Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Echocardiographic image texture has been demonstrated to reflect the physical properties of the tissue under examination. To evaluate the role of collagen in determining the echo pattern of the left ventricular wall, we studied nine hypertensive patients with left ventricular hypertrophy (left ventricular mass index > 125 gm/m2) and biopsy-proven different degrees of myocardial fibrosis by analyzing the echocardiographic examinations performed before the biopsy. Myocardial tissue was sampled under fluoroscopy and two-dimensional echo guidance in the interventricular septum. Collagen volume fraction (CVF; normal range up to 2%) was taken as an index of fibrosis. The echo patterns were assessed by analyzing standard two-dimensional parasternal long-axis echocardiograms recorded on videotape. Images were color-coded at 256 levels (0 = yellow, 256 = black) and digitized off-line onto a personal computer. The region of analysis was set using a selection tool (20 x 10 mm) in the general area of septum where the specimen was taken. For each selection a color-level histogram, representing the frequency distribution, was derived with estimates of the average pixel intensity (mCS), skewness (SK), kurtosis (K), and the broad band (Bb) of the echoes about the distribution. Echo-derived parameters in each patient were compared with corresponding CVF values. CVF was out of range in all patients, ranging from 2.6% to 7.6% (mean 4.3% +/- 1.6%). No correlation was found between CVF and mCS, whereas a significant correlation was found at end diastole between CVF and the parameters describing histogram morphology, respectively, SK (r = 0.73), K (r = 0.69), Bb (r = 0.72). These findings for the first time demonstrate in vivo in hypertensive patients with left ventricular hypertrophy an agreement between echo amplitude and histologically assessed collagen volume. Thus in our studied patients collagen content appears to be the major determinant of regional echo intensity, its increase resulting in a significant and progressive wider asymmetrical left shift (yellow) of the color histogram.
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PMID:Echocardiographic patterns of myocardial fibrosis in hypertensive patients: endomyocardial biopsy versus ultrasonic tissue characterization. 928 55

Rat serum mannose-binding protein (MBP-A) functions as part of the innate immune system by targetting complement toward potentially pathogenic microorganisms. In order to examine the molecular basis for complement activation, rat MBP-A has been overproduced in Chinese hamster ovary cells. Recombinant protein is post-translationally modified in the same way as the native lectin. Hydrodynamic studies indicate that MBP-A consists predominantly of covalent oligomers containing one to four copies of a subunit that comprises a trimer of polypeptides. These oligomers are non-interconverting and do not assemble into higher order structures at concentrations in excess of those normally found in serum. Disulfide bonds formed between cysteine residues at the N-terminal end of the collagen-like domain link polypeptides to form covalent oligomers. Analysis of wild-type MBP-A and MBP-A containing the substitution Cys6 --> Ser suggests that polypeptides within each trimeric structural unit are mostly linked by disulfide bonds between cysteine residues at positions 13 and 18 arranged in an asymmetrical configuration. Disulfide bonds involving Cys6 connect polypeptides within separate trimers. Analysis of chimeras between MBP-A and rat liver MBP (MBP-C) indicates that residues within the N-terminal region of the collagenous domain and the cysteine-rich domain of MBP-A enable assembly of trimers into higher order oligomers. The activity of MBP-A in a hemolytic complement fixation assay using mannan-coated sheep erythrocytes was approximately 20-fold greater than the activity of MBP-C. Analysis of the MBP chimeras and isolated oligomers of MBP-A reveals that the larger oligomers are more efficient at complement activation. These data indicate that the overall complement fixing activity of MBP-A is a function of the individual molecular activities of oligomers and their relative abundance within the serum.
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PMID:Molecular determinants of oligomer formation and complement fixation in mannose-binding proteins. 992 Sep 5

