Wide-range resistivity characterization of semiconductors with terahertz time-domain spectroscopy.

Resistivity is one of the most important characteristics in the semiconductor industry. The most common way to measure resistivity is the four-point probe method, which requires physical contact with the material under test. Terahertz time domain spectroscopy, a fast and non-destructive measurement method, is already well established in the characterization of dielectrics. In this work, we demonstrate the potential of two Drude model-based approaches to extract resistivity values from terahertz time-domain spectroscopy measurements of silicon in a wide range from about 10-3 Ωcm to 102 Ωcm. One method is an analytical approach and the other is an optimization approach. Four-point probe measurements are used as a reference. In addition, the spatial resistivity distribution is imaged by X-Y scanning of the samples to detect inhomogeneities in the doping distribution.

Targeting cathepsin S promotes activation of OLF1-BDNF/TrkB axis to enhance cognitive function.

BACKGROUND: Cathepsin S (CTSS) is a cysteine protease that played diverse roles in immunity, tumor metastasis, aging and other pathological alterations. At the cellular level, increased CTSS levels have been associated with the secretion of pro-inflammatory cytokines and disrupted the homeostasis of Ca2+ flux. Once CTSS was suppressed, elevated levels of anti-inflammatory cytokines and changes of Ca2+ influx were observed. These findings have inspired us to explore the potential role of CTSS on cognitive functions. METHODS: We conducted classic Y-maze and Barnes Maze tests to assess the spatial and working memory of Ctss-/- mice, Ctss+/+ mice and Ctss+/+ mice injected with the CTSS inhibitor (RJW-58). Ex vivo analyses including long-term potentiation (LTP), Golgi staining, immunofluorescence staining of sectioned whole brain tissues obtained from experimental animals were conducted. Furthermore, molecular studies were carried out using cultured HT-22 cell line and primary cortical neurons that treated with RJW-58 to comprehensively assess the gene and protein expressions. RESULTS: Our findings reported that targeting cathepsin S (CTSS) yields improvements in cognitive function, enhancing both working and spatial memory in behavior models. Ex vivo studies showed elevated levels of long-term potentiation levels and increased synaptic complexity. Microarray analysis demonstrated that brain-derived neurotrophic factor (BDNF) was upregulated when CTSS was knocked down by using siRNA. Moreover, the pharmacological blockade of the CTSS enzymatic activity promoted BDNF expression in a dose- and time-dependent manner. Notably, the inhibition of CTSS was associated with increased neurogenesis in the murine dentate gyrus. These results suggested a promising role of CTSS modulation in cognitive enhancement and neurogenesis. CONCLUSION: Our findings suggest a critical role of CTSS in the regulation of cognitive function by modulating the Ca2+ influx, leading to enhanced activation of the BDNF/TrkB axis. Our study may provide a novel strategy for improving cognitive function by targeting CTSS.

Anoxia-induced hippocampal LTP is regeneratively produced by glutamate and nitric oxide from the neuro-glial-endothelial axis.

Transient anoxia causes amnesia and neuronal death. This is attributed to enhanced glutamate release and modeled as anoxia-induced long-term potentiation (aLTP). aLTP is mediated by glutamate receptors and nitric oxide (·NO) and occludes stimulation-induced LTP. We identified a signaling cascade downstream of ·NO leading to glutamate release and a glutamate-·NO loop regeneratively boosting aLTP. aLTP in entothelial ·NO synthase (eNOS)-knockout mice and blocking neuronal NOS (nNOS) activity suggested that both nNOS and eNOS contribute to aLTP. Immunostaining result showed that eNOS is predominantly expressed in vascular endothelia. Transient anoxia induced a long-lasting Ca2+ elevation in astrocytes that mirrored aLTP. Blocking astrocyte metabolism or depletion of the NMDA receptor ligand D-serine abolished eNOS-dependent aLTP, suggesting that astrocytic Ca2+ elevation stimulates D-serine release from endfeet to endothelia, thereby releasing ·NO synthesized by eNOS. Thus, the neuro-glial-endothelial axis is involved in long-term enhancement of glutamate release after transient anoxia.

