine kidney (MDCK) cells. In this study, experiments were conducted to characterize the P2-purinoceptor subtype on MDCK cells responsible for stimulating inositol phosphate (IP) accumulation using a range of nucleotide analogues. In Ca2+- and Mg2+-free Krebs-Henseleit solution (KHS), ATP, UTP, and ATPgammaS caused an increase in IP accumulation as a function of concentration with comparable kinetics. The order of potency for the nucleotide analogues was UTP = ATPgammaS > ATP = 2-chloro ATP (Cl-ATP) >> alpha,beta-methylene ATP (alpha,beta-MeATP) = 2-methylthio ATP (2MeSATP). Selective agonists for P1-, P2X- and P2Y-purinoceptors, such as N6-cyclopentyl adenosine, AMP, alpha,beta-MeATP, and 2MeSATP, had little effect. Stimulation of MDCK cells with maximally effective concentrations of ATP and UTP showed no additive effect and furthermore, ATP, UTP, and ATPgammaS induced cross-desensitization of the IP response, suggesting that ATP and UTP act upon a common nucleotide receptor, i.e. a P2U-purinoceptor. In Ca2+- and Mg2+-containing KHS, the concentration-response curves of ATP, UTP, and ATPgammaS were shifted to the right of those obtained in Ca2+- and Mg2+-free buffer, and asymptotic maxima were not reached, indicating that ATP4- and not MgATP2- or CaATP2- was the active agonist. Pretreatment of MDCK cells with pertussis toxin (PTX) inhibited ATP- and UTP-induced IP accumulation in a concentration-dependent fashion but did not completely abolish the IP accumulation, indicating that a PTX-sensitive G protein was partially involved in the IP response. In conclusion, ATP- and UTP-stimulated IP accumulation in MDCK cells appears to be mediated through the activation of P2U-purinoceptors coupled to a G protein that is partially sensitive to PTX. A form of nucleotide uncomplexed with divalent ions such as ATP4- seems to be the preferential agonist form for the purinoceptors on MDCK cells.

Adenosine Triphosphate↗
PubMed1997

Effect of forskolin on bradykinin-induced calcium mobilization in cultured canine tracheal smooth muscle cells.

The effects of increases in intracellular adenosine 3':5'-cyclic monophosphate (cyclic AMP) on bradykinin (BK)-induced generation of inositol phosphates (IPs) and Ca2+ mobilization were investigated in canine cultured tracheal smooth muscle cells (TSMCs). Pretreatment of TSMCs with either forskolin or dibutyryl cyclic AMP attenuated BK-stimulated responses. The inhibitory effects of these agents produced both a depression of the maximal response and a shift to the right of the concentration-response curves of BK. The water-soluble forskolin analogue L-858051, 7-deacetyl-7 beta-(r-N-methylpiperazino)-butyryl forskolin, significantly attenuated BK-stimulated IPs accumulation, while 1,9-dideoxy forskolin, an inactive forskolin, had little effect on IPs response. Moreover, SQ-22536, 9-(tetrahydro-2-furanyl)-9-H-purin-6-amine, an inhibitor of adenylate cyclase, and both H-89, N-(2-aminoethyl)-5-isoquinolinesulfonamide, and HA-1004, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide, inhibitors of cyclic AMP-dependent protein kinase (PKA), reversed the ability of forskolin to attenuate BK-stimulated IPs accumulation. The KD and Bmax, values of the BK receptor for [3H]BK binding were not significantly changed by forskolin treatment for 30 min and 4 h. The AlF4(-)-induced IPs accumulation was attenuated by forskolin, indicating that G protein(s) are directly activated by AlF4- and uncoupled to phospholipase C by forskolin treatment. These results suggest that activation of cyclic AMP/PKA might inhibit the BK-stimulated PI breakdown and consequently reduce the [Ca2+]i increases or inhibit independently both responses, which is distal to the BK receptor in canine cultured TSMCs.

