住院老年病患者多病性和多药性研究

目的研究住院老年患者的多药性和多病性。方法选择2009～2012年期间5316例住院患者,依据患者年龄分为成人组和老年组,药物统计为出院前第1 d使用的药物数量,病种数以出院诊断为统计依据;同时使用≥5种药物为多药性,同时合并≥5种疾病为多病性。结果老年组平均使用药物为(10.5±9.2)种,成人组平均使用药物为(3.5±3.1)种,老年组显著多于成人组(P<0.01);不同年龄老年亚组平均使用药物为:65～74岁(6.5±6.4)种,75～84岁(9.6±9.2)种,≥85岁(11.4±10.2)种,65～74岁亚组与≥85岁亚组比较有显著差异(P<0.01)。老年组病种数为(8.3±4.8)种,成人组病种数为(3.8±3.2)种,老年组病种数比成人组病种数多(P<0.01)。不同年龄老年亚组病种数为:65～74岁(5.3±4.8)种,75～84岁(7.4±5.7)种,≥85岁(9.2±6.1)种,65～74岁亚组与≥85岁亚组比较有显著差异(P<0.01)。结论住院老年患者普遍存在多药性和多病性,高龄患者更突出。

住院老年高血压患者的多药性和多病性研究

目的研究住院老年高血压患者的多药性和多病性。方法 621例住院高血压患者依据电子病历记录被分为成人高血压组和老年高血压组。以高血压作为第一诊断患者为统计对象,药物计算为出院前1 d使用的药物数量,病种数以出院诊断为统计依据;同时使用5种或5种以上药物为多药性。结果成人高血压组使用药物(4.5±3.8)种,老年高血压组使用(10.4±6.3)种,老年高血压组使用药物数比成人高血压组高(P<0.01);老年人亚组使用药物:65～74岁使用(10.1±7.5)种,75～84岁使用(10.5±7.8)种,≥85岁使用(11.5±8.4)种,65～74岁亚组与≥85岁亚组比较有显著性差异(P<0.01)。老年高血压组病种数为(8.3±4.8)种,成人高血压组病种数为(7.8±4.3)种,老年高血压组病种数比成人高血压组病种数高(P<0.01)。老年人亚组病种数:65～74岁(6.3±3.5)种,75～84岁(6.7±4.2)种,≥85岁(7.3±4.4)种,65～74岁亚组与≥85岁亚组比较有显著性差异(P<0.01)。结论住院老年高血压患者普遍存在多药性和多病性,高龄患者更突出。

住院老年糖尿病患者的多药性研究

目的研究住院老年糖尿病患者的多药性和多病性。方法 2008年—2011年住院的老年糖尿病患者,依据我院的电子病历记录,分为成人糖尿病组和老年糖尿病组。以2型糖尿病作为第一诊断患者为统计对象。药物计算为出院前第1天使用的药物数量,病种数以出院诊断为统计依据;同时使用5种或5种以上药物为多药性。结果成人糖尿病组平均使用药物为6.3种,老年糖尿病组使用为11.2种,老年糖尿病组使用药物数、病种数高于成人糖尿病组(P<0.05),老年糖尿病亚组间无统计学意义。结论糖尿病患者普遍存在多药性和多病性,老年患者更突出,需要进一步优化治疗。

Comparative Assessment of Genetic Diversity of Peanut (Arachis hypogaea L.)Genotypes with Various Levels of Resistance to Bacterial Wilt Through SSR and AFLP Analyses

Bacterial wilt （BW） caused by Ralstonia solanacearum is an important constraint to peanut （Arachis hypogaea L.） production in several Asian and African countries, and planting BW-resistant cultivars is the most feasible method for controlling the disease. Although several BW-resistant peanut germplasm accessions have been identified, the genetic diversity among these has not been properly investigated, which has impeded efficient utilization. In this study, the genetic relationships of 31 peanut genotypes with various levels of resistance to BW were assessed based on SSR and AFLP analyses. Twenty-nine of 78 SSR primers and 32 of 126 AFLP primer combinations employed in this study were polymorphic amongst the peanut genotypes tested. The SSR primers amplified 91 polymorphic loci in total with an average of 3.14 alleles per primer, and the AFLP primers amplified 72 polymorphic loci in total with an average of 2.25 alleles per primer. Four SSR primers （14H06, 7G02, 3A8, 16C6） and one AFLP primer （P1M62） were found to be most efficient in detecting diversity. The genetic distance between pairs of genotypes ranged from 0.12 to 0.94 with an average of 0.53 in the SSR data and from 0.06 to 0.57 with an average of 0.25 in the AFLP data. The SSR-based estimates of the genetic distance were generally larger than that based on the AFLP data. The genotypes belonging to subsp, fastigiata possessed wider diversity than that of subsp, hypogaea. The clustering of genotypes based on the SSR and AFLP data were similar but the SSR clustering was more consistent with morphological classification ofA. hypogaea. Optimum diverse genotypes of both subsp, hypogaea and subsp.fastigiata can be recommended based on this analysis for developing mapping populations and breeding for high yielding and resistant cultivars.

