Scattering analysis of 2DEG carrier extracted by QMSA in undoped Al 0.25Ga0.75N/GaN heterostructures

Hall effect measurements on undoped Al0.25Ga0.75N/GaN heterostructures grown by a metalorganic chemical vapour deposition (MOCVD) technique have been carried out as a function of temperature (20-350 K) and magnetic field (0-1.5 T). Magnetic field dependent Hall data were analysed using the quantitative mobility spectrum analysis (QMSA) technique. The mobility and density within the two-dimensional electron gas (2DEG) at the Al 0.25Ga0.75N/GaN interface and within the underlying GaN layer were successfully separated by QMSA. Mobility analysis has been carried out using both the measured Hall data at a single field and the extracted data from QMSA. Analysis of the temperature-dependent mobility of 2DEG extracted from QMSA indicates that the interface roughness and alloy disorder scattering mechanisms are the dominant scattering mechanisms at low temperatures while at high temperatures only polar optical phonon scattering is the dominant mechanism. Al0.25Ga0.75N/GaN interface related parameters such as well width, deformation potential constant and correlation length were also accurately obtained from the fits of the simple analytical expressions of scattering mechanisms to the 2DEG mobility. © 2007 IOP Publishing Ltd

Discrimination between uterine serous papillary carcinomas and ovarian serous papillary tumours by gene expression profiling.

High-grade ovarian serous papillary cancer (OSPC) and uterine serous papillary carcinoma (USPC) represent two histologically similar malignancies characterised by markedly different biological behavior and response to chemotherapy. Understanding the molecular basis of these differences may significantly refine differential diagnosis and management, and may lead to the development of novel, more specific and more effective treatment modalities for OSPC and USPC. We used an oligonucleotide microarray with probe sets complementary to >10 000 human genes to determine whether patterns of gene expression may differentiate OSPC from USPC. Hierarchical cluster analysis of gene expression in OSPC and USPC identified 116 genes that exhibited >two-fold differences (P<0.05) and that readily distinguished OSPC from USPC. Plasminogen activator inhibitor (PAI-2) was the most highly overexpressed gene in OSPC when compared to USPC, while c-erbB2 was the most strikingly overexpressed gene in USPC when compared to OSPC. Overexpression of the c-erbB2 gene and its expression product (i.e., HER-2/neu receptor) was validated by quantitative RT-PCR as well as by flow cytometry on primary USPC and OSPC, respectively. Immunohistochemical staining of serous tumour samples from which primary OSPC and USPC cultures were derived as well as from an independent set of 20 clinical tissue samples (i.e., 10 OSPC and 10 USPC) further confirmed HER-2/neu as a novel molecular diagnostic and therapeutic marker for USPC. Gene expression fingerprints have the potential to predict the anatomical site of tumour origin and readily identify the biologically more aggressive USPC from OSPC. A therapeutic strategy targeting HER-2/neu may be beneficial in patients harbouring chemotherapy-resistant USPC

Gene expression profiles in primary ovarian serous papillary tumors and normal ovarian epithelium: identification of candidate molecular markers for ovarian cancer diagnosis and therapy.

With the goal of identifying genes with a differential pattern of expression between ovarian serous papillary carcinomas (OSPCs) and normal ovarian (NOVA) epithelium and using this knowledge for the development of novel diagnostic and therapeutic markers for ovarian cancer, we used oligonucleotide microarrays with probe sets complementary to 12,533 genes to analyze the gene expression profiles of 10 primary OSPC cell lines, 2 established OSPC cell lines (UCI-101, UCI-107) and 5 primary NOVA epithelial cultures. Unsupervised analysis of gene expression data identified 129 and 170 genes that exhibited >5-fold upregulation and downregulation, respectively, in primary OSPC compared to NOVA. Genes overexpressed in established OSPC cell lines had little correlation with those overexpressed in primary OSPC, highlighting the divergence of gene expression that occurs as a result of long-term in vitro growth. Hierarchical clustering of the expression data readily distinguished normal tissue from primary OSPC. Laminin, claudin 3, claudin 4, tumor-associated calcium signal transducers 1 and 2 (TROP-1/Ep-CAM, TROP-2), ladinin 1, S100A2, SERPIN2 (PAI-2), CD24, lipocalin 2, osteopontin, kallikrein 6 (protease M), kallikrein 10, matriptase (TADG-15) and stratifin were among the most highly overexpressed genes in OSPC compared to NOVA. Downregulated genes in OSPC included transforming growth factor-beta receptor III, platelet-derived growth factor receptor alpha, SEMACAP3, ras homolog gene family member I (ARHI), thrombospondin 2 and disabled-2/differentially expressed in ovarian carcinoma 2 (Dab2/DOC2). Differential expression of some of these genes, including claudin 3, claudin 4, TROP-1 and CD24, was validated by quantitative RT-PCR and flow cytometry on primary OSPC and NOVA. Immunohistochemical staining of formalin-fixed, paraffin-embedded tumor specimens from which primary OSPC cultures were derived further confirmed differential expression of CD24 and TROP-1/Ep-CAM markers on OSPC vs. NOVA. These results, obtained with highly purified primary cultures of ovarian cancer, highlight important molecular features of OSPC and may provide a foundation for the development of new type-specific therapies against this disease

