Improved membranes for the extraction of heavy metals

This work presents a series of experimental tests on new practical approaches in membrane design to improve extraction capacity and rate. We chose an extraction system involving Aliquat 336 as the extractant and Cd(II) as the metal ion to be extracted to demonstrate these new approaches. The core element in the new membrane assembly was the extractant loaded sintered glass filter. This membrane assembly provided a large interface area between the extractant and the aqueous solution containing metal ions. By recycling the aqueous solution through the membrane assembly, the extraction rate was significantly improved. The membrane assembly also offered good extraction capacity

Essential Role for miR-196a in Brown Adipogenesis of White Fat Progenitor Cells

Brown adipocytes can differentiate from white fat progenitor cells in mice exposed to cold or β3-adrenergic stimulation, and this process is regulated by a microRNA that regulates the expression of Hoxc8, a master regulator of brown adipogenesis

Dissection of the Transformation of Primary Human Hematopoietic Cells by the Oncogene NUP98-HOXA9

NUP98-HOXA9 is the prototype of a group of oncoproteins associated with acute myeloid leukemia. It consists of an N-terminal portion of NUP98 fused to the homeodomain of HOXA9 and is believed to act as an aberrant transcription factor that binds DNA through the homeodomain. Here we show that NUP98-HOXA9 can regulate transcription without binding to DNA. In order to determine the relative contributions of the NUP98 and HOXA9 portions to the transforming ability of NUP98-HOXA9, the effects of NUP98-HOXA9 on primary human CD34+ cells were dissected and compared to those of wild-type HOXA9. In contrast to previous findings in mouse cells, HOXA9 had only mild effects on the differentiation and proliferation of primary human hematopoietic cells. The ability of NUP98-HOXA9 to disrupt the differentiation of primary human CD34+ cells was found to depend primarily on the NUP98 portion, whereas induction of long-term proliferation required both the NUP98 moiety and an intact homeodomain. Using oligonucleotide microarrays in primary human CD34+ cells, a group of genes was identified whose dysregulation by NUP98-HOXA9 is attributable primarily to the NUP98 portion. These include RAP1A, HEY1, and PTGS2 (COX-2). Their functions may reflect the contribution of the NUP98 moiety of NUP98-HOXA9 to leukemic transformation. Taken together, these results suggest that the effects of NUP98-HOXA9 on gene transcription and cell transformation are mediated by at least two distinct mechanisms: one that involves promoter binding through the homeodomain with direct transcriptional activation, and another that depends predominantly on the NUP98 moiety and does not involve direct DNA binding

Proton Density Fat Suppressed MRI in 3T Increases the Sensitivity of Multiple Sclerosis Lesion Detection in the Cervical Spinal Cord

Purpose: Considering the number of multiple sclerosis (MS) patients referred for clinical spinal cord imaging, the optimization of imaging protocols plays a crucial role. We aimed to evaluate the use of proton density (PD) turbo spin-echo (TSE) with spectral attenuated inversion recovery (SPAIR) fat suppression and compare it with the currently recommended T2-TSE-SPAIR in sagittal plane in cervical spinal cord imaging. Methods: In this study 35 MS patients with clinically suspected or known spinal cord lesions were scanned on a 3.0T magnetic resonance imaging (MRI) system. In addition to the routine protocol, PD-TSE-SPAIR sequences were obtained to quantitatively and qualitatively evaluate lesion detectability and image quality compared to T2-TSE-SPAIR sequences. Quantitative analysis was based on measurements of lesion-to-cord contrast ratio (LCCR), lesion contrast-to-noise ratio (LCNR) and lesion dimensions and the qualitative analysis on ranking with a predetermined score scale. The presence of lesions in these sequences was verified in axial T2 multi-echo gradient echo images. Results: In quantitative analysis, the lesions on PD-TSE-SPAIR had statistically significantly higher contrast (p < 0.05), according to the statistical test of LCCR, LCNR calculated contrast and measured lesion dimensions. Qualitative analyses were congruent with quantitative results; the median rank of PD-TSE-SPAIR was significantly higher than T2-TSE-SPAIR (p < 0.05). Of the 34 detected lesions 9 (26%) were not visualized in T2-TSE-SPAIR sequence. Conclusion: Considering its superiority in contrast ratios and lesion dimensions when compared to T2-TSE-SPAIR in both qualitative and quantitative analyses, we therefore recommend PD-TSE-SPAIR as a pivotal sequence to evaluate demyelinating spinal cord lesions at 3T. © 2017, Springer-Verlag GmbH Germany

