Extralobar lung sequestration and hyaline membrane in the newborn: anatomo-pathologic findings and implications in the etiology of hyaline membrane disease.
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Autopsy↗
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[Letter: Hyaline membrane disease. Hyaline membrane and neonatal respiratory pathology].
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Complement System Proteins↗
The lipid and glycogen content of rabbit articular hyaline and non-articular hyaline cartilage.
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Journal Article↗
[Sclerosing hyaline necrosis of the liver, cytolytic hepatosis in chronic alcoholism: its cirrhoeg C/*339-53* A/Bertrand L, Pages A, Michel H: [Sclerosing hyaline necrosis of the liver, cytolytic hepatosis in chronic alcoholism: its cirrhogenic development].
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Adult↗
On the ultrastructure of hyalin, a cell adhesion protein of the sea urchin embryo extracellular matrix.
Hyalin is a large (ca. 350 x 10(3) kD by gel electrophoresis) molecule that contributes to the hyalin layer surrounding the sea urchin embryo. In previous work a mAb (McA Tg-HYL), specific for hyalin, was found to inhibit cell-hyalin adhesion and block morphogenesis of whole embryos (Adelson, D. L., and T. D. Humphreys. 1988. Development. 104:391-402). In this report, hyalin ultrastructure was examined via rotary shadowing. Hyalin appeared to be a filamentous molecule approximately 75-nm long with a globular "head" about 12 nm in diameter that tended to form aggregates by associating head to head. Hyalin molecules tended to associate with a distinct high molecular weight globular particle ("core"). In fractions containing the core particle often more than one hyalin molecule were seen to be associated with the core. The core particle maintained a tenacious association with hyalin throughout purification procedures. The site(s) of McA Tg-HYL binding to the hyalin molecule were visualized by decorating purified hyalin with the antibody and then rotary shadowing the complex. In these experiments, McA Tg-HYL attached to the hyalin filament near the head region in a pattern suggesting that more than one antibody binding site exists on the hyalin filament. From the ultrastructural data and from the cell adhesion data presented earlier we conclude that hyalin is a filamentous molecule that binds to other hyalin molecules and contains multiple cell binding sites. Attempts were made to demonstrate the existence of lower molecular weight hyalin precursors. Whilst no such precursors could be identified by immunoprecipitation of in vivo labeled embryo lysates, immunoprecipitation of in vitro translation products suggested such precursors (ca 40 x 10(3) kD) might exist.
Animals↗
Ultrastructure of hyaline, border, and vacuole cells in chick inner ear.
The sense organ for hearing in birds, the basilar papilla, is capable of replacing lost or damaged hair cells and supporting cells through regeneration. Potential candidates for precursor-cell populations include cells within the auditory receptor epithelium and nonsensory cells inferior to the sensory epithelium. Ultrastructural characteristics of hyaline cells, border cells, and vacuole cells, nonsensory cells which border or lie inferior to the receptor epithelium proper, were studied with transmission electron microscopy. Data were obtained from normal neonatal and adult chickens. Several rows of epithelial cells separate hyaline cells from inferiorly located organ supporting cells and hair cells. Ultrastructural characteristics and location of these epithelial cells differentiate them from organ supporting cells and hyaline cells; consequently, we have termed them "border cells." Synaptic specializations are observed between neural elements and border cells, and gap junctions are found between adjacent border cells, between border cells and neighboring organ supporting cells, and between juxtaposed border and hyaline cells. Hyaline cells, in contrast to border cells, are highly specialized. Dense bundles of filaments are present in hyaline cells from the basal one-half of the papilla, and an unusual structure, a rough tubular aggregate, is present in hyaline-cell cytoplasm. Pre- and postsynaptic specializations are observed between neural elements and hyaline cells, and gap-junctional complexes link neighboring hyaline cells. Vacuole cells lie inferior to the hyaline cells and rest on the inferior fibrocartilaginous plate. They are unspecialized morphologically. Their only remarkable morphological feature is the abundance of spherical vacuoles within their cytoplasmic matrix.
Animals↗
Hyaline droplet accumulation in rodent kidney proximal tubules: an association with histiocytic sarcoma.
