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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to investigate the healing process and the nature of the repaired tissue of injured articular cartilage. Full-thickness defects were made in the articular cartilage of the femoral condyles of 48 immature rats, and were examined by using light and transmission electron microscopes from one to 48 weeks after the injury. Under the light microscope, toluidine blue metachromasia was demonstrated in the deep matrix at 4 weeks after the injury. The repaired tissue was similar to the articular cartilage in controls at 12 weeks after the injury, but decreased number of cells and irregular surface were recognized in the specimen taken at 48 weeks after the injury. By electron microscopic examinations, at 12 weeks after the injury, cells in the repaired tissue were indistinguishable from chondrocytes, and the tidemark showed a fine structure similar to that in the articular cartilage in controls where many electron dense particles were observed. Collagen fibrils in the superficial layer were arranged in parallel to the articular surface. Three dimensional meshwork of collagen fibrils was also recognized in the intermediate and deep layers, but was inferior to that in the articular cartilage in controls. At 48 weeks after the injury, the surviving cells in the repaired tissue contained deposits of glycogen, large lipid droplets and vacuoles. Amianthoid change and fibrous long-spaced collagen were occasionally observed in the matrix. Collagen fibrils in the areas with poor cell population were smaller in diameter and loosely arranged. The above findings indicate that the anomalous arrangement of collagen fibrils is a main cause for the weakness of the repaired tissue to the mechanical load, resulting the degeneration.
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PMID:[Ultrastructural studies of healing process of injured articular cartilage]. 685 11

The pathogenesis of aneurysms formation and rupture is not clearly understood and is undoubtedly a multifactorial event. It is generally accepted that the aneurysm arises from an interaction between structural weakness of arterial wall and hemodynamic factors. Previous studies suggested the possible role of collagenolytic and elastolytic activities in aneurysm development, leading to extracellular matrix alteration. The content of collagen 3-hydroxypiridinium cross-links and elastase and collagenase activities were measured in 12 samples of intracranial aneurysms and in control specimens obtained from temporal superficial arteries and from autoptic samples of Willis Circle. Collagen content is significantly lower in aneurysm than in autoptic control samples (p < 0.01). The total amount of cross-links is significantly lower in ruptured aneurysms than in unruptured and autoptic controls (p < 0.01). Collagenase and elastase activities are significantly increased in ruptured cerebral aneurysms versus unruptured aneurysms (p < 0.01). Linear regression shows that an inverse relationship exists between cross-links content and both elastolytic (p = 0.0032) and collagenolytic (p < 0.001) activities in aneurysmal samples. Multiple regression shows that collagenase has a more important statistic impact (p = 0.027) than elastase (p = 0.08). The results of the study supports the hypothesis that an imbalance of protease-antiprotease homeostasis with elevated collagenolytic and elastolytic activities may represent the predisposing condition leading to aneurysms rupture through collagen depauperation and reduced cross-linkage of collagen fibres.
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PMID:Collagen cross-linkage, elastolytic and collagenolytic activities in cerebral aneurysms: a preliminary investigation. 969 37

Myogenic satellite cells are essential for postnatal muscle growth and the regeneration of muscle in response to injury. An understanding of how the extracellular matrix affects satellite cell activity, and the temporal and spatial expression of extracellular matrix macromolecules is largely unknown. In the avian genetic muscle weakness, low score normal (LSN), satellite cell proliferation and differentiation rates are significantly lower than that observed in normal chicken satellite cells, which may be attributed to a late embryonic increase in the expression of decorin. Satellite cell-derived morphological properties, collagen type I expression, and the spatial distribution of collagen type I were investigated during normal and LSN satellite cell proliferation and differentiation. These studies showed a decrease in LSN myotube length and the number of nuclei per myotube. Collagen type I expression was similar between the LSN and normal satellite cell cultures during the course of proliferation and differentiation. However, the spatial distribution of collagen type I was altered in the LSN cultures 48 h after the initiation of fusion. The LSN cultures exhibited a premature extracellular distribution of collagen type I compared to the normal satellite cells.
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PMID:Myotube morphology, and expression and distribution of collagen type I during normal and low score normal avian satellite cell myogenesis. 1022 11

