Flexible and Robust Core-Shell PANI/PVDF@PANI Nanofiber Membrane for High-Performance Electromagnetic Interference Shielding.

Developing high-performance electromagnetic interference (EMI) shielding materials that are lightweight and flexible and have excellent mechanical properties is an ideal choice for modern integrated electronic devices and microwave protection. Herein, we report the preparation of core-shell polyaniline (PANI)-based nanofiber membranes for EMI shielding through seed polymerization. Electrospinning a PANI solution leads to homogeneously dispersed PANI on the nanofiber surface, with abundant attachment sites for aniline through electrostatic adsorption and hydrogen bonding interaction, allowing PANI to grow on the nanofiber surfaces. This stable core-shell heterostructure provides more interfaces for reflecting and absorbing microwaves. The PANI/PVDF@PANI membranes achieved a shielding efficiency (SE) of 44.7 dB at a thickness of only 1.2 mm, exhibiting an exceptionally high specific EMI shielding effectiveness (SE/t) of 372.5 dB cm-1. Furthermore, the composite membrane exhibits outstanding mechanical stability, durability, air permeability, and moisture permeability, also making it suitable for applications such as EM shielding clothing.

Synergistic Optimization of Buried Interface by Multifunctional Organic-Inorganic Complexes for Highly Efficient Planar Perovskite Solar Cells.

For the further improvement of the power conversion efficiency (PCE) and stability of perovskite solar cells (PSCs), the buried interface between the perovskite and the electron transport layer is crucial. However, it is challenging to effectively optimize this interface as it is buried beneath the perovskite film. Herein, we have designed and synthesized a series of multifunctional organic-inorganic (OI) complexes as buried interfacial material to promote electron extraction, as well as the crystal growth of the perovskite. The OI complex with BF4- group not only eliminates oxygen vacancies on the SnO2 surface but also balances energy level alignment between SnO2 and perovskite, providing a favorable environment for charge carrier extraction. Moreover, OI complex with amine (- NH2) functional group can regulate the crystallization of the perovskite film via interaction with PbI2, resulting in highly crystallized perovskite film with large grains and low defect density. Consequently, with rational molecular design, the PSCs with optimal OI complex buried interface layer which contains both BF4- and -NH2 functional groups yield a champion device efficiency of 23.69%. More importantly, the resulting unencapsulated device performs excellent ambient stability, maintaining over 90% of its initial efficiency after 2000 h storage, and excellent light stability of 91.5% remaining PCE in the maximum power point tracking measurement (under continuous 100 mW cm-2 light illumination in N2 atmosphere) after 500 h.

Winter coexistence in herbivorous waterbirds: Niche differentiation in a floodplain, Poyang Lake, China.

The classical niche theory supports the idea that stable coexistence requires ecological differences between closely related species. However, information on waterbirds coexistence in the entirely landlocked freshwater system of Poyang Lake is not well understood, especially when the available biomass of their food in the area decreases. In this study, we tested the ecological segregation mechanisms in the 2015/2016 and 2016/2017 wintering periods among eight herbivorous waterbirds (including the Siberian crane Grus leucogeranus, hooded crane Grus monacha, white-naped crane Grus vipio, common crane Grus grus, greater white-fronted goose Anser albifrons, bean goose Anser fabalis, swan goose Anser cygnoides, and tundra swan Cygnus columbianus) at Poyang Lake. Using field observations and species niche and foraging habitat selection models, we investigated the abundance, distribution, and food sources of these eight waterbird species to quantify and compare their habitat use and ecological niches. Our results showed that niche segregation among the waterbirds, with respect to food types, time, and spatial location, allow them to coexist and use similar resources. The water level gradually receded in the sub-lakes of the Poyang Lake, which could provide food sources and various habitats for wintering herbivorous waterbirds to coexist. We demonstrated that the differences in habitat use could mitigate interspecific competition, which may explain the mechanism whereby waterbirds of Poyang Lake coexist during the wintering period, despite considerable overlap in the dietary niches of herbivorous waterbirds.

The International Teaching and Practice of Cryobiology and Biobankology Course in China.

