MH_dev_244

Hypothalamic regulation of the adenohypophyseal-testicular axis in the male chick embryo . An antibody against luteinizing hormone-releasing hormone ( P01148 ) as well as naloxone , an opioid antagonist , were added to the chorioallantoic membrane ( P62158 ) of 11.5- and 14.5- day-old male chick embryos and plasma testosterone ( T ) concentrations were determined . This protocol was designed to demonstrate : ( 1 ) Whether P01148 is essential in the regulation of the adenohypophyseal-testicular axis in the male embryo and ( 2 ) if P01148 is operative in this unit ' s function , are opiatergic pathways involved in the secretion of P01148 by the hypothalamus . Both anti - P01148 and naloxone lowered plasma T levels in 14.5- day-old embryos , but not 11.5- day-old embryos . This indicates that the hypothalamus , via P01148 , begins to regulate the pituitary-testicular unit at some time between Days 11.5 and 14.5 , i . e . , the hypothalamo-adenohypophyseal-testicular axis is established . The results also strongly suggest that the normal secretory pattern of P01148 is dependent upon opiatergic innervation of the hypothalamus at the same embryonic time .

Suppression of tumor growth and metastasis by a P17948 antagonizing peptide identified from a phage display library . Although the P15692 - Flk - 1 - pathway has been known as the major driving force of angiogenesis , new evidence has shown that P17948 / Flt - 1 plays important roles during the neovascularization under pathological conditions including tumor , atherosclerosis and arthritis . In search of Flt - 1 receptor antagonizing peptides , we screened a phage display 12 - mer-peptide library with recombinant Flt - 1 protein . Seven candidate peptides were identified that specifically bound to P15692 receptor Flt - 1 , of which peptide F56 ( WHSDMEWWYLLG ) almost abolished P15692 binding to receptor Flt - 1 in vitro . In vivo , F56 fused with P00374 ( P00374 - F56 ) inhibited angiogenesis in a P62158 assay . Moreover , P00374 - F56 significantly inhibited the growth of nodules of human gastric cancer cell line MGC - 803 in BALB / c nude mice . Histological analyses showed that necrosis of the implanted tumor was markedly enhanced following treatment with P00374 - F56 . In the severe combined immunodeficiency disease ( SCID ) mouse model for studying metastasis of the human breast cancer cell line BICR-H 1 , synthetic peptide F56 significantly inhibited tumor growth and lung metastases . Taken together , our results have demonstrated that peptide F56 , as a Flt - 1 receptor antagonist , fulfilled the antiangiogenic and antimetastatic effects by specifically interfering with the interaction between P15692 and receptor Flt - 1 . Thus , short peptide F56 may have clinical potential in tumor therapy .

DB09341 transporter - 2 ( P11168 ) promoter mediated transgenic insulin production reduces hyperglycemia in diabetic mice . P01308 production afforded by hepatic gene therapy ( HGT ) retains promise as a potential treatment for type 1 diabetes , but successful approaches have been limited . We employed a novel and previously untested promoter for this purpose , glucose transporter - 2 ( P11168 ) to drive insulin production via delivery by recombinant adeno-associated virus ( rAAV ) . In vitro , the P11168 promoter was capable of robust glucose-responsive expression in transduced HepG 2 human hepatoma cells . Therefore , rAAV constructs were designed to express the furin-cleavable human preproinsulin B10 gene , under the control of the murine P11168 promoter and packaged for delivery with rAAV expressing the type 5 capsid . DB00428 MEN - induced diabetic mice were subjected to hepatic portal vein injection immediately followed by implantation of a sustained-release insulin pellet to allow time for transgenic expression . All mice injected with the rAAV 5 - P11168 - fHPIB 10 virus remained euglycemic for up to 35 days post-injection , with 50 % euglycemic after 77 days post-injection . In contrast , mock-injected mice became hyperglycemic within 15 days post-injection following dissolution of the insulin pellet . Serum levels of both human insulin and C-peptide further confirmed successful transgenic delivery by the rAAV 5 - P11168 - fHPIB 10 virus . These findings indicate that the P11168 promoter may be a potential candidate for regulating transgenic insulin production for hepatic insulin gene therapy in the treatment of type I diabetes .

