Статті в журналах: "Elastin body"

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Nygaard, Rie Harboe, Scott Maynard, Peter Schjerling, Michael Kjaer, Klaus Qvortrup, Vilhelm A. Bohr, Lene J. Rasmussen, Gregor B. E. Jemec, and Michael Heidenheim. "Acquired Localized Cutis Laxa due to Increased Elastin Turnover." Case Reports in Dermatology 8, no. 1 (February 13, 2016): 42–51. http://dx.doi.org/10.1159/000443696.

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Cutis laxa is a rare disease characterized by abnormal skin wrinkling and laxity, due to decreased elastin synthesis or structural extracellular matrix defects. We have explored elastin metabolism in a case of adult onset cutis laxa localized to the upper body of a woman. For this purpose, we obtained skin biopsies from affected and unaffected skin areas of the patient and analyzed these with microscopy, polymerase chain reaction, western blotting and cell culture experiments. Skin from the affected area lacked elastin fibers in electron microscopy but had higher mRNA expression of elastin and total RNA. Levels of an apparent tropoelastin degradation product were higher in the affected area. Fibroblast cultures from the affected area were able to produce elastin and showed higher proliferation and survival after oxidative and UVB stress compared to fibroblasts from the unaffected area. In conclusion, we report a case of acquired localized cutis laxa with a lack of elastic fibers in the skin of the patient's upper body. The lack of elastic fibers in the affected skin was combined with increased mRNA expression and protein levels of elastin. These findings indicate that elastin synthesis was increased but did not lead to deposited elastic fibers in the tissue.

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Misra, Ashish, Abdul Q. Sheikh, Abhishek Kumar, Jiesi Luo, Jiasheng Zhang, Robert B. Hinton, Leslie Smoot та ін. "Integrin β3 inhibition is a therapeutic strategy for supravalvular aortic stenosis". Journal of Experimental Medicine 213, № 3 (8 лютого 2016): 451–63. http://dx.doi.org/10.1084/jem.20150688.

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The aorta is the largest artery in the body, yet processes underlying aortic pathology are poorly understood. The arterial media consists of circumferential layers of elastic lamellae and smooth muscle cells (SMCs), and many arterial diseases are characterized by defective lamellae and excess SMCs; however, a mechanism linking these pathological features is lacking. In this study, we use lineage and genetic analysis, pharmacological inhibition, explant cultures, and induced pluripotent stem cells (iPSCs) to investigate supravalvular aortic stenosis (SVAS) patients and/or elastin mutant mice that model SVAS. These experiments demonstrate that multiple preexisting SMCs give rise to excess aortic SMCs in elastin mutants, and these SMCs are hyperproliferative and dedifferentiated. In addition, SVAS iPSC-derived SMCs and the aortic media of elastin mutant mice and SVAS patients have enhanced integrin β3 levels, activation, and downstream signaling, resulting in SMC misalignment and hyperproliferation. Reduced β3 gene dosage in elastin-null mice mitigates pathological aortic muscularization, SMC misorientation, and lumen loss and extends survival, which is unprecedented. Finally, pharmacological β3 inhibition in elastin mutant mice and explants attenuates aortic hypermuscularization and stenosis. Thus, integrin β3–mediated signaling in SMCs links elastin deficiency and pathological stenosis, and inhibiting this pathway is an attractive therapeutic strategy for SVAS.

3

Robb, Bruce W., Hiroshi Wachi, Theresa Schaub, Robert P. Mecham, and Elaine C. Davis. "Characterization of an In Vitro Model of Elastic Fiber Assembly." Molecular Biology of the Cell 10, no. 11 (November 1999): 3595–605. http://dx.doi.org/10.1091/mbc.10.11.3595.

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Elastic fibers consist of two morphologically distinct components: elastin and 10-nm fibrillin-containing microfibrils. During development, the microfibrils form bundles that appear to act as a scaffold for the deposition, orientation, and assembly of tropoelastin monomers into an insoluble elastic fiber. Although microfibrils can assemble independent of elastin, tropoelastin monomers do not assemble without the presence of microfibrils. In the present study, immortalized ciliary body pigmented epithelial (PE) cells were investigated for their potential to serve as a cell culture model for elastic fiber assembly. Northern analysis showed that the PE cells express microfibril proteins but do not express tropoelastin. Immunofluorescence staining and electron microscopy confirmed that the microfibril proteins produced by the PE cells assemble into intact microfibrils. When the PE cells were transfected with a mammalian expression vector containing a bovine tropoelastin cDNA, the cells were found to express and secrete tropoelastin. Immunofluorescence and electron microscopic examination of the transfected PE cells showed the presence of elastic fibers in the matrix. Biochemical analysis of this matrix showed the presence of cross-links that are unique to mature insoluble elastin. Together, these results indicate that the PE cells provide a unique, stable in vitro system in which to study elastic fiber assembly.

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Del Prado Audelo, María Luisa, Néstor Mendoza-Muñoz, Lidia Escutia-Guadarrama, David Giraldo-Gomez, Maykel González-Torres, Benjamín Florán, Hernán Cortés, and Gerardo Leyva-Gomez. "RECENT ADVANCES IN ELASTIN-BASED BIOMATERIALS." Journal of Pharmacy & Pharmaceutical Sciences 23 (August 17, 2020): 314–32. http://dx.doi.org/10.18433/jpps31254.

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Elastin is one of the main components of the extracellular matrix; it provides resistance and elasticity to a variety of tissues and organs of the human body, besides participating in cellular signaling. On the other hand, elastin-derived peptides are synthetic biopolymers with a similar conformation and structure to elastin, but these possess the advantage of solubility in aqueous mediums. Due to their biological activities and physicochemical properties, elastin and related peptides may be applied as biomaterials to develop diverse biomedical devices, including scaffolds, hydrogels, and drug delivery systems for tissue engineering. Likewise, the combination of elastin with natural or synthetic polymers has demonstrated to improve the mechanical properties of biomedical products and drug delivery systems. Here we comprehensively describe the physicochemical properties and physiological functions of elastin. Moreover, we offer an overview of the use of elastin and its derivative polymers as biomaterials to develop scaffolds and hydrogels for tissue engineering. Finally, we discuss some perspectives on the employment of these biopolymers to fabricate new biomedical products.

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Tang, Xin. "Elastin-Like Polypeptides as Thermosensitive Polymer System." Advanced Materials Research 898 (February 2014): 296–99. http://dx.doi.org/10.4028/www.scientific.net/amr.898.296.

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Thermo-responsive elastin-like polypeptides (ELPs) were successfully obtained by inverse transition cycling (ITC) and recursive directional ligation (RDL). Six ELPs displayed thermal properties, depending on their sequence and chain length. It was found that the ELP[KV8F-4 and ELP[KV8F-8 were effective as thermosensitive materials at the body temperature with phase transition temperature from 35 to 45oC.

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Garner, Tyler, An Ouyang, Adam J. Berrones, Marilyn S. Campbell, Bing Du, and Bradley S. Fleenor. "Sweet potato (Ipomoea batatas) attenuates diet-induced aortic stiffening independent of changes in body composition." Applied Physiology, Nutrition, and Metabolism 42, no. 8 (August 2017): 802–9. http://dx.doi.org/10.1139/apnm-2016-0571.

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We hypothesized a sweet potato intervention would prevent high-fat (HF) diet−induced aortic stiffness, which would be associated with decreased arterial oxidative stress and increased mitochondrial uncoupling. Young (8-week old) C57BL/6J mice were randomly divided into 4 groups: low fat (LF; 10% fat), HF (60% fat), low-fat sweet potato (LFSP; 10% fat containing 260.3 μg/kcal sweet potato), or high-fat sweet potato diet (HFSP; 60% fat containing 260.3 μg/kcal sweet potato) for 16 weeks. Compared with LF and LFSP, HF- and HFSP-fed mice had increased body mass and percent fat mass with lower percent lean mass (all, P < 0.05). Sweet potato intervention did not influence body composition (all, P > 0.05). Arterial stiffness, assessed by aortic pulse wave velocity and ex vivo mechanical testing of the elastin region elastic modulus (EEM) was greater in HF compared with LF and HFSP animals (all, P < 0.05). Advanced glycation end products and nitrotyrosine abundance were greater in aortic segments from HF mice compared with LF and HFSP animals (all, P < 0.05). Aortic elastin and uncoupling protein 2 expressions, however, were reduced in HF compared with LF and HFSP mice (all, P < 0.05). Aortic segments cultured with 2,4-dinitrophenol (DNP), a mitochondrial uncoupler, for 72 h reduced the EEM of HF arteries compared with nontreated HF segments (P < 0.05). DNP had no effect on the EEM of aortic segments from HFSP mice. In conclusion, sweet potato attenuates diet-induced aortic stiffness independent of body mass and composition, which is associated with a normalization of arterial oxidative stress possibly due to mitochondrial uncoupling.

