Fully integrated wearable microneedle biosensing platform for wide-range and real-time continuous glucose monitoring.

Wearable microneedle sensors for continuous glucose monitoring (CGM) have great potential for clinical impact by allowing access to large data sets to provide individualized treatment plans. To date, their development has been challenged by the accurate wide linear range tracking of interstitial fluid (ISF) glucose (Glu) levels. Here, we present a CGM platform consisting of a three-electrode microneedle electrochemical biosensor and a fully integrated radio-chemical analysis system. The long-term performance of the robust CGM on diabetic rats was achieved by electrodepositing Prussian blue (PB), and crosslinking glucose oxidase (GOx) and chitosan to form a 3D network using glutaraldehyde (GA). After redox by GOx, PB rapidly decomposes hydrogen peroxide and mediates charge transfer, while the 3D network and graphite powder provide enrichment and release sites for Glu and catalytic products, enabling a sensing range of 0.25-35 mM. Microneedle CGM has high sensitivity, good stability, and anti-interference ability. In diabetic rats, CGM can accurately monitor Glu levels in the ISF in real-time, which are highly consistent with levels measured by commercial Glu meters. These results indicate the feasibility and application prospects of the PB-based CGM for the clinical management of diabetes. STATEMENT OF SIGNIFICANCE: This study addresses the challenge of continuous glucose monitoring system design where the narrow linear range of sensing due to the miniaturization of sensors fails to meet the monitoring needs of clinical diabetic patients. This was achieved by utilizing a three-dimensional network of glutaraldehyde cross-linked glucose oxidase and chitosan. The unique topology of the 3D network provides a large number of sites for glucose enrichment and anchors the enzyme to the sensing medium and the conductive substrate through covalent bonding, successfully blocking the escape of the enzyme and the sensing medium and shortening the electron transfer and transmission path.

Flowthrough Capture of Microplastics through Polyphenol-Mediated Interfacial Interactions on Wood Sawdust.

Nano-/microplastics accumulate in aquatic bodies and raise increasing threats to ecosystems and human health. The limitation of existing water cleanup strategies, especially in the context of nano-/microplastics, primarily arises from their complexity (morphological, compositional, and dimensional). Here, highly efficient and bio-based flowthrough capturing materials (bioCap) are reported to remove a broad spectrum of nano-/microplastics from water: polyethylene terephthalate (anionic, irregular shape), polyethylene (net neutral, irregular shape), polystyrene (anionic and cationic, spherical shape), and other anionic and spherical shaped particles (polymethyl methacrylate, polypropylene, and polyvinyl chloride). Highly efficient bioCap systems that adsorb the ubiquitous particles released from beverage bags are demonstrated. As evidence of removal from drinking water, the in vivo biodistribution of nano-/microplastics is profiled, confirming a significant reduction of particle accumulation in main organs. The unique advantage of phenolic-mediated multi-molecular interactions is employed in sustainable, cost-effective, and facile strategies based on wood sawdust support for the removal of challenging nano-/microplastics pollutions.

Green Tea Catechin EGCG Ameliorates Thioacetamide-Induced Hepatic Encephalopathy in Rats via Modulation of the Microbiota-Gut-Liver Axis.

SCOPE: Existing research suggests that (-)-epigallocatechin-3-gallate (EGCG), which is a natural tea catechin active substance, can protect against liver injury. However, its mechanism for hepatic encephalopathy (HE) treatment is still unclear. In this study, the role of EGCG in the amelioration of HE rats and the effect on the microbiota-gut-liver axis are mainly analyzed. METHODS AND RESULTS: Thioacetamide (TAA) is employed to induce the HE model in rats. The results of open field test show that EGCG restores locomotor activity and exploratory behavior. Histological and biochemical results demonstrate that EGCG ameliorates brain and liver damage, decreases the expression of pro-inflammatory cytokines, and increases the activity of antioxidant enzymes. Meanwhile, EGCG modulates the Nrf2 pathway and TLR4/NF-κB pathway to mitigate TAA-induced oxidative stress and inflammatory responses. Immunohistochemistry reveals protection of the intestinal barrier by EGCG upregulating the expression of occludin and zonula occludens-1. Furthermore, serum levels of ammonia and LPS are reduced. 16S rRNA analysis shows that EGCG treatment increases the abundance of beneficial bacteria (e.g., Bifidobacterium, Lactobacillus, and Limosilactobacillus). CONCLUSION: The above results reveal that EGCG has anti-oxidative stress and anti-inflammatory effects, and ameliorates the condition through the microbiota-gut-liver axis, with potential for the treatment of HE.