Attenuation of anti-tuberculosis therapy induced hepatotoxicity by Spirulina fusiformis , a candidate food supplement . Therapy using Isoniazid ( DB00951 ) and DB01045 MENMAX DB01045 MEN ( Q9HBH0 ) leads to induction of hepatotoxicity in some individuals undergoing anti-tuberculosis treatment . In this study , we assessed the effect of Spirulina fusiformis on DB00951 and Q9HBH0 induced hepatotoxicity in rats compared with hepatoprotective drug Silymarin . Induction of hepatotoxicity was measured by changes in the liver marker enzymes ( aspartate transaminase , alanine transaminase , and alkaline phosphatase ) . The antioxidant status was also analyzed in liver tissue homogenate and plasma by measurement of superoxide dismutase , catalase , glutathione-S-transferase , glutathione reductase , and lipid peroxidation levels . We also aimed to study the binding and interactions of the transcription factors Pregnane X Receptor ( O75469 ) and Farnesoid X Receptor ( Q96RI1 ) with DB00951 , Q9HBH0 , and representative active compounds of Spirulina fusiformis by in silico methods . The administration of DB00951 and Q9HBH0 resulted in significant ( p < 0.05 ) decrease in the antioxidant levels and total protein levels . There was also a significant ( p < 0.05 ) increase in the levels of liver marker enzymes . Spirulina fusiformis was seen to protect the parameters from significant changes upon challenge with DB00951 and Q9HBH0 in a dose-dependent manner . This was corroborated by histological examination of the liver . The results of the in silico analyses further support the wet lab results .

[ P08473 activity in the guinea pig model of asthma ] . P08473 exists in airway epithelial cells , smooth muscle , and submucosa near glands , and cleaves tachykinins to inactive metabolites , thereby reducing there effects . To study the role of enkephalinase in asthmatic response , we measured its activity in guinea pig model of asthma . When compared with the control values , the enkephalinase activity was reduced during in immediate asthmatic response ( Q92932 ) and late asthmatic response ( P10586 ) . Compared with the control values ( 100 % ) , each value was 79.7 % , 73.4 % in the trachea and 74.3 % , 55.7 % in the lung respectively . Tracheal muscle preparation taken from the control , Q92932 , and P10586 groups were made and mounted in oxygenated modified Krebs-Ringer solution . The response was monitored by isometric transducer . Concentration response curves to P20366 with or without phosphoramidon were obtained . The contractile responses of the P10586 groups were enhanced in potency and efficiency . DB02557 MEN potentiated the P20366 induced contraction of control and the Q92932 groups but was less potent in enhancing the contractile response in the P10586 group , showing less enkephalinase activity in the P10586 . These results suggest that the enkephalinase plays an important role in P10586 . In P10586 , the enkephalinase activity may be inhibited and the responsiveness of the smooth muscle to some bronchoconstrictor , such as tachykinins , may be increased .

Modulation of tachykinin and cytokine release in patients with coronary disease undergoing percutaneous revascularization . Plasma levels of DB05875 ( SP ) and neurokinin A ( P20366 ) tachykinin and of gamma interferon ( P01579 ) and tumor necrosis factor alpha ( P01375 ) cytokines were assayed in plasma obtained from peripheral blood of 19 patients presenting with stable chronic coronary stenosis and 12 patients with acute coronary syndrome ( ACS ) . Plasma samples were obtained before , during , and after percutaneous coronary intervention ( P05154 ) consisting of implantation of a metallic stent . Fourteen healthy subjects without any evident risk factors for coronary artery disease ( CAD ) were also included for comparison at basal time . We found that plasma levels of both P01579 and P01375 were significantly higher in patients with chronic or acute CAD than those in control subjects at the time of presentation . P20366 and P01579 levels were also significantly increased in ACS patients compared with those in patients with stable disease . The analysis performed during and after P05154 revealed that P01579 levels increased 15 min after stent implantation in both chronic and ACS patients and that P01375 levels increased in chronic patients only compared to basal values . In addition , a significant decrease of both P20366 and SPA levels 48 h after the end of the revascularization procedure was observed in ACS patients . These data suggest that modulation of tachykinin and / or cytokine release with proinflammatory activity in chronic or acute cardiac ischemia and during following coronary stenting might play an important role in heart tissue damage and in long-term inflammatory complications of P05154 .