Long stem revision versus short stem revision with plate osteosynthesis for Vancouver type B2 periprosthetic femoral fracture: a comparative study of eighty five cases.

PURPOSE: Periprosthetic femoral fractures (PPFs) around the hip are challenging complications in orthopaedic surgery, particularly Vancouver type B2 (VTB2) fractures. The surgical management of these fractures is crucial and depends on various factors. Cementless short taper stem with plate osteosynthesis is an alternative surgical technique. This study aims to compare the outcomes of this surgical technique with revision arthroplasty (RA) with long stem in the treatment of VTB2 PPFs. METHODS: This retrospective study was conducted in a single medical institute from February 2010 to May 2019. Patients who had received either total hip arthroplasty or bipolar hemiarthroplasty and subsequently developed a VTB2 PPF were included; patients who sustained intra-operative fractures or received a cemented stem previously were excluded from the analysis. The patients were divided into two groups: group I received RA with cementless long stem, while group II underwent RA with cementless short taper stem with plate osteosynthesis. Demographic data, radiographic and functional outcomes, and complications were analyzed between the two groups. RESULTS: A total of 85 patients diagnosed with VTB2 PPFs were included in the study. There were no significant differences between the two groups in terms of demographic data, including age, gender, mean follow-up times, estimated blood loss, and operative times. The radiographic results showed that there was no significant difference in the incidence of subsidence and implant stability between the two groups. However, group II tended to have less subsidence and periprosthetic osteolysis. Patients in group II had significantly better functional scores (mean Harris hip score: post-operative: 60.2 in group I and 66.7 in group ii; last follow-up: 77.4 in group 1 and 83.2 in group II (both p < 0.05)). There were no significant differences in the overall complication rate, including infection, dislocation, re-fracture, and revision surgery, between the two groups. CONCLUSIONS: Both surgical techniques, cementless long stem and cementless short taper stem with plate osteosynthesis, are effective in the treatment of Vancouver B2 PPFs, with no significant differences in outcomes or complications. However, patients in cementless short taper stem with plate osteosynthesis had better functional scores at both post-operative and the last follow-up.

The role of postoperative piriformis fossa and greater trochanter tubercle distance to predict cutout failure after cephalomedullary nail fixation.

BACKGROUND: This study investigated the association between postoperative piriformis fossa and greater trochanter tubercle distance (distance from the deepest point of piriformis fossa to the most lateral greater trochanter tubercle [PG]) and cutout failure after cephalomedullary nail (CMN) osteosynthesis for intertrochanter fracture (ITF). A rotating femur model was designed to analyze PG variation during femur rotation. METHODS: From 2005 to 2010, 311 patients diagnosed of ITF (Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association [AO/OTA] 31-A2 and A3) underwent CMN fixation at our institute were reviewed. Of these, 281 (90.3%) patients achieved union without complication, 21 (6.8%) had cutout failure, six (1.9%) had femoral head osteonecrosis, and three (1%) had nonunion during postoperative 2-year follow-up. The side difference of postoperative PG compared to contralateral uninjured hip (dPG) was analyzed between patients who had cutout failure and those who did not. In the rotating femur model, the PG was measured for every 2.5° increments of internal and external rotation from 0° to 50°. RESULTS: The dPG was significantly higher in the failure group (10.2 ± 4.2 vs 6.6 ± 3.5 mm, p <0.001). The odds ratio for lag screw cutout was 6.35 (95% CI, 1.10-11.6, p =0.003) for every 1 mm dPG increment. dPG exhibited high diagnostic performance in predicting cutout failure according to receiver operating characteristic curve analysis. The area under the curve was 0.774 (95% CI, 0.711-0.837). dPG yielded the greatest sensitivity (78.4%) and specificity (78.4%) to predict lag screw cutout when cutoff value being 8.65 mm. In rotating femur model, PG change from baseline demonstrated significant ( p <0.001) positive and negative correlation with increased external and internal rotation, respectively. CONCLUSION: Increased dPG is a risk factor of cutout failure for ITF osteosynthesis with CMN. In conjunction with tip-apex distance, fracture displacement, and reduction quality; dPG can help surgeons interpret postoperative radiograph and predict failure. However, it should be noticed that a proper and standard patient positioning is critical for accurate dPG measurement.

