Deficiency of RAB39B Activates ER Stress-Induced Pro-apoptotic Pathway and Causes Mitochondrial Dysfunction and Oxidative Stress in Dopaminergic Neurons by Impairing Autophagy and Upregulating α-Synuclein.

Deletion and missense or nonsense mutation of RAB39B gene cause familial Parkinson's disease (PD). We hypothesized that deletion and mutation of RAB39B gene induce degeneration of dopaminergic neurons by decreasing protein level of functional RAB39B and causing RAB39B deficiency. Cellular model of deletion or mutation of RAB39B gene-induced PD was prepared by knocking down endogenous RAB39B in human SH-SY5Y dopaminergic cells.

Trend and survival outcome in Taiwan cervical cancer patients: A population-based study.

Cervical cancer is one of the most common cancers in Taiwan. The aim of this study was to estimate the incidence of cervical cancer in Taiwan, the relationship between cervical cancer and previous co-morbidities, and the long-term trend of cervical cancer mortality differences in the rest of the world.This study was based on the data of cervical cancer in the National Health Insurance Research Database from 1997 to 2013, and estimated the annual prevalence and incidence of cervical cancer.

IL-17 deficiency attenuates acetaminophen-induced hepatotoxicity in mice.

Acetaminophen (APAP) overdose results in the production of reactive oxygen species (ROS), hepatocyte necrosis, and cell death, and leads to acute liver failure. Interleukin-17 (IL-17), a pro-inflammatory cytokine, plays a key role in the recruitment of neutrophils into sites of inflammation and subsequent damage after liver ischemia-reperfusion injury. In this study, we employed IL-17 knockout (KO) mice to investigate the role of IL-17 in APAP-induced hepatotoxicity.

Video laryngoscopy-assisted tracheal intubation in airway management.

Introduction: Video laryngoscopy-assisted tracheal intubation devices have become alternatives to traditional laryngoscopes in recent years. This review will provide information on commonly used video laryngoscopes and their clinical applications in airway management.

Areas Covered: In this review, the differences between video laryngoscopy and direct laryngoscopy, and the utilization of video laryngoscopes in specific clinical settings are discussed.

Tropisetron Protects Against Acetaminophen-Induced Liver Injury via Suppressing Hepatic Oxidative Stress and Modulating the Activation of JNK/ERK MAPK Pathways.

. To investigate the protective effects of tropisetron on acetaminophen- (APAP-) induced liver injury in a mice model. .

Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons.

Background: Several lines of evidence suggest that CCL2 could initiate the hyperalgesia of neuropathic pain by causing central sensitization of spinal dorsal horn neurons and facilitating nociceptive transmission in the spinal dorsal horn. The cellular and molecular mechanisms by which CCL2 enhances spinal pain transmission and causes hyperalgesia remain unknown. The substantia gelatinosa (lamina II) of the spinal dorsal horn plays a critical role in nociceptive transmission.

CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons.

Background: Inflammation or nerve injury-induced upregulation and release of chemokine CC chemokine ligand 2 (CCL2) within the dorsal root ganglion (DRG) is believed to enhance the activity of DRG nociceptive neurons and cause hyperalgesia. Transient receptor potential vanilloid receptor 1 (TRPV1) and tetrodotoxin (TTX)-resistant Na(v)1.8 sodium channels play an essential role in regulating the excitability and pain transmission of DRG nociceptive neurons.

Astringinin-mediated attenuation of the hepatic injury following trauma-hemorrhage.

Although astringinin administration under adverse circulatory conditions is known to be protective, the mechanism by which astringinin produces the salutary effects remains unknown. We hypothesize that astringinin administration in males following trauma-hemorrhage decreases cytokine production and protects against hepatic injury. Male Sprague-Dawley rats underwent trauma-hemorrhage (mean blood pressure: 40 mmHg for 90 min, then resuscitation).

The effect of warmed ropivacaine to body temperature on epidural sensory block characteristics.

Study Objective: To determine whether warmed (body temperature) ropivacaine increases the speed of onset of sensory block of epidural anesthesia.

Study Design: Prospective, randomized, double-blind study.

Setting: University hospital.

Effect of warm lidocaine on the sensory onset of epidural anesthesia: a randomized trial.

Background: Administration of local anesthetics at body temperature has been reported to shorten the onset time of regional block; however, studies examining the effects of warmed lidocaine on the onset of epidural anesthesia are limited. Here, we ascertain whether warming lidocaine solution to body temperature shortens the time to onset of epidural anesthesia.

