Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ultrastructure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources

Ultrastructural criteria for identification of mast cells and basophils in humans, guinea pigs, and mice.

Basophils and mast cells represent distinct populations that may express differences in function, biochemistry, and response to drugs. In this review, we define ultrastructural criteria useful in distinguishing basophils from mast cells in humans, the guinea pig, and the mouse. Although the ultrastructural features of normal mature basophils and mast cells are the main subject of this report, we also describe variations in basophil and mast cell ultrastructure that reflect the cells' functional activity or stage of maturation. Appreciation of such ultrastructural changes, which can strikingly alter the appearance of these cells, is particularly important in identifying basophils and mast cells in sites of inflammation. In addition to facilitating the accurate identification of basophils and mast cells in vivo, ultrastructural analysis has played an important role in in vitro studies of basophil and mast cell maturation and function. The morphology and biochemistry of these cells now can be studied either by analyzing highly purified populations derived from blood or tissues, notably the lung, or by examining cloned cell lines maintained in vitro. Exploitation of these important technical advances promises to rapidly increase our understanding of the roles of basophils and mast cells in health and disease.

Animals↗

Nasal ciliary ultrastructure and function in patients with primary ciliary dyskinesia compared with that in normal subjects and in subjects with various respiratory diseases.

In an attempt to establish the relevance of ciliary ultrastructure to the pathophysiologic aspects of respiratory tract disease, we compared quantitatively the ultrastructure and function of cilia from healthy subjects (atopic and nonatopic nonsmokers, asymptomatic smokers) and patients with a variety of respiratory diseases (cystic fibrosis, chronic rhinitis, bronchiectasis associated with hypogammaglobulinemia, chronic bronchitis) with cilia from patients with primary ciliary dyskinesia (PCD). In healthy subjects and patients with non-PCD respiratory disease, approximately 5% of the cilia evaluated had ultrastructural abnormalities. Ciliary beat frequency was significantly higher in the chronic rhinitis group (15.3 +/- 1.2 Hz) than in the other non-PCD groups, which were within the normal range (12.5 +/- 1.7 Hz), and in all non-PCD cases ciliary wave form was normal. In each of these groups, normal mucociliary transport had been previously demonstrated. By contrast, in patients with PCD, the proportion of cilia with ultrastructural abnormalities was significantly greater than in the normal subjects and those with non-PCD respiratory disease (p less than 0.0001). In addition, beat frequency was significantly reduced, ciliary wave form was grossly abnormal, and pulmonary and nasal mucociliary transport were virtually absent. These findings demonstrate the relevance of ciliary ultrastructural abnormalities to altered ciliary function and lend support to the primary role of the demonstrated abnormalities in the respiratory tract disease of PCD.

Adolescent↗

Thyrotropin-releasing hormone accelerates fetal mouse lung ultrastructural maturation via stimulation of extra thyroidal pathway.

Maternal administration of TSH-releasing hormone (TRH) in the euthyroid mouse accelerates fetal lung ultrastructural maturation. However, the mechanism(s) of TRH in fetal lung development remains unclear; it could be due to its neuroendocrine and/or neurotransmitter effects. Although the neuroendocrine effect of TRH is mediated via stimulation of the fetal pituitary-thyroid axis, the neurotransmitter effect is mediated via stimulation of fetal autonomic nervous system activity. In the hyt/hyt mouse there is a point mutation in the beta subunit of the TSH receptor in the thyroid gland of the Balb-c mouse. In these mice TSH does not bind to its receptors, leading ultimately to the development of primary hypothyroidism, which is transmitted as an autosomal recessive trait. A maturational delay in the lung ultrastructure of the hyt/hyt mouse fetus has been observed. This investigation was undertaken to study the effect of maternal TRH treatment on lung ultrastructural maturation in the hyt/hyt mouse fetus. If the effect of TRH is mediated via stimulation of fetal pituitary-thyroid axis, TRH treatment should not enhance lung maturity in the hyt/hyt fetus and vice versa. Adult hyt/hyt mice made euthyroid by triiodothyronine supplementation were mated to carry hyt/hyt pups. Saline or TRH (0.4 or 0.6 mg/kg/dose) was administered to the mother (i.p.) on d 16 and 17 (b.i.d.) and on d 18 of pregnancy 1 h before killing (term, approximately 20 d). The fetal lung electron micrographs were subjected to ultrastructural morphometric analysis of the number of lamellar bodies and glycogen/nuclear ratio in type II cells, and the alveolar/parenchymal ratio by Chalkley point counting with an interactive computerized image analyzer (Optimas, Bioscan). Fetal lungs exposed to the lower dose of TRH (n = 7) showed no significant difference in their ultrastructural maturation when compared with saline-treated controls (n = 5). However, fetal lungs exposed to a higher dose of TRH (n = 6) showed increased numbers of lamellar bodies per type II cell, an increase in the alveolar/parenchymal ratio, larger air spaces, thinner alveolar septa, presence of tubular myelin, and increased numbers of air-blood barriers. We conclude that the effect of TRH in accelerating fetal mouse lung maturation is at least in part mediated via stimulation of extra thyroidal pathways.

