Identification of the CAD gene from Eucalyptus urophylla GLU4 and its functional analysis in transgenic tobacco.

Cinnamyl alcohol dehydrogenase (CAD) catalyzes the final step in lignin biosynthesis. The genus Eucalyptus belongs to the family Myrtaceae, which is the main cultivated species in China. Eucalyptus urophylla GLU4 (GLU4) is widely grown in Guangxi. It is preferred for pulping because of its excellent cellulose content and fiber length. Based on GLU4 and CAD gene expression, a Eucalyptus variety low in lignin content should be obtained using transgenic technology, which could reduce the cost of pulp and improve the pulping rate, and have favorable prospects for application. However, the role and function of CAD in GLU4 is still unclear. In the present study, EuCAD was cloned from GLU4 and identified using bioinformatic tools. Subsequently, in order to evaluate its impact on lignin synthesis, a full-length EuCAD RNAi vector was constructed, and transgenic tobacco was obtained via Agrobacterium-mediated transformation. A significant decrease in CAD expression and lignin content in transgenic tobacco demonstrated a key role for EuCAD in lignin biosynthesis and established a regulatory role for RNAi. In our study, the direct molecular basis of EuCAD expression was determined, and the potential regulatory effects of this RNAi vector on lignin biosynthesis in E. urophylla GLU4 were demonstrated. Our results provide a theoretical basis for the study of lignin biosynthesis in Eucalyptus.

[A murine model of local allergic rhinitis].

OBJECTIVE: To establish the murine models of local allergic rhinitis (LAR) and allergic rhinitis (AR) by using ovalbumin (OVA), and to investigate the relationship between them. METHODS: Thirty BALB/c mice were divided into 5 groups, (1) the nasally sensitized group (group A1) that was challenged with OVA by a 10 d procedure, (2) the control group of A1 that was challenged with phosphate-buffered saline (PBS), (3) the nasally sensitized group (group A2) that was challenged with OVA by a 25 d procedure, (4)the control group of A2 that was challenged with PBS, (5) the intraperitoneally sensitized group (group B) .The numbers of sneezing after final challenge were counted, and the serum OVA-specific immunoglobulin E (OVA-sIgE), interleukin (IL) -4, IL-13, IL-5 levels in nasal lavage fluid were measured by ELISA. Hematoxylin-eosin staining was performed to evaluate the histological change of nose and lung tissues. Graph Pad Prism 6 software was used to analyze the data. RESULTS: Nasally sensitized group A1 displayed LAR symptoms of sneezing and eosinophilic infiltrating, but without increased OVA-sIgE in serum on day 10 compared with the control group of A1(t=0.697, P>0.05), OVA-sIgE in serum of group A2(2.710±1.406)ng/ml reached to statistical significance and with airway remodeling on day 25 compared with the control group of A2((0.221±0.080)ng/ml, t=4.329, P<0.05). IL-5 and IL-13 in nasal fluid showed a significant increase in the nasally sensitized group A1, compared with the group A2(t values were 2.442, 2.804, P values were less then 0.05). CONCLUSIONS: A short time intranasal instillation with OVA could establish LAR murine model, continuing OVA challenge could increase serum sIgE level and with airway remodeling. LAR mice show a unique characteristic by expressing higher IL-5 and IL-13 in nose than AR mice, but sIgE in serum remains at a normal level.

Long-term results of Taiwan Pediatric Oncology Group studies 1997 and 2002 for childhood acute lymphoblastic leukemia.