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Conley, Andrew J., Jussi J. Joensuu, Rima Menassa, and Jim E. Brandle. "Induction of protein body formation in plant leaves by elastin-like polypeptide fusions." BMC Biology 7, no. 1 (2009): 48. http://dx.doi.org/10.1186/1741-7007-7-48.

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RUBINI, ALESSANDRO, VINCENZO CATENA, DANIELE DEL MONTE, and EMANUELE LUIGI CARNIEL. "A REVIEW OF THE EFFECTS OF BODY TEMPERATURE VARIATIONS ON RESPIRATORY MECHANICS: MEASUREMENTS BY THE END-INFLATION OCCLUSION METHOD IN THE RAT." Journal of Mechanics in Medicine and Biology 15, no. 05 (October 2015): 1530006. http://dx.doi.org/10.1142/s0219519415300069.

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The temperature of body fluids is expected to affect tissues mechanical properties, including respiratory system tissues. This is because of the changes in airway smooth muscle tone and contractile properties, influencing airway frictional resistance to airflow, and because of the temperature effects on the stress–strain relationships of elastin and collagen, which determinates the elastic behavior of the lungs as reflected by their pressure–volume relationship. Alveolar surfactant biological and physical properties have also been shown to be affected by temperature changes, suggesting influences on the respiratory system hysteretic properties. Experimental works describing the effects of body temperature variations on respiratory mechanics are reviewed, including recent findings dealing with investigations on respiratory mechanics carried out by the end-inflation occlusion method in the rat. This method allows to determine, together with the elastance of the respiratory system, its resistive properties too. In particular, both the ohmic airway resistance due to frictional forces in the airway and the additional visco-elastic resistance exerted because of tissues stress-relaxation may be quantified. The effects of body temperature variations were assessed, and experimentally induced temperature increments and/or decrements allowed to conclude that respiratory system tissues stiffness, both the ohmic and the stress-relaxation linked resistances, and the hysteretic behavior of the respiratory system, decrease with temperature increments. The mechanisms responsible for these effects are analyzed.

9

Daugherty, Alan, Debra L. Rateri, Israel F. Charo, A. Phillip Owens, Deborah A. Howatt, and Lisa A. Cassis. "Angiotensin II infusion promotes ascending aortic aneurysms: attenuation by CCR2 deficiency in apoE−/− mice." Clinical Science 118, no. 11 (March 9, 2010): 681–89. http://dx.doi.org/10.1042/cs20090372.

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AngII (angiotensin II) induces atherosclerosis and AAAs (abdominal aortic aneurysms) through multiple proposed mechanisms, including chemotaxis. Therefore, we determined the effects of whole-body deficiency of the chemokine receptor CCR2 (CC chemokine receptor 2) on these diseases. To meet this objective, apoE (apolipoprotein E)−/− mice that were either CCR2+/+ or CCR2−/−, were infused with either saline or AngII (1000 ng·kg−1 of body weight·min−1) for 28 days via mini-osmotic pumps. Deficiency of CCR2 markedly attenuated both atherosclerosis and AAAs, unrelated to systolic blood pressure or plasma cholesterol concentrations. During the course of the present study, we also observed that AngII infusion led to large dilatations that were restricted to the ascending aortic region of apoE−/− mice. The aortic media in most of the dilated area was thickened. In regions of medial thickening, distinct elastin layers were discernable. There was an expansion of the distance between elastin layers in a gradient from the intimal to the adventitial aspect of the media. This pathology differed in a circumscribed area of the anterior region of ascending aortas in which elastin breaks were focal and almost transmural. All regions of the ascending aorta of AngII-infused mice had diffuse medial macrophage accumulation. Deficiency of CCR2 greatly attenuated the AngII-induced lumen dilatation in the ascending aorta. This new model of ascending aortic aneurysms has pathology that differs markedly from AngII-induced atherosclerosis or AAAs, but all vascular pathologies were attenuated by CCR2 deficiency.

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Boyce, Teresa Terpin, and Margot R. Roach. "The canine tail artery as a model for cerebral aneurysm studies." Canadian Journal of Physiology and Pharmacology 67, no. 1 (January 1, 1989): 34–39. http://dx.doi.org/10.1139/y89-006.

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The occluded canine tail artery, which comes off in the same plane as the aortoiliac junction, has been used as a flow model for cerebral aneurysms. These experiments were designed to determine if it is a realistic distensible model of human intracranial aneurysms. Distensibility studies were done on the aorta, and the iliac and tail arteries of four dogs. From these pressure–volume studies, tension–strain curves, elastances, and collagen slack were obtained. The tail artery is stiffer longitudinally and more distensible circumferentially than the other vessels. The iliac arteries and the aorta are not significantly different. The elastance of elastin and collagen is lower in the tail artery, and the collagen is more wavy circumferentially. Longitudinally, the collagen slack is least for the tail artery, and the elastance of elastin is not different in all three vessels. The number of elastin layers in the iliac and tail arteries seen in cross section is not significantly different, but the aorta is different from both these vessels. In another four dogs the aorta proximal to the trifurcation was cannulated and infused with saline to increase pressure. India ink marks were put on the surface to measure changes in length. Photographs were taken at intervals of 10 mmHg(1 mmHg = 133.3 Pa). This was done with the vessels tethered and untethered in the body and then taken out and studied with the same method in vitro. Arteries tethered in the body expanded circumferentially more than longitudinally. The tail artery becomes less distensible if untethered in the body and therefore acts more like an aneurysm. This makes it a good distensible flow model for aneurysm study. Even though the walls of the tail artery are thick and the geometry is not spherical, it is a reasonable model to study flow in aneurysms.Key words: elasticity, aorta, aneurysm, tethering, canine.

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Bartstra, Jonas W., Wilko Spiering, Jody M. W. van den Ouweland, Willem P. T. M. Mali, Rob Janssen, and Pim A. de Jong. "Increased Elastin Degradation in Pseudoxanthoma Elasticum Is Associated with Peripheral Arterial Disease Independent of Calcification." Journal of Clinical Medicine 9, no. 9 (August 26, 2020): 2771. http://dx.doi.org/10.3390/jcm9092771.

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Pseudoxanthoma elasticum (PXE) results in extensive fragmentation and calcification of elastin fibers in the peripheral arteries, which results in peripheral arterial disease (PAD). Current research focuses on the role of calcifications in the pathogenesis of PXE. Elastin degradation and calcification are shown to interact and may amplify each other. This study aims to compare plasma desmosines, a measure of elastin degradation, between PXE patients and controls and to investigate the association between desmosines and (1) arterial calcification, (2) PAD, and (3) PAD independent of arterial calcification in PXE. Plasma desmosines were quantified with liquid chromatography-tandem mass spectrometry in 93 PXE patients and 72 controls. In PXE patients, arterial calcification mass was quantified on CT scans. The ankle brachial index (ABI) after treadmill test was used to analyze PAD, defined as ABI < 0.9, and the Fontaine classification was used to distinguish symptomatic and asymptomatic PAD. Regression models were built to test the association between desmosines and arterial calcification and arterial functioning in PXE. PXE patients had higher desmosines than controls (350 (290–410) ng/L vs. 320 (280–360) ng/L, p = 0.02). After adjustment for age, sex, body mass index, smoking, type 2 diabetes mellitus, and pulmonary abnormalities, desmosines were associated with worse ABI (β (95%CI): −68 (−132; −3) ng/L), more PAD (β (95%CI): 40 (7; 73) ng/L), and higher Fontaine classification (β (95%CI): 30 (6; 53) ng/L), but not with arterial calcification mass. Lower ABI was associated with higher desmosines, independent from arterial calcification mass (β (95%CI): −0.71(−1.39; −0.01)). Elastin degradation is accelerated in PXE patients compared to controls. The association between desmosines and ABI emphasizes the role of elastin degradation in PAD in PXE. Our results suggest that both elastin degradation and arterial calcification independently contribute to PAD in PXE.

