scholarly journals Hypothyroidism Affects Vascularization and Promotes Immune Cells Infiltration into Pancreatic Islets of Female Rabbits

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Julia Rodríguez-Castelán ◽  
Margarita Martínez-Gómez ◽  
Francisco Castelán ◽  
Estela Cuevas
Keyword(s):  
Extracellular Matrix ◽  
Immune Cells ◽  
Islet Cells ◽  
Periodic Acid ◽  
Serum Glucose ◽  
Female Adult ◽  
General Observation ◽  
Periodic Acid Schiff ◽  
Islet Size ◽  
Pancreatic Edema

Thyroidectomy induces pancreatic edema and immune cells infiltration similarly to that observed in pancreatitis. In spite of the controverted effects of hypothyroidism on serum glucose and insulin concentrations, the number and proliferation of Langerhans islet cells as well as the presence of extracellular matrix are affected depending on the islet size. In this study, we evaluated the effect of methimazole-induced hypothyroidism on the vascularization and immune cells infiltration into islets. A general observation of pancreas was also done. TwelveChinchilla-breed female adult rabbits were divided into controln=6and hypothyroid groups (n=6, methimazole, 0.02% in drinking water for 30 days). After the treatment, rabbits were sacrificed and their pancreas was excised, histologically processed, and stained with Periodic Acid-Schiff (PAS) or Masson’s Trichrome techniques. Islets were arbitrarily classified into large, medium, and small ones. The external and internal portions of each islet were also identified. Student-t-test and Mann-Whitney-Utest or two-way ANOVAs were used to compare variables between groups. In comparison with control rabbits, hypothyroidism induced a strong infiltration of immune cells and a major presence of collagen and proteoglycans in the interlobular septa. Large islets showed a high vascularization and immune cells infiltration. The present results show that hypothyroidism induces pancreatitis and insulitis.

scholarly journals ANRIL regulates production of extracellular matrix proteins and vasoactive factors in diabetic complications

2018 ◽  
Vol 314 (3) ◽  
pp. E191-E200 ◽  
Author(s):  
Anu Alice Thomas ◽  
Biao Feng ◽  
Subrata Chakrabarti
Keyword(s):  
Extracellular Matrix ◽  
Periodic Acid ◽  
Urine Volume ◽  
Immunohistochemical Analysis ◽  
Diabetic Mouse ◽  
Chromosome 9 ◽  
Wild Type ◽  
Vegf Mrna ◽  
Periodic Acid Schiff ◽  
Ecm Proteins

noncoding RNAs (lncRNAs) have gained widespread interest due to their prevailing presence in various diseases. lncRNA ANRIL (a. k. a. CDKN2B-AS1) is located on human chromosome 9 (p21.3) and transcribed in opposite direction to the INK4b-ARF-INK4a gene cluster. It has been identified as a highly susceptible region for diseases such as coronary artery diseases and type 2 diabetes. Here, we explored its regulatory role in diabetic nephropathy (DN) and diabetic cardiomyopathy (DCM) in association with epigenetic modifiers p300 and polycomb repressive complex 2 (PRC2) complex. We used an ANRIL-knockout (ANRILKO) mouse model for this study. The wild-type and ANRILKO animals with or without streptozotocin-induced diabetes were monitored for 2 min. At the end of the time point, urine and tissues were collected. The tissues were measured for fibronectin (FN), type IV collagen (Col1α4), and VEGF mRNA and protein expressions. Renal function was determined by the measurement of 24-h urine volume and albumin/creatinine ratio at euthanasia. Renal and cardiac structures were investigated using periodic acid-Schiff stain and/or immunohistochemical analysis. Elevated expressions of extracellular matrix (ECM) proteins were prevented in ANRILKO diabetic animals. Furthermore, ANRILKO had a protective effect on diabetic mouse kidneys, as evidenced by lowering of urine volume and urine albumin levels in comparison with the wild-type diabetic animals. These alterations regulated by ANRIL may be mediated by p300 and enhancer of zeste 2 (EZH2) of the PRC2 complex. Our study concludes that ANRIL regulates functional and structural alterations in the kidneys and hearts in diabetes through controlling the expressions of ECM proteins and VEGF.

