Relevant bibliographies by topics / Tunnel staining

Academic literature on the topic 'Tunnel staining'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Tunnel staining"

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Inagaki, Yusuke, Kota Uematsu, Manabu Akahane, Yusuke Morita, Munehiro Ogawa, Tomoyuki Ueha, Takamasa Shimizu, Tomohiko Kura, Kenji Kawate, and Yasuhito Tanaka. "Osteogenic Matrix Cell Sheet Transplantation Enhances Early Tendon Graft to Bone Tunnel Healing in Rabbits." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/842192.

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The objective of this study was to determine whether osteogenic matrix cell sheets (OMCS) could induce bone formation around grafted tendons, thereby enhancing early stage tendon to bone tunnel healing in skeletally mature male Japanese white rabbits. First, the osteogenic potential of rabbit OMCS was evaluated. Then, the OMCS were transplanted into the interface between the grafted tendon and the bone tunnel created at the tibia. Histological assessments and biomechanical tensile testing were performed after 3 weeks. The rabbit OMCS showed high alkaline phosphatase (ALP) activity, positive staining of ALP, and osteogenic potential when transplanted subcutaneously with beta tricalcium phosphate disks. Newly formed bony walls and positive collagen type I staining were seen around the grafted tendon with OMCS transplantation, whereas such bony walls were thinner or less frequent without OMCS transplantation. Micro-computed tomography images showed significantly higher bone volume in the OMCS transplantation group. The pullout strength was significantly higher with OMCS (0.74±0.23 N/mm2) than without OMCS (0.58±0.15 N/mm2). These results show that OMCS enhance early tendon to bone tunnel healing. This method can be applied to cases requiring early tendon to bone tunnel healing after ligament reconstruction surgery.
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Mbegbu, Edmund C., Ikechukwu R. Obidike, and Ali A. Fouladi-Nashta. "Immunohistochemical Detection of Vasa Antigen and Apoptosis-Related DNA Fragmentation in Ovaries of Sheep Fetuses Prenatally Exposed to Vitamin D Deficiency." Acta Veterinaria 69, no. 3 (September 1, 2019): 262–74. http://dx.doi.org/10.2478/acve-2019-0022.

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Abstract The primordial germ cells (PGCs) in female animals are comprised of diplotene oocytes arrested in the first meiotic prophase. Expression of Vasa is one of the key factors required for subsequent resumption of development and recruitment of PGCs into the growing follicle class. Since vitamin D regulates recruitment of PGCs and developmental competence of ovarian follicles, this study was designed to investigate the expression of Vasa and rate of apoptosis in foetal ovaries prenatally restricted from dietary vitamin D. Nineteen sexually mature Welsh mountain ewes were randomly assigned to vitamin D deficient (VDD) and vitamin D control (VDC) diets from 17d before mating, up to 125d of gestation, when fetal ovaries were collected and fixed in formalin for immunohistochemistry and TUNEL assay. VDD ovaries had fewer healthy oocytes that could stain positive for Vasa as well as a lower integrated density value for DAB staining intensity. Conversely, TUNNEL staining in VDD animals showed a higher integrated density value and percentage of affected area (P<0.05). The present findings indicate that Vasa expression is decreased, while the rate of apoptosis increased in VDD fetal ovaries, and this may adversely affect resumption of growth and development of PGCs reserve.
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Rao, RohitS, Charudutt Kalamkar, Amrita Mukherjee, and BhavinK Patel. "Novel tunnel staining technique to reduce premature entry in manual small-incision cataract surgery." Indian Journal of Ophthalmology 70, no. 11 (2022): 4041. http://dx.doi.org/10.4103/ijo.ijo_1562_22.

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Wang, Rui, Bin Xu, and Hong-Gang Xu. "Up-Regulation of TGF-β Promotes Tendon-to-Bone Healing after Anterior Cruciate Ligament Reconstruction using Bone Marrow-Derived Mesenchymal Stem Cells through the TGF-β/MAPK Signaling Pathway in a New Zealand White Rabbit Model." Cellular Physiology and Biochemistry 41, no. 1 (2017): 213–26. http://dx.doi.org/10.1159/000456046.

