Research on spatial localization method of composite damage under strong noise.

In this paper, a damage spatial imaging approach based on novel signal extraction is suggested to reconstruct the Lamb wave response signal under strong noise and realize the spatial localization of damage. First, the Variable Mode Decomposition (VMD) parameters are optimized by the improved Grey Wolf optimization method (IGWO) to decompose the response signal. To rebuild the response signal, the correlation coefficient is used to choose the optimal modal component and the residual. To give the best wavelet function and transform level for adaptive denoising of the reconstructed signal without a reference signal, an enhanced Discrete Wavelet Transform (DWT) based on Shannon entropy is proposed. To achieve damage localization imaging, a damage spatial localization model is built utilizing a reconstruction algorithm for probabilistic inspection of damage (RAPID) approach and a convolutional neural network (CNN). The suggested method may successfully increase the signal-to-noise ratio (SNR) of the reconstructed response signal and lower the error of spatial localization under strong noise through experiments. The spatial localization of composite damage using Lamb wave under strong noise is expanded in this paper.

Fatigue Behavior of 3D Braided Composites Containing an Open-Hole.

The static and dynamic mechanical performances of notched and un-notched 3D braided composites were studied. The effect of longitudinal laid-in yarn was investigated in comparison with low braiding angle composites. The specimens were fatigue tested for up to millions of cycles, and the residual strength of the samples that survived millions of cycles was tested. The cross-section of the 3D braided specimens was observed after fatigue loading. It was found that the static and fatigue properties of low angle 3D braided behaved better than longitudinally reinforced 3D braided composites. For failure behavior, pure braids contain damage better and show less damage area than the braids with longitudinal yarns under fatigue loading. More cracks occurred in the 3D braided specimen with axial yarn cross-section along the longitudinal and transverse direction.

Prediction and Optimization of Electrospun Polyacrylonitrile Fiber Diameter Based on Grey System Theory.

This paper provides a new method for predicting the diameter of electrospun nanofibers. Based on the grey system theory, the effects of polyacrylonitrile mass fraction, voltage, flow rate, and receiving distance on fiber diameter were studied. The GM(1,1) (grey model) model and DNGM(1,1) (The DNGM (1,1) model is based on the whitening differential equation using parameters to Directly estimate the approximate Non-homogeneous sequence Grey prediction Model) model were established to predict fiber diameter by a single-factor change, and the results showed high prediction accuracy. The multi-variable grey model MGM(1,n) (MGM(1,n) is a Multivariate Grey prediction Model) was used for prediction of fiber diameter when multiple factors change simultaneously. The results showed that the average modeling fitting error is 8.62%. The background value coefficients of the MGM(1,n) model were optimized, the average modeling fitting error was reduced to 1.01%, and the average prediction error was reduced to 1.33%. Combining the fractional optimization with the background-value coefficient optimization, the optimal background-value coefficient α and the order r were selected. The results showed that the average modeling fitting error is 0.85%, and the average prediction error is 0.38%. The results demonstrate that the grey system theory can effectively predict the diameter of polyacrylonitrile electrospinning fibers with high prediction accuracy. This theory can increase the control of nanofiber diameters in production.

[Assessment of hematopoiesis and cytogenetics changes in interventional radiologists].

Objective: To investigate hematopoiesis and cytogenetics changes in staff of interventional radiology. Methods: A total of 121 intervention radiation workers, 245 common radiation workers and 100 medical personnel (healthy control) without exposure to radiation were enrolled in the study. The peripheral lymphocyte chromosomal aberrations and micronucleus were detected, and the result of white blood cells examination was analyzed. Results: Compared with common radiation group and healthy control group, decreases in white blood cells count, neutrophil ratio, and increase in lymphocyte ratio were observed in intervention radiation group (all P<0.05). Intervention radiation group had higher chromosome aberration rate and micronuclear rate than common radiation group and healthy control group (all P<0.05). Most common chromosome aberrations were dicentric chromosome, acentric ring, fragments and minute chromosome. Abnormal rates in chromosome aberration and micronucleus rates were increased with the rise of length of service, but no statistically significant difference was observed (P>0.05). Conclusion: Long term exposure to ionizing radiation may lead to changes in the human hematopoietic system and cause human chromosome aberration, and the severity of such injuries may be associated with the dose of ionizing radiation.

CNS targets support and sustain differentiation of cultured neuronal and retinal progenitor cells.