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Gutiérrez, Sonia P., Reza Saberianfar, Susanne E. Kohalmi, and Rima Menassa. "Protein body formation in stable transgenic tobacco expressing elastin-like polypeptide and hydrophobin fusion proteins." BMC Biotechnology 13, no. 1 (2013): 40. http://dx.doi.org/10.1186/1472-6750-13-40.

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Polańska, Adriana, Paulina Cieplewicz, Zygmunt Adamski, Ryszard Żaba, and Aleksandra Dańczak‑Pazdrowska. "The influence of ultraviolet radiation on the aging process of the skin." Journal of Face Aesthetics 2, no. 1 (February 10, 2019): 28–37. http://dx.doi.org/10.20883/jofa.8.

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Skin as the largest organ of the human body is constantly exposured to solar radiation. Photoaging describes the influence of ultraviolet radiation (UVR) on the skin exposed to light. A typical histopathological indicator of skin aging is the phenomenon of elastosis, which is the accumulation of amorphous elastin and tropoelastine in the reticular layer of the dermis. The presented study summarizes pathogenesis and clinical features related to chronic exposition of skin to UVR.

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Brüel, Annemarie, and Hans Oxlund. "Biosynthetic growth hormone changes the collagen and elastin contents and biomechanical properties of the rat aorta." Acta Endocrinologica 125, no. 1 (July 1991): 49–57. http://dx.doi.org/10.1530/acta.0.1250049.

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Abstract The biomechanical and biochemical properties of aortas from female rats treated with biosynthetic human GH (b-hGH) for 80 days were investigated. b-hGH was administered at a dose of 5 mg·kg−1·d−1. Treatment with b-hGH increased the body weight by 75% and the diameter of the aorta by 14% compared with the control group. The concentration of collagen and the relative amount of collagen type I were increased, and the concentration of elastin was decreased. Aortas from the b-hGH-treated group showed increased extensibility in the regions corresponding to physiological load values (i.e. 100-200 mmHg), and increased stiffness in regions with higher load values. The increased extensibility at low load values corresponds well with the loss of elastin, and the increased stiffness at higher load values with the increase of collagen and relative increase of collagen type I. These alterations induced by the growth hormone treatment might influence the elasticity and recoiling properties of the aorta.

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Carruthers, Jean, Gyasi Bourne, Michaela Bell, and Alan Widgerow. "Prospective, Randomized, Comparative Study of the Cutaneous Effects of a Topical Body Treatment Compared to a Bland Moisturizer." Aesthetic Surgery Journal 41, no. 9 (April 2, 2021): NP1188—NP1198. http://dx.doi.org/10.1093/asj/sjab161.

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Abstract Background Over time human skin thins and loses elasticity; topical treatments attempt to reverse this process. Objectives The aim of this study was to assess the efficacy of TransFORM Body Treatment (TFB) in skin rejuvenation compared to a bland moisturizer on the extensor and volar forearms. Methods Blinded participants were given 2 products to apply on the designated forearms with follow-up at 4, 8, and 12 weeks. Measurements included skin thickness, photography, dermatopathology, cutaneous elasticity determined by 2 different methods, and patient-reported outcomes. All were compared to baseline. Results Changes between bland moisturizer and TFB were recorded for the following parameters. (1) Roughness: extensor –0.09 mm for bland moisturizer and –0.26 mm for TFB (P = 0.174); volar 0.01 mm for bland moisturizer and –0.23 mm for TFB (P = 0.004). (2) Recoil velocity: volar –56°/sec for bland moisturizer and –24°/sec for TFB (P = 0.61); extensor –95°/sec for bland moisturizer and –63°/sec for TFB (P = 0.57). Retraction speed: volar –3.25 ms for bland moisturizer and –20.08 ms for TFB (P = 0.33); extensor –2.17 ms for bland moisturizer and –10.83 ms for TFB (P = 0.66). Histologically, TFB resulted in an increase in mucopolysaccharide content, new collagen, and number of elastin fibers in the papillary dermis. Changes in the Rao-Goldman score were also observed: volar –0.17 for bland moisturizer and –0.33 for TFB (P = 0.25); extensor –0.08 for bland moisturizer and –0.17 for TFB (P = 0.36). Conclusions Histology showed production of new collagen and elastin. Quantification of changes in skin thickness, skin retraction speed, and skin recoil velocity showed trends that agree with the visual data. Level of Evidence: 4

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Yu, Jing, Sean Mcleans, Hiromi Yanagisawa, C. Peter Winlove, Sally Roberts, Robert P. Mecham, and Jill Urban. "The importance of elastin and fibulin-5 on spine development: a study of elastin KO and fibulin-5 KO on the development of vertebral body and intervertebral disc." International Journal of Experimental Pathology 85, no. 1 (June 28, 2008): A29—A30. http://dx.doi.org/10.1111/j.0959-9673.2004.369am.x.

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Rabinovich, Roberto A., Bruce E. Miller, Karolina Wrobel, Kareshma Ranjit, Michelle C. Williams, Ellen Drost, Lisa D. Edwards, et al. "Circulating desmosine levels do not predict emphysema progression but are associated with cardiovascular risk and mortality in COPD." European Respiratory Journal 47, no. 5 (March 23, 2016): 1365–73. http://dx.doi.org/10.1183/13993003.01824-2015.

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Elastin degradation is a key feature of emphysema and may have a role in the pathogenesis of atherosclerosis associated with chronic obstructive pulmonary disease (COPD). Circulating desmosine is a specific biomarker of elastin degradation. We investigated the association between plasma desmosine (pDES) and emphysema severity/progression, coronary artery calcium score (CACS) and mortality.pDES was measured in 1177 COPD patients and 110 healthy control subjects from two independent cohorts. Emphysema was assessed on chest computed tomography scans. Aortic arterial stiffness was measured as the aortic–femoral pulse wave velocity.pDES was elevated in patients with cardiovascular disease (p<0.005) and correlated with age (rho=0.39, p<0.0005), CACS (rho=0.19, p<0.0005) modified Medical Research Council dyspnoea score (rho=0.15, p<0.0005), 6-min walking distance (rho=−0.17, p<0.0005) and body mass index, airflow obstruction, dyspnoea, exercise capacity index (rho=0.10, p<0.01), but not with emphysema, emphysema progression or forced expiratory volume in 1 s decline. pDES predicted all-cause mortality independently of several confounding factors (p<0.005). In an independent cohort of 186 patients with COPD and 110 control subjects, pDES levels were higher in COPD patients with cardiovascular disease and correlated with arterial stiffness (p<0.05).In COPD, excess elastin degradation relates to cardiovascular comorbidities, atherosclerosis, arterial stiffness, systemic inflammation and mortality, but not to emphysema or emphysema progression. pDES is a good biomarker of cardiovascular risk and mortality in COPD.

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Keeley, F. W., A. Elmoselhi, and F. H. Leenen. "Enalapril suppresses normal accumulation of elastin and collagen in cardiovascular tissues of growing rats." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1013—H1021. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1013.

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We have investigated the effect of enalapril, an angiotensin converting-enzyme (ACE) inhibitor, on the accumulation of ventricular and vascular collagen and elastin in young, growing rats. Beginning at either 4 or 10 wk of age, male Wistar rats were treated with enalapril for 2 or 5 wk. Enalapril treatment had no significant effect on body weight and small, generally non-significant effects on systolic and diastolic blood pressures. In contrast, young enalapril-treated animals showed a marked decrease in accumulation of total elastin and collagen in both large (aorta, renal, and carotid) and smaller (superior and large mesenteric) arteries, as well as a large reduction in total collagen in both left and right ventricles. This effect also was present but less pronounced in rats treated with enalapril beginning at 10 wk of age. These data indicate that inhibition of ACE activity during a period of rapid growth significantly reduces accumulation of vascular and ventricular connective tissue and suggests that angiotensin II may be important in normal cardiovascular development and growth.

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Zhang, Shoubing, and Enkui Duan. "Fighting against Skin Aging." Cell Transplantation 27, no. 5 (April 25, 2018): 729–38. http://dx.doi.org/10.1177/0963689717725755.