Adenine↗
PubMed1997

Inhibition of 5-hydroxytryptamine-induced phosphoinositide hydrolysis and Ca2+ mobilization in canine cultured tracheal smooth muscle cells by phorbol ester.

1. Regulation of the increase in inositol-1,4,5-trisphosphate (IP3) production and intracellular Ca2+ concentration ([Ca2+]i by protein kinase C (PKC) was investigated in canine cultured tracheal smooth muscle cells (TSMCs). Stimulation of TSMCs by 5-hydroxytryptamine (5-HT) caused an initial transient [Ca2+]i peak followed by a sustained elevation of [Ca2+]i in a concentration-dependent manner. 2. Pretreatment of TSMCs with phorbol 12-myristate 13-acetate (PMA, 1 microM) for 30 min blocked the 5-HT-induced IP3 formation and Ca2+ mobilization. This inhibition was reduced after the cells had been incubated with PMA for 8 h, and within 48 h the 5-HT-induced Ca2+ mobilization reached the same extent as control cells. 3. The concentration of PMA that gave half-maximal inhibition of 5-HT-induced increase in [Ca2+]i was 4 nM. Pretreatment of TSMCs with staurosporine (1 microM) of GF109203X (0.1 microM), PKC inhibitors, inhibited the ability of PMA to attenuate 5-HT-induced responses, suggesting that the inhibitory effect of PMA was mediated through the activation of PKC. 4. In parallel with the effect of PMA on 5-HT-induced IP3 formation and Ca2+ mobilization, the translocation and down-regulation of PKC isozymes were determined by Western blot analysis in TSMCs. Analysis of cell extracts by Western blotting with antibodies against different PKC isozymes revealed that TSMCs expressed PKC-alpha, beta I, beta II, delta, epsilon, theta and zeta. With PMA treatment of the cells for various times, translocation of PKC-alpha, beta I, beta II, delta, epsilon, and theta from the cytosol to the membrane was seen after 5 min, 30 min, 2 h, and 4 h treatment. However, 24 h treatment caused a partial down-regulation of these PKC isozymes PKC-zeta was not significantly translocated and down-regulated at any of the times tested. 5. In conclusion, these results suggest that activation of PKC may inhibit the receptor-mediated phosphoinositide hydrolysis and consequently attenuate the [Ca2+]i increase or inhibit both responses independently. The translocation of PKC-alpha, beta I, beta II, delta, epsilon, and theta induced by PMA caused an attenuation of 5-HT-stimulated IP3 accumulation and Ca2+ mobilization in TSMCs.

Animals↗
PubMed1997

Three-dimensional magnetic resonance cholangiopancreatography for evaluation of obstructive jaundice.

The purpose of this study was to assess the diagnostic value of magnetic resonance cholangiopancreatography (MRCP) in studying the anatomy, sites, and causes of obstructive jaundice. From September 1994 to May 1996 three-dimensional MRCP was performed on 31 patients with abdominal pain and obstructive jaundice with a fast spin-echo T2-weighted pulse sequence. The images were reconstructed using maximal intensity projection, AVERAGE and SURFACE algorithm processing techniques at a graphics workstation. All the reconstructed images were compared with those obtained using conventional cholangiographic techniques, such as endoscopic retrograde cholangiopancreatography, percutaneous transhepatic cholangiography and drainage, and intraoperative cholangiography. The patients' diagnoses included choledochal cyst (13), cholangiocarcinoma (five), choledocholithiasis (four), pancreatic head carcinoma (three), rhabdomyosarcoma (one), papillary Vater carcinoma (one), recurrent gastric carcinoma (one), ascaris (one), and biliary atresia (two). Extrahepatic biliary dilatation was present in all 13 patients with choledochal cyst; the pancreatic ducts and their entrance level to the common bile duct were observed in eight of these patients. The level of obstruction in patients with cholangiocarcinoma was well documented but the biliary tract of one patient with biliary atresia was not identified by MRCP. In one patient with biliary rhabdomyosarcoma, MRCP clearly delineated the extrabiliary extension of the tumor. In a patient with ascaris in the common bile duct an increase in signal intensity inside the digestive tract of the worm denoted fluid in its gut. Lithiasis was shown in all of the four patients with choledocholithiasis. Thus, MRCP is a useful tool in the assessment of biliary tract obstruction and its causes, and is a valuable addition to ultrasonography.

