Biomedical subjects

S Kaneko

Publications and source records attributed to S Kaneko.

At least 73 records · Page 4Linked to original sources

PubMed2001

Expression of angiogenic factors and tumor progression in human neuroblastoma.

PURPOSE: The growth and metastasis of malignant tumors is largely dependent on angiogenesis. Angiogenic factors produced by tumor cells are known to promote tumor angiogenesis. The aim of this study was to investigate which angiogenic factor is the most important in the progression of neuroblastoma (NB). PROCEDURE: The relative expression levels of vascular endothelial growth factor-A (VEGF-A), VEGF-C, basic fibroblast growth factor (bFGF), and platelet-derived endothelial growth factor (PD-ECGF/TP) were studied in 28 NB tumor specimens by real-time quantitative reverse transcriptase/polymerase chain reaction (RT-PCR). The relationships between the expression of these four angiogenic factors and stage, patient age, primary site, MYCN copy number, and lymph node metastasis were analyzed. RESULTS: High VEGF-A expression was correlated with stage 4 disease (blood-borne metastasis). No relationship between VEGF-A expression and age, primary site, MYCN copy number, or lymph node metastasis was found. The expression of VEGF-C, bFGF, or PD-ECGF/TP showed no correlation with stage, age, primary site, MYCN copy number, or lymph node metastasis. CONCLUSIONS: Our findings suggest that VEGF-A, but not VEGF-C, bFGF, or PD-ECGF/TP, may be associated with progression of NB. VEGF-A could be a target for antiangiogenic therapy for disseminated NB.

Angiogenesis Inducing Agents↗

PubMed2001

Protective effects of 1 alpha,25-(OH)(2)D(3) against the neurotoxicity of glutamate and reactive oxygen species in mesencephalic culture.

This study was undertaken to determine whether 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25-(OH)(2)D(3)], an active metabolite of vitamin D, protects dopaminergic neurons against the neurotoxic effects of glutamate and dopaminergic toxins using rat mesecephalic culture. Brief glutamate exposure elicited cytotoxicity in both dopaminergic and non-dopaminergic neurons. Pretreatment, but not co-administration, of 1 alpha,25-(OH)(2)D(3) protected both types of neurons against the cytotoxicity of glutamate in a concentration- and time-dependent manner. The neuroprotective effect of 1 alpha,25-(OH)(2)D(3) was inhibited by the protein synthesis inhibitor, cycloheximide. To investigate the mechanisms of these neuroprotective effects, we examined the effects of 1 alpha,25-(OH)(2)D(3) on neurotoxicity induced by calcium ionophore and reactive oxygen species (ROS). Pretreatment with 1 alpha,25-(OH)(2)D(3) protected both types of neurons against the cytotoxicity induced by A23187 in a concentration-dependent manner. Furthermore, 24-h pretreatment with 1 alpha,25-(OH)(2)D(3) concentration-dependently protected both types of neurons from ROS-induced cytotoxicity. A 24-h incubation with 1 alpha,25-(OH)(2)D(3) inhibited the increase in intracellular ROS level following H(2)O(2) exposure. A 24-h exposure to 1-methyl-4-phenylpyridium ion (MPP(+)) or 6-hydroxydopamine (6-OHDA) exerted selective neurotoxicity on dopaminergic neurons, and these neurotoxic effects were ameliorated by 1 alpha,25-(OH)(2)D(3). These results suggest that 1 alpha,25-(OH)(2)D(3) provides protection of dopaminergic neurons against cytotoxicity induced by glutamate and dopaminergic toxins by facilitating cellular functions that reduce oxidative stress.

1-Methyl-4-phenylpyridinium↗

PubMed2001

In vivo evaluation of bone-bonding of titanium metal chemically treated with a hydrogen peroxide solution containing tantalum chloride.