Animals↗

Ultrastructural pathological study of left ventricular myocardium in patients with isolated rheumatic mitral stenosis with normal or abnormal left ventricular function.

An electron microscopic study of left ventricular myocardium was carried out in 15 patients who had isolated rheumatic mitral stenosis, with particular reference to the relation among ultrastructural pathological findings, the severity of mitral stenosis and left ventricular function. They were divided into 2 groups based on left ventricular performance evaluated by 2-dimensional echocardiography and angiocardiography. The severity of mitral stenosis was determined by hemodynamic data and mitral valve areas measured by 2-dimensional echocardiography. Regardless of the level of left ventricular contractile function we consistently demonstrated varying degrees of ultrastructural pathological alterations of left ventricular muscle cells, involving the myofibrils, mitochondria, nuclei and other elements of the sarcoplasm and membranes surrounding the myocardial cells in all specimens examined. The ultrastructural pathological findings did not correlate with the severity of mitral stenosis reflected in the echocardiographic and hemodynamic data. However, those patients with abnormal left ventricular function always exhibited more extensive loss of myofibrils resulting from either disproportion of the mitochondria-to-myofibril ratio or myofibrillar degeneration. The present investigation provides the morphological data at the ultrastructural level to support the widely held concept of a myocardial factor i.e., the extent of myocardial involvement by the rheumatic process as the basic pathogenetic mechanism responsible for left ventricular dysfunction in patients with isolated rheumatic mitral stenosis. Furthermore, it is suggested that pathological alterations of myocardial ultrastructure were related to the extent of myocardial involvement by the rheumatic process rather than being structural adaptations in response to the hemodynamic derangement.

Adult↗

Ultrastructure and chaetotaxy of sensory receptors in the cercaria of a species of Allopodocotyle Pritchard, 1966 (Digenea: Opecoelidae).

Previous investigations of sensory systems in opecoelid cercariae have focused on chaetotaxy and ultrastructure of sensory receptors. They revealed chaetotaxic patterns within family, genus, and species as well as different receptors. Chaetotaxic and ultrastructural observations have rarely been combined. We investigated the ultrastructure of cercarial sensory receptors in conjunction with chaetotaxy and neuromorphology in a species of Allopodocotyle. Cercariae were treated with acetylthiocholine iodide and silver nitrate, and some were processed for light, scanning (SEM), and transmission (TEM) electron microscopy. Five nerve regions were distinguished. Chaetotaxy was consistent with that of other opecoelids. Five types of receptors were distinguished with SEM. Types differed in number of cilium-like structures (one or more), length of cilium-like structure (short, moderately long, or long), presence or absence of a tegumentary collar, and length of tegumentary collar (low, moderately low, or very high). Internal ultrastructure of some types revealed unsheathed cilium-like structures, basal body, and thickened nerve collars. Possible subtegumentary and sheathed receptors are introduced. Some receptor types were site-specific. For example, receptors with multiple cilium-like structures were concentrated on cephalic region whereas receptors with short cilium-like structure were widespread throughout most regions. Ultrastructure and site-specificity observations suggest that most receptors are mechanoreceptors.

Animals↗

Ultrastructural characterization of apoptosis in bovine lymphocytes exposed to Pasteurella haemolytica leukotoxin.

