Nanosecond Random Telegraph Noise in In-Plane Magnetic Tunnel Junctions.

We study the timescale of random telegraph noise (RTN) of nanomagnets in stochastic magnetic tunnel junctions (MTJs). From analytical and numerical calculations based on the Landau-Lifshitz-Gilbert and the Fokker-Planck equations, we reveal mechanisms governing the relaxation time of perpendicular easy-axis MTJs (p-MTJs) and in-plane easy-axis MTJs (i-MTJs), showing that i-MTJs can be made to have faster RTN. Superparamagnetic i-MTJs with small in-plane anisotropy and sizable perpendicular effective anisotropy show relaxation times down to 8 ns at negligible bias current, which is more than 5 orders of magnitude shorter than that of typical stochastic p-MTJs and about 100 times faster than the shortest time of i-MTJs reported so far. The findings give a new insight and foundation in developing stochastic MTJs for high-performance probabilistic computers.

Sphingosine 1-phosphate attenuates peroxide-induced apoptosis in HaCaT cells cultured in vitro.

BACKGROUND: Sphingosine 1-phosphate (S1P) is a sphingolipid mediator that elicits a wide array of physiological responses in various types of mammalian cells. Among the numerous biological activities elicited by S1P is protection from apoptotic cell death, which seems to take place through the cell-surface S1P receptor and the downstream phosphoinositide 3'-OH kinase (PI3-K)/Akt pathway. It is unclear whether and how S1P protects human keratinocytes from hydrogen peroxide (H2 O2 )-induced apoptosis. AIM: We investigated the effects of S1P on apoptotic cell death in HaCaT cells, spontaneously immortalized human keratinocytes. METHODS: HaCaT cells were treated with hydrogen peroxide (H2 O2 ) 1-2 mmol/L as an inducer of apoptosis. Cellular apoptosis was assessed with terminal dUTP nick-end labelling (TUNEL), WST-8 and immunoblot assays. RESULTS: In WST-8 and TUNEL assays, S1P pretreatment (1 µmol/L for 30 min) attenuated H2 O2 -induced cell death. Promotion of the cleavage of caspase-3 by H2 O2 was markedly attenuated when cells had been preincubated with S1P. S1P markedly potentiated phosphorylation (activation) of Akt in the presence of H2 O2 . Wortmannin, a selective inhibitor of the PI3-K/Akt pathway, significantly suppressed S1P-induced attenuation of caspase-3 cleavage promoted by H2 O2 . CONCLUSIONS: S1P, a sphingolipid mediator, attenuates H2 O2 -induced apoptosis of HaCaT cells, by promoting phosphorylation of the Akt pathway.

Synergistic effects of antibiotics and an N-acyl homoserine lactone analog on Porphyromonas gingivalis biofilms.

AIMS: To investigate the effects of the combined application of an N-acyl homoserine lactone (HSL) analog and antibiotics on biofilms of Porphyromonas gingivalis, a major pathogen of periodontal disease. METHODS AND RESULTS: Antibiotics used were cefuroxime, ofloxacin and minocycline. A flow-cell model was used for biofilm formation. Samples were divided into four groups: control, analog-treated, antibiotic-treated and combined application groups. Biofilm cell survival was determined using adenosine triphosphate (ATP) bioluminescence and confocal laser microscopy (CLSM). In the combined application group, the ATP count in biofilm cells was significantly decreased compared with the antibiotic-treated group (Games-Howell test, P < 0·05). A combination of cefuroxime and the analog was most effective against the P. gingivalis biofilm. CLSM observations revealed that the proportion of dead cells was highest in the combined application group. CONCLUSIONS: The combined application of the N-acyl HSL analog and antibiotics was effective at reducing the viability of P. gingivalis cells in biofilms. SIGNIFICANCE AND IMPACT OF THE STUDY: The combined application of the N-acyl HSL analog and antibiotics may be successful for eradicating infections involving bacterial biofilms, such as periodontitis.

