Biomechanical and Microstructural Analysis of Wildtype (C57BL6) Mouse Aorta

2011 ◽  
Author(s):  
Darren Haskett ◽  
Greg Johnson ◽  
Mohamad Azhar ◽  
Jonathan Vande Geest
Keyword(s):  
Disease Progression ◽  
Microstructural Analysis ◽  
Disease Process ◽  
Infrarenal Aorta ◽  
Unanswered Question ◽  
C57bl6 Mouse ◽  
Underlying Mechanisms ◽  
Mouse Aorta ◽  
Biomechanical Factors

It is generally accepted that the formation of an aneurysm in the infrarenal aorta is a complex and multi-factorial disease, however little is known about how biomechanical factors may play a role in the progression of aneurysmal disease. Although it is known that human aneurysmal tissue is remodeled in the disease process [1] and that such reorganization leads to altered function [2], the underlying mechanisms by which such changes remains an important unanswered question in the literature. The purpose of this study is to develop a means for determining the biomechanical alterations that occur within the aorta to better understand aneurysmal disease progression.

Progressive Alterations in Biomechanical Response of a Mouse Model of Aneurysm

2012 ◽  
Author(s):  
Darren Haskett ◽  
Urs Utzinger ◽  
Mohamad Azhar ◽  
Jonathan Vande Geest
Keyword(s):  
Mouse Model ◽  
Complex Disease ◽  
Mechanical Characteristics ◽  
Infrarenal Aorta ◽  
Unanswered Question ◽  
Significant Morbidity ◽  
Biomechanical Behavior ◽  
Abdominal Aortic ◽  
Biomechanical Response ◽  
Underlying Mechanisms

Abdominal aortic aneurysm (AAA) is a complex disease that leads to a localized dilation of the infrarenal aorta, the rupture of which is associated with significant morbidity and mortality, however the underlying mechanisms by which such changes remains an important unanswered question in the literature. Animal models of AAA can be used to study how changes in the microstructural and biomechanical behavior of aortic tissues develop as disease progresses in these animals. We chose here to investigate changes in mechanical characteristics with time in the established Apolipoprotein E deficient (ApoE−/−) angiotensin II (AngII) infused mouse model of AAA.

scholarly journals In-situ Experiments to Capture the Evolution of Microstructure During Phase Transformation of Titanium Under Dynamic Loading

2018 ◽  
Vol 183 ◽  
pp. 03020
Author(s):  
Benjamin M. Morrow ◽  
David R. Jones ◽  
Paulo A. Rigg ◽  
George T. Gray ◽  
Ellen K. Cerreta
Keyword(s):  
Phase Transformation ◽  
Dynamic Loading ◽  
Microstructural Analysis ◽  
Alpha Phase ◽  
Material Behavior ◽  
High Rate ◽  
Omega Phase ◽  
In Situ Experiments ◽  
Consistent Picture ◽  
Underlying Mechanisms

Under sufficient stresses, such as during dynamic loading, titanium experiences a phase transformation from hcp alpha phase to hexagonal omega phase. Omega phase is often retained in the microstructure after unloading, and has a strong influence on subsequent mechanical properties. Simulations suggest there are multiple pathways and underlying mechanisms for this transformation. Due to the incredibly short timescales involved, experimental measurements for model validation have been difficult. However, new capabilities at the Advanced Photon Source have enabled diffraction measurements during plate impact experiments to study the evolution of titanium during transformation. These high-rate data allow us to probe the mechanism and kinetics of phase transformations in new ways. Recent results will be presented and compared to post-mortem characterization of soft-recovered shocked specimens. Comparisons are made with previous tests where material was shock-loaded and soft recovered for microstructural analysis. Together these techniques create a consistent picture of material behavior during the shock-induced ff–! phase transformation in titanium.

CERVICAL SPONDYLOSIS

Neurosurgery ◽  
2007 ◽  
Vol 60 (suppl_1) ◽  
pp. S1-130-S1-136 ◽  
Author(s):  
Brian P. Witwer ◽  
Gregory R. Trost
Keyword(s):  
Cervical Spondylosis ◽  
Disease Process ◽  
Cord Compression ◽  
Surgical Decompression ◽  
Decision Making Process ◽  
Combined Approach ◽  
Surgical Decision ◽  
Technical Aspects ◽  
Biomechanical Factors ◽  
Surgical Decision Making

Abstract CERVICAL SPONDYLOSIS IS a result of degenerative changes of the cervical spine. Neurological symptoms of myelopathy result from the narrowing of the spinal canal, causing spinal cord compression. Surgical management of cervical stenosis requires an understanding of the interplay between multiple pathological and biomechanical factors contributing to this disease process. Surgical decompression can be addressed from a ventral, dorsal, or combined approach. The authors discuss the technical aspects of the surgical decision making process regarding the decision to approach the spine from a ventral or dorsal orientation.

