The proteoglycan skeleton of the Kurloff body as evidenced by Cuprolinic Blue staining

1994 ◽  
Vol 26 (7) ◽  
pp. 571-581 ◽  
Author(s):  
G. Landemore ◽  
M. Quillec ◽  
S. -E. Leta�ef ◽  
J. Izard
Keyword(s):  
Blue Staining ◽  
Cuprolinic Blue

scholarly journals Binding and endocytosis of thrombospondin and thrombospondin fragments in endothelial cell cultures analyzed by cuprolinic blue staining, colloidal gold labeling, and silver enhancement techniques.

1991 ◽  
Vol 39 (10) ◽  
pp. 1385-1394 ◽  
Author(s):  
W Völker ◽  
P Schön ◽  
P Vischer
Keyword(s):  
Endothelial Cells ◽  
Cell Surface ◽  
Colloidal Gold ◽  
Blue Staining ◽  
Heparin Binding ◽  
Binding Region ◽  
Silver Enhancement ◽  
Coated Pits ◽  
Gold Particles ◽  
Cuprolinic Blue

We investigated the distribution of thrombospondin-specific binding sites and the uptake of thrombospondin-gold conjugates in cultured porcine endothelial cells by light and electron microscopy. Colloidal gold marker and silver enhancement techniques were applied for cytochemical detection of monomeric thrombospondin and fragments of thrombospondin. Thrombospondin binds to granular and fibrillar structures and to sites of cell-cell contact on the cell surface, as indicated by many proteoglycan-cuprolinic blue precipitates. Cell migration tracks on the culture dish bottom are most heavily stained. Labeling of intact thrombospondin and of proteolytic fragments of thrombospondin with colloidal gold followed by silver intensification enables one to detect its binding and uptake in endothelial cells. Binding to the cell surface and uptake of thrombospondin-gold particles was inhibited by heparin but not by hyaluronic acid or chondroitin sulfate. The heparin binding region at the N-terminal end of the thrombospondin molecule proved to be essential for cell surface binding. Gold-conjugated thrombospondin fragments devoid of the heparin binding region were not internalized. After 60 min incubation at 37 degrees C, thrombospondin-gold particles accumulated in the lysosomal compartment close to the nucleus. In the presence of monensin and ammonium chloride, vesicles in this area are swollen and the concentration of particulate marker is reduced. Binding and uptake of thrombospondin by vascular endothelial cells appears to require linkage of the heparin binding region of the thrombospondin molecule to coated pits and heparan sulfate-rich molecules as receptors. Colloidal gold conjugation of thrombospondin fragments proved to be useful for cytochemical characterization of molecular domains.

Medial Smooth Muscle Cell Proliferation in the Balloon Injured Rabbit Aorta: Effect of a Thiazole Compound with Platelet Inhibitory Activity

1984 ◽  
Vol 51 (01) ◽  
pp. 075-078 ◽  
Author(s):  
R G Schaub ◽  
C A Simmons
Keyword(s):  
Smooth Muscle ◽  
Platelet Aggregation ◽  
Balloon Catheter ◽  
Rabbit Aorta ◽  
Surface Characteristics ◽  
Inhibitory Effect ◽  
Lesion Size ◽  
Blue Staining ◽  
Morphologic Characteristics ◽  
Time Period

SummaryTwenty-seven adult male New Zealand rabbits (3–4 kgs) were used in this study. Six rabbits received vehicle, 3 groups of 6 each received doses of 4,5-bis(p-methoxyphenyl)-2-(trifluoromethyl)- thiazole, (U-53,059), at 0.3 mg/kg, 3.0 mg/kg and 30.0 mg/kg/day respectively. Drug and vehicle doses were given orally each day starting 3 days before balloon injury and continuing for the entire 2 week time period. Three rabbits were used as nontreated sham controls. In the vehicle and U-53,059 treated groups aortae were denuded of endothelial cells by balloon catheter injury. Two weeks after injury platelet aggregation to collagen was measured and the aortae removed for analysis of surface characteristics by scanning electron microscopy and lesion size by morphometry. All doses of U-53,059 inhibited platelet aggregation. The 3.0 and 30.0 mg/kg groups had the greatest inhibitory effect. All balloon injured aortae had the same morphologic characteristics. All vessels had similar extent and intensity of Evan’s blue staining, similar areas of leukocyte/platelet adhesion, and a myointimal cell cover of transformed smooth muscle cells. The myointimal proliferative response was not inhibited at any of the drug doses studied.