FMR1 premutation and full mutation molecular mechanisms related to autism

Fragile X syndrome (FXS) is caused by an expanded CGG repeat (>200 repeats) in the 5′ un-translated portion of the fragile X mental retardation 1 gene (FMR1) leading to a deficiency or absence of the FMR1 protein (FMRP). FMRP is an RNA-binding protein that regulates the translation of a number of other genes that are important for synaptic development and plasticity. Furthermore, many of these genes, when mutated, have been linked to autism in the general population, which may explain the high comorbidity that exists between FXS and autism spectrum disorders (ASD). Additionally, premutation repeat expansions (55 to 200 CGG repeats) may also give rise to ASD through a different molecular mechanism that involves a direct toxic effect of FMR1 mRNA. It is believed that RNA toxicity underlies much of the premutation-related involvement, including developmental concerns like autism, as well as neurodegenerative issues with aging such as the fragile X-associated tremor ataxia syndrome (FXTAS). RNA toxicity can also lead to mitochondrial dysfunction, which is common in older premutation carriers both with and without FXTAS. Many of the problems with cellular dysregulation in both premutation and full mutation neurons also parallel the cellular abnormalities that have been documented in idiopathic autism. Research regarding dysregulation of neurotransmitter systems caused by the lack of FMRP in FXS, including metabotropic glutamate receptor 1/5 (mGluR1/5) pathway and GABA pathways, has led to new targeted treatments for FXS. Preliminary evidence suggests that these new targeted treatments will also be beneficial in non-fragile X forms of autism

Convergence insufficiency in idiopathic Parkinson\u27s disease responsive to levodopa

We report a patient with pathologically proven idiopathic Parkinson\u27s disease (IPD) who developed diplopia secondary to convergence insufficiency during his motor off periods. Diplopia resolved with onset of motor benefit from levodopa. Neuro-ophthalmologic examination demonstrated convergence insufficiency during motor off periods that was alleviated after onset of motor benefit from levodopa. This is the first reported case of convergence insufficiency in IPD responsive to levodopa

The effect of allopurinol pretreatment on intestinal hypoperfusion encountered after correction of intestinal volvulus

After reversal of blood flow following a prolonged period of ischemia, blood flow returns for a few seconds and is reduced afterward. This is called ''no-reflow phenomenon.'' Antioxidants such as allopurinol have been shown to prevent the occurrence of this phenomenon in organs other than the intestine. An experimental study was conducted to investigate the effect of allopurinol pretreatment on intestinal blood flow after correction of intestinal volvulus in rabbits. In group 1, baseline intestinal blood flow (IBF) was evaluated using radiolabeled red blood cells. In group 2, 720 degrees intestinal volvulus was created and IBF was evaluated 6 hours later. In group 3, intestinal volvulus was created and devolvulus was performed 6 hours later. Intraperitoneal isotonic saline was injected 60 minutes before correction of the volvulus. IBF was evaluated after correction of the volvulus. Group 4 had the same procedures as group 3, but allopurinol (200 mg/kg) was injected in place of the isotonic saline. IBF stopped 6 hours after volvulus. Compared with the baseline group, IBF was significantly lower in the group with volvulus + devolvulus (P < .01). The IBF of the allopurinol-treated group was significantly higher than that of the isotonic saline group (P < .01) and it did not differ significantly from that of the baseline group. Histopathological examination showed that intestinal volvulus leads to histological injury. The histological injury was more pronounced in the devolvulus group and was less severe in the allopurinol group in comparison to the isotonic saline pretreatment group (P < .01). It is concluded that allopurinol pretreatment prevents the intestinal hypoperfusion (no-reflow phenomenon) and histological injury encountered after correction of intestinal volvulus of 6 hours' duration. Copyright (C) 1996 by W.B. Saunders Compan

Giant left pheochromocytoma with vascular anomalies and pelvic horseshoe kidney: a case report

Abstract Background Pheochromocytoma is a neuroendocrine tumor, and its treatment is dependent on surgical resection. Due to the wide availability of cross-sectional imaging, pheochromocytomas are commonly seen as small tumors less than 10 cm in size and are mostly treated with minimally invasive surgery. Their concomitant presence with horseshoe kidney or other anatomical and vascular anomalies is rare. Herein, we present a surgically complex giant pheochromocytoma case who underwent an open left radical adrenalectomy. Case presentation A 41-year-old Hispanic female presented with a 12 × 8 cm left hypervascular adrenal mass, pelvic horseshoe kidney, and severely dilated large left retro-aortic renal vein which branched into a left adrenal vein, congested left ovarian vein, and left uterine plexus. She was managed with insulin and metformin for uncontrolled diabetes with an A1c level of 9% and doxazosin for persistent hypertension. Clinical diagnosis of pheochromocytoma was confirmed with elevated urine and serum metanephrine and normetanephrine. The pre-operative ACTH was within normal range with a normal dexamethasone suppression test and 24-hour urine free cortisol. The adrenalectomy of the highly aggressive adrenal mass was performed via open approach to obtain adequate surgical exposure. Due to the large size of the tumor and its significant involvement with multiple adjacent structures, coordination with multiple surgical teams and close hemodynamic monitoring by anesthesiology was required for successful patient outcomes including preservation of blood supply to the pelvic horseshoe kidney. The histopathological diagnosis was pheochromocytoma with negative surgical margins. The patient was followed at 1, 4, 12, and 24 weeks postoperatively. She had a normal postoperative eGFR and was able to discontinue antihypertensive and antidiabetic medications at four weeks. She had transient adrenal insufficiency, which resolved at five months. The horseshoe kidney was intact except for a minimal area of hypo-enhancement in the left superior renal moiety due to infarction, which was significantly improved at six months. Conclusion Our patient had a giant pheochromocytoma with anatomical variations complicating an already surgically challenging procedure. Nonetheless, with multiple provider collaboration, detailed pre-operative surgical planning, and meticulous perioperative monitoring, radical resection of the giant pheochromocytoma was safe and feasible with successful postoperative outcomes