纤维载体固定化红螺菌反应器处理发酵废液及其动力学模型

在充填软性纤维材料的玻璃柱式反应器中,利用Rhodopseudomonas polustris Y_6光合细菌(PSB)连续处理发酵废液。建立了该处理系统动力学模型。计算出模型参数:K_(?)=45.56mg/ml,μm=0.224h^(-1)。模型理论曲线与实验值较吻合。研究得出较适合的稀释率D_(opt)为0.129h^(-1),此时COD去除能力最大为1686.0ppm COD/h。本文为纤维载体固定化PSB处理有机废水提供了一些放大操作依据。

The Effect of Helicobacter Pylori Infection on Expression of hMSH2, hMLH1 and p53 in Gastric Carcinogenesis

Objective： To detect the expression of hMSH2, hMLH1 and p53 in gastric epithelial cells with and without Helicobactcr pylori （H. pylori） infection and investigate the relationship between H. pylori infection and these genes in gastric carcinogenesis. Methods： H. pylori infection was detected by rapid urease tests. Expression of hMSH2, hMLHland p53 in gastric cancer （GC） tissue, its adjacent mucosa, gastritic mucosa and normal mucosa was assessed by immunohistochemistry SP method. Results： Positive expression rate of hMSH2 in GC tissue （62.7%） was higher than those in adjacent mucosa （29.4%）, gastritic mucosa （32.4%） and normal mucosa （30.0%） （P〈0.001）. Positive rate of hMSH2 in poorly differentiated adenocarcinoma （76.4%） was higher than those in other carcinomas （54.3%, 53.1%） （P〈0.05）. Positive expression rate of hMLH1 in GC tissue （64.3%） mucosa （82.4%） and normal mucosa （80.0%） was lower than those in adjacent mucosa （84.4%）, gastritic （P〈0.01）. Positive rate of hMLH1 in mucoid carcinoma （43.7%） was lower than those in other carcinomas （78.2%, 64.7%） （P〈0.01）. Positive expression rate of p53 in GC tissue （51.9%） was higher than those in adjacent mucosa （3.1%）, gastritic mucosa （0.0%） and normal mucosa （0.0%） （P〈0.001）. Positive rate of p53 in well differentiated adenocarcinoma （32.6%） was lower than those in other carcinomas （58.8%, 68.7%） （P〈0.01）. Positive rates of hMSH2 and hMLH1 in GC with H. pylori infection were lower than those without the infection, respectively （P〈0.05）. Positive rate of p53 in GC with H. pylori infection （61.4%） was higher than that without the infection （40.6%） （P〈0.05）. Conclusion： Gastric carcinogenesis may be associated with abnormal expression of hMSH2, hMLH1 and p53; H. pylori infection affecting expression of these genes may be one of its carcinogenic mechanisms.

Adherent properties of Helicobacter pylori to human epithelial cells *

AIM To study the properties and factors of Helicobacter pylori adherence to human epithelial cells. METHODS The adherent properties of human epithelial cells were studied by using a group of isolated H. pylori strains, anti H. pylori monoclonal antibodies and varied pH environment in in vitro adherence model with HEp 2 cell.

Effects of Helicobacter pylori infection on gastric epithelial cell kinetics in patients with chronic renal failure

