Photoacoustic Effect of Near-Infrared Absorbing Organic Molecules via Click Chemistry.

Near-infrared dyes were developed to be contrast agents due to their ability to improve the productivity of photoacoustic (PA) imaging and photothermal therapy (PTT) treatments. During the article, we described in detail the PA and PT effects of a category of organic molecules. F-TCNQ could potentially cause a red-shift in the peak PA intensity.

Atomic oxygen effects on silvered polyimide films and their surface modification by poly(siloxane amic acid) ammonium salts.

The tolerance of silvered polyimide films synthesized by an self-metalization method against atomic oxygen (AO) was evaluated. The results showed that the mass loss of R-Ag/PI was markedly increased as the AO fluence increased; Ag/PI showed an identical trend. SEM data showed that the silver particles on the surfaces of R-Ag/PI and Ag/PI disappeared.

Inhibition of WNK3 Kinase Signaling Reduces Brain Damage and Accelerates Neurological Recovery After Stroke.

Background And Purpose: WNK kinases, including WNK3, and the associated downstream Ste20/SPS1-related proline-alanine-rich protein kinase (SPAK) and oxidative stress responsive 1 (OSR1) kinases, comprise an important signaling cascade that regulates the cation-chloride cotransporters. Ischemia-induced stimulation of the bumetanide-sensitive Na(+)-K(+)-Cl(-) cotransporter (NKCC1) plays an important role in the pathophysiology of experimental stroke, but the mechanism of its regulation in this context is unknown. Here, we investigated the WNK3-SPAK/OSR1 pathway as a regulator of NKCC1 stimulation and their collective role in ischemic brain damage.

Chronic high fat diet induces cardiac hypertrophy and fibrosis in mice.

Background: Obesity can cause pathological changes in organs. We determined the effects of chronic high fat diet (HFD) and intermittent fasting, a paradigm providing organ protection, on mouse heart.

Methods: Seven-week old CD1 male mice were randomly assigned to control, HFD and intermittent fasting groups.

Docosahexaenoic acid reduces ER stress and abnormal protein accumulation and improves neuronal function following traumatic brain injury.

In this study, we investigated the development of endoplasmic reticulum (ER) stress after traumatic brain injury (TBI) and the efficacy of post-TBI administration of docosahexaenoic acid (DHA) in reducing ER stress. TBI was induced by cortical contusion injury in Sprague-Dawley rats. Either DHA (16 mg/kg in DMSO) or vehicle DMSO (1 ml/kg) was administered intraperitoneally at 5 min after TBI, followed by a daily dose for 3-21 d.

Glutamate transporter type 3 mediates isoflurane preconditioning-induced acute phase of neuroprotection in mice.

A pre-exposure to isoflurane reduces ischemic brain injury in rodents (isoflurane preconditioning). This neuroprotection has acute and delayed phases. Our previous in vitro studies suggest that the acute phase may involve excitatory amino acid transporters (EAATs).

Chronic intermittent fasting improves cognitive functions and brain structures in mice.

Obesity is a major health issue. Obesity started from teenagers has become a major health concern in recent years. Intermittent fasting increases the life span.

Glutamate transporter type 3 knockout leads to decreased heart rate possibly via parasympathetic mechanism.

Parasympathetic tone is a dominant neural regulator for basal heart rate. Glutamate transporters (EAAT) via their glutamate uptake functions regulate glutamate neurotransmission in the central nervous system. We showed that EAAT type 3 (EAAT3) knockout mice had a slower heart rate than wild-type mice when they were anesthetized.

Isoflurane postconditioning reduces ischemia-induced nuclear factor-κB activation and interleukin 1β production to provide neuroprotection in rats and mice.

Application of isoflurane, a volatile anesthetic, after brain ischemia can reduce ischemic brain injury in rodents (isoflurane postconditioning). This study is designed to determine whether isoflurane postconditioning improves long-term neurological outcome after focal brain ischemia and whether this protection is mediated by attenuating neuroinflammation. Adult male Sprague-Dawley rats were subjected to a 90-min middle cerebral arterial occlusion (MCAO).

Isoflurane induces learning impairment that is mediated by interleukin 1β in rodents.

Postoperative cognitive decline is a clinical syndrome. Volatile anesthetics are commonly used during surgery. It is conceivable that volatile anesthetics may contribute to postoperative cognitive decline.

Contribution of microRNA-203 to the isoflurane preconditioning-induced neuroprotection.

A prior exposure to isoflurane, a common volatile anesthetic, provides neuroprotection (isoflurane preconditioning). To determine the role of microRNAs in this protection, we performed microRNA array assay on cerebral cortex harvested from rats exposed to isoflurane or isoflurane-exposed rat B35 neuron-like cells. We showed that isoflurane significantly increased microRNA-203 expression in B35 neuron-like cells.

Isoflurane preconditioning reduces oxygen-glucose deprivation-induced neuronal injury via B-cell lymphoma 2 protein.

A brief exposure to isoflurane prior to brain ischemia reduces ischemic brain injury in rodents. Here we showed that exposure of rat cerebral cortical neuronal cultures to 2% isoflurane for 30 min at 24 h before a 2-h oxygen-glucose deprivation (OGD) reduced the OGD-induced cell injury. This effect was abolished by HA14-1, a selective inhibitor of B-cell lymphoma 2 (Bcl-2) protein.