In the past 10 years, clinical biobanks have experienced increasing expansion in China. Demand for systematically educated biobanking professionals is a priority for Chinese biobanks' agenda. The cryobiology and biobankology course is the first semester-long course in China, designed and developed at Central South University with international cooperation. Leading professors were from China, the United States, United Kingdom, and Canada to teach the latest version of biobanking knowledge and skills around the globe. This course is a comprehensive elective course with six specific teaching modules, which is suitable for graduate students majoring in basic medical sciences, clinical medicine, life sciences, mechanical engineering, and biomedical engineering, who would like to seek biobanking careers in the future. Participants from China, Czech Republic, Ghana, Madagascar, Tanzania, South Sudan, and Israel attended the course. Through taking this course, students can broaden their international academic horizons and cultivate the ability to learn and apply the knowledge of biology, medicine, and engineering to analyze and explain the low-temperature biology and clinical samples-based research practice. At the same time, the course enables students to realize the importance of multidisciplinary fields of biobanking and the significance of innovative precision medicine research, and further enlightens students' enthusiasm to pursue biobanking professional careers, and in the future they can proudly call themselves "biobankers."

Stat3 in osteocytes mediates osteogenic response to loading.

Signal transducer and activator of transcription 3 (Stat3) is a member of the Stat family of proteins involved in signaling in many different cell types, including osteocytes. Osteocytes are considered major mechanosensing cells in bone due to their intricate dendritic networks able to sense changes in physical force and to orchestrate the response of osteoclasts and osteoblasts. We examined the role of Stat3 in osteocytes by generating mice lacking Stat3 in these cells using the Dmp-1(8kb)-Cre promoter (Stat3cKO mice). Compared to age-matched littermate controls, Stat3cKO mice of either sex (18 weeks old) exhibit reduced bone formation indices, decreased osteoblasts and increased osteoclasts, and altered material properties, without detectable changes in bone mineral density (BMD) or content of either trabecular or cortical bone. In addition, Stat3cKO mice of either sex show significantly decreased load-induced bone formation. Furthermore, pharmacologic inhibition of Stat3 in osteocytes in vitro with WP1066 blocked the increase in cytosolic calcium induced by ATP, a mediator of the cellular responses to sheer stress. WP1066 also increased reactive oxygen species (ROS) production in cultured MLO-Y4 osteocytes. These data demonstrate that Stat3 is a critical mediator of mechanical signals received by osteocytes and suggest that osteocytic Stat3 is a potential therapeutic target to stimulate bone anabolism.

Pin1 Is Regulated by CaMKII Activation in Glutamate-Induced Retinal Neuronal Regulated Necrosis.

In our previous study, we reported that peptidyl-prolyl isomerase 1 (Pin1)-modulated regulated necrosis (RN) occurred in cultured retinal neurons after glutamate injury. In the current study, we investigated the role of calcium/calmodulin-dependent protein kinase II (CaMKII) in Pin1-modulated RN in cultured rat retinal neurons, and in an animal in vivo model. We first demonstrated that glutamate might lead to calcium overloading mainly through ionotropic glutamate receptors activation. Furthermore, CaMKII activation induced by overloaded calcium leads to Pin1 activation and subsequent RN. Inactivation of CaMKII by KN-93 (KN, i.e., a specific CaMKII inhibitor) application can decrease the glutamate-induced retinal neuronal RN. Finally, by using an animal in vivo model, we also demonstrated the important role of CaMKII in glutamate-induced RN in rat retina. In addition, flash electroretinogram results provided evidence that the impaired visual function induced by glutamate can recover after CaMKII inhibition. In conclusion, CaMKII is an up-regulator of Pin1 and responsible for the RN induced by glutamate. This study provides further understanding of the regulatory pathway of RN and is a complementary mechanism for Pin1 activation mediated necrosis. This finding will provide a potential target to protect neurons from necrosis in neurodegenerative diseases, such as glaucoma, diabetic retinopathy, and even central nervous system diseases.

Calpain2 but not calpain1 mediated by calpastatin following glutamate-induced regulated necrosis in rat retinal neurons.

The purpose of this study is to investigate whether calpastatin (CAST) plays an important role in the regulated necrosis (RN) in rat retinal neurons under an excessive glutamate condition and furthermore to investigate whether this process is regulated by calapin1 and calpain2. In the present study, glutamate triggered CAST inhibition, calpain2 activation and retinal neuronal RN after injury. The application of CAST active peptide could provide protective effects against activated calpain2 mediated RN. However, the calpain1 activity was not changed in these processes. Finally, in vivo studies further confirmed the role of the CAST-calpain2 pathway in cellular RN in the rat retinal ganglion cell layer and inner nuclear layer after glutamate excitation. In addition, flash electroretinogram results provided evidence that the impaired visual function induced by glutamate could recover after CAST peptide treatment. This research indicated that excessive glutamate may lead to CAST inhibition and activated calpain2, but not calpain1 activation, resulting in RN.

