Effect of ultrasound transmission gel on ultrasound-guided fine needle aspiration cytological specimens of thyroid.

OBJECTIVE: To investigate prospectively the diagnostic impact of ultrasound coupling gel on thyroid specimens obtained under ultrasound guidance. METHODS: Patients presenting for ultrasound-guided fine needle aspiration (USG-FNA) of the thyroid were invited to participate in the study. Four specimens per nodule were collected: two using chlorhexdine wash and two using sterile, colourless ultrasound gel as couplant according to routine protocol. All slides were analysed in a blinded fashion by two senior cytologists for the presence or absence of ultrasound gel-induced artefacts. The presence of gel-induced artefacts between the two groups was analyzed using Pearson's chi-square test. Kappa statistics were used to measure the inter-rater agreement between the cytologists. RESULTS: Twenty thyroid nodules comprising 80 specimen slides were collected. On slides collected with gel, cytological artefacts were detected in 60-65% of cases compared with 10-15% of cases without gel (P<0.001). The inter-rater agreement between the two observers was very good (κ=0.84). Two of the 14 patients required repeat FNA due to non-diagnostic cytology results caused by inadequate sampling and gel-induced artefacts. CONCLUSIONS: Clinical cytopathologists, radiologists and sonographers should be aware of the potential for ultrasound gel to cause significant artefacts on cytological specimens. Our findings suggest that staff involved in USG-FNA cytology should remove the gel carefully before taking the aspirate.

Systematic investigation of absorption, fluorescence and laser properties of some p- and m-oligophenylenes.

Absorption, fluorescence and laser properties of ten selected aromatic compounds from the oligophenylene family are studied experimentally at room temperature (293 K). The first eight compounds are arranged in such way that odd numbered compounds reveal 1Lb --> 1A fluorescence, while even numbered compounds show 1La --> 1A fluorescence. All compounds are family related in pi-structure and are of the same degree of planarity and rigidity. The quantum yield of fluorescence, gamma, and the decay times, tau(f), of non-deaerated and deaerated cyclohexane solutions are measured. The oscillator strength, f(e), the fluorescence rate constant, Kf, natural lifetimes, tau(o)T, and intersystem crossing rate constant, K(ST), are calculated. The lowest 1Lb and 1La singlet and 3La, triplet (77 K) levels are determined. Investigations showed that transition from a polyphenyl molecule which shows 1La --> 1A fluorescence to a family related in the pi-structure molecule which reveals the 1Lb --> 1A fluorescence is accompanied by certain changes in all the fluorescence parameters. This indicates that gamma decreases, tau(f) increases, Kf and the FWRE of the fluorescence spectrum decrease. Moreover, K(ST) also decreases, sometimes very significantly. The decrease in the K(ST) value is explained by the fact that matrix elements of the spin-orbit coupling of the S alpha and Ti states are much lower in value than analogous elements of the spin-orbit coupling of Sp and Ti states. It is shown that all p-polyphenyles exhibit excellent laser action, while m-polyphenyles do not produce laser oscillation under any conditions. The values of K(ST) and other fluorescence parameters measured can be used for various practical purposes and theoretical considerations.

Stanniocalcin 2: characterization of the protein and its localization to human pancreatic alpha cells.

Stanniocalcin (STC) is a hormone that was originally identified in fish, where it inhibits calcium uptake by the gills and gut and stimulates phosphate adsorption by the kidney. Recently, two mammalian homologues of stanniocalcin were identified. The first (STC1) shows 61% identity to the fish stanniocalcins and appears to have a function similar to that of the fish stanniocalcins. The second homologue (STC2) is 30-38% identical to the fish stanniocalcins, and is characterized by unique cysteine and histidine motifs that are not found in the other stanniocalcins. We purified both the native hamster and recombinant human STC2 proteins and obtained a partial amino acid sequence of the hamster protein. Both proteins behave as a disulfide bonded homodimer, which undergoes post-translational modification(s). The STC2 gene was localized to human chromosome 5q35. Northern blot analysis revealed that the primary site of human STC2 production is the pancreas, and immunostaining localized the STC2 protein to a subpopulation of cells in the islet. Double immunostaining for STC2 and either insulin or glucagon revealed that STC2 protein is found in the alpha cells, but not the beta cells. We speculate that STC2 may play a role in glucose homeostasis.