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As the most voluminous organ of the body that is exposed to the outer environment, the skin suffers from both intrinsic and extrinsic aging factors. Skin aging is characterized by features such as wrinkling, loss of elasticity, laxity, and rough-textured appearance. This aging process is accompanied with phenotypic changes in cutaneous cells as well as structural and functional changes in extracellular matrix components such as collagens and elastin. In this review, we summarize these changes in skin aging, research advances of the molecular mechanisms leading to these changes, and the treatment strategies aimed at preventing or reversing skin aging.

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Schriver, Elise E., Jeffrey M. Davidson, Marilyn C. Sutcliffe, Bridget B. Swindell, and Gordon R. Bernard. "Comparison of Elastin Peptide Concentrations in Body Fluids from Healthy Volunteers, Smokers, and Patients with Chronic Obstructive Pulmonary Disease." American Review of Respiratory Disease 145, no. 4_pt_1 (April 1992): 762–66. http://dx.doi.org/10.1164/ajrccm/145.4_pt_1.762.

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Sahebjami, H., and J. MacGee. "Effects of starvation on lung mechanics and biochemistry in young and old rats." Journal of Applied Physiology 58, no. 3 (March 1, 1985): 778–84. http://dx.doi.org/10.1152/jappl.1985.58.3.778.

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Two groups of rats (young and old) were food-deprived for 3 wk and were compared with age-matched fed groups. Final body weight and dry and wet weights of lungs were significantly reduced in both young and old starved rats. As determined by saline volume-pressure (VP) curves, lungs of young starved rats accepted significantly less volume at all pressure levels compared with lungs of young fed rats. When expressed as a percent of maximum lung volume, the VP curve in young starved rats was significantly shifted upward at low lung volumes. In the old rats, the VP curves were similar in fed and starved rats. Total lung content of protein, DNA, crude connective tissue, hydroxyproline, and elastin were significantly reduced in young starved compared with young fed rats, whereas in old starved rats only protein and DNA contents were lower than those in old fed animals. It appears that in rapidly growing young rats starvation leads to growth retardation, loss of connective tissue components, and possibly reduction in tissue elastic forces at low lung volumes, whereas starvation has no significant effects on lung mechanics and connective tissue in old rats.

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Susic, D. "Cross-link breakers as a new therapeutic approach to cardiovascular disease." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 853–56. http://dx.doi.org/10.1042/bst0350853.

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Fibrillar proteins, such as collagens type I and III, and elastin are components of the extracellular matrix. They form an intricate widespread network that provides a basis for maintaining the physical structure of the heart and vessels and also play an important role in determining cardiovascular function. Physiologically, collagen and elastin fibres are enzymatically cross-linked to form matrix. In addition to these enzymatically formed cross-links, collagen fibres may be linked non-enzymatically, most notably by formation of AGEs (advanced glycation end-products). AGEs are formed by a reaction between reducing sugars and body proteins; they are formed increasingly in diabetes mellitus and hypertension and they accumulate with aging. There are several mechanisms whereby AGEs may affect cardiovascular structure and function. These include increased myocardial and vascular stiffness and (upon reaction with their receptors) inflammatory reactions, release of growth factors and cytokines, and increased oxidative stress. Therefore breaking AGEs appears as a promising tool in the therapy of cardiovascular injury related to diabetes, hypertension and aging. Breakers of AGE cross-links have been developed and one of them, alagebrium, has been extensively studied. This brief review discusses the formation of AGEs, their role in mediating cardiovascular injury, as well as the results of experimental and clinical studies involving alagebrium.

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Gourgas, Ophélie, Gregory B. Cole, Lisa D. Muiznieks, Simon Sharpe, and Marta Cerruti. "Effect of the Ionic Concentration of Simulated Body Fluid on the Minerals Formed on Cross-Linked Elastin-Like Polypeptide Membranes." Langmuir 35, no. 47 (November 15, 2019): 15364–75. http://dx.doi.org/10.1021/acs.langmuir.9b02542.

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Czekalla, Carolin, Karl-Heinz Schönborn, Nadine Döge, Sora Jung, Maxim E. Darvin, Jürgen Lademann, and Martina C. Meinke. "Impact of Body Site, Age, and Gender on the Collagen/Elastin Index by Noninvasive in vivo Vertical Two-Photon Microscopy." Skin Pharmacology and Physiology 30, no. 5 (2017): 260–67. http://dx.doi.org/10.1159/000477854.

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Simpson, Chartrisa LaShan, Jenna A. Mosier, and Narendra R. Vyavahare. "Osteoclast-Mediated Cell Therapy as an Attempt to Treat Elastin Specific Vascular Calcification." Molecules 26, no. 12 (June 15, 2021): 3643. http://dx.doi.org/10.3390/molecules26123643.

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Inflammation and stiffness in the arteries is referred to as vascular calcification. This process is a prevalent yet poorly understood consequence of cardiovascular disease and diabetes mellitus, comorbidities with few treatments clinically available. Because this is an active process similar to bone formation, it is hypothesized that osteoclasts (OCs), bone-resorbing cells in the body, could potentially work to reverse existing calcification by resorbing bone material. The receptor activator of nuclear kappa B-ligand (RANKL) is a molecule responsible for triggering a response in monocytes and macrophages that allows them to differentiate into functional OCs. In this study, OC and RANKL delivery were employed to determine whether calcification could be attenuated. OCs were either delivered via direct injection, collagen/alginate microbeads, or collagen gel application, while RANKL was delivered via injection, through either a porcine subdermal model or aortic injury model. While in vitro results yielded a decrease in calcification using OC therapy, in vivo delivery mechanisms did not provide control or regulation to keep cells localized long enough to induce calcification reduction. However, these results do provide context and direction for the future of OC therapy, revealing necessary steps for this treatment to effectively reduce calcification in vivo. The discrepancy between in vivo and in vitro success for OC therapy points to the need for a more stable and time-controlled delivery mechanism that will allow OCs not only to remain at the site of calcification, but also to be regulated so that they are healthy and functioning normally when introduced to diseased tissue.

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Kwon, Kyoo-Ri, Md Badrul Alam, Ji-Hyun Park, Tae-Ho Kim, and Sang-Han Lee. "Attenuation of UVB-Induced Photo-Aging by Polyphenolic-Rich Spatholobus Suberectus Stem Extract Via Modulation of MAPK/AP-1/MMPs Signaling in Human Keratinocytes." Nutrients 11, no. 6 (June 14, 2019): 1341. http://dx.doi.org/10.3390/nu11061341.

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It is well known that ultraviolet light activates mitogen-activated protein (MAP) kinase by increasing the reactive oxygen species (ROS) in the body, enhancing activating protein 1(AP-1) complexes (c-Jun and c-Fos), increasing matrix metalloproteinases (MMPs) and degrading collagen and elastin. In this study, we confirmed that polyphenolic rich Spatholobus suberectus (SS) stem extracts suppressed ultraviolet (UV)-induced photo-aging. The major active components of SS stem extracts were identified as gallic acid, catechin, vanillic acid, syringic acid and epicatechin. The aqueous and ethanolic extracts of the stem of SS (SSW and SSE, respectively) significantly reduced the elastase enzyme activity. Moreover, both extracts were suppressed the ROS generation and cellular damage induced by UVB in HaCaT cells. Our results also revealed that SSE could regulate the expression of MMPs, tissue inhibitor of matrix metalloproteinase (TIMP)-1, collagen type I alpha 1 (COL1A1), elastin (ELN) and hyaluronan synthase 2 (HAS2) at their transcriptional and translational level. Furthermore, SSE was blocked the UVB-induced phosphorylation of mitogen-activated protein kinases (MAPKs), nuclear factor-kappa B (NF-κB) and c-Jun. Moreover, combination of syringic acid, epicatechin and vanillic acid showed strong synergistic effects on elastase inhibition activity, in which the combination index (CI) was 0.28. Overall, these results strongly suggest that the polyphenolics of SSE exert anti-ageing potential as a natural biomaterial to inhibit UVB-induced photo-aging.

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Sahebjami, H., and D. Denholm. "Lung mechanics and connective tissue proteins in diabetic Bio-Breeding/Worcester Wistar rats." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1430–35. http://dx.doi.org/10.1152/jappl.1987.62.4.1430.