Histochemistry of the developing notochord, perichordal sheath and vertebrae in Danforth's short-tail (Sd) and normal C57BL/6 mice

Development ◽  
1980 ◽  
Vol 55 (1) ◽  
pp. 227-245
Author(s):  
Laurie G. Paavola ◽  
Doris B. Wilson ◽  
Elizabeth M. Center
Keyword(s):  
Extracellular Matrix ◽  
Alcian Blue ◽  
Periodic Acid ◽  
Mesenchymal Cell ◽  
Mesenchymal Cells ◽  
Periodic Acid Schiff ◽  
Short Tail ◽  
Cell Organization ◽  
Typical Distribution ◽  
Relationship Of

The development of the notochord, perichordal sheath and vertebrae was studied in C57BL/6 and Danforth's short-tail (Sd) mutant mice on days 9–14 of gestation, using histochemical stains to detect possible extracellular matrix (ECM) components or precursors. Stains used were periodic-acid Schiff (PAS) after diastase treatment (glycoproteins, neutral polysaccharides) and alcian blue (glycosaminoglycans). Embryos from C57BL/6Sfd mice were analyzed to establish a normal baseline. In 9-day normal (C57BL/6Sfd; + / + ) embryos the notochord is an uninterrupted structure and contains PAS-positive, diastaseresistant granules, whereas in abnormals (Sd/ + Sd/Sd) the notochord is discontinuous and exhibits few, if any, granules. A notochordal sheath is present in normal and abnormal embryos on day 10 and stains with PAS, alcian blue and aniline blue; subsequently, it increases in thickness in normal, but not defective, embryos. In normal embryos, the notochord shows dilatations, and notochordal cells become vacuolated from 13 to 14 days. In contrast, the notochordal fragments of abnormals never develop dilatations, nor do the cells vacuolate. Organization of mesenchymal cells into specific patterns is observed initially in 11-day normal embryos; further mesenchymal organization into vertebral and intervertebral disc analgen occurs during days 12–14. In abnormal embryos, disturbance of mesenchymal cell organization is evident as early as day 11, and by day 12 aberrant patterns of organization have emerged. Mesenchymal cells of abnormal embryos also lack the typical distribution of PAS-positive, diastase-resistant granules that occurs in normal specimens. The possible relationship of these granules in notochordal and mesenchymal cells to ECM materials is discussed.

scholarly journals Quantitative characterization of glomerular fibrosis with magnetic resonance imaging: a feasibility study in a rat glomerulonephritis model

2018 ◽  
Vol 314 (5) ◽  
pp. F747-F752 ◽  
Author(s):  
Christopher C. Conlin ◽  
Yufeng Huang ◽  
Brian Adam Jamison Gordon ◽  
Jeff L. Zhang
Keyword(s):  
Magnetic Resonance Imaging ◽  
Extracellular Matrix ◽  
Magnetic Resonance ◽  
Mesangial Cells ◽  
Periodic Acid ◽  
Renal Diseases ◽  
Glomerular Mesangial Cells ◽  
Resonance Imaging ◽  
Periodic Acid Schiff ◽  
Cortical Perfusion

Glomerular fibrosis occurs in the early stages of multiple renal diseases, including hypertensive and diabetic nephropathy. Conventional assessment of glomerular fibrosis relies on kidney biopsy, which is invasive and does not reflect physiological aspects such as blood perfusion. In this study, we sought to assess potential changes of cortical perfusion and microstructure at different degrees of glomerular fibrosis using magnetic resonance imaging (MRI). A rat model of glomerular fibrosis was induced by injecting anti-Thy-1 monoclonal antibody OX-7 to promote mesangial extracellular matrix proliferation. For six rats on day 5 and five rats on day 12 after the induction, we measured renal cortical perfusion and spin-spin relaxation time (T2) in a 3-Tesla MRI scanner. T2 reflects tissue microstructural changes. Glomerular fibrosis severity was evaluated by histological analysis and proteinuria. Four rats without fibrosis were included as controls. In the control rats, the periodic acid-Schiff (PAS)-positive area was 22 ± 1% of total glomerular tuft, which increased significantly to 56 ± 12% and 45 ± 10% in the day 5 and day 12 fibrotic groups, respectively ( P < 0.01). For the three groups (control, day 5, and day 12 after OX-7 injection), cortical perfusion was 7.27 ± 2.54, 3.78 ± 2.17, and 3.32 ± 2.62 ml·min−1·g−1, respectively, decreasing with fibrosis severity ( P < 0.01), and cortical T2 was 75.2 ± 4.6, 84.1 ± 3.0, and 87.9 ± 5.6 ms, respectively ( P < 0.01). In conclusion, extracellular matrix proliferation in glomerular mesangial cells severely diminished blood flow through the glomeruli and also altered cortical microstructure to increase cortical T2. The MRI-measured parameters are proven to be sensitive markers for characterizing glomerular fibrosis.