OBJECTIVE: To characterize ultrastructural changes of bovine lymphocytes exposed to Pasteurella haemolytica leukotoxin (LKT). SAMPLE POPULATION: Partially purified LKT from a wild type P. haemolytica A1 strain and inactive pro-LKT from an isogeneic mutant Phaemolytica strain. Isolated bovine lymphocytes were obtained from 2 healthy calves. PROCEDURE: Isolated bovine lymphocytes were incubated with various concentrations of LKT and pro-LKT for 3 hours at 37 C and examined by use of transmission electron microscopy. A cytochemical Klenow DNA fragmentation assay was used to examine lymphocytes for DNA fragmentation. RESULTS: Lymphocytes incubated with LKT at a high concentration (1.0 toxic U/ml) had ultrastructural evidence of cytoplasmic and nuclear membrane rupture and swelling or lysis of mitochondria. Low concentrations of leukotoxin (0.1 toxic U/ml) induced DNA fragmentation in 80% of lymphocytes. Ultrastructurally, these cells had nuclear membrane blebbing, cytoplasmic vaculation, chromatin condensation, nuclear fragmentation, and membrane-bound apoptotic bodies. Incubation of lymphocytes with LKT at extremely low concentrations (0.001 toxic U/ml) or with pro-LKT did not alter their ultrastructure. Inclusion of 0.5 mM ZnCl2 in the medium blocked leukotoxin-induced ultrastructural changes in bovine lymphocytes. CONCLUSIONS AND CLINICAL RELEVANCE: Low concentrations of LKT induce apoptosis and high concentrations induce oncotic cell lysis in bovine lymphocytes. The ability of low LKT concentrations to induce apoptosis in host leukocytes may allow bacteria to escape host immune surveillance and colonize the host.

Animals↗

Ultrastructural immunolabeling in diagnostic surgical pathology: illustrative cases.

Ultrastructural immunolabeling techniques can be reproducibly applied to resolve diagnostic dilemmas in surgical pathology. The technique utilized for processing and labeling the cases presented in this article is simple and reproducible. The specimens were fixed in Carson-Millonig phosphate-buffered 4% formaldehyde fixative and embedded in LR White resin following a well-described protocol. Immunogold labeling allows precise localization of antigenic sites without compromise of the underlying ultrastructural morphologic findings; thus detailed immunomorphologic assessment is achieved. Immunoelectron microscopy techniques permit clarification of doubtful immunocytochemistry results by labeling antigenic epitopes in cases in which light microscopy immunocytochemistry techniques fail to show unequivocal positive results (probably as a consequence of small amounts of detectable antigen present in the tissues). Not only does ultrastructural labeling permit identification of focally positive reactions essential for accurate diagnosis in a given case, but it also localizes the antigenic determinants to specific cellular sites, providing immunomorphologic correlation. The specificity of the interpreted results can then be judged accordingly. Overall, ultrastructural immunolabeling is more sensitive than light microscopic immunocytochemistry. Ultrastructural immunolabeling can play a crucial role in the characterization of some tumors that cannot be accurately classified with other diagnostic techniques, even when combined.

Calcitonin↗

Pineal parenchymal tumors: an ultrastructural study with prognostic implications.

The pineal gland is host to a spectrum of neoplasms. Those considered to be derived from or differentiating toward pineal parenchymal cells are rare. Traditionally, pineal parenchymal tumors (PPTs) have been divided into 3 types: pineocytomas, pineoblastomas, and mixed or transitional tumors. Their characterization has been far from adequate and no firm diagnostic criteria, light microscopic or ultrastructural, have been established. In an attempt to provide more precise prognostic diagnostic criteria, we undertook a detailed ultrastructural analysis of 17 PPTs and found them to exhibit light microscopic and ultrastructural features strikingly similar to those of pineal parenchymal cells in varying stages of development, ranging from undifferentiated primitive neuroepithelial cells to mature pineal parenchymal cells. We endorse classification of PPTs based on a combination of their light microscopic and ultrastructural features. Accordingly, PPTs can be divided into three categories: 1) pinealoblastoma, 2) PPTs of intermediate or mixed differentiation, and 3) pineocytoma, a tumor of mature-appearing pineocytes. In keeping with this classification, our 3 pinealoblastomas behaved as highly malignant tumors. A correlation of morphology and prognosis was less evident between intermediate tumors and pineocytomas, perhaps the result of considerable variation in surgical and other therapies. Evidence of neurosensory differentiation, a feature noted to a varying extent in all but the pineoblastomas, included club-shaped "nerve endings" in 7 tumors, small numbers of dense core granules in 8, clear vesicles in 7, and structures suggestive of synapses in 4. With the exception of 3 undifferentiated PPTs or pinealoblastomas lacking nerve endings, all pineocytomas exhibited some combination of these markers of neuronal specialization. In that the ultrastructural features of these PPTs were more indicative of their aggressiveness than was their degree of light microscopic differentiation or grade, we consider electron microscopy a useful adjunct, not only in diagnosis but also in therapeutic decision-making and prognostication.