Alkaptonuria is a rare disease of phenylalanine, aromatic amino acids, and tyrosine metabolism. Because of a genetic deficiency of the enzyme homogentisic acid oxidase, an accumulation of homogentisic acid causes ochronotic pigment deposition. The most common clinical manifestations are arthropathy, urinary calculi and discoloration, cutaneous and cartilaginous pigmentation, and cardiac valvular disease. Arthropathy and aortic stenosis are the most debilitating manifestations of the disease. A case of alkaptonuric aortic stenosis is described. A 75-year-old woman with a history of alkaptonuria presented in the emergency department with complaints of progressive dyspnea. Upon examination, the patient was hypertensive, tachypneic, and tachycardic with premature ventricular contractions. She had pitting edema of the lower extremities and complaints of generalized weakness. Chest x-rays revealed congestive heart failure and pulmonary edema. Diuretics were administered, and a continuous nitroglycerin infusion was initiated in the emergency department. The patient was admitted for further evaluation. The patient's respiratory status continued to decline. She was intubated endotracheally 1 day after admission. Subsequent cardiac evaluation revealed an ejection fraction of 35%, severe aortic stenosis, mild coronary artery disease, ischemic cardiomyopathy, and anteroapical akinesis. A dobutamine infusion was instituted for persistent hypotension, and renal dose dopamine was initiated for oliguric renal failure. The patient underwent an emergency operation for an aortic valve replacement with a Dacron patch 10 days after admission. Cardiopulmonary bypass and mild hypothermia were used during the procedure. The patient's hemodynamic status remained tenuous throughout the procedure. Although the first attempt to wean off cardiopulmonary bypass failed, the second attempt was successful with the aid of an intra-aortic balloon pump, inotropic support, and atrioventricular pacing. These measures were maintained during transport to the surgical intensive care unit. In the intensive care unit, the patient did not have an audible blood pressure or a palpable pulse without the support of the intra-aortic balloon pump and atrioventricular pacing. Coarse atrial fibrillation was the underlying electrocardiogram rhythm in the absence of atrioventricular pacing. Sodium bicarbonate was given without improvement. After discussion with the family, all life support measures were discontinued. The patient died 10 minutes after her arrival in the intensive care unit. Alkaptonuria's pathogenesis is manifested as both local and systemic in nature. Collagen vascular diseases share a similar pattern of multisystem involvement. Despite the negative outcome for the patient described, valuable insight can be obtained by studying this case and noting the anesthetic considerations specific to collagen vascular diseases in general.
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PMID:Alkaptonuric aortic stenosis: a case report. 1048 88

Adolescent meat-type poultry and cage layers exhibit a high incidence of bone problems that include bone weakness, deformity, breakage, and infection and osteoporosis-related mortalities. These problems include economic and welfare issues. To improve bone quality in poultry, it is essential to understand the physiological basis of bone maturity and strength in poultry. A complex array of factors that include structural, architectural, compositional, physiological, and nutritional factors interactively determine bone quality and strength. Bone is approximately 70% mineral, 20% organic, and 10% water. Collagen is the major organic matrix that confers tensile strength to the bone, whereas hydroxyapatite provides compressional strength. In recent years, the roles of different collagen crosslinks have been shown to be important in the increase of bone mechanical strength. Similarly, age-related glyco-oxidative modifications of collagen have been shown to increase the stiffness of collagen. These posttranslational modifications of matrix can affect bone quality as it would be affected by the changes in the mineralization process. Our studies show that the growth in the tibia continued until 25 wk of age, which correlated with the increase in the content of hydroxylysylpridinoline (HP) and lysylpyridinoline (LP), the collagen crosslinks. The tibia from 5-wk-old chicks were strong but brittle because of low collagen crosslinks and high mineral content. Bone maturity may relate to its crosslink content. Compared to crosslink content, bone density and ash content showed moderate increases during growth. The bones from younger turkeys were more susceptible to corticosteroid-induced stunting of growth, which also resulted in decreased bone strength. This review discusses how different factors can compromise bone strength by reducing growth, altering shape, affecting mineralization, and affecting collagen crosslinking.
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PMID:Factors regulating bone maturity and strength in poultry. 1090 Dec 6

The relationship between ageing and nutrition is considered with collagen as the intermediate target. Some data showed that diet restriction resulted in decreased collagen accumulation and collagen ageing. Conversely, being overweight reduced the lifespan and increased collagen ageing. Collagen ageing, which includes low turnover and glycoxidation, involves an increase in both stiffness and weakness. Their consequences concern all tissues including those with vital importance such as cartilage, heart ventricle or arterial wall.
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PMID:Collagen, ageing and nutrition. 1506 73

Ullrich's congenital muscular dystrophy (UCMD) is an autosomal recessive myopathy characterised by neonatal muscle weakness, proximal joint contractures and distal hyperlaxity. Mutations in the COL6A1, COL6A2 (21 q22.3) and COL6A3 (2 q37) genes, encoding the alpha 1, alpha 2 and alpha 3 chains of collagen VI, respectively, have been recently identified as responsible for UCMD in a total of 9 families. We investigated in detail the clinical and morphological phenotype of 15 UCMD patients from 11 consanguineous families showing potential linkage either to 21 q22.3 (6 families) or to 2 q37 (5 families). Collagen VI deficiency was confirmed on muscle biopsies or skin fibroblasts in 8 families. Although all patients shared a common phenotype, a great variability in severity was observed. Collagen VI deficiency in muscle or cultured fibroblasts was complete in the severe cases and partial in the milder ones, which suggests a correlation between the degree of collagen VI deficiency and the clinical severity in UCMD. No significant phenotypical differences were found between the families linked to each of the 2 loci, which confirms UCMD as a unique entity with underlying genetic heterogeneity.
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PMID:Collagen VI status and clinical severity in Ullrich congenital muscular dystrophy: phenotype analysis of 11 families linked to the COL6 loci. 1512 9