A New Method of Biostorage and Biopreservation for Human Amputated Extremities.

OBJECTIVES: We have explored a better method to preserve and store human medically amputated large size samples. The approach involved developing a special embalming solution and procedures for biopreservation and biostorage of a large-sized sample as a whole specimen rather than dissected small parts. Evaluation of the effect of our special embalming solution and procedures on whole human amputated extremities compared with excised small tissues was conducted. Histological and morphological techniques and elemental analyses were utilized to assess the effects of our new method using the special embalming solution. METHODS: Whole remains and excised tissues (skin, muscle, saphenous nerve, and femoral artery) were immersed in a special embalming solution for 6, 12, and 24 months, respectively. Then samples from whole remains and excised tissues were paraffin embedded and Hematoxylin-Eosin staining was performed. Transmission electron microscopy was performed to detect the microstructure of the samples. At the same time, concentrations of chemical elements in the embalming solution from whole remains and excised tissues were separately determined by using inductively coupled plasma atomic emission spectrometry. RESULTS: The morphological structure of tissues was well preserved at 6 and 12 months, and few chemical elements, especially trace elements, leached into the embalming fluid. The macroelements leached into the fluid earlier than the trace elements, but there were some differences in the ultrastructure after preservation for 24 months between tissues excised before and after embalming. Over time, the types and concentrations of chemical elements in the embalming fluid increased. The trace elements in the whole remains were preserved better than those in the removed tissues, and trace elements in muscles and femoral artery were better preserved than those in the skin and saphenous nerve. CONCLUSION: The special embalming fluid can preserve fresh amputated remains well for a short time (less than 24 months), and performs better for the whole remains than excised tissues. This specific embalming fluid should be further studied to achieve higher quality preservation of different tissues for a longer period of time.

Using drugs to target necroptosis: dual roles in disease therapy.

Necroptosis is programmed necrosis, a process which has been studied for over a decade. The most common accepted mechanism is through the RIP1-RIP3-MLKL axis to regulate necroptotic cell death. As a result of previous studies on necroptosis, positive regulation for promoting necroptosis such as HSP90 stabilization and hyperactivation of TAK1 on RIP1 is clear. Similarly, the negative regulation of necroptosis, such as through caspase 8, c-FLIP, CHIP, MK2, PELI1, ABIN-1, is also clear. Therefore, the promise of corresponding applications in treating diseases becomes hopeful. Studies have shown that necroptosis is involved in the development of many diseases, such as ischemic injury diseases in various organs, neurodegenerative diseases, infectious diseases, and cancer. Given these results, drugs that inhibit or trigger necroptosis can be discovered to treat diseases. In this review, we briefly introduce up to date concepts concerning the mechanism of necroptosis, the diseases that involve necroptosis, and the drugs that can be applied to treat such diseases.

Inhibition of HSP90α protects cultured neurons from oxygen-glucose deprivation induced necroptosis by decreasing RIP3 expression.

Heat shock protein 90α (HSP90α) maintains cell stabilization and regulates cell death, respectively. Recent studies have shown that HSP90α is involved in receptor interacting protein 3 (RIP3)-mediated necroptosis in HT29 cells. It is known that oxygen and glucose deprivation (OGD) can induce necroptosis, which is regulated by RIP3 in neurons. However, it is still unclear whether HSP90α participates in the process of OGD-induced necroptosis in cultured neurons via the regulation of RIP3. Our study found that necroptosis occurs in primary cultured cortical neurons and PC-12 cells following exposure to OGD insult. Additionally, the expression of RIP3/p-RIP3, MLKL/p-MLKL, and the RIP1/RIP3 complex (necrosome) significantly increased following OGD, as measured through immunofluorescence (IF) staining, Western blotting (WB), and immunoprecipitation (IP) assay. Additionally, data from computer simulations and IP assays showed that HSP90α interacts with RIP3. In addition, HSP90α was overexpressed following OGD in cultured neurons, as measured through WB and IF staining. Inhibition of HSP90α in cultured neurons, using the specific inhibitor, geldanamycin (GA), and siRNA/shRNA of HSP90α, protected cultured neurons from necrosis. Our study showed that the inhibitor of HSP90α, GA, rescued cultured neurons not only by decreasing the expression of total RIP3/MLKL, but also by decreasing the expression of p-RIP3/p-MLKL and the RIP1/RIP3 necrosome. In this study, we reveal that inhibition of HSP90α protects primary cultured cortical neurons and PC-12 cells from OGD-induced necroptosis through the modulation of RIP3 expression.