Self-Assembled Integrative Nutrient Carrier Platform Containing Green Tea Catechin for Short Bowel Syndrome Treatment.

Extensive resection of the small intestine leads to the development of short bowel syndrome (SBS), which reduces the effective absorptive surface area of the intestine and predisposes patients to emaciation, malnutrition, and other severe symptoms. Herein, green tea catechin (-)-epigallocatechin gallate (EGCG) and ferrous ions (Fe2+ ) are utilized to construct a nutrient carrier platform that self-assembles with nutrients to form phenolic-based nutrient complexes (PNCs). PNCs effectively prolong the residence and absorption time of nutrients in the intestine. Further this platform is applied to integrate full nutrient formula, an enteral nutrition (EN) preparation containing a range of full nutrient components. In an SBS rat model, the prepared phenolic-based integrative nutrient complexes (PINCs) enhance nutritional status, improve anemia and immune function, as well as facilitate the growth of remaining intestinal villi and crypts, and maintain the integrity of the intestinal barrier. In addition, PINCs enable the modulation of gut microbial dysbiosis, enrich the abundance of beneficial bacteria, and have no toxic effects after the long-term ingestion. These results provide a proof of principle for the use of polyphenol-based nanocomplexes as EN preparation, offering a feasible strategy for both nutritional support and therapeutic perspectives for SBS treatment.

Research and Forecast Analysis of Financial Stability for Policy Uncertainty.

The instability of financial market will have a great impact on money, bonds, and stocks and affect the economic development of society and people's lives. Therefore, it is very necessary for us to study and predict the financial stability. According to the forecast results, we will analyze and make a series of preparatory measures. First, we make a series of analyses on the structure and significance of policy uncertainty and financial stability. This paper introduces the advantages and disadvantages of the P/L model, the KLS signal method, and the BP neural network model for financial stability early warning, It is clearly pointed out that the BP neural network is more reliable and accurate, Then, the BP neural network, the ant colony algorithm, and the genetic algorithm are used to predict the opening price, closing price, highest price, and lowest price of KDJ index of Cathay Pacific Group's 5-day data. Compared with the real value, we find that the BP neural network is almost the smallest in forecasting the opening price and closing price, or the lowest price and the highest price, and has good stability, which once again proves the feasibility of applying the BP neural network to the research and prediction of financial stability.

A fluorometric and colorimetric method for determination of trypsin by exploiting the gold nanocluster-induced aggregation of hemoglobin-coated gold nanoparticles.

A dual-signal assay is described for the determination of trypsin based on the use of gold nanoparticles (AuNPs) that aggregate in the presence of gold nanoclusters (AuNCs) due to electrostatic interaction. This is accompanied by a color change from red to blue. However, if hemoglobin (Hb) is present in the solution, it will attach to the surface of AuNPs, thus preventing aggregation. The Hb-coated AuNPs quench the fluorescence of AuNCs. Trypsin can hydrolyze Hb and destroy the protective coating of Hb on the AuNPs. As a result, AuNP aggregation will occur after the addition of AuNCs, and the blue fluorescence of the AuNCs with 365 nm excitation and 455 nm maximum emission peak is recovered. Thus, trypsin can be determined by measurement of fluorescence emission intensity. Additionally, trypsin can be determined by the maximum absorption peak wavelength between 530 nm and 610 nm. Fluorescence increases linearly in the 10-2500 ng⋅mL-1 concentration range, and absorbance in the 20-2000 ng·mL-1 concentration range. The limits of detection are 4.6 ng·mL-1 (fluorometry) and 8.4 ng·mL-1 (colorimetry), respectively. The assay is sensitive and selective, and can be applied to the determination of trypsin in serum. Graphical abstract Schematic presentation of a fluorometric and colorimetric method for determination of trypsin. The presence of hemoglobin (Hb) protects AuNPs from agglomeration after adding AuNCs and the fluorescence of AuNCs is quenched. With trypsin present, trypsin destroys the coating of AuNPs by Hb. AuNPs aggregate again and the fluorescence recovers after the addition of AuNCs.

