Efficacy of a 7-day course of furazolidone, levofloxacin, and lansoprazole after failed Helicobacter pylori eradication

<p>Abstract</p> <p>Background</p> <p>Increasing resistance to clarithromycin and nitroimidazole is the main cause of failure in the <it>Helicobacter pylori </it>eradication. The ideal retreatment regimen remains unclear, especially in developing countries, where the infection presents high prevalence and resistance to antibiotics. The study aimed at determining the efficacy, compliance and adverse effects of a regimen that included furazolidone, levofloxacin and lansoprazole in patients with persistent <it>Helicobacter pylori </it>infection, who had failed to respond to at least one prior eradication treatment regimen.</p> <p>Methods</p> <p>This study included 48 patients with peptic ulcer disease. <it>Helicobacter pylori </it>infection was confirmed by a rapid urease test and histological examination of samples obtained from the antrum and corpus during endoscopy. The eradication therapy consisted of a 7-day twice daily oral administration of lansoprazole 30 mg, furazolidone 200 mg and levofloxacin 250 mg. Therapeutic success was confirmed by a negative rapid urease test, histological examination and 14C- urea breath test, performed 12 weeks after treatment completion. The Chi-square method was used for comparisons among eradication rates, previous treatments and previous furazolidone use.</p> <p>Results</p> <p>Only one of the 48 patients failed to take all medications, which was due to adverse effects (vomiting). Per-protocol and intention-to-treat eradication rates were 89% (95% CI- 89%–99%) and 88% (88–92%), respectively. Mild and moderate adverse effects were reported by 41 patients (85%). For patients with one previous treatment failure, the eradication rate was 100%. Compared to furazolidone-naïve patients, eradication rates were lower in those who had failed prior furazolidone-containing regimen(s) (74% vs. 100%, p = 0.002).</p> <p>Conclusion</p> <p>An empiric salvage-regimen including levofloxacin, furazolidone and lansoprazole is very effective in the eradication of <it>Helicobacter pylori</it>, particularly in patients that have failed one prior eradication therapy.</p

Incompetence of Neutrophils to Invasive Group A streptococcus Is Attributed to Induction of Plural Virulence Factors by Dysfunction of a Regulator

Group A streptococcus (GAS) causes variety of diseases ranging from common pharyngitis to life-threatening severe invasive diseases, including necrotizing fasciitis and streptococcal toxic shock-like syndrome. The characteristic of invasive GAS infections has been thought to attribute to genetic changes in bacteria, however, no clear evidence has shown due to lack of an intriguingly study using serotype-matched isolates from clinical severe invasive GAS infections. In addition, rare outbreaks of invasive infections and their distinctive pathology in which infectious foci without neutrophil infiltration hypothesized us invasive GAS could evade host defense, especially neutrophil functions. Herein we report that a panel of serotype-matched GAS, which were clinically isolated from severe invasive but not from non-invaive infections, could abrogate functions of human polymorphnuclear neutrophils (PMN) in at least two independent ways; due to inducing necrosis to PMN by enhanced production of a pore-forming toxin streptolysin O (SLO) and due to impairment of PMN migration via digesting interleukin-8, a PMN attracting chemokine, by increased production of a serine protease ScpC. Expression of genes was upregulated by a loss of repressive function with the mutation of csrS gene in the all emm49 severe invasive GAS isolates. The csrS mutants from clinical severe invasive GAS isolates exhibited high mortality and disseminated infection with paucity of neutrophils, a characteristic pathology seen in human invasive GAS infection, in a mouse model. However, GAS which lack either SLO or ScpC exhibit much less mortality than the csrS-mutated parent invasive GAS isolate to the infected mice. These results suggest that the abilities of GAS to abrogate PMN functions can determine the onset and severity of invasive GAS infection

Large amplitude oscillatory shear of pseudoplastic and elastoviscoplastic materials

We explore the utility of strain-controlled large amplitude oscillatory shear (LAOS) deformation for identifying and characterizing apparent yield stress responses in elastoviscoplastic materials. Our approach emphasizes the visual representation of the LAOS stress response within the framework of Lissajous curves with strain, strain-rate, and stress as the coordinate axes, in conjunction with quantitative analysis of the corresponding limit cycle behavior. This approach enables us to explore how the material properties characterizing the yielding response depend on both strain amplitude and frequency of deformation. Canonical constitutive models (including the purely viscous Carreau model and the elastic Bingham model) are used to illustrate the characteristic features of pseudoplastic and elastoplastic material responses under large amplitude oscillatory shear. A new parameter, the perfect plastic dissipation ratio, is introduced for uniquely identifying plastic behavior. Experimental results are presented for two complex fluids, a pseudoplastic shear-thinning xanthan gum solution and an elastoviscoplastic invert-emulsion drilling fluid. The LAOS test protocols and the associated material measures provide a rheological fingerprint of the yielding behavior of a complex fluid that can be compactly represented within the domain of a Pipkin diagram defined by the amplitude and timescale of deformation.National Science Foundation (U.S.) (Graduate Research Fellowship)United States. Defense Advanced Research Projects Agency (DARPA) (Chemical Robots program