Adiponectin Gene Variation -4522C/T Is Associated with Type 2 Diabetic Obesity and Insulin Resistance in Chinese

The authors investigated the possible association of -4522C/T variation of adiponectin gene with coronary heart disease （CHD） and type 2 diabetes mellitus （T2DM）. Genotyping of SNP --4522C/T in 304 patients with CHD, 389 patients with T2DM, and 405 age and sex-matched healthy control subjects was carried out by means of PCR-RFLP approach. No significant difference in the genotype or allele frequencies was found, either between patients with CHD and control subjects, or between patients with T2DM and control subjects. However, in the subgroup analysis, an association of the TAr genotype and T allele with type 2 diabetes combined with obesity （BMI ≥ 25 kg/m2） was found （P = 0.014 and P = 0.034, respectively）. Also the homeostasis model assessment of insulin resistance （HOMA-IR） in T2DM patients with T/T genotype was significantly higher than that in T2DM patients carrying C allele （P = 0.0069）. The authors＇ findings for the first time demonstrated that SNP --4522 in the adiponectin gene was associated with T2DM that combined with obesity and higher insulin resistance index in patients with T2DM. This indicated that the variation might associate with an increased susceptibility to type 2 diabetic obesity and insulin resistance. But -4522C/T polymorphism did not contribute to the susceptibility of CHD.

Immunologic pathogenesis of multiple sclerosis

Multiple sclerosis （MS） is an autoimmune disease. The etiology and pathogenesis of MS remain unclear. At present, there are substantial evidences to support the hypothesis that genetics plays a crucial role. The people who have genetic predisposing genes easily develop immune-mediated disorder, probably in conjunction with environmental factors. The aim of this review is to describe recent observations regarding the immunologic pathogenesis of MS.

Establishment and Application of a Multiplex PCR System for the Detection of Blast Resistance Genes Pi-ta and Pi-b in Rice

Rice blast is one of the important diseases in major rice producing areas of China. The main blast resistance genes Pi-ta and Pi-b showed broad-spectrum and durable resistance to rice blast in many rice growing areas of China, which have been widely utilized in rice breeding and commercial production. In this study, on the basis of detection and verification of the genotypes of 22 rice varieties har- boring known blast resistance genes （Pi-ta and Pi-b） and blast susceptibility genes （pi-ta and pi-b）, two multiple PCR systems for these genes were established by us- ing the functional markers of blast resistance genes Pi-ta and Pi-b as well as blast susceptibility genes pi-ta and pi-b, respectively. Specifically, multiple PCR system I could simultaneously detect blast resistance genes Pi-ta and Pi-b, while system II could detect simultaneously blast susceptibility genes pi-ta and pi-b. In addition, the genotypes of 336 high generation breeding materials were detected with these two multiple PCR systems. The results were highly consistent with those of conventional single mark detection, indicating that these two multiplex PCR systems were stable, reliable and time-saving. The established multiplex PCR systems may serve as a rapid and efficient method to identify and screen rice germplasm resources and can be applied in marker-assisted selection to polymerize multiple genes for blast resis- tance in rice breeding.

Liriodendrin protects SH-SY5Y cells from dopamine-induced cytotoxicity

Aim To investigate the effect of liriodendrin, an extract from Fraxinus sielboldiana blume belonging to the Oleaceae family, on dopamine-induced cytotoxicity in human neuroblastoma SH-SY5Y cells. Methods Cell viability was processed when treated with 50 μmol·L^-1 of dopamine for 24 h by MTT assay. Early apoptosis, late apoptosis/necrosis were analyzed by flow cytometry using Annexin V-FITC and propidium iodide （PI） double-staining, respectively. Generation of reactive oxygen species （ROS） was assessed by DCFH-DA, an oxidation-sensitive fluorescent probe. To evaluate mitochondrion membrane potential （Δψm） using flow cytometry with the fluorescent dye Rhodamine 123. The transcriptional level of P53 was studied using RT- PCR. Results The dopamine-induced loss of cell viability was significantly attenuated by liriodendrin treatment at the concentration of 10^-8, 10^-7, 10^-6, 10^-5 and 10^-4 mol·L^-1. The protective effects of liriodendrin （10^-7, 10^-6 and 10^-5 mol·L^-1） on dopamine-induced cytotoxicity may be ascribed to its anti-oxidative properties by reducing ROS level and anti-apoptotic effect via protection of Δψm. In addition, the effect of liriodendrin may involve the P53 pathway in apoptosis. Conclusion Liriodendrin may provide a useful therapeutic strategy for the treatment of neurodegenerative diseases such as Parkinson＇s disease （PD）

