Recurrent Vogt–Koyanagi–Harada disease with sensorineural hearing loss and choroidal thickening

We report a case of Vogt–Koyanagi–Harada (VKH) disease that recurred with sensorineural hearing loss and choroidal thickening. We measured the choroidal thickness using enhanced-depth imaging optical coherence tomography (EDI-OCT) in a patient with VKH during corticosteroid-tapering therapy. A 71-year-old male presented with fever, headache, and anorthopia associated with wavy choroidal folds and a serous retinal detachment (SRD). The EDI-OCT images showed choroidal thickening (>600 μm at the subfovea), and he was diagnosed with VKH disease. After treatment with pulsed intravenous methylprednisolone, the choroidal folds and SRD resolved and the choroidal thickness decreased. About 6 months after subsequent treatment with an oral corticosteroid started, headache, tinnitus, and sensorineural hearing loss developed, and increased choroidal thickness was observed without other evidence of increased ocular inflammation. A high-dose corticosteroid was injected and tapered, and the sensorineural hearing loss improved immediately and the choroidal thickness decreased. In the current case, sensorineural hearing loss occurred with recurrent VKH disease; however, there were no ocular inflammatory signs except for rebound choroidal thickening. Measuring the choroidal thickness using EDI-OCT can sensitively identify recurrent VKH disease.     

Laryngeal plexiform schwannoma as first symptom in a patient with neurofibromatosis type 2

Neurofibromatosis type 2 (NF2) is an autosomal dominant disorder characterized by bilateral vestibular schwannomas. The initial symptoms of NF2 are usually hearing loss and tinnitus caused by vestibular schwannomas. Although other intracranial, spinal, or skin tumors also occur in NF2, laryngeal lesions are very rare. We report a rare case of NF2 with laryngeal plexiform schwannoma as first symptom. A 38-year-old man presented with a smooth-surfaced submucosal supraglottic mass. Two round masses in the left chest wall and left supraclavicular fossa were noted incidentally during investigation of the laryngeal mass. Magnetic resonance imaging (MRI) findings for these masses were identical to those of the laryngeal mass. No typical symptoms related to NF2 were identified. Histologically, the laryngeal tumor represented plexiform schwannoma. We thus considered that the two round masses in the left chest wall and left supraclavicular fossa might also represent plexiform schwannomas. NF2 was suspected, as a high incidence of multiple plexiform schwannomas has been suggested for patients with NF2. MRI of brain lesions demonstrated bilateral vestibular schwannomas and multiple meningiomas. Finally, NF2 with laryngeal plexiform schwannoma was diagnosed. Recognizing that multiple plexiform schwannomas could be associated with NF2 is important.     

Carbon Monoxide Liberated from CO-Releasing Molecule (CORM-2) Attenuates Ischemia/Reperfusion (I/R)-Induced Inflammation in the Small Intestine

CORM-released CO has been shown to be beneficial in resolution of acute inflammation. The acute phase of intestinal ischemia-reperfusion (I/R) injury is characterized by oxidative stress-related inflammation and leukocyte recruitment. In this study, we assessed the effects and potential mechanisms of CORM-2-released CO in modulation of inflammatory response in the small intestine following I/R-challenge. To this end mice (C57Bl/6) small intestine were challenged with ischemia by occluding superior mesenteric artery (SMA) for 45 min. CORM-2 (8 mg/kg; i.v.) was administered immediately before SMA occlusion. Sham operated mice were injected with vehicle (0.25% DMSO). Inflammatory response in the small intestine (jejunum) was assessed 4 h following reperfusion by measuring tissue levels of TNF-α protein (ELISA), adhesion molecules E-selectin and ICAM-1 (Western blot), NF-κB activation (EMSA), along with PMN tissue accumulation (MPO assay) and leukocyte rolling/adhesion in the microcirculation of jejunum (intravital microscopy). The obtained results indicate that tissue levels of TNF-α, E-selectin and ICAM-1 protein expression, activation of NF-κB, and subsequent accumulation of PMN were elevated in I/R-challenged jejunum. The above changes were significantly attenuated in CORM-2-treated mice. Taken together these findings indicate that CORM-2-released CO confers anti-inflammatory effects by interfering with NF-κB activation and subsequent up-regulation of vascular pro-adhesive phenotype in I/R-challenged small intestine.     

