A case of left main bronchial rupture due to bronchocath tube

A 68-year-old woman underwent a right upper lobectomy for lung cancer. After resection, we noticed the left main bronchial rupture due to bronchocath tube (polyvinyl chloride double lumen tube). The lesion of the rupture was repaired by interrupted sutures with 4-0 prolene. Subsequent course of the patient was uneventful. Tracheobronchial rupture is rare complication of intubation with polyvinyl chloride double lumen tube. There are 6 cases of this complication last five years in Japan. The cause and prevention of this complications are described. It is important to use an adequate tube size, to prevent malposition of the tube and overinflation of the bronchial balloon.     

Biphasic effects of magnesium on the [3H]N-(1-(2-thienyl)cyclohexyl)-3,4-piperidine binding in the rat cerebral cortex

Mg2+ at micromolar concentrations greatly enhanced [3H]N-(1-(2-thienyl)cyclohexyl)-3,4-piperidine ([3H]TCP) binding to well-washed rat cortical membranes, whereas [3H]TCP binding was inhibited by Mg2+ at concentrations higher than 1 mM. In the presence of either L-glutamate (10 microM) or glycine (10 microM), 30 microM Mg2+ caused further stimulation of [3H]TCP binding, suggesting that a high-affinity site for Mg2+ is distinct from the glutamate or glycine binding site. These findings indicate that Mg2+ acts on at least two different recognition sites, e.g. a novel high-affinity site for Mg2+ which stimulates [3H]TCP binding and the Mg2+ recognition site located within the ion channel.     

Myogenic determination and differentiation of the mouse palatal muscle in relation to the developing mandibular nerve.

The vertebrate palatal muscles are derived from the cranial paraxial mesoderm and start myogenesis by the expression of myogenic regulatory factors (MRFs). Predetermined myogenic cells migrate from the cranial paraxial mesoderm into the branchial arches, followed by myogenic differentiation. The objective of this study was to elucidate whether the determination, migration, and differentiation of myogenic cells during the myogenesis of the palatal muscles, particularly the tensor veli palatini (TVP), are related to the extending mandibular nerve in mouse embryos. By immunohistochemical staining at embryonic day (E) 9.5, MyoD1 and myogenin have been expressed in the mandibular arch, into which the mandibular nerve had not yet extended. At E11.5, these myogenic cells encircled the extending mandibular nerve and were distributed from the distal and lateral to the trigeminal ganglion and into the mandibular arch to form the muscle plate, a girdle-like structure. By E12.5, these myogenic cells lost their girdle-like pattern, vacated the trunk area of the mandibular nerve, and were separated into several incompletely divided masses encircling the collateral branches of the mandibular nerve. The TVP started differentiation at E13.5 with the appearance of myofilaments and acetylcholinesterase (AchE), whereas the other palatal muscles began differentiation at E14.5. We defined the differentiation process of mouse palatal muscles into five stages based on the present findings. These results suggest that the determination and initial migration of the palatal myogenic cells into the mandibular arch occur before the mandibular nerve extends out of the trigeminal ganglion, whereas the myogenic cells migrating into the final sites of differentiation intimately relate to the extending nerve.     

Can antistress music tapes reduce mental stress?

The effects of so-called antistress music tapes on reduction of mental stress were examined using Cox and Mackay's SACL, Japanese edition (J-SACL). Fifty-two subjects were exposed to experimentally induced stressful situations and the J-SACL was administered before and after this stress exposure. The results indicated that: (1) music tapes in general could reduce both the stress and arousal factors of the J-SACL; (2) however, differential effects in stress reduction of antistress music tapes were not demonstrated; (3) stress-reducing effects were more prominent in stress than in arousal factors.     

Inhibitory effect of modified 5'-capped short RNA fragments on influenza virus RNA polymerase gene expression

We have shown previously that the 5'-capped short phosphodiester RNA fragments, Cap decoy, (Gm 12 nt) are potent inhibitors of influenza virus RNA polymerase gene expression. Here we investigate the modified capped RNA derivative containing phosphorothioate oligonucleotides (Cap decoy) as a potential influenza virus RNA polymerase inhibitor. The modified 5'-capped short phosphorothioate RNA fragments (Gms 12-15 nt) with the 5'-capped structure (m7GpppGm) were synthesized by T7 RNA polymerase. The 5'-capped short RNA fragments (Gms 12-15 nt) were encapsulated in liposome particulates and tested for their inhibitory effects on influenza virus RNA polymerase gene expression in the clone 76 cells. The 12-15 nt long Gms RNA fragments showed highly inhibitory effects. By contrast, the inhibitory effects of the 13 nt long short RNA fragments (Gm 13 nt) were considerably less in comparison with the 5'-capped short phosphorothioate RNA fragments (Gms 12-15 nt). In particular, the various Gms RNA chain lengths showed no significant differences in the inhibition of influenza virus RNA polymerase gene expression. Furthermore, the capped RNA with a phosphorothioate backbone was resistant to nuclease activity. These phosphorothioate RNA fragments exhibited higher inhibitory activity than the 5'-capped short RNA fragments (Gm 12 nt). These decoys may prove to be useful in anti-influenza virus therapeutics.     

Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts

We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves. Because BK production increases in myocardial ischemia, endogenous BK could foster NE release and associated arrhythmias. We tested this hypothesis in guinea pig and human myocardial ischemia models. BK administration (100 nM) markedly enhanced exocytotic and carrier-mediated NE overflow from guinea pig hearts subjected to 10- and 20-min ischemia/reperfusion, respectively. Ventricular fibrillation invariably occurred after 20-min global ischemia; BK prolonged its duration 3-fold. The BK B2 receptor antagonist HOE140 (30 nM) blocked the effects of BK, whereas the B1 receptor antagonist des-Arg9-Leu8-BK (1 microM; i.e., 2.5 x pA2) did not. When serine proteinase inhibitors (500 KIU/ml aprotinin and 100 microg/ml soybean trypsin inhibitor) were used to prevent the formation of endogenous BK, NE overflow and reperfusion arrhythmias were diminished. In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced. B2 receptor blockade abolished these effects but was ineffective if kininases were not inhibited. B2 receptor stimulation, by either exogenous or endogenous BK, also markedly enhanced carrier-mediated NE release in the human myocardial ischemia model; conversely, inhibition of BK biosynthesis diminished ischemic NE release. Because atherosclerotic heart disease impairs endothelial BK production, in myocardial ischemia BK could accumulate at sympathetic nerve endings, thus augmenting exocytotic and carrier-mediated NE release and favoring coronary vasoconstriction and arrhythmias.