Effects of N-acyl homoserine lactone analogues on Porphyromonas gingivalis biofilm formation.

BACKGROUND AND OBJECTIVE: The gram-negative anaerobic rod Porphyromonas gingivalis in oral biofilms is a primary etiological agent of periodontal disease. Biofilm formation of various gram-negative bacteria is regulated by a quorum-sensing circuit that relies on N-acyl homoserine lactones (HSLs). Some synthetic N-acyl HSL analogues act as quorum-sensing inhibitors and suppress biofilm formation in Pseudomonas aeruginosa. Development of chemical control agents against oral biofilms is necessary, because until now, biofilms have been removed only by mechanical debridement. The present study investigated the effect of N-acyl HSL analogues on P. gingivalis biofilm formation, with the aim of developing new drugs that inhibit oral biofilm formation. MATERIAL AND METHODS: A flow-cell model was used for P. gingivalis biofilm formation. Seventeen synthetic N-acyl HSL analogues were quantitatively assessed by spectrophotometry. The effects of three antagonistic compounds against P. gingivalis biofilm formation were further examined by confocal laser scanning microscopy, and investigated for primary attachment using spectrophotometry and phase contrast microscopy. RESULTS: Ten out of 17 analogues affected P. gingivalis biofilm formation. Three out of 10 analogues significantly decreased biofilm-forming cells (p < 0.05), and these biofilm structures were less well formed three-dimensionally. There were no quantitative or qualitative differences in cell attachment between the control and the three analogue-treated groups. CONCLUSION: Three synthetic N-acyl HSL analogues inhibited biofilm formation in P. gingivalis. We suggest that these analogues influence the development stage of P. gingivalis biofilm formation.

Statins induce S1P1 receptors and enhance endothelial nitric oxide production in response to high-density lipoproteins.

BACKGROUND AND PURPOSE: Sphingosine 1-phosphate (S1P) is a serum-borne naturally occurring sphingolipid, specifically enriched in high-density lipoprotein (HDL) fractions. S1P binds to G-protein-coupled S1P1 receptors to activate endothelial NO synthase (eNOS) in vascular endothelial cells. We explored whether and how statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, modulate expression of S1P1 receptors and endothelial responses for subsequent stimulation with S1P or with HDL. EXPERIMENTAL APPROACH: Protein expression and phosphorylation and mRNA expression in cultured bovine aortic endothelial cells (BAEC) were determined using immunoblots and reverse transcription PCR analyses, respectively. NO synthesis was assessed as nitrite production. KEY RESULTS: Stimulation of BAEC with pitavastatin or atorvastatin led to significant increases in S1P1-receptors, at levels of protein and mRNA, in a dose-dependent manner. When BAEC were treated with pitavastatin prior to stimulation with S1P or with normal human HDL, phosphorylation and activation of eNOS evoked by S1P or by HDL was enhanced. These effects of statins were counteracted by L-mevalonate and were mimicked by an inhibitor of geranylgeranyl transferase I, suggesting that inhibition of HMG-CoA reductase activity and subsequent decreases in protein geranylgeranylation may contribute to these actions of statins. Specific knock down of S1P1 receptors by small interfering RNA led to attenuation of eNOS responses to HDL. CONCLUSIONS AND IMPLICATIONS: Statins induce S1P1 receptors and potentiate responses of endothelial cells to HDL-associated sphingolipids, identifying a novel aspect of the pleiotropic actions of statins through which they may exert NO-dependent vascular protective effects.

A primitive myoglobin from Tetrahymena pyriformis: its heme environment, autoxidizability, and genomic DNA structure.