Methods: Eighty patients were randomly allocated into two groups of equal size.

Nocistatin and nociceptin exert opposite effects on the excitability of central amygdala nucleus-periaqueductal gray projection neurons.

Central amygdala nucleus (CeA)-periaqueductal gray (PAG) pathway is the component of descending antinociceptive circuitry. Nociceptin/orphanin FQ (N/OFQ) and nocistatin (NST) produce supraspinal pronociceptive and antinociceptive effects, respectively. We hypothesized that opposite effects of N/OFQ and NST on supraspinal pain modulation result from their opposing effects on the excitability of CeA-PAG projection neurons.

Acute unilateral parotid glands enlargement following endotracheal general anesthesia: report of two cases.

Acute parotid gland enlargement in association with general anesthesia is rare and has also been called anesthesia mumps. We present two patients who were scheduled for lumbar spine surgery under general anesthesia. Each developed acute unilateral parotid gland enlargement over one side of the face proven by sonography.

PINK1 mutants associated with recessive Parkinson's disease are defective in inhibiting mitochondrial release of cytochrome c.

Mutations in PTEN-induced kinase 1 (PINK1) gene cause recessive familial type 6 of Parkinson's disease (PARK6). We investigated molecular mechanisms underlying PINK1 neuroprotective function and PARK6 mutation-induced loss of PINK1 function. Overexpression of wild-type PINK1 blocked mitochondrial release of apoptogenic cytochrome c, caspase-3 activation and apoptotic cell death induced by proteasome inhibitor MG132.

Sitting position does not alter minimum alveolar concentration for desflurane.

Purpose: Hypotension is a common complication of the sitting position during anesthesia, and is often counteracted by decreasing anesthetic depth, thereby exposing patients to the risk of being inadequately anesthetized. Baroreceptor unloading and the consequent sympathoexcitation, as during head up tilt, decreases pain threshold and arouses the central nervous system (CNS), whereas hypotension exerts a direct CNS depressant effect. We estimated the minimal alveolar concentration (MAC) of desflurane for immobility in patients undergoing surgery in the sitting position, in comparison to MAC desflurane for patients having a similar type of surgery in the supine position.

Polyglutamine-expanded ataxin-7 decreases nuclear translocation of NF-kappaB p65 and impairs NF-kappaB activity by inhibiting proteasome activity of cerebellar neurons.

Our recent study indicated that polyglutamine-expanded ataxin-7-Q75 induced apoptotic death of cultured cerebellar neurons by downregulating Bcl-x(L) expression and activating mitochondrial apoptotic cascade. Mutant polyglutamine-expanded proteins are believed to impair the proteolytic function of ubiquitin-proteasome system by sequestering components of proteasomes. Proteasome degradation of IkappaBalpha permits nuclear translocation of NF-kappaB and is required for continuous NF-kappaB activity, which supports the survival of cultured cerebellar neurons by inducing Bcl-x(L) expression.

Labetalol pretreatment reduces blood pressure instability during surgical resection of pheochromocytoma.

Background: To evaluate the effect of pretreatment with the mixed alpha- and beta-adrenergic blocker, labetalol, on blood pressure instability during surgical resection of pheochromocytoma.

Methods: Blood pressure stability and surgical results were compared between patients in the saline (n = 11) and labetalol (n = 15) groups. Anesthesia was induced with fentanyl, sodium thiopental and atracurium, and maintained with isoflurane in a 50% oxygen/nitrous oxide mixture.

Efficacy of ultrasound-guided axillary brachial plexus block: a comparative study with nerve stimulator-guided method.

Background: The aim of this study was to compare the efficacy of axillary brachial plexus block using an ultrasound-guided method with the nerve stimulator-guided method. We also compared the efficacy of ultrasound-guided single-injection with those of double-injection for the quality of the block.

Methods: Ninety patients scheduled for surgery of the forearm or hand were randomly allocated into three groups (n = 30 per group), i.

Two C-terminal amino acids, Ser(334) and Ser(335), are required for homologous desensitization and agonist-induced phosphorylation of opioid receptor-like 1 receptors.

Various cellular signaling pathways induced by nociceptin activation of ORL1 (opioid receptor-like 1 receptor) develop homologous desensitization. Multiple lines of evidence suggest that agonist-induced phosphorylation of serine (Ser)/threonine (Thr) residues at intracellular carboxyl tail leads to homologous desensitization of G protein-coupled receptors. In the present study, we investigated the functional role played by C-terminal Ser/Thr residues in agonist-induced desensitization and phosphorylation of ORL1.