AIM： To evaluate the effects of Helicobacter pylori infection on gastric epithelial cell kinetics in patients with chronic renal failure （CRF）. METHODS： Forty-four patients were enrolled in this study and divided into four groups with respect to their Helicobacter pylori （H pylori） and CRF status. Groups were labeled as follows： la： normal renal function, H pylori negative （n = 12）, lb： normal renal function, H pylori positive （n = 11）, 2a： CRF, H pylori negative （n = 10）, 2b： CRF, H pylori positive （n = 11）. Upper gastrointestinal endoscopy was done in all the patients involved in the study. During endoscopical investigation, antral biopsy specimens were taken from each patient. In order to evaluate the cell apoptosis and proliferation in gastric epithelial cells, Bax and proliferating cell nuclear antigen （PCNA） labeling indexes （LI） were assessed with immunohistochemical staining method. RESULTS： For groups la, lb, 2a, and 2b, mean Bax LI was identified as 34.4±13.7, 44.1±16.5, 46.3±20.5, 60.7±13.8, respectively and mean PCNA LI was identified as 36.2±17.2, 53.6±25.6, 59.5±25.6, 67.2±22, respectively. When the one-way ANOVA test was applied, statistically significant differences were detected between the groups for both Bax LI （P = 0.004 〈0.01） and PCNA LI （P = 0.009 〈0.01）. When groups were compared further in terms of Bax LI and PCNA LI with Tukey＇s HSD test for multiple pairwise comparisons, statistically significant difference was observed only between groups la and 2b （P = 0.006 〈0.01）.CONCLUSION： In gastric epithelial cells, expression of both the pre-apoptotic protein Bax and the proliferation marker PCNA increase with H pylori infection. This increase is more evident in patients with uremia. These findings suggest that uremia accelerates apoptosis and proliferation in gastric epithelial cells.

Effect of Clostridium butyricum on fecal flora in Helicobacter pylori eradication therapy

AIM： To investigate the effect of probiotic bacterium, Clostridium butyricum MIYAIRI 588 strain （CBM） on the changes of the fecal flora in Helicobacter pylori （H pylon） treatment. METHODS： Thirty-five patients with gastric or duodenal ulcers positive for H pylori were randomized either to 1 wk amoxicillin, clarithromycin, lansoprazole （Group 1） or to the same regimen supplemented with CBM 7 d ahead of the triple therapy （Group 2）. Stool samples were collected before and 2, 4, 7, 15, and 22 d after the starting eradication therapy, and were examined intestinal flora. Patients were required to keep a diary record of their condition. RESULTS： Obligate anaerobes decreased significantly on d 2, 4, 8 and 15 in Group 1. On the other hand, they did not decrease significantly in Group 2. The Escherichia coli was dominant bacterium in Enterobacteriaceae, but that was replaced by other species such as Klebsiella and Enterobacter after eradication in Group 1. The change was suppressed in Group 2. Abdominal symptoms were less frequent in Group 2 than in Group 1. CONCLUSION： The combined use of CBM reduced the changes in the intestinal flora and decreased the incidence of gastrointestinal side effects.

Helicobacter pyloripromote gastric cancer cells invasion through a NF-κB and COX-2-mediated pathway

AIM: To examine the effects of Helicobacter pylori(Hpylori) infection on the invasiveness of gastric cancer cells,and to elucidate its mechanism. METHODS: Gastric carcinoma cells, MKN-45, were incubated with CagA-positive H pylori, and cell invasion was determined by Matrigel analysis.The expression of matrix metallopr-oteinase-9 (MMP-9),vascular endothelial growth factor (VEGF), and cyclooxygenase-2 (COX-2) were assessed by Western-blot analysis, and transcriptional activation of the COX-2 promoter was examined by measuring luciferase and β-galactosidase activities. Lastly,the proteinDNA interaction was confirmed by an electrophoretic mobility shift assay. RESULTS: The current studies showed that: (1) incubation of CagA-positive H pylori with MKN-45 cells significantly promotes gastric cancer cells invasion, and this effect is attenuated by pre-treatment with NS-398, a COX-2 inhibitor, or PDTC,a nuclear factor κB (NF-κB) inhibitor;(2) the induction of MKN-45 cells invasion by Hpylori is associated with increases in COX-2, MMP-9, and VEGF protein expression, and co-incubation of NS-398 or PDTC significantly reduces these effects;(3) H pylori infection transactivates COX-2 promoter activity and increases the binding of NF-κB to this promoter. CONCLUSION: Our data demonstrate that H pylori infection promotes gastric epithelial cells invasion by activating MMP-9 and VEGF expression. These effects appear to be mediated through a NF-κB and COX-2 mediated pathway, as COX-2 or NF-κB inhibitor significantly attenuate the invasiveness of gastric cancer cells and the expressions of MMP-9 and VEGF protein.

