Ectopic expression of follicle-stimulating hormone receptors in thyroid tumors

Introduction

In normal conditions follicle-stimulating hormone receptors (FSHR) are expressed in the ovary and the testis. They can also be expressed in gonadal tumors. However, recently we have found FSHR immunostaining in pituitary adenomas, adrenal tumors and neuroendocrine tumors (carcinoids). The aim of this study was to determine whether the same occurs in thyroid tumors.

Material and methods

Thirty-six samples of surgically excised thyroids were examined. Follicle-stimulating hormone receptors immunostaining was performed on paraffin sections using the rabbit anti-human FSHR polyclonal antibody raised against a 1-190 amino acid sequence from the human FSHR (sc-13935, Santa Cruz).

Results

Normal thyroid follicles do not show immunopositivity for FSHR. The same concerns the majority of benign lesions, diagnosed as hyperplasia nodularis or thyroid adenomas. However, positive FSHR immunostaining in some follicles was observed. In all but one thyroid cancer (15 papillary, 10 follicular cancers and one case of anaplastic thyroid cancer) 10–100% of tumor cells exhibit positive FSHR immunostaining. In about 40% of samples FSHR immunoreactivity can be observed also in the endothelia of intrathyroidal blood vessels. This immunopositivity was more frequent in the samples of thyroid cancers (13/27) than in benign lesions (2/9).

Conclusions

Ectopic positive FSHR immunostaining is also present in thyroid cancers, and, to a lesser degree, in benign lesions but not in the normal thyroid epithelium.     

Lung ultrasound—a new diagnostic modality in persistent tachypnea of infancy

Lung ultrasound (LUS) has been increasingly used in diagnosing and monitoring of various pulmonary diseases in children. The aim of the current study was to evaluate its usefulness in children with persistent tachypnea of infancy (PTI). This was a controlled, prospective, cross‐sectional study that included children with PTI and healthy subjects. In patients with PTI, LUS was performed at baseline and then after 6 and 12 months of follow‐up. Baseline results of LUS were compared to (a) baseline high‐resolution computed tomography (HRCT) images, (b) LUS examinations in control group, and (c) follow‐up LUS examinations. Twenty children with PTI were enrolled. B‐lines were found in all children with PTI and in 11 (55%) control subjects (P < .001). The total number of B‐lines, the maximal number of B lines in any intercostal space, the distance between B‐lines, and pleural thickness were significantly increased in children with PTI compared to controls. An irregularity of the pleural line was found in all patients with PTI and in none of the healthy children. There were no significant changes in LUS findings in patients with PTI during the study period. The comparison of HRCT indices and LUS findings revealed significant correlations between the mean lung attenuation, skewness, kurtosis and fraction of interstitial pulmonary involvement, and the number of B‐lines as well as the pleural line thickness. LUS seems to be a promising diagnostic tool in children with PTI. Its inclusion in the diagnostic work‐up may enable to reduce the number of costly, hazardous, and ionizing radiation‐based imaging procedures.     

Adipocyte dysfunction in rats with streptozotocin–nicotinamide‐induced diabetes

Administration of streptozotocin (STZ) and nicotinamide (NA) to adult rats allows for the induction of mild diabetes. However, this experimental model has not been fully characterized. This study was undertaken to determine the metabolic and secretory activity of adipose tissue in rats with STZ‐NA‐induced diabetes. Experiments were performed using epididymal adipocytes isolated from control and mildly diabetic rats. Lipogenesis, glucose transport as well as glucose and alanine oxidation, lipolysis, anti‐lipolysis, cAMP levels and adipokine secretion were compared in cells isolated from the control and diabetic rats. Lipogenesis, glucose transport and oxidation were diminished in the adipocytes of diabetic rats compared with the fat cells of control animals. However, alanine oxidation appeared to be similar in the cells of non‐diabetic and diabetic animals. Lipolytic response to low epinephrine concentrations was slightly increased in the adipocytes of diabetic rats; however, at higher concentrations of the hormone, lipolysis was similar in both groups of cells. The epinephrine‐induced rise in cAMP levels was higher in the adipocytes of STZ‐NA‐induced diabetic rats, even in the presence of insulin. Lipolysis stimulated by dibutyryl‐cAMP did not significantly differ, whereas anti‐lipolytic effects of insulin were mildly decreased in the cells of diabetic rats. Secretion of adiponectin and leptin was substantially diminished in the adipocytes of diabetic rats compared with the cells of control animals. Our studies demonstrated that the balance between lipogenesis and lipolysis in the adipose tissue of rats with mild diabetes induced by STZ and NA is slightly shifted towards reduced lipid accumulation. Simultaneously, adiponectin and leptin secretion is significantly impaired.     

The Complement Cascade and Renal Disease

Serum complement cascade, a part of innate immunity required for host protection against invading pathogens, is also a mediator of various forms of disease and injury. It is activated by classical, lectin, and alternative pathways that lead to activation of C3 component by C3 convertases, release of C3b opsonin, C5 conversion and eventually membrane attack complex formation. The tightly regulated activation process yields also C3a and C5a anaphylatoxins, which target a broad spectrum of immune and non-immune cells. The review discusses the involvement of the complement cascade in kidney disease pathogenesis and injury. The role of the complement pathways in autoantibody-mediated forms of glomerulonephritis (lupus nephritis, anti-glomerular basement membrane disease, anti-neutrophil cytoplasmic autoantibody-induced or membranoproliferative glomerulonephritis, membranous nephropathy), C3 glomerulopathy, atypical forms of hemolytic uremic syndrome, ischemic-reperfusion injury of transplanted kidney, and antibody-mediated renal allograft rejection are discussed. The disturbances in complement activation and regulation with underlying genetics are presented and related to observed pathology. Also promising strategies targeting the complement system in complement-related disorders are mentioned.