Polyglutamine-expanded ataxin-7 activates mitochondrial apoptotic pathway of cerebellar neurons by upregulating Bax and downregulating Bcl-x(L).

Spinocerebellar ataxia type 7 (SCA7) is an autosomal dominant neurodegenerative disorder caused by polyglutamine-expanded ataxin-7. In the present investigation, we expressed disease-causing mutant ataxin-7-Q75 in the primary neuronal culture of cerebellum with the aid of recombinant adenoviruses. Subsequently, this in vitro cellular model of SCA7 was used to study the molecular mechanism by which mutant ataxin-7-Q75 induces neuronal death.

Glutamate transporter function of rat hippocampal astrocytes is impaired following the global ischemia.

Astroglial glutamate transporters, GLT-1 and GLAST, play an essential role in removing released glutamate from the extracellular space and are essential for maintaining a low concentration of extracellular glutamate in the brain. It was hypothesized that impaired function of glial glutamate transporters induced by transient global ischemia may lead to an elevated level of extracellular glutamate and subsequent excitotoxic neuronal death. To test this hypothesis, in the present study, we performed whole-cell patch-clamp recording of hippocampal CA1 astrocytes in control or postischemic slices, and measured glutamate transporter activity by recording glutamate-evoked transporter currents.

Heterodimerization of opioid receptor-like 1 and mu-opioid receptors impairs the potency of micro receptor agonist.

Nociceptin activation of ORL1 (opioid receptor-like 1 receptor) has been shown to antagonize mu receptor-mediated analgesia at the supraspinal level. ORL1 and mu-opioid receptor (muR) are co-expressed in several subpopulations of CNS neurons involved in regulating pain transmission. The amino acid sequence of ORL1 also shares a high degree of homology with that of mu receptor.

Reproducible hepatic dysfunction following separate anesthesia with sevoflurane and desflurane.

Both desflurane and sevoflurane have individually been reported to induce hepatic dysfunction; however hepatic dysfunction after administration of both of them separately in a single patient has not previously been reported. As their metabolites differ in nature, we considered that it would be unlikely that their combined use would cause sensitization and induce hepatic dysfunction. We report on the first patient with reproducible liver dysfunction after sevoflurane and desflurane.

Functional analysis of connexin-26 mutants associated with hereditary recessive deafness.

The physiological importance of connexin-26 (Cx26) gap junctions in regulating auditory function is indicated by the finding that autosomal recessive DFNB1 deafness is associated with mutations of the Cx26 gene. To investigate the pathogenic role of Cx26 mutation in recessive hearing loss, four putative DFNB1 Cx26 mutants (V84L, V95M, R127H, and R143W) were stably expressed in N2A cells, a communication-deficient cell line. In N2A cells expressing (R127H) Cx26 gap junctions, macroscopic junctional conductance and ability of transferring neurobiotin between transfected cells were greatly reduced.

Identification of two C-terminal amino acids, Ser(355) and Thr(357), required for short-term homologous desensitization of mu-opioid receptors.

Our recent study suggests that a cluster of Ser/Thr residues (T(354)S(355)S(356)T(357)) at the intracellular carboxyl tail of rat mu-opioid receptor (MOR1) is required for the development of short-term homologous desensitization. To investigate the functional role played by individual serine or threonine residue of this (TSST) cluster in the agonist-induced mu-opioid receptor desensitization, point mutant (T354A), (S355A), (S356A) and (T357A) mu-opioid receptors were prepared and stably expressed in human embryonic kidney 293 cells (HEK 293 cells). Similar to wild-type mu-opioid receptors, mutant (T354A) and (S356A) mu-opioid receptors stably expressed in HEK 293 cells developed homologous desensitization after 30 min pretreatment of DAMGO ([D-Ala(2),N-methyl-Phe(4),Gly-ol(5)]enkephalin), a specific mu-opioid receptor agonist.

Elevated vascular resistance after labetalol during resection of a pheochromocytoma (brief report).

Purpose: To report a case of pheochromocytoma exhibiting an increase in systemic vascular resistance index (SVRI) and decreased cardiac index (CI) after use of labetalol.

Clinical Features: A 36-yr-old male underwent adrenectomy for pheochromocytoma. Midazolam 5 mg, fentanyl 100 microg and labetalol 20 mg were administrated intravenously for premedication upon arrival in the operating theatre.