Biomedical subjects

M Shimada

Publications and source records attributed to M Shimada.

At least 217 records · Page 12Linked to original sources

PubMed1999

Induction of L-phenylalanine ammonia-lyase and suppression of veratryl alcohol biosynthesis by exogenously added L-phenylalanine in a white-rot fungus phanerochaete chrysosporium

The effects of exogenously added L-phenylalanine (L-Phe) on the activities of L-phenylalanine ammonia-lyase (PAL) and 3, 4-dimethoxybenzyl alcohol (veratryl alcohol, VA) biosynthesis in ligninolytic cultures of Phanerochaete chrysosporium were investigated. Increasing PAL activity was detected in low nitrogen (LN) culture but not in high nitrogen (HN) culture. The addition of L-Phe into the LN culture caused a 25-fold increase in enzyme activity, which clearly shows that L-Phe, a substrate of the enzyme, served as an inducer of PAL. The increase in activity of PAL triggered by nitrogen starvation was correlated with biosynthesis of VA. However, PAL induced by the added L-Phe did not promote VA biosynthesis but suppressed the biosynthesis probably due to NH(4)(+) released from L-Phe.

Journal Article↗

PubMed1999

Chemosensitivity and p53-dependent apoptosis in epithelial ovarian carcinoma.

BACKGROUND: Although p53 gene mutation frequently is observed in ovarian carcinoma, the function of the p53 gene in chemosensitivity has not been defined conclusively. The objective of the current study was to elucidate the relation between chemotherapy-induced apoptosis through the p53 pathway and chemosensitivity to ovarian carcinoma. METHODS: Tumor samples were obtained from 24 patients with epithelial ovarian carcinoma before and after chemotherapy with cisplatin, doxorubicin, and cyclophosphamide. Mutations in the p53 gene were screened by polymerase chain reaction-single-strand conformation polymorphism analysis and determined by cycle sequencing. Expression of the p53, Bax, and bcl-2 proteins and proliferating cell nuclear antigen (PCNA) were determined by immunohistochemical staining. Apoptotic cells were detected by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick-end labeling method. RESULTS: Of the 24 patients, 12 responded to chemotherapy and 12 did not. p53 gene mutation was observed in ten nonresponders and two responders. The incidence of p53 protein expression in tumors with the gene mutation was 58% (7 of 12) and was 17% (2 of 12) in tumors without the gene mutation. A significant reverse correlation between apoptotic index (AI) and labeling index (LI), determined by the percentage of PCNA positive cells, was observed in tumors after chemotherapy. AI was found to increase significantly after chemotherapy in tumors with the wild-type p53 gene (3.84 +/- 1.64 vs. 7.13 +/- 5.23) but LI did not change in either tumor type. The expression of Bax protein was significantly greater in tumors with the wild-type p53 gene after chemotherapy. bcl-2 protein expression did not relate to p53 gene status before or after chemotherapy. CONCLUSIONS: The current study suggests that p53-dependent apoptosis in tumors is strongly related to the chemosensitivity in epithelial ovarian carcinoma.

Apoptosis↗

PubMed1999

Experimental mumps virus-induced hydrocephalus: viral neurotropism and neuronal maturity.

In order to elucidate the relationship between virus neurotropism and neuronal maturity, two experiments were performed. First, mumps virus infectivity was compared among the different developmental stages of hamster brains inoculated with mumps virus by examining the immunohistochemical distribution of mumps virus antigen. Second, brain lesions resulting from mumps virus infection during the period of neuronal migration were histologically and ultrastructurally analyzed. Three groups of Syrian hamsters, Group E12 (fetuses on the 12th day of gestation), and Groups P2 and P30 (2 and 30 days old, respectively), were injected with mumps virus intraplacentally or intracerebrally. In Group P30, mumps virus antigen was observed specifically in ependymal cells and the choroid plexus. In addition to these areas, in Group P2, some neurons in layers II and III of the cerebral cortex also showed virus antigen immunoreactivity. In Group E12, mumps virus antigen accumulated primarily in the neuroepithelial cells within the ventricular zone. Neither specific intranuclear changes related to viral replication nor the formation of complete virions and nucleocapsids was observed. We conclude that mumps virus neurotropism to hamster brains is dependent on the degree of neuronal maturity and that mumps virus can induce an abortive infection and resultant neuronal cell necrosis in the immature developing hamster brain.