The long-term outcome of 1390 children with acute lymphoblastic leukemia (ALL), treated in two successive clinical trials (Taiwan Pediatric Oncology Group (TPOG)-ALL-97 and TPOG-ALL-2002) between 1997 and 2007, is reported. The event-free survival improved significantly (P=0.0004) over this period, 69.3+/-1.9% in 1997-2001 to 77.4+/-1.7% in 2002-2007. A randomized trial in TPOG-97 testing L-asparaginase versus epidoxorubicin in combination with vincristine and prednisolone for remission induction in standard-risk (SR; low-risk) patients yielded similar outcomes. Another randomized trial, in TPOG-2002, showed that for SR patients, two reinduction courses did not improve long-term outcome over one course. Decreasing use of prophylactic cranial irradiation in the period 1997-2008 was not associated with increased rates of CNS relapse, prompting complete omission of prophylactic cranial irradiation from TPOG protocols, beginning in 2009. Decreased use of etoposide and cranial irradiation likely contributed to the low incidence of second cancers. High-risk B-lineage ALL, T-cell, CD10 negativity, t(9;22), infant, and higher leukocyte count were consistently adverse factors, whereas hyperdiploidy >50 was a consistently favorable factor. Higher leukocyte count and t(9;22) retained prognostic significance in both TPOG-97 and TPOG-2002 by multivariate analysis. Although long-term outcome in TPOG clinical trials is comparable with results being reported worldwide, the persistent strength of certain prognostic variables and the lower frequencies of favorable outcome predictors, such as ETV6-RUNX1 and hyperdiploidy >50, in Taiwanese children warrant renewed effort to cure a higher proportion of patients while preserving their quality of life.

Treatment results of the TPOG-NHL92 protocols for childhood non-Hodgkin's lymphomas in Taiwan: a report from the Taiwan Pediatric Oncology Group (TPOG)

A nation-wide chemotherapeutic trial for childhood non-Hodgkin's lymphoma (NHL) was conducted by the Taiwan Pediatric Oncology Group (TPOG). Four TPOG-NHL92 protocols based on stage and histology were activated in 1992: TPOG-92LD (treatment duration: 8 months) was used for localized (stages I/II) NHL with any histology, 92LB (2 years), 92SNC (5 months), and 92LC (1 year) for advanced (stages III/IV) lymphoblastic (LB), small non-cleaved cell (SNC), and large cell (LC) lymphoma, respectively. From January 1992 through June 1998, 200 children with newly diagnosed NHL from 13 member hospitals of TPOG were enrolled. There were 140 boys and 60 girls. Their ages at diagnosis ranged from 2.4 months to 18.3 years with a median of 8.2 years. There were 54 (27.3%) patients with LB, 94 (47.5%) with SNC including B-cell acute lymphoblastic leukemia (B-ALL), and 50 (25.2%) with LC. Stages I, II, III, and IV (including B-ALL) of the disease comprised 5%, 10%, 43%, and 42% of cases, respectively. There were 176 patients eligible for evaluation of treatment results. The remission rate of induction was 82.4%, induction failed in 22 (12.5%) patients, and nine patients died during induction. As of August 31, 1999, 26 patients relapsed, six died during remission, one patient developed secondary acute myelomonocytic leukemia, and 105 patients remained in continuous remission with a median remission duration of 49 months. The event-free survival (EFS) at 7 years was 63.5%, 61.5% and 65% for LB, SNC, and LC groups (P = 0.8298). The 7-year EFS for stages I/II, III, and IV of the disease was 73%, 68.9%, and 50.3% (P = 0.0212), respectively. We concluded that following the strategy of stratification of therapy, only disease stages had prognostic significance in this study. More efforts are needed to improve our treatment results.

Seroprevalence of cytotoxin-associated gene A positive Helicobacter pylori strains in Changle, an area with very high prevalence of gastric cancer in south China.