Control of phenylalanine and tyrosine metabolism by phosphorylation mechanisms . A system for the parallel determination of enzyme phosphorylation and expressed activity in rat liver cells , and its application to studies of phenylalanine hydroxylase and tyrosine aminotransferase , is described . DB00120 MEN hydroxylase is phosphorylated by agents which stimulate cyclic AMP - and Ca2 + - dependent protein kinase activity . The phosphorylation site ( s ) appear to be the same for both kinases . Phosphorylation is accompanied by increased metabolic flux at low , physiologically relevant , substrate concentrations . P01308 and spermine both inhibit the phosphorylation of the enzyme , possibly by increasing dephosphorylation . P17735 is phosphorylated in liver cell incubations but the rate is slow and insensitive to additions to the medium . No parallel changes in flux could be detected . Both enzymes are subject to complex regulatory mechanisms , short - and long-term . Their activities may be coordinated in vivo by control exerted at the level of the plasma membrane where both amino acids share the same transport processes . Determination of the control coefficients for the several components indicates that membrane transport may be a major limitation on flux .

Cribriform-morular variant of papillary thyroid carcinoma in an 8 - year-old girl : a case report with immunohistochemical and molecular testing . The description of the histological features and the immunohistochemical and molecular analyses of a case of cribriform-morular variant of papillary thyroid carcinoma in an 8 - year-old girl with a family history of adenomatous polyposis is presented . The neoplasm was multifocal and bilateral , with a mixed pattern of solid , trabecular , and morular areas . The neoplasm showed angioinvasive behavior , extracapsular infiltration with extension to the perythyroidal muscles , and lymph node metastases . Tumor cells were positive for P62158 5.2 , cytokeratins 5/6 , Q15669 - 1 , HBME - 1 , galectin - 3 , and β-catenin . In addition , the molecular tests did not reveal P15056 mutations , P07949 / PTC rearrangement , P25054 mutation , or P01116 mutation .

Identification of insulin-stimulated phosphorylation sites on calmodulin . P01308 enhances calmodulin phosphorylation in vivo . To determine the insulin-sensitive phosphorylation sites , phosphocalmodulin was immunoprecipitated from Chinese hamster ovary cells expressing human insulin receptors ( CHO / IR ) . P62158 was constitutively phosphorylated on serine , threonine , and tyrosine residues , and insulin enhanced phosphate incorporation on serine and tyrosine residues . Phosphocalmodulin immunoprecipitated from control and insulin-treated CHO / IR cells , and calmodulin phosphorylated in vitro by the insulin receptor kinase and casein kinase II were resolved by two-dimensional phosphopeptide mapping . Several common phosphopeptides were detected . The phosphopeptides from the in vitro maps were eluted and phosphoamino acid analysis , manual sequencing , strong cation exchange chromatography , and additional proteolysis were performed . This strategy demonstrated that DB00135 - 99 and DB00135 - 138 were phosphorylated in vitro by the insulin receptor kinase and DB00156 - 79 , DB00133 - 81 , DB00133 - 101 and DB00156 - 117 were phosphorylated by casein kinase II . In vivo phosphorylation sites were identified by comigration of phosphopeptides on two-dimensional maps with phosphopeptides derived from calmodulin phosphorylated in vitro and by phosphoamino acid analysis . This approach revealed that DB00135 - 99 and DB00135 - 138 of calmodulin were phosphorylated in CHO / IR cells in response to insulin . Additional sites remain to be identified . The identification of the insulin-stimulated in vivo tyrosine phosphorylation sites should facilitate the elucidation of the physiological role of phosphocal-modulin .