Aging↗

PubMed1999

Analysis of the chicken TBP-like protein(tlp) gene: evidence for a striking conservation of vertebrate TLPs and for a close relationship between vertebrate tbp and tlp genes.

TLP (TBP-like protein), which is a new protein dis-covered by us, has a structure similar to that of the C-terminal conserved domain (CCD) of TBP, although its function has not yet been elucidated. We isolated cDNA and genomic DNA that encode chicken TLP (cTLP) and determined their structures. The predicted amino acid sequence of cTLP was 98 and 91% identical to that of its mammalian and Xenopus counterparts, respectively, and its translation product was ubiquitously observed in chicken tissues. FISH detection showed that chicken tlp and tbp genes were mapped at 3q2.6-2.8 and 3q2.4-2.6 of the same chromosome, respectively. Genome analysis revealed that the chicken tlp gene was spliced with five introns. Interestingly, the vertebrate tbp genes were also found to be split by five introns when we focused on the CCDs, and their splicing points were similar to those of tlp. On the contrary, another TBP-resembling gene of Drosophila, trf1, is split by only one intron, as is the Drosophila 's tbp gene. These results support our earlier assumption that vertebrate TLPs did not directly descend from Drosophila TRF1. On the basis of these results together with phylogenetical exam-ination, we speculate that tlp diverged from an ancestral tbp gene through a process of gene duplication and point mutations.

Amino Acid Sequence↗

PubMed1999

Heparin-binding epidermal growth factor-like growth factor mRNA expression in neonatal rat brain with hypoxic/ischemic injury.

The neuronal expression of mRNA of heparin-binding epidermal growth factor-like growth factor (HB-EGF) was investigated in immature rat brains. Two rat models were used in this study. One was a hypoxic/ischemic (HI) brain injury model, and the other was an N-methyl-d-aspartate (NMDA) intracerebral injection model. The former model was made by permanent ligation of the left carotid artery and subsequent exposure to 2 h of hypoxia. After the HI insult, the HB-EGF mRNA was assessed by a Northern blot analysis. The levels of transcripts for HB-EGF in the cerebral cortex and the hippocampus of the ligated side were significantly higher than those of non-treated rats from 3 to 24 h after the insult. The spatial distribution of the mRNA of HB-EGF was also studied using in situ hybridization. Three to 24 h after the hypoxia, hybridization signals were intense in neuronal cytoplasm on the ligated side, but a focally decreased signal was seen in infarcted areas. Strongly increased mRNA expression was observed in the neurons surrounding the infarct. These results indicate that a neonatal HI insult induces a neuronal upregulation of HB-EGF immediately after hypoxia. In the latter model, the intracerebral NMDA injection also induced an immediate, strong upregulation of HB-EGF transcripts. Our results indicate that HB-EGF may act as a neuroprotective factor in the immature brain with HI injury by modulating the neurotoxic process which is mediated by overactivation of the NMDA receptor.

Animals↗

PubMed1999

Activation of the mouse inositol 1,4,5-trisphosphate receptor type 1 promoter by AP-2.

Inositol 1,4,5-trisphosphate receptor (IP3R) functions as a Ca2+ channel that increases the intracellular Ca2+ upon binding to inositol trisphosphates. IP3R is expressed ubiquitously and consists of a multigene family. Since the type 1 IP3R (IP3R1) is highly expressed in the cerebellar Purkinje cells and moderately in hippocampus in the mammalian central nervous system (CNS), it is regarded as a neural member of this gene family. In this work, we investigated transcriptional regulation of the mouse ip3r1 gene. A DNaseI footprinting assay demonstrated that a sequence from -95 to -75, designated as box-II, was a binding site for a cerebellum-enriched factor. A consensus sequence for AP-2 was located in box-II. An electrophoretic mobility shift assay with anti-AP-2 antibody revealed that AP-2 is capable of binding to box-II. Deletion analysis of box-II showed that flanking sequences beside the box-II motif were required for the stable binding. We demonstrated by transient luciferase assay that exogenously expressed AP-2 activated box-II-dependent transcription. Moreover, we showed that endogenous AP-2 induced by retinoic acid also activated transcription via box-II in P19 cells. In-situ hybridization of the mouse brain revealed that AP-2 was predominantly expressed in the cerebellar Purkinje cells and hippocampal CA1 region, where IP3R1 is also highly expressed. From these observations, AP-2 binding to box-II is thought to be responsible for IP3R1 gene regulation in the CNS.