Wrinkles are a major topic in dermocosmetology; the purpose of this work has been to go deeper into the knowledge of cutaneous damage underlying these modifications of skin surface. Up to now, the number of published works about the histological structure of wrinkles is not very large. Therefore to complete the findings, we studied 46 subjects of both sexes, between 57 and 98-year-old, enabling us to obtain 157 skin biopsies of wrinkles (face) and sun-protected areas (abdomen). We used different histological techniques involving histochemistry, immunohistochemistry, electron microscopy and quantification by image analysis in addition to classic standard techniques. This study has allowed us to confirm published structural modifications of wrinkles, but also to display many other original alterations. The increased thinning of the epidermis atrophied with age is confirmed by the study of desmoplakins outlining the cellular contours of keratinocytes. Such a thinning is accompanied by a decrease in several markers of epidermal differentiation at the bottom of the wrinkles: filaggrin, keratohyalin granules and transglutaminase I, disturbing desquamation and the capacity of the horny layer to retain water. The dermoepidermal junction is modified by a decrease of collagen IV and VII, which, combined with fewer and fewer oxytalan fibres under wrinkles, weakens this interface. The deposition of abnormal elastotic tissue in the dermis, with an interruption of these deposits under wrinkles and an atrophy of dermal collagen more pronounced under wrinkles, boosts the magnitude and depth of wrinkles. The composition of the other dermal constituents is also altered with, more particularly, a marked decrease of chondroitin sulphates in the papillary dermis under wrinkles, combined with an asymmetrical variation of glycosaminoglycans on both edges of wrinkles. The atrophy of the hypodermis, also more marked under wrinkles, with a thickening of fibrous lines, also makes the depth of wrinkles more pronounced. Wrinkle formation appears at the same time as numerous modifications in different cutaneous structures, which may be mutually amplified. Such a study by pointing out altered elements in skin physiology, makes the development of specific treatments possible in order to mitigate this unwelcome cutaneous deterioration.
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PMID:A histological study of human wrinkle structures: comparison between sun-exposed areas of the face, with or without wrinkles, and sun-protected areas. 1035 68

HLA-B27 is highly linked with a group of human diseases called spondyloarthropathies (SpA). Many of these disorders begin after an infection with an enterobacteria. The symptoms seen in patients with spondyloarthropathies are inflammatory pain in the spine and asymmetrical arthritis of lower limbs. Additional symptoms related to SpA include inflammation in the eyes, bowel, and skin. The autoantigen(s) in SpA are not known. Proteins such as collagen and proteoglycans have been thought to be potent autoantigens in arthritidis including B27-associated human diseases. Type II collagen is a common denominator among eyes and joints, affected tissues in B27-linked diseases. Moreover, a few reports indicated CII specific T cells and antibodies in patients with spondyloarthropathies. We and others have previously described development of spontaneous arthritis and nail disease in HLA-B27 transgenic animals. To determine whether CII may be a target antigen in the B27-linked diseases, B27 + m beta 2 m% (HLA-B27) transgenic mice lacking mouse beta 2m with and without human beta 2m) mice were immunized with type II collagen inside the barrier facility. Male HLA-B27 transgenic mice developed collagen-induced arthritis compared to transgene negative littermates or female counterparts. There was no difference in the incidence of arthritis in HLA-B27 transgenic mice with and without human beta 2m. Our data suggest that beta 2m free heavy chain of HLA-B27 may present soluble antigens such as type II collagen to trigger specific T cells contributing in the development of arthritis. Our data also suggest that CII may be a potential target antigen in the cartilage during the disease process.
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PMID:HLA-B27 transgenic mice are susceptible to collagen-induced arthritis: type II collagen as a potential target in human disease. 1071 6

Pulsed magnetic field (PMF) stimulation was applied to mammalian neurons in vitro to influence axonal growth and to determine whether induced current would direct and enhance neurite growth in the direction of the current. Two coils were constructed from individual sheets of copper folded into a square coil. Each coil was placed in a separate water-jacketed incubator. One was energized by a waveform generator driving a power amplifier, the other was not energized. Whole dorsal root ganglia (DRG) explant cultures from 15-day Sprague-Dawley rat embryos were established in supplemented media plus nerve growth factor (NGF) at concentrations of 0-100 ng/mL on a collagen-laminin substrate. Dishes were placed at the center of the top and bottom of both coils, so that the DRG were adjacent to the current flowing in the coil. After an initial 12 h allowing DRG attachment to the substrate floor, one coil was energized for 18 h, followed by a postexposure period of 18 h. Total incubation time was 48 h for all DRG cultures. At termination, DRG were histochemically stained for visualization and quantitative analysis of neurite outgrowth. Direction and length of neurite outgrowth were recorded with respect to direction of the current. PMF exposed DRG exhibited asymmetrical growth parallel to the current direction with concomitant enhancement of neurite length. DRG cultures not PMF exposed had a characteristic radial pattern of neurite outgrowth. These results suggest that PMF may offer a noninvasive mechanism to direct and promote nerve regeneration.
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PMID:Directed and enhanced neurite growth with pulsed magnetic field stimulation. 1079 56