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We studied lungs of spontaneously diabetic Bio-Breeding/Worcester (BB/W) Wistar rats which resemble human insulin-dependent diabetes mellitus. Compared with the age-matched control group, the body weight of the diabetic rats tended to be smaller and lung wet and dry weight were similar, but lung dry weight, relative to body weight and to lung wet weight, was significantly larger. Both air and saline lung volumes were reduced in the diabetic rats, and volume-pressure (V-P) curves expressed as a percent of maximal lung volume were significantly shifted downward and to the right of those in the control group over the midportion. Total DNA and RNA contents were similar in both groups, whereas protein content and concentration and protein/DNA and RNA/DNA ratios were significantly reduced in the diabetic rats. In contrast, content and concentration of 4-hydroxy-L-proline, elastin, and crude connective tissue were significantly higher in the diabetic group. We conclude that the increase in connective tissue proteins in the BB/W rats is most likely responsible for the shift in the V-P curves.

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Karlinsky, J. B., R. H. Goldstein, B. Ojserkis, and G. L. Snider. "Lung mechanics and connective tissue levels in starvation-induced emphysema in hamsters." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 2 (August 1, 1986): R282—R288. http://dx.doi.org/10.1152/ajpregu.1986.251.2.r282.

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The effect of starvation on lung mechanics, morphometry, and levels of connective tissue components was determined in young adult golden Syrian hamsters. A base-line control, fed control, and starved group were studied. Fed group animals increased body weight by 13%, but dry lung weight did not increase above that of the base-line controls. The total lung capacity when transpulmonary pressure was at 25 cmH2O (TLC25) also increased by 20% above base-line controls. The mean TLC25 of the starved group was greater than that of the base-line control group but less than that of the fed control group (P less than 0.05). Volume-corrected air-filled volume pressure (VP) curves of the three groups were similar. Volume-corrected saline-filled VP curves were identical in the three groups. Total lung collagen, elastin, glycosaminoglycan, and protein were similar in the three groups. Air space size was significantly increased and mean internal surface area was significantly decreased in the starved group compared with the base-line and fed controls. No evidence of alveolar wall destruction was evident by light or electron microscopy. We conclude that severe starvation of young adult hamsters produces air space enlargement without changes in lung elastic recoil. The mechanism of alveolar wall remodeling is not yet understood in this model of emphysema.

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Orton, Lisa Schichtel, and Paul F. Brodie. "Engulfing mechanics of fin whales." Canadian Journal of Zoology 65, no. 12 (December 1, 1987): 2898–907. http://dx.doi.org/10.1139/z87-440.

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The grooved throat wall of fin whales, Balaenoptera physalus, extends tremendously during feeding causing the whale to expand its profile from a cigar shape to the shape of an elongated, bloated tadpole. Ventral groove blubber associated with the engulfing feeding mechanism can be extended reversibly to as much as 4 times its resting length in the circumferential direction, and to 1.5 times its resting length along the long axis of the body. The muscle in the throat wall can be reversibly extended up to 3 times its resting length. Both these tissues have large amounts of the protein elastin in their microstructures that may function in retracting the expanded buccal cavity. Calculations of forces contributing to the expansion of the buccal cavity show that the engulfing process in feeding can be powered solely by the speed of swimming.

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Czekalla, Carolin, Karl Heinz Schönborn, Nadine Döge, Sora Jung, Maxim E. Darvin, Jürgen Lademann, and Martina C. Meinke. "Body regions have an impact on the collagen/elastin index of the skin measured by non-invasive in vivo vertical two-photon microscopy." Experimental Dermatology 26, no. 9 (April 11, 2017): 822–24. http://dx.doi.org/10.1111/exd.13283.

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31

Roth, Sarah. "Tension Headaches: An Investigation into Their Causes from a Naturopathic Perspective." Biofeedback 44, no. 1 (March 1, 2016): 4–14. http://dx.doi.org/10.5298/1081-5937-44.1.01.

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A thorough understanding of the physiological processes that underlie muscle tension is foundational to any discussion on environments and substances that alter such a process. The fascial web, an interconnection of the various fascia, extends throughout the entire body and acts to link every area of the body together and connect external and internal structures. It is the fascial tissue that transmits forces locally (i.e., between muscle and bone or between muscle and ligament) and distally, thereby creating muscle contraction in interconnected but distant areas of the body. Fascia is composed of various cell types, fibers (elastin, collagen, and reticular), and a fluid-like ground substance that is rich in proteoglycans. Fascial tissue responds both acutely and chronically to its environment via adaptations in both collagen and proteoglycan structure. Acutely, this results in the normal contraction of muscles and resultant movement, such as looking down at one's feet while walking, but chronically it can result in chronic pain syndromes, including tension headaches, due to tensegrity (tensional integrity) changes in the fascial framework. This can occur as a response to repetitive strain or acute injury. The purpose of this discussion is to provide an overview of some of the many influences on muscle tension from the perspective of a naturopathic doctor. I will use tension headaches as an example, though the principles discussed here may be extended to many different chronic pain syndromes.

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Nagai, A., M. Katayama, W. M. Thurlbeck, R. Matsui, S. Yasui, and K. Konno. "Effect of indomethacin on lung development in postnatal rats: possible role of prostaglandin in alveolar formation." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 1 (January 1, 1995): L56—L62. http://dx.doi.org/10.1152/ajplung.1995.268.1.l56.

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We administered 1.3 mg ip of indomethacin, a prostaglandin synthetase inhibitor, per 100 g body wt to male rat pups daily on postnatal days 4-13 and examined their lungs on day 14. Indomethacin administration produced abnormal lung structure with diminished alveolar air, increased alveolar duct air, increased mean linear intercept (gas-exchanging wall distance), diminished gas-exchanging surface area and surface-to-volume ratio, increased septal wall thickness, diminished the number of alveolar crests, and increased the number of lamellar bodies in alveolar type II cells. However, this procedure did not alter quantitative lung growth (normal lung weights, volumes, and DNA and protein contents). Tissue prostaglandin content was decreased. The total amount of lung collagen or elastin was unchanged, but when collagen was analyzed into soluble and insoluble components, soluble collagen was increased. Supplementation with 1.0 g of prostaglandin E2 per 100 g body wt to animals treated with indomethacin reduced the abnormalities in pulmonary architecture. We conclude that indomethacin affects lung structure in growing rats and that it is an unusual model in that lung growth is normal, but lung development is abnormal. We also suggest that prostaglandins may play a significant role in alveolar formation in postnatal lung development in rats.

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Xuan, Yue, and Zhaoyan Zhang. "Influence of Embedded Fibers and an Epithelium Layer on the Glottal Closure Pattern in a Physical Vocal Fold Model." Journal of Speech, Language, and Hearing Research 57, no. 2 (April 2014): 416–25. http://dx.doi.org/10.1044/2013_jslhr-s-13-0068.

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Purpose The purpose of this study was to explore the possible structural and material property features that may facilitate complete glottal closure in an otherwise isotropic physical vocal fold model. Method Seven vocal fold models with different structural features were used in this study. An isotropic model was used as the baseline model, and other models were modified from the baseline model by either embedding fibers aligned along the anterior–posterior direction in the body or cover layer, adding a stiffer outer layer simulating the epithelium layer, or a combination of the 2 features. Phonation tests were performed with both aerodynamic and acoustic measurements and high-speed imaging of vocal fold vibration. Results Compared with the isotropic one-layer model, the presence of a stiffer epithelium layer led to complete glottal closure along the anterior–posterior direction and strong excitation of high-order harmonics in the resulting acoustic spectra. Similar improvements were observed with fibers embedded in the cover layer, but to a lesser degree. The presence of fibers in the body layer did not yield noticeable improvements in glottal closure or harmonic excitation. Conclusion This study shows that the presence of collagen and elastin fibers and the epithelium layer may play a critical role in achieving complete glottal closure.

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Li, Jun, Azhar Masood, Man Yi, Mandy Lau, Rosetta Belcastro, Julijana Ivanovska, Robert P. Jankov, and A. Keith Tanswell. "The IGF-I/IGF-R1 pathway regulates postnatal lung growth and is a nonspecific regulator of alveologenesis in the neonatal rat." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 9 (May 1, 2013): L626—L637. http://dx.doi.org/10.1152/ajplung.00198.2012.