Adolescent↗

Immunophenotype and ultrastructural studies in blast crisis of chronic myeloid leukemia.

Thirty-four patients with chronic myeloid leukemia in blast crisis (CML-BC) were evaluated for lineage differentiation with immunological markers and the presence of ultrastructural peroxidase. Eighteen (52.9%) were found to have myeloid blast crisis. Cytochemically, myeloperoxidase (MPO) could be detected only in six patients on light microscopy while in the remaining 12 patients, myeloid differentiation was confirmed only by demonstration of MPO either at ultrastructural level or by the reactivity with anti myeloperoxidase (anti MPO) antibody. Six (17.6%) had lymphoid blast crisis as identified by lymphoid specific markers (CD19; CD10; CD7; CD4) along with the absence of myeloid markers. Heterogenous blast cell populations with mixed lineage differentiation were seen in 4 (11.7%) patients. These cases showed both lymphoid (CD19, CD10) and myeloid (anti MPO and ultrastructural MPO) characteristics. A single case of megakaryoblastic blast crisis was identified with positivity for CD41 and CD42 along with the presence of platelet peroxidase at the ultrastructural level. Five cases (14%) of CML blast crisis remained unclassifiable. These results suggest that blast crisis in CML show an arrest of differentiation at an early stage when compared to de novo acute leukemias. This is particularly evident from the fact that MPO could only be demonstrated ultrastructurally or with anti MPO antibody in the majority of patients with myeloid differentiation. It is expected that utilisation of molecular studies including immunoglobulin and T-cell receptor gene rearrangement and m-RNA expression for myeloperoxidase will provide a better insight into the level of differentiation for the presently unclassifiable cases of CML-blast crisis.

Antigens, CD↗

Ultrastructural studies of gastrointestinal stromal tumors.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors in the gastrointestinal tract (GIT). Although interstitial cells of Cajal has been suggested as origin of this tumor, the cytological and ultrastructural features of GISTs are heterogeneous and unclear. A total 10 cases of normal gastrointestinal tissue (control), 13 GISTs of the stomach (8), small intestine (3), mesocolon (1) and liver (1), and 2 gastrointestinal autonomic nervous tumor (GANT) of small intestine were ultrastructurally studied. Normal interstitial cells of Cajal (ICC) were abundantly present around the myenteric plexuses or individually scattered through the wall of GIT. ICC was characterized by slender cytoplasmic processes, well-developed endoplasmic reticulum (ER), mitochondria, Golgi apparatus, caveolae and intermediate filaments. The GISTs and GANTs had overlapping ultrastructures. The most common and important ultrastructural features of GISTs were rich villous cytoplasmic processes, dispersed intermediate filaments and abundant SER, and those of GANTs were neurosecretory granules and skenoid fibers. Compared with ICC, the GISTs and GANTs had remarkably reduced caveolae and gap junctions. Our study suggested that ultrastructural analysis gives much information to investigate lineage differentiation of neoplastic cells and make a differential diagnosis of these tumors from other mesenchymal tumors and between GISTs and GANTs.

Adult↗

Ultrastructural and ERG findings in mice with adenomatous polyposis coli gene disruption.