Antidepressant-like effect of Cordyceps sinensis in the mouse tail suspension test

Cordyceps sinensis (CS) has been known as a component of traditional medicines that elicit various biological effects such as anti-fatigue, immunomodulatory, and hypoglycemic actions. Since it has been well-established that fatigue is closely related to depression, we used the tail suspension test (TST) in mice to examine the antidepressant-like effects of hot water extract (HWCS) and supercritical fluid extract (SCCS) of CS. Immobility time in the TST was reduced by administration of SCCS (2.5-10 ml/kg, p.o.) dose-dependently though it was not reduced by treatment with HWCS (500-2000 mg/kg, p.o.). Neither HWCS nor SCCS altered locomotor activity in the open field test, excluding the possibility that the effect of SCCS is due to activation of locomotion. Pretreatment with prazosin (an adrenoreceptor antagonist) or sulpiride (a dopamine D2 receptor antagonist) reduced the effect of SCCS on the immobility time. In contrast, pretreatment with p-chlorophenylalanine (p-CPA, a serotonin synthesis inhibitor) did not alter the anti-immobility effect of SCCS. The last finding is consistent with an additional observation that SCCS had no effect on head twitch response induced by 5-hydroxy-L-tryptophan in mice. Taken altogether, these results suggest that SCCS may elicit an antidepressant-like effect by affecting the adrenergic and dopaminergic systems, but not by affecting the serotonergic system.     

Effects of alcohol consumption on traumatic brain injury

It has been well known that alcohol consumption affects traumatic brain injury. The mechanism of detrimental effect of ethanol on traumatic brain injury has not been clarified. This review focused on the relationship among traumatic brain injury, ethanol and aquaporin-4. We have reported that ethanol increased brain edema after brain contusion and decreased survival rates in rats. It was suggested that increasing brain edema by ethanol after brain contusion may be caused by oxidative stress. Brain edema consists of cytotoxic brain edema, vasogenic brain edema, interstitial brain edema and osmotic edema. Ethanol mainly increases cytotoxic brain edema. Both alcohol consumption and brain contusion cause oxidative stress. Antioxidant treatment decreases cytotoxic brain edema. Aquaporin-4, an water channel, was increased by ethanol 24 hr after traumatic brain injury in rat. The aquaporin-4 inhibitor decreased brain edema after brain contusion and increased survival rates under ethanol consumption. Aquaporin-4 may have strict relation between ethanol and brain edema increasing after brain contusion.     

Ethanol-induced hyponatremia augments brain edema after traumatic brain injury

Alcohol consumption augments brain edema by expression of brain aquaporin-4 after traumatic brain injury. However, how ethanol induces brain aquaporin-4 expression remains unclear. Aquaporin-4 can operate with some of ion channels and transporters. Therefore, we hypothesized that ethanol may affect electrolytes through regulating ion channels, leading to express aquaporin-4. To clarify the hypothesis, we examined role of AQP4 expression in ethanol-induced brain edema and changes of electrolyte levels after traumatic brain injury in the rat. In the rat traumatic brain injury model, ethanol administration reduced sodium ion concentration in blood significantly 24 hr after injury. An aquaporin-4 inhibitor recovered sodium ion concentration in blood to normal. We observed low sodium ion concentration in blood and the increase of brain aquaporin-4 in cadaver with traumatic brain injury. Therefore, ethanol increases brain edema by the increase of aquaporin-4 expression with hyponatremia after traumatic brain injury.     

Navigation surgery for pancreatic disease using multislice computed tomography

In navigation surgery, preoperatively acquired image data are used so that surgical instruments can be guided inside the body while their location is displayed on a computer monitor. It is used in cranial nerve and spinal surgery. In the field of abdominal surgery, however, surgical manipulations in the target area cause major changes in the displayed images compared with those obtained preoperatively, and therefore, with the exception of certain organs, navigation surgery is difficult to apply. In general, this type of surgery aims to use intraoperative image information to improve surgical precision, carry out the preoperative plan accurately, and avoid dangerous areas. Three-dimensional images of the vascular architecture obtained with multislice computed tomography (MS-CT) make it possible to visualize arteries, the portal vein, bile duct, and even the pancreatic duct from any angle, which cannot be done with conventional angiography. Accurate positional relationships in the affected region can be determined preoperatively by manipulating multiplanar reconstruction images at a work station. MS-CT is extremely useful in navigation for safe performance of all types of pancreatectomy.     

Therapeutic potential of PRL-3 targeting and clinical significance of <Emphasis Type=Italic>PRL-3</Emphasis> genomic amplification in gastric cancer

Background  

Phosphatase of regenerating liver-3 (PRL-3) has deserved attention as a crucial molecule in the multiple steps of metastasis. In the present study, we examined the mechanisms regulating PRL-3 expression, and assessed the clinical potential of PRL-3-targeted therapy in gastric cancer.