Loss of oxytocin receptors in hilar mossy cells impairs social discrimination.

Hippocampal oxytocin receptor (OXTR) signaling is crucial for discrimination of social stimuli to guide social recognition, but circuit mechanisms and cell types involved remain incompletely understood. Here, we report a role for OXTR-expressing hilar mossy cells (MCs) of the dentate gyrus in social stimulus discrimination by regulating granule cell (GC) activity. Using a Cre-loxP recombination approach, we found that ablation of Oxtr from MCs impairs discrimination of social, but not object, stimuli in adult male mice. Ablation of MC Oxtr increases spontaneous firing rate of GCs, synaptic excitation to inhibition ratio of MC-to-GC circuit, and GC firing when temporally associated with the lateral perforant path inputs. Using mouse hippocampal slices, we found that bath application of OXTR agonist [Thr4,Gly7]-oxytocin causes membrane depolarization and increases MC firing activity. Optogenetic activation of MC-to-GC circuit ameliorates social discrimination deficit in MC OXTR deficient mice. Together, our results uncover a previously unknown role of MC OXTR signaling for discrimination of social stimuli and delineate a MC-to-GC circuit responsible for social information processing.

Gastric vagal afferent signaling to the basolateral amygdala mediates anxiety-like behaviors in experimental colitis mice.

Inflammatory bowel disease (IBD) is a relapsing-remitting disorder characterized by chronic inflammation of the gastrointestinal (GI) tract. Anxiety symptoms are commonly observed in patients with IBD, but the mechanistic link between IBD and anxiety remains elusive. Here, we sought to characterize gut-to-brain signaling and brain circuitry responsible for the pathological expression of anxiety-like behaviors in male dextran sulfate sodium-induced (DSS-induced) experimental colitis mice. We found that DSS-treated mice displayed increased anxiety-like behaviors, which were prevented by bilateral GI vagal afferent ablation. The locus coeruleus (LC) is a relay center connecting the nucleus tractus solitarius to the basolateral amygdala (BLA) in controlling anxiety-like behaviors. Chemogenetic silencing of noradrenergic LC projections to the BLA reduced anxiety-like behaviors in DSS-treated mice. This work expands our understanding of the neural mechanisms by which IBD leads to comorbid anxiety and emphasizes a critical role of gastric vagal afferent signaling in gut-to-brain regulation of emotional states.

Implementing the AAOS Guidelines for Screening of Developmental Dysplasia of the Hip Before the Age of 6 Months in Taiwan.

BACKGROUND: The prevalence of developmental dysplasia of the hip (DDH) has been considered to be low in East Asia, but this may be incorrect because of inconsistent diagnostic definitions and testing criteria. In 2015, the AAOS released guidelines for systematic screening for DDH in newborns. We implemented these guidelines and compared DDH incidence and outcomes before and after their implementation. METHODS: We used a historic comparison cohort of newborns with DDH between July 2015 and May 2017 before guideline implementation (the preguideline group); their data were retrieved using electronic medical records. In this group, the newborns received general hip screening without systemic follow-up. The postguideline group included newborns who were screened for hip dysplasia and followed up per the AAOS guidelines between July 2017 and May 2019. Their data were prospectively collected. The primary outcome in the postguideline group was DDH incidence. Other outcomes included rates of referral, surgery, and complications, and DDH prognosis. RESULTS: The preguideline and postguideline groups included 3534 and 2663 newborns, respectively, of whom 49 (1.1%) and 225 (8.4%), respectively, were referred to the pediatric orthopaedic clinic enrolled. In the postguideline group, 35 patients were diagnosed as having DDH (incidence: 1.3%, 95% CI: 0.8%-1.9%). Both the incidence and referral rates were significantly higher in the postguideline group than in the preguideline group. Furthermore, the mean age at referral was 6.7±10.06 months and 0.9±0.25 months in the preguideline and postguideline groups, respectively, indicating a potential for early treatment in the postguideline group. Finally, the female sex was identified as a risk factor for residual hip dysplasia at 6 months of age. CONCLUSION: DDH incidence in East Asia seems comparable to that in Western countries. Implementing the AAOS guidelines increased the diagnosis rate and opportunity for early treatment initiation, thus potentially avoiding surgical intervention. Nevertheless, residual DDH may be detected in some patients at 6 months of age, particularly in female infants. LEVEL OF EVIDENCE: Level IV.