Superior colliculus (SC) is the target of retinal neurons, allowing them to form connections. Cultured stem cells/progenitors can potentially be used as donor tissue to reconstruct degenerated retina including perhaps replacing lost ganglion cells in glaucoma. In which case, it will be essential for these cells to integrate with the central nervous system targets. Here, we have investigated if the mid-brain region containing superior colliculus (SC) provides a permissive environment for the survival and differentiation of neural progenitors, including retinal progenitor cells propagated in cultures. Neural (NPCs) and retinal progenitor cells (RPCs) from green fluorescent protein (GFP) transgenic mice were cultured. Passage two through four neural and retinal progenitor cells were subsequently cocultured with the SC organotypic slices and maintained in culture for 17 and eight days respectively. Differentiation of the neurons was studied by immunocytochemistry for retinotypic neuronal markers. Retinal progenitor cells cocultured with SC slices were able to differentiate into various neuronal morphologies. Some cocultured progenitor cells differentiated into neurons as suggested by class III ß tubulin immunoreactivity. In addition, specific retinotypic neuronal differentiation of RPC was detected by immunoreactivity for calbindin and PKC. SC provides a permissive environment that supports survival and differentiation of the progenitor cells.

Effect of oxidative preconditioning on neural progenitor cells.

Neural progenitor cells (NPCs) have drawn attention because they offer possible treatment for neurodegenerative disorders in the form of regenerative therapy or transplantation. NPCs adapt and change in response to the cues in the pathological environment. We assessed the effect of pre-exposure to non-cytotoxic levels of oxidative stress, a common pathogenic factor in a number of neurological disorders, on the cell viability and neurosphere morphology of NPCs derived from the periventricular zone of mice brain. Neural progenitor cell viability and neurosphere morphology (neurosphere number, size and chain migration) were assessed in response to cytotoxic levels of oxidative stress in the presence or absence of preconditioning with non-cytotoxic doses of hydrogen peroxide (H(2)O(2)). Preconditioning with non-cytotoxic levels of H(2)O(2) provided significant protection against subsequent exposure to lethal doses of H(2)O(2). Preconditioning also modulated alteration in the neurosphere morphology in response to oxidative stress. Oxidative stress increased chain migration and neurosphere size while decreasing neurosphere numbers, specially in the cultures that were preconditioned with higher doses of H(2)O(2). Non-cytotoxic exposure to oxidative stress can evoke endogenous cytoprotection in NPCs. Redox signaling plays a role in other cellular functions of NPCs, namely the chain migration of NPCs from neurospheres, perhaps as a result of its effect on cell differentiation.

Safety and efficacy of a novel cannabinoid chemotherapeutic, KM-233, for the treatment of high-grade glioma.

OBJECTIVE: To test in vitro and in vivo the safety and efficacy of a novel chemotherapeutic agent, KM-233, for the treatment of glioma. METHODS: In vitro cell cytotoxicity assays were used to measure and compare the cytotoxic effects of KM-233, Delta(8)-tetrahydrocannabinol (THC), and bis-chloroethyl-nitrosurea (BCNU) against human U87 glioma cells. An organotypic brain slice culture model was used for safety and toxicity studies. A human glioma-SCID mouse side-pocket tumor model was used to test in vivo the safety and efficacy of KM-233 with intratumoral and intra-peritoneal administration. RESULTS: KM-233 is a classical cannabinoid with good blood brain barrier penetration that possesses a selective affinity for the CB2 receptors relative to THC. KM-233 was as efficacious in its cytotoxicity against human U87 glioma as Delta(8)-tetrahydrocannabinol, and superior to the commonly used anti-glioma chemotherapeutic agent, BCNU. The cytotoxic effects of KM-233 against human glioma cells in vitro occur as early as two hours after administration, and dosing of KM-233 can be cycled without compromising cytotoxic efficacy and while improving safety. Cyclical dosing of KM-233 to treat U87 glioma in a SCID mouse xenograft side pocket model was effective at reducing the tumor burden with both systemic and intratumoral administration. CONCLUSION: These studies provide both in vitro and in vivo evidence that KM-233 shows promising efficacy against human glioma cell lines in both in vitro and in vivo studies, minimal toxicity to healthy cultured brain tissue, and should be considered for definitive preclinical development in animal models of glioma.

Regulation of myeloid leukemia factor-1 interacting protein (MLF1IP) expression in glioblastoma.

