Tracheal Bronchus Detected During General Anesthesia: A Case Report.

A tracheal bronchus is a congenital abnormality of the tracheobronchial tree in which a displaced or accessory bronchus arises from the trachea superior to its bifurcation. We herein report a case in which a tracheal bronchus was incidentally found after induction of general anesthesia, and we discuss the potential airway management problems that may have ensued. An 80-year-old man was scheduled for buccal mucosa resection and abdominal skin grafting for treatment of squamous cell carcinoma of the left buccal mucosa.

Unexpected Anesthetic Circuit Leak Attributed to Improper Use of a Tube Holder: A Case Report.

Leaks involving the anesthesia circuit can cause significant complications including hypoxia and hypoventilation. We present a case of a circuit leak caused by damage to the corrugated tubing attributed to improper use of the tube holder. A 58-year-old male was scheduled for resection of a palatal tumor under an intubated general anesthetic.

Rapid elevation of brain-derived neurotrophic factor production in the bilateral trigeminal ganglia by unilateral transection of the mental nerve in mice.

Objectives: Previous spinal nerve injury studies have reported brain-derived neurotrophic factor (BDNF) mRNA upregulation in either the ipsilateral dorsal root ganglion (DRG) neurons or both the contralateral and ipsilateral DRG neurons from early period after peripheral nerve injury. This BDNF elevation induces hyperalgesia in the injured and/or uninjured sites, but this detailed mechanism remains unknown. This study aimed to investigate the BDNF mRNA expression in bilateral DRG neurons caused by unilateral nerve injury and to explore the possible mechanisms by which nitric oxide (NO) mediates BDNF production in the DRG, resulting in contralateral hyperalgesia.

Protracted delay in taste sensation recovery after surgical lingual nerve repair: a case report.

Introduction: Lingual nerve injury is sometimes caused by dental treatment. Many kinds of treatment have been reported, but many have exhibited poor recovery. Here the authors report changes in somatosensory and chemosensory impairments during a long-term observation after lingual nerve repair.

Functional serotonin and histamine receptor subtypes in porcine ciliary artery in comparison with middle cerebral artery.

Functional serotonin (5-HT) and histamine receptor subtypes were investigated in porcine middle cerebral and ciliary arteries. An H(1) antagonist, mepyramine, antagonized histamine-induced responses with pK(B) values of 8.91-9.

Potentiation by neuropeptide Y of histamine H1 receptor-mediated contraction in rat blood vessels.

Histamine-induced contraction and its potentiation by neuropeptide Y were investigated in rat blood vessels. Rat arteries and veins constricted with single concentrations of histamine dose-dependently (0.1-100 microM).

Potentiation by neuropeptide Y of 5HT2A receptor-mediated contraction in porcine coronary artery.

Potentiation by neuropeptide Y of serotonin (5-HT)-induced vasoconstriction was investigated in porcine coronary artery. 5-HT caused concentration-dependent contraction through 5-HT2A receptors. Neuropeptide Y (30 nM) significantly increased the 5HT-induced contraction by 16+/-5% in arteries with intact endothelium.

Neuropeptide Y selectively potentiates alpha1-adrenoceptor-mediated contraction through Y1 receptor subtype in rat femoral artery.

The aim of this study was to investigate the synergism between neuropeptide Y and other vasoconstrictors (phenylephrine and serotonin) and which neuropeptide Y receptor subtype is responsible for the neuropeptide Y-induced potentiation. Exogenous neuropeptide Y (10 nM) potentiated alpha1-adrenoceptor-mediated (PE-induced) contraction in rat femoral artery permissively without its direct action, but not in the thoracic aorta. In contrast, neuropeptide Y produced no change in serotonin-induced contraction in both arteries.

Marked neuropeptide Y-induced contractions via NPY-Y1 receptor and its desensitization in rat veins.

The aim of this study was to investigate neuropeptide Y (NPY)-induced vasoconstrictions in rat blood vessels and which NPY receptor subtype is involved in vasoconstrictions. NPY produced marked contractions in rat common jugular, brachial, portal, femoral and tail veins, and vena cava inferior, whereas it produced little or no contractions in rat common carotid, brachial, femoral and tail arteries, and thoracic and abdominal aortae. The maximal NPY-induced contractions were larger than maximal phenylephrine (PE)-induced contractions in the veins.

Neuropeptide Y-induced contraction and its desensitization through the neuropeptide Y receptor subtype in several rat veins.

Exogenous neuropeptide Y produced marked contractions in rat isolated common jugular, brachial, and caudal veins, while it produced little or no contractions in common carotid, brachial, and caudal arteries. Neuropeptide Y (30 nM) produced larger contractions in these veins than did phenylephrine (1 microM), with maximal contractions through the neuropeptide Y receptor and the alpha1-adrenoceptor, respectively. In contrast, neuropeptide Y (30 nM) produced smaller contractions than did phenylephrine (1 microM) in the arteries.

Leptin-induced transactivation of NPY gene promoter mediated by JAK1, JAK2 and STAT3 in the neural cell lines.

Neuropeptide Y (NPY) plays an important role in the central and sympathetic regulation of food intake and blood pressure. Although the NPY gene expression is regulated by a number of agents such as leptin, the mechanism responsible for leptin-induced regulation of the transcription of the NPY gene remains to be explored. In this study, the NPY gene promoter was transactivated by leptin in N18TG2, NG108-15 and PC12 cells which expressed the functional leptin receptor.