Preparation and Characterization of a Composite Dust Suppressant for Coal Mines.

In an effort to effectively control coal dust pollution and thereby reduce the harm of coal dust to human health, we prepared a highly efficient composite dust suppressant. First, dynamic contact angle and zeta potential measurements were used to select sodium dodecyl sulfonate (SDS) over sodium carboxymethyl cellulose and trisodium methyl silicon as the complementary additive to soy protein isolate for the dust suppressant. We employed viscosity and wind erosion resistance tests to compare the performance of the composite dust suppressant with three common, commercially available suppressants. As the concentration of the composite dust suppressant was increased, the viscosity increased, reaching a maximum value of 22.7 mPa·s at a concentration of 5 wt%. The 5 wt% concentration of the composite dust suppressant provided the lowest wind erosion rate (20.62%) at a wind speed of 12 m/s. The composite dust suppressant also had good bonding performance and wind erosion resistance. Scanning electron microscopy, X-ray diffraction, and thermogravimetric analysis were used to characterize the properties of the dust suppressants. The dust suppressant, which had a crystal-like structure, could easily capture coal dust and form an effective package. In addition, the density of the dust suppressant film increased as its crystallinity increased. The increased density was beneficial in that it enabled the dust suppressant to form a hard, solidified shell on the surface of coal dust, which improved dust suppression. The composite dust suppressant also had good thermal stability.

Long course hyperbaric oxygen stimulates neurogenesis and attenuates inflammation after ischemic stroke.

Several studies have provided evidence with regard to the neuroprotection benefits of hyperbaric oxygen (HBO) therapy in cases of stroke, and HBO also promotes bone marrow stem cells (BMSCs) proliferation and mobilization. This study investigates the influence of HBO therapy on the migration of BMSCs, neurogenesis, gliosis, and inflammation after stroke. Rats that sustained transient middle cerebral artery occlusion (MCAO) were treated with HBO three weeks or two days. The results were examined using a behavior test (modified neurological severity score, mNSS) and immunostaining to evaluate the effects of HBO therapy on migration of BMSCs, neurogenesis, and gliosis, and expression of neurotrophic factors was also evaluated. There was a lower mNSS score in the three-week HBO group when compared with the two-day HBO group. Mobilization of BMSCs to an ischemic area was more improved in long course HBO treatments, suggesting the duration of therapy is crucial for promoting the homing of BMSCs to ischemic brain by HBO therapies. HBO also can stimulate expression of trophic factors and improve neurogenesis and gliosis. These effects may help in neuronal repair after ischemic stroke, and increasing the course of HBO therapy might enhance therapeutic effects on ischemic stroke.

Attenuating inflammation but stimulating both angiogenesis and neurogenesis using hyperbaric oxygen in rats with traumatic brain injury.

BACKGROUND: Inflammation, angiogenesis, neurogenesis, and gliosis are involved in traumatic brain injury (TBI). Several studies provide evidence supporting the neuroprotective effect of hyperbaric oxygen (HBO2) therapy in TBI. The aim of this study was to ascertain whether inflammation, angiogenesis, neurogenesis, and gliosis during TBI are affected by HBO2 therapy. METHODS: Rats were randomly divided into three groups: TBI + NBA (normobaric air: 21% O2 at 1 absolute atmospheres), TBI + HBO2, and Sham operation + NBA. TBI + HBO2 rats received 100% O2 at 2.0 absolute atmospheres for 1 hr/d for three consecutive days. Behavioral tests and biochemical and histologic evaluations were done 4 days after TBI onset. RESULTS: TBI + NBA rats displayed: (1) motor and cognitive dysfunction; (2) cerebral infarction and apoptosis; (3) activated inflammation (evidenced by increased brain myeloperoxidase activity and higher serum levels of tumor necrosis factor-α); (4) neuronal loss (evidenced by fewer NeuN-positive cells); and (5) gliosis (evidenced by more glial fibrillary protein-positive cells). In TBI + HBO2 rats, HBO2 therapy significantly reduced TBI-induced motor and cognitive dysfunction, cerebral infarction and apoptosis, activated inflammation, neuronal loss, and gliosis. In addition, HBO2 therapy stimulated angiogenesis (evidenced by more bromodeoxyuridine-positive endothelial and vascular endothelial growth factor-positive cells), neurogenesis (evidenced by more bromodeoxyuridine-NeuN double-positive and glial cells-derived neurotrophic factor-positive cells), and overproduction of interleukin-10 (an anti-inflammatory cytokine). CONCLUSIONS: Collectively, these results suggest that HBO2 therapy may improve outcomes of TBI in rats by inhibiting activated inflammation and gliosis while stimulating both angiogenesis and neurogenesis in the early stage.