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The growing interest and clinical translation of alpha particle (α) therapies brings with it new challenges to assess target cell engagement and to monitor therapeutic effect. Noninvasive imaging has great potential to guide α-treatment and to harness the potential of these agents in the complex environment of disseminated disease. Poly(ADP) ribose polymerase 1 (PARP-1) is among the most abundantly expressed DNA repair enzymes with key roles in multiple repair pathways—such as those induced by irradiation. Here, we used a third-generation PARP1-specific radiotracer, [18F]-PARPZ, to delineate castrate resistant prostate cancer xenografts. Following treatment with the clinically applied [225Ac]-PSMA-617, positron emission tomography was performed and correlative autoradiography and histology acquired. [18F]-PARPZ was able to distinguish treated from control (saline) xenografts by increased uptake. Kinetic analysis of tracer accumulation also suggests that the localization of the agent to sites of increased PARP-1 expression is a consequence of DNA damage response. Together, these data support expanded investigation of [18F]-PARPZ to facilitate clinical translation in the ⍺-therapy space.

Urinary metabolomics is a useful non-invasive tool for large-scale screening of disease-related metabolites. However, no comprehensive urinary metabolomic analysis of vitiligo is presently available. To investigate the urine metabolic pattern of vitiligo patients, we conducted a combined cross-sectional and prospective self-control cohort study and an untargeted urinary metabolomic analysis. In the cross-sectional study, 295 vitiligo patients and 192 age‐ and sex‐matched controls were enrolled, and 71 differential metabolites between two groups were identified. Pathway enrichment analysis revealed that drug metabolism-cytochrome P450, biopterin metabolism, vitamin B9 (folate) metabolism, selenoamino acid metabolism, and methionine and cysteine metabolism showed significant enrichment in vitiligo patients compared with the status in healthy controls. In the self-control cohort, 46 active vitiligo patients were recruited to analyse the urinary metabolic signatures after treatment. All of these patients were asked to undertake follow-up visits every 2 months three times after first consulting and the disease stage was evaluated compared with that at the last visit. Folate metabolism, linoleate metabolism, leukotriene metabolism, alkaloid biosynthesis, and tyrosine metabolism were predicted to be involved in vitiligo activity. Our study is the first attempt to reveal urinary metabolic signatures of vitiligo patients and provides new insights into the metabolic mechanisms of vitiligo.

Frontal lobe epilepsy (FLE) is the second most common type of the focal epilepsies. Our understanding of this disease has been revolutionized over the past decade, but variable treatment outcomes persist and the underlying functional mechanisms responsible for this have yet to be deciphered. This study was designed to determine how intrinsic brain connectivity related to treatment response in patients with FLE. 50 patients with FLE and 28 healthy controls were enrolled in this study and underwent functional MRI at baseline. At the end of 12-month follow up period, all patients with FLE were classified, based on their responses to AEDs treatment, into drug-responsive and drug-refractory groups. The amplitude of low-frequency fluctuation (ALFF) was calculated amongst the three groups in order to detect regional neural function integration. The responsive group showed decreased ALFF only in the left ventromedial prefrontal cortex (vmPFC), while the refractory group showed decreased ALFF in the left vmPFC, right superior frontal gyrus (SFG), and supramarginal gyrus (SMG) relative to healthy controls. In addition, both the responsive and refractory groups showed increased ALFF in the precuneus and postcentral gyrus when compared to the healthy controls. Furthermore, the refractory group exhibited significantly decreased ALFF in the left vmPFC, right SFG and SMG, relative to the responsive group. Focal spontaneous activity, as assessed by ALFF, was associated with response to antiepileptic treatment in patients with FLE. Patients with refractory frontal lobe epilepsy exhibited decreased intrinsic brain activity. Our findings provide novel neuroimaging evidence into the mechanisms of medically-intractable FLE at the brain level.