Since recognition during the last decade that certain renal carcinogens can initially cause an accumulation of hyaline (protein) droplets in proximal tubules of male rats, it has become appropriate to establish whether this phenomenon of protein overload can also occur in rodent kidneys unrelated to chemical treatment. Kidney tissue from a number of selected rodent studies held in the National Toxicology Program (NTP) or Food and Drug Administration (FDA) archives were evaluated for hyaline droplet accumulation in proximal tubules. The survey concentrated on rats and mice of both sexes bearing hematopoietic tumors, as our preliminary observations had suggested this direction of study. The tissues of 101 Sprague-Dawley, 25 Osborne-Mendel, and 70 Fischer 344 rats and 96 B6C3F1 mice were examined. These animals provided an assortment of tumors including histiocytic sarcoma, lymphocytic lymphoma, mononuclear cell leukemia, and sarcoma. Hyaline droplet accumulation, primarily involving the P2 segment of proximal tubules, was diagnosed in 96% of rats with histiocytic sarcoma (74/77 cases in Sprague-Dawley, 17/18 in Osborne-Mendels, 7/7 in Fischers) and in 55% of B6C3F1 mice with histiocytic sarcoma (18/33 cases). There appeared to be a qualitative correlation between hyaline droplet accumulation and degree of tumor burden. Thus, in cases negative for hyaline droplets, the tumor was often confined to a single location, while increasing involvement of proximal segments beyond P2 occurred with more extensive multi-organ dissemination of the tumor. By immunohistochemistry on 11 cases of rat and 8 cases of mouse histiocytic sarcoma, the protein in hyaline droplets was identified as lysozyme, a known major secretory product of monocytes and macrophages. The hyaline droplets were negative for alpha 1-antitrypsin, alpha 2u-globulin, rat or mouse immunoglobulin, and albumin. More sparsely scattered droplets and granules present in proximal tubules of Fischer rats with mononuclear cell leukemia were negative for lysozyme but positive for either iron or lipofuscin pigment. The study establishes a clear association between renal tubule hyaline droplet and lysozyme accumulation in rats and mice with histiocytic sarcoma. Hyaline droplets secondary to neoplasia should be distinguished from chemically-induced hyaline droplet nephropathy in the male rat involving alpha 2u-globulin.
Animals↗
Lymph node hyalinization in elderly Japanese.
Lymph node hyalinization has been comprehensively investigated using specimens obtained from elderly Japanese and white Americans. Onion-peel lesions and associated meshwork areas were often found in the medullary sinus of the thoracic node (mediastinal-type hyalinization), while eosinophilic, glassy and spotty lesions were consistently seen in B lymphocyte areas of the pelvic node (pelvic-type hyalinization). The mediastinal-type hyalinization was comprised of thin collagen fibrils (ca 50 nm in diameter), whereas the pelvic-type hyalinization had thick fibrils (ca 150 nm in diameter). This difference seemed to be consistent with a difference in composite collagen fibrils of vascular walls between the thoracic and pelvic regions. The pelvic-type hyalinization was often or sometimes seen in other nodes, such as cervical, axillary, abdominal and inguinal nodes, especially in white Americans. The mediastinal-type hyalinization, usually in combination with a sinus filled with anthracotic macrophages, tended to be observed in Japanese more frequently than in white Americans. Anthracosis seemed to be connected to the pathogenesis of the hyalinization. On the other hand, because the lesion was weakly positive for Factor VIII immunohistochemistry and because lesions were located along thin vessels, the pelvic-type hyalinization seemed to originate from vascular degeneration in the nodal cortex. Due to the high incidence and large proportion in total volume of the node, the hyalinization seems to be one of the major events that diminish the nodal filtration function and ruin the node with aging.
Aged↗
Cardiovascular risk factors and hyalinization of renal arterioles at autopsy. The Honolulu Heart Program.