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Background/Aims: This study aimed to explore the role of TGF-β in tendon-to-bone healing after anterior cruciate ligament (ACL) reconstruction using bone marrow-derived mesenchymal stem cells (BMSCs) through the TGF-β/MAPK signaling pathway in a New Zealand white rabbit model. Methods: A total of 72 healthy male New Zealand white rabbits were selected for these experiments. Flow cytometry and immunofluorescence were used to detect the expression of BMSC surface markers, and qRT-PCR was performed to detect TGF-β mRNA expression. The ACL reconstruction model was established with autografts. The rabbits were randomly divided into the following groups: inhibition of TGF-β (inhibition), over-expression of TGF-β (over-expression), empty vector and untreated (n = 18 per group). Hematoxylineosin (HE) staining, toluidine blue staining and Masson trichrome staining were conducted to observe any chondrocyte-like cell growth, and biomechanical tests were used to calculate the maximum load and rigidity. Three-dimensional CT imaging and Western blotting were applied to detect changes in bone tunnel size and bone density and the expression levels of TGF-β/MAPK signaling pathway-related proteins, respectively. Results: CD90 and CD44 were positively expressed, while CD11b was not detected. Compared with the empty vector and untreated groups, TGF-β mRNA expression was significantly decreased in the inhibition group but increased in the over-expression group; the latter group had a larger number of fibroblasts, a tighter tendon-bone interface, an increased number of chondrocyte-like cells and fibrochondrocytes, and more collagen fibers than the inhibition, empty vector and untreated groups. Compared with the empty vector and untreated groups, the maximum load and rigidity; the CT values of bone tunnel and bone tunnel margin; and the protein expression levels of TGF-β, p-ERK1/2, p-p38, p-JNK, c-jun and c-myc were significantly down-regulated in the inhibition group but up-regulated in the over-expression group. Conclusion: Our study indicated that up-regulating TGF-β expression in BMSCs from New Zealand white rabbits could promote tendon-to-bone healing after ACL reconstruction by regulating the TGF-β/MAPK signaling pathway.
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Khanna, Rohit K., Mark L. Rosenblum, Jack P. Rock, and Ghaus M. Malik. "Prolonged external ventricular drainage with percutaneous long-tunnel ventriculostomies." Journal of Neurosurgery 83, no. 5 (November 1995): 791–94. http://dx.doi.org/10.3171/jns.1995.83.5.0791.

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✓ External ventricular drainage has been used extensively for management of several neurosurgical disorders. The main limitation of this procedure has been the high risk of infection, especially with prolonged drainage. In an effort to minimize the risk of infection, the authors have used a new ventriculostomy technique that involves tunneling the ventricular catheter subcutaneously to an exit site in the lower chest or upper abdomen. This report describes the results of this procedure on 100 consecutive cases. Patients requiring emergency ventriculostomies had short-tunnel ventriculostomies placed at the bedside that were converted to long-tunnel ventriculostomies in the operating room within 5 days. The average duration of drainage was 18.3 days (range 5–40 days). Cerebrospinal fluid was routinely sent for Gram staining and culture to monitor for infection. Prophylactic antibiotic medications were administered only perioperatively. No infection was observed during the first 16 days of drainage in any patient. The overall incidence of infection was 4% and blockage occurred in 6% of the cases. In this series the incidence of ventricular infection was 2.37 per 1000 ventricular drainage days, one of the lowest reported incidences of infection in the literature. This procedure provides a simple and effective method of maintaining long-term ventricular drainage with a very low risk of infection or blockage.
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Wang, Xinxin, Peng Shen, Dezhi Tang, Hao Xu, Hongfu Qiu, Tao Wu, and Xiang Gao. "Effects of Qi-Fang-Xi-Bi-Granules on Cartilage Morphology and C/ebpαPromoter Methylation in Rats with Knee Osteoarthritis." Evidence-Based Complementary and Alternative Medicine 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/2074976.