Inhibition of isoflurane-induced increase of cell-surface redistribution and activity of glutamate transporter type 3 by serine 465 sequence-specific peptides.

Excitatory amino acid transporters (EAAT) transport glutamate into cells to regulate glutamate neurotransmission and to maintain nontoxic extracellular glutamate levels for neurons. We showed previously that the commonly used volatile anesthetic isoflurane increases the transporting activity of EAAT3, the major neuronal EAAT. This effect requires a protein kinase C (PKC) α-mediated and S465-dependent EAAT3 redistribution to the plasma membrane.

Glutamate transporter type 3 knockout reduces brain tolerance to focal brain ischemia in mice.

Excitatory amino-acid transporters (EAATs) transport glutamate into cells under physiologic conditions. Excitatory amino-acid transporter type 3 (EAAT3) is the major neuronal EAAT and also uptakes cysteine, the rate-limiting substrate for synthesis of glutathione. Thus, we hypothesize that EAAT3 contributes to providing brain ischemic tolerance.

Delayed treatment with isoflurane attenuates lipopolysaccharide and interferon gamma-induced activation and injury of mouse microglial cells.

Background: Isoflurane pretreatment can induce protection against lipopolysaccharide and interferon gamma (IFNgamma)-induced injury and activation of mouse microglial cells. This study's goal was to determine whether delayed isoflurane treatment is protective.

Methods: Mouse microglial cells were exposed to various concentrations of isoflurane for 1 h immediately after the initiation of lipopolysaccharide (10 or 1000 ng/ml) and IFNgamma (10 U/ml) stimulation or to 2% isoflurane for 1 h at various times after initiation of the stimulation.

Isoflurane induces a postconditioning effect on bovine pulmonary arterial endothelial cells exposed to oxygen-glucose deprivation.

Application of volatile anesthetics during the onset of reperfusion reduced ischemia-induced cardiac and brain injury (anesthetic postconditioning). This study was designed to evaluate whether volatile anesthetics induced a postconditioning effect in endothelial cells. Bovine pulmonary arterial endothelial cell (BPAEC) cultures were exposed to oxygen-glucose deprivation, a condition to simulate ischemia in vitro, for 3 h.

Protective effects of TREK-1 against oxidative injury induced by SNP and H2O2.

Aim: TREK-1 (TWIK-related K+ channel-1) is a 2-pore-domain K+ channel subtype. The present study investigated the role of TREK-1 in cell death induced by oxidative stress.

Methods: The cell viability of wild-type Chinese hamster ovary (CHO) and TREK-1-transfected CHO cells (TREK-1/CHO cells) was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in the presence of sodium nitroprusside (SNP) or hydrogen peroxide (H2O2).

Postconditioning with isoflurane reduced ischemia-induced brain injury in rats.

Background: Preexposure of brain to isoflurane, a commonly used anesthetic, induces ischemic tolerance. This phenomenon is called isoflurane preconditioning. However, it is not known whether isoflurane application after ischemia provides neuroprotection.

Isoflurane preconditioning increases B-cell lymphoma-2 expression and reduces cytochrome c release from the mitochondria in the ischemic penumbra of rat brain.

We and others have shown that prior exposure to the volatile anesthetic isoflurane induces ischemic tolerance in the brain. Our results also suggest that isoflurane preconditioning reduces cell apoptosis in the penumbral region of rat brain. We designed this study to determine whether isoflurane preconditioning decreased mitochondria-dependent cell apoptosis.

Isoflurane preconditioning improves long-term neurologic outcome after hypoxic-ischemic brain injury in neonatal rats.

Background: Preconditioning the brain with relatively safe drugs seems to be a viable option to reduce ischemic brain injury. The authors and others have shown that the volatile anesthetic isoflurane can precondition the brain against ischemia. Here, the authors determine whether isoflurane preconditioning improves long-term neurologic outcome after brain ischemia.

Selective alteration of expression of Na+/Ca2+ exchanger isoforms after transient focal cerebral ischemia in rats.

The Na+/Ca2+ exchanger (NCX) is an antiporter located in the plasma membrane of many cells, which can maintain the intracellular Ca(2+) homeostasis. Some studies have shown the close relationship of NCX and cerebral ischemia. But controversial results were obtained.

[A simple and repeatable model of subarachnoid hemorrhage in rats].

Aim: To build a simple and repeatable animal model of subarachnoid hemorrhage (SAH).

Methods: SAH was produced by passing a nylon thread up through the right internal carotid artery and piercing a hole in the right anterior cerebral artery. At 12 h and 24 h after SAH operation, the rats were evaluated with rotarod test and the behavior scale (5-point scale).

Enhanced expressions of arachidonic acid-sensitive tandem-pore domain potassium channels in rat experimental acute cerebral ischemia.

To further explore the pathophysiological significance of arachidonic acid-sensitive potassium channels, RT-PCR and Western blot analysis were used to investigate the expression changes of TREK channels in cortex and hippocampus in rat experimental acute cerebral ischemia in this study. Results showed that TREK-1 and TRAAK mRNA in cortex, TREK-1 and TREK-2 mRNA in hippocampus showed significant increases 2 h after middle cerebral artery occlusion (MCAO). While the mRNA expression levels of the all three channel subtypes increased significantly 24 h after MCAO in cortex and hippocampus.