The myelodysplasia/myeloid leukemia factor 1-interacting protein MLF1IP is a novel gene which encodes for a putative transcriptional repressor. It is localized to human chromosome 4q35.1 and is expressed in both the nuclei and cytoplasm of cells. Northern and Western blot analyses have revealed MLF1IP to be present at very low amounts in normal brain tissues, whereas a number of human and rat glioblastoma (GBM) cell lines demonstrated a high level expression of the MLF1IP protein. Immunohistochemical analysis of rat F98 and C6 GBM tumor models showed that MLF1IP was highly expressed in the tumor core where it was co-localized with MLF1 and nestin. Moreover, MLF1IP expression was elevated in the contralateral brain where no tumor cells were detected. These observations, together with previous data demonstrating a role for MLF1IP in erythroleukemias, suggest a possible function for this protein in glioma pathogenesis and potentially in other types of malignancies.

Up-regulation of neuropoiesis generating glial progenitors that infiltrate rat intracranial glioma.

To investigate adult neural stem cell (NSC) biology in relation to glioma, the C6 glioma cell line was tagged with green fluorescent protein (GFP) and inoculated into the brain of adult rats. The in vivo biological response of the brain to glioma was studied using immunohistochemical analysis of the subventricular zone (SVZ), peritumoral areas, and glioma. Nestin immunoreactive cells were found infiltrating glioma, but the distribution of abnormal immunoreactivity was restricted to the dorsal and medial border of the tumor relative to the ipsilateral ventricle. The SVZ was found to be hypertrophic, hypercellular, and up-regulated nestin expression. Furthermore, a dense contiguous population of nestin immunoreactive cells could be found streaming from ipsilateral dorsal tip of the SVZ, tracking along the ventral margin of the corpus callosum, and fanning out to encompass and infiltrate the proximal tumor border. Although most cells were either nestin or glial fibrillary acidic protein (GFAP) immunoreactive in the SVZ and along the ventral margin of the corpus callosum, the number of cells co-expressing both markers increased proportionally as the tumor was approached so that the predominant cell population along the proximal tumor border was GFAP immunoreactive. Finally, we demonstrated that a significant proportion of cells found in areas of abnormal immunoreactivity were proliferating, especially in peritumoral areas. In summary, there is an induction of neuropoietic activity in a rat intracranial glioma model that results in an infiltration and accumulation of abnormal nestin and GFAP expressing cells with proliferative potential along the dorsal and medial border of intracranial C6 glioma.

Correlation of N-cadherin expression in high grade gliomas with tissue invasion.

Cadherins are Ca2+-dependent cell adhesion molecules that play an important role in tissue construction and morphogenesis in multicellular organisms. Over the last few years, reports have emerged in the literature describing the involvement of cadherins in tumor invasion and metastasis. Cadherins typically demonstrate up and down-regulation according to the biological needs of the tissue. Additionally, up-regulation of N-cadherin is thought to be important for tumor formation in early stages of tumor development. We studied N-cadherin in surgical specimens of patients with primary glioblastoma by microarray analysis and found that N-cadherin mRNA expression is up-regulated compared to normal brain. To study the effects of N-cadherin expression on invasion and metastasis in vitro and in vivo, we overexpressed N-cadherin in the rat C6 glioma cell line which normally has low levels of N-cadherin. We found that up-regulation of N-cadherin resulted in a slight decreased adhesion to type IV collagen, fibronectin, and laminin, but statistically significant decreased adhesion to type I collagen. Furthermore, increased expression of N-cadherin correlated with a dramatic decrease in invasive behavior in extracellular matrix invasion assays. We then proceeded to study these cell lines in vivo in a rat intracranial glioma model, and found that N-cadherin expression inversely correlated with invasion into surrounding tissues, irregular margins, and extracranial invasion. In summary, these data collectively demonstrate that N-cadherin levels are important in the malignant behavior of gliomas, and may serve as a prognostic indicator for patients with high-grade gliomas.

Recombinant vesicular stomatitis virus vectors as oncolytic agents in the treatment of high-grade gliomas in an organotypic brain tissue slice-glioma coculture model.