Third-line rescue therapy for Helicobacter pylori infection

H pylori gastric infection is one of the most prevalent infectious diseases worldwide. The discovery that most upper gastrointestinal diseases are related to Hpylori infection and therefore can be treated with antibiotics is an important medical advance. Currently, a first-line triple therapy based on proton pump inhibitor （PPI） or ranitidine bismuth citrate （RBC） plus two antibiotics （darithromycin and amoxicillin or nitroimidazole） is recommended by all consensus conferences and guidelines. Even with the correct use of this drug combination, infection can not be eradicated in up to 23% of patients. Therefore, several second line therapies have been recommended. A 7 d quadruple therapy based on PPI, bismuth, tetracycline and metronidazole is the more frequently accepted. However, with second-line therapy, bacterial eradication may fail in up to 40% of cases. When Hpylori eradication is striclly indicated the choice of further treatment is controversial. Currently, a standard third-line therapy is lacking and various protocols have been proposed. Even after two consecutive failures, the most recent literature data have demonsbated that Hpylori eradication can be achieved in almost all patients, even when antibiotic susceptibility is not tested. Different possibilities of empirical treatment exist and the available third-line strategies are herein reviewed.

Latest insights into the effects of Helicobacter pylori infection on gastric carcinogenesis

There appears to be the strong association between Helicobacter pylori （H pylori） and gastric cancer. We reviewed the latest evidences about the effects of H pylori infection on gastric carcinogenesis, classified into epidemiology, dynamics of gastric mucosal changes, DNA damages, virulence factors, host factors, and source of gastric malignancy. Through the considerable progress made in research into virulence factors resulting from differences between Hpylori strains, such as cagA positivity, as well as into host factors, such as gene polymorphisms, a diverse spectrum of H pyloriassociated diseases, including gastric cancer, is beginning to lend itself to elucidation. The impact of the novel hypothesis advanced by Houghton et al proposing bonemarrow derived stem cells （BMDC） as a potential source of gastric malignancy on evolving research remains to be seen with interest. Further progress in research into H pylori eradication as a viable prophylaxis of gastric cancer, as well as into the mechanisms of gastric carcinogenesis, is to be eagerly awaited for the current year and beyond.

Helicobacter pylori-infected animal models are extremely suitable for the investigation of gastric carcinogenesis

Although various animal models have been developed to clarify gastric carcinogenesis, apparent mechanism of gastric cancer was not clarified in recent years. Since the recognition of the pathogenicity of Helocobacter pylori（H pylori）, several animal models with H pylori infection have been developed to confirm the association between Hpylori and gastric cancer. Nonhuman primate and rodent models were suitable for this study. Japanese monkey model revealed atrophic gastritis and p53 mutation after long-term infection of Hpylori. Mongolian gerbil model showed the development of gastric carcinoma with H pylori infection alone, as well as with combination of chemical carcinogens, such as N-methyl- N-nitrosourea and N-methyl-N-nitro-N＇-nitrosoguanidine. The histopathological changes of these animal models after H pylori inoculation are closely similar to those in human beings with Hpylori infection. Eradication therapy attenuated the development of gastric cancer in Hpylori- infected Mongolian gerbil. Although several features of animal models differ from those seen in human beings, these experimental models provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of Hpylon infection and assist the planning of eradication therapy to prevent gastric carcinoma.