Genetic predisposition to inflammation:a new risk factor of Alzheimer's disease

Inflammation has been shown to play an important role in the progression of Alzheimer＇s disease （AD）. Recent epidemical study indicates that the incidence of AD in some populations is substantially influenced by the gene polymorphisms of the inflammation mediators. Meanwhile, an ensured risk factor, the ApoE ε4 allele is also reported to directly promote inflammation. Accordingly, it appears that an individual genetic background has partly determined his predisposition for AD by the extent of the inflammation response to the chronic stimulus by β-amyloid peptide （Aβ） deposits and other antigen stressor in the elderly. Hence we present a hypothesis that the inflammation genotypes may contribute to AD susceptibility. This may provide a new orientation both for future identification of individuals at risk and for personalized medication.

Drug-induced liver injury:Is it somehow foreseeable?

The classic view on the pathogenesis of drug-induced liver injury is that the so-called parent compounds are made hepatotoxic by metabolism (formation of neosubstances that react abnormally), mainly by cytochromes P-450 (CYP), with further pathways, such as mitochondrial dysfunction and apoptosis, also playing a role. Risk factors for drug-induced liver injury include concomitant hepatic diseases, age and genetic polymorphisms of CYP. However, some susceptibility can today be predicted before drug administration, working on the common substrate, by phenotyping and genotyping studies and by taking in consideration patients' health status. Physicians should always think of this adverse effect in the absence of other clear hepatic disease. Ethical and legal problems towards operators in the health care system are always matters to consider.

Polymorphisms of some cytokines and chronic hepatitis B and C virus infection

AIM： To study the relationship between the polymorphisms in some cytokines and the outcome of hepatitis B virus （HBV） and hepatitis C virus （HCV） infection. METHODS： Samples were obtained from 203 patients infected with HBV and/or HCV while donating plasma in 1987, and 74 controls were obtained from a rural area of North China. Antibodies to HBV or HCV antigens were detected by enzyme-linked imrnunoassay. The presence of viral particles in the serum was determined by nested reverse-transcriptase polymerase chain reaction （PCR）. Hepatocellular injury, as revealed by alanine aminotransferase （ALT） and aspartate aminotransferase level, was detected by a Beckman LX-20 analyzer. DNA was extracted from blood cells. Then, the single nucleotide polymorphisms of IL-2-330, IFN-γ＋874, IL-10-1082/-592 and IL-4-589 were investigated by restriction fragment length polymorphism-PCR or sequence specific primer-PCR.RESULTS： Persistent infection with HBV, HCV, and HBV/HCV coinfection was associated with IL-2-330 TT genotype and T allele, IFN-γ＋874 AA genotype, and IL-10-1082 AA genotype. The clinical outcome of HBV and/or HCV infection was associated with IL-2-330 TT genotype and T allele, IFN-γ＋874 AA genotype, and IL-10-1082 AA genotype. IL-2-330 GG genotype frequency showed a negative correlation with clinical progression, IL-10-1082 AA genotype frequency showed a positive correlation and IL-10-1082 AG genotype frequency showed a negative correlation with clinical progression. HCV RNA positive expression was associated with IL-10-1082 AA genotype and the A allele frequency. Abnormal serum ALT level was associated with IL-10-592 AC genotype frequency and IL-4-589 CC genotype, CT genotype, and the C allele. CONCLUSION： These results suggest that polymorphisms in some cytokine genes influence persistent HBV and HCV infection, clinical outcome, HCV replication, and liver damage.