Macroglia-derived thrombospondin 2 regulates alterations of presynaptic proteins of retinal neurons following elevated hydrostatic pressure.

Many studies on retinal injury and repair following elevated intraocular pressure suggest that the survival ratio of retinal neurons has been improved by various measures. However, the visual function recovery is far lower than expected. The homeostasis of retinal synapses in the visual signal pathway is the key structural basis for the delivery of visual signals. Our previous studies found that complicated changes in the synaptic structure between retinal neurons occurred much earlier than obvious degeneration of retinal ganglion cells in rat retinae. The lack of consideration of these earlier retinal synaptic changes in the rescue strategy may be partly responsible for the limited visual function recovery with the types of protective methods for retinal neurons used following elevated intraocular pressure. Thus, research on the modulatory mechanisms of the synaptic changes after elevated intraocular pressure injury may give new light to visual function rescue. In this study, we found that thrombospondin 2, an important regulator of synaptogenesis in central nervous system development, was distributed in retinal macroglia cells, and its receptor α2δ-1 was in retinal neurons. Cell cultures including mixed retinal macroglia cells/neuron cultures and retinal neuron cultures were exposed to elevated hydrostatic pressure for 2 h. The expression levels of glial fibrillary acidic protein (the marker of activated macroglia cells), thrombospondin 2, α2δ-1 and presynaptic proteins were increased following elevated hydrostatic pressure in mixed cultures, but the expression levels of postsynaptic proteins were not changed. SiRNA targeting thrombospondin 2 could decrease the upregulation of presynaptic proteins induced by the elevated hydrostatic pressure. However, in retinal neuron cultures, elevated hydrostatic pressure did not affect the expression of presynaptic or postsynaptic proteins. Rather, the retinal neuron cultures with added recombinant thrombospondin 2 protein upregulated the level of presynaptic proteins. Finally, gabapentin decreased the expression of presynaptic proteins in mixed cultures by blocking the interaction of thrombospondin 2 and α2δ-1. Taken together, these results indicate that activated macroglia cells may participate in alterations of presynaptic proteins of retinal neurons following elevated hydrostatic pressure, and macroglia-derived thrombospondin 2 may modulate these changes via binding to its neuronal receptor α2δ-1.

The potential combinational effect of miR-34a with celecoxib in osteosarcoma.

Advanced osteosarcoma (OS) is usually treated by preoperative and postoperative chemotherapy, but there are a very limited number of active agents. Celecoxib (Cel) is a COX-2-selective nonsteroidal anti-inflammatory drug and its antitumoral effect has been shown widely in a variety of cancers including OS cells in vitro. However, the potential combinational effect of Cel with other biological therapy has not been reported in OS cells. In this study, the effects of Cel, miR-34a mimics, and their combination on cell proliferation (MTT assay), migration (in-vitro scratch assay), invasion (transwell assay), mRNA (real-time PCR), and protein (Western blot) expression of associated signal transductions were investigated in cultured MG63 cells. The results showed that miR-34a mimics transfection and Cel treatment significantly decreased cell viability, migration, and invasion in MG63 cells, with their combination being more effective. In contrast, miR-34a inhibitors transfection exerted an effect opposite to miR-34a mimics on cell viability, migration, and invasion. The antitumoral effects of miR-34a, Cel, and their combination were observed in significant up-regulated expression of PTEN and GSK-3ß, down-regulated expression of ROCK1, Notch1, and MMP9 as well as Akt Ser phosphorylation. Our data suggested that miR-34a exerts a combinational effect with Cel on the cell proliferation, migration, and invasion in OS cells through regulating Notch1/ROCK1-PTEN-Akt-GSK-3ß signaling and MMP9 gene expression.