Mutations in the three collagen VI genes COL6A1, COL6A2 and COL6A3 cause Bethlem myopathy and Ullrich congenital muscular dystrophy (UCMD). UCMD, a severe disorder characterized by congenital muscle weakness, proximal joint contractures and marked distal joint hyperextensibility, has been considered a recessive condition, and homozygous or compound heterozygous mutations have been defined in COL6A2 and COL6A3. In contrast, the milder disorder Bethlem myopathy shows clear dominant inheritance and is caused by heterozygous mutations in COL6A1, COL6A2 and COL6A3. This model, where dominant mutations cause mild Bethlem myopathy and recessive mutations cause severe UCMD was recently challenged when a patient with UCMD was shown to have a heterozygous in-frame deletion in COL6A1. We have studied five patients with a clinical diagnosis of UCMD. Three patients had heterozygous in-frame deletions in the N-terminal region of the triple helical domain, one in the alpha1(VI) chain, one in alpha2(VI) and one in alpha3(VI). Collagen VI protein biosynthesis and assembly studies showed that these mutations act in a dominant negative fashion and result in severe collagen VI matrix deficiencies. One patient had recessive amino acid changes in the C2 subdomain of alpha2(VI), which prevented collagen VI assembly. No collagen VI mutations were found in the fifth patient. These data demonstrate that rather than being a rare cause of UCMD, dominant mutations are common in UCMD, now accounting for four of the 14 published cases. Mutation detection in this disorder remains critical for accurate genetic counseling of patients and their families.
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PMID:Dominant collagen VI mutations are a common cause of Ullrich congenital muscular dystrophy. 1556 6

In ascending aorta aneurysms, there is an enlargement of the whole vessel, whereas aortic dissections (ADs) are characterized by the cleavage of the wall into 2 sheets at the external half. We searched if alterations in collagen could be related to these diseases. Sections of aortas from 14 case patients with acute dissections, 10 case patients with aneurysms, and 9 control subjects were stained with picrosirius. Slides were analyzed under polarized microscopy to evaluate the structure of collagen fibers. The proportion of collagen was calculated in each half of the medial layer by color detection in a computerized image analysis system. Collagen appearance under polarized light was consistent with collagenolysis. The mean collagen proportions at the inner and outer halves, respectively, were 0.50 +/- 0.13 and 0.40 +/- 0.08 in the control group, 0.20 +/- 0.10 and 0.18 +/- 0.12 in the AD group, and 0.33 +/- 0.12 and 0.19 +/- 0.12 in the aneurysm group. The AD (P < .01) and control (P = .04) groups had less collagen at the external half; no difference was found in the aneurysm group (P = .71). In both halves, there was less collagen in the case patients than in the control subjects (all P < .01), but at the internal half, the decrease was significantly greater in the case patients with aneurysms than in those with dissections (P = .03; at the external half, P = .99). Aortic dissections and aneurysms show a decrease in collagen content that could be related to a weakness of the wall underlying the diseases, but the locations of the decrease differ: in dissections, it is situated mostly at the external portion of the media (site of cleavage), whereas in aneurysms, it is more diffuse, consistent with the global enlargement.
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PMID:Collagen is reduced and disrupted in human aneurysms and dissections of ascending aorta. 1826 28

Collagen gel scaffolds can potentially be utilized as cell seeded systems for skin tissue engineering. However, its dramatic contraction after being mixed with cells and its mechanical weakness are the drawbacks for its application to skin engineering. In this study, a compressed collagen gel scaffold was fabricated through the rapid expulsion of liquid from reconstituted gels by the application of 'plastic compression'(PC) technique. Both compressed and uncompressed gels were characterized with their gel contraction rate, morphology, the viability of seeded cells, their mechanical properties and the feasibility as a scaffold for constructing tissue-engineered skin. The results showed that the compression could significantly reduce the contraction of the collagen gel and improve its mechanical property. In addition, seeded dermal fibroblasts survived well in the compressed gel and seeded epidermal cells gradually developed into a stratified epidermal layer, and thus formed tissue engineered skin. This study reveals the potential of using compressed collagen gel as a scaffold for skin engineering.
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PMID:Compressed collagen gel as the scaffold for skin engineering. 2030 Aug 56


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