People with epilepsy (PWE) have an increased suicide prevalence. This study aimed to identify the risk factors for suicidal tendency among PWE in West China. A nested case–control study was designed in a cohort of patients with epilepsy (n = 2087). In total, 28 variates were calculated. In the univariate analysis, unemployment, low income, seizure frequency, seizure-free time, infectious or structural etiology, levetiracetam or phenobarbital use, anxiety, depression, and stigma were associated with suicidal tendency. A multivariate analysis indicated that unemployment (odds ratio [OR] 5.74, 95% confidence interval [CI] 2.13–15.48), levetiracetam use (OR 2.80, 95%CI 1.11–7.05), depression (C-NDDI-E score ≥ 13; OR 3.21, 95%CI 1.26–8.21), and stigma (SSCI score ≥ 16; OR 6.67, 95%CI 1.80–24.69) were independently associated with suicidal tendency. Conditional inference tree analysis indicated that SSCI and C-NDDI-E scores could effectively identify patients with suicidal tendency. Thus, this study suggests that unemployment, levetiracetam use, depression, and stigma are independent risk factors for suicidal tendency in PWE in China.

Sugarcane is the most important sugar and biofuel crop. MADS-box genes encode transcription factors that are involved in developmental control and signal transduction in plants. Systematic analyses of MADS-box genes have been reported in many plant species, but its identification and characterization were not possible until a reference genome of autotetraploid wild type sugarcane specie, Saccharum spontaneum is available recently. We identified 182 MADS-box sequences in the S. spontaneum genome, which were annotated into 63 genes, including 6 (9.5%) genes with four alleles, 21 (33.3%) with three, 29 (46%) with two, 7 (11.1%) with one allele. Paralogs (tandem duplication and disperse duplicated) were also identified and characterized. These MADS-box genes were divided into two groups; Type-I (21 Mα, 4 Mβ, 4 Mγ) and Type-II (32 MIKCc, 2 MIKC*) through phylogenetic analysis with orthologs in Arabidopsis and sorghum. Structural diversity and distribution of motifs were studied in detail. Chromosomal localizations revealed that S. spontaneum MADS-box genes were randomly distributed across eight homologous chromosome groups. The expression profiles of these MADS-box genes were analyzed in leaves, roots, stem sections and after hormones treatment. Important alleles based on promoter analysis and expression variations were dissected. qRT-PCR analysis was performed to verify the expression pattern of pivotal S. spontaneum MADS-box genes and suggested that flower timing genes (SOC1 and SVP) may regulate vegetative development.

The high coercivity of Nd–Fe–B magnets can also be obtained in the Ce–Fe–B magnets fabricated via the dual-main-phase (DMP) method in which the high abundance Ce was used to substitute Nd(Pr). The inhomogeneous distributions of the matrix grains in the DMP magnet play a key role in the enhanced magnetic performance. Compared with the single-phase magnet, more grain boundary phases encapsulating the matrix 2:14:1 grain are formed in the DMP magnet, which reduce the exchange coupling between adjacent magnetic grains. The switching field distribution and the interaction field distribution of the Ce–Fe–B magnets were determined by the first-order-reversal curves (FORC). The switching field peaks around 6 kOe, 11 kOe and 12 kOe in the FORC distribution indicate that three major reversal components coexist for the DMP magnet. The overlapp of the second and third switching field peaks reveals the presence of a pinning interaction within individual magnetic grains with a core–shell structure, which further improve the coercivity of the magnet.

This paper investigates the possibility of saving a network that is predicted to have a cascading failure that will eventually lead to a total collapse. We model cascading failures using the recently proposed KQ model. Then predict an impending total collapse by monitoring critical slowing down indicators and subsequently attempt to prevent the total collapse of the network by adding new nodes. To this end, we systematically evaluate five node addition rules, the effect of intervention delay and network degree heterogeneity. Surprisingly, unlike for random homogeneous networks, we find that a delayed intervention is preferred for saving scale free networks. We also find that for homogeneous networks, the best strategy is to wire newly added nodes to existing nodes in a uniformly random manner. For heterogeneous networks, however, a random selection of nodes based on their degree mostly outperforms a uniform random selection. These results provide new insights into restoring networks by adding nodes after observing early warnings of an impending complete breakdown.