Adolescent↗
PubMed1996

Regulation of 5-hydroxytryptamine-induced calcium mobilization by cAMP-elevating agents in cultured canine tracheal smooth muscle cells.

The effects of increases in cellular adenosine 3'5'-cyclic monophosphate (cAMP) on 5-hydroxytryptamine-(5-HT-) induced generation of inositol phosphates (IPs) and increases in intracellular Ca2+ ([Ca2+]i) were investigated using canine cultured tracheal smooth muscle cells (TSMCs). Cholera toxin and forskolin induced concentration- and time-dependent cAMP formation with half-maximal effects (-logEC50) produced at concentrations of 7.0 +/- 0.5 and 4.9 +/- 0.4 respectively. Pretreatment of TSMCs with either forskolin or dibutyryl cAMP inhibited 5-HT-stimulated responses. Even after treatment for 24h, these agents still inhibited the 5-HT-induced Ca2+ mobilization. The inhibitory effects of these agents produced both depression of the maximal response and a shift to the right of the concentration response curves of 5-HT. The water-soluble forskolin analogue L-858051 [7-deacetyl-7beta-(gamma-N-methylpiperazino)-butyryl forskolin] significantly inhibited the 5-HT-stimulated accumulation of IPs. In contrast, the addition of 1,9-dideoxy forskolin, an inactive forskolin analogue, had little effect on this response. Moreover, SQ-22536 [9-(tetrahydro-2-furanyl)-9-H-purin-6-amine], an inhibitor of adenylate cyclase, and both H-89 [N-(2-aminoethyl)-5-isoquinolinesulphonamide] and HA-1004[N-(2-guanidinoethyl)-5-isoquinolinesulphonamide], inhibitors of cAMP-dependent protein kinase (PKA), attenuated the ability of forskolin to inhibit the 5-HT-stimulated accumulation of IPs. These results suggest that activation of cAMP/PKA was involved in these inhibitory effects of forskolin. The AlF4--induced accumulation of IPs was inhibited by forskolin, suggesting that G protein(s) are directly activated by AlF4-- and uncoupled from phospholipase C by forskolin treatment. These results suggest that activation of cAMP/PKA might inhibit the 5-HT-stimulated phosphoinositide breakdown and consequently reduce the [Ca2+]i increase or inhibit both responses independently.

Adenine↗
PubMed1996

Effect of cAMP elevating agents on carbachol-induced phosphoinositide hydrolysis and calcium mobilization in cultured canine tracheal smooth muscle cells.