Ultrastructure of the Parotid Gland of the Nine-Banded Armadillo

1977 ◽  
Vol 35 ◽  
pp. 640-641
Author(s):  
J. R. Ruby
Keyword(s):  
Endoplasmic Reticulum ◽  
Parotid Gland ◽  
Periodic Acid ◽  
Acinar Cells ◽  
Duct System ◽  
Parotid Glands ◽  
Dasypus Novemcinctus ◽  
Anterior Portion ◽  
Periodic Acid Schiff ◽  
Thin Sections

Parotid glands were obtained from five adult (four male and one female) armadillos (Dasypus novemcinctus) which were perfusion-fixed. The glands were located in a position similar to that of most mammals. They extended interiorly to the anterior portion of the submandibular gland.In the light microscope, it was noted that the acini were relatively small and stained strongly positive with the periodic acid-Schiff (PAS) and alcian blue techniques, confirming the earlier results of Shackleford (1). Based on these qualities and other structural criteria, these cells have been classified as seromucous (2). The duct system was well developed. There were numerous intercalated ducts and intralobular striated ducts. The striated duct cells contained large amounts of PAS-positive substance.Thin sections revealed that the acinar cells were pyramidal in shape and contained a basally placed, slightly flattened nucleus (Fig. 1). The rough endoplasmic reticulum was also at the base of the cell.

Detection of Carriers in Glanzmann's Thrombasthenia

1983 ◽  
Vol 49 (03) ◽  
pp. 182-186
Author(s):  
G T E Zonneveld ◽  
E F van Leeuwen ◽  
A Sturk ◽  
J W ten Cate
Keyword(s):  
Bleeding Time ◽  
Periodic Acid ◽  
Type I ◽  
Clot Retraction ◽  
Periodic Acid Schiff ◽  
Glanzmann’S Thrombasthenia ◽  
Aggregation Response ◽  
Glanzmann's Thrombasthenia ◽  
Sds Page ◽  
Reduced State

SummaryQuantitative glycoprotein (GP) analysis of whole platelets or platelet membranes was performed by SDS-polyacrylamide gelelectrophoresis (SDS-PAGE) and periodic acid Schiff staining in the families of two unrelated Glanzmann’s thrombasthenia (GT) patients. Each family consisted of two symptom free parents, a symptom free daughter and a GT daughter. All symptom free members had a normal bleeding time, clot retraction and platelet aggregation response to adenosine 5’-diphosphate (ADP), collagen and adrenalin. Platelet Zw* antigen was normally expressed in these subjects. GT patiens, classified as a type I and II subject, showed reduced amounts of GP lib and of GP nia. Analysis of isolated membranes in the non-reduced state, however, showed that the amount of GP Ilia was also reduced in three of the four parents, whereas one parent (of the GT type I patient) and the two unaffected daughters had normal amounts of GP Ilia. Quantitative SDS-PAGE may therefore provide a method for the detection of asymptomatic carriers in GT type I and II.