Synchronous mucinous tumors of the appendix and the ovary associated with pseudomyxoma peritonei . A clinicopathologic study of six cases with comparative analysis of P01116 mutations . Mucinous tumors of the ovary are often associated with mucinous tumors of the appendix . It has not been clearly determined whether they are independent or metastatic neoplasms . A clinicopathologic study and a comparative analysis of P01116 mutations were done in six cases of synchronous ovarian and appendiceal tumors . The clinicopathologic features ( simultaneous presentation , bilaterality or right-sided predominance , similar histopathologic findings , presence of pseudomyxoma peritonei ) suggested that they were primary appendiceal tumors metastatic to the ovaries . DNA was extracted from formalin-fixed , paraffin-embedded tissue , and target sequences were amplified in vitro by the polymerase chain reaction . Mutations were detected by the presence of restriction fragment length polymorphism , artificially introduced by the use of mutant amplimers . The pattern of P01116 mutations was identical in the ovarian and appendiceal tumors of all patients . Four patients had a P19440 --> Q6IB77 ( DB00145 MEN --> DB00128 ) transition and one a P19440 --> GTT ( DB00145 MEN --> DB00161 ) transversion , all detected in codon 12 . No mutation was found in the sixth patient in either the ovarian or the appendiceal tumor . Because P01116 mutations are considered to represent an early event in tumorigenesis , our results support a clonal nature for both tumors and suggest that they are not independent tumors but rather originate one from another .

DB00171 - sensitive potassium channel activation induces angiogenesis in vitro and in vivo . Intense research is conducted to identify new molecular mechanisms of angiogenesis . Previous studies have shown that the angiogenic effects of hydrogen sulfide ( H2S ) depend on the activation of DB00171 - sensitive potassium channels ( KATP ) and that P23582 ( P09543 ) , which can act through KATP , promotes endothelial cell growth . We therefore investigated whether direct KATP activation induces angiogenic responses and whether it is required for the endothelial responses to P09543 or vascular endothelial growth factor ( P15692 ) . Chick chorioallantoic membrane ( P62158 ) angiogenesis was similarly enhanced by the direct KATP channel activator 2 - nicotinamidoethyl acetate ( SG - 209 ) and by P09543 or P15692 . The KATP inhibitors glibenclamide and 5 - hydroxydecanoate ( 5 - HD ) reduced basal and abolished P09543 - induced P62158 angiogenesis . In vitro , the direct KATP openers nicorandil and SG - 209 and the polypeptides P15692 and P09543 increased proliferation and migration in bEnd . 3 mouse endothelial cells . In addition , P15692 and P09543 induced cord-like formation on Matrigel by human umbilical vein endothelial cells ( HUVECs ) . All these in vitro endothelial responses were effectively abrogated by glibenclamide or 5 - HD . In HUVECs , a small-interfering RNA-mediated decrease in the expression of the inwardly rectifying potassium channel ( Kir ) 6.1 subunit impaired cell migration and network morphogenesis in response to either SG - 209 or P09543 . We conclude that 1 ) direct pharmacologic activation of KATP induces angiogenic effects in vitro and in vivo , 2 ) angiogenic responses to P09543 and P15692 depend on KATP activation and require the expression of the Kir 6.1 KATP subunit , and 3 ) KATP activation may underpin angiogenesis to a variety of vasoactive stimuli , including H2S , P15692 , and P09543 .