BACKGROUND: Helicobacter pylori, especially the CagA-positive strains, are closely associated with peptic ulcers and gastric cancers. We performed a large scale gastric cancer screening project and examined the prevalence of H. pylori and CagA-positive strains in Changle, China, an area with one of the World's highest gastric cancer mortality. We also compared the prevalence with that in Hong Kong which has one-tenth of the gastric cancer mortality of that in Changle. METHODS: A total of 2424 subjects in Changle and 523 subjects in Hong Kong had endoscopic examination and venesection. Sera were tested for anti-H. pylori antibody and anti-CagA antibody and correlated with endoscopic findings. RESULTS: In Changle, 80. 9% of the subjects were H. pylori carriers. Out of 551 carriers, 408 (74%) were positive for anti-CagA antibody. A total of 76% and 87% of the asymptomatic and gastric cancer patients were positive for anti-CagA antibody, respectively (P > 0.05). Compared to Hong Kong, there was a significantly (P < 0.0001) higher prevalence of CagA-positive strains in asymptomatic subjects in Changle (76%) than in Hong Kong (28%), but not in peptic ulcers or gastric cancers. CONCLUSIONS: Subjects in Changle had a high prevalence of H. pylori infection and a high prevalence of the CagA-positive strains. The contrast in the prevalence of CagA-positive strains, in asymptomatic subjects in two areas with differing gastric cancer mortality, supports the pathogenic role of CagA-positive strains in gastric carcinogenesis.

Differential Helicobacter pylori infection rates in two contrasting gastric cancer risk regions of South China. China Gastric Cancer Study Group.

BACKGROUND: Carriers of Helicobacter pylori are believed to have a three- to six-fold increased risk of developing gastric cancer. We have recently conducted a simultaneous cross-sectional population study on the prevalence of H. pylori infection in a cohort of asymptomatic adult volunteers in two contrasting gastric cancer risk regions of South China, Hong Kong and Changle of Fujian. Their mean annual gastric cancer mortality has been approximately 7.5 and 75/100 000 population, respectively, since the beginning of the last decade. The aim of this study was to evaluate if H. pylori prevalence bears any relationship to gastric cancer mortality rates in these two southern regions of China. METHODS: Sera were obtained from 397 volunteers in Hong Kong. They were tested for anti-H.pylori immunoglobulin (Ig) G antibody by using a commercial enzyme-linked immunosorbent assay (ELISA) kit. Volunteers of Changle (1456) had upper endoscopy examination and were also tested for anti-H. pylori IgG antibody by the same ELISA method. RESULTS: The overall H. pylori infection prevalence was significantly higher in Changle (80.4%) than in Hong Kong (58.4%; P< 0.01). The high prevalence is associated with more atrophic gastritis. The overall risk of gastric cancer in people of Changle is approximately five-fold that of Hong Kong (adjusted odds ratio 4.9, 95% CI 2.5-9.8). CONCLUSIONS: It is concluded that the prevalence of H. pylori infection rates bear a direct relationship to gastric cancer mortality rates in these two southern regions of China. Thus, H. pylori most likely plays a significant aetiopathogenetic role in gastric carcinogenesis in subjects living in Changle.

Differential north to south gastric cancer-duodenal ulcer gradient in China. China Ulcer Study Group.

There are suggestions that duodenal ulcer protects individuals from gastric cancer and that rice is ulcerogenic while wheat is gastro-protective. We aimed to examine the relationship of gastric cancer, duodenal and gastric ulcers in different geographical regions in China and identified dietary risk factors for duodenal ulcer and gastric cancer. The prevalence of peptic ulcer and gastric cancer among symptomatic patients in eight major cities, four each from the north and the south representing all the six defined regions of China were studied. Endoscopy and case records over a 10 year period were reviewed and cases of confirmed duodenal and gastric ulcer and gastric cancer, together with the total number of endoscopies performed per year, were recorded. Rates were expressed as cases/1000 endoscopies. Results were compared to another epidemiological study on diet and mortality in the same regions in China conducted at the same time. Duodenal ulcer rates were 2.4-fold higher in southern China than northern China, whereas gastric cancer rates were 1.6-fold higher in the north than in the south. Correlation studies showed for the first time an inverse linear relationship between the gastric cancer rates and the duodenal ulcer rates (r=-0.8076, P=0.015), as well as the duodenal ulcer: gastric ulcer ratios (r=-0.9133, P=0.002). Gastric ulcer rates were higher in southern China but did not correlate with the gastric cancer rates (r=0.1455, P=0.731). Duodenal ulcer rates were found to be related to daily rice intake (r=0.8554, P=0.029) and inversely related to daily wheat flour intake (r=-0.8472, P=0.033). Gastric cancer rates were not related to any dietary risk factors tested. We concluded there was an inverse relationship between gastric cancer rates and duodenal ulcer rates. Although duodenal ulceration and gastric cancer are both linked to Helicobacter pylori infection, the findings of this study indicate independent additional aetiological factors for the pathogenesis of these conditions. Dietary factors such as rice or wheat intake may play a role.