scholarly journals Cervical ossification of the posterior longitudinal ligament and its post surgical outcome analysis

2020 ◽  
Vol 8 (3) ◽  
pp. 816
Author(s):  
Vipul Kumar Gupta ◽  
T. Narsimha Rao
Keyword(s):  
Anterior Approach ◽  
Posterior Approach ◽  
Tertiary Care ◽  
Disease Process ◽  
Posterior Longitudinal Ligament ◽  
Functional Improvement ◽  
Outcome Analysis ◽  
Biomechanical Factors ◽  
Surgical Group

Background: Ossification of the posterior longitudinal ligament (OPLL) is a complex multi-factorial disease process having both metabolic and biomechanical factors. The objective of this study was to assess the surgical out come and post operative functional improvement in patients with cervical OPLL at a tertiary care centre.Methods: This prospective observational study included 35 patients undergoing surgery for cervical OPLL in the department of neurosurgery, Care hospitals Hyderabad from October 2015 to October 2016 with follow up at 3months and 6 months.Results: Total 35 patients who underwent surgery, majority (77.15%) were males and (22.85%) were female. The age of the patients was between 30 to 70 years. The most common type of OPLL was found to be segmental and mixed type. Nurick grade improved by 1.12 in anterior approach vs 0.66 in posterior approach. Recovery rates observed in anterior approach is 57.72% while in posterior surgical approach it is 48.87%. No complication was observed in this study.Conclusions: OPLL is more common in males as compared to females. The average age of presentation is sixth decade. Younger patients have better outcomes. The most common variant of OPLL is segmental.  The recovery rate achieved from anterior approach are better than those from the posterior approach. Improvement in NURICKS score is more in anterior surgical group than in posterior surgical group. No complications seen in this study. No mortality seen in this study.

scholarly journals P62 accumulates through neuroanatomical circuits in response to tauopathy propagation

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
François-Xavier Blaudin de Thé ◽  
Benjamin Lassus ◽  
Ari W. Schaler ◽  
Stephanie L. Fowler ◽  
Chris N. Goulbourne ◽  
...  
Keyword(s):  
Disease Progression ◽  
Brain Regions ◽  
In Vitro Models ◽  
Tau Pathology ◽  
Neuron Models ◽  
Protein Clearance ◽  
Underlying Mechanisms ◽  
Tau Aggregation

AbstractIn Alzheimer’s disease and related tauopathies, trans-synaptic transfer and accumulation of pathological tau from donor to recipient neurons is thought to contribute to disease progression, but the underlying mechanisms are poorly understood. Using complementary in vivo and in vitro models, we examined the relationship between these two processes and neuronal clearance. Accumulation of p62 (a marker of defective protein clearance) correlated with pathological tau accumulation in two mouse models of tauopathy spread; Entorhinal Cortex-tau (EC-Tau) mice where tau pathology progresses in time from EC to other brain regions, and PS19 mice injected with tau seeds. In both models and in several brain regions, p62 colocalized with human tau in a pathological conformation (MC1 antibody). In EC-Tau mice, p62 accumulated before overt tau pathology had developed and was associated with the presence of aggregation-competent tau seeds identified using a FRET-based assay. Furthermore, p62 accumulated in the cytoplasm of neurons in the dentate gyrus of EC-Tau mice prior to the appearance of MC1 positive tauopathy. However, MC1 positive tau was shown to be present at the synapse and to colocalize with p62 as shown by immuno electron microscopy. In vitro, p62 colocalized with tau inclusions in two primary cortical neuron models of tau pathology. In a three-chamber microfluidic device containing neurons overexpressing fluorescent tau, seeding of tau in the donor chamber led to tau pathology spread and p62 accumulation in both the donor and the recipient chamber. Overall, these data are in accordance with the hypothesis that the accumulation and trans-synaptic spread of pathological tau disrupts clearance mechanisms, preceding the appearance of obvious tau aggregation. A vicious cycle of tau accumulation and clearance deficit would be expected to feed-forward and exacerbate disease progression across neuronal circuits in human tauopathies.