Methylene Blue Test in Assessing Disease Free Margins in Lingual Carcinoma Resection

2018 ◽  
Vol 68 (12) ◽  
pp. 2879-2880
Author(s):  
Razvan Hainarosie ◽  
Viorel Zainea ◽  
Mura Hainarosie ◽  
Catalina Pietrosanu ◽  
Irina Ionita ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Young Patients ◽  
Blue Staining ◽  
Resection Margins ◽  
Methylene Blue Test ◽  
Lingual Carcinoma ◽  
Disease Free

Lingual squamous cell carcinoma is one of the most frequent localization of the oral carcinomas. The tongue neoplasia represents nearly 40% of the oral carcinomas. Recent studies showed an increasing trend of lingual carcinoma in young patients. Several staining tests have been described to early detect the disease. After detection, disease free margins resection will increase the survival rate. This study aims to analyze the methylene blue staining test in achieving disease free resection margins in lingual squamous cell carcinoma.

The Use of Methylene Blue Staining Test in Determining the CSF Leaks Location of the Anterior Skull Base

2018 ◽  
Vol 69 (6) ◽  
pp. 1376-1377
Author(s):  
Razvan Hainarosie ◽  
Teodora Ghindea ◽  
Irina Gabriela Ionita ◽  
Mura Hainarosie ◽  
Cristian Dragos Stefanescu ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Cerebrospinal Fluid ◽  
Intrathecal Injection ◽  
Diagnostic Procedures ◽  
Blue Staining ◽  
Csf Leak ◽  
Glucose Content ◽  
Csf Rhinorrhea ◽  
Cerebrospinal Fluid Rhinorrhea ◽  
Csf Leakage

Cerebrospinal fluid rhinorrhea represents drainage of cerebrospinal fluid into the nasal cavity. The first steps in diagnosing CSF rhinorrhea are a thorough history and physical examination of the patient. Other diagnostic procedures are the double ring sign, glucose content of the nasal fluid, Beta-trace protein test or beta 2-transferrin. To establish the exact location of the defect imagistic examinations are necessary. However, the gold standard CSF leakage diagnostic method is an intrathecal injection of fluorescein with the endoscopic identification of the defect. In this paper we analyze a staining test, using Methylene Blue solution, to identify the CSF leak�s location.

scholarly journals Physical and mechanical properties of rubberwood (Hevea brasiliensis) dyed with Lasiodiplodia theobromae

2019 ◽  
Vol 65 (1) ◽  
Author(s):  
Boshi Zhao ◽  
Zhiming Yu ◽  
Yang Zhang ◽  
Chusheng Qi
Keyword(s):  
Mass Loss ◽  
Water Absorption ◽  
Hevea Brasiliensis ◽  
Ph Value ◽  
Energy Dispersive Spectrometer ◽  
Physical And Mechanical Properties ◽  
Blue Staining ◽  
Loss Ratio ◽  
Lasiodiplodia Theobromae ◽  
Infrared Spectrometer

AbstractBlue staining on rubberwood (Hevea brasiliensis) is a common kind of defect. There currently exists much research focused on the prevention and control of blue staining. However, little research has been concentrated on the utilization of blue staining for green dyeing. The research conveyed in this paper primarily used Lasiodiplodia theobromae to dye rubberwood, and used scanning electron microscope (SEM), energy-dispersive spectrometer (EDS), X-ray diffraction (XRD), and fourier transform infrared spectrometer (FTIR) to analyze the commission internationale eclairage (CIE) L*a*b* value of color, the contact angle, the pH value, 24-h water absorption, mass loss ratio, and compressive strength in increments between 5 and 40 days. The results found that the color of rubberwood became darker and more uniform, and that the surface dyed with fungi can reach a super-hydrophobic state. With the increase of time, the pH value of rubberwood changed from acidic to alkaline. Furthermore, hyphae entered the wood mainly through vessels for their large pore diameter, and reduced water absorption. Mass loss ratio increased gradually between 5 and 40 days. The research in this paper concludes that the microorganism was an effective method of wood dyeing, and lays a foundation for further research.