Helicobacter infection in hepatocellular carcinoma tissue

AIM： To investigate whether Helicobacter species （Helicobacter spp.） could be detected in hepatocellular carcinoma （HCC） tissue.METHODS： Liver samples from 28 patients with hepatocellular carcinoma （HCC） diagnosed by histopathology were studied. Twenty-two patients with other liver diseases （5 with liver trauma, 7 with cavernous liver hemangioma, 6 with liver cyst and 4 with hepatolithiasis）, 25 patients with gastric cancer, 15 with colonic cancer and 15 with myoma of uterus served as controls. Two piceces of biopsy were obtained from each patient. One was cultured for Helicobacter spp. and extraction of DNA, the other was prepared for scanning electron microscopy （SEM） and in situ hybridization. The samples were cultured on Columbia agar plates with microaerobic techniques. Helicobacter spp. in biopsy from the studied subjects was detected by polymerase chain reaction （PCR） with Helicobacter spp. 16S rRNA primers. Amplified products were identified by Southern hybridization and sequenced further. Besides, other genes （vacA, cagA） specific for Helicobacter pylori （H pylorO were also detected by PCR. Helicobacter spp. in biopsies was observed by SEM. Transmission electron microscopy （TEM） was performed to identify the cultured positive Helicobacter spp. The presence of Helicobacter spp. was detected by in situ hybridization to confirm the type of Helicobacter. RESULTS： The positive rate of He/icobacter cultured in HCC and gastric cancer tissue was 10.7% （3/28） and 24%（6/25）, respectively. Helicobacter microorganisms were identified further by typical appearance on Gram staining, positive urease test and characteristic colony morphology on TEM. The bacterium was observed in adjacent hepatocytes of the two HCC samples by SEM.The number of cocci was greater than that of bacilli. The bacterium was also found in four gastric cancer samples. PCR showed that the positive rate of HCC and gastric cancer samples was 60.7% and 72% respectively, while the controls were negative （P〈 0.01）. The PCR-amplified products were identified by Southern hybridization and sequenced. The homology to 16S rRNA of H pylon was 97.80%. The samples were verified by in situ hybridization for Helicobacter spp. 16S rRNA-mRNA and proved to be Hpylori positive. There was no statistical significance between HCC and gastric cancer （P〉 0.05）, but the positive rate of HCC and controls had statistical significance （P〈0.01）. Only 3 HCC samples and 2 gastric cancer samples of the cagA genes were detected. None of the samples reacted with primers for vacA in the two groups. As for the genotype of H pylori, type II had preference over type I. CONCLUSION： Helicobacter infection exists in liver tissues of HCC patients. Helicobacter spp. infection is related with HCC, which needs further research.

CagA+ H pylori infection is associated with polarization of T helper cell immune responses in gastric carcinogenesis

AIM:To characterize the immune responses including local and systemic immunity induced by infection with H pylori,especially with CagA+ H pylori strains and the underlying immunopathogenesis. METHODS:A total of 711 patients with different gastric lesions were recruited to determine the presence of H pylori infection and cytotoxin associated protein A (CagA),the presence of T helper (Th) cells and regulatory T (Treg) cells in peripheral blood mononuclear cells (PBMCs),expression of plasma cytokines,and RNA and protein expression of IFN-γ and IL-4 in gastric biopsies and PBMCs were determined by rapid urease test,urea 14C breath test,immunoblotting test,flow cytometry ,real time RT-PCR and immunohistochemistry. RESULTS:Of the patients,629 (88.47%) were infected with H pylori ; 506 (71.16%) with CagA+ and 123 (17.30%) with CagA- strains. Among patients infected with CagA+ H pylori strains,Th1-mediated cellular immunity was associated with earlier stages of gastric carcinogenesis,while Th2-mediated humoral immunity dominated the advanced stages and was negatively associated with an abundance of Treg cells. However,there was no such tendency in Th1/Th2 polarization in patients infected with CagA- H pylori strains and those without H pylori infection. CONCLUSION:Polarization of Th cell immune responses occurs in patients with CagA+ H pyloriinfection,which is associated with the stage and severity of gastric pathology during the progression of gastric carcinogenesis. This finding provides further evidence for a causal role of CagA+ H pylori infection in the immunopathogenesis of gastric cancer.

