Amyloid Fibers Increase Free Radicals of Synthetic Melanin.

Functional amyloid fibers are crucial in melanogenesis, but their roles are incompletely understood. In particular, their relationship with intrinsic spin characters of melanin remains unexplored. Here, we show that adding an amyloid scaffold greatly augments the spin density in synthetic melanin. It also brings about concurrent alterations in water dispersibility, bandgaps, and radical scavenging properties of the synthetic melanin, which facilitates its applications in solar water remediation and protection of human keratinocytes from UV irradiation. This work provides implications in the unrevealed role of functional amyloid in melanogenesis and in the origin of the superiority of natural melanin toward its synthetic variants in terms of the spin-related properties.

Acute unilateral anesthesia mumps after hysteroscopic surgery under general anesthesia: a case report.

Acute unilateral parotid gland swelling after general anesthesia, anesthesia mumps is rare and when occurred, it is associated with the patient's position and with long-lasting surgery. The exact mechanism or etiology has not been fully established but stasis of gland secretion, blockage of Stensen's duct by direct compression, or retrograde flow of air by increased the oral cavity pressure are suspicious reasons. We experienced a case of soft tissue swelling in the left preauricular and submandibular regions in a 40-year-old female patient after short-lasting, hysteroscopic myomectomy performed in the lithotomy position with no suspicious predisposing factor. It is required to pay attention on the fact that even with the usual face mask ventilation can lead to the development of anesthesia mumps.

Antidepressants modulate glycine action in rat hippocampus.

Antidepressants are drugs that relieve symptoms of depressive disorders. Fluoxetine, tianeptine, and milnacipran are different types of antidepressants, and they have widely been used for relieving of depression symptoms. In the present study, the effects of fluoxetine, tianeptine, and milnacipran on the glycine-induced ion current by nystatin-perforated patch clamp and on the amplitude of field potential in the hippocampal CA1 region by multichannel extracellular recording, MED64, system, were studied. In the present results, fluoxetine, tianeptine, and milnacipran reduced glycine-induced ion current in the hippocampal CA1 neurons in nystatin-perforated patch clamp method. These drugs enhanced the amplitude of the field potential in the hippocampal CA1 region in MED64 system. These results suggest that antidepressants may increase neuronal activity by enhancing field potential through inhibition on glycine-induced ion current.

Analysis of expert consultation referrals to the Korean Society of Anesthesiologists (KSA): a comparison of procedural sedation and general anesthesia.

PURPOSE: Procedural sedation during diagnostic or therapeutic procedures is currently widely used by clinicians across a broad range of specialties. However, procedural sedation is a poorly controlled practice in many countries, often performed in potentially unsafe environments. METHODS: In 2009, the Legislation Committee of the Korean Society of Anesthesiologists, based on expert consultation referrals provided by police departments, civil courts, and criminal courts, initiated the construction of database to compile all anesthesia-related adverse events. Using this database (July 2009 to April 2012), we have compared causative mechanisms and injury patterns in procedural sedation (Sedation) cases (N = 25) with those in general anesthesia (GA) cases (N = 29). RESULTS: The severity of injury in Sedation cases was similar to that in GA cases, with death occurring in 72.0 % of cases. Hypoxia secondary to airway obstruction or respiratory depression was the most common specific mechanism of Sedation-related injuries (64.0 %). In-depth analysis of pre-procedural evaluation and intraoperative monitoring revealed a common lack of vigilance in the Sedation cases, and most injuries were judged as preventable with better monitoring. Non-anesthesiologist administration of propofol (NAAP) was performed in the great majority of Sedation cases (88.0 %). CONCLUSION: Our analysis of procedural sedation based on anesthesia-related adverse events compiled in the national database revealed a high severity of patient injury similar to that due to general anesthesia. Most procedural sedations were shown to be poorly controlled without adequate pre-procedural patient evaluation or intraoperative monitoring. Thus, it is essential to establish proper practical guidelines for procedural sedation and ensure strict adherence to these guidelines, especially during the NAAP.

Hepatic ischemic preconditioning provides protection against distant renal ischemia and reperfusion injury in mice.