Concentrations and health risks of heavy metals in soils and crops around the Pingle manganese (Mn) mine area in Guangxi Province, China.

Heavy metal concentrations in agricultural fields and their ecological risks are a source of extensive concern worldwide. A field survey was conducted to investigate the present situation and health risks of heavy metals (Mn, Pb, Zn, Cu, and Cd) and crops (corn, green soybean, sweet potato, persimmon, cassava, and Chinese chestnut) around the Pingle manganese (Mn) mine site in Guangxi Province, China, which was abandoned 20 years ago. The results showed that the ranges of Mn, Pb, Zn, Cu, and Cd were 2706.54-6760.16, 229.37-275.84, 160.39-215.48, 58.11-75.30, and 5.78-6.98 mg kg-1, respectively, which were approximately 15.38-38.41, 11.76-14.15, 2.12-2.85, 2.09-2.71, and 21.64-28.75 times greater than their respective background values. Most of these concentrations exceeded the national standard for soil quality (grade 2) developed by the Ministry of Environmental Protection of China (1995). Contamination assessments based on the single contamination index (Pi), Nemerow multi-factor index (Pcom), and potential ecological risk index (RI) showed that the sampled soils were severely polluted with these heavy metals, especially Pb and Cd. Similarly, the crops were enriched with Pb and Cd, with concentrations of 10.22-41.78 and 2.33-5.37 mg kg-1, respectively, which were much higher than the threshold values of the national food standards. Contamination assessments with Pi and Pcom also showed that the crops were severely polluted with Pb and Cd. The bioaccumulation factor values for Cd were highest among the heavy metals, with an average mean of 0.66 in these six crops, demonstrating that Cd readily accumulates in these crops. An assessment showed that the health risk for adults living in the mining-impacted areas was significant. Our study strongly recommends that heavy metal contamination in agricultural soils and crops grown around the Pingle Mn mining-affected areas should be treated to mitigate the health risks.

microRNA-99a Reduces Lipopolysaccharide-Induced Oxidative Injury by Activating Notch Pathway in H9c2 Cells.

microRNA-99a (miR-99a) is recently recognized as a key regulator in various cancers and cardiovascular diseases. In the present study, we sought to investigate the effects of miR-99a in rat cardiomyocyte H9c2 cells against oxidative injury induced by lipopolysaccharide (LPS).MTT assay, reactive oxygen species (ROS) assay, flow cytometry and lactate dehydrogenase (LDH) assay were respectively used to explore viability, ROS levels, apoptosis, and cell death in H9c2 cells. Quantitative PCR (qRT-PCR) was performed to confirm the expression of miR-99a. Western blot was performed to determine the expression of Notch pathway factors.LPS could significantly suppress viability and increase cell death, apoptosis, and ROS level (P < 0.05). However, miR-99a could significantly increase the viability and decrease apoptosis and ROS level of H9c2 cells (P < 0.05). Overexpression of miR-99a could activate a Notch pathway and regulate the expression of B-cell CLL/lymphoma 2 (BCL2) and cleaved caspase 3.Our study found that overexpression of miR-99a could attenuate LPS-induced oxidative injury in H9c2 cells, possibly via a Notch pathway. These findings suggest that miR-99a may be a key factor in cardiomyocyte oxidative injury and could be a new therapeutic strategy for cardiovascular diseases.