H pylori and host interactions that influence pathogenesis

H py/ori is probably the most prevalent human pathogen worldwide. Since it was initially suggested in 1983 by Marshall and Warren to be implicated in gastritis and peptic ulcer disease, H pylori has also been implicated in gastric carcinoma and was classified as a class I carcinogen. In the last two decades, a noteworthy body of research has revealed the multiple processes that this gram negative bacterium activates to cause gastroduodenal disease in humans. Most infections are acquired early in life and may persist for the life of the individual. While infected individuals mount an inflammatory response that becomes chronic, along with a detectable adaptive immune response, these responses are ineffective in clearing the infection. Hpylori has unique features that allow it to reside within the harsh conditions of the gastric environment, and also to evade the host immune response. In this review, we discuss the various virulence factors expressed by this bacterium and how they interact with the host epithelium to influence pathogenesis.

Retinol-binding protein, acute phase reactants and Helicobacter pylori infection in patients with gastric adenocarcinoma

AIM： To determine the serum levels of c-reactive protein （CRP）, transferrin （TRF）, a2-macroglobulin （A2M）, ceruloplasmin （CER）, al-acid glycoprotein （AAG）, prealbumin （P-ALB） and retinol-binding protein （RBP） in gastric carcinoma patients and to explore their possible correlation with underlying Helicobacter pylori （H pylon） infection. METHODS： We measured the serum levels of CRP, TRF, A2M, CER, AAG, P-ALB, and RBP in 153 preoperative patients （93 males; mean age： 63.1±11.3 years） with non-cardia gastric adenocarcinoma and 19 healthy subjects. RESULTS： The levels of CRP, CER, RBP, and AAG in cancer patients were significantly higher than those in healthy controls （P〈0.0001）, while no difference was found regarding the TRF, P-ALB, and A2M levels. Cancer patients with H py/ori infection had significantly lower RBP values compared to non-infected ones （P〈0.0001） and also higher values of CRP and AAG （P = 0.09 andP = 0.08, respectively）. CONCLUSION： High serum levels of CRP, CER and AAG in cancer patients do not seem to be related to H pylori infection. Retinol-binding protein seems to discriminate between infected and non-infected patients with gastric carcinoma. Further studies are needed to explore if it is directly involved in the pathogenesis of the disease or is merely an epiphenomenon.

Effect of drug treatment on hyperplastic gastric polyps infected with Helicobacter pylorh A randomized, controlled trial

AIM： To study the effects of drug treatment on hyperplastic gastric polyps infected with Helicobacter pylori （H pylori. METHODS： Forty-eight patients with hyperplasticgastric polyps （3-10 mm in diameter） infected with Hpylori were randomly assigned to a treatment group （n = 24） which received proton-pump inhibitor （omeprazole or lansoprazole）, clarithromycin, bismuth citrate and tinidazole, and a control group （n = 24） which received protective agent of gastric mucosa （tepretone） . Patients underwent endoscopy and H pylori examination regularly before enrollmentand 1-12 mo after treatment. RESULTS： Twenty-two patients in the treatment group and 21 in the control group completed the entire test protocol. In the treatment group, polyps disappeared 1-12 mo （average, 6.5 ± 1.1 too） after the treatment in 15 of 22 patients （68.2%） and H pylori infection was eradicated in 19 of the 22 patients （86.4%）. However, 12 months after the study, no change in polyps or H pylori status was seen in any controls （^bp 〈 0.01）. CONCLUSION： Most hyperplastic gastric polyps disappear after eradication of H pylori.