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Objective. To investigate the effects of Qi-Fang-Xi-Bi-Granules (QFXBGs) on cartilage morphology and methylation of C/ebpα(CCAAT/enhancer binding proteinα) at the promoter region.Methods. Knee osteoarthritis (KOA) modeling was performed in rats in accordance with Hulth’s method, and control group received sham operation. Eight weeks after KOA modeling, the rats in the KOA modeling group were further divided into 6 groups. Each group was given the appropriate drug. After 8 weeks, half of the rats were used for Micro-CT scan, HE staining, ABH/OG staining, immunohistochemistry, and TUNNEL staining of the knee joint tissue, and the other half were used to examine C/ebpαpromoter methylation.Results. The three dose groups of QFXBGs all showed lower degrees of surface fissures and flaking, thicker cartilage layer, and restored chondrocyte and subchondral bone morphology, compared with the KOA model group. C/ebpα-22 promoter methylation levels in the high- and low-dose groups were significantly higher than that in the KOA modeling group (p<0.05), while C/ebpα-2 promoter methylation level in the medium-dose group was significantly higher than that in the KOA modeling group (p<0.05).Conclusions. QFXBGs may alleviate articular cartilage degeneration through promoting C/ebpα-2 or C/ebpα-22 methylation at specific promoter sites.
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Joseph, Oliver C., Oleg Uryasev, John P. McNamara, and Apostolos P. Dallas. "TIBIAL NERVE PERINEURAL INJECTIONS AT THE POSTERIOR TARSAL TUNNEL." Journal of Musculoskeletal Research 16, no. 03 (September 2013): 1350014. http://dx.doi.org/10.1142/s0218957713500140.

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Introduction: Posterior tarsal tunnel syndrome (PostTTS) refers to compression of the tibial nerve (TN) within this tunnel. PostTTS is most commonly secondary to entrapment with subsequent inflammation. As it is true with other entrapment-type neuropathies, corticosteroids could provide therapeutic relief. To the authors' knowledge, the feasibility of such injections using ultrasound guidance has not been described in the literature. We hypothesize that one can inject the TN perineural space immediately proximal to the posterior tarsal tunnel utilizing ultrasonography US-guidance. Methods: This research was a pilot study using four cadaveric models. US was utilized to image the proximal posterior tarsal tunnel. Perineural injections of methylene blue were performed with subsequent dissection. Injections were designated as accurate (referring to nerve staining) and precise (referring to dye localization). Results: One cadaver was precluded due to pronounced musculoskeletal abnormality. 5-of-6 (83%) injections were accurate and 6-of-6 (100%) precise. Conclusion: Initial attempt was inaccurate and precise, while later injections were both accurate and precise. The most apparent source of error was from one cadaver's pronounced musculoskeletal deformity, which precluded successful injections bilaterally. Of the three cadavers unaffected by musculoskeletal deformity, accuracy was 5-of-6 (83%) and precision was 6-of-6 (100%). While surgery is the definitive treatment for refractory PostTTS, therapeutic effect of corticosteroid injections has not been evaluated in this patient population. Such injections could provide symptomatic relief and postpone surgical intervention. Small sample size not withstanding the results suggest that TN perineural injections are feasible under US-guidance. This study suggests that US-guidance can increase accuracy and precision and is a potential adjunct to the treatment. Future study will expand the initial data set and categorize consistent protocol. Subsequent translational research will then be sought to evaluate therapeutic efficacy in this patient population.
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Kramer, Adriel A., Arnold-Peter C. Weiss, Hans-J. Barrach, and Edward Akelman. "VARIATIONS IN THE QUANTITY OF TYPE II COLLAGEN IN CARPAL TUNNEL SYNDROME AND TRIGGER FINGER." Hand Surgery 01, no. 02 (July 1996): 95–101. http://dx.doi.org/10.1142/s0218810496000178.