Mechanics of Post Constrained Recovery Residual Stress Produced by NiTi

2019 ◽  
Author(s):  
Muhammad Istiaque Haider ◽  
Armin Yazdi ◽  
Maysam Rezaee ◽  
Li Chih Tsai ◽  
Nathan Salowitz
Keyword(s):  
Residual Stress ◽  
Microstructural Analysis ◽  
Small Strain ◽  
Load Cycle ◽  
Large Strains ◽  
Self Healing ◽  
Minor Variation ◽  
Residual Stress State ◽  
Continuous Application ◽  
Underlying Mechanisms

Abstract Recent research has revealed that Nickel Titanium (NiTi) shape memory alloys can produce residual stresses after undergoing constrained recovery and returning to their low temperature, martensitic state while still constrained. The nature and underlying mechanisms that cause this post constrained recovery residual stress (PCRRS) are not well understood. This paper presents experimental research and results seeking to further understand the PCRRS. Experiments were performed on multiple formulations of NiTi subjected to: 1) Cyclic loading and training before producing PCRRS, 2) Repeated thermomechanical loading with large strains followed by a thermal cycle to create and re-generated the PCRRS, and 3) Creation of the PCRRS followed by repeated cycles of small, 0.5% strains. Experiments found that the training in 1) did not significantly alter the ability to produce PCRRS or its magnitude. Straining samples from the PCRRS state could reduce the residual stress state to zero stress, but the PCRRS could be recreated by repeating thermal actuation with the only significant variation being a reduction in magnitude for the first to second cycle. Multiple small strain cycles applied from the PCRRS state caused an incremental reduction in residual stress. The full PCRRS could be re-created by repeating the initial thermomechanical cycle. The values of the residual stress varied across the first 3 sets of cycles, but from the third set onward the response stabilized. These results indicate that the primary mechanisms for generating a PCRRS are stable and recoverable with only minor and diminishing variations due to training or repeated regeneration of the PCRRS. Grain boundary stabilization and similar mechanisms may be responsible for the minor variation between the first few regenerations of the PCRRS. The incremental reduction in the residual stress after exposure to small 0.5% strains must be due to a recoverable process like partial and accumulating detwinning of the NiTi with each load cycle. Further work is underway to perform microstructural analysis of samples in the various states to further the theorized material states. The ability to generate and control PCRRS has the potential to find new application and advance capabilities in fields like self-healing and fatigue resistant materials by generating stresses without the continuous application of heat energy. New forms of actuation could also be developed based on the potential energy stored in a structure through PCRRS.

scholarly journals Env-Specific IgA from Viremic HIV-Infected Subjects Compromises Antibody-Dependent Cellular Cytotoxicity

2015 ◽  
Vol 90 (2) ◽  
pp. 670-681 ◽  
Author(s):  
María Julia Ruiz ◽  
Yanina Ghiglione ◽  
Juliana Falivene ◽  
Natalia Laufer ◽  
María Pía Holgado ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Disease Progression ◽  
Acute Infection ◽  
Protective Role ◽  
Cellular Cytotoxicity ◽  
Antibody Dependent Cellular Cytotoxicity ◽  
Elite Controllers ◽  
Before And After ◽  
Adcc Assay ◽  
Underlying Mechanisms

ABSTRACTElucidating the factors that modulate HIV-specific antibody-dependent cellular cytotoxicity (ADCC) will help in understanding its role in HIV immunity. The aim of this study was to determine whether IgA could modify the magnitude of ADCC in HIV infection, abrogating its protective role. Plasma samples from 20 HIV-positive (HIV+) subjects enrolled during primary HIV infection (PHI), 10 chronically infected subjects (chronic), and 7 elite controllers (EC) were used. ADCC was determined by using a fluorometric ADCC assay, before and after removal of plasma IgA. Data were analyzed by using nonparametric statistics. ADCC was documented in 80% of PHI enrollment samples and in 100% of PHI 12-month, chronic, and EC samples; it peaked after acute infection, reached a plateau in chronic infection, and decreased after initiation of antiretroviral treatment (ART). Significant associations between ADCC and disease progression were found only after removal of plasma IgA from 12-month PHI samples: the magnitude of ADCC not only increased after IgA removal but also correlated with CD4+T-cell preservation. This work provides evidence that gp120-specific IgA was capable of modifying ADCC responses during natural HIV infection for the first time and adds to similar evidence provided in other settings. Furthermore, it underscores the complexity of the ADCC phenomenon and will help in an understanding of its underlying mechanisms.IMPORTANCEAlthough the induction of ADCC-mediating antibodies in HIV-infected subjects has been extensively documented, the association of these antibodies with protection from disease progression is poorly understood. Here, we demonstrate that plasma IgA is a factor capable of modifying the magnitude of IgG-mediated ADCC in HIV infection, mitigating its beneficial effect. These results help in understanding why previous studies failed to demonstrate correlations between ADCC and disease progression, and they also contribute to the notion that an HIV vaccine should stimulate the production of ADCC-mediating IgG antibodies but not IgA.

scholarly journals Markers predicting progression of human immunodeficiency virus-related disease.