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IGF-I, IGF-II, and the IGF-I receptor are widely distributed throughout the neonatal rat lung on days 4, 7, 10, and 14 of life, with a similar abundance at each of these time points. Injection of 20 μg/g of a truncated soluble IGF-I receptor on days 2 and 5 of life, to decoy ligand away from the endogenous IGF-I receptor, reduced lung weight and lung-to-body weight ratio, reduced lung tissue fraction, and impaired alveolar formation, as assessed by secondary crest formation and mean linear intercepts on day 7 of life. Lung procollagen I content and elastin fiber density were also reduced. Injection of 100 μg/day of neutralizing anti-IGF-I, to prevent IGF-I from binding to the IGF-I receptor, on days 3, 4, and 5 of life reduced tissue fraction and elastin fiber density and impaired alveolar formation on day 6 of life. Both interventions reduced total lung cell and secondary crest cell DNA synthesis and small vessel counts per unit area, but these effects were lost after normalization to the reduced tissue fraction. These findings are consistent with a role for IGF-I binding to the IGF-I receptor in postnatal lung growth and on alveologenesis through a nonspecific positive effect on DNA synthesis. Injection of 100 μg/day of neutralizing anti-IGF-II, to prevent IGF-II from binding to the IGF-I receptor, on days 3, 4, and 5 of life had no effect on total lung cell DNA synthesis per unit area on day 6 of life, and a role for IGF-II in postnatal alveologenesis was not further pursued.

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Keller, Jennifer, Maurizio Mandala, Peter Casson, and George Osol. "Endothelial Dysfunction in a Rat Model of PCOS: Evidence of Increased Vasoconstrictor Prostanoid Activity." Endocrinology 152, no. 12 (October 25, 2011): 4927–36. http://dx.doi.org/10.1210/en.2011-1424.

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Clinical research demonstrates an association between polycystic ovary syndrome (PCOS) and endothelial dysfunction, a pathological state widely believed to be a hallmark of vascular disease; the underlying pathways, however, have not been defined. The purpose of this study was to characterize endothelial function in resistance arteries in a novel rat model of PCOS. Female rats were randomized at 3–4 wk to implantation of a 7.5-mg, 90-d dihydrotestosterone (DHT) pellet or a matched placebo. At 15–16 wk, experiments were performed on isolated mesenteric resistance arteries using a pressurized arteriograph. Endothelial function was assessed by the vasodilatory response of preconstricted arteries to acetylcholine (ACh) in the absence and presence of inhibitors for cyclooxygenase (indomethacin) and the thromboxane prostanoid receptor antagonist (SQ29,548). Distensibility was evaluated by measuring vessel diameter from 3–100 mm Hg, and elastin/collagen content was calculated on formalin-fixed vessels. Serum steroid levels were analyzed by sensitive RIA. DHT-induced PCOS rats were heavier, cycled irregularly, and had elevated blood pressure and smaller arterial lumens than controls. Furthermore, DHT vessels showed significantly reduced vasodilatory efficacy to ACh (with no change in sensitivity), reduced distensibility, and increased elastin content compared with controls. Within DHT animals, maximal dilation correlated negatively to DHT levels (r = −0.72) but not to body weight. Preincubation with either indomethacin or SC29,548 abrogated the dysfunction and restored full efficacy to ACh (P < 0.05). This is the first report to demonstrate the presence of endothelial dysfunction in a hyperandrogenic rat model of PCOS and to identify the role of vasoconstrictor prostanoids, allowing for more targeted research regarding the development of disease and potential therapeutic interventions.

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Rosellini, Elisabetta, Denise Madeddu, Niccoletta Barbani, Caterina Frati, Costanza Lagrasta, Federico Quaini, and Maria Grazia Cascone. "SDF-1 Molecularly Imprinted Biomimetic Scaffold as a Potential Strategy to Repair the Infarcted Myocardium." Open Biomedical Engineering Journal 15, no. 1 (August 11, 2021): 45–56. http://dx.doi.org/10.2174/1874120702115010045.

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Background: In situ cardiac tissue engineering aims to heal the infarcted myocardium by guiding tissue regeneration within the patient body. A key step in this approach is the design of a bioactive scaffold, able to stimulate tissue repair at the site of damage. In the development of bioactive scaffolds, molecular imprinting nanotechnology has been recently proposed as a new functionalization strategy. Objectives: In this work, Molecularly Imprinted Particles (MIP) with recognition properties towards the stromal-derived factor-1 (SDF-1) were synthesized, characterized and used for the functionalization of a biomimetic scaffold. MIP are expected to favor the enrichment of the SDF-1 bioactive molecule within the scaffold, thereby promoting myocardial regeneration. Methods: MIP were obtained by precipitation polymerization, using the SDF-1 molecule as a template. Alginate/gelatin/elastin sponges were fabricated by freeze-drying and functionalized by MIP deposition. Morphological, physicochemical and functional analyses were performed both on MIP and on MIP-modified scaffolds. A preliminary biological in vitro investigation was also carried out using rat cardiac progenitor cells (rCPCs). Results: Imprinted nanoparticles with an average diameter between 0.6 and 0.9 µm were obtained. Infrared analysis of MIP confirmed the expected chemical structure. Recognition and selectivity tests showed that MIP were able to selectively recognize and rebind the template, even after their deposition on the scaffold. In vitro biological tests showed that cell adhesion to the scaffold was promoted by MIP functionalization. Conclusion: Results obtained in the present study suggest that biomimetic alginate/gelatin/elastin sponges, functionalized by MIP with recognition properties towards SDF-1, could be successfully used for tissue engineering approaches to repair the infarcted heart.

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Lages, Renata Bandeira, Joseilson Barbosa Nunes, and Yves Viana Ramalho Oliveira. "Estruturação da face por meio dos fios de polidioxanona – relato de caso." Simmetria Orofacial Harmonizaton in Science 2, no. 7 (2021): 8–13. http://dx.doi.org/10.24077/202124813.

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Many facial rejuvenation techniques have been discovered for people looking for a younger look. In this context, the facelift using support threads made of polydioxanone (PDO) presented itself as a technique that, in addition to producing excellent postoperative results, is a minimally invasive procedure. It can neutralize the effects of aging by providing support and stimulation to the tissues of the areas around the patient’s problem, as there is the production of collagen and elastin. The present study aims to present a clinical case of a 68-year-old white female patient who had as main complaint the sagging and ptosis of the skin, the appearance of tiredness and falling of the corners of the lip, in which the PDO spiculated threads were inserted, reporting the changes caused on the face. The result was satisfactory, with improvement of the skin’s flaccidity, and the elevation of the labiolomental groove and the accumulation of fat in the mandibular body, with minimal side effects, being an effective and safe technique.

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Goergen, Craig J., Bonnie L. Johnson, Joan M. Greve, Charles A. Taylor, and Christopher K. Zarins. "Increased Anterior Abdominal Aortic Wall Motion: Possible Role in Aneurysm Pathogenesis and Design of Endovascular Devices." Journal of Endovascular Therapy 14, no. 4 (August 2007): 574–84. http://dx.doi.org/10.1177/152660280701400421.

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Purpose: To determine whether variations in aortic wall motion exist in mammalian species other than humans and to consider the potential implications of such variations. Methods: M-mode ultrasound was used to measure abdominal aortic wall motion in 4 animal species [mice (n=10), rats (n=8), rabbits (n=7), and pigs (n=5)], and humans (n=6). Anterior wall displacement, posterior wall displacement, and diastolic diameter were measured. The ratio of displacement to diameter and cyclic strain were calculated. Results: Body mass varied from 24.1±2.4 g (mouse) to 61.8±13.4 kg (human); aortic diameter varied from 0.53±0.07 mm (mouse) to 1.2±1 mm (human). Anterior wall displacement was 2.5 to 4.0 times greater than posterior among the species studied. The ratios of wall displacement to diastolic diameter were similar for the anterior (range 9.40%–11.80%) and posterior (range 2.49%–3.91%) walls among species. The ratio of anterior to posterior displacement (range 2.47–4.03) and aortic wall circumferential cyclic strain (range 12.1%–15.7%) were also similar. An allometric scaling exponent was experimentally derived relating anterior wall (0.377±0.032, R2=0.94) and posterior wall (0.378±0.037, R2=0.93) displacement to body mass. Conclusion: Abdominal aortic wall dynamics are similar in animals and humans regardless of aortic size, with more anterior than posterior wall motion. Wall displacement increases linearly with diameter, but allometrically with body mass. These data suggest increased dynamic strain of the anterior wall. Increased strain, corresponding to increased elastin fatigue, may help explain why human abdominal aortic aneurysms initially develop anteriorly. Aortic wall motion should be considered when developing endovascular devices, since asymmetric motion may affect device migration, fixation, and sealing.

