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1.
Diagn Pathol ; 10: 196, 2015 Oct 26.
Article in English | MEDLINE | ID: mdl-26503236

ABSTRACT

BACKGROUND: Nodular follicular lesions of thyroid gland comprise benign and malignant neoplasms, as well as some forms of hyperplasia. "Follicular" refers to origin of cells and in the same time to growth pattern - building follicles. Nodular follicular thyroid lesions have in common many morphological features, therefore attempts were made to define additional criteria for distinction between follicular adenoma, follicular carcinoma and follicular variant of papillary carcinoma. Increasing number of immunohistochemical markers is in the continual process of evaluation. METHODS: Tissue microarrays incorporating, total 201 cases, out of which 122 malignant and 79 benign follicular lesions, including neoplastic and non-neoplastic, were constructed and immunostained with antibodies to CD56, CK19, Galectin-3, HBME-1. Tissue cores were exclusively being acquired from tumour/lesion on interface with normal thyroid tissue. A systematic review of literature was done for period from the year 2001 to present time. RESULTS: All analysed markers may make a difference between benign lesions/tumours from differentiated thyroid carcinomas (p = <0.01, for all markers). Expression of all markers is significantly higher in papillary carcinoma than in follicular adenoma (p < 0.01). Statistically significant difference in expression of Galectin-3 and CD56 between follicular carcinoma and follicular adenoma was registered (p = 0.043; p = 0.028, respectively). The only marker which expression showed statistically significant difference between adenoma and carcinoma of Hurthle cells was Galectin 3 (p = 0.041). CK19 and HBME-1 were significantly expressed more in papillary carcinoma as compared to follicular carcinoma. CONCLUSION: Galectin 3 is most sensitive marker for malignancy, while loss of expression of CD56 is very specific for malignancy. Expected co-expression for combination of markers in diagnosis of follicular lesions decreases sensitivity and increases specificity for malignancy.


Subject(s)
Adenocarcinoma, Follicular , Biomarkers, Tumor , CD56 Antigen , Galectin 3 , Keratin-19 , Thyroid Neoplasms , Adult , Aged , Female , Humans , Male , Middle Aged , Adenocarcinoma, Follicular/diagnosis , Adenocarcinoma, Follicular/metabolism , Biomarkers, Tumor/analysis , Biomarkers, Tumor/metabolism , Carcinoma, Papillary/pathology , CD56 Antigen/metabolism , Galectin 3/metabolism , Keratin-19/metabolism , Thyroid Neoplasms/diagnosis , Thyroid Neoplasms/metabolism
2.
Med Oncol ; 25(4): 458-61, 2008.
Article in English | MEDLINE | ID: mdl-18214715

ABSTRACT

Two patients with lymphoplasmacytic lymphoma, and monoclonal proteins of IgM in one, and IgG and lambda light chains in the second patient, nephrotic syndrome and acute renal failure are reported. A 58-year-old man previously treated for pre-B acute lymphoblastic leukemia, developed 3 years later nephrotic syndrome as a complication of lymphoplasmacytic lymphoma and high-paraprotein IgM kappa type. Immunofluorescent analysis of kidney biopsy showed extensive IgM and light kappa chain deposits, which caused membranoproliferative glomerulonephritis. Treatment with cyclophosphamide was ineffective and patient died 2 months later. The second patient is a 42-year-old female diagnosed with lymphoplasmacytic lymphoma and paraprotein IgG lambda type. The course of the disease was fulminant with developing nephrotic syndrome and fatal acute renal failure. Immunofluorescent and light microscopic studies of kidney biopsy showed signs of immunotactoid glomerulonephritis with deposits of IgG and C3. Hemodyalises and cytostatic therapy were without response and she died after 45 days.


Subject(s)
Acute Kidney Injury/complications , Lymphoma, Non-Hodgkin/complications , Nephrotic Syndrome/complications , Waldenstrom Macroglobulinemia/complications , Acute Kidney Injury/pathology , Acute Kidney Injury/physiopathology , Adult , Fatal Outcome , Female , Fluorescent Antibody Technique , Humans , Immunoglobulin G , Immunoglobulin M , Immunohistochemistry , Lymphoma, Non-Hodgkin/pathology , Lymphoma, Non-Hodgkin/physiopathology , Male , Middle Aged , Nephrotic Syndrome/pathology , Nephrotic Syndrome/physiopathology , Waldenstrom Macroglobulinemia/physiopathology
3.
J Pharmacol Sci ; 100(1): 34-40, 2006 Jan.
Article in English | MEDLINE | ID: mdl-16404133

ABSTRACT

Radial artery (RA) is increasingly used as graft for coronary artery bypass grafting due to its good long-term patency. However, the mechanism of peri- and post-operative spasm is still unclear. Because of that, the aim of our study is to analyze the contractility of RA and to determine whether the presence of functional endothelium alters its contractile properties. Contractions of isolated RA rings were provoked by exogenously applied vasoconstrictors or by electrical field stimulation (EFS, 20 Hz). The order of vasoconstrictors potency based on their EC50 values was as follows: angiotensin II > phenylephrine > 5-hydroxytriptamine. Presence of endothelium increased both EC50 and maximal contraction to phenylephrine and angiotensin II, but inhibited reactivity of RA to 5-hydroxytriptamine. Spontaneous rhythmic contractions (SRC, <4 mHz) and EFS-induced contractions of RA are endothelium-independent and weaker than contractions induced by exogenously applied vasoconstrictors. Our study concludes that RA shows marked sensitivity and reactivity to angiotensin II, phenylephrine, and 5-hydroxytriptamine. Further investigations are necessary to answer why angiotensin II and phenylepehrine induce stronger contractions in the presence of endothelium. In addition, SRC as well as contractions of neurogenic origin may take part in developing vascular spasm of RA.


Subject(s)
Radial Artery/drug effects , Vasoconstriction , Angiotensin II/pharmacology , Dose-Response Relationship, Drug , Electric Stimulation , Endothelium, Vascular/drug effects , Humans , In Vitro Techniques , Muscle, Smooth, Vascular/drug effects , Phenylephrine/pharmacology , Serotonin/pharmacology , Time Factors , Vasoconstrictor Agents/pharmacology
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