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Carpal tunnel syndrome (CTS) and trigger finger (TF) are two related disorders which involve alterations in the normal mechanical loading of tendon sheath pulleys. This study examines the presence of Type II collagen in the carpal ligament and A-1 pulley by Western blotting to determine the extent of cartilage metaplasia that may occur in these tissues. Cyanogen bromide peptides generated from tissue supplied from 77 patients were separated by SDS-PAGE and transferred to nitrocellulose. The membranes were stained with the E1E5 monoclonal antibody and collagen levels were quantified. All specimens were found to contain at least small amounts of Type II collagen. Approximately 15 percent of the samples from patients with carpal tunnel syndrome and trigger finger were found to contain significantly elevated levels of Type II collagen. All specimens with high levels of Type II collagen were found in female patients. These increases may indicate the presence of cartilage metaplasia enabling the tissue to counteract compressive loads. With further study, tissue staining techniques using monoclonal antibodies may provide useful clinical information on severity or long-term outcome prognosis.
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Wang, Joon Ho, and Byung Hoon Lee. "Mediolateral Differences of Proteoglycans Distribution at the ACL Tibial Footprint: Experimental Study of 16 Cadaveric Knees." BioMed Research International 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/3762580.

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This study aimed to identify the staining pattern of ACL attachment blended with cartilage of the medial tibial plateau at the tibial insertion and histologically characterize the tibial footprint. Sixteen fresh frozen cadaveric knees (mean age: 52.0±6.2 years) were used for this study. The specimens were bisected in the coronal plane, in accordance with the fiber orientation of the ACL tibial attachment. Adjacent sections were then stained with hematoxylin and eosin (H&E) to observe the morphology of the ACL insertion and with fast green and Safranin-O protocols to evaluate for collagen and proteoglycans (PG). The insertion area on the tibial footprint was divided into five zones in the medial to lateral direction, which was determined by division of the section from most prominent medial tibial spine to most lateral margin of ACL attachment. Then rectangular area with a vertical length that is twice the width of respective five zones was set. Stained areas of all images were quantified positively by using ImageJ software, and the value for staining area measured was defined in percentage by multiplying whole image area by 100. The mean proportion of Safranin-O staining is significantly greater nearer to the medial tibial spine (59% in zone 1, 32% in zone 2, 13% in zone 3, 13% in zone 4, and 4% in zone 5, P<0.001). The medial section of the tibial insertion area grew in size and increased in PG staining with more densely organized collagen arrangement with more fibrocartilage cells. The ACL tibial insertion showed a medially eccentric staining pattern by histological evaluation of the ACL attachment to cartilage. Our histological results of the eccentric biomaterial property in the medial tibial spine of ACL insertion area can be considered in making a more functional anatomic tibial tunnel placement.
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Zhao, YuHan, and QingHong Cheng. "Exogenous H2S Protects against Septic Cardiomyopathy by Inhibiting Autophagy through the AMPK/mTOR Pathway." Contrast Media & Molecular Imaging 2022 (June 10, 2022): 1–8. http://dx.doi.org/10.1155/2022/8464082.

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Background. Given the cardioprotective role of autophagy, this study aimed to investigate the protective effect of exogenous H2S (NaHS) on infectious cardiomyopathy through the inhibition of the AMPK/mTOR pathway. Methods. In this study, sepsis models were established by cecal ligation and puncture (CLP) induction in vivo and intraperitoneal injection of NaHS was performed. Autophagy- and apoptosis-related proteins were observed by western blot, isolated myocardial tissue morphology was observed by hematoxylin-eosin (H&E) staining, and myocardial apoptosis was evaluated by the tunnel method. The ultrastructure of autophagy was observed by using an electron transmission electron microscope. Results. In an SD rat model of cecum ligation puncture-induced sepsis, the level of autophagy-related proteins was significantly increased, and hematoxylin and eosin staining showed irregular myocardial bands and swollen cardiomyocytes. Following NaHS treatment, the level of autophagy-related proteins decreased, and electron transmission microscopy revealed decreased autophagosomes. Echocardiography suggested an increase in ejection fraction and significant relief of myocardial inhibition. Conclusions. Our results suggest that NaHS treatment can attenuate the cellular damage caused by excessive autophagy through the AMPK/mTOR pathway.
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Dissertations / Theses on the topic "Tunnel staining"