Upregulated Expression of TRIM32 Is Involved in Schwann Cell Differentiation, Migration and Neurite Outgrowth After Sciatic Nerve Crush.

Tripartite motif containing 32 (TRIM32), a member of the tripartite motif (TRIM) family, plays an indispensable role in myoblast proliferation. It also regulates neuron and skeletal muscle stem cell differentiation. Although it is of great importance, we know little about the roles of TRIM32 during peripheral nervous system injury. Here, we examined the dynamic changes of TRIM32 in acute sciatic nerve crush (SNC) model. After crush, TRIM32 rapidly increased and reached the climax at 1 week but then gradually declined to the normal level at 4 weeks post-injury. Meanwhile, we observed similar changes of Oct-6. What is more, we found co-localization of TRIM32 with S100 and Oct-6 in 1-week-injured tissues using double immunofluorescent staining. In further vitro experiments, enhancive expression of TRIM32 was detected during the process of cyclic adenosine monophosphate (cAMP)-induced Schwann cell differentiation and nerve growth factor (NGF)-induced PC12 cell neurite outgrowth. More interestingly, specific si-TRIM32-transfected RSC96 cells exhibited obvious reduction in the ability of migration. Taken together, we inferred that upregulated TRIM32 was not only involved in the differentiation and migration of Schwann cells but the neurite elongation after SNC.

SCY1-Like 1-Binding Protein 1 (SCYL1BP1) Suppressed Sciatic Nerve Regeneration by Enhancing the RhoA Pathway.

SCY1-like 1-binding protein 1 (SCYL1BP1) is first identified as an interacting protein with SCYL1. Since SCYL1BP1 is a soluble protein with coiled-coil domains known to be relevant with transcriptional regulation, it has been found to activate the transcription of murine double minute 2 (MDM2) and participate in neurite outgrowth and regeneration. However, the role and mechanism of SCYL1BP1 in peripheral nerve system lesion and repair are still unknown. Here in vitro, our work demonstrated that SCYL1BP1 inhibited cAMP-induced primary Schwann cell differentiation and suppressed nerve growth factor-mediated neurite outgrowth in PC12 cells by enhancing the RhoA pathway. Furthermore, we found that pretreatment with a Rho kinase inhibitor Y-27632 resulted in partial rescue of Schwann cell differentiation and neurite outgrowth. In vivo experiments showed that SCYL1BP1 could also suppress nerve fiber regeneration. In conclusion, we speculated that SCYL1BP1 participated in Schwann cell (SC) differentiation and neurite outgrowth in the sciatic nerve after crush by regulating the RhoA pathway.

[Multi-slice CT angiography in the diagnosis of lesions of mesenteric artery and mesenteric vein].

OBJECTIVE: To evaluate the value of multi-slice CT angiography (MSCTA) in the diagnosis of super mesenteric artery (SMA) and super mesenteric vein (SMV), and discuss the 3D reconstruction method for detecting mesenteric vessel lesions. METHODS: Thirty-three patients suffering from mesenteric vessel diseases were analyzed. There were 14 SMA lesions, including 9 thromboses, 3 dissecting aneurysms, 1 pseudoaneurysm, and 1 malrotation. There were 19 SMV thromboses. The 3D reconstruction included volume rendering (VR), maximum intensity projection (MIP), and multi-planner reformation (MPR). RESULTS: The lesions appeared clear by MSCTA in the 33 patients. The SMA thrombosis was shown clear in the MIP in all 9 patients, and only 4 of them were detected in the VR. There was significant difference between MIP andVR in detecting SMA thrombosis (P=0.0294). Three dissecting aneurysms were best shown in the MPR; 1 pseudoaneurysm and 1 malrotation were clearly manifested in the VR. The thrombosis of SMV was clearly shown by both MIP and MPR in all 19 patients. Collateral vessels were clearly shown in the MIP in 12 patients; the collateral vessels were detected by VR only in 5, and the other 7 failed to show the collateral vessels. There was significant difference between the MIP and the VR in showing lateral collateral vessels (P=0.0046). CONCLUSION: Both lesions of SMA and SMV can be detected by MSCTA. MIP is an ideal reconstruction method for SMA thrombosis and collateral vessels around the SMV.