Regulation and therapeutic targeting of peptide-activated receptor guanylyl cyclases . Cyclic GMP is a ubiquitous second messenger that regulates a wide array of physiologic processes such as blood pressure , long bone growth , intestinal fluid secretion , phototransduction and lipolysis . Soluble and single-membrane-spanning enzymes called guanylyl cyclases ( GC ) synthesize cGMP . In humans , the latter group consists of P16066 , P20594 , P25092 , GC-E and P51841 , which are also known as P16066 , P20594 , StaR , Ret 1 - GC and Ret 2 - GC , respectively . Membrane GCs are activated by peptide ligands such as atrial natriuretic peptide ( P01160 ) , B-type natriuretic peptide ( DB04899 ) , P23582 ( P09543 ) , guanylin , uroguanylin , heat stable enterotoxin and GC-activating proteins . DB04899 and carperitide are clinically approved peptide-based drugs that activate P16066 . CD-NP is an experimental heart failure drug that primarily activates P20594 but also activates P16066 at high concentrations and is resistant to degradation . Inactivating mutations in P20594 cause acromesomelic dysplasia type Maroteaux dwarfism and chromosomal mutations that increase P09543 concentrations are associated with Marfanoid-like skeletal overgrowth . Pump-based P09543 infusions increase skeletal growth in a mouse model of the most common type of human dwarfism , which supports P09543 / P20594 - based therapies for short stature diseases . DB08890 MEN is a peptide activator of P25092 that stimulates intestinal motility and is in late-stage clinical trials for the treatment of chronic constipation . This review discusses the discovery of cGMP , guanylyl cyclases , the general characteristics and therapeutic applications of P16066 , P20594 and P25092 , and emphasizes the regulation of transmembrane guanylyl cyclases by phosphorylation and DB00171 .

DB00227 - stimulated superinduction of P16581 , P05362 and P19320 in P01375 activated human vascular endothelial cells . Inhibitors of P04035 ( statins ) reveal important pharmacological effects in addition to reducing the plasma LDL cholesterol level . In the pathogenesis of arteriosclerosis , transendothelial migration of various leukocytes including monocytes is a crucial step . We , therefore , investigated the expression of P16581 , intercellular cell adhesion molecule - 1 ( P05362 ) and vascular cell adhesion molecule - 1 ( P19320 ) in vascular endothelial cells as influenced by lovastatin . Human umbilical vein endothelial cells ( HUVECs ) express significant amounts of selectins and cell adhesion molecules ( CAMs ) within a few hours after stimulation with P01375 . This effect is potentiated by 100-200 % when the cells are pretreated with 0.1- 2.5 microM lovastatin . The lovastatin-mediated increase in the cytoplasm and at the cell surface is dose-dependent and significant at lovastatin concentrations comparable to plasma levels in patients under lovastatin treatment . The lovastatin-potentiated increase of P16581 and CAMs is correlated with a corresponding increase of selectin - and P62158 - specific mRNA . We conclude that , in vivo , statin treatment could trigger an enhanced recruitment of macrophages that might support the cholesteryl ester efflux from the arteriosclerotic plaque .

Selective modulation of promoter recruitment and transcriptional activity of PPARgamma . P37231 ( PPARgamma ) is a nuclear receptor regulated by the insulin-sensitizing thiazolidinediones ( TZDs ) . We studied selective modulation of endogenous genes by PPARgamma ligands using microarray , RNA expression kinetics , and chromatin immunoprecipitation ( ChIP ) in 3T3 - Q9NUQ9 adipocytes . We found over 300 genes that were significantly regulated the TZDs pioglitazone , rosiglitazone , and troglitazone . TZD-mediated expression profiles were unique but overlapping . Ninety-one genes were commonly regulated by all three ligands . TZD time course and dose-response studies revealed gene - and TZD-specific expression kinetics . PEPCK expression was induced rapidly but Q16654 expression was induced gradually . DB00197 MEN EC50 values for PEPCK , Q16654 , and P41220 regulation were greater than those for pioglitazone and rosiglitazone . TZDs differentially induced histone acetylation of and PPARgamma recruitment to target gene promoters . Selective modulation of PPARgamma by TZDs resulted in distinct expression profiles and transcription kinetics which may be due to differential promoter activation and chromatin remodeling of target genes .

