The benefit of the bismuth add-on to the 2-week clarithromycin-based triple regimen for Helicobacter pylori eradication: a propensity score-matched retrospective study.

BACKGROUND: Bismuth salt is bacteriostatic and bactericidal against Helicobacter pylori (H. pylori). Little is known about the benefit of bismuth itself. Recently in Korea, government regulation changed to allow bismuth add-on to conventional triple eradication regimens. Study aimed the additional benefit of the bismuth add-on to the 2-week clarithromycin-based triple regimen for H. pylori eradication. METHODS: A single-centered retrospective review of electronic medical records was conducted in Seoul, Korea. Treatment-naïve H. pylori infected subjects treated with the clarithromycin-based triple regimen were consecutively enrolled. After propensity score matching, 118 subjects who were treated with rabeprazole 20 mg, amoxicillin 1 g, and clarithromycin 500 mg twice daily for 14 days (PAC) and matched 118 subjects with PAC plus bismuth subcitrate potassium 300 mg twice daily for 14 days (PACB) were included in the final analysis. The primary endpoint was the eradication success rates in each group.Article title: Kindly check and confirm the edit made in the article title.Yes, I agree with the article title.  RESULTS: The eradication success rates were 91.5% (86.4-96.6%) for PACB regimen and 81.4% (74.2-88.5%) for PAC in the intention-to-treat analysis, and 97.3% (94.2-100%) for PACB and 88.1% (81.9-94.3%) for PAC in the per-protocol analysis. The relative risk of eradication failure for PACB over PAC was calculated as 0.184 (0.0492-0688, p value = 0.005) in multiple regression logistic analysis. Compliance and adverse event incidence were not different between the two groups.Author names: Please confirm if the author names are presented accurately and in the correct sequence (given name, middle name/initial, family name). Author 1 Given name: [Da Wit], Last name: [Shin]. Author 2 Given name: [Dae Young], Last name: [Cheung]. Author 3 Given name: [Ji Hee], Last name: [Song]. Author 4 Given name: [Fan Hee], Last name: [Lee]. Author 5 Given name: [Jin Il], Last name: [Kim]. Yes. I found the names presented are accurate and in the correct sequence. Author 1 Given name: [Da Wit], Last name: [Shin].Author 2 Given name: [Dae Young], Last name: [Cheung].Author 3 Given name: [Ji Hee], Last name: [Song].Author 6 Given name: [Han Hee], Last name: [Lee].Author 7 Given name: [Jin Il], Last name: [Kim]. CONCLUSION: The bismuth add-on to the 2-week clarithromycin-based triple regimen increased the eradication success rate.

Performance of Balloon-Assisted Enteroscopy for Non-ERCP Indications in Patients with Surgically Altered Gastrointestinal Anatomy.

BACKGROUND AND AIMS: Surgically altered gastrointestinal (GI) tract anatomy hinders deep enteroscopy. While enteroscopy-assisted endoscopic retrograde cholangiopancreatography (ERCP) in patients with altered GI anatomy has been heavily investigated, the role of non-ERCP balloon-assisted enteroscopy (BAE) has yet to be fully elucidated.Please check and confirm the author names and initials are correct. Also, kindly confirm the details in the metadata are correct.I have checked all you asked and have no correction.  Thank you. METHODS: A multicenter retrospective study of non-ERCP BAEs in patients with surgically altered GI tract anatomy at two tertiary academic hospitals was performed from January 2006 to December 2020. Altered GI tract anatomy was defined by surgical reconstruction affecting the length, angle, or overall trajectory of the endoscope during the intended approach. The main outcome measurements included technical success rate, diagnostic and therapeutic yields, and complication rate.Please check the edit made in the title of the article and correct if necessary.No more correction. Thank you. RESULTS: A total of 68 patients with surgically altered GI tract anatomy underwent 56 antegrade and 24 retrograde non-ERCP BAE procedures. The technical success rate was 86.2% in both, including 83.9% via antegrade approach and 91.7% via retrograde approach. Antegrade approach in Roux-en-Y anatomy was associated with the lowest success rate of 77.8%, whereas retrograde approach in patients with colon resection resulted in the highest rate of 100%. The diagnostic and therapeutic yields of non-ERCP BAE were 79.4% and 82.9%, respectively. The diagnostic yields varied according to the procedural indications. The major complication was luminal perforation in one case (1.3%). CONCLUSIONS: Non-ERCP BAE is effective and safe via both antegrade and retrograde approaches with a high technical success rate and diagnostic and therapeutic yields in patients with surgically altered GI tract anatomy.

