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The management of achalasia remains controversial, with little consensus on the optimal patient treatment pathway. In our own esophageal unit, we offer pneumatic dilatation as the initial therapy in most patients as first-line therapy. In this study, we aimed to examine the safety and efficacy of our own approach to the management of patients with a diagnosis of achalasia, examining symptomatic outcomes, patient satisfaction, and need for further intervention, as well as examining patient factors associated with treatment failure. Sixty-seven consecutive patients underwent pneumatic dilatation as first-line therapy (53% male, mean age 46 years). All attended regular outpatient follow-up (mean 37, range 3–132 months). Twenty-five percent of patients required a second intervention because of symptom recurrence, at a median period of 4.5 months. Symptomatic outcomes were excellent or good in 80%. Significant predictors of treatment failure and poor symptom score included a younger age at the time of diagnosis and increased esophageal diameter on barium swallow. This study suggests that pneumatic dilatation is a safe and effective approach as first-line therapy in patients with newly diagnosed achalasia. [ABSTRACT FROM AUTHOR]

Evaluates the effects of aspirin, cardioselective beta-blocker, and pravastatin on patients after elective and abdominal aortic aneurysm repair and femoral-distal revascularization of critically ischemic legs. Detection of a higher limb salvage rate; Improvement in the outcome of patients with the use of these drugs.

Aims: Both endotoxin/Lipopolysaccharide (LPS) tolerance and BLP tolerance represent an essential control mechanism during sepsis. We have previously demonstrated that BLP tolerance is superior to LPS tolerance in protecting against septic shock-induced mortality, however, the underlying mechanisms involved in BLP tolerance are not clear. In this study, we investigated the alterations in inflammatory signal transduction pathways following BLP tolerance. Methods: BLP tolerance and LPS tolerance in human THP-1 monocytic cells were induced in either serum-present or serum-free culture system to evaluate the involvement of soluble CD14. Tolerized cells were further stimulated with high doses of BLP or LPS. TNF-α and IL-6 levels were determined by ELISA. Toll-like receptor 2 (Tlr 2), mitogen-activated protein kinases (MAPK), including ERK, JNK, and P38 kinase were detected by western blotting. NF-kB activation was assessed by transfection of the pNFkB-Luciferase reporter vector and electrophoretic mobility shift assay (EMSA). A number of MAPK and NF-kB inhibitors were also used to determine which signal pathway was involved in BLP tolerance. Results: BLP-tolerized monocytes had a significant reduction in TNF-α production in response to high doses of BLP (41 ± 9 pg mL-1 versus 2341 ± 537 pg mL-1 in nontolerized cells, P < 0.01), or LPS (30 ± 7.5 pg mL-1 versus 1001 ± 147 pg mL-1 in nontolerized cells, P < 0.01). Using a specific CD14 blocking mAb and a serum-free culture system revealed that induction of BLP tolerance was independent of both membrane CD14 and soluble CD14. BLP tolerance as well as LPS tolerance inhibited phosphorylation of ERK, JNK, and p38 kinase, and activation of NF-kB in response to subsequent BLP or LPS stimulation. There was a marked downregulation of Tlr 2 expression in BLP tolerized cells, whereas LPS tolerance did not affect Tlr 2 expression. Conclusions: These results indicate that LPS + BLP tolerance share similar intracellular mechanisms. The critical difference between each peptide relates to differential expression of Tlr 2 amd Tlr 4. [ABSTRACT FROM AUTHOR]