Mesenteric cysts and mesenteric venous thrombosis leading to intestinal necrosis in pregnancy managed with laparotomy: A case report and review of the literature

Background: Mesenteric cyst is a rare clinical entity especially in pregnancy; therefore, few cases have been reported in the literature. The standard method of their treatment is surgical excision either with laparotomy or laparoscopy. In addition, mesenteric vein thrombosis is a rare and life-threatening condition in pregnancy and needs immediate treatment because it can lead to intestinal necrotic ischemia. This is the first report of the coexistence of mesenteric cysts and mesenteric vein thrombosis during gestation. Case presentation: A 27-year-old Greek woman, gravida 2 para 1, presented at 10 weeks' gestation to the Emergency Unit of our hospital complaining of diffuse abdominal pain which deteriorated the last 3 days, which was localized in her right iliac fossa, along with vomiting. She had undergone open laparotomy and right salpingo-oophorectomy at the age of 23 due to an ovarian cyst. Besides this, her personal and family medical history was unremarkable. She had never received oral contraceptives or any hormone therapy. On arrival, a clinical examination revealed tenderness on palpation of her right iliac fossa, without rebound tenderness or muscle guarding. Within 10 hours of hospitalization, her symptoms deteriorated further with rebound tenderness during the examination, tachycardia, and a drop of 12 units in her hematocrit value. An emergency laparotomy was performed. Two mesenteric cysts and a 60 cm necrotic part of her intestine were revealed intraoperatively. In the postoperative period, she complained of acute abdominal pain, tachycardia, and dyspnea. Computed tomography imaging revealed mesenteric vein thrombosis and pulmonary thromboembolism. She was treated with low molecular weight heparin and she was discharged on the 11th postoperative day. Conclusions: To the best of our knowledge, this is the first report in the literature of a simultaneous mesenteric cyst and mesenteric vein thrombosis in pregnancy. It is known that pregnancy is a state of hypercoagulation and clinicians should bear in mind this rare clinical condition in their diagnostic algorithm for acute abdominal pain. © 2017 The Author(s)

The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia

In leukemogenesis, several genetic changes conferring a proliferative and/or survival advantage to hematopoietic progenitor cells in addition to a block in differentiation are required. Here, we demonstrate that overexpression of the wild-type (wt) Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions (NUP98-HOXA10 and NUP98-HOXD13) to induce aggressive acute myeloid leukemia (AML). We used a mouse transplantation model to show their synergism in cotransduced bone marrow cells as well as in a cellular model of leukemic progression. Furthermore, our data support the finding that Meis1 overexpression leads to marked elevation in Flt3 transcription and extend it to the context of NUP98-HOX-induced leukemia. Together, these results support a multistep model where the synergism between NUP98-HOX and wt-Flt3 is the result of the ability of Flt3 to increase proliferation of myeloid progenitors blocked in differentiation by NUP98-HOX fusions and reveal a direct role for wt-Flt3 in the pathobiology of AML. Given the similarities in the leukemogenic role of native HOX and NUP98-fused HOX genes, our results underscore the clinical significance of the recurrent co-overexpression of wt-FLT3 and HOX in human leukemia and suggest that specific FLT3 inhibitors could be useful in treatment of HOX-induced AML or acute lymphoblastic leukemia (ALL)