scholarly journals Iron accumulation in the oculomotor nerve of the progressive supranuclear palsy brain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hansol Lee ◽  
Myung Jun Lee ◽  
Eun-Joo Kim ◽  
Gi Yeong Huh ◽  
Jae-Hyeok Lee ◽  
...  
Keyword(s):  
High Resolution ◽  
Progressive Supranuclear Palsy ◽  
Oculomotor Nerve ◽  
Iron Accumulation ◽  
Blue Staining ◽  
Normal Brain ◽  
Myelinated Fiber ◽  
Healthy Controls ◽  
Icp Ms

AbstractAbnormal iron accumulation around the substantia nigra (SN) is a diagnostic indicator of Parkinsonism. This study aimed to identify iron-related microarchitectural changes around the SN of brains with progressive supranuclear palsy (PSP) via postmortem validations and in vivo magnetic resonance imaging (MRI). 7 T high-resolution MRI was applied to two postmortem brain tissues, from one normal brain and one PSP brain. Histopathological examinations were performed to demonstrate the molecular origin of the high-resolution postmortem MRI findings, by using ferric iron staining, myelin staining, and two-dimensional laser ablation-inductively coupled plasma-mass spectrometry (LA-ICP-MS) imaging. In vivo iron-related MRI was performed on five healthy controls, five patients with Parkinson’s disease (PD), and five patients with PSP. In the postmortem examination, excessive iron deposition along the myelinated fiber at the anterior SN and third cranial nerve (oculomotor nerve) fascicles of the PSP brain was verified by LA-ICP-MS. This region corresponded to those with high R2* values and positive susceptibility from quantitative susceptibility mapping (QSM), but was less sensitive in Perls’ Prussian blue staining. In in vivo susceptibility-weighted imaging, hypointense pixels were observed in the region between the SN and red nucleus (RN) in patients with PSP, but not in healthy controls and patients with PD. R2* and QSM values of such region were significantly higher in patients with PSP compared to those in healthy controls and patients with PD as well (vs. healthy control: p = 0.008; vs. PD: p = 0.008). Thus, excessive iron accumulation along the myelinated fibers at the anterior SN and oculomotor nerve fascicles may be a pathological characteristic and crucial MR biomarker in a brain with PSP.

Lif Deficiency Leads to Iron Transportation Dysfunction in Ameloblasts

2021 ◽  
pp. 002203452110119
Author(s):  
L. Fan ◽  
Y.J. Ou ◽  
Y.X. Zhu ◽  
Y.D. Liang ◽  
Y. Zhou ◽  
...  
Keyword(s):  
Tooth Development ◽  
Iron Status ◽  
Acid Resistance ◽  
Blue Staining ◽  
Maturation Stage ◽  
Wild Type ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Stem Cell Pluripotency ◽  
Underlying Mechanisms

Leukemia inhibitory factor (LIF), a member of the interleukin 6 family of cytokines, is involved in skeletal metabolism, blastocyst implantation, and stem cell pluripotency maintenance. However, the role of LIF in tooth development needs to be elucidated. The aim of the present study was to investigate the effect of Lif deficiency on tooth development and to elucidate the functions of Lif during tooth development and the underlying mechanisms. First, it was found that the incisors of Lif-knockout mice had a much whiter color than those of wild-type mice. Although there were no structural abnormalities or defective mineralization according to scanning electronic microscopy and computed tomography analysis, 3-dimensional images showed that the length of incisors was shorter in Lif−/− mice. Microhardness and acid resistance assays showed that the hardness and acid resistance of the enamel surface of Lif−/− mice were decreased compared to those of wild-type mice. In Lif−/− mice, whose general iron status was comparable to that of the control mice, the iron content of the incisors was significantly reduced, as confirmed by energy-dispersive X-ray spectroscopy (EDS) and Prussian blue staining. Histological staining showed that the cell length of maturation-stage ameloblasts was shorter in Lif−/− mice. Likewise, decreased expression of Tfrc and Slc40a1, both of which are crucial proteins for iron transportation, was observed in Lif−/− mice and Lif-knockdown ameloblast lineage cell lines, according to quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot. Moreover, the upregulation of Tfrc and Slc40a1 induced by Lif stimulation was blocked by Stattic, a signal transducer and activator of transcription 3 (Stat3) signaling inhibitor. These results suggest that Lif deficiency inhibits iron transportation in the maturation-stage ameloblasts, and Lif modulates expression of Tfrc and Slc40a1 through the Stat3 signaling pathway during enamel development.

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