Animals↗

PubMed1999

Structure and expression of the rat CYP3A1 gene: isolation of the gene (P450/6betaB) and characterization of the recombinant protein.

A P450 gene (P450/6betaB) of the CYP3A subfamily was isolated from a rat genomic library. Nucleotide sequencing of the exons revealed a high similarity with P450PCN1 cDNA (Gonzalez et al. (1985), J. Biol. Chem. 260, 7345-7441), but differed in 41 nucleotides, resulting in 11 changes and 2 deletions of amino acid residues. The P450/6betaB spanned about 30 kbp and consisted of 13 exons, and was in exon number and size identical with CYP3A2 gene except in the 6th exon, which was shorter than that of CYP3A2. 6beta-B mRNA, which may be transcribed from P450/6betaB, was detected on Northern blotting and by reverse transcription-polymerase chain reaction (RT-PCR). Profiles of the developmental change and induction by a treatment with several chemicals were very similar to those of P450PCN1 mRNA reported previously. P450PCN1 mRNA and gene, however, were not detected by PCR in rats. To determine whether P450/6betaB encodes an active protein, a cDNA was isolated and expressed. Expression of 6beta-B cDNA in COS-1 cells was carried out and revealed that the recombinant protein comigrated with purified P4506beta-4 previously identified as CYP3A1. The recombinant 6beta-B protein showed similar turnover rate and regioselectivity for testosterone with purified P4506beta-4 by the simultaneous addition of NADPH-cytochrome P450 reductase and cytochrome b5. These data suggest that P450/6betaB encodes an active P450 form corresponding to CYP3A1 and P450PCN1 reported previously does not exist in rats.

Amino Acid Sequence↗

PubMed1999

Melain G, a cysteine protease from green fruits of the bead tree, Melia azedarach: a protease affected by specific amino acids at P3 position.

A protease (melain G) was isolated from the greenish fruits of the bead tree, Melia azedarach var. japonica Makino. Melain G shares 110 identical amino acid residues (50%) with papain, 112 (51%) with actinidain, and 91 (41%) with stem bromelain. From the sites cleaved in the oxidized insulin B-chain and synthetic oligopeptide substrates by melain G, the enzyme preferred small amino acid residues such as Gly or Ser at the P2 position and negatively charged residues such as glutamic or cysteic acid at the P3 position. This is clearly different from the specificity of papain, which prefers the large hydrophobic amino acid residues such as Phe, Val, and Leu at the P2 position. Accordingly, it is presumed that the bottom of the S2 pocket of melain G is shallow due to the presence of a Phe residue, and a bulky P2 substrate (for example Phe residue) is not preferred by the enzyme. Negatively charged residues at the P3 position of substrates well suited the S3 site of melain G for making a salt bridge. It is likely that Arg61 is the S3 position of melain G by analogy with papain.

Amino Acid Sequence↗

PubMed1999

Isolation of cDNA, chromosome mapping, and expression of the human TBP-like protein.

TBP is an essential factor for eukaryotic transcription. In this study, we identified a human cDNA encoding 21-kDa TBP-like protein (TLP). The TLP ORF, carrying 186 amino acids, covered the entire 180 amino acids of the C-terminal conserved domain of human TBP with 39% identity and 76% similarity. FISH determined that human tlp gene was located at chromosome 6 region q22.1-22.3. Northern blot analysis demonstrated that TLP mRNAs were expressed in various human tissues ubiquitously. We found that the TLP proteins exist in multiple mammalian cells and chicken cells. Although the Drosophila TBP-related factor (TRF) is a neurogenesis-related transcription factor, expression of TLP was nearly constant throughout the neural differentiation of P19 cells. Unlike TRF, TLP did not bind to the TATA-box nor direct transcription initiation in vitro. Similarity between TRF and TLP was considerably lower (35 in alignment score) than that between Drosophila TBP and human TBP (88 in alignment score). Multiple amino acids critical for the TBP function were deleted or substituted in TLP. We suggest that TLP is not a bona fide vertebrate counterpart nor a direct descendant of TRF.

Amino Acid Sequence↗

PubMed1999

Palmar and plantar pads and flexion creases of genetic polydactyly mice (Pdn).