Detection of H.pylori DNA in gastric epithelial cells by in situ hybridization

AIM: To investigate the presence of H.pylori DNA within gastric epithelial cells in patients with H.pylori infection and its possible carcinogenic mechanism. METHODS: Total 112 patients, with pathologically confirmed chronic superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, atypical hyperplasia or gastric cancer were studied. Among them, 28 were H.pylori negative and 84 H.pylori positive. H.pylori DNA in gastric epithelial cells was detected by GenPoint catalyzed signal amplification system for in situ hybridization. RESULTS: In the H.pylori positive group, zero out of 24 chronic superficial gastritis (0.0%), four out of 25 precancerous changes (16.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the nucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells were progressively increased in chronic superficial gastritis, precancerous changes and gastric cancer groups (chi(2)=12.56, P=0.002); One out of 24 chronic superficial gastritis (4.2%), eleven out of 25 precancerous changes (44.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (chi(2)=10.86, P=0.004). In the H.pylori negative group, only one patient with gastric cancer was found H.pylori DNA in the nucleus of gastric epithelial cells; Only two patients, one patient with precancerous changes and another with gastric cancer, showed H.pylori DNA in the cytoplasm of gastric epithelial cells. Furthermore, H.pylori DNA must have been in the cytoplasm as long as it existed in the nucleus of gastric epithelial cells. CONCLUSION: H.pylori DNA exists both in the nucleus and the cytoplasm of gastric epithelial cells in patients with H.pylori infections. The pathological progression from chronic superficial gastritis, precancerous changes to gastric cancer is associated with higher positive rates of H.pylori DNA presence in the nucleus of gastric epithelial cells.

Causal role of Helicobacter pylori infection in gastric cancer: An Asian enigma

Helicobacter pylori （H pylori） has been etiologically linked to gastric cancer. H pylori infection is more frequent in less developed Asian countries like India, Bangladesh, Pakistan, and Thailand and is acquired at early age than in more developed Asian countries like Japan and China. Frequency of gastric cancer, however, is very low in India, Bangladesh, Pakistan and Thailand compared to that in Japan and China. Similar enigma has been reported from Africa as compared to the West. Seroprevalence of HpyloN infection in adult populations of India, Bangladesh, Pakistan and Thailand varies from 55% to 92%. In contrast, seroprevalence of H pylon in Chinese and Japanese adults is 44% and 55%, respectively. Annual incidence rate of gastric cancer in India, Bangladesh, and Thailand is 10.6, 1.3, 7.1 per 100 000 populations, respectively; in contrast, that in China and Japan is 32-59 and 80-115 per 100 000 populations, respectively. Several studies from India failed to show higher frequency of H pylori infection in patients with gastric cancer than controls. Available evidences did not support difference in H pylori strains as an explanation for this enigma. Despite established etiological role of H pylon, situation is somewhat enigmatic in Asian countries because in countries with higher frequency of infection, there is lower rate of gastric cancer. Host＇s genetic makeup and dietary and environmental factors might explain this enigma. Studies are urgently needed to solve this issue.

Helicobacter pylori eradication to prevent gastric cancer: underlying molecular and cellular mechanisms

Numerous cellular and molecular events have been described in development of gastric cancer. In this artide, we overviewed roles of Helicobacter pylori （H pylori） infection on some of the important events in gastric carcinogenesis and discussed whether these cellular and molecular events are reversible after cure of the infection. There are several bacterial components affecting gastric epithelial kinetics and promotion of gastric carcinogenesis. The bacterium also increases risks of genetic instability and mutations due to NO and other reactive oxygen species. Epigenetic silencing of tumor suppressor genes such as RUNX3 may alter the frequency of phenotype change of gastric glands to those with intestinal metaplasia. Host factors such as increased expression of growth factors, cytokines and COX-2 have been also reported in non-cancerous tissue in Hpylori-positive subjects. It is noteworthy that most of the above phenomena are reversed after the cure of the infection. However, some of them including overexpression of COX-2 continue to exist and may increase risks for carcinogenesis in metaplastic or dysplastic mucosa even after successful H pylori eradication. Thus, H pylori eradication may not completely abolish the risk for gastric carcinogenesis. Efficiency of the cure of the infection in suppressing gastric cancer depends on the timing and the target population, and warrant further investigation.