Natural progression of the pubofemoral distance with age and its correlation with future acetabular index.

OBJECTIVES: This study investigated the progression of pubofemoral distance (PFD) with age and assessed the correlation between PFD and late acetabular index (AI) measurements. METHODS: This prospective observational study was conducted between January 2017 and December 2021. We enrolled 223 newborns who underwent the first, second, and third hip ultrasounds, and pelvis radiograph at a mean age of 18.6 days, 3.1 months, 5.2 months, and 6.8 months, respectively. The difference between PFD measured at serial ultrasounds and the correlation with AI were analyzed. RESULTS: The PFD increased significantly (p < 0.001) at serial measurements. The mean PFD at the first, second, and third ultrasounds were 3.3 (2.0-5.7), 4.3 (2.9-7.2), and 5.1 (3.3-8.0) mm, respectively. The PFD at three ultrasounds were all significantly (p < 0.001) and positively correlated with AI, with the Pearson correlation coefficients being 0.658, 0.696, and 0.753 for the first, second, and third ultrasounds, respectively. Using AI as reference, the diagnostic ability of PFD was calculated by the areas under the receiver operating characteristic curve, which was 0.845, 0.902, and 0.938 for the first, second, and third PFD, respectively. For the first, second, and third ultrasounds, PFD cutoff values of ≥ 3.9, ≥ 5.0, and ≥ 5.7 mm, respectively, yielded the greatest sensitivity and specificity in predicting late abnormal AI. CONCLUSION: The PFD naturally progresses with age and is positively correlated with AI. The PFD has potential for predicting residual dysplasia. However, the cutoff for abnormal PFD values may require adjustment according to the patient's age. KEY POINTS: • The pubofemoral distance measured in hip ultrasonography naturally increases as the infant's hips mature. • The early pubofemoral distance demonstrates a positive correlation with late acetabular index measurements. • The pubofemoral distance may help physicians predict abnormal acetabular index. However, the cutoff for abnormal pubofemoral distance values may require adjustment according to patient's age.

Identification of Scoparone from Chinese Olive Fruit as a Modulator of Macrophage Polarization.

Chinese olive (Canarium album L.) has been highlighted for its remarkable health benefits. We previously showed that the ethyl acetate fraction of Chinese olive (COE) is an effective anti-inflammatory agent. In this study, we used a luciferase-based RAW 264.7 cell platform to detect the transcriptional activity of NF-κB, a key mediator of inflammation, and the promoter activity of its downstream target, COX-2. Through functional-oriented screening using these platforms, we further divided COE into several subfractions. Subsequently, we used silica gel column chromatography for purification, and the active compounds were separated and isolated by thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC). The structure of the resulting compound with high anti-inflammatory activity was then identified as scoparone. Our results showed that scoparone not only inhibited lipopolysaccharide (LPS)-induced secretion of nitric oxide and suppressed M1 macrophage markers (iNOS, Il-6, Ccl2, and Tnf-α) but also markedly decreased the production of pro-inflammatory cytokines (IL-6, CCL2, and TNF-α). Treatment with scoparone significantly reduced the protein level of TNF-α in LPS-treated bone-marrow-derived macrophages (BMDMs). In addition, scoparone promoted macrophages toward an M2 anti-inflammatory phenotype, as determined by the significantly increased gene expression of M2 macrophage markers (Arg1, Ym1, Mrc1, Il-10, and Cd206) and the protein level of Arg1. This study indicates that COE fruit has high therapeutic potential for various inflammatory diseases as a result of switching the macrophage phenotype from pro-inflammatory M1 to anti-inflammatory M2.

