656 research outputs found

    Primary hepatic neuroendocrine carcinoma: report of two cases and literature review.

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    Background: Primary hepatic neuroendocrine carcinoma (PHNEC) is extremely rare. The diagnosis of PHNEC remains challenging-partly due to its rarity, and partly due to its lack of unique clinical features. Available treatment options for PHNEC include surgical resection of the liver tumor(s), radiotherapy, liver transplant, transcatheter arterial chemoembolization (TACE), and administration of somatostatin analogues. Case presentation: We report two male PHNEC cases and discuss the diagnosis and treatment options. Both cases presented with abdominal pain; case two also presented with symptoms of jaundice. The initial diagnosis for both cases was poorly differentiated grade 3 small-cell neuroendocrine carcinoma, based on imaging characteristics and the pathology of liver biopsies. Final diagnoses of PHNEC were arrived at by ruling out non-hepatic origins. Case one presented with a large tumor in the right liver lobe, and the patient was treated with TACE. Case two presented with tumors in both liver lobes, invasions into the left branch of hepatic portal vein, and metastasis in the hepatic hilar lymph node. This patient was ineligible for TACE and was allergic to the somatostatin analogue octreotide. This limited treatment options to supportive therapies such as albumin supplementation for liver protection. Patient one and two died at 61 and 109 days, respectively, following initial hospital admission. Conclusions: We diagnosed both cases with poorly differentiated grade 3 small-cell PHNEC through imaging characteristics, immunohistochemical staining of liver biopsies, and examinations to eliminate non-hepatic origins. Neither TACE nor liver protection appeared to significantly extend survival time of the two patients, suggesting these treatments may be inadequate to improve survival of patients with poorly differentiated grade 3 small-cell PHNEC. The prognosis of poorly differentiated grade 3 small-cell PHNEC is poor due to limited and ineffective treatment options. BMC Clin Pathol 2018 Mar 1; 18:3

    Effect of β-nerve growth factor on differentiation of endothelial progenitor cells in rats

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    Purpose: To investigate the effect of recombinant adenovirus-mediated human β-nerve growth factor (Ad-EGFP-hβ-NGF) on the differentiation of endothelial progenitor cells (EPCs) in rats.Methods: The successfully constructed Ad-EGFP-hβ-NGF and its negative control Ad-EGFP were infected into the isolated and purified rat EPCs to observe their morphological changes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the levels of vascular endothelial growth factor (VEGF), von Willebrand factor (vWF) and basic fibroblast growth factor (bFGF) in different rat EPC culture solutions. Western blot was performed to determine the expression of tyrosine kinase receptor A (TrKA) protein in different groups of EPCs.Results: Primary fibrous EPCs were converted into epithelium-like cells. After infection with Ad-EGFPhβ- NGF for 1 week, some EPCs became round and exhibited neural stem cell-like changes. The expression levels of VEGF, vWF and bFGF in the Ad-EGFP-hβ-NGF infection group were significantly higher than those in the control group (p < 0.01). TrKA protein in Ad-EGFP-hβ-NGF infection was also significantly up-regulated compared with that in the negative control and blank control groups (p <0.01).Conclusion: β-NGF up-regulates the expression of TrKA receptor protein and secretion of angiogenic growth factors (i.e., VEGF, vWF and bFGF), thereby promoting the differentiation of rat EPCs, which may contribute to angiopoiesis or vascular repair.Keywords: β-Nerve growth factor, Endothelial progenitor cells, Angiogenic growth factors, Tyrosine kinase receptor A, Cell differentiatio

    New structures of Fe3S for rare-earth-free permanent magnets

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    We applied an adaptive genetic algorithm (AGA) to search for low-energy crystal structures of Fe3S. A number of structures with energies lower than that of the experimentally reported Pnma and I-4 structures have been obtained from our AGA searches. These low-energy structures can be classified as layer-motif and column-motif structures. In the column-motif structures, Fe atoms self-assemble into rods with a bcc type of underlying lattice, which are separated by the holes terminated by S atoms. In the layer-motif structures, the bulk Fe is broken into slabs of several layers passivated by S atoms. Magnetic property calculations showed that the column-motif structures exhibit reasonably high uniaxial magnetic anisotropy. In addition, we examined the effect of Co doping to Fe3S and found that magnetic anisotropy can be enhanced through Co doping

    The Chinese (Cantonese) Montreal Cognitive Assessment in Patients with Subcortical Ischemic Vascular Dementia