The dental basement membrane (BM) putatively mediates epithelial-mesenchymal interactions during tooth morphogenesis and cytodifferentiation. Type IV collagen alpha chains, a major network-forming protein of the dental BM, was studied and results disclosed distinct expression patterns at different stages of mouse molar germ development. At the dental placode and bud stage, the BM of the oral epithelium expressed alpha 1, alpha 2, alpha 5 and alpha 6 chains while the gubernaculum dentis, in addition to the above four chains, also expressed a 4 chain. An asymmetrical expression for alpha 4, alpha 5 and alpha 6 chains was observed at the bud stage. At the early bell stage, the BM associated with the inner enamel epithelium (IEE) of molar germ expressed alpha 1, alpha 2 and alpha 4 chains while the BM of the outer enamel epithelium (OEE) expressed only alpha 1 and a 2 chains. With the onset of dentinogenesis, the collagen a chain profile of the IEE BM gradually disappeared. Howeverfrom the early to late bell stage, the gubernaculum dentis consistently expressed alpha 1, alpha 2, alpha 5 and a 6 chains resembling fetal oral mucosa. These findings suggest that stage- and position-specific distribution of type IV collagen alpha subunits occur during molar germ development and that these changes are essential for molar morphogenesis and cytodifferentiation.
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PMID:Localization of type IV collagen a 1 to a 6 chains in basement membrane during mouse molar germ development. 1173 42

We describe the arrangement of white muscle fibers and tendinous myoseptal structures and the relation of these structures to each other in order to provide an anatomical framework for discussions and experimental research on fish swimming mechanics. For the three major craniate groups, the petromyzontids, myxinids and gnathostomes, we identify three conditions that differ remarkably. Myxinids are characterized by asymmetrical myosepta with long cones. Within a single myoseptum these are connected by collagenous fibers that are almost oriented longitudinally. Distinct tendons are absent in myxinid myosepta. Petromyzontid myosepta lack cones and distinct myoseptal tendons, whereas gnathostomes bear cones and distinct tendinous structures: the lateral band, epineural (epipleural) tendon and myhabdoid tendon. Myoseptal fibers of petromyzontids and myoseptal tendons of gnathostome myosepta are firmly anchored in the skin. Myxinids lack firm myoseptal-skin-connections. Their muscular arrangement is neither comparable to that of petromyzontids nor to that of gnathostomes. The latter two bear archlike arrangements of muscle fibers spanning several segments that are hypothesized to play a role during bending. In gnathostomes, archlike helical muscle fiber arrangements (HMFAs) are present that span the length of several body segments and are multiply intersected by myosepta. Hence, a series of tendinous lateral bands of myosepta is embedded in HMFAs. The posterodorsally oriented HMFAs are underlain by posteroventrally oriented crossing muscle fibers (CMFs). Bending may be generated by contraction of the muscle fibers belonging to an HMFA and the simultaneous counteraction of CMFs. Moving caudally, this anterior muscle fiber arrangement gradually changes, eventually becoming the posterior muscle fiber arrangement. This pattern suggests that the function of the myomeres will also change. Three additional putative roles of myoseptal tendons can be deduced from their relations to white muscle fibers in gnathostomes (and in part in petromyzontids): (1) Posterior transmission of anteriorly generated muscular forces via lateral bands and/or myorhabdoid tendons. These tendons are more robust posteriorly. Anterior and posterior cones appear to play an important role in force transmission. (2) Pulling on collagen fibers of the skin via lateral bands and myorhabdoid tendons, suggesting a transmission of muscular forces that puts the skin into tension. (3) Resisting radial expansion of contracting muscle fibers by epineural (epipleural) tendons. By the latter two mechanisms modulation of body stiffness is likely to be achieved.
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PMID:Spatial arrangement of white muscle fibers and myoseptal tendons in fishes. 1248 90

