This paper introduces the working principle of the blood circle treatment system outside the body. A monitoring instrument of plasma leakage suited for the blood circle treatment system outside the body is developed based on the absorption spectrum experiments of plasma leakage. Photoelectric detection technology and virtual instrumentation are utilized in the development. A series of detecting experiments of waste solution containing plasma with continuously changing concentration show the monitoring system possesses a relatively high sensitivity. Moreover, the experiments of continual detection with plasma concentration at one certain point indicate the monitoring system has a quite good stability. The monitoring instrument is adapted to dynamically detecting the plasma leakage when the blood circle treatment system outside the body is working.

Objective To analyze the hemodynamic changes of cerebral arterial collateral circulation and distal perfusion of cerebral arteries after external carotid artery occlusion (EICAO).Methods Ninety-six patients with EICAO were selected as the case group,of which 46 cases of left EICAO (group A),50 cases of right EICAO (group B) and 30 normal volunteers were selected as the control group.Color Doppler ultrasonography (TCD) was used to detect peak systolic velocity (Vs) in the middle cerebral artery (MCA),end diastolic velocity (Vd),mean blood flow velocity (Vm),pulsatility index (PI),hemodynamic parameters of arteries,and opening rate of grade Ⅰ anterior communicating artery (ACOA) and posterior communicating artery (PCOA).Results There were significant differences in Vs,Vm,Vd,and PI among group A,B and C (F =56.046,31.027,39.283,18.614,49.658,24.992,15.035,22.069,P＜ 0.001).The Vs,Vd,Vm,and PI of the left MCA in the group A were significantly lower than those of the left side in the control group (P＜0.01);the Vs,Vd,Vm,and PI of the right MCA in the group B were significantly lower than those of the right side in the control group (P＜0.01).In group A and B,the open rate of simple ACOA in the stage Ⅰ collateral circulation was 26.09％ and 30.00％.The open rate of PCOA alone was 23.91％ and 36.00％,respectively,and the concurrent opening rate of ACOA and PCOA was 36.96％ and 30.00％,respectively,There was no significant difference in the open rate of grade Ⅰ collateral circulation among the three types of blood vessels (x2 =0.223,2.881,0.808,P=0.637,0.090,0.369).The incidence of cerebral infarction at the MCA donor site in the group A was 60.87％ on the left side and 8.70％ on the right side.The data of the left side was significantly higher than that of the right side (x2 =57.165,P＜0.001).The incidence of cerebral infarction at the MCA in the group B was 14.00％ on the left side and 60.00％ on the right side,and the data of the fight side was significantly higher than that of the left side (x2 =43.436,P＜ 0.001).Conclusion Although there is a higher grade Ⅰ collateral circulation opening rate in patients with EICAO,the MCA blood supply area of the distal internal carotid artery is still in a state of low blood flow perfusion,and the incidence of cerebral infarction is also high,so opening the grade Ⅰ collateral circulation does not completely reduce the risk of cerebral infarction in these patients,and these patients are still at high risk of cerebral infarction.

Objective:Neonatal mice hypoxia model was established to observe the responses of the main neural cell types in cognition-related brain areas.Methods:Pups at postnatal day 2(P2)were subjected to 10％oxygen for suc-ceeding 5 days,and harvested at different development stage for histologic study.Immunofluorescence histochemistry was used to compare the changes of oligodendrocyte density,mature oligodendrocyte ratio and myelin protein level in corpus callosum(CC)and motor cortex(M1)after hypoxia,as well as the expression changes of excitatory and inhibi-tory neurons in anterior cingulate cortex(ACC),hippocampus(Hippo)and sensory cortex(S1).Furthermore,the density changes of different types of inhibitory intermediate neurons,microglia and astrocytes in ACC were compared.At the same time,the effect of hypoxia on the expression of synaptic proteins was also detected.Results:Quantitative immunofluorescence results showed lower myelin protein levels and mature oligodendrocyte ratio in CC and M1 of hypoxic mice compared with control mice.There was no significant difference in the number of excitatory neurons in ACC,but the number of gamma-aminobutyric acid(GABA)neurons in ACC,Hippo,and S1 were significantly reduced,especially parvalbumin neuron,ssomatostatin neurons,and vasoactive intestinal polypeptide neurons in ACC.The number of excitatory synapses labeled by vesicular glutamate transporter 1(VGluT1)and inhibitory synapses labeled by gephyrin were significantly decreased in ACC of hypoxic mice.Although there was no significant difference in astrocyte and microglia numbers,microglia were activated after hypoxic injury.Conclusion:Chronic hypoxia will lead to changes in the development of oligodendrocytes and interneurons,impair synapse formation.These results provide an important experimental basis for exploring the neural mechanism of diseases related to abnormal brain intelligence devel-opment.