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Russell, Anthony P. "The morphological basis of weight-bearing in the scansors of the tokay gecko (Reptilia: Sauria)." Canadian Journal of Zoology 64, no. 4 (April 1, 1986): 948–55. http://dx.doi.org/10.1139/z86-144.

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The scansors (subdigital, lamellar, scalelike structures) of gekkonid lizards bear adhesive setae and during locomotion on smooth surfaces must bear the weight of the animal. Thus, the body weight is supported by the integument and relatively large tensile stresses are imposed upon the skin at these times. In order that the relatively delicate integument is not damaged or stripped away from underlying tissues, precise linkages at transition zones occur. The setae themselves consist of material of high tensile strength, the epidermal–dermal junction is an extremely tight bond and the stratum compactum of the dermis provides a direct connection between the epidermis and the lateral digital tendon complex. The latter, in turn, connects directly to the skeleton by way of the metacarpo- or metatarso-phalangeal joint capsules. Additionally, elastin fibrils in the dermis and the collagen fibrils of the dermis and lateral digital tendon network are aligned in parallel with the long axis of each digit and are arranged to permit controlled distortion of the exposed scansorial surfaces.

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McClintock, Dana E., Barry Starcher, Mark D. Eisner, B. Taylor Thompson, Doug L. Hayden, Gwynne D. Church, and Michael A. Matthay. "Higher urine desmosine levels are associated with mortality in patients with acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L566—L571. http://dx.doi.org/10.1152/ajplung.00457.2005.

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Desmosine is a stable breakdown product of elastin that can be reliably measured in urine samples. We tested the hypothesis that higher baseline urine desmosine would be associated with higher mortality in 579 of 861 patients included in the recent Acute Respiratory Distress Syndrome Network trial of lower tidal volume ventilation ( 1 ). We also correlated urine desmosine levels with indexes of disease severity. Finally, we assessed whether urine desmosine was lower in patients who received lower tidal volumes. Desmosine was measured by radioimmunoassay in urine samples from days 0, 1, and 3 of the study. The data were expressed as a ratio of urine desmosine to urine creatinine to control for renal dilution. The results show that higher baseline ( day 0) urine desmosine-to-creatinine concentration was associated with a higher risk of death on adjusted analysis (odds ratio 1.36, 95% confidence interval 1.02–1.82, P = 0.03). Urine desmosine increased in both ventilator groups from day 0 to day 3, but the average rise was higher in the 12-ml/kg predicted body weight group compared with the 6-ml/kg predicted body weight group ( P = 0.053, repeated-measures model). In conclusion, patients with acute lung injury ventilated with lower tidal volumes have lower urine desmosine levels, a finding that may reflect reduced extracellular matrix breakdown. These results illustrate the value of evaluating urinary biological markers that may have prognostic and pathogenetic significance in acute lung injury.

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Khayat, Rana Osama S., Kirsty J. Shaw, Gary Dougill, Louise M. Melling, Glenn R. Ferris, Glen Cooper, and Robyn A. Grant. "Characterizing wing tears in common pipistrelles (Pipistrellus pipistrellus): investigating tear distribution, wing strength, and possible causes." Journal of Mammalogy 100, no. 4 (June 4, 2019): 1282–94. http://dx.doi.org/10.1093/jmammal/gyz081.

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Abstract Bats have large, thin wings that are particularly susceptible to tearing. Anatomical specializations, such as fiber reinforcement, strengthen the wing and increase its resistance to puncture, and an extensive vasculature system across the wing also promotes healing. We investigated whether tear positioning is associated with anatomy in common pipistrelles (Pipistrellus pipistrellus). Wing anatomy was described using histological techniques, imaging, and material testing. Tear information, including type, position, time in rehabilitation, and possible causes, was collected from rehabilitators of injured bats across the United Kingdom. Results suggest that the position of the plagiopatagium (the most proximal wing section to the body), rather than its anatomy, influenced the number, location, and orientation of wing tears. While material testing did not identify the plagiopatagium as being significantly weaker than the chiropatagium (the more distal sections of the wing), the plagiopatagium tended to have the most tears. The position of the tears, close to the body and toward the trailing edge, suggests that they are caused by predator attacks, such as from a cat (Felis catus), rather than collisions. Consistent with this, 38% of P. pipistrellus individuals had confirmed wing tears caused by cats, with an additional 38% identified by rehabilitators as due to suspected cat attacks. The plagiopatagium had the lowest number of blood vessels and highest amounts of elastin fibers, suggesting that healing may take longer in this section. Further investigations into the causes of tears, and their effect on flight capabilities, will help to improve bat rehabilitation.

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Konischeva, A. Yu, V. B. Gervazieva, and S. A. Mazurina. "CLINICAL AND IMMUNOLOGICAL INFLAMMATORY PATTERNS OF BRONCHIAL ASTHMA IN OBESE PATIENTS." Journal of microbiology epidemiology immunobiology 1, no. 1 (August 23, 2019): 59–63. http://dx.doi.org/10.36233/0372-9311-2019-1-59-63.

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We aimed to investigate immunological patterns of inflammation and autoimmunity, in bronchial asthma (BA) associated with obesity. Materials and methods. 109 people aged from 17 to 58 years with various body weights have been examined in total, including 64 individuals with allergic diseases as bronchial asthma (BA) and allergic rhinitis (AR). We performed the measurement of the body mass index according to WHO criteria, and evaluation of the asthma severity and comorbid conditions. In the samples of peripheral blood we measured biochemical tests (cholesterol and its fractions), spontaneous and PHA-induced production of cytokines: IL-4, IL-10, IL-17, TNF-, and serum levels of C-reactive protein (CRP), leptin, total IgE and IgE-autoAT, specific for a number of tissue AH (epithelial keratin, collagen 3 and 6 types, elastin and myosin). Results. Our study showed that in both groups of adults, the obesity was associated with increasing of acute phase proteins, CRP, leptin and TNF-α in serum, being most enhanced in asthma group. Individuals with excess body weight are characterized by significantly an increased level of acute phase proteins (Westergren ESR, CRP) and pro-inflammatory cytokines (TNF-α) in serum, thereby confirming the involvement of systemic inflammation in the obesity pathogenesis. The phenotype of BA with obesity is characterized by overproduction of CRP and leptin, along with increased spontaneous production of IL-4 and TNF-α, and also revealed sIgE to self-antigen as keratin, that in total could indicate more prominent inflammatory pathways with the impairment of immune regulation in this endotype of patients. Conclusion. The revealed associations confirm the link between obesity, as a chronic inflammatory condition, with atopy and development of asthma with further immune-mediated inflammation of the conduction airways.

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Nickel, Brian T., Mitchell R. Klement, Colin Penrose, Cynthia L. Green, Michael P. Bolognesi, and Thorsten M. Seyler. "Dislocation rate increases with bariatric surgery before total hip arthroplasty." HIP International 28, no. 5 (May 13, 2018): 559–65. http://dx.doi.org/10.1177/1120700017752567.

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Introduction: Annually in the USA, 113,000 patients with refractory obesity undergo bariatric surgery (BS), and a subset does so in order to lower body mass index to become a more desirable total hip arthroplasty (THA) candidate. This study aims to evaluate THA risk with and without bariatric surgery. Methods: 12,160 patients were identified in a claim-based review of the entire Medicare database with ICD-9 codes to identify patients in three groups. Patients who underwent BS prior to THA (Group I: 1,545 experimental group) and two control groups that did not undergo BS but had either a body mass index >40 (Group II: 6,918 bariatric control) or <25 (Group III: 3,697 normal weight control). Preoperative demographics/comorbidities and short-term medical (30 day) and long-term surgical (90-day and 2-year) complications were evaluated. Results: Group I had female predominance, youngest age, and highest incidence of: deficiency anaemia, cardiovascular disease, liver disease, diabetes, polysubstance abuse, psychiatric disorders and smoking. At 2 years, Group I had approximately twice the dislocation and revision risk compared to both Groups II and III; Groups I and II had over four times the risk of infection and wound complications compared to Group III. Conclusion: In the Medicare population, these patients continue to have complication rates similar to and sometimes greater than obese patients with no prior bariatric surgery. Greater dislocation risk is possibly due to ligamentous laxity related to decreased collagen/elastin and/or component malposition due to intraoperative visualisation challenges.

