Design parameters and treatment efficiency of a retrofit bioretention system on runoff nitrogen removal.

Mixed media design is key factor that affects the operation of bioretention systems. In this study, four types of modifiers, namely, water treatment residual (WTR), green zeolite, fly ash, and coconut bran, were mixed with traditional bioretention soil (65% sand + 30% soil + 5% sawdust, by mass). Consequently, four kinds of modified media were obtained. Ten pilot-scale bioretention basins were constructed by setting different configurations. The steady infiltration rates of the modified packing bioretention systems were 3.25~62.78 times that of plant soil, which was 2.88~55.75 m/day. Results showed that the average concentration removal (ACR) of both mixed and layered fly ash and WTR were better than those of the other media, and the effects could reach over 61.92%. In the bioretention basins with WTR as the modifier, the treatment efficiency of nitrogen under the submerged zone height of 150 mm was relatively optimal, and ACR could reach 65.46%. Outflow total nitrogen (TN) load was most influenced by inflow load, and the correlation coefficient was above 0.765. Relative to the change of inflow concentration (IC), the change of recurrence interval (RI) and discharge ratio (DR) was more sensitive to TN load reduction. The reduction rate of TN load decreased by approximately 15% when the recurrence interval increased from 0.5 to 3 years. It decreased by approximately 12% when the discharge ratio increased from 10 to 20. This study will provide additional insights into the treatment performance of retrofit bioretention systems, and thus, can guide media and configuration design, effect evaluation, and related processes.

Overexpression of miR-381 relieves neuropathic pain development via targeting HMGB1 and CXCR4.

MicroRNA are significant regulators of neuropathic pain development. Neuroinflammation contributes a lot to the progression of neuropathic pain. miR-381 is involved in various pathological processes. However, the role of miR-381 in neuropathic pain development remains barely understood. Therefore, in our study, we aimed to investigate the effects of miR-381 on the process of neuropathic pain progression by establishing a rat model using chronic sciatic nerve injury (CCI). Here, we observed that miR-381 was dramatically decreased in CCI rats. Up-regulation of miR-381 strongly reduced neuropathic pain behaviors including mechanical and thermal hyperalgesia. In addition, inflammatory cytokine expression, including IL-6, IL-10 and TNF-α were significantly repressed by overexpression of miR-381. High mobility group box 1 protein (HMGB1) and Chemokine CXC receptor 4 (CXCR4) participate in neuropathic pain development. In our present study, HMGB1 and CXCR4 were predicted as direct targets of miR-381 by employing bioinformatics analysis. Overexpression of miR-381 was able to restrain the expression of HMGB1 and CXCR4 greatly. The direct correlation between HMGB1 and CXCR4 and miR-381 was confirmed in our research. Furthermore, we found that HMGB1 and CXCR4 were increased in CCI rats time-dependently. Moreover, it was demonstrated that silence of HMGB1 and CXCR4 in CCI rats depressed neuropathic pain progression greatly. In conclusion, it was indicated that miR-381could inhibit neuropathic pain development through targeting HMGB1 and CXCR4.

Epileptiform response of CA1 neurones to convulsant stimulation by cyclothiazide, kainic acid and pentylenetetrazol in anaesthetized rats.

We have previously reported that cyclothiazide (CTZ) evokes epileptiform activities in hippocampal neurons and induces seizure behavior. Here we further studied in vivo the sensitivity of the hippocampal CA1 neurons in response to CTZ in epileptogenesis in comparison with two other classic convulsants of kainic acid (KA) and pentylenetetrazol (PTZ). CTZ administered intracerebral ventricle (i.c.v.) induced epileptiform activities from an initial of multiple evoked population spikes, progressed to spontaneous spikes and finally to highly synchronized burst activities in hippocampal CA1 neurons. PTZ, when given by subcutaneously, but not by intracerebral ventricle injection, evoked similar progressive epileptiform activities. In contrast, KA given by i.c.v. induced a quick development of epileptiform burst activities and then shortly switched to continuous high frequency firing as acute status epilepticus (ASE). Pharmacologically, alprazolam, a high-potency benzodiazepine ligand, inhibited CTZ and PTZ, but not KA, induced epileptiform burst activities while GYKI 53784, an AMPA receptor antagonist, suppressed CTZ and KA but not PTZ evoked epileptiform activities. In conclusion, CTZ and PTZ induced epileptiform activities are most likely to share a similar progressive pattern in hippocampus with GABAergic mechanism dominant in epileptogenesis, while CTZ model involves additional glutamate receptor activation. KA induced seizure in hippocampus is different to that of both CTA and PTZ. The results from this study indicate that hippocampal neurons respond to various convulsant stimulation differently which may reflect the complicated causes of the seizure in clinics.

Nitric oxide inhibits excitatory vagal afferent input to nucleus tractus solitarius neurons in anaesthetized rats.

OBJECTIVE: Endogenous nitric oxide (NO) has been implicated in the regulation of neuronal activity which mediates cardiovascular reflexes. However, there is controversy concerning the role of NO in the nucleus tractus solitarius (NTS). The present study aims to elucidate the possible physiological role of endogenous NO in modulating the excitatory vagal afferent input to NTS neurons. METHODS: All the experiments in the rat were conducted under anaesthetic conditions. Ionophoresis method was used for the application of NO donor or nitric oxide synthase (NOS) inhibitor, and single unit recording method was employed to detect the effects of these applications on vagal afferent- or cardio-pulmonary C-fibre reflex-evoked neuronal excitation in NTS. RESULTS: Ionophoresis applications of L-arginine (L-Arg), a substrate of NOS, and sodium nitroprusside (SNP), a NO donor, both attenuated the vagal afferent-evoked discharge by (51.5+/-7.6)% (n = 17) and (68.3+/-7.1)% (n = 9), respectively. In contrast, application of D-Arg at the same current exerted no overall effect on this input. Also, both L-Arg and SNP inhibited spontaneous firing of most of the recorded neurons. In contrast, ionophoresis application of N(G)-nitro-L-arginine methyl ester (L-NAME) enhanced vagal afferent-evoked excitation by (66.3+/-11.4)% (n = 7). In addition, ionophoresis application of L-Arg and SNP significantly attenuated cardio-pulmonary C-fibre reflex-induced excitation in the tested NTS neurons. CONCLUSION: Activation of local NO pathway in the NTS could suppress vagal afferent-evoked excitation, suggesting that NO is an important neuromodulator of visceral sensory input in the NTS.