Attempts to gain a better understanding of the relationship between the epidermal ridge patterns (dermatoglyphics) and flexion creases on the volar aspects of human hands and feet and specific medical disorders led to a search for a suitable animal model, allowing studies of the fetal development of the pertinent structures. A common experimental animal, the rat (Rattus norvegicus), was found to be an excellent candidate, owing to the strong resemblance of the volar pads and flexion creases on its palmar and plantar surfaces to those of human subjects. A hereditary preaxial polydactyly mouse (Pdn) provides an opportunity to study the effects of this malformation on the surrounding morphological structures and, specifically, on the volar pads, i.e., the sites over which the dermatoglyphic patterns develop. The hands and feet of the wild-type (+/+) mice show no anomalies, and their major pad and flexion crease configurations correspond to those of normal rats. The heterozygous (Pdn/+) mice, in spite of having a thumb/big toe with a duplicated distal phalanx on their hands/feet, did not display any alterations in palmar/plantar pads. The homozygous (Pdn/Pdn) mice have a protrusion in the thenar area and one to three supernumerary digits on the preaxial portion of both the hands and feet. The effect of these anomalies was found to be limited to the pad and flexion crease configurations in the preaxial areas; the postaxial sites were not affected. The original number of pads on the thenar/first interdigital areas of Pdn/Pdn mice was apparently identical to that of the +/+ and Pdn/+mice. The preaxial protrusion, however, affected the number, size, and location of the pads observed in the newborn mice, resulting in varying pad configurations, such as fused and scattered pads or a pad cluster formed by gathering the neighboring pads. These pad modifications were induced by the preaxial plantar/palmar protrusion only and were not affected by the presence of supernumerary preaxial digits. In view of the similarities in the morphology and fetal development of human and mouse distal limbs, the present study is relevant to human subjects, particularly to the understanding of the significance of dermatoglyphic variations in individuals with specific medical disorders. Future studies of naturally occurring or experimentally induced limb malformations in mice or rats should provide valuable insights into the development of human hands and feet and into factors contributing to their congenital anomalies.

Animals↗

PubMed1999

Multicenter study of paroxysmal dyskinesias in Japan--clinical and pedigree analysis.

To investigate the clinical features of paroxysmal dyskinesias and carry out a pedigree analysis, we conducted a multicenter survey in Japan. A questionnaire was mailed to 229 medical institutions. A total of 150 patients with paroxysmal kinesigenic choreoathetosis (PKC), including 53 sporadic cases and 97 affected individuals from 32 pedigrees, were identified. The mean age of onset of PKC was 8.8 years, and 80% of the cases were men. Of the 32 pedigrees with familial occurrence, 18 (56%) were compatible with an autosomal-dominant inheritance (AD) with complete penetrance, and seven (22%) had AD with incomplete penetrance; the remaining seven were sibling recurrence cases with apparently healthy parents. In six of seven familial cases with incomplete penetrance, the disease gene was thought to be transmitted by clinically unaffected females. Paroxysmal dystonic choreoathetosis (PDC) was found in five cases, including two sporadic cases and three affected individuals from two pedigrees; the mean age of onset was 0.6 years, and a male predominance was noted (male:female = 4:1). There was one case of paroxysmal hypnogenic dyskinesia and one case of paroxysmal exertion-induced dyskinesia. There is an unexplained male predominance for paroxysmal dyskinesias. When the genetic defect of patients with paroxysmal dyskinesias is identified, the pathophysiology of the disease will become more clear.

Adolescent↗

PubMed1999

Evaluation of a hybrid artificial liver using a polyurethane foam packed-Bed culture system in dogs.

BACKGROUND AND AIMS: We developed a polyurethane foam packed-bed culture system of hepatocyte spheroids as a hybrid artificial liver (PUF-HAL), which was effective for recovery from liver failure in rat experiments. In this report, the design of a scaled-up PUF-HAL for dogs is described and evaluated using a dog acute liver failure model. METHODS: Warm ischemic liver failure was induced with a portocaval shunt in each dog. The dogs were divided into two groups: (1) a control group (N = 4), in which each dog was attached to a PUF-HAL without hepatocytes for 9 h, and (2) a HAL group (N = 5), in which each dog was attached to a PUF-HAL with hepatocytes. Blood pressure, blood ammonia, blood glucose, serum creatinine, and other parameters related to liver function were compared between the two groups. RESULTS: In the HAL group, blood ammonia and serum creatinine levels were significantly lower, and blood pressure and blood glucose levels significantly higher, than those in the control group. CONCLUSIONS: The scaled-up PUF-HAL developed for large animals is useful as a liver support system in the dog acute liver failure model.