Apatite formation on implants is important in achieving a direct bonding to bone tissue. We recently showed that titanium metal chemically treated with a hydrogen peroxide solution containing tantalum chloride has the ability to form a hydroxyapatite layer in simulated body fluid which had inorganic ion composition similar to human blood plasma. In this study, a pure titanium cylinder (4.0 mm in diameter, 20.0 mm in length) treated with this method was implanted into a hole (4.2 mm in diameter) in a rabbit's tibia. After implantation for predetermined periods up to 16 weeks, the specimens were extracted with bone tissue, and were examined by push-out test to evaluate the shearing force between the implant and bone tissue. The results were compared with those of non-treated pure titanium. Eight weeks after surgery, the shearing force of the treated titanium implanted in the 4.2 mm-hole was significantly higher than that of non-treated titanium, although the surface roughness was not changed after the treatment. Scanning electron microscopic (SEM) observation and energy-dispersive X-ray (EDX) microanalysis showed that the bone comes very close to the surface of the treated titanium. Moreover, the shearing force was higher for the implanted sample in the 4.0 mm-hole than that in the 4.2 mm-hole. Thus, it is confirmed that the treatment with hydrogen peroxide solution containing tantalum chloride provides higher bonding ability on titanium implants in vivo.

Animals↗

PubMed2001

Gene therapy for hepatocellular carcinoma using two recombinant adenovirus vectors with alpha-fetoprotein promoter and Cre/lox P system.

Tissue-specific promoter has been used for cancer-specific suicide gene therapy, but its transcriptional activity is relatively low. For more efficient gene therapy of hepatocellular carcinoma, a simultaneous infection method of two recombinant adenoviruses was developed, in which one carried Cre gene under the control of alpha-fetoprotein promoter and the other a potent expression unit activated by Cre. When the vectors with lacZ reporter gene were introduced systematically into mouse models of disseminated tumors, specific and enhanced gene expression was observed exclusively in hepatocellular carcinomas both in the liver and in the lung. Next, using herpes simplex virus thymidine kinase, the anti-tumor effect was examined. Although in cultured cells, 60-300-fold expression of enzymatic activity and enhanced ganciclovir sensitivity was obtained compared with that of the single recombinant adenovirus directly driven by alpha-fetoprotein promoter, there was no significant anti-tumor effect for subcutaneous tumor on athymic mice. The lack of anti-tumor effect in mice could be explained by insufficient simultaneous transduction of the two vectors in the tumors, since it was found that a high multiplicity of infection was required to activate this system. Some strategies to overcome this dose limitation are needed, at least in the case of hepatocellular carcinoma.

Adenoviridae↗

PubMed2001

Cloning and characterization of the 5'-flanking region of human cytokeratin 19 gene in human cholangiocarcinoma cell line.

BACKGROUND/AIMS: The regulatory mechanism of cell-specific gene expression in cholangiocytes has not been sufficiently evaluated. In this study, we characterized the 5'-flanking region of the cytokeratin 19 gene expressed specifically in cholangiocytes. METHODS: We cloned a 2952-bp fragment in the 5'-flanking region of cytokeratin 19 and evaluated the regulatory mechanism of gene expression in this region by assaying transient expression of reporter gene and DNA footprinting. RESULTS: This segment of the 5'-flanking region of the human cytokeratin 19 gene shows an intense transcriptional activity in the cholangioma cell line KMBC, which was about 10 times its activity in the osteosarcoma cell line Saos-2, which does not express cytokeratin 19. From the results of reporter assays, important transcription regulatory elements are considered to be located in the segments from -2249 to -2050 bp and from -732 bp to the first ATG, and six protein-binding sites were detected in the segment from -732 bp to the first ATG by the DNA footprinting technique. CONCLUSIONS: Sp1 site, CCAAT box, and TATA box were present in the segment from -374 to the first ATG, and they are considered to constitute a cholangiocyte-specific promoter.

Base Sequence↗

PubMed2001

Surgical results of skull base surgery for the treatment of head and neck malignancies involving skull base: multi-institutional studies on 143 cases in Japan.