Can misoprostol and omeprazole reduce nicotine and ethanol induced gastric mucosal injury? A quantitative macroscopic and microscopic analysis in rats.

We compared the effects of misoprostol, omeprazole and methylcellulose (control) on gastric mucosal injury induced by nicotine and/or ethanol. The results demonstrate that misoprostol and omeprazole each significantly reduce macroscopic injury and deep injury at a microscopic level (P < 0.05) induced by nicotine alone, ethanol alone or a combination of ethanol and nicotine. Misoprostol and omeprazole each reduced the leakage of fluorescein isothiocyanate-albumin into the interstitium in the gastric mucosa. Misoprostol and omeprazole are each effective in preventing injury induced by nicotine and ethanol and vascular factors are involved.

The gastric cytoprotective action of adenosine and prostaglandin E2 in rabbits.

The direct protective action of adenosine and prostaglandin E2 (PGE2) was examined in an isolated gastric gland preparation in rabbits. Ethanol (8%, v/v) incubation markedly increased the release of lactate dehydrogenase (LDH) and number of non-viable glands in the preparation. Both effects were prevented by PGE2 preincubation in a concentration (10(-6), 1.4 x 10(-5) or 2.8 x 10(-5) M)-dependent manner. The protective action was smaller in adenosine-treated groups, and yet the highest concentration (10(-4) M) of the compound also significantly inhibited the cytotoxic effects of ethanol. These findings indicate that both adenosine and PGE2 possess cytoprotective action on gastric glands in rabbits, but the former compound exerts its action beyond physiological concentrations. It is concluded that endogenous PGE2, but not adenosine may act as an ulcer modulator in the stomach.

Peripheral T-cell lymphoma in childhood: a report of five cases in Taiwan.

We encountered five children with peripheral T-cell lymphoma (PTL) at National Taiwan University Hospital (NTUH) from 1985-1989. The patients were four boys and one girl, aged between 5 and 13 years. The duration of prediagnostic symptoms varied from 1 month to 5 years. All had pyrexia and lymphadenopathy; one had a prolonged history of granulomatosis with repeated infection. Four had hepatosplenomegaly. One patient presented with diffuse pulmonary infiltration and impending respiratory failure. All patients were negative for human T-cell leukemia virus (HTLV)-I antibody, and positive for HBsAg. Four patients who had EBV-viral capsid antigen (VCA) IgG and who were IgM tested were positive for EBV-VCA IgG, but only two had evidence of active EBV infection. Tumor cell markers were examined and showed the following phenotypes: all patients were CD2, CD3, and CD7 positive but CD19 and CD20 negative; three patients were CD4 positive and CD8 negative; the other two patients were CD4 negative and CD8 positive. Four patients died 2-7 months after diagnosis. The remaining patient received allogeneic bone marrow transplantation and has survived free of disease for more than 22 months after transplant. Our five cases reconfirm the high frequency of diagnostic delay, the heterogenous immunophenotypes, high mortality, and poor responsiveness to conventional therapy for PTL. Bone marrow transplantation in the early stage might be a possible cure of this disease.

Long-term observation of pediatric aplastic anemia.