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    Background: Subcortical ischemic vascular dementia (SIVD) has been proposed as the most frequent subtype of vascular cognitive impairment. The aim of this study was to evaluate the psychometric properties of the Chinese (Cantonese) Montreal Cognitive Assessment (CC- MoCA) in patients with SIVD in the Guangdong Province of China. Methods: 71 SIVD patients and 60 matched controls were recruited for the CC-MoCA, Mini Mental State Examination and executive clock drawing tasks. Receiver-operating characteristic curve analyses were performed to determine optimal sensitivity and specificity of the CC-MoCA total score in differentiating mild vascular dementia (VaD) patients from moderate VaD patients and controls. Results: The mean CC-MoCA scores of the controls, and mild and moderate VaD patients were 25.2 ± 3.8, 16.4 ± 3.7, and 10.0 ± 5.1, respectively. In our study, the optimal cutoff value for the CC-MoCA to be able to differentiate patients with mild VaD from controls is 21/22, and 13/14 to differentiate mild VaD from moderate VaD. Conclusion: The CC-MoCA is a useful cognitive screening instrument in SIVD patients

    GeV antiproton/gamma-ray excesses and the WW-boson mass anomaly: three faces of ∼60−70\sim 60-70 GeV dark matter particle?

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    For the newly discovered WW-boson mass anomaly, one of the simplest dark matter (DM) models that can account for the anomaly without violating other astrophysical/experimental constraints is the inert two Higgs doublet model, in which the DM mass (mSm_{S}) is found to be within ∼54−74\sim 54-74 GeV. In this model, the annihilation of DM via SS→bbˉSS\to b\bar{b} and SS→WW∗SS\to WW^{*} would produce antiprotons and gamma rays, and may account for the excesses identified previously in both particles. Motivated by this, we re-analyze the AMS-02 antiproton and Fermi-LAT Galactic center gamma-ray data. For the antiproton analysis, the novel treatment is the inclusion of the charge-sign-dependent three-dimensional solar modulation model as constrained by the time-dependent proton data. We find that the excess of antiprotons is more distinct than previous results based on the force-field solar modulation model. The interpretation of this excess as the annihilation of SS→WW∗SS\to WW^{*} (SS→bbˉSS\to b\bar{b}) requires a DM mass of ∼40−80\sim 40-80 (40−6040-60) GeV and a velocity-averaged cross section of O(10−26) cm3 s−1O(10^{-26})~{\rm cm^3~s^{-1}}. As for the γ\gamma-ray data analysis, rather than adopting the widely-used spatial template fitting, we employ an orthogonal approach with a data-driven spectral template analysis. The fitting to the GeV γ\gamma-ray excess yields DM model parameters overlapped with those to fit the antiproton excess via the WW∗WW^{*} channel. The consistency of the DM particle properties required to account for the WW-boson mass anomaly, the GeV antiproton excess, and the GeV γ\gamma-ray excess suggest a common origin of them.Comment: 8 page

    Major adverse cardiovascular events associated with testosterone treatment: a pharmacovigilance study of the FAERS database

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    Background and purpose: Testosterone is an essential sex hormone in maintaining masculine characteristics, which is prescribed for male hypogonadism as testosterone replacement treatment (TRT). Herein, we investigated long-standing controversies about the association between TRT and major adverse cardiovascular events (MACEs), based on real world adverse event (AE) reports, registered in the Food and Drug Administration Adverse Event Reporting System (FAERS).Methods: Publicly available FAERS data from 1 January 2004 to 31 December 2022 were retrieved from the Food and Drug Administration (FDA) website. The data mining protocol including the reporting odds ratio (ROR) and the Bayesian confidence propagation neural network (BCPNN) was applied to analyze overreporting caused by risk factors and MACEs, including TRT, morbidities, and ages. The ROR and the BCPNN were also applied to investigate the annually developing trend of pharmacovigilance (PV) signals in the real world, retrospectively.Results: A total of 3,057 cases referring to MACEs, with a median age of 57 years old (yo), were identified from 28,921 cases of testosterone users. MACEs related to PV signals have emerged since 2014, including cardiac death, non-fatal myocardial infarction, and non-fatal stroke. Myocardial infarction (MI) (ROR: 9.46; IC025: 3.08), acute myocardial infarction (AMI) (ROR: 16.20; IC025: 3.72), ischemic cardiomyopathy (ROR: 11.63; IC025: 2.20), and cardiomyopathy (ROR: 5.98; IC025: 1.96) were the most significant signals generated, and weaker signals included cardiac failure acute (ROR: 4.01; IC025: 0.71), cardiac arrest (ROR: 1.88; IC025: 0.56), and ventricular fibrillation (VF) (ROR: 2.38; IC025: 0.38). The time-to-onset (TTO) of MACEs was calculated with a median of 246 days for AMI.Conclusion: For myocardial infarction and cardiomyopathy, TRT statistically tended to increase the risk of MACEs, while for cardiac arrhythmia, cardiac failure, and stroke, TRT demonstrated beneficial effects among the population with morbidities, such as testosterone deficiency (TD), diabetes mellitus (DM), and hypertension. MACEs were rare but led to serious outcomes including significant increase in death and disability. Since 2018, and before 2014, reports referring to TRT associated with MACEs were relatively scarce, which indicated that there might be a considerable number of cases that went unrecorded, due to neglection. Health workers and testosterone users might pay more attention to testosterone-induced MACEs
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