We analyzed 143 cases of skull base surgery collected from the eight institutions of the Study Group supported by the Grant-in-Aid for Cancer Research from the Ministry of Health and Welfare of Japan. Histologically, the most common type was squamous cell carcinoma (n = 78), which was followed by olfactory neuroblastoma (n = 16) and adenoid cystic carcinoma (n = 16). The most frequent surgical approach was frontal craniotomy (n = 66), followed by front-temporal craniotomy (n = 54) and infratemporal fossa approach (n = 8). For repair of dura matter, fascia lata was used in 37 cases. galeopericranial flap in 35 and temporal muscle fascia in 16. The 5-year survival rate by Kaplan-Meier method of nose and paranasal sinus carcinoma (n = 119) was 48%. As for histological classification, the survival rates were both 65%) in adenoid cystic carcinoma (n = 12) and bone soft tissue malignancy (n = 10), 62% in olfactory neuroblastoma (n = 16), 46% in squamous cell carcinoma (n = 62) and 33% in adenocarcinoma (n = 11). All the three cases of malignant melanoma died within 1 year, so we considered skull base surgery to be contraindicated for this disease. Complications were observed in 62 out of the 143 cases (43%); local infection was most frequent in 29 cases. liquorrhea in 18, abscess in 16, necrosis of the flap and meningitis in ten cases, DIC in four, rupture of the internal carotid artery in two and cerebral thrombosis in one. Death caused directly by surgery was in ten cases (7%). It is important that a multi-center registry be maintained to have a large enough database for comparison of results, and prognosis for each histological entity and further define the role of multidisciplinary treatment.

Adult↗

PubMed2001

Long-term observations of two siblings with Lafora disease treated with zonisamide.

We have reported long-term clinical follow-up for two siblings with Lafora disease, a brother and sister, one of whom autopsied. Both siblings had repeated attacks of severe myoclonus, tonic and tonic-clonic convulsions, and intractable status epilepticus. The addition of orally administered zonisamide brought about striking effective seizure control for about 12-14 years in both patients, relieving not only myoclonus and generalized tonic-clonic seizures but also intractable status epilepticus.

Adult↗

PubMed2001

Automatic discriminative sensitivity inside temporal window of sensory memory as a function of time.

Neural representation of preceding sound-patterns stored in the human brain, as reflected by mismatch negativity (MMN) related to the automatic discriminative process, is restricted to a duration of 160-170 ms due to the short form of auditory sensory memory termed the temporal window of integration (TWI). To examine the temporal uniformity of deviation-sensitivity inside TWI of sensory memory, magnetic MMN (MMNm) responses were measured with a dual 37-channel magnetometer for complex sounds of 170 ms duration containing an omitted (silent) segment. Frequent standard stimuli (probability of 80%) consisted of five tone segments. Deviant stimuli were different from standard stimuli in that one of four segments was occasionally (probability of 5%) omitted and replaced by a silent segment. The stimulus duration of 170 ms was intended to correspond to the postulated duration of TWI. When the silent segment occurred later in deviant stimulus, the MMNm peak amplitude was attenuated and MMNm peak latency, measured from the onset of each silent segment, was delayed. Thus, automatic deviation-detection sensitivity declines nonlinearly toward the end of TWI in auditory sensory memory. In the second experiment, two types of deviant stimuli, which differed from each other only in the period after the occurrence of the silent segment, elicited MMNm with the same peak latency but with a different peak amplitude. Thus, mismatch process is triggered at the moment of change but still lasts after the detection of deviation. In other words, both standard and deviant stimuli are treated as a unitary event within a TWI.

Acoustic Stimulation↗

PubMed2001

Involvement of IL-10, an anti-inflammatory cytokine in murine liver injury induced by Concanavalin A.