A myoglobin-like protein isolated from Tetrahymena pyriformis is composed of 121 amino acid residues. This is much smaller than sperm whale myoglobin by 32 residues, suggesting a distinct origin from the common globin gene. We have therefore examined this unique protein for its structural, spectral and stability properties. As a result, the rate of autoxidation of Tetrahymena oxymyoglobin (MbO(2)) was found to be almost comparable to that of sperm whale MbO(2) over a wide range of pH 4-12 in 0.1 M buffer at 25 degrees C. Moreover, both pH profiles exhibited the remarkable proton-assisted process, which can be performed in sperm whale myoglobin by the distal (E7) histidine as its catalytic residue. These kinetic observations are also in full accord with spectral examinations for the presence of a distal histidine in ciliated protozoa myoglobin. At the same time, we have isolated the globin genes both from T. pyriformis and Tetrahymena thermophila, and found that there is no intron in their genomic structures. This is in sharp contrast to previous reports on the homologous globin genes from Paramecium caudatum and Chlamydomonas eugametos. Rather, the Tetrahymena genes seemed to be related to the cyanobacterial globin gene from Nostoc commune. These contracted or truncated globins thus have a marked diversity in the cDNA, protein, and genomic structures.

Amelioration of severity of myocardial injury by a nitric oxide donor in rabbits fed a cholesterol-rich diet.

OBJECTIVES: This study compared the effect of a nitric oxide donor on limiting the size of infarct resulting from myocardial ischemia-reperfusion between atherosclerotic and nonatherosclerotic models. BACKGROUND: Endothelial-derived relaxation in coronary arteries affected by ischemia is substantially impaired after reperfusion, and this impairment may exacerbate the myocardial ischemia-reperfusion injury. In animals with experimental atherosclerosis, release of endothelial-derived relaxing factor is also decreased, and the propagation of myocardial infarction could be exacerbated. METHODS: We examined the extent of myocardial injury induced by ischemia (30 min) and reperfusion (48 hr) in rabbits fed a cholesterol-rich (1%) or normal diet for 10 weeks. We also evaluated the effect of a nitric oxide donor (S-nitroso-N-acetylpenicillamine [SNAP], a nitric oxide precursor (L-arginine) or a degradation product of SNAP (N-acetylpenicillamine) on infarct size in these models. RESULTS: Severity of myocardial injury was significantly exacerbated in cholesterol-fed rabbits (75.2 +/- 4.4% [mean +/- SEM]) compared with that in non-cholesterol-fed rabbits (53.2 +/- 5.2%). This exacerbation was prevented by treatment with SNAP (50.2 +/- 6.4%) but not with L-arginine (70.5 +/- 6.0%) or N-acetylpenicillamine (70.4 +/- 4.8%) in cholesterol-fed-rabbits. However, SNAP did not limit infarct size in non-cholesterol-fed rabbits (60.8 +/- 4.2%). The rate-pressure product was similar during the course of the experiment in all the groups. CONCLUSIONS: Myocardial damage induced by ischemia-reperfusion was significantly exacerbated in rabbits fed a long-term cholesterol-rich diet but was effectively reversed by treatment with a nitric oxide donor. However, this agent did not limit infarct size in normal rabbits. Thus, a nitric oxide donor reduces myocardial infarct size in atherosclerotic but not in nonatherosclerotic rabbits.

Vascular angiotensin-converting enzyme activity in cholesterol-fed rabbits: effects of enalapril.

Many reports have shown inhibitory effects of angiotensin-converting enzyme (ACE) inhibitors on the progression of atherosclerotic plaque lesions in vascular tissue of experimental models. However, no report has shown alterations of ACE activity in vascular tissue during the process of atherosclerosis. We measured ACE activity in plasma and aortic tissue in rabbits fed a cholesterol-rich (1%) or normal diet for 10 weeks. We also evaluated the blood pressure response to angiotensin (Ang) I and II. These data were compared in untreated rabbits and in rabbits receiving chronic treatment with an ACE inhibitor, enalapril (3 mg/kg/day for 10 weeks). ACE activity in aortic tissue, but not in plasma, in cholesterol-fed rabbits was gradually but significantly increased compared with that in noncholesterol-fed rabbits even after the 4-week feeding period, when no atherosclerotic lesion was observed in the aortic tissue. Treatment with enalapril for 10 weeks, but not 4 weeks, significantly reduced the ACE activity in aortic tissue in association with the reductions in the elevated Ang II level and the atherosclerotic plaque area of the aortic tissue. These results indicated that ACE activity in aortic tissue was increased during the early phase of atherosclerotic process.