Peroxisome-proliferator activator receptor-gamma activation decreases attachment of endometrial cells to peritoneal mesothelial cells in an in vitro model of the early endometriotic lesion . The aim of this study was to investigate whether peroxisome proliferator-activated receptor ( Q07869 ) - gamma activation has an effect on the attachment of endometrial cells to peritoneal mesothelial cells in a well-established in vitro model of the early endometriotic lesion . The endometrial epithelial cell line EM42 and mesothelial cell line LP9 were used for this study . EM42 cells , LP9 cells or both were treated with the P37231 agonist ciglitazone ( CTZ ) at varying concentrations ( 10 , 20 and 40 microM ) x 48 h with subsequent co-culture of EM42 and LP9 cells . The rate of EM42 attachment and invasion through LP9 cells was then assessed and compared with control ( EM42 and LP9 cells co-cultured without prior treatment with CTZ ) . Next , attachment of CTZ-treated and untreated EM42 cells to hyaluronic acid ( HA ) , a cell adhesion molecule ( P62158 ) on peritoneal mesothelial cells , were assessed . Although there was no difference in EM42 attachment when LP9 cells alone were treated with CTZ , treatment of EM42 cells with 40 microM CTZ decreased EM42 attachment to LP9 cells by 27 % ( P < 0.01 ) . Treatment of both EM42 and LP9 cells with 40 microM CTZ decreased EM42 attachment to LP9 by 37 % ( P < 0.01 ) . Treatment of EM42 cells with 40 microM CTZ decreased attachment to HA by 66 % ( P = 0.056 ) . CTZ did not decrease invasion of EM42 cells through the LP9 monolayer . CTZ may inhibit EM42 cell proliferation . In conclusion , CTZ significantly decreased EM42 attachment to LP9 cells and HA in an in vitro model of the early endometriotic lesion .

Plasmodium falciparum dihydrofolate reductase alleles and pyrimethamine use in pregnant Ghanaian women . Drug resistance in Plasmodium falciparum affects prevention of malaria in pregnancy . In a cross-sectional study of 530 pregnant Ghanaian women , P . falciparum dihydrofolate reductase ( P00374 ) gene mutations linked with pyrimethamine resistance were assessed and associations with pyrimethamine intake were analyzed . P . falciparum infected 69 % of women without pyrimethamine use , 59 % of those who had a history of pyrimethamine consumption but a negative urine test , and 53 % of individuals with a positive urine test . Eighty-one percent , 43 % , and 74 % of the isolates contained the mutations DB00174 - 108 , DB00167 - 51 , and DB00125 - 59 , respectively . DB00156 - 108 occurred in 8 % . DB00205 MEN use was associated with increased frequencies of DB00174 - 108 and DB00125 - 59 but not of DB00167 - 51 or DB00156 - 108 . In women with prophylaxis , wild-type parasites were absent and anemia tended to be more common with an increasing number of P00374 gene mutations . DB00205 MEN appears to be not adequately effective in this part of Ghana , most likely due to the predominance of resistant parasites . Selection for resistance following insufficient prophylaxis could possibly affect the efficacy of future intermittent sulfadoxine-pyrimethamine treatment .