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Xu, Jie, Shuangshuang Zheng, Xueyan Hu, Liying Li, Wenfang Li, Roxanne Parungao, Yiwei Wang, Yi Nie, Tianqing Liu, and Kedong Song. "Advances in the Research of Bioinks Based on Natural Collagen, Polysaccharide and Their Derivatives for Skin 3D Bioprinting." Polymers 12, no. 6 (May 29, 2020): 1237. http://dx.doi.org/10.3390/polym12061237.

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The skin plays an important role in protecting the human body, and wound healing must be set in motion immediately following injury or trauma to restore the normal structure and function of skin. The extracellular matrix component of the skin mainly consists of collagen, glycosaminoglycan (GAG), elastin and hyaluronic acid (HA). Recently, natural collagen, polysaccharide and their derivatives such as collagen, gelatin, alginate, chitosan and pectin have been selected as the matrix materials of bioink to construct a functional artificial skin due to their biocompatible and biodegradable properties by 3D bioprinting, which is a revolutionary technology with the potential to transform both research and medical therapeutics. In this review, we outline the current skin bioprinting technologies and the bioink components for skin bioprinting. We also summarize the bioink products practiced in research recently and current challenges to guide future research to develop in a promising direction. While there are challenges regarding currently available skin bioprinting, addressing these issues will facilitate the rapid advancement of 3D skin bioprinting and its ability to mimic the native anatomy and physiology of skin and surrounding tissues in the future.

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Keyes, Joseph T., Stacy M. Borowicz, Jacob H. Rader, Urs Utzinger, Mohamad Azhar, and Jonathan P. Vande Geest. "Design and Demonstration of a Microbiaxial Optomechanical Device for Multiscale Characterization of Soft Biological Tissues with Two-Photon Microscopy." Microscopy and Microanalysis 17, no. 2 (January 13, 2011): 167–75. http://dx.doi.org/10.1017/s1431927610094341.

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AbstractThe biomechanical response of tissues serves as a valuable marker in the prediction of disease and in understanding the related behavior of the body under various disease and age states. Alterations in the macroscopic biomechanical response of diseased tissues are well documented; however, a thorough understanding of the microstructural events that lead to these changes is poorly understood. In this article we introduce a novel microbiaxial optomechanical device that allows two-photon imaging techniques to be coupled with macromechanical stimulation in hydrated planar tissue specimens. This allows that the mechanical response of the microstructure can be quantified and related to the macroscopic response of the same tissue sample. This occurs without the need to fix tissue in strain states that could introduce a change in the microstructural configuration. We demonstrate the passive realignment of fibrous proteins under various types of loading, which demonstrates the ability of tissue microstructure to reinforce itself in periods of high stress. In addition, the collagen and elastin response of tissue during viscoelastic behavior is reported showing interstitial fluid movement and fiber realignment potentially responsible for the temporal behavior. We also demonstrate that nonhomogeneities in fiber strain exist over biaxial regions of assumed homogeneity.

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Drabek, Charles M., and Jennifer M. Burns. "Heart and aorta morphology of the deep-diving hooded seal (Cystophora cristata)." Canadian Journal of Zoology 80, no. 11 (November 1, 2002): 2030–36. http://dx.doi.org/10.1139/z02-181.

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An investigation of the heart morphology of 8 male and 15 female hooded seals (Cystophora cristata) revealed that the heart is proportionately large and the aortic bulb is larger than that reported for most seals. Hooded seals of all ages have large hearts (0.64% of the body mass) and the right ventricle is proportionately longer and more muscular than reported for other seals. The bulb of the ascending aorta shows the large-diameter characteristic of seals capable of making long deep dives, and is constricted to a diameter of less than one-third in the descending aorta. In addition, the ascending aorta has a much greater concentration of elastin fibers than does the descending aorta. In combination with the large right ventricle, these features probably serve to increase lung perfusion during the hooded seal's surface recovery, and to maintain a high blood pressure throughout the cardiac cycle during diving bradycardia. That there was no substantive difference in the heart morphology of pups, yearlings, and adults, suggests that these features are important in the development of diving behavior, and agrees with the rapid behavioral and physiological development of hooded seal neonates.

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Kovar, Jana, Karen E. Willet, Alison Hislop, and Peter D. Sly. "Impact of postnatal glucocorticoids on early lung development." Journal of Applied Physiology 98, no. 3 (March 2005): 881–88. http://dx.doi.org/10.1152/japplphysiol.00486.2004.

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Inhaled glucocorticoid treatment during the first 2 yr of life is controversial because this is a period of major structural remodeling of the lung. Rabbits received aerosolized budesonide (Bud; 250 μg/ml) or injected dexamethasone (Dex; 0.05 mg·ml−1·kg−1) between 1 and 5 wk of age. Treatment with Bud caused specific growth retardation of the lung. Dex but not Bud affected the mechanical properties of the lung parenchyma, when corrected for lung volume. Small peripheral airway walls in both glucocorticoid groups were thinner and had fewer alveolar attachment points with greater distance between attachments than controls, but collagen content was not affected by glucocorticoids. Dex led to reduced body weight, lung volume, alveolar number, and surface area. The alveolar size and number and elastin content, when related to lung volume, was not affected by Bud, suggesting normal structural development but inhibition of total growth. Arterial wall thickness and diameter were affected by Bud. This study demonstrates that developing lungs are sensitive to inhaled glucocorticoids. As such, the use of glucocorticoids in young infants and children should be monitored with caution and only the lowest doses that yield significant clinical improvement should be used.

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Hlaváček, Ivan. "Shape optimization of an elasto-perfectly plastic body." Applications of Mathematics 32, no. 5 (1987): 381–400. http://dx.doi.org/10.21136/am.1987.104269.

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Aysa, Noor Hadi. "Elastic Properties of Undegradable Nanocomposites at Human Body Temperature Using as Prosthetics." NeuroQuantology 18, no. 1 (January 30, 2020): 32–36. http://dx.doi.org/10.14704/nq.2020.18.1.nq20104.

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Nevado, Rosa M., Magda R. Hamczyk, Pilar Gonzalo, María Jesús Andrés-Manzano, and Vicente Andrés. "Premature Vascular Aging with Features of Plaque Vulnerability in an Atheroprone Mouse Model of Hutchinson–Gilford Progeria Syndrome with Ldlr Deficiency." Cells 9, no. 10 (October 8, 2020): 2252. http://dx.doi.org/10.3390/cells9102252.

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Hutchinson–Gilford progeria syndrome (HGPS) is among the most devastating of the laminopathies, rare genetic diseases caused by mutations in genes encoding nuclear lamina proteins. HGPS patients age prematurely and die in adolescence, typically of atherosclerosis-associated complications. The mechanisms of HGPS-related atherosclerosis are not fully understood due to the scarcity of patient-derived samples and the availability of only one atheroprone mouse model of the disease. Here, we generated a new atherosusceptible model of HGPS by crossing progeroid LmnaG609G/G609G mice, which carry a disease-causing mutation in the Lmna gene, with Ldlr−/− mice, a commonly used preclinical atherosclerosis model. Ldlr−/−LmnaG609G/G609G mice aged prematurely and had reduced body weight and survival. Compared with control mice, Ldlr−/−LmnaG609G/G609G mouse aortas showed a higher atherosclerosis burden and structural abnormalities typical of HGPS patients, including vascular smooth muscle cell depletion in the media, adventitial thickening, and elastin structure alterations. Atheromas of Ldlr−/−LmnaG609G/G609G mice had features of unstable plaques, including the presence of erythrocytes and iron deposits and reduced smooth muscle cell and collagen content. Ldlr−/−LmnaG609G/G609G mice faithfully recapitulate vascular features found in patients and thus provide a new tool for studying the mechanisms of HGPS-related atherosclerosis and for testing therapies.

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