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INAGAKI-TACHIBANA, EIKO, TAKAMITSU TSUKAHARA, KAZUHIKO KAJI, RYOJI EGUCHI, HIROAKI KANAZAWA, HISAYOSHI HAYASHI, and YUICHI SUZUKI. "INVOLVEMENT OF DNA FRAGMENTATION OF ENTEROCYTES IN MUCOSAL INJURY TO A MOUSE JEJUNUM INCUBATED IN USSING CHAMBERS." Nagoya University School of Medicine, 2009. http://hdl.handle.net/2237/11332.

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Kunz, Tina. "The Role of Cyclooxygenase-2 in Models of Epilepsy and Traumatic Brain Injury : Effects of Selective Cyclooxygenase-2 Inhibitors." Doctoral thesis, Uppsala University, Department of Pharmaceutical Biosciences, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2543.

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Cyclooxygenase-2 (COX-2) catalyses prostaglandin synthesis from arachidonic acid during inflammation. COX-2 is expressed in the normal brain and is induced in neurological disorders. There is evidence that COX-2 is involved in secondary events leading to cell death in the brain. The first objective was to study the expression of COX-2 in the brain after kainate (KA)-induced limbic seizures and brain trauma caused by controlled cortical contusion (CCC) and fluid percussion injury (FPI). COX-2 mRNA and protein were strongly induced by limbic seizures in the hippocampus, amygdala and piriform cortex. CCC and FPI resulted in an upregulation of COX-2 mainly in the dentate gyrus and cortex, with differences in expression levels in these regions between the models. The second objective was to evaluate the effects of selective COX-2 inhibitors on delayed cell death. Limbic seizures induced cell death in parts of the hippocampus, amygdala and functionally connected regions. Treatment with the selective COX-2 inhibitor rofecoxib 8 h after KA injection significantly reduced hippocampal cell death. Pre-treatment with the COX-2 inhibitor nimesulide augmented acute seizures with increased mortality and thus the effect of nimesulide on delayed cell death could not be evaluated. Effects of rofecoxib on trauma-induced cell death were studied in the FPI model. FPI induced delayed cell death mainly in the ipsilateral cortex and bilaterally in the dentate gyrus. Rofecoxib treatment, starting directly after injury was caused, had no protective effect against cell death.

The results suggest that COX-2 inhibition may be both detrimental and beneficial and largely dependent on the time schedule of treatment. COX-2 inhibitors might thus be of value as a neuroprotective treatment approach, provided that the role of COX-2 and the time course of effects of its metabolites in the brain are elucidated.

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Myers, Jonathan. "Changing the tune : conceptualising the effects of the global financial crisis on stakeholder perceptions of corporate value." Thesis, University of Hertfordshire, 2019. http://hdl.handle.net/2299/21101.

