Frandsenriley1370
The electrophysiological finding confirmed by biochemical results that showed malondialdehyde and nitric oxide levels increased and superoxide dismutase and catalase activities decreased after occlusion in cochlea tissue.
This study showed that bilateral common carotid artery occlusion increases cochlear oxidative stress and induces hearing loss in rats.
This study showed that bilateral common carotid artery occlusion increases cochlear oxidative stress and induces hearing loss in rats.
MicroRNAs (miRNAs or miRs) are non-coding RNAs. Studies have shown that miRNAs are expressed aberrantly in stroke. The miR1 enhances ischemic damage, and a previous study has demonstrated that reduction of miR1 level has a neuroprotective effect on the Middle Cerebral Artery Occlusion (MCAO). Since apoptosis is one of the important processes in neural protection, the possible effect of miR1 on this pathway has been tested in this study. Post-ischemic administration of miR1 antagomir reduces infarct volume via bcl-w and bad expression.
Rats were divided into four experimental groups sham, control, positive control, and antagomir treatment group. One hour after MCAO surgery, the rats were received intravenously (Tail vein) 0.1 mL Normal Saline (NS), 0.1 mL rapamycin, and 300 pmol/g miR1 antagomir (soluble in 0.1 mL normal saline) in control, positive control, and treatment group, respectively. Twenty-four hours after reperfusion infarct volume was measured. The expression of miR1, bcl-w, and bad were analyzed using real-time PCR in sham, control, and treated groups.
Our results indicate that administration of miR1 antagomir reduces infarct volume significantly, it also decreases miR1 and bad expression while increases bcl-w expression.
Understanding the precise neuroprotective mechanism of miR1 antagomir can make it a proper treatment and an innovative approach for stroke therapy.
Understanding the precise neuroprotective mechanism of miR1 antagomir can make it a proper treatment and an innovative approach for stroke therapy.
To evaluate Low-Molecular-weight (LMW) DNA as a possible prognostic biomarker in acute ischemic and hemorrhagic stroke.
LMW DNA samples were isolated from plasma and cerebrospinal fluid by phenol deproteinization, analyzed by gradient polyacrylamide electrophoresis and quantified by spectrophotometry.
Two common types of stroke, i.e. ischemic and hemorrhagic, differ by the temporal dynamics of cell-free DNA (cfDNA) accumulation. In hemorrhagic stroke, an initial increase in LMW DNA levels, most likely reflects an extent of the tissue damage, while in ischemic patients, the LMW DNA levels increase in parallel with the damage caused by hypoxia and subsequent compensatory reperfusion.
These time-course data specify optimal assessment windows with maximum differentiating power for stroke outcomes 24-48 hours post-event for ischemic stroke, and as close as possible to the moment of hospital admission for hemorrhagic stroke. These data also indicate the role of apoptosis in the formation of ischemic focus.
These time-course data specify optimal assessment windows with maximum differentiating power for stroke outcomes 24-48 hours post-event for ischemic stroke, and as close as possible to the moment of hospital admission for hemorrhagic stroke. These data also indicate the role of apoptosis in the formation of ischemic focus.
Hepcidin is the main modulator of systemic iron metabolism, and its role in the brain has been clarified recently. Studies have shown that hepcidin plays an important role in neuronal iron load and inflammation. This issue is of significance because neuronal iron load and inflammation are pathophysiological processes that are highly linked to neurodegeneration. Moreover, the activity of hepcidin has recently been manipulated to recover the neuronal impairment caused by brain inflammation in animal models.
Streptozotocin (STZ) was used to induce type 1 diabetes. selleck chemicals Male Wistar rats (n = 40) with a weight range of 200-250 g were divided into control, diabetic, diabetic + insulin, and diabetic + dalteparin groups. Dalteparin (100 mg/kg IP) and insulin (100 mg/kg SC) were administered for 8 weeks. At the end of the experiment, Y-maze and passive avoidance tasks were carried out. The animals were perfused randomly and their hippocampal tissue was isolated for the analysis of markers such as lipid peroxidation like the existing knowledge of therapeutics to reduce cognitive impairment in diabetes and is suggested to be a potential therapeutic agent in diabetes.
Diabetic encephalopathy is described as any cognitive and memory impairments associated with hippocampal degenerative changes, including the neurodegenerative process and decreased number of living cells. Mitochondrial diabetes (MD) appears following activation of mutant mitochondrial DNA and is a combination of diabetes and cognitive deficit. In this research, we showed the correlation of diabetic encephalopathy, dysfunctional mitochondria, and changes in the expression of axonal transport proteins (KIF5b, Dynein).
Twenty-four male Wistar rats were divided into three groups (n=8 in each group)1. Control + saline; 2. Diabetic, and 3. Diabetic + insulin. Before starting the experiments, the animals with blood sugar lower than 150 mg/dL entered the study. Diabetes induction was carried out by Intraperitoneal (IP) Streptozotocin (STZ) administration. Fasting Blood Sugar (FBS) and body weight was checked after the first week and at the end of the eighth week. Then, behavioral studies (elevated plus maze, Y-matic encephalopathy.
KIF5b mRNA up-regulation in hippocampal neurons of STZ-diabetic rats is a factor that can be involved in abnormal axonal transport and decreased MMP, leading to impairment of mitochondrial function. These manifestations showed mitochondrial dysfunction in diabetes and resulted in abnormal behavioral tests and diabetic encephalopathy.
Ventral Tegmental Area (VTA) dopamine neurons play an important role in reward mechanisms of food intake, and VTA dopamine receptors exist on the terminal of glutamatergic and GABAergic neurons and regulate Gamma-Aminobutyric Acid (GABA) and glutamate release. To our knowledge, no evidence indicates any role for VTA D1 dopamine receptors in regular chow intake.
In this paper, different dose of SKF38393, a D1 receptor agonist, was microinjected in VTA of 18-h food deprived-conscious rats and food intake was measured.
Our results revealed that VTAmicroinjected SKF383993 increased regular chow intake in a dose-dependent manner. The SKF3833 stimulatory effect persisted over 2 h post-injection. The results showed that the SKF38393, at doses less than 5 μg, did not affect locomotor activities.
VTA D1-like and/or serotonergic receptors may be involved in regulatory pathways. the current study suggests that VTA D1-like and/or serotonergic receptors not only affects food reward but is also involved in regulatory mechanisms of regular feeding.