Fifty-nine verified cases of acquired aplastic anemia (AA), diagnosed at the Pediatric Department of the National Taiwan University Hospital from 1977 to 1987, were reviewed and analyzed. The demographic features showed a high relative incidence (acute myelogenous leukemia/AA ratio, 2.2/1), a high percentage of non-severe AA (39%) and a high association with hepatitis (20.8%). No evidence of hepatitis A, B or C virus infection was found in five cases of hepatitis-associated AA. No sex preponderance was noted in this pediatric series. The 10-year projected survival rate of the total series approached 55%. The crude two-year-survival and two-year-transfusion-free-survival rates were 59% and 44%, respectively, in the conservative therapy group treated with androgens and steroids; 36% and 32%, respectively, in patients with severe AA in the conservative therapy group; and 73% and 64%, respectively, in the aggressive therapy group treated with cyclosporin, anti-lymphocyte globulin or bone marrow transplant. The major causes of death were hemorrhage (44%) and infection (56%) in the conservative therapy group; but in the aggressive therapy group, two out of three deaths were related to therapeutic complications. Multivariate analysis of prognostic factors revealed that severity and treatment modality were independent risk factors. Only two out of 31 patients who survived more than two years (long-term survivors) experienced late mortalities. At two, five, seven and 10 years after diagnosis, 61%, 55%, 41% and 40% of the long-term survivors had inadequate hematopoietic recovery.

Nicotine induced gastric injury. A quantitative macroscopic and microscopic analysis of the protective effects of sucralfate and feeding.

Nicotine, while an important component of cigarettes, does not cause gross gastric mucosal damage, although its microscopic effect remains unknown. We have evaluated the histology and the microvascular permeability of (a) the effect of nicotine alone or in combination with ethanol on the gastric mucosa of rats and (b) the effect of feeding and sucralfate on the mucosa of rats treated with nicotine and ethanol. Mucosal injury was assessed histologically by the depth of injury and microvascular permeability by the leakage of fluorescein isothiocyanate-labelled albumin. Our results show that nicotine induced microscopic mucosal damage and accentuated the damage induced by alcohol. The damaging effects on mucosa of nicotine and ethanol, alone or in combination, were reduced by pretreatment with sucralfate. Similarly, feeding reduced the degree of mucosal injury. Nicotine and ethanol increased leakage of albumin into the interstitium and the leakage was reduced after sucralfate pretreatment. This study substantiates the adverse effect of smoking on mucosal damage. Vascular factors are probably involved in the pathogenesis.

The effect of misoprostol, omeprazole and sucralfate on nicotine- and ethanol-induced gastric injury and gastric mucosal blood flow: a comparative study.

Nicotine, which is thought to be responsible for part of the pharmacological effect of smoking, exacerbates gastric mucosal injury in rats. The effects of misoprostol (12.5 micrograms to 100 micrograms), omeprazole (12.5 mg to 100 mg) and sucralfate (50 to 400 mg) on gastric mucosal blood flow and mucosal injury induced by nicotine were studied in an ex vivo gastric chamber preparation in rats. Rats were pretreated with nicotine (25 micrograms/mL orally) for 10 days and ethanol was added to the gastric chamber preparation. Laser Doppler flowmetry was used to measure the gastric mucosal blood flow and mucosal damage (ulcer index) was assessed by the area of haemorrhagic lesions. The ulcer index was significantly higher in rats pretreated with nicotine. Treatment with misoprostol and omeprazole lowered the ulcer index significantly compared with controls. The peak and summation blood flows were lower in nicotine-treated rats but failed to reach statistical significance. The peak blood flow (blood flow at 45 min) and the summation blood flow were significantly higher with all doses of sucralfate, misoprostol and omeprazole than in controls (P less than 0.05). The increase in gastric mucosal blood flow was significantly higher with sucralfate and misoprostol than with omeprazole. We conclude that sucralfate, misoprostol and omeprazole prevent nicotine- and ethanol-induced gastric mucosal damage and are accompanied by an increase in gastric mucosal blood flow. This indicates that smoking exacerbates gastric mucosal injury and that cytoprotective and site-protective agents can reduce injury by these noxious agents.