Complete chloroplast genome of Sphagnum subsecundum Nees from Korea.

We determined the complete chloroplast genome sequence of the peatmoss Sphagnum subsecundum Nees from Mt. Halla in Korea. The total size of the chloroplast genome was 140,136 bp, and it consisted of a large single-copy region (LSC) of 98,064 bp, a small single-copy region (SSC) of 21,388 bp, and two copies of inverted repeat (IRa and IRb) regions of 10,342 bp each. The genome encoded a set of 130 genes, comprising 85 protein-coding genes, 37 tRNA genes, and 8 rRNA genes. This species formed a monophyletic clade with S. orientale and S. lenese as the result of ML phylogenetic analysis based on whole gemone sequence of 15 species including one outgroup species.

The complete chloroplast genome sequence of Lilium tsingtauense Gilg (sect. Martagon, Liliaceae).

Lilium tsingtauense Gilg, known as Twilight Lily and distributed in Korea and eastern China, possessed a 151,983 bp chloroplast genome (cpDNA) sequence composed of a large single copy (81,424 bp), a small single copy (17,575 bp), and two inverted repeat regions (26,492 bp each). This cpDNA encoded 81 protein-coding genes, 30 tRNAs and four rRNAs. In contrast to the overlaps between ycf1 and ndhF at the IR/SSC junctions in other Lilium species, there was no record of this pattern in L. tsingtauense. Moreover, variable poly A sequences located downstream of start codon caused different annotations of cemA among Lilium species.

Change of distribution and timing of bite force after botulinum toxin type A injection evaluated by a computerized occlusion analysis system.

PURPOSE: The aim of this study was to determine the force distribution and pattern of mastication after injection of botulinum toxin type A (BTX-A) into both masseter muscles. The hypothesis to be tested was that the difference between right and left balance of occlusal force diminishes over time following BTX-A injection. MATERIALS AND METHODS: Fifteen patients were submitted to BTX-A injection therapy for subjective masseter hypertrophy. A total of 25 U of BTX-A (50 U in total) was injected into two points located 1 cm apart at the center of the lower one-third of both masseter muscles. All patients were examined using the T-Scan occlusion analysis system before and 4, 8, 12, and 24 weeks after BTX-A injection. RESULTS: A significant change in force balance was found between the right and left sides over time and the difference between the two sides decreased with the time post-injection, reaching a minimum at 12 weeks. Comparison of the force balance between the anterior and posterior occlusions revealed no significant difference at any of the time points. The occlusion and disclusion times (right and left sides) did not differ significantly with time since BTX-A injection. CONCLUSION: A decline in the difference in the clenching force between the left and right sides was found with increasing time up to 12 weeks following BTX-A injection.

ROS/Epac1-mediated Rap1/NF-kappaB activation is required for the expression of BAFF in Raw264.7 murine macrophages.