Effects of H pylori therapy on erythrocytic and iron parameters in iron deficiency anemia patients with H pylori-positive chronic gastristis

AIM： To elucidate the influences of Hpylori infection on oral iron treatment for iron deficiency anemia （IDA）.METHODS： A total of 86 patients were divided into two groups： group A, receiving ferrous succinate combined with triple therapy for H pylori eradication, and group B （control）, treated with ferrous succinate only. During treatment of IDA, dynamic changes in hemoglobin （Hb） level, mean corpuscular volume （MCV）, mean corpuscular hemoglobin （MCH）, serum iron （SI）, and serum ferritin （SF） were compared between the groups.RESULTS： Hb was slightly higher in group A at d 14 alter the start of triple therapy for H pylori eradication （P 〉 0.05）. After the therapy, the increase of Hb in group A became significantly faster than that in group B （P 〈 0.05）. At d 56, the mean Hb in group A returned to the normal level, however, in group B, it was lower than that in group A （P 〈 0.05） although it had also increased compared with that before oral iron treatment. The MCV and MCH in group A recovered to the normal level, and were much higher than those in group B （P 〈 0.05） at d 21. In Group B, the MCV and MCH remained at lower than normal levels until d 42 alter the start of therapy. And then, they reached a plateau in both groups and the differences disappeared （P 〉 0.05）. The SF in group A was higher than that in group B （P 〈 0.05） 28 d alter the treatment and its improvement was quicker in group A （P 〈 0.05）, and the difference between the two groups was even more significant （P 〈 0.01） at d 56. The SI in group A was higher than that in group B （P 〈 0.05） at d 14 and this persisted until d 56 when the follow-up of this research was finished.CONCLUSION： Treatment of H pylori can enhance the efficacy of ferrous succinate therapy in IDA patients with Hpylori-positive chronic gastritis.

Discrepancies between primary physician practice and treatment guidelines for Helicobacterpylori infection in Korea

AIM： To evaluate the attitude of primary care physicians in the diagnosis and treatment of Helicobacter pylori （fl pylori） infection. METHODS： Primary care physicians in the Seoul metropolitan area answered self-administered questionnaire from January to March 2003. RESULTS： One hundred and eight doctors responded to the questionnaire. The most frequent reasons for testing H pylori infection were gastric and duodenal ulcers （93.5% and 88.9%, respectively）. For patients with Hplori positive dyspepsia, 28.7% of doctors always tried to eradicate the worm and 34.4% treated selectively. A large proportion （28.7%） of primary care physicians treated H pylori on a patient＇s request basis. Only 9.3% of primary care physicians always conducted follow-up testing after treating H pylori infection. When H pylori was not cleared by the first treatment, 40.7% of doctors reused the same regimen, 16.7% changed to another triple regimen and 25% to a quadruple regimen. CONCLUSION： It has been well documented that the issuance of guidelines alone has little impact on practice. Communication between primary care physicians and gastroenterologists in the form of continuous medical education is required.

Bactericidal and anti-adhesive properties of culinary and medicinal plants against Helicobacter pylori

AIM： To investigate the bactericidal and anti-adhesive properties of 25 plants against Helicobacter pylori （H pylon）. METHODS： Twenty-five plants were boiled in water to produce aqueous extracts that simulate the effect of cooking. The bactericidal activity of the extracts was assessed by a standard kill-curve with seven strains of H pylori. The anti-adhesive property was assessed by the inhibition of binding of four strains of FITC-labeled Hpylori to stomach sections. RESULTS： Of all the plants tested, eight plants, including Bengal quince, nightshade, garlic, dill, black pepper, coriander, fenugreek and black tea, were found to have no bactericidal effect on any of the isolates. Columbo weed, long pepper, parsley, tarragon, nutmeg, yellow-berried nightshade, threadstem carpetweed, sage and cinnamon had bactericidal activities against Hpylori, but total inhibition of growth was not achieved in this study. Among the plants that killed H pylori, turmeric was the most efficient, followed by cumin, ginger, chilli, borage, black caraway, oregano and liquorice. Moreover, extracts of turmeric, borage and parsley were able to inhibit the adhesion of H pylori strains to the stomach sections. CONCLUSION： Several plants that were tested in our study had bactericidal and/or anti-adhesive effects on Hpylori. Ingestion of the plants with anti-adhesive properties could therefore provide a potent alternative therapy for H pylori infection, which overcomes the problem of resistance associated with current antibiotic treatment.