In this work, three dianhydrides with similar chemical structures, 3,3 0 ,4,4 0 -benzophenone tetracarboxylic dianhydride (BTDA), 4,4 0 -oxydiphthalic anhydride (ODPA), and pyromellitic dianhydride (PMDA), are employed for the crosslinking modification of poly(vinyl alcohol) (PVA) membranes for ethanol dehydration via pervaporation. The changes in crosslinking degree, surface hydrophilicity, and glass-transition temperature are investigated and compared. Compared to the pure PVA membrane, all crosslinked membranes show higher fluxes but lower separation factors, because of the higher fractional free volume and the lower hydrophilicity by the crosslinking of the PVA matrix, respectively. In addition, all crosslinked PVA membranes exhibit similar flux, and the separation factor presents a decreasing order of PVA/PMDA-2 > PVA/ODPA-2 > PVA/BTDA-2, which is in the reverse order of their hydrophilicity, probably because of the reduction in the swelling resistance. With the PMDA content increasing from 0.01 to 0.04 mol/(kg PVA) in the PVA/PMDA crosslinked membranes, the crosslinking degree is enhanced and the hydrogen bonding is weakened, resulting in a flux increase from 120.2 to 190.8 g m 22 h 21 , but the separation factor declines from 306 to 58. This work is believed to provide useful insight on the chemical modification of PVA membranes for pervaporation and other membrane-based separation applications.
With an increase of elderly population, aging-related diseases such as hypertension, arteriosclerosis and different forms of dementia are also increased. 1) One of these diseases is vascular dementia (VD). VD is a step-wise deterioration in intellectual powers that appear as different areas of the brain are damaged by loss of blood supply.2,3) The conventional concept of VD is that of multi-infarct dementia, 3,4) arising from chronic cerebral ischemia and various vascular changes in the brain.5) It is reported that the reduction in cerebral blood flow and abnormal energy metabolism occurred in chronic cerebral ischemia can induce the accumulation of NO and ROS which lead to neurons injury in selective, vulnerable regions of the brain, especially the hippocampus and cerebral cortex, accompanied by cognitive decline and some motor disorders. [6][7][8] In oriental medicine, many traditional Chinese drugs have been used clinically for treatment of ischemic cerebrovascular disease. 9) Breviscapine is extracted from the traditional Chinese drug Erigeron Breviscapus (vant.) Hand.-Mazz and mainly composed of Scutellarein, Plantaginin and Pyromeconic acid. 10,11) The injection preparation of breviscapine has been used in clinic to treat cardiovascular diseases, cerebral infarction and stroke in China. 3,10,11) The clinical reports suggested that the injection of breviscapine (0.5 mg/kg, i.v. gtt, qd, 15 d) possess neuroprotective action and improves learning and memory in cerebrovascular diseases.12,13) Although the curative effect of breviscapine in cerebral infarction and cerebral ischemia is obvious, there is no data available for this drug in treatment of VD. In this study, the effects of chronic treatment with breviscapine on the learning deficits, neuronal injury and antioxidative properties in VD rats were investigated. MATERIALS AND METHODS Animal Models and Drug AdministrationThe vascular dementia models were made from the male Wistar rats (6 weeks, 230Ϯ10 g), which were obtained from the Experimental Animals Center of Tongji Medical College, Huazhong University of Science and Technology. Wistar rats were subjected to permanent occlusion of bilateral common carotid arteries to induce chronic cerebral ischemia and mimic the VD models.14) The experimental protocols were approved by the Committee of Animal Care of Huazhong University of Science and Technology.The injection of breviscapine (Bre, Bath No. z5302066, China) was purchased from Kunming Long-Jin Pharmaceutical Co., Ltd. Tacrine (9-amino-1,2,3,4-tetrahydroacridine HCl), a reference drug for behavioral test, was purchased from Sigma (St. Louis, MO, U.S.A.) and dissolved in physiological saline. Fifteen days after surgery, the male Wistar rats were randomly divided into three groups, e.g., sham-operated group, model group, Bre-treated group and tacrine-treated group. The Bre-treated group was administered with breviscapine (2 mg/kg, i.p., equal 0.33 mg/kg adult dose, once a day). Tacrine was administered intraperitoneally at a dosage of 3 mg/kg. The sham-ope...