Transcription factor Snai1-1 induces osteosarcoma invasion and metastasis by inhibiting E-cadherin expression.

Osteosarcoma (OS) is a type of primary malignant bone tumor with a high propensity for local recurrence and distant metastasis. A previous study showed Snail-1 is highly expressed in OS cells. The present study aimed to investigate the association between the transcription factor Snai1 and E-cadherin in OS. SaOS2 OS cells were transfected either with a plasmid expressing short hairpin RNA (shRNA) specific for the Snai1-1 gene (SaOS2-shRNA) or a negative control plasmid (SaOS2-Mock). The expression levels of E-cadherin and Snai1-1 in the transfected and control cells were determined by quantitative polymerase chain reaction and western blot analysis. In addition, the study was extended to evaluate the migratory and invasive properties of the cells through a Transwell experiment. The results show that E-cadherin was expressed at a high level in the SaOS2-shRNA cells, which were much less migratory and invasive than the control cells. Overexpression of Snai1-1 in OS is associated with tumor progression, possibly through the suppression of E-cadherin expression and induction of the process of epithelial-mesenchymal transition, which contributes to the proceeding invasion and metastasis of OS cells.

Involvement of upregulated SYF2 in Schwann cell differentiation and migration after sciatic nerve crush.

SYF2 is a putative homolog of human p29 in Saccharomyces cerevisiae. It seems to be involved in pre-mRNA splicing and cell cycle progression. Disruption of SYF2 leads to reduced α-tubulin expression and delayed nerve system development in zebrafish. Due to the potential of SYF2 in modulating microtubule dynamics in nervous system, we investigated the spatiotemporal expression of SYF2 in a rat sciatic nerve crush (SNC) model. We found that SNC resulted in a significant upregulation of SYF2 from 3 days to 1 week and subsequently returned to the normal level at 4 weeks. At its peak expression, SYF2 distributed predominantly in Schwann cells. In addition, upregulation of SYF2 was approximately in parallel with Oct-6, and numerous Schwann cells expressing SYF2 were Oct-6 positive. In vitro, we observed enhanced expression of SYF2 during the process of cyclic adenosine monophosphate (cAMP)-induced Schwann cell differentiation. SYF2-specific siRNA-transfected Schwann cells did not show significant morphological change in the process of Schwann cell differentiation. Also, we found shorter and disorganized microtubule structure and a decreased migration in SYF2-specific siRNA-transfected Schwann cells. Together, these findings indicated that the upregulation of SYF2 was associated with Schwann cell differentiation and migration following sciatic nerve crush.

FBP1 and p27kip1 expression after sciatic nerve injury: implications for Schwann cells proliferation and differentiation.

Far Upstream Element (FUSE) Binding Protein 1 (FBP1), first identified as a single-stranded DNA (ssDNA) binding protein that binds to the FUSE, could modulate c-myc mRNA levels and also has been shown to regulate tumor cell proliferation and replication of virus. Typically, FBP1 could active the translation of p27kip1 (p27) and participate in tumor growth. However, the expression and roles of FBP1 in peripheral system lesions and repair are still unknown. In our study, we found that FBP1 protein levels was relatively higher in the normal sciatic nerves, significantly decreased and reached a minimal level at Day 3, and then returned to the normal level at 4 weeks. Spatially, we observed that FBP1 had a major colocation in Schwann cells and FBP1 was connected with Ki-67 and Oct-6. In vitro, we detected the decreased level of FBP1 and p27 in the TNF-α-induced Schwann cells proliferation model, while increased expression in cAMP-induced Schwann cells differentiation system. Specially, FBP1-specific siRNA-transfected SCs did not show fine and longer morphological change after cAMP treatment and had a decreased motility compared with normal. At 3 days after cAMP treatment and SC/neuron co-cultures, p27 was transported to cytoplasm to form CDK4/6-p27 to participate in SCs differentiation. In conclusion, we speculated that FBP1 and p27 were involved in SCs proliferation and the following differentiation in the sciatic nerve after crush by transporting p27 from nucleus to cytoplasm.