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Could shareholder primacy, with its assumed short-termist practices, have had its day when it comes to managerial activity centered on creating corporate value? Many business and opinion leaders appear to take this position, not least Jack Welch who famously declared 'shareholder primacy is the dumbest idea in the world!' Indeed, in a post-Crash economy has a wider stakeholder focus with a longer-term outlook superseded any business notions of shareholder primacy and wealth maximization? This research examines these possibilities through a consideration of the narrative companies produce, such as annual reports. From this corpus material, an assessment is made of whether UK managers' perceptions about corporate value generation changed over the period covering the worldwide financial crisis, with respect to their relative favouring of shareholders and stakeholders. The corpus of narrative material used is visualized as a conceptual space in which a conversation reflecting perceptual bias to the generation of corporate value occurs. To explore such corpuses, in order to compare narratives at points either side of the 2008 Crash, a new methodology was devised called narrative staining. Hence, a detection and visual mapping over the period was made possible of managers' changing perceptions concerning primacy (shareholder or stakeholder orientation) with its mediation by termism (a short or long-term bias). Termism is also originally conceived as part of a larger temporal category, which includes a sense of urgency to act (urgent versus non-urgent) that is similarly examined. The investigation reveals that over time perceptual change about value creation happened, though in unanticipated ways. Companies pre-Crash were often short-term stakeholder oriented then moved post-Crash to a long-term shareholder orientation. A focus for this study was the corporate domain, consisting of a selection of FT250 companies. However, managerial perceptions about corporate value creation are influenced not simply by the conversation of the corporate domain but rather by a multi-actor conversation taking place throughout the business environment. To comprehend this effect, the research mines further corpuses that comprise the UK's regulatory domain (hard and soft law), the press (Financial Times and other newspapers), and relevant peripheral stakeholder organizations (including the Confederation of British Industry, the Institute of Directors, and the Trades Union Congress). These organizations demonstrated more complex, unforeseen, perceptual effects as the financial crisis proceeded with many aligning according to their political or business agenda, which also impacted any sense of urgency to act they had. There appears to be no previous attempt at an extensive and multivariate analysis of this nature. And the findings challenge prevalent characterizations of shareholder and stakeholder behaviour. Moreover, the research shows that utilizing a wide set of stakeholder corpuses acts a viable proxy for broader financial perspectives amongst UK organizations. The technique of narrative staining therefore provides insights, hitherto inaccessible, for assessing and consolidating large-scale perceptual bias regarding value creation across the economy. The technique also has significant potential for other applications.
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Saggu, Sarabjit Kaur. "Aspects of retinal and optic nerve pathology after excitotoxic retinal injury." Thesis, 2011. http://hdl.handle.net/2440/71304.

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A large body of evidence supports the notion that excitotoxicity plays a major role in the pathogenesis of a number of neurological diseases, including central nervous system (CNS) ischaemia, Alzheimer's disease, motor neurone disease, and glaucoma. In the global population 60 years of age and over, these diseases are among the leading causes of mortality and morbidity. Although the site of excitotoxic injury is principally at the level of the cell body (perikaryal), understanding the secondary effects on the neuronal axon is important because axonopathy is a documented early feature of these common neurological conditions; hence, an understanding of the pattern and mechanisms of secondary axonal degeneration after excitotoxic perikaryal injury could provide novel detection and treatment strategies in the early phase of neurological disease. The retina and optic nerve, as approachable regions of the CNS, provide a unique anatomical substrate to investigate axonal degeneration after perikaryal excitotoxic injury. Spatiotemporal changes in the retina and optic nerve were studied after injection of 20nM of Nmethyl-D-Aspartate (NMDA) in the left eye of the rat with the saline-injected right eye serving as the control. Temporal changes in the morphology of retina and optic nerve were studied by light and electron microscopy. Progressive retinal damage beginning at 72 hrs, seen as thinning of the inner retina and cell loss in the ganglion cell layer, showed strong correlation (R= 0.949) with degenerative changes in the optic nerve; the distal optic nerve segment displayed significantly more axon loss, axon swellings and myelin damage than the proximal segment (p<0.05), suggestive of a 'dying-back type degeneration'. Beginning at 24 hrs, electron microscopy demonstrated various features of necrosis in retinal ganglion cells (RGCs): mitochondrial and endoplasmic reticulum swelling, disintegration of polyribosomes, rupture of membranous organelle and formation of myelin bodies. Ultrastructural damage in the optic nerve, which began at 72 hrs, mimicked the changes of Wallerian degeneration, where early nodal-paranodal disturbances were followed by the appearance of three major morphological variants: watery degeneration, dark degeneration, and demyelination. Features suggestive of RGC regeneration in the form of dendritic sprouting after acute excitotoxic injury were also demonstrated at day 7. Immunohistochemistry revealed glial cell responses and changes to the axon transport system. Excitotoxic injury resulted in progressive activation of macroglia (Müller cells and astrocytes) and microglial cells in the retina and optic nerve as demonstrated by increased glial-fibrillary-acidic protein (GFAP) and ED-1 immunolabelling as early as 72 hrs. Interxonal glial cells in the optic nerve also showed increased β-amyloid precursor protein (β-APP) beginning at 72 hrs. Impairment of slow axonal transport at 72 hrs resulted in decrease anterograde transport of neurofilament-light (NF-L) to the axon terminal and hence their accumulation in proximal neuron (seen as NF-L rich spheroids). This fundamental research revealed a pathological picture of Wallerian-like degeneration after perikaryal excitotoxic injury in the CNS. This novel finding is consistent with recent evidence of a labile axonal 'survival' factor, nicotinamide mononucleotide adenylyltransferase 2,(Nmnat2) produced by the neuronal cell body. Further study is required to test the hypothesis that a lack of Nmnat2 is the mechanism by which axons degenerate after excitotoxic perikaryal injury.
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2011
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Conference papers on the topic "Tunnel staining"