PURPOSE: In order to continue the previous morphological studies of eyes from mice with adenomatous polyposis coli (APC) gene mutation at codon 1638, we determined the ultrastructural and electrophysiologic characteristics of these eyes. METHODS: Thirty-eight eyes from 20 mice heterozygous for APC gene mutation and 22 eyes from 11 wild-type mice were examined by light microscopy. Six APC-modified eyes without light microscopic abnormalities, four APC-modified eyes with focal light microscopic abnormalities, and four wild-type eyes were examined by electron microscopy. Electroretinograms were recorded from four APC-modified and three wild-type mice. RESULTS: Four of 38 APC-modified eyes demonstrated ultrastructural evidence of focal RPE cells with increased melanosome production and atrophy. Other areas of the RPE in these four eyes demonstrated no ultrastructural abnormalities. Three APC-modified eyes demonstrated electron and light microscopic evidence of RPE hyperplasia. Electron microscopic examination of APC-modified eyes without light microscopic evidence of abnormalities demonstrated no ultrastructural differences from age-matched controls. Electroretinography demonstrated no differences in the b-wave or c-wave amplitudes between APC-modified and wild-type mice. CONCLUSIONS: While light microscopic RPE alterations are observed in these APC-modified mice, the absence of a generalized, ultrastructural murine RPE defect is in contradistinction to observations in electron microscopic investigations of humans with colonic polyposis, pigmented ocular fundus lesions, and APC gene mutations between codons 463 and 1444. Our results in mice with APC mutation at codon 1638, however, are consistent with a previously identified association between the expression of pigmented ocular fundus lesions and region-specific mutation in the human APC gene. The APC protein may possess a physiologic function for both retinal and RPE development.

Adenomatous Polyposis Coli↗

[Comparison of endometrial histology and ultrastructure during different ovarian stimulation protocols in hamsters].

OBJECTIVE: To evaluate the influence of ovarian stimulation by pregnant mare's serum gonadotropin(PMSG) with or without gonadotropin releasing hormone agonist (GnRH-a) on endometrial histology and ultrastructure in hamsters. METHODS: Thirty hamsters were randomly allocated into 3 groups. (1) LA + PMSG group: Leuprolide acetate (LA) was given first for desensitizing the pituitary, then PMSG added for ovarian stimulation. (2) PMSG group was injected with PMSG only. (3) Control group was given with saline of same volume as groups LA + PMSG and PMSG on the same time schedule. Endometrial histology and ultrastructure were investigated by light microscope and electron microscope. RESULTS: Comparing to the controls, the changes of endometrial histology in group of LA + PMSG was not significantly different, but its ultrastructure had marked atterations: mitochondria swelling, undifferentiated crista and no basket-like structure. Delayed endometrial maturation was frequently found in group PMSG (P < 0.01), and the ultrastructure showed poorly developed mitochondria. CONCLUSION: The degree of endometrial maturation varied considerably with different ovarian stimulation protocols. Ovarian stimulation with GnRH-a was better than PMSG alone, because the protocol LA + PMSG, in hamsters, facilitated the formation of a physiologic endometrium. But the protocol with GnRH-a still had a negative effect on endometrial ultrastructure.

Animals↗

Ultrastructural, immunologic and clinical follow-up of five patients with HCL treated with interferon (IFN) for more than three years.

BACKGROUND: Treatment results in HCl have been improved by the use of alpha-IFN, which is now the standard first-line therapy for this disease, but the mechanism of IFN action is still unclear. It is known, however, that IFN is able to induce hematologic, immunological and phenotype membrane changes which parallel the patients' (pts) clinical response. The aim of our study was to correlate the clinical response to IFN treatment with ultrastructural and phenotype membrane changes in hairy cells (HCs), in order to elucidate the mechanism of IFN action at the cell level. METHODS: We assessed the phenotype membrane and ultrastructural changes induced in HCs by long-term alpha-IFN treatment in five pts with HCL; membrane-bound Il 2-R on PHA-stimulated PBL, the release of IL 2-R by PHA-stimulated PBL and the serum levels of s-IL 2-R were also determined in one pt. RESULTS: The surface immunological phenotype, mainly the HCL-related surface antigen CD25, changed after IFN treatment, dropping from abnormally high to normal values. Furthermore, IFN treatment induced ultrastructural changes in HCs, consisting mainly of a sharp reduction in, up to the almost complete disappearance of, the hairy projections: very few, if any, short, thick villi persisted. The ultrastructural changes in HCs paralleled clinical and hematologic response to IFN treatment in such a way that IFN alone may be considered the cause of these changes. As far as detection of the membrane-bound IL 2-R p55 chain on PHA-stimulated PBL is concerned, the expression of p55 is very high on the membrane of HCs; a high level of serum s-IL 2-R was also found in the HCL pt studied before IFN treatment, whereas the release of IL 2-R by PHA-stimulated PBL was higher than normal, but not significantly. Two of our pts, who did not respond or responded very poorly clinically to IFN treatment, should probably be considered cases of HCL "variants". CONCLUSIONS: The phenotype membrane and the ultrastructural changes in HCs very closely paralleled the patients' clinical responses to IFN, suggesting that both the immunologic and the morphologic changes induced in HCs by in vivo IFN treatment are a direct counterpart of its biologic effect.