Changes in the Foxj1 expression of Schwann cells after sciatic nerve crush.

Foxj1 is a member of the Forkhead box family of transcription factors expressed in multiple tissues during development and a major regulator of cilia development. It was reported that Foxj1 has a significant up-regulation after traumatic brain injury and plays an important role in central nervous system injury and repair. However, its expression and function in the peripheral nervous system lesion are not well understood. In this study, we investigated the spatiotemporal expression of Foxj1 in a rat sciatic nerve crush model. After never injury, we observed that Foxj1 had a significant up-regulation from 1 day, peaked at day 3 and then gradually decreased to the normal level at 4 weeks. At its peak expression, Foxj1 expressed mainly in Schwann cells (SCs) of the distal sciatic nerve segment from injury, but had few co-localizations in axons. Besides, the peak expression of Foxj1 was in parallel with proliferating cell nuclear antigen (PCNA), and numerous SCs expressing Foxj1 were PCNA positive. Collectively, we hypothesized that peripheral nerve crush-induced up-regulation of Foxj1 in the sciatic nerve was associated with Schwann cells proliferation.

Dynamic changes of Jab1 and p27kip1 expression in injured rat sciatic nerve.

Jun activation domain-binding protein (Jab1) is a multifunctional protein that participates in affecting signaling pathway, controlling cell proliferation and apoptosis, and regulating genomic instability and DNA repair, and acts as a key subunit of COP9 signalosome. p27kip1, a member of the Cip/Kip family of cyclin-dependent kinase inhibitors, was shown to inhibit the enzymatic activity of cyclin-CDK complexes, resulting in cell-cycle arrest at G1. Recent studies have shown that Jab1 directly binds to p27kip1 and induces nuclear export and subsequent degradation in a variety of human cancers, while the association and function of Jab1 and p27kip1 in nervous system lesion and regeneration remain unclear. Here, we performed a sciatic nerve injury model in adult rats and studied the dynamic changes of Jab1 and p27kip1 expression by Western blot. Sciatic nerve crush (SNC) resulted in a significant upregulation of Jab1 and a downregulation of p27kip1. Besides, we observed that Jab1 was expressed widely in Schwann cells (SCs) and had few co-localization in axons by double immunofluorescence staining. In addition, the peak expression of Jab1 was parallel with proliferating cell nuclear antigen (PCNA), and numerous SCs expressing Jab1 were PCNA-positive. Results obtained by co-immunoprecipitation and double labeling further showed their interaction in the sciatic nerve. Thus, these results suggested that Jab1 and p27kip1 may be involved in the pathophysiology of sciatic nerve after SNC.

The member of high temperature requirement family HtrA2 participates in neuronal apoptosis after intracerebral hemorrhage in adult rats.

The members of high-temperature requirement (HtrA) family are evolutionarily conserved serine proteases that combine a trypsin-like protease domain with at least one PDZ interaction domain. HtrA2, a special one, is mainly located in mitochondria and required for maintaining homeostasis. Once released into cytoplasm, HtrA2 contributes to apoptosis via caspase-dependent and -independent pathways. Accumulating evidence has showed its pro-apoptotic effect in cancers and central nervous system (CNS) diseases. However, the distribution and function of HtrA2 in CNS diseases remains to be further explored. To investigate HtrA2's roles in the pathophysiology of intracerebral hemorrhage (ICH), an ICH rat model was established and assessed by behavioral tests. Western blot and immunohistochemistry revealed a remarkable up-regulation of HtrA2 surrounding the hematoma after ICH; and immunofluorescence showed HtrA2 was strikingly increased in neurons, but not in astrocytes and oligodendrocytes. Terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling staining suggested the involvement of HtrA2 in neuronal apoptosis after ICH. Additionally, HtrA2 co-localized with active-caspase-3 around the hematoma and the expression of active-caspase-3 was parallel with that of HtrA2 in a time-dependent manner. Furthermore, hemin was used to stimulus a neuronal cell line PC12 to mimic ICH model in vitro. We analyzed the relationship of HtrA2 with X-linked inhibitor of apoptosis protein (XIAP) in PC12 cells by Western blot, immunofluorescence and co-immunoprecipitation. The connection of HtrA2 with XIAP was strengthened in apoptotic cells after hemin treatment. Thus, we speculated that HtrA2 might exert an important function in regulating caspase-dependent neuronal apoptosis through interacting with XIAP following ICH.