High-entropy alloys have attracted much attention due to their unique microstructures and excellent properties. Since their invention more than ten years ago, research attention has been mainly focused on the study of multicomponent alloys with equiatomic or near-equiatomic compositions. Here we propose a novel design of non-equiatomic medium-entropy alloys that contain one matrix element and several equiatomic alloying elements. To verify the utility of this new design, a series of Co-free Fex(CrNiAl)100−x (at.%, 25 ≤ x ≤ 65) medium-entropy alloys were designed from the much-studied FeNiCrCoAl high-entropy alloy. Detailed characterization reveals that the alloys exhibit novel two-phase microstructures consisting of B2-ordered nanoprecipitates and BCC-disordered matrix. As the alloys deviate far from equiatomic composition, the structure of the nanoprecipitates transfers from a spinodal-like intertwined structure to a nanoparticle dispersed structure. Previous parametric approaches to predict phase formation rules for high-entropy alloys are unable to describe the phase separation behaviors in the studied alloys. Our findings provide a new route to design medium-entropy alloys and also demonstrate a strategy for designing nanostructured alloys from multicomponent alloy systems through simple variations in non-equiatomic compositions.

Periventricular nodular heterotopia (PNH) is a neural migration disorder which often presents clinically with seizures. However, the underlying functional neural basis of PNH is still unclear. We aimed to explore the underlying pathological mechanism of PNH by combining both whole brain functional connectivity (FC) and seed-based FC analyses. We utilized resting-state fMRI to measure functional connectivity strength (FCS) in 38 patients with PNH-related epilepsy and 38 control subjects. The regions with FCS alterations were selected as seeds in the following FC analyses. Pearson correlation analyses were performed to explore associations between these functional neural correlates and clinical features. In comparison with controls, PNH patients showed lower FCS in bilateral insula (P

Implementing selective-area p-type doping through ion implantation is the most attractive choice for the fabrication of GaN-based bipolar power and related devices. However, the low activation efficiency of magnesium (Mg) ions and the inevitable surface decomposition during high-temperature activation annealing process still limit the use of this technology for GaN-based devices. In this work, we demonstrate successful p-type doping of GaN using protective coatings during a Mg ion implantation and thermal activation process. The p-type conduction of GaN is evidenced by the positive Seebeck coefficient obtained during thermopower characterization. On this basis, a GaN p-i-n diode is fabricated, exhibiting distinct rectifying characteristics with a turn-on voltage of 3 V with an acceptable reverse breakdown voltage of 300 V. Electron beam induced current (EBIC) and electroluminescent (EL) results further confirm the formation of p-type region due to Mg ion implantation and subsequent thermal activation. This repeatable and uniform manufacturing process can be implemented in mass production of GaN devices for versatile power and optoelectronic applications.

This study aimed to investigate the impact of timing interval to start AED withdraw (TIW) after surgery on the seizure outcome in non-neoplastic drug resistant epilepsy (DRE). TIW were divided into three groups (respectively

The aim of the current study was to find the epileptic focus and examine its causal relationship to other brain regions in children with new-onset benign childhood epilepsy with centrotemporal spikes (BECTS). Resting-state functional magnetic resonance imaging (fMRI) was performed in 66 children with BECTS and 37 matched control children. We compared the amplitude of low frequency fluctuation (ALFF) signals between the two groups to find the potential epileptogenic zone (EZ), then used Granger causality analysis (GCA) to explore the causal effects of EZ on the whole brain. Children with BECTS had significantly increased ALFF in the right Broca’s area, and decreased ALFF in bilateral fusiform gyrus. The patients also showed increased driving effect from the EZ in Broca’s area to the right prefrontal lobe, and decreased effects to the frontal lobe and posterior parts of the language network. The causal effect on left Wernicke’s area negatively correlated with verbal IQ (VIQ) score. Our research on new-onset BECTS patients illustrates a possible compensatory mechanism in the language network at early stages of BECTS, and the negative correlation of GCA and VIQ suggest the disturbance of epileptiform activity on language. These findings shed light on the mechanisms of and language dysfunction in BECTS.