B-cell activating factor (BAFF) plays a role for the maturation and the maintenance of B cells. Lipopolysaccharide (LPS) activates toll-like receptor 4 (TLR4)-dependent signal transduction, which resulted in BAFF expression through nuclear factor kappa B (NF-κB) activation. Here, we investigated whether BAFF expression could be regulated by p65 phosphorylation through the production of reactive oxygen species (ROS) or cyclic AMP (cAMP) in Raw264.7 murine macrophages. mBAFF expression was reduced by ROS scavengers and it was increased by dibutyl-cAMP, a cAMP analogue. mBAFF expression and mBAFF promoter activity were increased by co-transfection of p65 but they were reduced by p65-small interference (si) RNA. Serine (Ser) 276 phosphorylation of p65 was increased by LPS-mediated PKA activation or by the treatment with forskolin, adenylate cyclase activator and dibutyl-cAMP. In contrast, p65 phosphorylation at Ser276 was decreased by ROS scavengers. H(2)O(2) increased intracellular cAMP concentration, significantly. While no increase in p65 phosphorylation at Ser276 was detected by the treatment with H(2)O(2), CREB and p65 phosphorylation at Ser133 and Ser536 was observed, respectively. It implicates that p65 phosphorylation at Ser276 is independent of ROS-induced cAMP production. As another cAMP effector protein was cAMP-responsive guanine nucleotide exchange factor (Epac), a Rap GDP exchange factor, NF-κB was activated by the treatment with 8-(4-chloro-phenylthio)-2'-O-methyladenosine-3',5'-cyclic monophosphate (CPT) that is an activator to Epac. Epac1-mediated Rap1 was activated by the treatment with H(2)O(2) but it was inhibited by ROS scavengers. CPT induced p65 phosphorylation at both Ser276 and Ser536. CPT also increased not only mBAFF expression but mBAFF promoter activity. Data demonstrate that TLR4-mediated mBAFF expression was resulted from the crosstalk of p65 phosphorylation at Ser536 and Ser276 through ROS- and/or cAMP-mediated signal transduction. It suggests for the first time that ROS/Epac1-mediated Rap1/NF-κB pathway could be required for BAFF expression.

Actin-sequestering protein, thymosin-beta-4 (TB4), inhibits caspase-3 activation in paclitaxel-induced tumor cell death.

Thymosin-beta-4 (TB4) as an actin-sequestering peptide has been detected outside of cells in blood plasma or in wound fluid. TB4 induces tumor metastasis and paclitaxel resistance, which is the most significant obstacle to successful therapy in tumors. Here we investigated the inhibitory effect of TB4 peptides on tumor cell death by paclitaxel. The effect of TB4 peptides was assayed by the measurement of caspase-3 activity, G2/M arrest, and Bcl-2 phosphorylation. Cell survival rate was increased and caspase-3 activity was decreased by the treatment with TB4 peptides. In contrast, small interfering RNA (siRNA) of TB4 inhibited cell viability and augmented caspase-3 activity. Significant changes in Bcl-2 phosphorylation were detected by TB4 peptide treatment or by the overexpression of TB4 gene in Hela cells. The reduced population in G2/M phase by TB4 peptide treatment was correlated with the decreased expression of cyclin B1. The data were confirmed in gastric tumor cell lines, SNU 638 (low TB4 level) and SNU 668 (high TB4 level), which were established from clinically isolated gastric tumors. In conclusion, soluble TB4 peptides produced in cancer cells could be an obstacle to treat tumors with paclitaxel. Therefore, TB4 could be a novel target to control paclitaxel resistance.

ERK activation by thymosin-beta-4 (TB4) overexpression induces paclitaxel-resistance.

The development of paclitaxel-resistance in tumors is one of the most significant obstacles to successful therapy. Thymosin-beta-4 (TB4) has been known as actin-sequestering protein and functions in tumor metastasis. Here, we overexpressed TB4 in HeLa cells (TB4-HeLa) and examined the effect of TB4 in paclitaxel-induced cell death. TB4-HeLa cells showed a higher growth rate and a lower percentage of basal apoptosis than HeLa cells. TB4-HeLa cells were more resistant to paclitaxel-induced cell death than HeLa cells. TB4 transcript expression with paclitaxel treatment was dose-dependently increased in HeLa cells but that was not in TB4-HeLa cells. Small interfering RNA (siRNA) of TB4 inhibited HeLa cell growth and enhanced paclitaxel-induced cell death. Basal ERK phosphorylation was elevated and basal p38 kinase phosphorylation was reduced in paclitaxel non-treated TB4-HeLa cells. When treated with paclitaxel, cell death and resistance-induction were independent of ERK and p38 kinase activation. Paclitaxel-resistance of TB4-HeLa cells was overcome by the inhibition of basal ERK activity with PD98059 pre-treatment. The inhibition of basal p38 kinase activity with SB203580 pre-treatment attenuated the paclitaxel-induced HeLa cell death. In conclusion, TB4 induced paclitaxel-resistance through the elevation of basal level of ERK phosphorylation. Therefore, TB4 could be a novel target to regulate paclitaxel-resistance.