Genetic diversity of the hepatitis C virus: Impact and issues inthe antiviral therapy

The hepatitis C Virus (HCV) presents a high degree of genetic variability which is explained by the combination of a lack of proof reading by the RNA dependant RNA polymerase and a high level of viral replication. The re- sulting genetic polymorphism defines a classification in clades, genotypes, subtypes, isolates and quasispecies. This diversity is known to reflect the range of responses to Interferon therapy. The genotype is one of the pre- dictive parameters currently used to define the antiviral treatment strategy and the chance of therapeutic suc- cess. Studies have also reported the potential impact of the viral genetic polymorphism in the outcome of antivi- ral therapy in patients infected by the same HCV geno- type. Both structural and non structural genomic regions of HCV have been suggested to be involved in the Inter- feron pathway and the resistance to antiviral therapy. In this review, we first detail the viral basis of HCV diversity. Then, the HCV genetic regions that may be implicated in resistance to therapy are described, with a focus on the structural region encoded by the E2 gene and the non- structural genes NS3, NS5A and NS5B. Both mechanisms of the Interferon resistance and of the new antiviral drugs are described in this review.

Phase I/II enzyme gene polymorphisms and esophageal cancer risk: A meta-analysis of the literature

AIM:Phase I/II enzymes metabolize environmental carcinogens and several functional polymorphisms have been reported in their encoding genes. Although their significance with regard to esophageal carcinogenicity has been examined epidemiologically, it remains controversial. The present systematic review of the literature was performed to clarify associations. METHODS: Eligible studies were case-control or cohort studies published until September 2004 that were written in any language. From PubMed and a manual review of reference lists in relevant review articles, we obtained 16 studies related to the CYP1A1 Ile-Val substitution in exon 7, CYP1A1 MspI polymorphisms, CYP2E1 Rsal polymorphisms, GSTM1 null type, GSTT1 null type and GSTP1 Ilel04Val. All were of case-control design. Summary statistics were odds ratios (ORs) comparing heterozygous-, homozygous-non-wild type or these two in combination with the homozygous wild type, or the null type with the non-null type for GSTM1 and GSTT1, A random effect model was used to estimate the summary ORs. A meta-regression analysis was applied to explore sources of heterogeneity. RESULTS: Individuals with the Ile-Val substitution in CYP1A1 exon 7 had increased esophageal cancer risk, with ORs (95%CI) compared with lie/lie of 1.37 (1.09-1.71), 2.52 (1.62-3.91) and 1.44 (1.17-1.78) for Ile-Val, Val/Val genotype and the combined group. No significant association was found between esophageal cancer risk and the other genetic parameters. CONCLUSION: A significant association exists between the CYP1A1 Ile-Val polymorphism and risk of esophageal cancer. Polymorphisms that increase the internal exposure to activated carcinogens may increase the risk of esophageal cancer.

Effect of cytokine gene polymorphism on histological activity index, viral load and response to treatment in patients with chronic hepatitis C genotype 3

AIM： To investigate the association between cytokine gene polymorphism and disease status in chronic hepatitis C genotype 3 by liver biopsy, ALl, HCV RNA levels and response to treatment. METHODS： Patients with chronic hepatitis C genotype 3 were analyzed for single nucleotide polymorphisms of interleukin （IL）-10, IL-1 beta, interferon-gamma （IFN-y）, tumor necrosis factor-alpha （TNF-y） and transforming growth factor-beta （TGF-β） by polymerase chain reaction using sequence-specific oligonucleotide primers. Liver biopsies were assessed by modified histological activity index （HAI） scoring system using a scale of 0-18 for grading the necro-inflammatory activity and 0-6 for staging the fibrosis. HCV RNA levels were determined by bDNA assay. The patients were treated with interferon alpha and ribavirin for 6 mo. Sustained virological response was assessed 6 mo after the completion of the treatment. RESULTS： Out of the 40 patients analyzed, 26 were males. Mean age was 40.5±12.5 years （range 18- 65 years）. The frequencies of different dimorphic polymorphisms based on single nucleotide substitution were as follows： IL-10-1082 G/A 85%, A/A 12.5%, G/ G 2.5%; IL-10-819 A/C 87.5%, C/C 10%, A/A 2.5%; IL-10-592 C/A 72.5%, C/C 27.5%; IL-1 C 90%, U 10%; IFN-874 T/A 50%, T/T 27.5%, A/A 22.5%; TNF-308 A/G 95%, G/G 5%; TGF-10 T/C 52.5%, C/C 35%, T/T 12.5%. The mean grades of necroinflammatory activity of different genotypes of IL-10 at promoter site -1082 were A/A = 3.6, A/G = 5.0, and G/G = 10.0 and the difference was significant （P = 0.029）. The difference in the stage of disease at a scale of 0-6 was A/A 0.8, A/G 2.3, and G/G 4.0 （P = 0.079）. The difference in the HAI seemed to be related to the presence of allele -1082G.For IL-10 -819 genotypes, mean scores of fibrosis were A/A = 6.0, A/C = 2.2, and C/C = 1.0 （P = 0.020） though the inflammatory activity was not much different. No significant differences in HAI were noted among polymorphisms of other cytokines. Moreover, ALT and HCV RNA levels were not significantly different among different cytokine polymorphisms. There was a significant correlation of HAI and HCV RNA levels with the duration of disease. TGFI3 -10 genotype CC patients had a better end of treatment response than those with other genotypes （P = 0：020）. Sustained virological response to the treatment was not influenced by the cytokine polymorphism. No effect of other factors like viral load, degree of fibrosis, gender, steatosis, was observed on sustained virological response in this population infected with genotype 3. CONCLUSION： There is no significant correlation between cytokine polymorphisms and HAI except for the polymorphisms of anti-inflammatory cytokine IL-10, which may influence hepatic inflammatory activity and fibrosis in patients with chronic hepatitis C genotype 3. Sustained virological response in this genotype does not seem to be influenced by cytokine gene polymorphisms.