A mechanism of liver injury such as, viral hepatitis or autoimmune hepatitis is considered to involve the impairment of hepatocytes mainly mediated by T-cell immunity, but the roles of a variety of cytokines involved in regulation remain unclarified. We investigated the involvement of various cytokines, particularly, interleukin-10 (IL-10) which is considered to be an anti-inflammatory cytokine, in a murine model of experimental liver injury induced by Concanavalin A (Con A). The model of liver injury was made by intravenous injection of Con A (0.5 &mgr;g) through the caudal vein in 6-week-old female BALB/c mice weighting 20 g. By collecting blood before and at 1, 3, 6, 12 and 24 h after the injection of Con A, alanine aminotransferase (ALT) levels were sequentially measured, and liver tissue was sampled to examine liver injury. Furthermore, TNF-alpha, IL-4 and IL-10 levels were sequentially determined by enzyme-linked immunosorbent assay (ELISA). Serum ALT significantly increased between 3 and 24 h after the Con A injection, and spotty necrosis was histologically observed, suggesting mild liver injury. TNF-alpha and IL-4 increased soon after the injection of Con A. IL-10 increased bimodally soon after and at 12 h after the Con A injection. After neutralizing antibodies (1 &mgr;g) to IL-10 were intraperitoneally injected into the same model at 6 h before Con A treatment, serum ALT levels and the histology of the liver were examined 12 h after the Con A injection. ALT was significantly higher in the group treated with anti-IL-10 antibody (130.7+/-33.5 IU per I) than in the non-treated group (56.5+/-3.5 IU per I) (P<0.05). Histological examination showed spotty necrosis in the group treated with anti-IL-10 antibody. These results suggest that IL-10 has inhibitory effect on liver injury in a murine model of Con A-induced experimental liver injury mediated by cellular immunity.

Journal Article↗

PubMed2001

Occlusal hypofunction causes changes of proteoglycan content in the rat periodontal ligament.

The biological functions of proteoglycans and glycosaminoglycans are closely associated with mechanical stress on the tissue. In order to reveal the relationship between proteoglycans in the periodontal ligament and mechanical stress such as occlusal stimuli, occlusal hypofunction of rat unilateral mandibular molars was induced by extraction of the opposing first, second and third maxillary molars. Immunohistochemical analyses were performed using antibodies for chondroitin sulfate, decorin, biglycan, heparan sulfate and keratan sulfate, and hyaluronic acid-binding protein. Chondroitin sulfate, observed more strongly in the cervical side than in the apical side of the periodontal ligament of the unextracted sides of mandible, and uniformly present in the extracellular matrix of the periodontal ligament, decreased significantly from 1 wk post-extraction of the antagonists, with a decrease in thickness and disarrangement in fibrous components. Decorin core protein, uniformly present in the periodontal ligament of the unextracted sides, decreased as early on as 2 d post-extraction. Heparan sulfate, mainly localized on the cell surface of vascular endothelial cells and osteoclastic cells as well as in the extracellular matrix of the unextracted sides, decreased significantly in association with the decreased number of blood vessels and osteoclastic cells as early on as 2 d post-extraction. Biglycan, keratan sulfate and hyaluronic acid, uniformly distributed in the periodontal ligament of the unextracted sides, showed little change after the extraction. These results demonstrate that occlusal hypofunction causes tissue remodeling of the periodontal ligament, with a significant decrease of chondroitin sulfate, decorin and heparan sulfate.

Animals↗

PubMed2001

Effects of genetic polymorphism of CYP1A2 inducibility on the steady-state plasma concentrations of trazodone and its active metabolite m-chlorophenylpiperazine in depressed Japanese patients.