Aged↗

[Ultrastructural characteristics of rat adrenal cortex cultured cells in the norm and after calcium ionophore A23187 and adrenocorticotropic hormone application].

The ultrastructure of a fasciculata-reticularis zone cells of a rat adrenal cortex in norm, and after application of adrenocorticotropic hormone (ACTH) and calcium ionophore A23187 was investigated. In the control it has been revealed three types of cells which differed on the ultrastructure. ACTH or ionophore A23187 application resulted in disappearance of a difference in ultrastructure of cells of different types, also all cells got morphological attributes of accelerated steroidogenesis. The probable role of cells with different types of ultrastructure for fasciculata-reticularis zone function, and also prospective participation of calcium ions in ACTH influences on ultrastructure of a fasciculata-reticularis zone is discussed.

Adrenal Cortex↗

Functional role of test cells in swimming larvae of Ascidia malaca: ultrastructural and cytochemical investigations.

The functional role played by test cells in larvae of various ascidian species consists in depositing sub-microscopic structures known as ornaments and/or proteoglycan substances on the larval test surface. According to the data reported in the literature, the deposition of ornaments together with proteoglycan substances on the larval test would render the latter hydrophilic and thus allow the larva to swim being immersed in water. Ornament deposition on the larval test does not occur in all the ascidian species. Ultrastructural investigations made on larvae belonging to the Cionidae and Ascididae families, for instance, have failed to evidence the presence of ornaments on the test. For these ascidian families it has been hypothesized that in swimming larvae test cells secrete an amorphous substance that would allow them to adhere to the larval test. In order to ascertain the functional role played by test cells in swimming larvae of the Ascididae family, the presently reported ultrastructural and cytochemical investigations have been made on larvae of Ascidia malaca. Besides suggesting that test cells, tightly adherent to the test surface, present an amoeboidic behaviour, the ultrastructural investigations have evidenced that these cells are still metabolically active. Their cytoplasm, characterized by the presence of a Golgi apparatus actively involved in synthesis, is almost entirely filled with very large granules; some of them gradually empty their contents turning into vacuoles containing scarce residues of electrondense particles. The present ultrastructural observations support the hypothesis that the adhesion of test cells on the larval test could be very likely eased by the secretion of substances synthesized by the Golgi and released through pseudopodes which test cells then wedge into the test. The cytochemical investigations were based on a reaction (fixation in glutaraldehyde-tannic acid) which evidences the presence, at the ultrastructural level, of proteoglycan substances such as glycosaminoglycans (Singley and Solursh, 1980). The reaction has given positive results in test cell granules undergoing emptying, on the outer membrane of the same cells, and on the outer cuticular layer C1 of the larval test. The present investigations, besides confirming the absence of ornament deposition on the test surface by test cells of Ascidia malaca swimming larvae, have evidenced that the secretion products deposited on the larval test surface by test cells consist of glycosaminoglycans, i.e. proteoglycan substances. In agreement with the data reported in the literature, it is hypothesized that the deposition of glycosaminoglycans on the surface of Ascidia malaca larval test makes the larval tunic hydrophilic and thus the larva is able to swim being immersed in water.

Animals↗

Ultrastructural alterations in renal tissues of rabbits induced by diclofenac sodium (Voltaren).