IBD5 polymorphisms in inflammatory bowel disease: Association with response to infliximab

AIM: Inflammatory bowel diseases (IBD) are multifactorial pathologies of unknown etiology. One susceptibility locus, IBD5, has been mapped to chromosome 5q31. We analyzed our Spanish cohorts of Crohn's disease (CD) and ulcerative colitis (DC) patients to determine whether this locus is associated with IBD, and to ascertain the main clinical phenotype influenced by this risk factor. The kind of interaction, either genetic heterogeneity or epistasis, between this IBD5 susceptibility region and the NOD2/CARD15 gene mutations was studied as well. Finally, we assessed whether this locus can predict response to infliximab therapy. METHODS: A case control study was performed with 274 CD and 211 UC patients recruited from a single center and 511 healthy ethnically matched controls. Two polymorphisms were genotyped in the IBD5 locus and three in the CARD15/NOD2 gene. RESULTS: Our results evidence association only with CD especially with the fistulizing phenotype and in the absence of NOD2/CARD15 variants (mutant allele frequency in patients vs controls: OR = 2.03, 95% CI = 1.35-3.06, P<0.01). The frequency of the IBD5 homozygous mutant genotype significantly increased in CD patients lacking response to infliximab (RR = 3.88, 95% CI = 1.18-12.0, P<0.05). UC patients overall do not show association with 5q31 polymorphisms, although a similar trend to the one observed in CD is found within the worse prognosis group. CONCLUSION: The IBD5 variants may enhance an individual carrier's risk for CD, mainly in the absence of the NOD2/CARD15 mutations and in fistulizing patients. The data presented suggest the potential role of the 5q31 polymorphisms as markers of response to infliximab.

Impact of lipoprotein lipase gene polymorphisms on ulcerative colitis

AIM： To examine the influence of lipoprotein lipase （LPL） gene polymorphism in ulcerative colitis （UC） patients.METHODS： Peripheral blood was obtained from 131 patients with UC and 106 healthy controls for DNA extraction. We determined LPL gene polymorphisms affecting the enzyme at Ser447stop, as well as Hind Ⅲ and Pvu Ⅱ polymorphisms using PCR techniques. PCR products were characterized by PCR-RFLP and direct sequencing. Polymorphisms were examined for association with clinical features in UC patients. Genotype frequencies for LPL polymorphisms were also compared between UC patients and controls.RESULTS： In patients with onset at age 20 years or younger, C/G and G/G genotypes for Ser447stop polymorphism were more prevalent than C/C genotype （OR = 3.13, 95% CI = 0.95-10.33）. Patients with H^＋/- or H^-/- genotype for Hind Ⅲ polymorphism also were more nu merous than those with H^＋/＋ genotype （OR = 2.51, 95% CI = 0.85-7.45）. In the group with H^＋/＋ genotype for Hind Ⅲ polymorphism, more patients had serum triglyceride concentrations over 150 mg/dL than patients with H^＋/- or H^- genotype （P 〈 0.01, OR = 6.46, 95% CI = 1.39-30.12）. Hypertriglycemia was also more prevalent in patients with P^＋/＋ genotypes for Pvu Ⅱ polymorphism （P 〈 0.05, OR = 3.0, 95% CI = 1.06-8.50）. Genotype frequency for LPL polymorphism did not differ significantly between UC patients and controls.

