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Background Effects of octreotide on post-endoscopic retrograde cholangiopancreatography pancreatitis have been studied in many clinical trials. These trials have yielded inconclusive results. Results of more recent studies using larger doses, however, seem to be more optimistic. Aim To examine effects of octreotide at different doses on PEP. Methods A comprehensive search of relevant databases, including Medline, Embase, the Cochrane Controlled Trials Register, the Cochrane Library and Science Citation Index yielded 18 randomized controlled trials (RCTs). Trials were divided into two groups according to the total dosage of octreotide: <0.5 mg (OCT1), ≥0.5 mg (OCT2). The rate of PEP was analysed using a fixed effect model. Results At doses of ≥0.5 mg, octreotide reduced the rate of PEP. In the OCT2 group, analysis revealed a statistically significant difference on PEP between the octreotide group and the controls (3.4% vs. 7.5%, pooled OR = 0.45; 95% CI: 0.28–0.73; P = 0.001, NNT = 25). In the OCT1 group, the rate of PEP was similar between patients receiving octreotide and the controls (7.2% vs. 6.0%, pooled OR = 1.23; 95% CI: 0.80–1.91; P = 0.35). Conclusion Octreotide is effective in preventing PEP, but only at sufficient doses (≥0.5 mg). [ABSTRACT FROM AUTHOR]

The article focuses on a study which examined the mechanical properties and shape-memory behaviors of poly(L-actide-co-e-caprolactone) (PCLA) copolymers. It notes that a variety of chemical compositions were used to synthesize a series of biodegradable PCLA copolymers. Results of the study showed that the copolymer compositions influenced the mechanical properties significantly. It also found a decline in the tensile strength of copolymers due to an increase in e-caprolactone content.

The successful fabrication of InAlSb/InAs and InAlSb/InAsSb HFETs using recessed gate technology is reported. Epitaxial growth, device fabrication and characterisation are discussed in this Letter. A comparison of the two kinds of HFETs shows that the use of Sb in the InAs channel layer can effectively reduce the gate leakage resulting from the band‐to‐band tunnelling. This improvement is primarily because of increased separation between the conduction band edge of the InAsSb channel layer and the valence band edge of the InAlSb top barrier layer. An InAlSb/InAsSb HFET with 2 μm gate length and 50 μm gate width shows ID = 596 mA/mm and gm = 1 S/mm. [ABSTRACT FROM AUTHOR]

We have studied Ca2+ homeostasis in a unique model of human neurons, the NT2N cell, which differentiates from a human teratocarcinoma cell line, NTera2/C1.D1 by retinoic acid treatment. When perifused with Krebs-HEPES buffer containing 2.5 mM CaCl2, fura-2 loaded NT2N cells produced spontaneous cytosolic Ca2+ oscillations, or Ca2+ transients. These cytosolic Ca2+ transients were not blocked by antagonists of glutamate (6-cyano-7-nitroquinoxaline-2,3-dione and D(-)-2-amino-5-phosphonopentanoic acid) or muscarinic (atropine) receptors. Omission of extracellular Ca2+ completely abolished Ca2+ oscillations and decreased the average Ca2+ level from 106 +/- 14 nM to 59 +/- 8 nM. Addition of the L-type Ca2+ channel blocker nifedipine (1 or 10 microM) or of the N-type inhibitor omega-conotoxin GVIA (5 microM) significantly, although incompletely, suppressed Ca2+ oscillations, while omega-conotoxin MVIIC (5 microM), a selective antagonist of P- and Q-channels, had no effect. Ni2+, at 100 microM, a concentration selective for T-type channels, did not inhibit Ca2+ transients. Non-specific blockage of Ca2+ channels by higher concentrations of Ni2+ (2-5 mM) or Co2+ (1 mM) abolished Ca2+ oscillations completely. The endoplasmic reticulum Ca2+-ATPase inhibitor, thapsigargin (1 microM), slightly decreased Ca2+ oscillation frequency, and induced a small transitory increase in the average cytosolic Ca2+ concentration. The mRNAs of L- (alpha1D subunit) and N-type (alpha1B subunit) Ca2+ channel were present in NT2N cells, while that of a T-type Ca2+ channel (alpha1-subunit) was not present in the NT2N cells as shown by reverse transcription-polymerase chain reaction. In conclusion, NT2N neuronal cells generate cytosolic Ca2+ oscillations mainly by influx of extracellular Ca2+ through multiple channels, which include L- and N-type channels, and do not require activation of glutamate or muscarinic receptors.