Ammonia↗

PubMed1999

Correlation of anatomic and hemodynamic features with aortic valve leaflet deformity in doubly committed subarterial ventricular septal defect.

The records of 153 patients with doubly committed subarterial ventricular septal defect (DCVSD) who underwent intracardiac repair were analyzed to evaluate factors responsible for aortic valve leaflet deformity. The patients were divided into two groups according to their echocardiographic and angiographic features as well as anatomic findings at operation: DCVSD without (17/153, 11.1%) and with arterial valve offsetting (136/153, 88.9%). Aortic regurgitation (AR) was much more prevalent in the patients with (50.0%) than in those without leaflet deformity (2.2%, P < 0.01). Arterial valve offsetting is one of the major contributing factors to the development of leaflet deformity, accounting for 5.9% in the patients without offsetting and 46.3% in those with offsetting (P < 0.01). Among the patients with arterial valve offsetting, the pulmonary-to-systemic pressure ratio was significantly higher (P < 0.01) in the patients without (0.76 +/- 0.14) than in those with leaflet deformity (0.36 +/- 0.12), suggesting that pulmonary hypertension might prevent the aortic valve leaflet from prolapsing in DCVSD. In addition, increased severity of aortic valve leaflet deformity and subsequent AR were observed with increasing age. These results suggest that aging and the presence of arterial valve offsetting as well as the absence of pulmonary hypertension might be factors responsible for aortic valve leaflet deformity and subsequent AR in DCVSD. The anatomic and hemodynamic features in DCVSD have a great impact on the development of aortic valve leaflet deformity and subsequent AR.

Adolescent↗

PubMed1999

The mechanism of hepatic graft protection against reperfusion injury by prostaglandin E1.

The purpose of this study was to evaluate the effect of prostaglandin E1 (PGE1) on protecting against hepatic endothelial cell damage and increasing graft viability after cold preservation and reperfusion, using an isolated perfused rat liver (IPRL) model. The grafts were divided into three groups, according to the cold preservation time and PGE1 administration, namely: 4h preservation (group 1, n = 9), 6h preservation (group 2, n = 9), and 6h preservation followed by PGE1 infusion (group 3, n = 9). After cold storage, the grafts were put on the recirculating IPRL system, then reperfused for 120 min at 37 degrees C with oxygenated Krebs-Henseleit buffer containing hyaluronic acid (HA). To examine the function of the sinusoidal endothelial cells and hepatocytes, serial measurements of HA, tumor necrosis factor-alpha (TNFalpha), thromboxane B2 (TXB2), acid phosphatase, and conventional parameters in the perfusate were made. After perfusion, the trypan blue exclusion test was performed to assess the presence of any microscopic sinusoidal lining cell damage. In group 3, the bile output and HA clearance were significantly greater, while glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, TNFalpha, TXB2, and acid phosphatase in the perfusate were significantly lower than in group 2. Histologically, less endothelial cell damage and hepatocyte damage than in group 2 was also confirmed. These results therefore suggest that the improvement of hepatic graft viability by PGE1 administration is mainly due to sinusoidal endothelial cell protection.

Acid Phosphatase↗

PubMed1999

Does preoperative chemotherapy cause adverse effects on the perioperative course of patients undergoing esophagectomy for carcinoma?

The aim of this study was to clarify whether preoperative chemotherapy caused adverse effects on the perioperative course of patients undergoing esophagectomy. A total of 42 esophageal cancer patients were entered into a randomized trial and were analyzed. Twenty-one patients were assigned to immediate surgery (Surgery Group). The other 21 received two 5-day courses of chemotherapy comprising cisplatin (70 mg/m2) on day 1, and fluorouracil (700 mg/m2) and leucovorin (20 mg/m2) on each of days 1 to 5 (chemotherapy group). Hospital mortality comprised of one patient (2.3%) who had undergone an operation in the beginning of this series at 21 days after chemotherapy. Thereafter, the interval between the chemotherapy and operation was prolonged, with the average being 35 +/- 7 days. Preoperatively, both the lymphocyte counts and serum albumin levels were not increased in the chemotherapy group of patients even though their body weights increased. In the chemotherapy group, the operation time and the blood loss were increased and, on the 1st postoperative day, the development of systemic inflammatory response syndrome was high but the level of C-reactive protein was low. The incidence of positive microbial cultures of sputum and/or wound discharge within 8 postoperative days was higher in the chemotherapy group (42.9%) than in the surgery group (4.8%). The host defense damage caused by chemotherapy may be prolonged and may show adverse effects in patients undergoing esophagectomy in the early postoperative period. Minimally, a 4-week interval between the completion of chemotherapy and operation is recommended for preventing surgical mortality related to the preoperative chemotherapy.