An adjuvant effect of poly A - poly U on production of antibodies to DNA in rabbits.

The effect of polyadenylate-polyuridylate copolymer (poly A-poly U) on the formation of anti-DNA antibodies in rabbits was investigated. 1) Poly A-poly U proved to be an effective adjuvant for production of antibodies to DNA. These were elicited in rabbits at high titer and were formed at an early stage of immunizations. 2) The antiserum obtained reached potently with denatured DNA, but with neither methylated bovine serum albumin (MBSA) used as carrier protein nor poly A-poly U used as adjuvant. This was demonstrable both by C-fixation and double diffusion tests. 3) The antibodies occurred exclusively in the IgG fraction separated by Sephadex G-200 column chromatography.

delta-Aminolevulinate synthetases in the liver cytosol fraction and mitochondria of mice treated with allylisopropylacetamide and 3,5-dicarbethoxyl-1,4-dihydrocollidine.

Hepatic delta-aminolevulinate (ALA) synthetase was induced in mice by the administration of allylisopropylacetamide (AIA) and 3,5-dicarbethoxy-1,4-dihydrocollidine (DDC). In both cases, a significant amount of ALA synthetase accumulated in the liver cytosol fraction as well as in the mitochondria. The apparent molecular weight of the cytosol ALA synthetase was estimated to be 320,000 by gel filtration, but when the cytosol ALA synthetase was subjected to sucrose density gradient centrifugation, it showed a molecular weight of 110,000. In the mitochondria, there were two different sizes of ALA synthetase with molecular weights of 150,000 and 110,000, respectively; the larger enzyme was predominant in DDC-treated mice, whereas in AIA-treated mice and normal mice the enzyme existed mostly in the smaller form. When hemin was injected into mice pretreated with DDC, the molecular size of the mitochondrial ALA synthetase changed from 150,000 to 110,000. The half-life of ALA synthetase in the liver cytosol fraction was about 30 min in both the AIA-treated and DDC-treated mice. The half-life of the mitochondrial ALA synthetase in AIA-treated mice and normal mice was about 60 min, but in DDC-treated mice the half-life was as long as 150 min. The data suggest that the cytosol ALA synthetase of mouse liver is a protein complex with properties very similar to those of the cytosol ALA synthetase of rat liver, which has been shown to be composed of the enzyme active protein and two catalytically inactive binding proteins, and that ALA synthetase may be transferred from the liver cytosol fraction to the mitochondria with a size of about 150,000 daltons, followed by its conversion to enzyme with a molecular weight of 110,000 within the mitochondria. The process of intramitochondrial enzyme degradation seems to be affected in DDC-treated animals.

Effects of administration of cobalt chloride and cobalt protoporphyrin on delta-aminolevulinate synthase in rat liver.

Cobalt protoporphyrin inhibited the drug-induced increase of delta-aminolevulinate synthase as well as its transfer from the cytosol fraction to the mitochondria in rat liver in a similar way to protoheme. Cobalt chloride given to animals in a large dose exhibited similar effects. Cobalt protoporphyrin was isolated from the liver of rats treated with cobalt chloride. The observed regulatory effects of cobalt chloride with respect to the induction and the intracellular translocation of delta-aminolevulinate synthase may be mediated by cobalt protoporphyrin synthesized in vivo.

Circadian rhythm of serotonin levels in planarians.