Nephrosclerosis, commonly found in subjects with hypertension and diabetes, is marked by hyalinization of arterioles and fibroplasia of small arteries in the renal cortex. Cardiovascular risk factors that predicted subsequent hyalinization of renal arterioles at autopsy were identified, using data from the Honolulu Heart Program, a prospective epidemiological study of cardiovascular disease (CVD) in Japanese-American men. Among 8006 participants at baseline, 1381 died between 1965 and 1982; 285 of these had a protocol autopsy, and 150 had assessments of arteriolar hyalinization from renal tissue. Subjects were categorized into four groups on the basis of the number of hyalinized arterioles per square centimeter of renal tissue, and CVD risk factor levels and proportions were compared across these groups with the use of general linear models and logistic regression. Multivariate assessment using logistic regression demonstrated that diastolic blood pressure (DBP) and glucose level were positively associated and alcohol intake was negatively associated with an elevated degree of renal arteriolar hyalinization, independent of other CVD risk factors. The odds ratios for elevated hyalinization associated with a 10-mm Hg increase in DBP, a 20-mg/dL increase in glucose level, and a 30-mL/d increase in alcohol intake were 1.97 (95% confidence interval [CI] = 1.24-3.12), 1.23 (95% CI = 1.07-1.41), and 0.24 (95% CI = 0.11-0.55), respectively. Associations were similar when prevalent cases of CVD were excluded and when autopsy selection bias was taken into account. Renal arteriolar hyalinization was also more strongly associated with atherosclerosis in the larger cerebral vessels (Spearman's r = .59, P < .001) than in the coronary arteries (r = .16, P = .073) and aorta (r = .24, P = .022). Hyalinization was significantly related to cardiovascular-renal mortality, and this association was accounted for by other CVD risk factors. These findings suggest that blood pressure, glucose level, and alcohol intake are independent predictors of hyalinization in renal arterioles and that this type of renal vasculopathy may be a marker for atherosclerosis in other vascular regions, particularly the cerebral vessels. The protective association involving alcohol and the possibility that renal arteriolar hyalinization may be an indicator of cerebral atherosclerosis may warrant investigation in other populations.
Age Factors↗
Polypeptide composition and organization of the sea urchin extraembryonic hyaline layer.
The protein composition and organization of the sea urchin extraembryonic hyaline layer was examined. Hyalin and a polypeptide of 45 kilodaltons (kDa) were present in hyaline layers isolated from 1-h-old embryos through to the pluteus larva stage. In contrast, several polypeptide species ranging in size from 175 to 32 kDa either decreased in amount or disappeared from the layer as embryonic development proceeded. Concomitant with the changes in composition, hyaline layers became progressively more refractory to dissolution by washing in Ca2+, Mg2(+)-free seawater. Incubation of intact layers, isolated from 1-h-old embryos, with proteinase K resulted in the selective digestion of hyalin and was accompanied by release of the 45-kDa polypeptide from the layers. Washing intact layers in 20 mM Tris (pH 8.0) also resulted in the selective removal of hyalin and the 45-kDa polypeptide. The Ca2(+)-precipitable protein hyalin, alone among the hyaline layer polypeptides, bound the Ca2(+)-antagonist ruthenium red. These results suggest a structural organization within the hyaline layer that is both heterogenous and dynamic throughout embryonic development.
Animals↗
Lattice theory analysis of the relationship of hyaline membrane disease and fetal pneumonia in 96 perinatal autopsies.
A previous study of hyaline membrane disease of the newborn demonstrated that the hyaline membrane was derived from necrotic epithelial cells, and it was suggested that a no flow-reflow episode affecting the pulmonary circulation might account for the cell necrosis. An unexpected statistical finding in that study was a highly significant negative correlation between hyaline membrane disease and chorioamnionitis. Because it seemed to us that fetal infection could be expected to produce the circulatory pathophysiology suggested to produce hyaline membrane disease, we reexamined the issue by reviewing a group of autopsied infants. Data were collected on clinicopathologic variables from 42 stillborn and 54 liveborn infants less than or equal to 12 h of age with lung and placenta slides available for review. Correlations and multivariate regression analysis showed that the inflammatory responses in membranes, cord, and lung are interrelated but that hyaline membrane disease develops independently. However, lattice theory analysis, which represents the pathogenesis of a progressive disease process as edges along a mathematical lattice or hyperdimensional cube, showed that this separation was not absolute. Despite the negative correlation of hyaline membrane disease and fetal pneumonia, there were 10 (10%) patients with both conditions and a total of 19 (20%) with hyaline membrane disease and inflammation of membranes, cord, and/or lung. We suggest that the coexistence of hyaline membrane disease and fetal pneumonia in some patients implies a possible pathogenetic relationship between the two entities. Given the nature of the two processes, it seems likely that the direction of causality is that fetal pneumonia would give rise to the hyaline membrane disease of the newborn.