The role of HSPA12B in regulating neuronal apoptosis.

Heat shock protein A12B (HSPA12B) is the newest member of a recently defined subfamily of proteins distantly related to the 70-kDa family of heat shock proteins (HSP70) family. HSP70s play a crucial role in protecting cells, tissues, organs and animals from various noxious conditions. Here we studied the dynamic expression changes and localization of HSPA12B after middle cerebral artery occlusion (MCAO) with reperfusion induced ischemic insult processes in adult rats. Apoptosis, as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, was also increased in the peri-ischemic cortex compared to non-ischemic hemisphere. The expression of HSPA12B was strongly induced in the ischemic hemisphere of MCAO reperfusion rats in vivo. In vitro studies indicated that the up-regulation of HSPA12B may be involved in oxygen-glucose deprivation-induced PC12 cell death. And knockdown of HSPA12B in cultured differentiated PC12 cells by siRNA showed that HSPA12B inhibited the expression of active caspase-3. Collectively, these results suggested that HSPA12B may be required for protecting neurons from ischemic insults.

Increased expression of Gem after rat sciatic nerve injury.

Gem belongs to the Rad/Gem/Kir subfamily of Ras-related GTPases, whose expression is induced in several cell types upon activation by extracellular stimuli. Two functions of Gem have been demonstrated, including regulation of voltage-gated calcium channel activity and inhibition of Rho kinase-mediated cytoskeletal reorganization, such as stress fiber formation and neurite retraction. Because of the essential relationship between actin reorganization and peripheral nerve regeneration, we investigated the spatiotemporal expression of Gem in a rat sciatic nerve crush (SNC) model. After never injury, we observed that Gem had a significant up-regulation from 1 day, peaked at day 5 and then gradually decreased to the normal level. At its peak expression, Gem expressed mainly in Schwann cells (SCs) and macrophages of the distal sciatic nerve segment, but had few colocalization in axons. In addition, the peak expression of Gem was in parallel with PCNA, and numerous SCs expressing Gem were PCNA positive. Thus, all of our findings suggested that Gem may be involved in the pathophysiology of sciatic nerve after SNC.

Transcription initiation factor IIB involves in Schwann cell differentiation after rat sciatic nerve crush.

Transcription Initiation Factor IIB (TFIIB), as a general transcription factor, plays an essential role in preinitiation complex assembly and transcription initiation by recruiting RNA polymerase II to the promoter. However, its distribution and function in peripheral system lesion and repair were still unknown. Here, we investigated the spatiotemporal expression of TFIIB in an acute sciatic nerve crush model in adult rats. Western blot analysis revealed that TFIIB was expressed in normal sciatic nerve. It gradually increased, reached a peak at the seventh day after crush, and then returned to the normal level at 4 weeks. We observed that TFIIB expressed mainly increased in Schwann cells and co-localized with Oct-6. In vitro, we induced Schwann cell differentiation with cyclic adenosine monophosphate (cAMP) and found that TFIIB expression was increased in the differentiated process. TFIIB-specific siRNA inhibited cAMP-induced Schwann cell morphological change and the expression of P0. Collectively, we hypothesized peripheral nerve crush-induced upregulation of TFIIB in the sciatic nerve was associated with Schwann cell differentiation.