The effects of a genetic polymorphism of inducibility of cytochrome P450 (CYP) 1A2 on the steady-state plasma concentrations of trazodone and its active metabolite, m-chlorophenylpiperazine, were studied in order to clarify if these steady-state plasma concentrations are dependent on the CYP1A2 polymorphism. Fifty-eight Japanese depressed patients received trazodone 150 mg/day at bedtime. The steady-state plasma concentrations of trazodone and m-chlorophenylpiperazine were measured in duplicate using high performance liquid chromatographic method, and were corrected to the mean body weight for analyses. A point mutation from guanine (wild type) to adenine (mutated type) at position -2964 in the 5'-flanking region of CYP1A2 gene was identified by polymerase chain reaction fragment length polymorphism method. The mean steady-state plasma concentration of trazodone, but not m-chlorophenylpiperazine was significantly (P<0.05) lower in smokers than in non-smokers. Twenty-two smokers had 16 homozygotes of the wild type allele, 5 heterozygotes of the wild type and mutated alleles, and one homozygote of the mutated allele. There was no significant difference in the mean steady-state plasma concentration of trazodone or m-chlorophenylpiperazine between smokers with no mutation and those with mutation, although one homozygote of the mutated allele had the highest steady-state plasma concentration of trazodone in smokers. The present study thus suggests that CYP1A2 polymorphism does not necessarily have predictive value of the steady-state plasma concentration of trazodone or m-chlorophenylpiperazine in most of the smokers treated with trazodone.

Adult↗

PubMed2001

The gene encoding a newly discovered protein, chorein, is mutated in chorea-acanthocytosis.

Chorea-acanthocytosis is a neurodegenerative disorder with peripheral red cell acanthocytosis. Linkage of chorea-acanthocytosis to chromosome 9q21 has been found. We refined the locus region and identified a previously unknown, full-length cDNA encoding a presumably structural protein, which we called chorein. We found a deletion in the coding region of the cDNA leading to a frame shift resulting in the production of a truncated protein in both alleles of patients and in single alleles of obligate carriers.

Chorea↗

PubMed2001

Pharmacological discrimination between effects of carbamazepine on hippocampal basal, Ca(2+)- and K(+)-evoked serotonin release.

To elucidate mechanisms of hippocampal serotonin release and possible mechanisms of clinical action of carbamazepine (CBZ), we determined interaction between antagonists of N-type (omega-conotoxin GVIA:GVIA), P-type (omega-agatoxin IVA:IVA) Ca(2+) channels, Na(+) channel (tetrodotoxin: TTX) and CBZ on hippocampal basal, Ca(2+)- and K(+)-evoked serotonin releases, using microdialysis in freely moving rats. Basal release was reduced by TTX, GVIA and IVA (GVIA>IVA). Ca(2+)-evoked release was reduced by GVIA but unaffected by TTX and IVA. K(+)-evoked release was reduced by TTX, GVIA and IVA (GVIA<IVA). TTX inhibited actions of IVA and GVIA on respective basal and K(+)-evoked releases, without affecting Ca(2+)-evoked release. Perfusion with 100 microM CBZ (estimated-concentration in hippocampal tissue: 19+/-2 microM) enhanced basal and Ca(2+)-evoked releases, but reduced K(+)-evoked release, whereas 1000 microM CBZ (estimated-concentration in hippocampal tissue: 188+/-16 microM) reduced three types of releases. Under condition of pretreatment with 100 and 1000 microM CBZ, TTX unaffected basal and K(+)-evoked releases. Under condition of pretreatment with 100 microM CBZ, IVA and GVIA unaffected basal and K(+)-evoked releases, respectively, but GVIA reduced basal, Ca(2+)-evoked releases and IVA also reduced K(+)-evoked release. Under condition of pretreatment with 1000 microM CBZ, GVIA unaffected three types of releases, and IVA unaffected basal release but reduced K(+)-evoked release. These findings contribute towards the possible mechanisms of concentration-dependent antiepileptic action of CBZ, which possibly inhibits Na(+) channel related neurotransmitter release mechanisms during K(+)-evoked stage, and simultaneously enhances N-type Ca(2+) channel related basal serotonin release at the resting stage.

Animals↗

PubMed2001

Determination of effects of antiepileptic drugs on SNAREs-mediated hippocampal monoamine release using in vivo microdialysis.