Multisession Anodal Transcranial Direct Current Stimulation Enhances Adult Hippocampal Neurogenesis and Context Discrimination in Mice.

Transcranial direct current stimulation (tDCS) is a promising noninvasive neuromodulatory treatment option for multiple neurologic and psychiatric disorders, but its mechanism of action is still poorly understood. Adult hippocampal neurogenesis (AHN) continues throughout life and is crucial for preserving several aspects of hippocampal-dependent cognitive functions. Nevertheless, the contribution of AHN in the neuromodulatory effects of tDCS remains unexplored. Here, we sought to investigate whether multisession anodal tDCS may modulate AHN and its associated cognitive functions. Multisession anodal tDCS were applied on the skull over the hippocampus of adult male mice for 20 min at 0.25 mA once daily for 10 d totally. We found that multisession anodal tDCS enhances AHN by increasing the proliferation, differentiation and survival of neural stem/progenitor cells (NSPCs). In addition, tDCS treatment increased cell cycle reentry and reduced cell cycle exit of NSPCs. The tDCS-treated mice exhibited a reduced GABAergic inhibitory tone in the dentate gyrus compared with sham-treated mice. The effect of tDCS on the proliferation of NSPCs was blocked by pharmacological restoration of GABAB receptor-mediated inhibition. Functionally, multisession anodal tDCS enhances performance on a contextual fear discrimination task, and this enhancement was prevented by blocking AHN using the DNA alkylating agent temozolomide (TMZ). Our results emphasize an important role for AHN in mediating the beneficial effects of tDCS on cognitive functions that substantially broadens the mechanistic understanding of tDCS beyond its well-described in hippocampal synaptic plasticity.SIGNIFICANCE STATEMENT Transcranial direct current stimulation (tDCS) has been shown to effectively enhance cognitive functions in healthy and pathologic conditions. However, the mechanisms underlying its effects are largely unknown and need to be better understood to enable its optimal clinical use. This study shows that multisession anodal tDCS enhances adult hippocampal neurogenesis (AHN) and therefore contributes to enhance context discrimination in mice. Our results also show that the effect of tDCS on AHN is associated with reduced GABAergic inhibition in the dentate gyrus. Our study uncovers a novel mechanism of anodal tDCS to elicit cognitive-enhancing effects and may have the potential to improve cognitive decline associated with normal aging and neurodegenerative disorders.

Ba3.5Cu7.55In1.15Se9: A Wide-Bandgap Copper Indium Selenide Reveals Strong Luminescence and Third-Harmonic Generation.

A new copper indium selenide, Ba3.5Cu7.55In1.15Se9, was synthesized by the KBr flux reaction at 800 °C. The compound crystallizes with orthorhombic Pnma, a = 46.1700(12) Å, b = 4.26710(10) Å, c = 19.8125(5) Å, and Z = 8. The structural framework mainly consists of four sites of cubane-type defective M4Se3 (M = Cu, Cu/In) units with disordered Cu+/In3+ ions present at the part corner of each unit. The single crystal emits intense photoluminescence at 657 nm with a relative quantum yield (RQY) 0.2 times that of rhodamine 6G powder. The compound belongs to a direct band gap at 1.91 eV, analyzed by Tauc's plot, and the energy is close to the PL position. The Hall effect measurement on a pressed pellet reveals an n-type conductivity with a carrier concentration of 3.358 × 1017 cm-3 and a mobility of 24.331 cm2 V-1 s-1. Furthermore, the compound produces a strong nonlinear third-harmonic generation (THG), with an χS(3) value of 1.3 × 105 pm2/V2 comparable to 1.6 × 105 pm2/V2 for AgGaSe2 measured at 800 nm.