Stage-dependent inhibition of Plasmodium falciparum by potent Ca2 + and calmodulin modulators . The effects of Ca2 + channel blockers , verapamil , nicardipine and diltiazem , and of potent calmodulin ( P62158 ) inhibitors , trifluoperazine ( Q9HCM9 ) , calmidazolium , W - 7 and W - 5 , on Plasmodium falciparum in culture were examined . Among Ca2 + blockers , nicardipine was the most potent with the 50 % inhibitory concentration ( IC50 ) of 4.3 microM at 72 h after culture . Parasites were more sensitive to calmidazolium and W - 7 with IC50 of 3.4 and 4.5 microM , respectively , than to Q9HCM9 and W - 5 . All Ca2 + blockers and P62158 inhibitors suppressed parasite development at later stages . DB00622 SUB , diltiazem , calmidazolium and W - 5 also retarded parasite development at earlier stages and / or subsequent growth following pretreatment . Verapamil , nicardipine , Q9HCM9 and calmidazolium reduced erythrocyte invasion by merozoites . Fluorescence microscopy with the cationic fluorescent dye rhodamine 123 revealed that nicardipine , Q9HCM9 and calmidazolium depolarized both the plasma membrane and mitochondrial membrane potentials of the parasite . It is therefore considered that although all Ca2 + and P62158 antagonists tested here influence parasite development at later stages , they are multifunctional , having effects not directly associated with Ca2 + channels or P62158 .

Use of P01148 antagonists in reproductive medicine . Gonadotrophin-releasing hormone ( DB00644 ) plays a key role in the secretion of gonadotrophins , follicle-stimulating hormone ( DB00094 ) and luteinizing hormone ( LH ) , which regulate steroidogenesis and folliculogenesis . Two DB00644 antagonists , DB00050 and DB06785 MEN , deprived of histaminergic side-effects , have been introduced into ovarian stimulation protocols to prevent premature LH surges and proved their safety in clinical trials . At present , most of the published studies have not found significant differences in follicular recruitment , oocyte quality , and so on , except for a decrease in pregnancy and implantation rates in in vitro fertilization and embryo transfer ( IVF-ET ) cycles when the DB00644 antagonist rather than the agonist was used . This decrease in pregnancy rates was in relation with a necessary learning curve of the physicians . Another possibility is the impact of the DB00644 antagonist on endometrium through its P30968 ; this effect was cancelled after cryopreserved embryo transfers because the pregnancy rates were similar between DB00644 antagonist and agonist in this case . DB00644 antagonists were also interesting in poor responders and polycystic ovarian syndrome , where the agonists have not permitted to obtain the better results in IVF-ET cycles . Similarly , the DB00644 antagonists could prevent the LH surge in the intrauterine insemination cycles .

[ Antibacterial activity of 16 antibiotics against Helicobacter pylori ] . The susceptibilities of 24 Helicobacter pylori isolates , which were originated from clinical materials , to 5 beta-lactam antibiotics [ benzylpenicillin ( DB01053 ) , ampicillin ( DB00415 ) , cephalothin ( DB00456 ) , ceftazidime ( DB00438 ) , cefotiam ( DB00229 ) and imipenem ( IPM ) ] , two macrolides [ clarithromycin ( P62158 ) and rokitamycin ( RKM ) ] , two aminoglycosides [ amikacin ( AMK ) and gentamicin ( GM ) ] , two new quinolones [ ciprofloxacin ( CPFX ) and levofloxacin ( LVFX ) ] , two tetracycline [ tetracycline ( TC ) and minocycline ( MINO ) ] , rifampicin ( Q9HBH0 ) and chloramphenicol ( CP ) were tested . All of the isolates showed similar susceptibilities against beta-lactam antibiotics . However , MICs of DB00229 and DB00438 were two - to four-fold higher than those of DB01053 , DB00415 , DB00456 and IPM , MICs of rokitamycin for the tested strains were higher than those of clarithromycin . MICs of CPFX and LVFX showed two-modal distributions . The first peak of distributions was observed between 0.06 to 0.5 microgram / ml and second one was between 4 to 16 micrograms / ml . These distributions suggested that MIC values of 4 to 16 micrograms / ml could result from the expression of a resistance mechanism . In addition , some of H . pylori strains were observed drug resistances between CP and AMK , new quinolones and AMK respectively . From the molecular epidemiological study , cryptic plasmids were detected from the 3 isolates among 24 strains tested .