Autopsy↗
["Hyaline-cell chondroid syringoma." Morphological, immunohistochemical and ultrastructural study of a case and review of the literature].
Chondroid syringoma represents the cutaneous counterpart of mixed tumor ("pleomorphic adenoma") of salivary glands, therefore it is also termed mixed tumor of the skin. The presence of hyaline cells in mixed tumors of salivary gland is a very well known event. Tumors mainly or exclusively composed of hyaline cells are termed myoepitheliomas of hyaline type, accordingly to their alleged myoepithelial origin. Scanty components of hyaline cells in chondroid syringomas of the skin have also been observed since more than a decade. However chondroid syringomas mainly or exclusively composed of hyaline cells have been reported only very recently. If the hyaline cells of chondroid syringomas are myoepithelial or epithelial in origin is still a matter of debate, we prefer to retain the descriptive label "hyaline cell-rich chondroid syringoma" as originally conceived by JA Ferrero and AG Nascimento the patronimic authors of the entity. A case of hyaline cell-rich chondroid syringoma is reported on in a white male patient aged 64, which occurred on the external ear of 1-year duration. This case was studied immunohistochemically and ultrastructurally. Both immunoprofile which included reactivity for vimentin, low molecular weight cytokeratins, S-100 protein, GFAP (focally), alfa-smooth actin and muscle-specific actin, and ultrastructural features including evidence of intermediate filaments (non-bundling filaments, tonofilaments), desmosomes, and thin filaments of actin type sustain a myoepithelial differentiation for hyaline cells of this tumor and site. The authors also remark the importance of being aware of this new entity during the diagnostic practice for avoiding misinterpretation. A list of condition to be taken into account in differential diagnosis is also given.
Adenoma, Pleomorphic↗
Ultrastructure of early mineral deposition during hyaline layer formation in rat molars.
There is no consensus on whether the first mineralized layer, the hyaline layer, that is juxtaposed to root dentine is a variety of dentine or cementum or even a tissue of epithelial origin. Some suggest that there is no intermediate tissue between the acellular extrinsic fibre cementum (AEFC) and the root dentine. Here, to study hyaline layer formation and mineralization we examined by transmission electron microscopy the early stages of root development in upper molars from 10 to 13 day old Wistar rats. In addition to conventionally processed material, undemineralized and unstained sections were examined, which showed the deposition of fine mineral crystals in contact with the mineralized surface of root dentine. Early mineralization of the hyaline layer occurred in the region of the inner basement membrane, which persisted between the inner cellular layer of Hertwig's epithelial root sheath and the outer mineralized root dentine. When the root sheath began its fragment, collagen fibrils from the developing periodontal ligament began to insert into the mineralising hyaline layer, which was 0.5-0.8 micron wide. As the fragmentation of the root sheath HERS increased, more collagen fibrils appeared intermingled with the mineralising hyaline layer. In more advanced stages, when the hyaline layer had become fully mineralized and the formation of the AEFC began, the hyaline layer could no longer be identified. Thus, the hyaline layer is clearly discernible at early stages of periodontal development. Subsequently, it is masked by intermingling of cementum and dentine and therefore it is not possible to detect it in the formed roots of rat molars.
Animals↗
Hyaline bodies of odontogenic cysts: histological, histochemical and electron microscopic studies.
Hyaline bodies of odontogenic cyst were examined by histological, histochemical and electron microscopic observations. They were seen only in odontogenic cysts and their prevalence was 6.9% in 576 cases of the cysts. They occurred most frequently within the epithelial lining, but a few bodies were observed in the connective tissue walls. Histochemical reactions of hyaline bodies were similar to those of dental cuticles, but differed from keratin. Ultrastructurally, hyaline bodies were typed into two forms: lamellated and homogeneous. The lamellated bodies were composed of alternate electron-dense and electron-lucent layers. The homogeneous bodies were occasionally formed around granular material, mineralized masses and cholesterol clefts. Hyaline bodies adjoined epithelial cells via a basal lamina-like structure and half-desmosomes. Epithelial cells containing well-developed, rough surfaced, endoplasmic reticulum were seen adjacent to hyaline bodies. Ferritin-like granules were found in the cytoplasm of epithelial cells near hyaline bodies. By electron probe X-ray microanalysis, inorganic elements within the ferritin-like granules were the same in constitution as those in the outermost electron-dense layer of the lamellated bodies. By scanning electron microscopy, hyaline bodies displayed ellipsoidal and stick-like shapes. The present study suggested that hyaline bodies are particular products formed by odontogenic epithelium.