OBJECT: The purpose of this study was to evaluate both replication-competent and replication-restricted recombinant vesicular stomatitis virus (VSV) vectors as therapeutic agents for high-grade gliomas by using an organotypic brain tissue slice-glioma coculture system. METHODS: The coculture system involved growing different brain structures together to allow neurons from these tissues to develop synaptic connections similar to those found in vivo. Rat C6 or human U87 glioma cells were then introduced into the culture to evaluate VSV as an oncolytic therapy. The authors found that recombinant wild-type VSV (rVSV-wt) rapidly eliminated C6 glioma cells from the coculture, but also caused significant damage to neurons, as measured by a loss of microtubule-associated protein 2 immunoreactivity and a failure in electrophysiological responses from neurons in the tissue slice. Nonetheless, pretreatment with interferon beta (IFNbeta) virtually eliminated VSV infection in healthy tissues without impeding any oncolytic effects on tumor cells. Despite the protective effects of the IFNbeta pretreatment, the tissue slices still showed signs of cytopathology when exposed to rVSV-wt. In contrast, pretreatment with IFNbeta and inoculation with a replication-restricted vector with its glycoprotein gene deleted (rVSV-deltaG) effectively destroyed rat C6 and human U87 glioma cells in the coculture, without causing detectable damage to the neuronal integrity and electrophysiological properties of the healthy tissue in the culture. CONCLUSIONS: Data in this study provide in vitro proof-of-principle that rVSV-deltaG is an effective oncolytic agent that has minimal toxic side effects to neurons compared with rVSV-wt and therefore should be considered for development as an adjuvant to surgery in the treatment of glioma.

Blink-related sensorimotor anatomy in the rat.

Protection of the eye and maintenance of the precorneal tear film depend on sensory innervation of the cornea and eyelids and motor innervation of muscles involved in closing and opening the eyes. Using a variety of fluorescent and transganglionic tracers, the sensorimotor innervation of blink-related orbital and periorbital structures was studied in Sprague-Dawley rats. The orbicularis oculi muscle surrounded the entire palpebral fissure and was innervated by motoneurons located along the dorsal cap of the ipsilateral facial motor nucleus. Upper and lower eyelid orbicularis oculi motoneurons were strictly ipsilateral and co-extensive, but upper eyelid orbicularis oculi motoneurons were, on average, slightly rostral and lateral to lower eyelid orbicularis oculi motoneurons. Facial motoneurons supplying the frontoscutularis, a muscle that helps to elevate the upper eyelid, were located in the medial division of the ipsilateral facial motor nucleus. Presumptive type Abeta afferents from the cornea terminated most prominently at the junction of the first cervical segment and the spinal trigeminal nucleus, pars caudalis. There was a second concentration of corneal terminations at the junction of pars caudalis and pars interpolaris of the spinal trigeminal nucleus. Sparse projections to the spinal trigeminal nucleus, pars oralis and the principal trigeminal nucleus were also detected. Presumptive type Abeta afferents from the eyelids terminated throughout the rostrocaudal extent of the spinal trigeminal nucleus with a heavy concentration within laminae III and IV of the first cervical segment. Presumptive types Adelta and C terminals from the eyelids were virtually limited to laminae I and II of the first cervical segment. Central terminations from the frontal nerve were present in the principal trigeminal nucleus and throughout the spinal trigeminal nucleus, but were most prominent within the dorsal horn of the first cervical segment. Our comprehensive description of blink-related sensorimotor anatomy in rats will provide a foundation for future physiological studies of blinking.

Localization of preganglionic neurons that innervate choroidal neurons of pterygopalatine ganglion.

PURPOSE: The pterygopalatine ganglion (PPG) receives preganglionic input from the superior salivatory nucleus (SSN) of the facial motor complex and is the main source of parasympathetic input to the choroid in mammals. The present study was undertaken to determine in rats the location and neurotransmitters of SSN neurons innervating those PPG neurons that target the choroid and to determine the location and neurotransmitters of the PPG choroidal neurons themselves. METHODS: Retrograde labeling from rat choroid using a fluorescent tracer, in combination with immunofluorescence labeling for nitric oxide synthase (NOS), vasoactive intestinal polypeptide (VIP), and choline acetyltransferase (ChAT), was used to characterize the location and neurotransmitters of choroidal PPG neurons. To identify SSN neurons that innervate the choroidal PPG neurons, the Bartha strain of the retrograde transneuronal tracer pseudorabies virus (PRV-Ba) was injected into rat choroid, and immunolabeling for NOS or ChAT was used to characterize their neurochemistry. RESULTS: Fluorescent retrograde labeling showed that PPG neurons projecting to the choroid contained NOS, VIP, and ChAT and were widely distributed in PPG and its preganglionic root, the greater petrosal nerve. SSN neurons were ChAT(+), and a subset of them was found to contain NOS. PRV-Ba transneuronal retrograde labeling revealed that choroidal preganglionic neurons were localized to the rostral medioventral part of the ipsilateral SSN. The choroidal SSN neurons were ChAT(+) and appeared largely to correspond to the NOS(+) neurons of the SSN. CONCLUSIONS: These results show that preganglionic neurons in rats that are presumed to regulate choroidal blood flow through the PPG reside within the rostral medioventral SSN, and that NOS is a marker for these SSN neurons.