The effects of increases in intracellular adenosine 3',5'-cyclic monophosphate (cAMP) on carbachol-induced generation of inositol phosphates (IPs) and increases in intracellular Ca2+ ([Ca2+]i) were investigated in canine cultured tracheal smooth muscle cells (TSMCs). The cAMP elevating agents, cholera toxin (CTX) and forskolin, induced concentration- and time-dependent cAMP formation with half-maximal effects (-logEC50) at concentrations of 7.6 +/- 1.3 g/ml and 4.8 +/- 0.9 M, respectively. Forskolin caused a concentration-dependent inhibition of carbachol-induced increase in [Ca2+]i with half-maximal inhibition (-logEC50) at 5.2 +/- 0.7 M. Pretreatment of TSMCs with either CTX (10 micrograms/ml, 4 h), forskolin (10-100 microM, 30 min), or dibutyryl cAMP (1 mM, 30 min) inhibited carbachol-stimulated Ca2+ mobilization and IPs accumulation. The inhibitory effects of these agents produced both depression of the maximal response and a shift to the right of the concentration-response curve of carbachol without changing the EC50 values. After treatment with forskolin for 24 h, carbachol-induced IPs accumulation and Ca2+ mobilization were close to those of control group. SQ-22536 [9-(tetrahydro-2-furanyl)-9H-purin-6-amine, 10 microM], an inhibitor of adenylate cyclase, and HA-1004 [N-(2-guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride, 50 microM], an inhibitor of cAMP-dependent protein kinase (PKA), attenuated the ability of forskolin to inhibit carbachol-induced IPs accumulation. Moreover, the inactive analogue of forskolin, 1,9-dideoxy forskolin, did not inhibit these responses evoked by carbachol, suggesting that activation of cAMP/PKA was involved in these inhibitory effects of forskolin. The KD and Bmax values of the muscarinic receptor (mAChR) for [3H]-N-methyl scopolamine binding were not significantly changed by forskolin treatment for 30 min and 24 h, suggesting that the inhibitory effect of forskolin is distal to the mAChR. The locus of this inhibition was further investigated by examining the effect of forskolin treatment on AIF4(-)-stimulated IPs accumulation in canine TSMCs. The AIF4(-)-induced response was inhibited by forskolin, supporting the notion that G protein(s) are directly activated by AIF4- and uncoupled to phospholipase C by forskolin treatment. We conclude that cAMP elevating agents inhibit carbachol-stimulated generation of IPs and Ca2+ mobilization in canine cultured TSMCs. Since generation of IPs and increases in [Ca2+]i are very early events in the activation of mAChRs, attenuation of these events by cAMP elevating agents might well contribute to the inhibitory effect of cAMP on tracheal smooth muscle formation.

Adenine↗
PubMed1996

Precore mutant of hepatitis B virus prevails in acute and chronic infections in an area in which hepatitis B is endemic.

By using an amplification-created restriction site method, the precore TAG mutant of hepatitis B virus was detected in 6 (75%) of 8 acute fulminant hepatitis B patients, 7 (58%) of 12 acute self-limiting hepatitis B patients, 35 (81%) of 43 hepatitis B virus surface antigen carriers with fulminant hepatitis, and 42 (70%) of 60 hepatitis B virus surface antigen carriers with chronic hepatitis. The precore TAG mutant prevails in acute and chronic hepatitis B of various severity in this area where hepatitis B is endemic.

Acute Disease↗
PubMed1996

Non-O1 Vibrio cholerae bacteremia in patients with cirrhosis: 5-yr experience from a single medical center.

OBJECTIVES: To assess the clinical features and susceptibility of cirrhotic patients to non-O1 Vibrio cholerae bacteremia and to provide our therapeutic experiences in this rare and high lethal infection. METHODS: Twenty-eight blood culture isolates of non-O1 V. cholerae were identified by our clinical microbiology laboratory between July 1989 and June 1994. Patients with underlying cirrhosis and the aforementioned bacteremia were retrospectively reviewed. RESULTS: Twenty-one cirrhotic patients (16 male, five female; mean age, 50.9 yr; range 28-67 yr) were identified and classified as Child B (6 cases) and Child C (15 cases). Bacteremic episodes occurred most often from March to September. Seafood ingestion (seven cases) and seawater exposure (two cases) were risk factors, but nosocomial infections were also noted in six cases. Presenting symptoms and signs included ascites (95.2%), fever (81%), abdominal pain (52.4%), diarrhea (33.3%), and cellulitis with bullae formation (19%). Concurrent spontaneous bacterial peritonitis was determined in 10 cases, seven with positive ascites cultures. Antibiotic therapy (either cephalothin with gentamicin or ceftriaxone alone) cured most of the bacteremic episodes. The overall case-fatality rate was 23.8%, but 75% of the deaths were observed in patients with skin manifestation. CONCLUSIONS: Patients with decompensated cirrhosis are susceptible to non-O1 V. cholerae bacteremia and should not ingest raw seafood or expose skin wounds to salt water. A high index of suspicion and early administration of antibiotics may lower the mortality rate.