We investigated the incidence, perioperative risk factors, and outcomes of postoperative acute kidney injury (AKI) in neurosurgical critically ill patients. A prospective multicenter cohort study was conducted, enrolling adult patients who underwent neurosurgical procedure and admitted to the neurosurgical intensive care units (ICU). Postoperative AKI was diagnosed within 7 days after surgery based on the Kidney Disease Improving Global Outcomes criteria. Of 624 enrolled patients, postoperative AKI occurred in 84 patients. AKI was associated with increased rates of ICU and in-hospital mortality, postoperative renal replacement therapy, postoperative tracheotomy, and postoperative tracheal reintubation. Patients who developed AKI had higher total ICU costs, prolonged length of hospital and ICU stay, and longer duration of postoperative mechanical ventilation. Multivariate analysis identified postoperative reoperation (adjusted odds ratio [OR] 5.70 [95% CI, 1.61–20.14]), postoperative concentration of serum cystatin C (adjusted OR 4.53 [95% CI, 1.98–10.39]), use of mannitol during operation (adjusted OR 1.97 [95% CI, 1.13–3.43]), postoperative APACHE II score (adjusted OR 1.11 [95% CI, 1.06–1.16]), and intraoperative estimated blood loss (adjusted OR 1.04 [95% CI, 1.00–1.08]) as independent risk factors for postoperative AKI. Postoperative AKI in neurosurgical critically ill cohort is prevalent and associated with adverse in-hospital outcomes.

Parkinson’s disease (PD) and Parkinsonism are common neurodegenerative disorders with continuously increasing prevalence, causing high global burdens. However, data concerning the comorbidity burden of patients with PD or Parkinsonism in China are lacking. To investigate the health condition and comorbidity burden, a total of 3367 PD and 823 Parkinsonism patients were included from seven tertiary hospitals in seven cities across China from 2003 to 2012. Their comorbidity burden was collected and quantified by the Elixhauser Comorbidity Index (ECI) and Charlson Comorbidity Index (CCI). The comorbidity spectra differed between PD and Parkinsonism patients. Compared with PD patients, Parkinsonism patients were older (69.8 ± 11.5 vs. 67.9 ± 11.4, P P P P P

It is well known that mutations in the gene coding for amyloid precursor protein are responsible for autosomal dominant forms of Alzheimer’s disease. Proteolytic processing of the protein leads to a number of metabolites including the amyloid beta peptide. Although brain amyloid precursor protein expression and amyloid beta production are associated with the pathophysiology of Alzheimer’s disease, it is clear that amyloid precursor protein is expressed in numerous cell types and tissues. Here we demonstrate that amyloid precursor protein is involved in regulating the phenotype of both adipocytes and peripheral macrophages and is required for high fat diet-dependent weight gain in mice. These data suggest that functions of this protein include modulation of the peripheral immune system and lipid metabolism. This biology may have relevance not only to the pathophysiology of Alzheimer’s disease but also diet-associated obesity.

The cerebral haemodynamic status of idiopathic generalized epilepsy (IGE) is a very complicated process. Little attention has been paid to cerebral blood flow (CBF) alterations in IGE detected by arterial spin labelling (ASL) perfusion magnetic resonance imaging (MRI). However, the selection of an optimal delay time is difficult for single-delay ASL. Multi-delay multi-parametric ASL perfusion MRI overcomes the limitations of single-delay ASL. We applied multi-delay multi-parametric ASL perfusion MRI to investigate the patterns of postictal cerebral perfusion in IGE patients with absence seizures. A total of 21 IGE patients with absence seizures and 24 healthy control subjects were enrolled. IGE patients exhibited prolonged arterial transit time (ATT) in the left superior temporal gyrus. The mean CBF of IGE patients was significantly increased in the left middle temporal gyrus, left parahippocampal gyrus and left fusiform gyrus. Prolonged ATT in the left superior temporal gyrus was negatively correlated with the age at onset in IGE patients. This study demonstrated that cortical dysfunction in the temporal lobe and fusiform gyrus may be related to epileptic activity in IGE patients with absence seizures. This information can play an important role in elucidating the pathophysiological mechanism of IGE from a cerebral haemodynamic perspective.