Aged↗

PubMed1999

Long-term results of the fenestrated Fontan operation. Progress of patients with patent fenestrations.

The fenestrated Fontan operation was introduced as a modification of the "completed" Fontan operation for patients with high risk factors, and low operative mortality has frequently been reported. However, use of the umbrella device is now restricted, and this procedure should be performed without subsequent closure. In this paper, we review our clinical experience with this procedure and discuss ongoing problems. Sixteen patients (4 tricuspid atresia and 12 other cardiac anomalies including 5 cases of univentricular heart) underwent the fenestrated Fontan operation (7 atriopulmonary and 9 total cavopulmonary connection). All of them have some risk factors for a completed Fontan operation. There were three early deaths of the 16. Two experienced an anticipated thromboembolic accident, one of which involved the pulmonary aspect while the other involved the arterial aspect. Patients who survived the operation have progressed well and have a clinical status of New York Heart Association class I, with the exception of one late death due to congestive heart failure. There have been no thromboembolic accidents in this group during the late follow-up period. Spontaneous closures of the fenestrations were noted in two patients. The late mean Qp/Qs value in patients with patent fenestrations was 0.80 +/- 0.1, SaO2 was 88.8 +/- 5.6%, and right atrial pressure was 9.7 +/- 3.8 mmHg. No major problems have been encountered in patients with a patent fenestration over extended periods. A modified Fontan operation to fit a permanently open fenestration may be considered as a final surgical option for certain high-risk patients.

Adolescent↗

PubMed1999

A case of anorexia nervosa with hyperbilirubinaemia in a patient homozygous for a mutation in the bilirubin UDP-glucuronosyltransferase gene.

UNLABELLED: Gilbert syndrome was diagnosed in a girl with anorexia nervosa and unconjugated hyperbilirubinaemia. Since the patient was starved and hyperbilirubinaemic, the loading test was not used for the diagnosis but analysis of the bilirubin UDP-glucuronosyltransferase gene (UGT1A1) instead. The patient was homozygous for a missense mutation that replaced guanine with adenine at nucleotide number 211 (211G-->A: G71R). The unconjugated hyperbilirubinaemia was apparently induced by the fasting state. Homozygous missense mutations of the gene have been generally recognized as responsible for Crigler-Najjar syndrome type II; the results obtained here, however, confirm that Gilbert syndrome may also be caused by a homozygous missense mutation of UGT1A1. CONCLUSION: Since anorexia nervosa patients are in a fasting state, they may show moderate unconjugated hyperbilirubinaemia if they have Gilbert syndrome. Gene analysis of such cases will rule out hepatic damage. Homozygous missense mutations of the bilirubin-UDP-glucuronosyltransferase gene cause not only Crigler-Najjar syndrome type II but also Gilbert syndrome.

Anorexia Nervosa↗

PubMed1999

Rare occurrence of colorectal cancer metastasis in livers infected with hepatitis B or C virus.

BACKGROUND: The rarity of the occurrence of metastatic malignancy in injured liver has been noted by many observers. However, since the clinicopathological features of primary carcinoma and the etiology of liver disease of these patients vary greatly, this phenomenon may not be universal. METHODS: We evaluated the relationship between either hepatitis B virus (HBV) or hepatitis C virus (HCV) infection and the incidence of colorectal liver metastasis in 438 patients undergoing surgical treatment for advanced colorectal carcinoma. RESULTS: The liver function of the patients in the infection group (n = 37) was significantly worse than that of those in the noninfection group (n = 401). The incidences of tumor recurrence in the lung or peritoneum were comparable between the two groups. However, the percentage of patients with liver metastases in the infection group (3 of 37, 8.1%) was significantly lower (P <0.05) than that of those in the noninfection group (85 of 401, 21.2%). The patients in the infection group tended to survive longer than the patients in the noninfection group. CONCLUSIONS: We herein report an initial finding that colorectal carcinoma rarely metastasizes to livers infected with HBV or HCV.

Aged↗