1. To elucidate possible mechanisms underlying the effects of carbamazepine (CBZ), valproate (VPA) and zonisamide (ZNS) on neurotransmitter exocytosis, the interaction between these three antiepileptic drugs (AEDs) and botulinum toxins (BoNTs) on basal, Ca(2+)- and K(+)-evoked release of dopamine (DA) and serotonin (5-HT) were determined by microdialysis in the hippocampus of freely moving rats. 2. Basal release of monoamine was decreased by pre-microinjection of the syntaxin inhibitor, BoNT/C, but only weakly affected by the synaptobrevin inhibitor, BoNT/B. Ca(2+)-evoked release was inhibited by BoNT/C selectively. K(+)-evoked release was reduced by BoNT/B predominantly and BoNT/C weakly. 3. Perfusion with low and high concentrations of CBZ and ZNS increased and decreased basal monoamine release, respectively. Perfusion with VPA increased basal 5-HT release concentration-dependently, whereas basal DA release was affected by VPA biphasic concentration-dependently, similar to CBZ and ZNS. This stimulatory action of AEDs on basal release was inhibited by BoNT/C predominantly. 4. Ca(2+)-evoked monoamine release was increased by low concentrations of CBZ, ZNS and VPA, but decreased by high concentrations. These effects of the AEDs on Ca(2+)-evoked release were inhibited by BoNT/C, but not by BoNT/B. 5. K(+)-evoked monoamine release was reduced by AEDs concentration-dependently. The inhibitory effect of these three AEDs on K(+)-evoked release was inhibited by BoNT/B, but not by BoNT/C. 6. These findings suggest that the therapeutic-relevant concentration of CBZ, VPA and ZNS affects exocytosis of DA and 5-HT, the enhancement of syntaxin-mediated monoamine release during resting stage, and the inhibition of synaptobrevin-mediated release during depolarizing stage.

Animals↗

PubMed2001

Enhanced anti-tumor effects of herpes simplex virus thymidine kinase/ganciclovir system by codelivering monocyte chemoattractant protein-1 in hepatocellular carcinoma.

The therapeutic efficacy of herpes simplex virus thymidine kinase/ganciclovir (HSV-tk/GCV) system in many types of tumors is unsatisfactory due to the insufficient spread of gene transfer and insufficient cell killing. In the current study, we investigated whether adenovirally delivered monocyte chemoattractant protein (MCP)-1 potentiates the antitumor effects of the HSV-tk/GCV system in hepatocellular carcinoma (HCC) cells. Subcutaneous tumor foci of the human HCC cell line, HuH7, established in athymic mice were directly transduced with a recombinant adenovirus (rAd) harboring an HSV-tk gene driven by a human alpha-fetoprotein promoter, followed by GCV administration. Subsequently, another rAd expressing MCP-1 under the universal CAG promoter was injected. The growth of tumors was markedly suppressed by codelivering HSV-tk and MCP-1 genes compared to that by either HSV-tk/GCV or MCP-1 delivery. In the tumor tissues, monocyte/macrophage infiltration was detected immunohistochemically. The antitumor effects of the rAd expressing MCP-1 were markedly reduced by the administration of carrageenan, a compound known to inactivate macrophage. These results indicate that adenovirally delivered MCP-1 enhanced the antitumor effects of the HSV-tk/GCV system synergistically by recruitment/activation of macrophages in tumor tissues, suggesting an effective immunotherapy for HCC and other lineages of tumors when used adjuvantly with a suicide gene.

Animals↗

PubMed2001

HVJ-liposome-mediated transfection of HSVtk gene driven by AFP promoter inhibits hepatic tumor growth of hepatocellular carcinoma in SCID mice.