Swim bladder mycosis in farmed rainbow trout Oncorhynchus mykiss caused by Phoma herbarum and experimental verification of pathogenicity

2020 ◽  
Vol 138 ◽  
pp. 237-246 ◽  
Author(s):  
J Řehulka ◽  
A Kubátová ◽  
V Hubka
Keyword(s):  
Rainbow Trout ◽  
Histopathological Examination ◽  
Periodic Acid ◽  
Bladder Wall ◽  
Swim Bladder ◽  
Cell Reactivity ◽  
Periodic Acid Schiff ◽  
Posterior Portion ◽  
Hepatic Congestion ◽  
Phoma Herbarum

In this study, spontaneous swim bladder mycosis was documented in a farmed fingerling rainbow trout from a raceway culture system. At necropsy, the gross lesions included a thickened swim bladder wall, and the posterior portion of the swim bladder was enlarged due to massive hyperplasia of muscle. A microscopic wet mount examination of the swim bladder contents revealed abundant septate hyphae, and histopathological examination showed periodic acid-Schiff-positive mycelia in the lumen and wall of the swim bladder. Histopathological examination of the thickened posterior swim bladder revealed muscle hyperplasia with expansion by inflammatory cells. The causative agent was identified as Phoma herbarum through morphological analysis and DNA sequencing. The disease was reproduced in rainbow trout fingerlings using intraperitoneal injection of a spore suspension. Necropsy in dead and moribund fish revealed extensive congestion and haemorrhages in the serosa of visceral organs and in liver and abdominal serosanguinous fluid. Histopathological examination showed severe hepatic congestion, sinusoidal dilatation, Kupffer cell reactivity, leukostasis and degenerative changes. Fungi were disseminated to the liver, pyloric caeca, kidney, spleen and heart. Although infections caused by Phoma spp. have been repeatedly reported in fish, species identification has been hampered by extensive taxonomic changes. The results of this study confirmed the pathogenicity of P. herbarum in salmonids by using a reliably identified strain during experimental fish infection and provides new knowledge regarding the course of infection.

Erdheim-Chester Disease Presenting with Histiocytic Colitis and Cytokine Storm

2017 ◽  
Vol 26 (2) ◽  
pp. 183-187
Author(s):  
George P. Christophi ◽  
Yeshika Sharma ◽  
Quader Farhan ◽  
Umang Jain ◽  
Ted Walker ◽  
...  
Keyword(s):  
Periodic Acid ◽  
Poor Response ◽  
Rare Type ◽  
Periodic Acid Schiff ◽  
Hematopoietic Stem ◽  
Hemodynamic Compromise ◽  
Erdheim Chester Disease ◽  
Erdheim Chester ◽  
Chester Disease ◽  
Segmental Colitis

Background: Non-Langerhans histiocytosis is a group of inflammatory lymphoproliferative disorders originating from non-clonal expansion of hematopoietic stem cells into cytokine-secreting dendritic cells or macrophages. Erdheim-Chester Disease (ECD) is a rare type of non-Langerhans cell histiocytosis characterized by tissue inflammation and injury caused by macrophage infiltration and histologic findings of foamy histiocytes. Often ECD involves the skeleton, retroperitoneum and the orbits. This is the first report documenting ECD manifesting as segmental colitis and causing cytokine-release syndrome.Case presentation: A 68-year old woman presented with persistent fever without infectious etiology and hematochezia. Endoscopy showed segmental colitis and pathology revealed infiltration of large foamy histiocytes CD3-/CD20-/CD68+/CD163+/S100- consistent with ECD. The patient was empirically treated with steroids but continued to have fever and developed progressive distributive shock.Conclusion: This case report describes the differential diagnosis of infectious and immune-mediated inflammatory and rheumatologic segmental colitis. Non-Langerhans histiocytosis and ECD are rare causes of gastrointestinal inflammation. Prompt diagnosis is imperative for the appropriate treatment to prevent hemodynamic compromise due to distributive shock or gastrointestinal bleeding. Importantly, gastrointestinal ECD might exhibit poor response to steroid treatment and other potential treatments including chemotherapy, and biologic treatments targeting IL-1 and TNF-alpha signaling should be considered.Abbreviations: AFB: acid-fast bacilli; ECD: Erdheim-Chester Disease; IBD: inflammatory bowel disease; PASD: periodic acid-Schiff with diastase; TB: tuberculosis

scholarly journals Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation

2008 ◽  
Vol 295 (2) ◽  
pp. H691-H698 ◽  
Author(s):  
Alex Y. Tan ◽  
Shengmei Zhou ◽  
Byung Chun Jung ◽  
Masahiro Ogawa ◽  
Lan S. Chen ◽  
...  
Keyword(s):  
Pulmonary Vein ◽  
Sinus Node ◽  
Periodic Acid ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Atrial Arrhythmias ◽  
Periodic Acid Schiff ◽  
Stellate Ganglia ◽  
Ectopic Beats