High-Fat Diet Exacerbates Autistic-Like Restricted Repetitive Behaviors and Social Abnormalities in CC2D1A Conditional Knockout Mice.

Autism spectrum disorder (ASD) represents a heterogeneous group of neurodevelopmental disorders characterized by deficits in social communication, social interaction, and the presence of restricted repetitive behaviors. The cause of ASD involves complex interactions between genetic and environmental factors. Haploinsufficiency of the Coiled-coil and C2 domain containing 1A (Cc2d1a) gene is causally linked to ASD, and obesity has been associated with worse outcomes for ASD. High-fat diet (HFD) feeding leads to the development of obesity and metabolic dysfunction; however, the effect of HFD on pre-existing autistic-like phenotypes remains to be clarified. Here, we report that male Cc2d1a conditional knockout (cKO) mice fed with HFD, from weaning onwards and throughout the experimental period, show a marked aggravation in autistic-like phenotypes, manifested in increased restricted repetitive behaviors and impaired performance in the preference for social novelty, but not in sociability and cognitive impairments assessed using the object location memory, novel object recognition, and Morris water maze tests. HFD feeding also results in increased numbers of reactive microglia and astrocytes, and exacerbates reductions in dendritic complexity and spine density of hippocampal CA1 pyramidal neurons. Furthermore, we demonstrate that chronic treatment with minocycline, a semisynthetic tetracycline-derived antibiotic, rescues the observed behavioral and morphological deficits in Cc2d1a cKO mice fed with HFD. Collectively, these findings highlight an aggravating role of HFD in pre-existing autistic-like phenotypes and suggest that minocycline treatment can alleviate abnormal neuronal morphology and behavioral symptoms associated with ASD resulted from the interplay between genetic and environmental risk factors.

A dorsal CA2 to ventral CA1 circuit contributes to oxytocinergic modulation of long-term social recognition memory.

BACKGROUND: Social recognition memory (SRM) is the ability to distinguish familiar from novel conspecifics and is crucial for survival and reproductive success across social species. We previously reported that oxytocin (OXT) receptor (OXTR) signaling in the CA2/CA3a of dorsal hippocampus is essential to promote the persistence of long-term SRM, yet how the endogenous OXT system influences CA2 outputs to regulate long-term SRM formation remains unclear. METHODS: To achieve a selective deletion of CA2 OXTRs, we crossed Amigo2-Cre mice with Oxtr-floxed mice to generate CA2-specific Oxtr conditional knockout (Oxtr-/-) mice. A three-chamber paradigm test was used for studying SRM in mice. Chemogenetic and optogenetic targeting strategies were employed to manipulate neuronal activity. RESULTS: We show that selective ablation of Oxtr in the CA2 suffices to impair the persistence of long-term SRM but has no effect on sociability and social novelty preference in the three-chamber paradigm test. We find that cell-type specific activation of OXT neurons within the hypothalamic paraventricular nucleus enhances long-term SRM and this enhancement is blocked by local application of OXTR antagonist L-368,899 into dorsal hippocampal CA2 (dCA2) region. In addition, chemogenetic neuronal silencing in dCA2 demonstrated that neuronal activity is essential for forming long-term SRM. Moreover, chemogenetic terminal-specific inactivation reveals a crucial role for dCA2 outputs to ventral CA1 (vCA1), but not dorsal lateral septum, in long-term SRM. Finally, targeted activation of the dCA2-to-vCA1 circuit effectively ameliorates long-term SRM deficit observed in Oxtr-/- mice. CONCLUSIONS: These findings highlight the importance of hippocampal CA2 OXTR signaling in governing the persistence of long-term SRM and identify a hippocampal circuit linking dCA2 to vCA1 necessary for controlling long-term SRM formation.

Factors associated with mortality in patients with super-refractory status epilepticus.