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Shah, Amit K., Li-Jen Yuan, Peter A. Torzilli, and C. T. Christopher Chen. "Strain Is the Major Factor for Chondrocyte Death in Articular Cartilage Under Static Load." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43059.

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Several studies have shown that stress, strain, and stress/strain rate at certain levels can kill chondrocytes, but the major factor is unclear. The objective of this study was to determine the effects of strain and stress on chondrocyte death. Bovine cartilage explants (5 mm) at the age of 2 and 24 month were indented (3 mm) at 3.12, 6.25 and 12.5 MPa to reach a final strain of 15, 30, 45, 60 and 75%. Cell death in the center and on the edges of the indented region was assessed at 0, 3 and 7 days post-loading, and quantified using commercially available software. Our results showed cell death in the center region increased with strain (p&lt;0.001) but decreased with age (p&lt;0.001). Cell death at the edges of the indented region was greater than that of the center (p&lt;0.001), and increased with strain (p&lt;0.001). With post-load incubation, a decrease of cell death was found in the explant loaded with 60 and 75%. Cells with positive TUNEL-staining and positive M30-staining were consistently seen in the middle and deep zones in the center region 3 days after load removal. This suggests that two types of cell injury/death (necrosis and apoptosis) occur simultaneously. Linear regression and ANOVA suggest that strain is the major factor for chondrocyte death under static load.
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Kulik, M. J., D. S. Shenoda, and C. R. Forest. "A Low-Cost, Two-Axis, Precision Robot for Automated Fluorescence In-Situ Hybridization Assays." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-13272.

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Genetics research often relies on experiments that require repetitive, time-consuming handling of small volumes of liquid (1 mL) and biomass (10–20 μL) such as fluorescence in-situ hybridization (FISH), β-galactosidase staining, immunohisto chemistry, skeletal and tunel assays. Often manual, these experiments are time intensive and error-prone. We report on the design, fabrication, and testing of a low-cost, two-axis, precision robot for FISH assays on whole mice embryos. The robot can complete 20 successive embryo immersions in unique isothermal solutions in minutes for 6 samples. Repeatability of the orthogonal axes is 66 and 214 μm, near the measurement uncertainty limit and sufficient for operation. Accuracy is achieved by systematic error compensation. Low-cost and precision are obtained using design and manufacturing techniques and processes, resulting in a cost of 15% of comparable instruments (e.g., InsituStain, Intavis Bioanalytical Instruments). This design demonstrates a simple, automated platform to perform a typically manual experimental genetics technique.
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Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.

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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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