In the freshwater planarian Dugesia japonica, which belongs to the most primitive metazoan phylum, serotonin (5-hydroxytryptamine) was detectable by both immunohistochemistry and high-performance liquid chromatography (HPLC) with fluorometric detection. Immunohistochemical studies showed that serotonin was localized primarily in the cephalic ganglion (brain), in the main nerve cords extending posteriorly from the brain and in the commissure axons connecting the main nerve cords. HPLC with fluorometric detection analysis revealed that the serotonin levels of planarians maintained under a 12:12h light:dark cycle showed significant diurnal variations with a trough in the middle of the dark phase. In constant darkness, the serotonin levels fluctuated with a circadian rhythm. These results demonstrate the existence of a circadian timekeeping mechanism in the planarian.

Inhibitory effects of azelastine and tranilast on leukotriene B4 and leukotriene C4 generation by rat colonic mucosa.

Anti-allergic drugs such as sodium cromoglycate are known to be effective for the treatment of ulcerative colitis (UC). Because leukotriene (LT) production is considered to play an important role in the pathophysiology of UC, we examined the effect of the anti-allergic drugs, azelastine and tranilast, and the 5-lipoxygenase inhibitor, AA861, on LTB4 and LTC4 production by isolated rat colonic mucosa treated with the calcium ionophore, A23187. Preincubation of colonic mucosa with AA861 (10(-4) M) or azelastine (10(-4) M) significantly reduced AA23187-induced LTB4 (p < 0.01 and p < 0.05, respectively) and LTC4 (p < 0.01) production. Pretreatment with tranilast (10(-3) M) also significantly reduced A23187-induced LTC4 production (p < 0.05). These findings suggest that azelastine and tranilast can inhibit LT production in colonic mucosa and may be beneficial in the treatment of patients with UC.

Effects of n-3 polyunsaturated fatty acids on indomethacin-induced changes in eicosanoid production and blood flow in the gastric mucosa of rats.

We investigated the effects of n-3 polyunsaturated fatty acids (PUFAs) on non-steroidal anti-inflammatory drug (NSAID)-induced changes in microcirculation and eicosanoid production in the gastrointestinal mucosa. We measured gastric mucosal blood flow using laser Doppler flowmetry, assessed the fatty acid composition in the mucosal phospholipids, and quantified the production of prostaglandin E2 (PGE2), leukotriene B4, and leukotriene C4 (LTB4 and C4) from the mucosa with the stimulation of calcium ionophore 20 min after an injection of indomethacin or vehicle in rats fed a diet containing different compositions of alpha-linolenic acid. Four weeks after the initiation of the test diet the arachidonic acid level in gastric mucosal phospholipids was significantly lower in the perilla group than in the other three groups. Conversely, alpha-linolenic acid and eicosapentaenoic acid (EPA) were significantly higher in the perilla group than in the other three groups. The percent of gastric mucosal blood flow in the three groups administered indomethacin were significantly lower than that in the control group injected with vehicle alone. The percent of gastric mucosal blood flow in the perilla group was significantly higher than that in the corn group. LTB4 and LTC4 production from the gastric mucosa in the soybean and corn groups were significantly higher than those in the control group, and the LTC4 production in the perilla group was significantly lower than that in the corn group. There were no significant differences in PGE2 production among the four groups. Our results suggest that alpha-linolenic acid affectively suppressed the indomethacin-induced decreases in gastric mucosal blood flow by increasing EPA and decreasing the levels of arachidonic acid and LTC4 in the gastric mucosa.

Proteins recognized by antibodies against isolated cytological heterochromatin from rat liver cells change their localization between cell species and between stages of mitosis (interphase vs metaphase).