Suicide gene therapy using ganciclovir (GCV) with transfection of the herpes thymidine kinase (HSVtk) gene has been studied for cancer therapy. The present study demonstrates an efficient method of suicide gene therapy for multiple hepatic tumors, involving repetitive transfection of the HSVtk gene driven by the alpha-fetoprotein (AFP) promoter using hemagglutinating virus of Japan (HVJ)-liposomes. AFP-producing cells (HUH7) and AFP-nonproducing cells (LS180) were injected subcutaneously (s.c.) to establish tumors in nude mice. Two plasmid constructs, bacterial LacZ gene driven by the AFP promoter (AFPLacZ), and HSVtk gene driven by the AFP promoter (AFPTK1) were encapsulated into the HVJ-liposome and used. When AFPLacZ was injected into the s.c. tumors, expression of LacZ gene was confined to HUH7 tumors. Repeated transfection of AFPTK1 followed by GCV treatment markedly suppressed growth of HUH7 tumors, and apoptosis of HUH7 cells was recognized in the tumor. Next, HUH7 cells were injected into the portal vein in severe combined immunodeficiency mice to establish a hepatic tumor model. After inoculation with the tumor, HVJ-liposomes containing the AFPTK1 plasmid vector were injected into the portal vein via the splenic hilum, followed by GCV treatment. This gene therapy significantly inhibited the growth of tumors in the liver and markedly improved survival. Three injections of the AFPTK1 plasmid vector completely inhibited tumor growth. This procedure seems to have great potential for the treatment of multiple hepatic tumors.

Animals↗

PubMed2001

Importance of achieving complete necrosis during the first treatment for hepatocellular carcinoma to prevent bone metastasis: a prospective study.

BACKGROUND AND AIMS: Recent advances in the treatment of hepatocellular carcinoma (HCC) have changed the importance of bone metastasis during the follow up of such patients. In the present study, we investigated risk factors for bone metastasis after treatment for HCC. METHODS: Two hundred and two patients with HCC were diagnosed as free of bone metastasis by technecium 99m-methylene diphosphonate bone scintigraphy and were followed prospectively after treatment of the primary lesions (follow-up period 2-146 months; median 20 months). We statistically analyzed the risk factors for bone metastasis using the clinical characteristics at the time of first treatment. RESULTS: Multiple tumors (P < 0.005), main tumor size > 5 cm in diameter (P < 0.005), the presence of distant metastasis (P < 0.005), elevation of serum alpha-fetoprotein (> 100 ng/mL; P < 0.05), chemotherapy (P < 0.05) and insufficient therapeutic response (P < 0.0005) were identified as risk factors for bone metastasis by univariate analyses. Insufficient therapeutic response and main tumor size > 5 cm in diameter (both P < 0.05) were identified as independent predisposing factors for bone metastasis. CONCLUSIONS: Complete necrosis of primary HCC during the first treatment is important to prevent subsequent bone metastasis.

Aged↗

PubMed2001

Sociomedical aspects of epileptic patients: their employment and marital status.

We examined the employment and marital status of adult patients with epilepsy who did not have mental retardation and who had been treated at Hirosaki University Hospital, Hirosaki, Japan, for more than 5 years. The present study included 278 patients (142 males and 136 females) ranging from 20 to 60 years of age. We investigated the occupational status of the subjects and found that 168 had permanent jobs, but 41 patients were unemployed at the time of this survey. The proportion of the patients whose seizures were controlled at the time of this survey was 68% (114/168) in the group having permanent jobs, and 22% (9/41) in the unemployed group. Forty cases answered that they had resigned from their jobs due to occurrence of epileptic seizures. Of these patients, 13 were dismissed and 27 resigned voluntarily due to the potential for seizures. As to relationship between jobs and neuropsychiatric complications, the incidence of a past history of psychotic states in the unemployed group was significantly higher than that in the employed group. As to marital status, 13 males and 16 females (n = 29) had experienced divorce. Seven cases (two males and five females) had answered that epilepsy had been the reason for their divorce. We conclude that epilepsy or epileptic seizures have various negative effects on the patient's social life.

Adult↗