The Keap1/Nrf2 pathway is a master regulator of antioxidant, anti-inflammatory, and other cytoprotective mechanisms important in protection from kidney disease. For the first time in kidney disease, we describe the use of Keap1 hypomorphic mice, which possess Nrf2 hyperactivation. We exposed these mice and wild type controls to ischemia/reperfusion injury (IRI). The initial tubular injury at 24 hours post-IRI appeared to be unaffected, with the only observed difference being a decrease in inflammatory cytokine expression in the hypomorphs. However, we noted significant improvement in serum creatinine in the hypomorphs at 3 and 10 days after injury, and renal fibrosis was dramatically attenuated at the late timepoint. Assessment of Nrf2-regulated targets (GSTM1, GSTP1, NQO1) revealed higher expression in the hypomorphs at baseline. While injury tended to suppress these genes in wild-type mice, the suppression was attenuated or reversed in Keap1 hypomorphs, suggesting that protection in these mice was mediated by increased Nrf2 transcriptional activity. To assess the generalizability of our findings, we subjected the hypomorphs to unilateral ureteral obstruction (UUO) and again found significant protection and increased expression of Nrf2 targets. Overall, these results support the conclusion that the Nrf2 pathway is protective in a variety of kidney diseases.

Evidence suggest that overexpression of hypoxia-inducible factor-1α (HIF-1α) is linked to multidrug resistance of epilepsy. Here we explored whether aberrant expression of HIF-1α is regulated by miRNAs. Genome-wide microRNA expression profiling was performed on temporal cortex resected from mesial temporal lobe epilepsy (mTLE) patients and age-matched controls. miRNAs that are putative regulator of HIF-1α were predicted via target scan and confirmed by real-time quantitative polymerase chain reaction (RT-qPCR). Mimics or miRNA morpholino inhibitors were transfected in astrocytes and luciferase reporter assay was applied to detect HIF-11α expression. Microarray profiling identified down-regulated miR-153 as a putative regulator of HIF-1α in temporal cortex resected from surgical mTLE patients. RT-qPCR confirmed down-regulation of miR-153 in plasma of mTLE patients in an independent validation cohort. Knockdown of miR-153 significantly enhanced expression of HIF-1α while forced expression of miR-153 dramatically inhibited HIF-1α expression in pharmacoresistant astrocyte model. Luciferase assay established that miR-153 might inhibit HIF-1α expression via directly targeting two binding sites in the 3′UTR region of HIF-1α transcript. These data suggest that down-regulation of miR-153 may contribute to enhanced expression of HIF-1α in mTLE and serve as a novel biomarker and treatment target for epilepsy.

This study was designed to explore the association between elevated platelet to lymphocyte ratio (PLR) and prognosis of patients with non-small cell lung cancer (NSCLC) by meta-analysis. A total of 11 studies with 3,430 subjects were included and the combined hazard ratio (HR) and 95% confidence intervals (95% CI) were calculated. The data showed that elevated PLR predicted poor overall survival (OS) (HR = 1.42; 95% CI: 1.25–1.61, p 2 = 63.6, Ph = 0.002) and poor disease-free survival (DFS)/progression-free survival (PFS) (HR = 1.19; 95% CI: 1.02–1.4, p = 0.027; I2 = 46.8, Ph = 0.111). Subgroup analysis showed elevated PLR did not predict poor OS in patients included in large sample studies (HR = 1.44; 95% CI: 0.94–2.21, p = 0.098) whereas petients with Caucasian ethnicity (HR = 1.59; 95% CI: 1.27–1.98, p 180 (HR = 1.61; 95% CI: 1.3–1.99, p

