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Background: Persistent hyperparathyroidism after kidney transplantation has been associated with adverse outcomes. Parathyroidectomy is the definitive treatment approach, but the success of parathyroidectomy relies on the accurate preoperative localization of the culprit parathyroid lesions. Simultaneous intrathyroidal parathyroid adenomas and multifocal papillary thyroid carcinoma present important diagnostic challenges. Here, we describe a patient with kidney transplantation who underwent successful surgery after being evaluated with functional and structural imaging.Case Presentation: A 53-year-old man presented with potentially malignant multifocal thyroid nodules by ultrasonography 2 years after kidney transplantation. The patient had hypercalcaemia and persistent hyperparathyroidism. Thyroid papillary carcinoma was confirmed in the left thyroid nodules by fine-needle aspiration biopsy. The right superior thyroid hypoechoic nodule was 1.2 cm in size and showed marked uptake of the tracer 99mTcO4-sestamibi during single-photon emission computed tomography/computed tomography (SPECT/CT); additionally, a cystic parathyroid lesion without tracer uptake was present behind the left superior pole of the thyroid. The histological examination demonstrated the coexistence of right intrathyroidal parathyroid adenomas, left cystic parathyroid nodular hyperplasia and multifocal papillary thyroid carcinoma. At the 6-month follow-up, the serum calcium levels were within the normal range, and the patient's kidney function remained stable.Conclusions: Simultaneous intrathyroidal parathyroid adenomas and multifocal papillary thyroid carcinoma in a patient with kidney transplantation is a rare clinical scenario. Physicians must be aware that the combination of functional (SPECT/CT) and structural (ultrasonography) imaging is highly successful in diagnosing patients with coexistent intrathyroidal parathyroid adenomas and papillary thyroid carcinoma. [ABSTRACT FROM AUTHOR]

Background: Cumulative evidences demonstrated the aberrant overexpression of Small Nucleolar RNA Host Gene 12 (SNHG12) in diverse human cancer. However, the expression status and involvement of SNHG12 in renal cell carcinoma is still elusive. Methods: The expression of SNHG12 was determined by q-PCR. The transcriptional regulation was interrogated by luciferase reporter assay. Cell viability was measured with CCK-8 kit. The anchorage-independent was evaluated by soft agar assay. Cell apoptosis was analyzed by Annexin V/7-AAD double staining. The migration and invasion were determined by trans-well assay and wound scratch closure. The in vivo tumor growth was monitored in xenograft mice model. Protein expression was quantified by immunoblotting. Results: SNHG12 was aberrantly up-regulated in renal carcinoma both in vivo and in vitro. High expression of SNHG12 associated with poor prognosis. Deficiency of SNHG12 significantly suppressed cell viability, anchorage-independent growth and induced apoptosis. In addition, SNHG12 silencing inhibited migrative and invasive in vitro and xenograft tumor growth in vivo. Mechanistically, SNHG12 modulated HIF1α expression via competing with miR-199a-5p, which consequently contributed to its oncogenic potential. MiR-199a-5p inhibition severely compromised SNHG12 silencing-elicited tumor repressive effects. Conclusion: Our data uncovered a crucial role of SNHG12-miR-199a-5p-HIF1α axis in human renal cancer. [ABSTRACT FROM AUTHOR]

Background: The objective of this study was to compare the dose distributions of RapidArc (RA), static gantry intensity-modulated radiotherapy (IMRT), and three-dimensional conformal radiotherapy (3DCRT) as adjuvant radiotherapy modalities for the treatment of gastric cancer.Methods: Fifteen patients with gastric cancer that underwent limited lymphadenectomy of perigastric lymph nodes were included in this study. Dosimetric values for a total dose of 45 Gy (1.8 Gy/day) were calculated for the RapidArc, IMRT, and 3DCRT modalities. The following parameters were compared: D99%, D1%, V95%, V107%, and conformity and homogeneity index values (CI and HI, respectively) for the planned target volume (PTV). Dose volume histogram (DVH) and dose distribution of the organs at risk (OAR), as the maximal dose to the spinal cord, V30 and V40 of the small bowel, and V20, V30 of liver and kidney were also assessed respectively.Results: RA, IMRT, and 3DCRT all achieved desirable PTV coverage. However, RA and IMRT significantly decreased D1% and V107%, and provided better CI and HI values compared with 3DCRT (P <0.05). Moreover, RA also achieved a significantly lower maximum dose for the spinal cord, liver V30, and kidney V20 compared to IMRT and 3DCRT; while the mean dose for these three organ types did not differ for the RA, IMRT, and 3DCRT plans.Conclusions: Both RA and IMRT achieved favorable PTV coverage compared to 3DCRT. In addition, RA achieved better dosimetry than IMRT and 3DCRT, and provided better protection for the spinal cord, liver, and kidneys. [ABSTRACT FROM AUTHOR]

Background: Glutathione S-transferases (GSTs) play an important role in metabolizing anti-epileptic drugs (AEDs) in liver. Expressions of GSTs in brain, which may result in poor efficacy of AEDs, have not been well studied. Using clinical cortex specimen from 32 intractable epileptic subjects and 8 non-epileptic controls, the present study investigated the correlation between GSTs and intractable epilepsy.Results: Three different GST isoforms (alpha, mu, and pi) were detected with immunohistochemistry. GST-alpha expression was not seen in any cortex specimens. Sixty three percent (63%) of control and 53% of intractible epileptic specimens showed GST-mu immunoreactivity. No significant difference in intensity of GST-mu staining was observed between these two groups. GST-pi expression was found in endothelial cells and glial cells/astrocytes. Fifty percent (50%) of the control patients and 66% of the epileptic patients were GST-pi positive. The grading of epileptic patients was significantly higher than that of control patients (p < 0.01).Conclusion: High levels of GST-pi in endothelial cells and glial cells/astrocyte correlate to medical intractable epilepsy, suggesting that GST-pi contributes to resistance to AED treatment. [ABSTRACT FROM AUTHOR]