Adult↗
PubMed1996

Hypoxemia in a cirrhotic patient caused by hepatopulmonary syndrome: a case report.

Hepatopulmonary syndrome (HPS) is the triad of liver disease, pulmonary vascular dilatation, and abnormal arterial oxygenation. We report a case with progressive orthodeoxia and platypnea who was proven to have HPS after serial investigations, including autopsy. This 61-year-old male is a case of alcoholic liver cirrhosis without any documented cardiopulmonary disorders before. However, he suffered from progressive dyspnea in his last one-year life. During that period, progressive severe hypoxemia, orthodeoxia and platypnea were detected. Serial non-invasive diagnostic approaches, including two-dimensional contrast enhanced echocardiography and technetium-99m labeled macroaggregated albumin (MAA) lung perfusion scanning, were performed and showed positive evidence of intrapulmonary shunting. Direct evidence of intrapulmonary vascular dilatation was finally proven by autopsy. Although this syndrome is not rare, clinical awareness of the association between liver disease and arterial oxygen desaturation is still inadequate. We report a case proved by typical clinical manifestation and complete investigation and review the literature to emphasize this important disorder.

Cyanosis↗
PubMed1996

Clinical challenge--an experience of spontaneous transmural rupture of the oesophagus in Taiwan.

In Taiwan, spontaneous oesophageal rupture is uncommon but the outcome is often lethal because of failure to make an early diagnosis. We have analysed clinical data, management and the risk factors that affect mortality for a consecutive series of 11 patients who had spontaneous oesophageal perforation between 1983 and 1994. The primary symptom was chest or abdominal pain, which was present in 100% of patients; 91% of patients had abnormal chest x-ray (63% pleural effusion, 46% pneumomediastinum, 37% subcutaneous emphysema). In our series of patients the lower thoracic area was the most common location of the perforation (80% of patients. There were no statistically significant differences in mortality due to age, underlying disease, perforation size, location or surgical methods. A poor prognosis seems to be correlated with the time elapsed between the perforation and treatment (especially if > 72 hours) (p < 0.05), respiratory failure (p < 0.05), and heavy contamination of the mediastinum (p < 0.05). The clinical findings depend on the location and time of perforation. History, chest x-ray and oesophagogram are the most useful diagnostic tools. Early diagnosis and treatment are mandatory for these patients.

Adult↗
PubMed1995

Risk factors of hepatocellular carcinoma with familial tendency.

Family history of hepatocellular carcinoma (HCC) has been identified as a risk factor of HCC. The pathogenesis is still uncertain. In order to evaluate the risk factors and to detect the small HCC. 721 asymptomatic family members (419 males and 302 females with a mean age of 40.21 years) of the index cases of HCC received a series of examinations including: serum GOT, GPT, alpha-fetoprotein (AFP). HBsAg, Anti-HCV, and abdominal ultrasonography (US). Of the 18 patients with liver tumor detected by US. 6 were proved to be HCC, 8 were hemangioma, and the nature of the rest was undetermined. The US found 22 with cirrhosis, 24 with chronic liver disease, 133 with fatty liver, and 14 with a liver cyst. The incidence of HCC in our study was 0.96% in males (4 of 419 cases), and 0.66% in females (2 of 302 cases) which was much higher than that in the general population of Taiwan (0.025% in males and 0.01% in females). The positive rate of HBsAg in the participants, including all the newly detected HCC patients, was 46.5% (335 cases) which was also higher than the prevalence in Taiwan (15-20%). Male, sibling and liver cirrhosis seemed to have higher risk. These results suggest that family members of patients with HCC have a high risk of developing HCC. The hepatitis B virus may be the most important link. Early diagnosis is possible by screening the family members by means of AFP and abdominal US.

Adult↗
PubMed1994

Absence of precore stop mutant in chronic dual (B and C) and triple (B, C, and D) hepatitis virus infection.

