ABSTRACT
This work investigated adsorptive removal of calcium ion (Ca2+) by virtue of Na(+) -conditioned clinoptilolite simulating the process of softening for industrial hot-water system. Influential factors such as the activation/regeneration of sorbent and solution pH were tested. The kinetics/thermodynamics for adsorption of Ca2+ were analyzed and discussed. Results showed that: (1) The adsorption rate was in good agreement with the pseudo-second order kinetic models, and the process of adsorption better followed the Langmuir model; (2) Higher solution temperature allowed an enhanced efficiency on Ca2+ removal, albeit the maximum adsorption capacity of Na(+)-conditioned clinoptilolite was hardly affected; (3) The process of adsorption was dominated by chemisorption, and also characterized by entropy increase with spontaneous/endothermic nature; (4) Solution temperature was suggested to be controlled within the range of 6 to 10, and more than 9 times of sorbent regeneration could be ensured for an effective adsorption towards Ca2+ with initial concentration less than 20 mg x L(-1). It was demonstrated that the activated clinoptilolite should be a promising alternative adsorbent for industrial hot-water softening.
Subject(s)
Calcium/isolation & purification , Water Softening/methods , Zeolites/chemistry , Adsorption , Hydrogen-Ion Concentration , Ions , Kinetics , Solutions , Temperature , Thermodynamics , Water , Water Pollutants, Chemical , Water PurificationABSTRACT
Herpes simplex virus type 1 (HSV-1) enters productive infection after infecting epithelial cells, where it controls the host nucleus to make viral proteins, starts viral DNA synthesis and assembles infectious virions. In this process, replicating viral genomes are organized into replication centers to facilitate viral growth. HSV-1 is known to use host factors, including host chromatin and host transcription regulators, to transcribe its genes; however, the invading virus also encounters host defense and stress responses to inhibit viral growth. Recently, we found that HSV-1 replication centers recruit host factor CTCF but exclude γH2A.X. Thus, HSV-1 replication centers may selectively recruit cellular factors needed for viral growth, while excluding host factors that are deleterious for viral transcription or replication. Here we report that the viral replication centers selectively excluded modified histone H3, including heterochromatin mark H3K9me3, H3S10P and active chromatin mark H3K4me3, but not unmodified H3. We found a dynamic association between the viral replication centers and host RNA polymerase II. The centers also recruited components of the DNA damage response pathway, including 53BP1, BRCA1 and host antiviral protein SP100. Importantly, we found that ATM kinase was needed for the recruitment of CTCF to the viral centers. These results suggest that the HSV-1 replication centers took advantage of host signaling pathways to actively recruit or exclude host factors to benefit viral growth.
Subject(s)
DNA Replication , Herpes Simplex/metabolism , Herpesvirus 1, Human/genetics , Viral Proteins/metabolism , Antigens, Nuclear/genetics , Antigens, Nuclear/metabolism , Autoantigens/genetics , Autoantigens/metabolism , CCCTC-Binding Factor , Cell Line , Herpes Simplex/enzymology , Herpes Simplex/genetics , Herpes Simplex/virology , Herpesvirus 1, Human/metabolism , Histones/genetics , Histones/metabolism , Host-Pathogen Interactions , Humans , Protein Binding , RNA Polymerase II/genetics , RNA Polymerase II/metabolism , Repressor Proteins/genetics , Repressor Proteins/metabolism , Viral Proteins/geneticsABSTRACT
AIM OF THE STUDY: Recent studies have revealed that ginsenoside Rb1 (GRb1) is neuroprotective for cerebral ischemia. However, the mechanism underlying of this function is unclear. We assessed whether this neuroprotective effect of GRb1 was mediated by the levels of brain-derived neurotrophic factor (BDNF), by the levels of caspase-3 proteins and by induced neurogenesis in rats following transient cerebral ischemia or not. MATERIALS AND METHODS: Cerebral ischemia was prepared by a 2 h occlusion of the middle cerebral artery and reperfusion, followed by infusion of GRb1 (40 mg/kg) and saline (GRb1 and ischemia groups, respectively). All rats were sacrificed at 3 and 12 h, 1, 2, 3, 5, and 10 days after reperfusion. Normal and sham-operated rats were used in control group. Modified Neurological Severity Scores (mNSS) test and hematoxylin and eosin staining were respectively performed to evaluate neurological function and histological feature. Immunohistochemistry was used to identify intrinsic neurogenesis by nestin antibody. Western blotting was used to detect BDNF and caspase-3 protein content. RESULTS: GRb1 infusion after cerebral ischemia significantly promoted recoveries of neurological functions at 3 and 5 days after reperfusion compared to ischemic rats. The number of nestin-positive cells was apparently increased after GRb1 infusion compared to ischemia rats at given time. Moreover, BDNF was significantly increased in GRb1-treated rats compared to ischemia rats at different time points. In contrast, GRb1 infusion after the onset of reperfusion, caspase-3 at a given time was significantly reduced compared to ischemia rats, but still significantly increased compared to control rats. CONCLUSIONS: Promotion of the neurogenesis and regulation of the expressions of BDNF and caspase-3 may be involved in GRb1-induced neuroprotection against cerebral ischemia.