The body of a Japanese flounder (Paralichthys olivaceus) changes from a symmetrical to an asymmetrical form during metamorphosis. To obtain detailed information on the mechanisms of the migration of the right eye to the left side, soft and hard tissues in the head of larval flounders were examined using transmission electron microscopy (TEM). Retrorbital vesicles (Rvs) are pairs of sac-like structures under the eyes. It has been suggested that the asymmetrical development of Rvs, with the right (blind) one being bigger than the left, is the driving force behind eye migration. The present study revealed that the ultrastructure of the Rv sheath is quite similar to that of a lymphatic capillary. Thus, it is possible that the Rv is a part of the lymph system, and is probably related to the secondary vascular system in teleosts. If we assume that the Rv sheath has a high permeability to liquid, similar to lymphatic capillaries, it is not plausible that the active expansion of the Rv pushes the eyeball. On the other hand, the pseudomesial bar (Pb) is a bone that is unique to flounders and is present only on the right (blind) side. At the beginning of eye migration, an aggregation of fibroblast-like cells is observed in the dermis under the right eye, where the Pb will subsequently be formed. These cells have a well-developed rough endoplasmic reticulum (rER) and mitochondria, and are probably responsible for formation of the thick layers of collagen fibrils around them. Since it is unlikely that the active expansion of the Rv causes eye migration, the role played by the Pb and its rudiment becomes more significant in right eye migration in the Japanese flounder becomes more significant.
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PMID:Fine structure of soft and hard tissues involved in eye migration in metamorphosing Japanese flounder (Paralichthys olivaceus). 1280 50

Hypertrophic cardiomyopathy is an autosomal dominant disease characterized by asymmetrical left ventricular hypertrophy, myocyte disarray, interstitial fibrosis, and small vessel disease. More than 100 mutations in 10 genes, all encoding for sarcomeric proteins, have been identified as responsible for this disease. While the etiology of hypertrophic cardiomyopathy has been extensively elucidated, its pathogenesis is not completely understood. Mutated proteins are incorporated in the sarcomere and impair myocyte contractility. This probably triggers the compensatory local release of trophic factors, which influence the development of the typical anatomical features of the disease. Modifying genes or the effect of environmental or local factors is likely to play a role. Interstitial fibrosis is a morphological characteristic of hypertrophic cardiomyopathy and, increasing chamber stiffness, is an important determinant of diastolic dysfunction. Studies on transgenic animals with hypertrophic cardiomyopathy emphasize the role of interstitial fibrosis in this disease. Recently our group has shown that collagen turnover, evaluated through serum markers of collagen metabolism, is more active in patients with hypertrophic cardiomyopathy than in normal subjects and that patients with passive diastolic dysfunction accumulate collagen I. These studies are potentially relevant as they allow to assess the effects of therapy with cardioreparatory drugs.
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PMID:[Myocardial interstitial fibrosis and diastolic dysfunction in hypertrophic cardiomyopathy]. 1465 60

The study of cystic cavities and collagen fibers fragmentation is useful to for a better knowledge of pathogenesis and surgical therapy of medial ascending aortic degeneration. Thus, the aim of this study was to describe by scanning electron microscopy the surfaces and shape of the cysts, measure their area, and identify microcystic spaces related to this degenerative disease. Scanning electron microscopy analysis was performed in 16 out of 36 patients who underwent surgery for ascending aorta dilatation with associated aortic valve disease. The aortic medial wall showed a cribrose appearance at low magnification (x50-100) and the intima was effuse. At high magnification (x500-2000), small cavities (clefts) lined by normal or fragmented elastic fibers and large cavities (pseudocystes) with anfractuous borders lined by fragmented elastic fibers and smooth muscle cells were observed. Furthermore, in the outer media wall microvessels lined by endothelium were also observed. These changes were lacking or less pronounced in normal aorta. SEM allows one to better identify the pathological cavities and to differentiate them from microvessels. These pathological cavities are more numerous and larger in the convexity than in the concavity of the aorta in according to our previous morphological and morphometric findings in asymmetrical aorta dilatation.
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PMID:Scanning electron microscopy of aortic medial changes in aortic ascending dilatation. 1547 26


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