Facile synthesis of telechelic poly(phenylene sulfide)s by means of electron-deficient aromatic sulfonium electrophiles.

We report the facile synthesis of telechelic poly(phenylene sulfide) (PPS) derivatives bearing functional groups at both termini. α,ω-Dihalogenated dimethyl-substituted PPS were obtained in high yield with a high degree of end-functionalization by using soluble poly(2,6-dimethyl-1,4-phenylenesulfide) (PMPS) and 4,4'-dihalogenated diphenyl disulfide (X-DPS, X = Cl, Br) as a precursor and an end-capping agent, respectively. Further end-functionalization is achieved through cross-coupling reactions; particularly, the Kumada-Tamao cross-coupling reaction of bromo-terminated telechelic PMPS and a vinylated Grignard reagent afforded end-vinylated PMPS with thermosetting properties. This synthetic approach can be applied to the preparation of various aromatic telechelic polymers with the desired structures and functionalities.

Transcending the Trade-off in Refractive Index and Abbe Number for Highly Refractive Polymers: Synergistic Effect of Polarizable Skeletons and Robust Hydrogen Bonds.

High-refractive-index polymers (HRIPs) are attractive materials for the development of optical devices with high performances. However, because practical components and structures for HRIPs are limited from the viewpoint of synthetic techniques, it has proved difficult using traditional strategies to enhance the refractive index (RI) of HRIPs to more than a certain degree (over 1.8) while maintaining their visible transparency. Here, we found that poly(phenylene sulfide) (PPS) derivatives featuring both methylthio and hydroxy groups can simultaneously exhibit balanced properties of an ultrahigh RI of n D = 1.85 and Abbe number of νD = 20 owing to the synergistic effect of high molar refraction and dense intermolecular hydrogen bonds (H-bonds). This brand new strategy is anticipated to contribute to the development of HRIPs displaying ultrahigh RI with adequate Abbe numbers beyond the empirical n D-νD threshold, which has not been achieved to date.

An atypical case of fulminant interstitial pneumonitis induced by carbamazepine.

Carbamazepine is a therapeutic anticonvulsant, used to manage pain. We often use it to treat trigeminal and post-herpes zoster neuralgias. Interstitial pneumonitis (IP) is a known adverse consequence of using carbamazepine, with bronchiolitis obliterans and organizing pneumonitis. (BOOP) drug-induced IP as typical examples. Here we described a patient with post-herpes zoster neuralgia, who suffered from drug-induced acute IP that differed from cases typically induced by carbamazepine.

Isoflurane inhibits protein kinase Cgamma and calcium/calmodulin dependent protein kinase ii-alpha translocation to synaptic membranes in ischemic mice brains.

Volatile anesthetics isoflurane possibly improves the ischemic brain injury. However, its molecular actions are still unclear. In ischemia, protein kinase C (PKC)gamma and calcium/calmodulin dependent protein kinase II (CaMKII)-alpha are persistently translocated from cytosol to cell membranes, and diminish these translocation suggested to be neuroprotective. We thus tested a hypothesis that isoflurane inhibits PKCgamma and CaMKII-alpha translocation after ischemic brain insults. C57Bl/6J male mice were made to inhale 1 or 2 MAC isoflurane, after which 3 or 5 min cerebral ischemia was induced by decapitation. The sampled cerebrum cortex was then homogenized and centrifuged into crude synaptosomal fractions (P2), cytosolic fractions (S3), and particulate fractions (P3). CaMKII-alpha and PKCgamma levels of these fractions were analyzed by immunoblotting. PKCgamma and CaMKII-alpha are translocated to synaptic membrane from cytosol by cerebral ischemia, although isoflurane significantly inhibited such translocation. These results may explain in part the cellular and molecular mechanisms of neuroprotective effects of isoflurane.

[Neuroprotective effects of novel derivatives of vasoactive intestinal peptide and pituitary adenylate cyclase-activating peptide in two brain ischemic models on mice].

BACKGROUND: Vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase-activating peptide (PACAP), are members of a VIP/secretin/glucagon family. These peptides were demonstrated to possess the neuroprotective properties. However, these peptides are not suited to be developed as a medicine for brain ischemia because of their susceptibilities to endopeptidases. METHODS: We examined the effects of IK 312548 (IK), VIP derivative, and Ac-PACAP, PACAP derivative, on the 10 min two-vessel occlusion (2 VO) model in C 57 BL/6 N mice lacking a part of the posterior communicating artery, and the 30 min middle cerebral artery occlusion (MCAO) model in ICR mice. A 10 ml x kg(-1) dose of each derivative (final concentration; 1 fmol x kg(-1) and 100 pmol x kg(-1)) was injected intraperitoneally (i.p.) to each animal just after the preparation of brain ischemia. RESULTS: In 2 VO experiments, the number of neuronal cells in hippocampus was significantly reduced. However IK and Ac-PACAP treatments inhibited such reductions of neuronal cells in a dose-dependent manner. Particularly, between 1 pmol x kg(-1) and 100 pmol x kg(-) IK, and also between 10 fmol x kg(-1) and 1 pmol x kg(-1) Ac-PACAP significantly protected neuronal cell loss. In MCAO experiments, more than 60% of hemisphere was damaged. By treatment of IK (1-100 pmol x kg(-1)) and Ac-PACAP (1 fmol-1 pmol x kg(-1)), the range of brain damage decreased in a dose-dependent manner. CONCLUSIONS: Ac-PACAP and IK after the brain ischemia could pass the blood-brain barrier and protect brain cell damage.