Electron Probe Microanalysis↗
Nonhomogeneous immunostaining of hyaline membranes in different manifestations of diffuse alveolar damage.
PURPOSE: To determine the nature of hyaline membranes in different manifestations of diffuse alveolar damage, [pulmonary and extrapulmonary acute respiratory distress syndrome], and idiopathic [acute interstitial pneumonia]. MATERIALS AND METHODS: Pulmonary specimens were obtained from 17 patients with acute respiratory distress syndrome and 9 patients with acute interstitial pneumonia. They were separated into 3 different groups: (a) pulmonary diffuse alveolar damage (pDAD) (n = 8), consisting only of pneumonia cases; (b) extrapulmonary diffuse alveolar damage (expDAI) (n = 9), consisting of sepsis and septic shock cases; and (c) idiopathic diffuse alveolar damage (iDAD) (n = 9), consisting of idiopathic cases (acute interstitial pneumonia). Hyaline membranes, the hallmark of the diffuse alveolar damage histological pattern, were examined using various kinds of antibodies. The antibodies used were against surfactant apoprotein-A (SP-A), cytokeratin 7 (CK7), cytokeratin 8 (CK8), alpha smooth muscle actin (alpha-SMA), cytokeratin AE1/AE3 (AE1/AE3), and factor VIII-related antigen (factor VIII). RESULTS: Pulmonary diffuse alveolar damage showed the largest quantity of hyaline membranes (12.65% +/- 3.24%), while extrapulmonary diffuse alveolar damage (9.52% +/- 3.64%) and idiopathic diffuse alveolar damage (7.34% +/- 2.11%) showed intermediate and lower amounts, respectively, with the difference being statistically significant between pulmonary and idiopathic diffuse alveolar damage (P < 0.05). No significant difference was found for hyaline membranes Sp-A immunostaining among pulmonary (15.36% +/- 3.12%), extrapulmonary (16.12% +/- 4.58%), and idiopathic (13.74 +/- 4.20%) diffuse alveolar damage groups. Regarding factor VIII, we found that idiopathic diffuse alveolar damage presented larger amounts of immunostained hyaline membranes (14.12% +/- 6.25%) than extrapulmonary diffuse alveolar damage (3.93% +/- 2.86%), with this difference being statistically significant (P < 0.001). Equally significant was the difference for progressive decrease of cytokeratin AE1/AE3 immunostaining in hyaline membranes present in the extrapulmonary diffuse alveolar damage (5.42% +/- 2.80%) and idiopathic diffuse alveolar damage (0.47% +/- 0.81%) groups (P < 0.001). None of the groups stained for cytokeratin CK-7, CK-8, vimentin, or a anti-smooth muscle actin. CONCLUSIONS: This study showed that only the epithelial/endothelial components (SP-A, factor VIII, and AE1/AE3) of the alveolar/capillary barrier are present in hyaline membranes formation in the 3 groups of patients with diffuse alveolar damage. The significant difference in the expression of factor VIII-related antigen and cytokeratin AE1/AE3 in the expDA versus iDAD groups as well as the significant difference in the amount of hyaline membranes present in the pDAD versus iDAD groups are suggestive of a local and specific lesion with different pathways (direct, indirect, or idiopathic), depending on the type of diffuse alveolar damage.
Analysis of Variance↗
Triple-phase dynamic MRI of intratumoral vessel density and hyalinization grade in uterine leiomyomas.