It remains unclear how infantile febrile seizures (FS) enhance adult seizure susceptibility. Here we showed that the transient increase of interleukin-1β (IL-1β) after prolonged FS promoted adult seizure susceptibility, which was blocked by interleukin-1 receptor antagonist (IL-1Ra) within a critical time window. Postnatal administered IL-1β alone mimicked the effect of FS on adult seizure susceptibility. IL-1R1 knockout mice were not susceptible to adult seizure after prolonged FS or IL-1β treatment. Prolonged FS or early-life IL-1β treatment increased the expression of cannabinoid type 1 receptor (CB1R) for over 50 days, which was blocked by IL-1Ra or was absent in IL-1R1 knockout mice. CB1R antagonist, knockdown and endocannabinoid synthesis inhibitor abolished FS or IL-1β-enhanced seizure susceptibility. Thus, this work identifies a pathogenic role of postnatal IL-1β/IL-1R1 pathway and subsequent prolonged prominent increase of endocannabinoid signaling in adult seizure susceptibility following prolonged FS and highlights IL-1R1 as a potential therapeutic target for preventing the development of epilepsy after infantile FS.

This study was aimed to investigate the prognostic value of neutrophil-to-lymphocyte ratio (NLR) in patients with prostate cancer (PCa). A meta-analysis including 14 publications (15 cohorts) with 16,266 patients was performed to evaluate the association between NLR and overall survival (OS), progression-free survival (PFS)/recurrence-free survival (RFS) in PCa using hazard ratio (HR) and 95% confidence intervals (95% CI). The combining data showed that increased NLR predict poor OS (HR = 1.38, 95%CI: 1.22–1.56) and PFS/RFS (HR = 1.24, 95%CI 1.05–1.46) in PCa. Stratified analysis by PCa type, sample size, ethnicity and NLR cut-off value revealed that NLR showed consistent prognostic value in metastatic castration-resistant prostate cancer (mCRPC) patients and predict poor PFS/RFS in Asians, but not in Caucasians. These statistical data suggested that increased NLR could predict poor prognosis in patients with PCa.

The formation of glial scar impedes the neurogenesis and neural functional recovery following cerebral ischemia. Histamine showed neuroprotection at early stage after cerebral ischemia, however, its long-term effect, especially on glial scar formation, hasn’t been characterized. With various administration regimens constructed for histidine, a precursor of histamine, we found that histidine treatment at a high dose at early stage and a low dose at late stage demonstrated the most remarkable long-term neuroprotection with decreased infarct volume and improved neurological function. Notably, this treatment regimen also robustly reduced the glial scar area and facilitated the astrocyte migration towards the infarct core. In wound-healing assay and transwell test, histamine significantly promoted astrocyte migration. H2 receptor antagonists reversed the promotion of astrocyte migration and the neuroprotection provided by histidine. Moreover, histamine upregulated the GTP-bound small GTPase Rac1, while a Rac1 inhibitor, NSC23766, abrogated the neuroprotection of histidine and its promotion of astrocyte migration. Our data indicated that a dose/stage-dependent histidine treatment, mediated by H2 receptor, promoted astrocyte migration towards the infarct core, which benefited long-term post-cerebral ischemia neurological recovery. Therefore, targeting histaminergic system may be an effective therapeutic strategy for long-term cerebral ischemia injury through its actions on astrocytes.

Subcortical ischemic vascular dementia (SIVD) caused by chronic cerebral hypoperfusion develops with progressive white matter and cognitive impairments, yet no effective therapy is available. We investigated the temporal effects of minocycline on an experimental SIVD exerted by right unilateral common carotid arteries occlusion (rUCCAO). Minocycline treated at the early stage (day 0–3), but not the late stage after rUCCAO (day 4–32) alleviated the white matter and cognitive impairments and promoted remyelination. The actions of minocycline may not involve the inhibition of microglia activation, based on the effects after the application of a microglial activation inhibitor, macrophage migration inhibitory factor and co-treatment with lipopolysaccharides. Furthermore, minocycline treatment at the early stage promoted the proliferation of oligodendrocyte progenitor cells (OPCs) in subventricular zone, increased OPC number and alleviated apoptosis of mature oligodendrocytes in white matter. In vitro, minocycline promoted OPC proliferation and increased the percentage of OPCs in S and G2/M phases. We provided direct evidence that early treatment is critical for minocycline to alleviate white matter and cognitive impairments after chronic cerebral hypoperfusion, which may be due to its robust effects on OPC proliferation and mature oligodendrocyte loss. So, early therapeutic time window may be crucial for its application in SIVD.