Super-refractory status epilepticus (SRSE) is a critical condition in which seizures persist despite anesthetic use for 24 h or longer. High mortality has been reported in patients with SRSE, but the cause of death remains unclear. We investigated the factors associated with mortality, including clinical characteristics, SE etiologies and severities, treatments, and responses in patients with SRSE in a 13-year tertiary hospital-based retrospective cohort study comparing these parameters between deceased and surviving patients. SRSE accounted for 14.2% of patients with status epilepticus, and 28.6% of SRSE patients died. Deceased patients were mostly young or middle-aged without known systemic diseases or epilepsy. All deceased patients experienced generalized convulsive status epilepticus and failure of anesthetic tapering-off, significantly higher than survivors. An increased number of second-line anesthetics besides midazolam was observed in the deceased (median, 3, interquartile range 2-3) compared to surviving (1, 1-1; p = 0.0006) patients with prolonged use durations (p = 0.047). For mortality, the cut-off number of second-line anesthetics was 1.5 (AUC = 0.906, p = 0.004). Deceased patients had significantly higher renal and cardiac complications and metabolic acidosis than survivors. In SRSE management, multi-anesthetic use should be carefully controlled to avoid systemic complications and mortality.

Facile and Green Process to Synthesize a Three-Dimensional Network Few-Layer Graphene/Carbon Nanotube Composite for Electromagnetic Interference Shielding.

We propose an environmentally friendly liquid exfoliation approach and subsequent freeze-drying process for constructing a three-dimensional (3D) carbon-based network by using few-layer graphene (FLG) and carbon nanotubes (CNTs) for electromagnetic interference (EMI) shielding applications. Systematic characterizations-such as X-ray diffraction, scanning electron microscopy, and transmission electron microscopy-as well as Raman characterization and EMI shielding tests were performed. The results indicated that the as-synthesized 3D-FLG/CNT composite obtained through the freeze-drying process exhibited excellent electromagnetic interference shielding. The shielding effect of FLG could be improved from 15 to 22 dB by introducing CNTs. The CNTs inhibited restacking of FLG in the structure. We also compared two drying processes: oven drying and freeze-drying. The freeze-drying technique markedly improved the shielding effect of FLG/CNTs from 22 to 36 dB. The composition-optimized 3D-FLG/CNT composite could be a candidate material for use in EMI shielding.

Association between early sonographic findings and acetabular index at the age of 6 months: a prospective observational study.

BACKGROUND: This study investigated the association between early Graf classification and femoral head coverage (FHC) with the acetabular index (AI) at the age of 6 months. METHODS: A prospective observational study was conducted between 2017-2018. Patients requiring Pavlik harness treatment and patients with syndromic dislocation or neurogenic dislocation were excluded. In total, 169 newborns with the first ultrasound performed at the mean age of 12.3 (0-15) days, the second ultrasound performed at the mean age of 3.2 (2.5-4.1) months, and the AI measured at the age of 6.6 (4.3-7.1) months were enrolled. The correlation between the AI and first and second alpha angles and FHC measurements, and the correlation of dysplasia in early ultrasound with dysplasia in the AI were analyzed. RESULTS: At the first ultrasound, only the FHC (P = .02) demonstrated a significant negative correlation with the AI. At the second ultrasound, both the alpha angle (P < .01) and FHC (P < .01) demonstrated a significant negative correlation with the AI. With the AI as a reference, the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were found to be 77%, 7%, 5%, and 81%, respectively, for the first Graf; 91%, 37%, 9%, and 98%, respectively, for the first FHC measurement; 82%, 90%, 35%, and 99%, respectively, for the second Graf; and 95%, 97%, 68% and 99%, respectively, for the second FHC measurement. CONCLUSIONS: FHC and alpha angle exhibited significant negative correlations with the AI at six months, both ultrasound parameters may have the potential to predict AI in DDH screening. Compared to the ultrasound measurements taken at 2 weeks, Graf and FHC at 3 months demonstrated superior sensitivity, specificity, PPV, and NPV to detect abnormal AI. The best timing to perform ultrasound examination may need further research.