1994 ◽  
Vol 7 (1) ◽  
pp. 14-28 ◽  
Author(s):  
C M Tsoukas ◽  
N F Bernard
Keyword(s):  
Human Immunodeficiency Virus ◽  
Immune System ◽  
Hiv Infection ◽  
Disease Progression ◽  
Opportunistic Infections ◽  
Surrogate Marker ◽  
Disease Process ◽  
Surrogate Markers ◽  
Hiv Disease ◽  
Immunodeficiency Virus

Human immunodeficiency virus (HIV) interacts with the immune system throughout the course of infection. For most of the disease process, HIV activates the immune system, and the degree of activation can be assessed by measuring serum levels of molecules such as beta 2-microglobulin and neopterin, as well as other serum and cell surface phenotype markers. The levels of some of these markers correlate with clinical progression of HIV disease, and these markers may be useful as surrogate markers for development of clinical AIDS. Because the likelihood and timing of development of clinical AIDS following seroconversion, for any particular individual, are not readily predictable, the use of nonclinical disease markers has become critically important to patient management. Surrogate markers of HIV infection are, by definition, measurable traits that correlate with disease progression. An ideal marker should identify patients at highest risk of disease progression, provide information on how long an individual has been infected, help in staging HIV disease, predict development of opportunistic infections associated with AIDS, monitor the therapeutic efficacy of immunomodulating or antiviral treatments, and the easily quantifiable, reliable, clinically available, and affordable. This review examines the current state of knowledge and the role of surrogate markers in the natural history and treatment of HIV infection. The clinical usefulness of each marker is assessed with respect to the criteria outlined for the ideal surrogate marker for HIV disease progression.

Does ossification of the posterior longitudinal ligament progress after laminoplasty? Radiographic and clinical evidence of ossification of the posterior longitudinal ligament lesion growth and the risk factors for late neurologic deterioration

2012 ◽  
Vol 17 (6) ◽  
pp. 512-524 ◽  
Author(s):  
Kyle M. Fargen ◽  
J. Bridger Cox ◽  
Daniel J. Hoh
Keyword(s):  
Disease Progression ◽  
Disease Process ◽  
Posterior Longitudinal Ligament ◽  
Outcome Data ◽  
Posterior Surgery ◽  
Progressive Growth ◽  
Lesion Growth ◽  
Delayed Neurological Deterioration ◽  
Surgical Treatments

Ossification of the posterior longitudinal ligament (OPLL) is a disease process characterized by progressive growth and calcification resulting in spinal canal compromise and serious neurological sequelae in advanced cases. Historically, OPLL has most commonly been treated with posterior surgical decompression. Although this procedure indirectly decompresses the spinal cord, it does not address the offending pathological entity, and further growth of the lesion may result in delayed neurological deterioration. This fact is particularly relevant because a number of long-term studies have revealed both longitudinal and transverse disease progression in individuals treated both surgically and conservatively. Despite these high rates of radiographically documented progression, however, the rate of neurological decline in patients undergoing posterior surgery with laminoplasty is low. In this article, the authors review the pathophysiology of OPLL, evidence of disease progression, and outcome data addressing conservative and surgical treatments.

Pearls and pitfalls: Cold-induced urticaria

2020 ◽  
Vol 41 (4) ◽  
pp. 301-304
Author(s):  
David C. Mari ◽  
Taylor A. Banks
Keyword(s):  
Differential Diagnosis ◽  
Complex Disease ◽  
Clinical Course ◽  
Disease Process ◽  
Rapid Onset ◽  
Periodic Syndrome ◽  
Younger Patients ◽  
Systemic Reactions ◽  
Pertinent Information ◽  
Underlying Mechanisms

Background: Cold-induced urticaria can take place either due to direct cold exposure, cryoglobulinemia, or genetic component (such as cryopyrin-associated periodic syndrome), which leads to the rapid onset of urticaria and/or angioedema. It is more common in younger patients and more likely to affect females compared with males. Objective: To increase awareness of such systemic reactions of anaphylaxis and provide a focused review of the differential diagnosis, underlying mechanisms, broad workup, and management of this disease process for allergy/immunology fellows, residents, general physicians, and general practitioners. Methods: Pertinent information was included from the patient's clinical course. Also, a review of the available literature to include additional references that were obtained by using the works cited in the most up-to-date reviews was completed. Results: A case of a patient with cold-induced urticaria with common sequela was presented, followed by a discussion of the pathophysiology, diagnosis and its differential diagnosis, workup, and management. Conclusion: Cold-induced urticaria is a complex disease with several different catalysts. Providers should be aware of the different forms of cold-induced urticaria and recognize the risk for anaphylaxis in this patient population. Pearls and pitfalls of the diagnosis and management are provided.

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