Although various imaging studies have focused on detecting the cerebral function underlying psychogenic non-epileptic seizures (PNES), the nature of PNES remains poorly understood. In this study, we combined the resting state fMRI with fractional amplitude of low-frequency fluctuations (fALFF) and functional connectivity based on the seed voxel linear correlation approach to examine the alterations of regional and inter-regional network cerebral functions in PNES. A total of 20 healthy controls and 18 patients were enrolled. The PNES patients showed significantly increased fALFF mainly in the dorsolateral prefrontal cortex (DLPFC), parietal cortices and motor areas, as well as decreased fALFF in the triangular inferior frontal gyrus. Thus, our results add to literature suggesting abnormalities of neural synchrony in PNES. Moreover, PNES exhibited widespread inter-regional neural network deficits, including increased (DLPFC, sensorimotor and limbic system) and decreased (ventrolateral prefrontal cortex) connectivity, indicating that changes in the regional cerebral function are related to remote inter-regional network deficits. Correlation analysis results revealed that the connectivity between supplementary motor area and anterior cingulate cortex correlated with the PNES frequency, further suggesting the skewed integration of synchronous activity could predispose to the occurrence of PNES. Our findings provided novel evidence to investigate the pathophysiological mechanisms of PNES.

Fe3O4 and Fe nanowires are successfully fabricated by electrospinning method and reduction process. Wiry microstructures were achieved with the phase transformation from α-Fe2O3 to Fe3O4 and Fe by partial and full reduction, while still preserving the wire morphology. The diameters of the Fe3O4 and Fe nanowires are approximately 50–60 nm and 30–40 nm, respectively. The investigation of microwave absorption reveals that the Fe3O4 nanowires exhibit excellent microwave absorbing properties. For paraffin-based composite containing 50% weight concentration of Fe3O4 nanowires, the minimum reflection loss reaches −17.2 dB at 6.2 GHz with the matching thickness of 5.5 mm. Furthermore, the calculation shows that the modulus of the ratio between the complex permittivity and permeability |e/μ| is far away from unity at the minimum reflection loss point, which is quite different from the traditional opinions.

Fe3O4 and Fe nanowires are successfully fabricated by electrospinning method and reduction process. Wiry microstructures were achieved with the phase transformation from α-Fe2O3 to Fe3O4 and Fe by partial and full reduction, while still preserving the wire morphology. The diameters of the Fe3O4 and Fe nanowires are approximately 50–60 nm and 30–40 nm, respectively. The investigation of microwave absorption reveals that the Fe3O4 nanowires exhibit excellent microwave absorbing properties. For paraffin-based composite containing 50% weight concentration of Fe3O4 nanowires, the minimum reflection loss reaches −17.2 dB at 6.2 GHz with the matching thickness of 5.5 mm. Furthermore, the calculation shows that the modulus of the ratio between the complex permittivity and permeability |ε/μ| is far away from unity at the minimum reflection loss point, which is quite different from the traditional opinions.

Activation of β-catenin, the principal mediator of canonical Wnt signaling, is a common pathologic finding in a wide variety of chronic kidney diseases (CKD). While β-catenin is induced predominantly in renal tubular epithelium in CKD, surprisingly, depletion of tubular β-catenin had little effect on the severity of renal fibrosis. Interestingly, less apoptosis was detected in interstitial fibroblasts in knockout mice, which was accompanied by a decreased expression of Bax and Fas ligand (FasL). Tubule-specific knockout of β-catenin diminished renal induction of matrix metalloproteinase (MMP-7), which induced FasL expression in interstitial fibroblasts and potentiated fibroblast apoptosis in vitro. These results demonstrate that loss of tubular β-catenin resulted in enhanced interstitial fibroblast survival due to decreased MMP-7 expression. Our studies uncover a novel role of the tubular β-catenin/MMP-7 axis in controlling the fate of interstitial fibroblasts via epithelial-mesenchymal communication.