How long should telomeres be?

What began as a study of the "end-replication problem" took on a new dimension as it became clear that telomeres are a "molecular clock" of replication in human somatic cells. Here we review the biology of telomeres in vitro and in vivo, in mice and humans. We suggest that, in humans, telomeres are involved in the biology of aging and pathobiology of disorders of aging, including cancer and cardiovascular disease. We also propose that the underlying dynamics of telomere biology is in line with broad principles of evolutionary theories.     

Clinical evaluation of four one-week triple therapy regimens in eradicating Helicobacter pylori infection

AIM:To evaluate clinical efficacy of four one-week tripletherapies in eradicating Helicobacter pylori infection.METHODS:In this clinical trial,132 patients with duodenalulcer and chronic gastritis were randomly divided into fourgroups,and received treatment with OAC (omeprazole20mg amoxicillin 1000mg clarithromycin 250mg),OFC(omeprazole 20mg furazolidone 100mg clarithromycin250mg),OFA (omeprazole 20mg furazolidone 100mg amoxicillin 1000mg) and OMC (omeprazole 20mg metronidazole 200mg clarithromycin 250mg),respectively.Each drug was taken twice daily for one week.The ~(13)C ureabreath test was carried out 4-8 weeks after treatment todetermine the success of H pylori eradication.RESULTS:A total of 127 patients completed the treatment.The eradication rate for H pylori infection was 90.3%,90.9%,70.9% and 65.6%,respectively in OAC,OFC OMCand OFA groups.CONCLUSION:A high eradication rate can be achievedwith one-week OAC or OFC triple therapy.Thus,one-week triple therapies with OAC and OFC are recommendedfor Chinese patients with duodenal ulcers and chronicgastritis.     

What consideration should be given to Helicobacter pylori in treating nonsteroidal anti-inflammatory drug ulcers?

Although Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) both cause peptic ulcers, they do so by different mechanisms so any interaction is not necessarily harmful. H. pylori has been shown to enhance gastric mucosal prostaglandin synthesis, while NSAIDs suppress it Pragmatically, there is no compelling evidence in favour of H. pylori eradication in all patients who take NSAIDs. As a broad generalisation, in therapeutic studies of NSAID users, those who have no ulcer at trial entry are more prone to ulcer development if they are H. pylori-positive. By contrast, in those who have ulcers at baseline, H. pylori-positive individuals are less likely to develop ulcers, particularly if taking acid-suppressive therapy. Trials of H. pylori eradication therapy tend to replicate this dichotomy. In one study of patients starting NSAIDs for the first time, with no ulcer history and no baseline ulcer, use of bismuth-based eradication therapy was associated with a lower incidence of gastric ulcer at 2 months. Conversely, in a study of patients with endoscopically proven ulcers and/or troublesome dyspepsia, proton pump inhibitor based eradication treatment had no effect on outcome (of acid suppression) over 6 months. H. pylori eradication has been associated with significantly slower healing of gastric ulcers compared with patients who did not undergo eradication. However, the effect of H. pylori eradication on healing of NSAID-associated duodenal ulcers does not appear to be so dramatic, and limited evidence suggests that it may be possible to prevent H. pylori-associated duodenal ulcer by eradicating the infection. An evidence-based approach to treatment would suggest that NSAID users should undergo H. pylori eradication therapy if they have a duodenal ulcer, whether or not they continue NSAIDs. Because COX-2 inhibitors appear not to be ulcerogenic, management of H. pylori in patients taking these drugs can be based upon the same risk assessment as in patients not taking anti-arthritis drugs. H. pylori eradication should not be used universally or in high-risk gastric ulcer patients who require management with acid suppression.     

How aggressive should initial therapy for rheumatoid arthritis be?

SIR, The report of Matteson et al. [1] concerning their experiencewith 111 rheumatoid arthritis (RA) patients who were treatedprimarily with hydroxychloroquine continues a long line of carefulclinical investigation by the authors. We were surprised, however,by their characterization of patients     

How closely is Helicobacter pylori infection related to gastroduodenal lesions?

BACKGROUND/AIMS: Various studies have indicated a relationship between Helicobacter pylori infection and upper gastrointestinal lesions, but this relationship needs to be assessed in individuals not seeking medical treatment for complaints. METHODOLOGY: We screened community residents for H. pylori infection and upper gastrointestinal lesions during an annual mass health examination aiming to determine relationships between infection and lesions. In 932 examinees we performed a 13C-urea breath test for H. pylori infection, and assessed degree of gastric atrophy by measuring pepsinogen I and II in serum. In 738 subjects we also performed upper gastrointestinal radiography with or without endoscopy. RESULTS: Prevalence of H. pylori infection increased with age, and the ratio of serum pepsinogen I to II decreased with age. Prevalence of H. pylori infection did not differ significantly between subjects with and without radiographically or endoscopically evident lesions. Of H. pylori-positive subjects with peptic ulcer, 73.2% had no recurrence of ulcer despite absence of medical treatment. CONCLUSIONS: Prolonged H. pylori infection was associated with atrophy of the gastric mucosa, but little relationship was evident between H. pylori infection and development or recurrence of peptic ulcer.     

Furazolidone therapy for Helicobacter pylori： Is it effective and safe？

Some aspects related with the use of furazolidone as a rescue therapy for Helicobacter pylori （H pylorl） infection should be remarked, especially regarding its potential oncologic risk. The inclusion of furazolidone in a treatment regimen for H pylori infection is, at least, controversial, and it does not appear to be safe.