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The use of iodine as a photolabile passivating agent for photochemical modification of silicon surfaces is demonstrated. X-ray photoelectron spectroscopy measurements show that iodine termination using iodine dissolved in benzene leads to Si surfaces exhibiting higher iodine surface coverages and lower levels of carbon contamination than previous methods. When exposed to 514 nm light in the presence of a suitable reactive molecule, such as an organic alkene, the surface iodine is removed and the reactive molecule links to the silicon surface. The results of experiments in which the polarization and angle of the incident light were varied show that the reaction mechanism is mediated by absorption of light in the bulk Si. A much greater photoattachment efficiency is obtained on heavily doped n-type silicon than on p-type silicon. It is proposed that on n-type silicon samples the photogenerated minority carriers (holes) accumulate near the surface, making the surface more susceptible to nucleophilic attack by the alkene molecules. The use of this method for photopatterning a Si surface with specific reactive groups is demonstrated.

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BackgroundBrain derived neurotrophic factor (BDNF) is one of the most important regulatory proteins in the pathophysiology of major depressive disorder (MDD). Increasing numbers of studies have reported the relationship between serum/plasma BDNF and antidepressants (ADs). However, the potential effects of several classes of antidepressants on BDNF concentrations are not well known. Hence, our meta-analyses aims to review the effects of differential antidepressant drugs on peripheral BDNF levels in MDD and make some recommendations for future research.MethodsElectronic databases including PubMed, EMBASE, the Cochrane Library, Web of Science, and PsycINFO were searched from 1980 to June 2016. The change in BDNF levels were compared between baseline and post-antidepressants treatment by use of the standardized mean difference (SMD) with 95% confidence intervals (CIs). All statistical tests were two-sided.ResultsWe identified 20 eligible trials of antidepressants treatments for BDNF in MDD. The overall effect size for all drug classes showed that BDNF levels were elevated following a course of antidepressants use. For between-study heterogeneity by stratification analyses, we detect that length of treatment and blood samples are significant effect modifiers for BDNF levels during antidepressants treatment. While both SSRIs and SNRIs could increase the BDNF levels after a period of antidepressant medication treatment, sertraline was superior to other three drugs (venlafaxine, paroxetine or escitalopram) in the early increase of BDNF concentrations with SMD 0.53(95% CI = 0.13–0.93; P = 0.009).ConclusionsThere is some evidence that treatment of antidepressants appears to be effective in the increase of peripheral BDNF levels. More robust evidence indicates that different types of antidepressants appear to induce differential effects on the BDNF levels. Since sertraline makes a particular effect on BDNF concentration within a short amount of time, there is potential value in exploring its relationship with BDNF and its pharmacological mechanism concerning peripheral blood BDNF. Further confirmatory trials are required for both observations.