Relationship between Crohn’s disease, infection with Mycobacterium avium subspecies paratuberculosis and SLC11A1 gene polymorphisms in Sardinian patients

AIM： To study the association between Crohn＇s disease （CD）, Mycobacterium avium subspecies paratubercuolsis （MAP）, and genetic factors by examining the role of natural resistance-associated macrophage protein 1 （NRAMP1） gene polymorphisms （now SLCllA1） in Sardinian patients with CD and controls. METHODS： Thirty-seven CD patients and 34 controls with no inflammatory bowel disease （IBD） were recruited at the University of Sassari after giving written consent. Six SCL11A1 polymorphisms previously reported to be the most significantly associated with IBD were searched. M, pafatubefculosis was identified by IS900 PCR and sequencing. Logistic regression was used to calculate odds ratios （OR） for the associations among CD, presence of MAP, and 6 loci described above.＇ RESULTS： For the first time, a strong association was observed between polymorphisms at NRAMP1 locus 823C/T and CD. While CD was strongly associated with both NRAMP1 and MAP, NRAMP1 polymorphisms and MAP themselves were not correlated. CONCLUSION： Combined with previous work on the NOD2/CARD15 gene, it is clear that the interplay of genetic, infectious, and immunologic factors in the etiology of CD is complex.

Genetic polymorphisms in non-alcoholic fatty liver disease:Clues to pathogenesis and disease progression

The spectrum of non-alcoholic fatty liver disease(NAFLD) ranges from simple steatosis through steatohepatitis to advanced f ibrosis and cirrhosis.Although the reason why only a minority of patients develop progressive forms of disease still remains largely unclear,recent research has identified genetic factors as a possible basis for this variation in disease presentation.Most of the studies have been focused on f inding associations between advanced disease forms and selected single nucleotide polymorphisms in genes encoding various proteins involved in disease pathogenesis.Although there are many limitations regarding the study design and interpretation of published data,further carefully planned studies together with implementation of new genetic technologies will likely bring new insights into disease pathogenesis and potential benefits to the management of patients with NAFLD.

Clinical analysis of multiple primary malignancies in the digestive system: A hospital-based study

AIM： To analyze the characteristics of multiple primary malignancies （MPMs） of digestive system; including incidence, types of tumor combinations, time intervals between development of multiple tumors, clinical course,and prognostic factors affecting survival and mortality.METHODS： Data from a total of 129 patients treated from January 1991 to December 2000 for pathologically proved MPMs, including at least one originating from the digestive system, were reviewed retrospectively.RESULTS： Among 129 patients, 120 （93.02%） had two primary cancers and 9 （6.98%） had three primary cancers. The major sites of MPMs of the digestive system were large intestine, stomach, and liver. Associated nondigestive cancers included 40 cases of gynecological cancers, of which 31 were carcinoma of cervix and 10 cases of genitourinary cancers, of which 5 were bladder cancers. Other cancers originated from the lung, breast,nasopharynx, larynx, thyroid, brain, muscle, and skin.Reproductive tract cancers, especially cervical, ovarian,bladder, and prostate cancers were the most commonlyassociated non-G! cancers, followed by cancer of the lung and breasts. Forty-three cases were synchronous, while the rest （86 cases） were metachronous cancers. Staging of MPMs and treatment regimes correlated with the prognosis between survival and non-survival groups.CONCLUSION： As advances in cancer therapy bring about a progressively larger percentage of long-term survivors, the proportion of patients with subsequent primary lesions will increase. Early diagnosis of these lesions, based on an awareness of the possibility of second and third cancers, and multidiscipiinary treatment strategies will substantially increase the survival of these patients.

Diversity of Gram negative bacteria antagonistic against major pathogens of rice from rice seed in the tropic environment

With the use of a seed washing technique, more than 4000 Gram negative bacteria were isolated by two improved isolation methods from 446 batches of 1 kg rice seed samples obtained from 22 provinces in the Philippines. They were initially characterized on the basis of colony morphology and results of biochemical and pathogenicity tests. Six hundred and fifty two strains were further identified by Biolog, from which 133 were selected for fatty acid methyl ester (FAME) analysis together with 80 standard reference!strains. Sixteen species or types of Pseudomonas and 17 genera of non pseudomonads were identified, more than one third of which have not been recorded in rice. The most predominant species observed were P. putida and P. fulva. About 17% of the strains of Pseudomonas and 2% of the non pseudomonads were antagonistic to one or more fungal or bacterial pathogens of rice. Rice seed is an important source of biological control agents.