Infant leukemia: an analysis of nine Chinese patients.

A study was made of the cellular and molecular characteristics of nine Chinese infants, consecutively presenting with acute leukemia. Five cases were acute lymphoblastic leukemia (ALL); four were acute nonlymphoblastic leukemia (ANLL). Hyperleukocytosis, hepatosplenomegaly, and poor response to conventional therapy were common features, and CNS involvement was detected at diagnosis in three cases. The blast cells from all five cases with ALL expressed early B-cell markers, i.e., HLA-DR+, CD19+, but CD10-. Terminal deoxynucleotidyl transferase (TdT) was present in blasts from four of the five cases and periodic acid-Schiff staining in blasts from two patients only. The leukemic cells of one patient also showed positive nonspecific esterase activity and expressed myeloid-associated antigens CD33 (My9), CD11 (OkM1), and CD14 (My4 and Mo2). Molecular analysis of leukemic cell DNA from this and two other patients showed rearrangement of the immunoglobulin (Ig) heavy-chain genes, but without any evidence of kappa light-chain gene rearrangement. T-cell receptor (TCR) genes remained in the germline configuration in these cases. Cytogenetic analysis showed translocation t(4;11) (q21;q23) in all four cases studied. In the group of ANLL, three cases belonged to the M4 and one to the M2 subtype. Chromosomal abnormality involving 11q23 was also detected in two patients: t(11;17)(q23;q11) and del(11)(q14q23) in each case respectively. Neither Ig nor TCR gene rearrangement was present in blast cells from patients with ANLL. The data indicate that chromosomal rearrangement of band 11q23 was quite common in Chinese infants with either form of leukemia, a finding that may have pathogenetic implications.

The influence of acute or chronic nicotine treatment on ethanol-induced gastric mucosal damage in rats.

The influences of acute or chronic nicotine pretreatment on ethanol-induced changes on gastric secretion, mucosal blood flow (GMBF), and glandular mucosal damage were studied in anesthetized rats. Ethanol administration decreased gastric acid secretion and GMBF, which were accompanied by a marked increase in gastric mucosal damage. Acute nicotine incubation 2 or 4 mg dose-dependently elevated both the titratable acid in the luminal solution and the gastric secretory volume; it also prevented the depressive action on GMBF and gastric mucosal damage in ethanol-treated animals. Chronic nicotine treatment for 10 days reduced the inhibitory action of ethanol on gastric acid secretion; the higher dose (25 micrograms/ml drinking water) potentiated the decrease of GMBF and the ulcerogenic property of ethanol. However, chronic treatment with the lower dose (5 micrograms/ml drinking water) had the opposite effects; it also markedly increased the gastric secretory volume. It is concluded that acute nicotine pretreatment elevates, whereas chronic nicotine pretreatment differentially affects GMBF. These effects could account for their protective or preventive actions on ethanol ulceration. The increase in nonacid gastric secretory volume by nicotine could partially explain its antiulcer effect. Furthermore, the acid secretory state of the stomach appears unrelated to the ulcerogenic property of ethanol.

An analysis of risk factor and survival in childhood acute lymphoblastic leukemia.