We previously demonstrated that there are acute and delayed phases of renal protection against renal ischemia and reperfusion (IR) injury with renal ischemic preconditioning (IPC). This study assessed whether hepatic IPC could also reduce distant renal IR injury through the blood stream-mediated supply of reactive oxygen species (ROS). Male C57BL/6 mice were randomly divided into four groups: group I, sham operated including right nephrectomy; group II (IR), left renal ischemia for 30 min and reperfusion injury; group III (IPC-IR), hepatic ischemia for 10 min followed by 10 min of reperfusion before left renal IR injury; group IV (MPG - IPC + IR), pretreated with 100 mg/kg N-(2-mercaptopropionyl)-glycine (MPG) 15 min before hepatic IPC and left renal IR injury. Renal function, histopathologic findings, proinflammatory cytokines, and cytoprotective proteins were evaluated 15 min or 24 hr after reperfusion. Hepatic IPC attenuated the expression of proinflammatory cytokines, tumor necrosis factor α, intercellular adhesion molecule 1, and induced inducible nitric-oxide synthase, and the phosphorylation of Akt in the murine kidney. Renal function was better preserved in mice with hepatic IPC (group III) than groups II or IV. Hepatic IPC protects against distant renal IR injury through the blood stream-delivery of hepatic IPC-induced ROS, by inducing cytoprotective proteins, and by inhibiting inflammatory reactions.

Low dose ketamine reduces the induction of ERK1/2 and CREB signaling protein in a neuropathic pain model of rats.

BACKGROUND: In addition to causing the loss of voluntary sensory and motor function, spinal cord injury (SCI) often creates a state of central neuropathic pain. Rats given SCI display increases in the activated form of transcription factors ERK 1/2 MAPK and CREB in the spinal cord, which correspond to allodynia in a model of neuropathic pain. This study was conducted to determine if low dose ketamine had an effect on the activation of ERK 1/2 and CREB in the development of neuropathic pain. METHODS: This study was conducted to evaluate ERK 1/2 and CREB protein in a sham operated (control) group, neuropathic pain and normal saline (NP + NS) group and neuropathic pain and ketamine (NP + Keta) group. To accomplish this, male Sprague-Dawley rats were anesthetized and then subjected to L5-L6 spinal nerve ligation (SNL, neuropathic rats). The total amounts of ERK 1/2 and CREB protein were then assessed by western blot analysis. In addition, changes in the amounts of ERK 1/2 and CREB mRNA were evaluated by RT-PCR. RESULTS: There was a significant increase in the amount of ERK 1/2 and CREB in the NP + NS group when compared with the sham group. However, the amount of ERK 1/2 and CREB protein induced due to SNL were significantly reduced by continuous infusion with ketamine in the NP + Keta group. CONCLUSIONS: The results of this study revealed a positive linkage between NMDA receptors and the ERK-CREB signaling pathway. Therefore, NMDA receptors could be the target of future therapeutic approaches. Additionally, the results of the present study provide additional evidence that low dose ketamine effectively prevents and treats central neuropathic pain following SNL.

Intrathecal clonidine reduces hypersensitivity after nerve injury by a mechanism involving spinal m4 muscarinic receptors.

UNLABELLED: alpha2-Adrenergic agonists reduce mechanical and thermal hypersensitivity in animals with nerve injury and effectively treat neuropathic pain in humans. Previous studies indicate a reliance of alpha2-adrenergic agonists in this setting on spinal cholinergic activation and stimulation of muscarinic receptors. The subtype(s) of muscarinic receptors in the spinal cord that produces antinociception in normal animals is controversial, and those involved in reducing hypersensitivity and interacting with alpha2-adrenergic systems after nerve injury are unstudied. To examine this, the left L5 and L6 spinal nerves were tightly ligated in rats, resulting in reduction in withdrawal threshold to punctate mechanical stimuli. Intrathecal clonidine, 15 micro g, returned the withdrawal threshold to normal. Using highly specific m1 and m4 antagonists, we observed no reduction in the effect of clonidine by the m1 antagonist, but inhibition of clonidine's effect by the m4 antagonist. Western analysis revealed no difference in quantitative expression of m1 and m4 receptor protein in the dorsal spinal cord of spinal nerve-injured animals compared with sham-operated controls, suggesting this interaction with m4 receptors does not reflect an increase in receptor expression. IMPLICATIONS: Neuraxial clonidine is an effective adjunct in the treatment of neuropathic pain and increases acetylcholine concentrations in cerebrospinal fluid in humans. These data in animals suggest that spinal m4 type muscarinic receptors are important to the effect of clonidine in treating hypersensitivity to touch after nerve injury.