Pin1 Promotes Regulated Necrosis Induced by Glutamate in Rat Retinal Neurons via CAST/Calpain2 Pathway.

The purpose of the current study was to investigate whether peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (Pin1) can interact with calpastatin (CAST) and regulate CAST/calpain2, under excessive glutamate conditions, and subsequently regulate necrosis in rat retinal neurons. Glutamate triggered CAST/calpain2-mediated necrosis regulation in primary cultured retinal neurons, as demonstrated by propidium iodide-staining and lactate dehydrogenase assay. Co-IP results and a computer simulation suggested that Pin1 could bind to CAST. Western blot, real-time quantitative polymerase chain reaction, immunofluorescence, and phosphorylation analysis results demonstrated that CAST was regulated by Pin1, as proven by the application of juglone (i.e., a Pin1 specific inhibitor). The retinal ganglion cell 5 cell line, combined with siRNA approach and flow cytometry, was then used to verify the regulatory pathway of Pin1 in CAST/calpain2-modulated neuronal necrosis that was induced by glutamate. Finally, in vivo studies further confirmed the role of Pin1 in CAST/calpain2-modulated necrosis following glutamate excitation, in the rat retinal ganglion cell and inner nuclear layers. In addition, a flash electroretinogram study provided evidence for the recovery of impaired visual function, which was induced by glutamate, with juglone treatment. Our work aims to investigate the involvement of the Pin1-CAST/calpain2 pathway in glutamate-mediated excitotoxicity.

Blood vessel wall-derived endothelial colony-forming cells enhance fracture repair and bone regeneration.

Endochondral bone formation requires new blood vessel formation, and endothelial progenitor cells (EPCs) may play a role in this process. Endothelial colony-forming cells (ECFCs), one subtype of EPCs, isolated from the microvasculature of rat lungs, exhibited cell surface antigen markers and gene products characteristic of endothelial cells and displayed high proliferative potential and an ability to form vessel-like network structures in vitro. The aim of this study was to evaluate whether ECFCs facilitate bone healing during fracture repair and stimulate bone regeneration. When type I collagen sponge containing ECFCs were surgically wrapped around the fractured femurs of rats, newly formed bone mineral at the site of fracture was 13% greater (P = 0.01) and energy to failure was 46% greater (P = 0.01) compared to sponge-wrapped fractures without ECFCs. When ECFCs in type I collagen sponge were surgically implanted into the bone defective area, more new vessels formed locally in comparison with sponge-alone controls and new bone tissues were seen. Further, co-implantation of ECFCs and hydroxyapatite/tricalcium phosphate (HA/TCP) scaffolds at the bone defective sites stimulated more new bone tissues than HA/TCP scaffold alone. These results show that cell therapy with vessel wall-derived ECFCs can induce new vessel formation, stimulate new bone formation, and facilitate bone repair and could be a useful approach to treat non-union fractures and bone defects.

Osteoblast/osteocyte-specific inactivation of Stat3 decreases load-driven bone formation and accumulates reactive oxygen species.

Signal transducers and activators of transcription 3 (Stat3) is a transcription factor expressed in many cell types including osteoblasts, osteocytes, and osteoclasts. STAT3 mutations cause a rare human immunodeficiency disease that presents reduced bone mineral density and recurrent pathological fractures. To investigate the role of Stat3 in load-driven bone metabolism, two strains of osteoblast/osteocyte-selective Stat3 knockout (KO) mice were generated. Compared to age-matched littermate controls, this selective inactivation of Stat3 significantly lowered bone mineral density (7-12%, p<0.05) as well as ultimate force (21-34%, p<0.01). In ulna loading (2.50-2.75N with 120 cycles/day at 2Hz for 3 consecutive days), Stat3 KO mice were less responsive than littermate controls as indicated by reduction in relative mineralizing surface (rMS/BS, 47-59%, p<0.05) and relative bone formation rate (rBFR/BS, 64-75%, p<0.001). Furthermore, inactivation of Stat3 suppressed load-driven mitochondrial activity, which led to an elevated level of reactive oxygen species (ROS) in cultured primary osteoblasts. Taken together, the results support the notion that the loss-of-function mutation of Stat3 in osteoblasts and osteocytes diminishes load-driven bone formation and impairs the regulation of oxidative stress in mitochondria.