OBJECTIVE: Although diclofenac sodium (Voltaren) is one of the most frequently prescribed non-steroidal anti-inflammatory drugs (NSAIDs) worldwide for the treatment of inflammation and pain; data on the ultrastructural alterations in renal tissues due to its chronic exposure are limited. Therefore, the present study was designed to identify the ultrastructural renal alterations induced by diclofenac sodium. METHODS: The experiment was conducted at the animal house of the Department of Zoology, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia during the period from April 2003 to June 2003. A total of 30 male rabbits were exposed to intraperitoneal injection with a daily dose of diclofenac sodium (1.5 mg/kg body weight) for 70 days to investigate the resultant ultrastructural alterations in renal tissues. RESULTS: In comparison with the respective control rabbits, chronic exposure to therapeutic doses of diclofenac sodium produced significant ultrastructural renal alterations, which involved swelling and cristolysis of the mitochondria, marked dilatation of the endoplasmic reticulum, detachment of ribosomes, increased lysosomal structures, nuclear chromatin condensation in the tubular cells, thickening of the glomerular basement membranes, distention of glomerular capillaries, which showed lodgment of neutrophils, mesangial and endothelial cell proliferation in the glomeruli, swelling and fusion of the glomerular podocytes foot processes with focal obliteration of the filtration slits. CONCLUSION: The obtained results indicate that chronic exposure to diclofenac sodium produces significant ultrastructural alterations in renal tissues.

Animals↗

[Study on the changes of electrocardiogram and ultrastructural in heroin dependence in rats].

OBJECTIVE: To study the changes of electrocardiograms (ECG) and myocardial ultrastructure in heroin dependence in rats, in order to reveal the mechanisms of the myocardial injury by heroin. METHODS: Establish heroin addict model in SD mice, investigate the changes in electrocardiograms, HE staining and myocardial ultrastructure. RESULTS: The electrocardiograms of the addict group had prominently changes, main expressions: heart rate decreased, P wave and T wave amplitude reduced and duration increased, S-T reduced and duration increased, QT interval prolongation, these changes indicated that myocardium had been injured, myocardial ischemia, ventricle function declined. These difference was significant (P<0.05) between before inject heroin and after inject heroin. Transformations in the ultrastructure: nuclear concentrate, reduce, nuclear membrane shrink, chromatin agglutinate, mitochondria cristal had disorder formation, disappeared or hollowed, these indicated that heroin could cause pathological changes in myocardial ultrastructure. CONCLUSION: Above-mentioned changes indicated that heroin can injure myocardium, and the changes of myocardial ultrastructure suggested that myocardial apoptosis may be one of the mechanisms of the myocardial injury by heroin.

Animals↗

Ultrastructural characteristics of axons in traumatic neuromas of the human lingual nerve.

AIMS: To determine the ultrastructural characteristics of axons in traumatic neuromas of the human lingual nerve during the surgical removal of lower third molar teeth and to establish whether any characteristics were different between patients with dysesthesia and patients without dysesthesia. METHODS: Transmission electron microscopy was used to determine the ultrastructural morphological characteristics of human lingual nerve neuromas (n = 34) removed at the time of microsurgical nerve repair. From a sample population of myelinated and nonmyelinated fibers within the neuromas, fiber diameter, myelin thickness, g-ratio, and the number of mitochondria per axon were quantified. Comparisons were made with normal control lingual nerve specimens (n = 8) removed at the time of organ donor retrieval. RESULTS: Significant differences in ultrastructural morphology were found between the neuromas and control nerves. The neuromas contained a higher proportion of small (2- to 8-microm diameter) myelinated nerve fibers than controls, and the mean myelinated fiber diameter was significantly lower in neuromas than in controls. Mean myelin sheath thickness was significantly thinner in neuromas (0.6 +/- 0.1 microm) than in controls. However, the g-ratio, which is a measure of the myelination status of the nerve fibers in relation to their diameter, was found to be similar in each group, suggesting a normal process of myelination in the damaged axons. Nonmyelinated axon diameter was also significantly smaller in the neuromas than in the controls, and Schwann cells were found to sheathe more nonmyelinated axons in neuromas than in controls. The ratio of nonmyelinated to myelinated axons was significantly higher in neuromas than in controls. However, no significant differences were found between patients with dysesthesia and those without dysesthesia. CONCLUSION: Damage to the lingual nerve results in marked changes to axon diameter, myelin sheath thickness, and Schwann cell-axon relationships. These ultrastructural changes could contribute to the altered electrophysiological properties of axons trapped within neuromas. However, no significant differences in the ultrastructural characteristics studied were found between specimens from patients with or without symptoms of dysesthesia.

Adolescent↗