The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein ( n = 11), right atrium ( n = 5), left atrium ( n = 2), and the vein of Marshall ( n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells ( P < 0.05) and sympathetic nerves ( P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

scholarly journals Immune Cell Modulation of the Extracellular Matrix Contributes to the Pathogenesis of Pancreatic Cancer

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 901
Author(s):  
Ramiz S. Ahmad ◽  
Timothy D. Eubank ◽  
Slawomir Lukomski ◽  
Brian A. Boone
Keyword(s):  
Pancreatic Cancer ◽  
Extracellular Matrix ◽  
Immune Cells ◽  
Immune Cell ◽  
Treatment Strategies ◽  
Stellate Cells ◽  
Pancreatic Stellate Cells ◽  
Ductal Adenocarcinoma ◽  
Cellular Mechanisms ◽  
Novel Treatment Strategies

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with a five-year survival rate of only 9%. PDAC is characterized by a dense, fibrotic stroma composed of extracellular matrix (ECM) proteins. This desmoplastic stroma is a hallmark of PDAC, representing a significant physical barrier that is immunosuppressive and obstructs penetration of cytotoxic chemotherapy agents into the tumor microenvironment (TME). Additionally, dense ECM promotes hypoxia, making tumor cells refractive to radiation therapy and alters their metabolism, thereby supporting proliferation and survival. In this review, we outline the significant contribution of fibrosis to the pathogenesis of pancreatic cancer, with a focus on the cross talk between immune cells and pancreatic stellate cells that contribute to ECM deposition. We emphasize the cellular mechanisms by which neutrophils and macrophages, specifically, modulate the ECM in favor of PDAC-progression. Furthermore, we investigate how activated stellate cells and ECM influence immune cells and promote immunosuppression in PDAC. Finally, we summarize therapeutic strategies that target the stroma and hinder immune cell promotion of fibrogenesis, which have unfortunately led to mixed results. An enhanced understanding of the complex interactions between the pancreatic tumor ECM and immune cells may uncover novel treatment strategies that are desperately needed for this devastating disease.

scholarly journals The potential renal toxicity of silver nanoparticles after repeated oral exposure and its underlying mechanisms

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Hamed Nosrati ◽  
Manijeh Hamzepoor ◽  
Maryam Sohrabi ◽  
Massoud Saidijam ◽  
Mohammad Javad Assari ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Molecular Mechanisms ◽  
Renal Toxicity ◽  
Periodic Acid ◽  
Critical Role ◽  
Oral Exposure ◽  
Control Group ◽  
Rt Pcr ◽  
Periodic Acid Schiff

Abstract Background Silver nanoparticles (AgNPs) can accumulate in various organs after oral exposure. The main objective of the current study is to evaluate the renal toxicity induced by AgNPs after repeated oral exposure and to determine the relevant molecular mechanisms. Methods In this study, 40 male Wistar rats were treated with solutions containing 30, 125, 300, and 700 mg/kg of AgNPs. After 28 days of exposure, histopathological changes were assessed using hematoxylin-eosin (H&E), Masson’s trichrome, and periodic acid-Schiff (PAS) staining. Apoptosis was quantified by TUNEL and immunohistochemistry of caspase-3, and the level of expression of the mRNAs of growth factors was determined using RT-PCR. Results Histopathologic examination revealed degenerative changes in the glomeruli, loss of tubular architecture, loss of brush border, and interrupted tubular basal laminae. These changes were more noticeable in groups treated with 30 and 125 mg/kg. The collagen intensity increased in the group treated with 30 mg/kg in both the cortex and the medulla. Apoptosis was much more evident in middle-dose groups (i.e., 125 and 300 mg/kg). The results of RT-PCR indicated that Bcl-2 and Bax mRNAs upregulated in the treated groups (p < 0.05). Moreover, the data related to EGF, TNF-α, and TGF-β1 revealed that AgNPs induced significant changes in gene expression in the groups treated with 30 and 700 mg/kg compared to the control group. Conclusion Our observations showed that AgNPs played a critical role in in vivo renal toxicity.

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