Sequences of hepatitis B virus (HBV) precore regions from 7 patients with HBV and hepatitis C virus (HCV) dual infection and 2 with HBV, HCV, and hepatitis D virus (HDV) triple infection were analyzed. Two patients, 1 with only acute HBV infection and 1 with only chronic HBV infection, were also included for comparison. All patients had antibodies against HBV e antigen (anti-HBe) except 1 with chronic hepatitis B and C. No precore stop mutation at codon 28 (TGG to TAG mutation) was found in 21 cloned sequences from the 7 patients with HBV and HCV infection, nor in 11 cloned sequences from 2 patients with HBV, HCV, and HDV infection. However, mutations in other positions of the precore region were observed in 2 patients with hepatitis B and C. In both cases, precore sequences with mutations in different positions were obtained from the same serum sample. No mutations were observed in other positions of the precore region in the 2 patients with hepatitis B, C, and D. The presence of anti-HBe in these patients was probably due to the low level of HBV replication and not to the presence of the precore stop mutant.

Adult↗
PubMed1994

Cholangiography of icteric type hepatoma.

OBJECTIVES: Icteric type hepatoma caused by floating tumor debris in the major bile duct was rare. Such cases were often incorrectly identified as biliary carcinoma or choledocholithiasis until pathological proof. The goal of this study was to analyze the cholangiograms of icteric type hepatomas, and to identify the characteristic cholangiographic features of this rare disease. METHODS: A retrospective analysis of 20 cholangiographies of icteric type hepatomas during a 10-yr period was carried out. RESULTS: There were 15 males and five females in this series. Seventeen (85%) patients were hepatitis B virus carriers, and liver cirrhosis was detected in 16 (80%) patients. Serum alpha-fetoprotein levels in 13 (65%) of the patients were over 400 ng/ml. The cholangiographic findings included: 1) intraductal filling defects resulting in partial or complete obstruction and ductal dilation in 14 cases (70%), 2) abrupt complete obstruction of the common hepatic duct with an irregular cut surface in three cases (15%), and 3) tumor encasement and stricture of the biliary system in three cases (15%). Management of these patients included hepatic resection, choledochotomies with T tube stenting, or PTCD. Most of them died within one-half year after diagnosis, but one patient in our series, who received hepatic resection, survived more than 70 months. CONCLUSIONS: It is important to recognize this group of patients. Because with proper management, good palliation or cure is possible. The cholangiographic appearances, when taken alone, are not diagnostic of icteric type hepatomas. Once these cholangiograms are seen in patients with associated risks of developing a hepatoma, such as liver cirrhosis, chronic viral hepatitis, and elevated serum alpha-fetoprotein, however, an icteric type hepatoma should be suspected.

Adult↗
PubMed1994

Separation of thoracopagus conjoined twins. A case report.

A pair of thoracopagus conjoined twins with a connection at the atrioventricular groove of both hearts and a huge conjoined liver were surgically separated. An aortopulmonary shunt was created for Twin B, a victim of complex congenital heart disease with hypoplastic right heart syndrome, who died 5 hours later. However, Twin A survived after prolonged endotracheal intubation and parenteral nutrition. He survived for 7 months, and went home, but finally died of sepsis. In reviewing 47 pairs of surgically separated thoracopagus conjoined twins, in 30 pairs of type A (Leachman's classification, completely separate hearts), 42 patients survived (70%); in 5 pairs of type B (atrial connection only), one patient survived (10%); in 9 pairs of type C (both atrial and ventricular interconnections), none survived; in 3 pairs of unknown type, 2 survived. Total survival rate of surgically separated thoracopagus conjoined twins was 47.9%. The survival rate was 38.2% in those operated in the neonatal period (n = 34) and 63.6% in those operated over 1 month of age (n = 44) (p = 0.016). In conclusion, thoracopagus conjoined twins are rare. Although its separation carries a high risk, especially in those with cardiac connection, this report confirmed that separation is still feasible under proper preparation and planning.

Electrocardiography↗