The band structures of one-dimensional photonic crystals containing a defect layer with a negative refractive index are studied, showing that the defect modes possess three types of dispersion: positive, zero, and negative types. Based on these three types of dispersion, practical designs for large incident angle filters without polarization effect and for narrow frequency and sharp angular filters are suggested. Moreover, the splitting of one degenerate defect mode into multiple defect modes is observed in the band gap when the parameters of the defect layer vary. This mode splitting phenomenon can be used to design multiple channeled filters or filters with a rectangular profile. The dispersion multiplicity of the defect modes can be understood by an approximate formula, and the critical condition for the defect mode splitting is also analyzed. Based on these analyses, practical optimization design of omnidirectional filter is also suggested.
Selective stimulation of inhibitory A1 and facilitatory A2a adenosine receptor subtypes located in the nucleus of the solitary tract (NTS) powerfully inhibits cardiopulmonary chemoreflex (CCR) control of regional sympathetic outputs via different mechanisms: direct inhibition of glutamate release and facilitation of an inhibitory neurotransmitter release, respectively. However, it remains unknown whether adenosine naturally released into the NTS has similar inhibitory effects on the CCR as the exogenous agonists do. Our previous study showed that adenosine is released into the NTS during severe hemorrhage and contributes to reciprocal changes of renal (decreases) and adrenal (increases) sympathetic nerve activity observed in this setting. Both A1 and A2a adenosine receptors are involved. Therefore, we tested the hypothesis that, during severe hemorrhage, CCR control of the two sympathetic outputs is attenuated by adenosine naturally released into the NTS. We compared renal and adrenal sympathoinhibitory responses evoked by right atrial injections of 5HT3 receptor agonist phenylbiguanide (2-8 μg/kg) under control conditions, during hemorrhage, and during hemorrhage preceded by blockade of NTS adenosine receptors with bilateral microinjections of 8-(p-sulfophenyl) theophylline (1 nmol/100 nl) in urethane/chloralose anesthetized rats. CCR-mediated inhibition of renal and adrenal sympathetic activity was significantly attenuated during severe hemorrhage despite reciprocal changes in the baseline activity levels, and this attenuation was removed by bilateral blockade of adenosine receptors in the caudal NTS. This confirmed that adenosine endogenously released into the NTS has a similar modulatory effect on integration of cardiovascular reflexes as stimulation of NTS adenosine receptors with exogenous agonists.
Cognitive impairment is a primary feature of many neuropsychiatric disorders and there is a need for new therapeutic options. Catechol-O-methyltransferase (COMT) inhibitors modulate cortical dopaminergic function and have been proposed as potential cognitive enhancers. Unfortunately, currently available COMT inhibitors are not good candidates due to either poor blood-brain barrier penetration or severe toxicity. To address the need for safe, brain-penetrant COMT inhibitors, we tested multiple novel COMT inhibitors in a set of preclinical in vivo efficacy assays to determine their viability as potential clinical candidates. We found that multiple COMT inhibitors, exemplified by LIBD-1 and LIBD-3, significantly modulated dopaminergic function measured as decreases in homovanillic acid (HVA) and increases in 3,4-Dihydroxyphenylacetic acid (DOPAC), two dopamine metabolites, in cerebrospinal fluid (CSF) and the frontal cortex. Additionally, we found the LIBD-1 significantly improved cognitive flexibility in a rat attentional set-shifting assay (ASST), an effect previously seen with the COMT inhibitor tolcapone. These results demonstrate that LIBD-1 is a novel COMT inhibitor with promising in vivo activity and the potential to serve as a new therapy for cognitive impairment.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.