Role of beta-arrestin in mediating agonist-promoted G protein-coupled receptor internalization.

beta-Arrestins are proteins that bind phosphorylated heterotrimeric GTP-binding protein (G protein)-coupled receptors (GPCRs) and contribute to the desensitization of GPCRs by uncoupling the signal transduction process. Resensitization of GPCR responsiveness involves agonist-mediated receptor sequestration. Overexpression of beta-arrestins in human embryonic kidney cells rescued the sequestration of beta 2-adrenergic receptor (beta 2AR) mutants defective in their ability to sequester, an effect enhanced by simultaneous overexpression of beta-adrenergic receptor kinase 1. Wild-type beta 2AR sequestration was inhibited by the overexpression of two beta-arrestin mutants. These findings suggest that beta-arrestins play an integral role in GPCR internalization and thus serve a dual role in the regulation of GPCR function.

An iron-sulfur cluster plays a novel regulatory role in the iron-responsive element binding protein.

Post-transcriptional regulation of genes important in iron metabolism, ferritin and the transferrin receptor (TfR), is achieved through regulated binding of a cytosolic protein, the iron-responsive element binding protein (IRE-BP), to RNA stem-loop motifs known as iron-responsive elements (IREs). Binding of the IRE-BP represses ferritin translation and represses degradation of the TfR mRNA. The IRE-BP senses iron levels and accordingly modifies binding to IREs through a novel sensing mechanism. An iron-sulfur cluster of the IRE-BP reversibly binds iron; when cytosolic iron levels are depleted, the cluster becomes depleted of iron and the IRE-BP acquires the capacity to bind IREs. When cytosolic iron levels are replete, the IRE-BP loses RNA binding capacity, but acquires enzymatic activity as a functional aconitase. RNA binding and aconitase activity are mutually exclusive activities of the IRE-BP, and the state of the iron-sulfur cluster determines how the IRE-BP will function.

A regulated RNA binding protein also possesses aconitase activity.

A clone for the iron-responsive element (IRE)-binding protein (IRE-BP) has been transfected and expressed in mouse fibroblasts. The IRE-BP gene product binds IREs with high affinity and specificity. Amino acid alignments reveal that the IRE-BP is 30% identical to mitochondrial aconitase. The 18 active site residues of mitochondrial aconitase are identical to those in the IRE-BP, suggesting that the IRE-BP may possess aconitase activity. After purification of native IRE-BP and immunoaffinity purification of transfected and expressed IRE-BP, we demonstrate that the purified IRE-BP has aconitase activity.

Combination chemotherapy as single modality therapy for stage IE and IIE thyroid lymphoma.

Three women presented with malignant thyroid lymphoma (stage IE and IIE) that was associated with Hashimoto's thyroiditis. Each patient was treated with combination chemotherapy (two patients received cyclophosphamide/adriamycin/vincristine/prednisolone, one patient received methotrexate/adriamycin/cyclophosphamide/vincristine/prednisolone/ble omy cin) as the primary mode of therapy. One patient underwent incomplete excisional surgery and received chemotherapy. A complete clinical and radiological remission was achieved in all patients, in spite of evidence of extensive extrathyroidal invasion in two patients. The chemotherapy was well-tolerated, producing minimal toxicity. All the patients are alive and remain free of tumour recurrence 26 to more than 38 months after diagnosis. These results suggest that combination chemotherapy can be employed successfully as a single modality treatment for stage IE and IIE thyroid lymphomas, even when significant extrathyroidal invasion is present. The treatment of thyroid lymphoma is reviewed with emphasis on the potential role for chemotherapy as the primary modality.

CT scan and surgery in subdural empyema: a case report.

A high index of suspicion is required to pick up cases of subdural empyema in clinical practice. CT scan may be normal in the initial stages. Early neurosurgical intervention is desirable to reduce mortality and morbidity in this condition.

Benign congenital intracardiac thyroid and polycystic tumor causing right ventricular outflow tract obstruction and conduction disturbance.

A patient with a rare intracardiac tumor arising from the right side of the interventricular septum who developed conduction disturbances and symptoms of right ventricular outflow tract obstruction is reported. The patient was successfully treated with insertion of a permanent pacemaker and surgical removal of the tumor after two-dimensional echocardiography diagnosed the intracardiac mass. Pathologic examination confirmed the benign nature of the tumor and showed the unusual features of both ectopic thyroid and benign congenital polycystic tumor.

Ventricular tachycardia and sudden death in myotonic dystrophy: clinical, electrophysiologic and pathologic features.

A 37 year old man who presented with a cardiomyopathy, conduction defects and atrial and ventricular arrhythmias was found to have the neuromuscular manifestations of myotonic dystrophy. Despite implantation of a permanent cardiac pacemaker, antiarrhythmic drug therapy and antiarrhythmic surgery, sudden death occurred. The results of electrophysiologic studies, coronary arteriography and pathologic findings are described. This case confirms previous observations that ventricular arrhythmias, in addition to atrial arrhythmias and conduction disturbances, are cardiac manifestations of myotonic dystrophy and can lead to sudden death.