Background::Heterotaxy (HTX) is a thoracoabdominal organ anomaly syndrome and commonly accompanied by congenital heart disease (CHD). The aim of this study was to analyze rare copy number variations (CNVs) in a HTX/CHD cohort and to examine the potential mechanisms contributing to HTX/CHD.Methods::Chromosome microarray analysis was used to identify rare CNVs in a cohort of 120 unrelated HTX/CHD patients, and available samples from parents were used to confirm the inheritance pattern. Potential candidate genes in CNVs region were prioritized via the DECIPHER database, and PNPLA4 was identified as the leading candidate gene. To validate, we generated PNPLA4-overexpressing human induced pluripotent stem cell lines as well as pnpla4-overexpressing zebrafish model, followed by a series of transcriptomic, biochemical and cellular analyses. Results::Seventeen rare CNVs were identified in 15 of the 120 HTX/CHD patients (12.5%). Xp22.31 duplication was one of the inherited CNVs identified in this HTX/CHD cohort, and PNPLA4 in the Xp22.31 was a candidate gene associated with HTX/CHD. PNPLA4 is expressed in the lateral plate mesoderm, which is known to be critical for left/right embryonic patterning as well as cardiomyocyte differentiation, and in the neural crest cell lineage. Through a series of in vivo and in vitro analyses at the molecular and cellular levels, we revealed that the biological function of PNPLA4 is importantly involved in the primary cilia formation and function via its regulation of energy metabolism and mitochondria-mediated ATP production. Conclusions::Our findings demonstrated a significant association between CNVs and HTX/CHD. Our data strongly suggested that an increased genetic dose of PNPLA4 due to Xp22.31 duplication is a disease-causing risk factor for HTX/CHD.

Objective To investigate the relationship between interleukin-1β (IL-1β) and miR-185-5p in the process of joint injury in acute gouty arthritis (AGA). Methods The serum miR-185-5p levels of 89 AGA patients and 91 healthy volunteers were detected by real-time quantitative PCR. The correlation between miR-185-5p expression level and VAS score or IL-1β expression level was evaluated by Pearson correlation coefficient method. Receiver operating characteristic (ROC) curve was used to evaluate the diagnostic value of miR-185-5p in AGA. THP-1 cells were induced by sodium urate (MSU) to construct an in vitro acute gouty inflammatory cell model. After the expression level of miR-185-5p in THP-1 cells was upregulated or downregulated by transfection of miR-185-5p mimics or inhibitors in vitro, inflammatory cytokines of THP-1 cells, such as IL-1β, IL-8 and tumor necrosis factor α (TNF-α), were detected by ELISA. The luciferase reporter gene assay was used to determine the interaction between miR-185-5p and the 3'-UTR of IL-1β. Results Compared with the healthy control group, the expression level of serum miR-185-5p in AGA patients was significantly reduced. The level of serum miR-185-5p was negatively correlated with VAS score and IL-1β expression level. The area under the curve (AUC) was 0.905, the sensitivity was 80.17% and the specificity was 83.52%. Down-regulation of miR-185-5p significantly promoted the expression of IL-1β, IL-8 and tumor necrosis factor (TNF-α), while overexpression of miR-185-5p showed the opposite results. Luciferase reporter gene assay showed that IL-1β was the target gene of miR-185-5p, and miR-185-5p negatively regulated the expression of IL-1β. Conclusion miR-185-5p alleviates the inflammatory response in AGA by inhibiting IL-1β.
Humans ; 3' Untranslated Regions ; Arthritis, Gouty/genetics* ; Interleukin-1beta/genetics* ; Interleukin-8 ; Luciferases ; MicroRNAs/genetics* ; Tumor Necrosis Factor-alpha