To study the survival and prognostic factor of childhood acute lymphoblastic leukemia, 78 newly-diagnosed cases between January 1982 and June 1987 in National Taiwan University Hospital were reviewed and analyzed. They were stratified into two groups, i.e. standard-risk (SR) and high-risk (HR), according to their pre-treatment leukocyte count and age. Following induction therapy, 97% of the SR patients and 80% of the HR patients attained complete remission. In the SR group, the 2- and 3-year failure-free survival rates were 37% and 24%, with a median survival of 16 months. In the HR group, failure-free survival at the second and third year were 11% and 4%, respectively, with a median survival of 5.3 months. Three factors are strongly related to induction failure, i.e. high leukocyte counts (greater than 50*10(9)/1), massive hepatomegaly and large lymph nodes. Univariate analysis of failure-free survival showed six variables with significant detrimental effects on eventual outcomes, i.e. high leukocyte counts (greater than 50*10(9)/1), meningeal leukemia, marked lymphadenopathy, age younger than 2 years and older than 10 years, massive hepatomegaly (greater than 6 cm), and high LDH level (greater than 800 u/1). However, statistical survival models should also determine the joint effects of the prognostic factors so that the relative importance of each factor can be assessed. High initial leukocyte count, disclosed by multivariate analysis, was the single most important factor detrimental to the continuance of complete remission (P = 0.0004). Preliminary results also revealed poor compliance and early relapse in this study. Possible causes of early failure are discussed. Conceptual education for family members, as well as management with effective cytoreductive therapies are urgently needed.

Dyskeratosis congenita preceded by severe aplastic anemia: report of one case.

Dyskeratosis congenita is a rare hereditary disease which usually manifests with skin hyperpigmentation, nail dystrophy, and leukoplakia of the mucous membrane (triad). This report describes a six-year-old boy with severe aplastic anemia who was later diagnosed to have dyskeratosis congenita. His unusual presentation was pancytopenia followed by leukoplakia of the tongue, hyperpigmentation of the skin and dystrophy of the nails. Treatment with horse anti-human lymphocyte immunoglobulin (ALG) for his aplastic anemia was not effective.

Extrahepatic biliary obstruction caused by cancer of non-liver origin in children: report of 5 cases.

Obstructive jaundice secondary to external compression of the extrahepatic bile duct caused by tumor of non-liver origin was found in 5 of 199 consecutive children with cancer between 1986 and 1988 at the Department of Pediatrics, National Taiwan University Hospital. Of the 5 patients, 2 had non-Hodgkin's lymphoma and the other 3 had acute promyelocytic leukemia, histiocytosis X and neuroblastoma, respectively. Extrahepatic biliary obstruction occurred as part of the initial presentation of malignancy in 3 cases, and later in the course of disease in the other 2 cases. In each instance, abdominal ultrasonography and computed tomography revealed dilatation of intrahepatic biliary trees due to mass compressing effects. A huge multilobulated tumor and multiple enlarged lymph nodes near the porta hepatis were found in all 3 patients who underwent an exploratory laparotomy. Wedge biopsy of the liver showed no cancer cell invasion. One case died before chemotherapy had commenced. The other 4 patients received chemotherapy and 3 of them received additional radiotherapy. Although jaundice and tumor regressed dramatically with this mode of treatments, subsequent recurrence of tumor without jaundice rapidly ensued in 3 patients. They all died, except 1 case, within 18 months from the occurrence of jaundice. This suggests that these patients were in an advanced stage of disease and should be diagnosed early and treated vigorously. Accordingly, cancer of non-liver origin, although rare, should be considered in the differential diagnosis of obstructive jaundice if survival is to be improved in these cancer children.

Late onset hemorrhagic cystitis after allogeneic bone marrow transplantation.

Three patients with acute myeloblastic leukemia, thalassemia major and aplastic anemia experienced hemorrhagic cystitis on the 23rd, 35th and 36th day respectively after allogeneic bone marrow transplantation. The conditioning regimens before transplantation comprised cyclophosphamide with or without busulfan and total lymphoid irradiation. The hematuria lasted from 5 to 45 days and then subsided after treatment. Multiple factors including the toxicity of chemotherapeutic agents, viral infection and graft-versus-host reactions may contribute to late onset hemorrhagic cystitis after allogeneic bone marrow transplantation. Adequate treatment to minimize urothelial damage from chemotherapy, screening for viral infection and controlling graft-versus-host disease are mandatory in decreasing the complication of late-onset hemorrhagic cystitis after bone marrow transplantation.