TNFα-mediated necroptosis in brain endothelial cells as a potential mechanism of increased seizure susceptibility in mice following systemic inflammation.

BACKGROUND: Systemic inflammation is a potent contributor to increased seizure susceptibility. However, information regarding the effects of systemic inflammation on cerebral vascular integrity that influence neuron excitability is scarce. Necroptosis is closely associated with inflammation in various neurological diseases. In this study, necroptosis was hypothesized to be involved in the mechanism underlying sepsis-associated neuronal excitability in the cerebrovascular components (e.g., endothelia cells). METHODS: Lipopolysaccharide (LPS) was used to induce systemic inflammation. Kainic acid intraperitoneal injection was used to measure the susceptibility of the mice to seizure. The pharmacological inhibitors C87 and GSK872 were used to block the signaling of TNFα receptors and necroptosis. In order to determine the features of the sepsis-associated response in the cerebral vasculature and CNS, brain tissues of mice were obtained for assays of the necroptosis-related protein expression, and for immunofluorescence staining to identify morphological changes in the endothelia and glia. In addition, microdialysis assay was used to assess the changes in extracellular potassium and glutamate levels in the brain. RESULTS: Some noteworthy findings, such as increased seizure susceptibility and brain endothelial necroptosis, Kir4.1 dysfunction, and microglia activation were observed in mice following LPS injection. C87 treatment, a TNFα receptor inhibitor, showed considerable attenuation of increased kainic acid-induced seizure susceptibility, endothelial cell necroptosis, microglia activation and restoration of Kir4.1 protein expression in LPS-treated mice. Treatment with GSK872, a RIP3 inhibitor, such as C87, showed similar effects on these changes following LPS injection. CONCLUSIONS: The findings of this study showed that TNFα-mediated necroptosis induced cerebrovascular endothelial damage, neuroinflammation and astrocyte Kir4.1 dysregulation, which may coalesce to contribute to the increased seizure susceptibility in LPS-treated mice. Pharmacologic inhibition targeting this necroptosis pathway may provide a promising therapeutic approach to the reduction of sepsis-associated brain endothelia cell injury, astrocyte ion channel dysfunction, and subsequent neuronal excitability.

CYFIP1 Dosages Exhibit Divergent Behavioral Impact via Diametric Regulation of NMDA Receptor Complex Translation in Mouse Models of Psychiatric Disorders.

BACKGROUND: Gene dosage imbalance caused by copy number variations (CNVs) is a prominent contributor to brain disorders. In particular, 15q11.2 CNV duplications and deletions have been associated with autism spectrum disorder and schizophrenia, respectively. The mechanism underlying these diametric contributions remains unclear. METHODS: We established both loss-of-function and gain-of-function mouse models of Cyfip1, one of four genes within 15q11.2 CNVs. To assess the functional consequences of altered CYFIP1 levels, we performed systematic investigations on behavioral, electrophysiological, and biochemical phenotypes in both mouse models. In addition, we utilized RNA immunoprecipitation sequencing (RIP-seq) analysis to reveal molecular targets of CYFIP1 in vivo. RESULTS: Cyfip1 loss-of-function and gain-of function mouse models exhibited distinct and shared behavioral abnormalities related to autism spectrum disorder and schizophrenia. RIP-seq analysis identified messenger RNA targets of CYFIP1 in vivo, including postsynaptic NMDA receptor (NMDAR) complex components. In addition, these mouse models showed diametric changes in levels of postsynaptic NMDAR complex components at synapses because of dysregulated protein translation, resulting in bidirectional alteration of NMDAR-mediated signaling. Importantly, pharmacological balancing of NMDAR signaling in these mouse models with diametric Cyfip1 dosages rescues behavioral abnormalities. CONCLUSIONS: CYFIP1 regulates protein translation of NMDAR and associated complex components at synapses to maintain normal synaptic functions and behaviors. Our integrated analyses provide insight into how gene dosage imbalance caused by CNVs may contribute to divergent neuropsychiatric disorders.