Heterochromatin in the cell nucleus seems to concentrate various proteins, such as Drosophila heterochromatin protein 1, which maintain the repressed state of gene expression. However, it still remains obscure how protein composition related to chromatin structure is different between heterochromatin and euchromatin in interphase nuclei. We isolated cytological heterochromatin from sonicated interphase nuclei obtained from rat liver cells and prepared antisera against it. The dense heterochromatic bodies seen in the preparation of intact nuclei were duplicated in a relatively pure form during the preparation of heterochromatin. In the sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis, differences between the fractions of heterochromatin and euchromatin were noted by their protein composition. Isolated heterochromatin was then digested by DNase after partial digestion with trypsin and its dense structure changed to become highly sensitive to DNase. The prepared antibodies reacted with the heterochromatin region of rat liver cell nuclei and isolated cytological heterochromatin; however, they did not react with euchromatin. Using immunohistochemistry, the antibodies bound to each cell nucleus in all tissues observed; some cell types were distinguished by their differential stainability (e.g. staining in the cytoplasm). Staining of the mitotic cells showed that the proteins recognized by the antibodies were localized in the cytoplasm and, in part, on the chromosomes. Based on the results of molecular cloning from rat liver cDNA library using the antibodies as a probe, it seemed that the antibodies mainly recognized two proteins similar to arginase and general vesicular transport factor p115, respectively. The results obtained from these experiments reveal that some proteins located in the heterochromatin of interphase liver cell nuclei seem to play important roles in condensing a portion of the chromatin structure during interphase and suggest that proteins composing heterochromatin might be changed according to cell types or the stage of the cell cycle.

Correlation of prostaglandin E2 production and gastric acid secretion in infants with hypertrophic pyloric stenosis.

PURPOSE: The aim of this study was to evaluate the relationship between gastric acid secretion and prostaglandin E2 (PGE2) generation in gastric mucosa and the role of PGE2 in the pathogenesis of hypertrophic pyloric stenosis (HPS). METHODS: The authors measured the levels of PGE2 and gastric acidity in the gastric juice of HPS patients before and after a Ramstedt operation. RESULTS: The PGE2 concentration in the gastric juice of nine HPS patients before the Ramstedt operation was significantly higher than that of eight controls, and the concentration significantly decreased after the operation. A significant inverse correlation between the PGE2 concentration and the pH level in the gastric juice was shown in HPS patients before and after the operation. CONCLUSION: These results suggest that the enhanced generation of PGE2 in gastric mucosa in cases of HPS is a secondary phenomenon caused by hyperacidity and is not responsible for the pathogenesis of HPS.

Hepatectomy of cavernous hemangioma with constitutional indocyanine green excretory defect.

The constitutional ICG excretory defect with marked ICG retention in spite of other normal hepatic functions has not been so rare in Japan. However, there is no previous report of hepatectomy in a patient with this disease. We describe a successful case of hepatectomy for cavernous hemangioma with this disease and use of technetium-99m diethylenetriaminepentaacetic acidgalactosyl-human serum albumin (99mTC-GSA) liver scintigraphy as the preoperative assessment of the liver functional reserve. In our case, ICGR15 was more than 55%, however, a modified receptor index obtained from 99mTC-GSA liver scintigraphy was normal. Left lateral segmentectomy of the liver was performed without any perioperative complications. Hepatectomy of patients with the constitutional ICG excretory defect is possible if modified receptor index value obtained from 99mTC-GSA scintigraphy is within the normal range.

Synchronous gastric cancer associated with hepatocellular carcinoma: a study of 10 patients.

BACKGROUND/AIMS: Little information regarding synchronous gastric cancer (GC) associated with hepatocellular carcinoma (HCC) is available. The aim of this study was to clarify the clinicopathologic features of synchronous GC associated with HCC, and we also discuss the diagnostic and therapeutic issues regarding them. METHODOLOGY: In a series of 396 patients with GC and 340 patients with HCC, we investigated the clinicopathologic features of the patients with synchronous GC associated with HCC (HCC group; n=10). They were compared to the patients with resected GC without HCC (non-HCC group) which was divided into 2 groups: with chronic hepatic disease (CHD: CHD group; n=15) and without CHD (Control group; n=345). RESULTS: The HCC group consisted of 10 of the 396 patients with GC (2.6%), and of 340 with HCC (2.9%). Eight node-negative early GC and 2 advanced GC cases were observed in the HCC group. Nine of these GC (90%) were well-differentiated adenocarcinoma. The tumor sizes of the HCC group were significantly smaller than those of the control group (p<0.05). The incidences of intestinal type and early GC in the HCC group were significantly higher than those in the control group, (p<0.05). However, there were no significant differences in any parameters between the HCC group and CHD group. With regard to early GC, there were no significant differences in any parameters, excluding the site of GC in the CHD group, between the HCC group and non-HCC group. Eight in the HCC group were surgically resected, and the post-operative period of these patients was uneventful. Although there were no significant differences in survival after surgery among the 3 groups, the survival of the patients with early GC in the HCC group was significantly worse than that in the control group (p<0.01). CONCLUSIONS: The clinicopathologic features of synchronous GC associated with HCC are not very aggressive in most patients probably because of the early detection, and those of early GC with HCC appeared to resemble that of GC with CHD. Since early GC may not influence the clinical outcome of HCC patients, limited gastric resection can be recommended even when curative surgery for HCC is performed. By contrast, when advanced GC is present, curative gastrectomy with lymphadenectomy would be advisable to improve the long-term survival.