OBJECTIVE: Our purpose was to clarify the relationship between the tissue vascularity shown on triple-phase dynamic MRI and the number of intratumoral vessels and degree of hyalinization, which are two histopathologic changes in leiomyoma. SUBJECTS AND METHODS. The subjects were 10 premenopausal patients with 20 leiomyomas who had undergone surgery without preoperative gonadotropin-releasing hormone analogue treatment. Intratumoral vessel density was determined by the mean number of intratumoral vessels with at least one smooth-muscle layer in the optic fields magnified 100 times. Hyalinization grade was determined by the severity of hyalinization, histopathologically classified in three grades. The enhancement index (EI) of the leiomyoma was calculated using the formula EI(t) = [S(t) - S(0)] / S(0), where S(0) is the signal intensity on pre-enhanced T1-weighted images and S(t) is the signal intensity on each dynamic phase image (t = 20, 60, and 180 sec) [corrected]. The histopathologic parameters of intratumoral vessel density and hyalinization grade were compared with the enhancement indexes obtained from the triple-phase dynamic MRI. RESULTS: We found positive correlations between intratumoral vessel density and EI(60) and between intratumoral vessel density and EI(180) (in both cases, p = 0.0028 and r = 0.69). We found significant differences among the mean enhancement indexes for each hyalinization grade at all dynamic phases (p < 0.01). The leiomyomas with lower intratumoral vessel densities tended to show greater hyalinization. CONCLUSION: Our results showed that leiomyomas with only slight hyalinization or with abundant vessels were well enhanced, but the leiomyomas with severe hyalinization enhanced poorly.
Adult↗
Presynaptic terminals in hyaline cells of normal and overstimulated chick inner ears.
Hyaline cells are non-sensory epithelial cells of the vibrating part of the basilar membrane of chicks; they receive an extensive efferent innervation. Although these anatomical features suggest roles in auditory transduction, very little is known about the function of these cells. One possible way to understand function is by lesion experiments. We used synapsin-specific antibodies to study changes that occur in the pattern of efferent innervation in hyaline cells after lesion of the sensory epithelium induced by acoustic overstimulation. We found only small changes in hyaline cells after such trauma. These included a small increase in size and a small decrease in density of nerve terminals on hyaline cells. This suggests that hyaline cells and their nerve terminals are less susceptible to acoustic trauma than hair cells. Using neurofilament-specific antibodies we found little or no trauma-induced change in the density of nerve fibres that cross the basilar papilla and reach the hyaline cell region. This finding suggested that trauma to the hair cells does not necessarily lead to changes in the efferent fibres that cross the papilla and extend into the hyaline cell region. Using the trauma and the morphological parameters studied here, it appears that a moderate lesion in the hair cell region in the avian inner ear does not influence the hyaline cells or their innervation.
Acoustic Stimulation↗
Rapid postexposure decay of alpha 2u-globulin and hyaline droplets in the kidneys of gasoline-treated male rats.
Unleaded gasoline induces nephropathy, characterized by rapid accumulation of hyaline (protein resorption) droplets in epithelial cells of the renal proximal convoluted tubules, only in male rats. The hepatic synthesis of the male rat-specific protein alpha 2u-globulin, a constituent of renal hyaline droplets, is unaltered by gasoline treatment (Olson et al., 1987). Renal alpha 2u-globulin content increased to 210% of control within 18 h of a single oral dose of gasoline (2.0 ml/kg); maximal levels (320% of control) were attained following gasoline administration for 3 d. Increases in renal alpha 2u-globulin caused by gasoline were accompanied by concurrent proliferation of hyaline droplets. However, within 3 d of terminating gasoline administration renal alpha 2u-globulin content decreased to the same level as that in unexposed rats, although renal hyaline droplet number returned to pretreatment levels somewhat more slowly. The conjoint effect of postexposure recovery and estradiol (an inhibitor of hepatic alpha 2u-globulin synthesis) administration was also determined in male rats. On postexposure d 3, 6, and 9, estradiol treatment (1 mg/kg, sc, 4 d, starting on d 9 of gasoline treatment) decreased renal alpha 2u-globulin content to 75%, 59%, and 48%, respectively, of that in rats allowed to recover from gasoline with no hormone treatment. Hepatic alpha 2u-globulin content in estradiol-treated rats was decreased by 74%, 97%, and 96% at the same intervals. Estradiol treatment during recovery from gasoline also appeared to increase the removal of accumulated hyaline droplets from the renal cortex. Thus, accumulation of alpha 2u-globulin-containing hyaline droplets after subacute exposure of male rats to gasoline is rapidly reversible, dependent on continuous exposure to gasoline and maintenance of the normal rate of hepatic alpha 2u-globulin synthesis. These results emphasize the dynamic state of renal cortical hyaline droplets and suggest strongly that gasoline hydrocarbons cause hyaline droplet accumulation by prolonging the half-time of degradation of alpha 2u-globulin.
Alpha-Globulins↗