Palliative gastrectomy for advanced gastric cancer.

BACKGROUND/AIMS: Although palliative gastrectomy for advanced gastric cancer may be favorable in selected patients presenting with bleeding and obstruction, little has been reported about the clinical significance of palliative gastrectomy, including prognosis. METHODOLOGY: A retrospective comparison between 84 patients with palliative gastrectomy (PG group) and 100 patients with unresectable operation (UO group) for advanced gastric cancer was carried out. RESULTS: The incidence of serosal invasion, peritoneal dissemination, hepatic and lymph node metastases, and undifferentiated tissue type in the UO group were significantly higher than in the PG group. Median survival after operation in the PG group (20.6 months) was significantly longer than in the UO group (5.7 months). Also, in stage IVb patients, median survival time in the PG group (10.2 months) was significantly longer than in the UO group (5.0 months). However, median survival in the patients with synchronous liver metastasis between PG (8.4 months) and UO (4.6 months) groups was not significantly different. Survival rates after operation of 6 months, 1 year and 2 years in all patients between the palliative gastrectomy group versus UO group were 83.6% versus 38.3% (P < 0.01), 63.0% versus 9.3% (P < 0.01) and 35.2% versus 0% (P < 0.01), respectively. CONCLUSIONS: Palliative gastrectomy compared to unresectable operation may be effective for improvement of prognosis even if stage IVb patients with peritoneal dissemination and/or distant lymph node metastasis. However, it may be unfavorable on survival of patients with synchronous liver metastasis.

Postoperative chemotherapy in elderly patients with advanced gastric cancer.

BACKGROUND/AIMS: The definitive efficacy of postoperative chemotherapy in elderly patients with advanced gastric cancer has not been established. The aim of this study is to evaluate prognosis in elderly patients with advanced gastric cancer and the effect of postoperative chemotherapy on prognosis. METHODOLOGY: Fifty-three patients, 75 years of age or older who underwent curative surgery for advanced gastric cancer were divided into 14 patients with postoperative chemotherapy (chemotherapy group) and 39 patients without postoperative chemotherapy (control group). Chemotherapy regimens were as follows: oral 5-FU alone (n = 11), intravenous mitomycin plus 5-FU: MF (n = 2), and MF plus oral 5-FU (n = 1). No prior chemotherapy or radiation was given. RESULTS: There were no significant differences of clinical and pathological backgrounds between the two groups. The rate of death due to recurrent carcinoma was 50.0% in the chemotherapy group and 43.6% in the control group, the difference being insignificant. Although the median survival time of the chemotherapy group (40.4 months) was longer than in the control group (31.7 months), a significant difference did not exist between the groups. The 1-, 3-, and 5-year survival rates did not significantly differ between the chemotherapy group versus the control group, 85.7% versus 82.1%, 42.9% versus 51.3%, and 35.7% versus 46.2%, respectively. CONCLUSIONS: Postoperative chemotherapy did not contribute to prolong survival in elderly patients with advanced gastric cancer mainly because the incidence of recurrent carcinoma was not reduced.