Adult ovarian and sellar region mixed germ cell tumor: a case report and literature review

Mixed germ cell tumors (mGCTs) involving both the ovaries and sellar region have been rarely reported; thus, they pose significant challenges in clinical management. Our report of a case of a 26-year-old female with left ovarian mGCTs (dysgerminoma + yolk sac tumor) who presented with postoperative headaches and blurred vision contributes new information to the literature on treating mGCTs, which can lead to standardized regimens and sequencing guidelines. A physical examination revealed right temporal hemianopia, and elevated levels of alpha-fetoprotein were detected in serum and cerebrospinal fluid. Magnetic resonance imaging (MRI) of the sellar region revealed a space-occupying lesion. Pathological examination of the tumor after endoscopic transnasal resection confirmed the diagnosis of mGCTs (germinomas + yolk sac tumor). The patient received adjuvant chemotherapy and radiotherapy at reduced dosages. During follow-up, tumor markers remained within normal limits, and there was no evidence of tumor recurrence on sellar region MRI. This case highlights the rarity of the simultaneous occurrence of ovarian and sellar region mGCTs and emphasizes the importance of accurate diagnosis and multidisciplinary management

Comparison of commercial solutions for Low Power Wide Area IoT

Low Power Wide Area (LPWA) technology is an important field for innovation in Internet of Things(IoT) that enables ubiquitous IoT. Target applications of LPWA technology are with low power consumption, large connections, and low cost. These applications have tremendous market potential, as they will be in the center of building an “everything-connected” world. The first step in realizing it will be connecting the end terminals to the network, a domain that has plenty of different access technologies. This thesis compares commercial access solutions for LPWA IoT network by considering the technical, business and market factors with literature review and case studies. The technologies include two categories, proprietary LPWA technologies and cellular LPWA technologies. The main proprietary technologies include SIGFOX and LoRa, while cellular technologies mainly include NB-IoT and eMTC. The result of this thesis reveals that proprietary and cellular technologies will have different uses and therefore different markets. Cellular LPWA solutions will be deployed on carrier-class network, while proprietary LPWA solutions are deployed with fast and flexible means in enterprise-specific applications, such as in smart cities and industries related to them

A Spectral Feature Based Convolutional Neural Network for Classification of Sea Surface Oil Spill

Spectral characteristics play an important role in the classification of oil film, but the presence of too many bands can lead to information redundancy and reduced classification accuracy. In this study, a classification model that combines spectral indices-based band selection (SIs) and one-dimensional convolutional neural networks was proposed to realize automatic oil films classification using hyperspectral remote sensing images. Additionally, for comparison, the minimum Redundancy Maximum Relevance (mRMR) was tested for reducing the number of bands. The support vector machine (SVM), random forest (RF), and Hu’s convolutional neural networks (CNN) were trained and tested. The results show that the accuracy of classifications through the one dimensional convolutional neural network (1D CNN) models surpassed the accuracy of other machine learning algorithms such as SVM and RF. The model of SIs+1D CNN could produce a relatively higher accuracy oil film distribution map within less time than other models

Bending Properties of Cold-Formed Thin-Walled Steel/Fast-Growing Timber Composite I-Beams

A cold-formed, thin-walled steel/fast-growing timber composite system has recently been presented for low-rise buildings. It aims to increase the use of fast-growing wood as a green building material in structures, thus contributing to the transformation of traditional buildings. This study proposed a composite I-beam combined with fast-growing radiata pine and cold-formed thin-walled U-shaped steel. A four-point bending test was used to measure the bending properties of steel–timber composite I-beams under various connection methods. Based on experimental results, this study examined the specimen’s failure mechanism, mechanical properties, and strain development. In addition, a method for calculating flexural bearing capacity based on the superposition principle and transformed section method was suggested. It is evident from the results that fast-growing timber and cold-formed thin-walled steel can have significant composite effects. Different connecting methods significantly impact beams’ failure mode, stiffness, and bearing capacity. Furthermore, the theoretical method for calculating the flexural bearing capacity of composite beams differs from the test value by less than 10%. This paper’s research encourages the applications of fast-growing wood as light residential components, and it serves as a reference for the development, production, and engineering of steel–timber composite structural systems

Triple conversion strategy to build anti-de-icing sheets for the leading edge of the rotor blade

Aircraft anti-icing and de-icing, aimed at reducing energy consumption, is a compelling technology that enables a plethora of eco-friendly energy applications to overcome long-standing crisis challenges. In this study, we present a tri-conversion strategy, inspired by superhydrophobicity, photothermal conversion, and electrothermal conversion, to develop an all-weather, high-efficiency, and low-energy rotor leading edge anti-icing and de-icing patch. The experimental samples not only possess stable superhydrophobic photothermal conversion capabilities but also achieve a 610-second delay in droplet icing, a 1-second nitrogen blow for frost, and a low ice adhesion strength of 11.6 KPa. Under one sun illumination, it can achieve a stable 54-second static melt and 37-second dynamic melt. With a connection to a 24 V DC stabilized power supply, it showcases an excellent 146-second de-icing capability. The synergistic action of multiple barriers enhances the anti-icing and de-icing performance. This work not only provides rational design principles for high-energy consumption de-icing but also offers insights into harnessing the power of nature for photothermal conversion de-icing

Exosomal MicroRNA Expression Profiling Analysis of the Effects of Lycium Barbarum Polysaccharide on Gestational Diabetes Mellitus Mice

Objective. Gestational diabetes mellitus (GDM) is a pathological condition, affecting an increasing number of pregnant women worldwide. Safe and effective treatment for GDM is very important for the public health. In this study, we utilized a high-fat diet-induced GDM model to evaluate the effects of LBP on GDM and examined the changes of exosomal microRNA expression profiling to decipher the potential underlying mechanism of LBP. Methods. Female C57BL/6J mice were fed a control diet, HFD, or 150 mg/kg LBP-supplemented HFD for 6 weeks before conception and throughout gestation. Oral glucose tolerance test and plasma lipid levels were determined, and liver histopathology was assessed. Sequencing was used to define the microRNA expression profiling of plasma exosomes in the three groups of mice, and protein expression levels of the candidate target genes were analyzed. Results. LBP significantly relieved glucose intolerance, abnormal plasma lipid levels, and pathomorphological changes of liver histopathology in HFD-induced GDM mice. Moreover, we found that this effect of LBP was mediated by downregulation of the increase of 6 miRNAs (miR-93-3p, miR-188-5p, miR-466k, miR-1188-5p, miR-7001-3p, and miR-7115-5p) and reversing the increase of the protein expression of CPT1A, which is the target gene of miR-188-5p. Conclusions. Our findings provide novel insights into the biological activities of LBP in the treatment of GDM

Systemic inflammatory response syndrome in patients with severe fever with thrombocytopenia syndrome: prevalence, characteristics, and impact on prognosis

Abstract Background Severe fever with thrombocytopenia syndrome (SFTS) is an emerging zoonosis with a high fatality rate in China. Previous studies have reported that dysregulated inflammatory response is associated with disease pathogenesis and mortality in patients with SFTS. This investigation aimed to evaluate the prevalence and characteristics of systemic inflammatory response syndrome (SIRS), and its impact on prognosis. Methods Data on demographic characteristics, comorbid conditions, clinical manifestations, laboratory parameters, and survival time of patients with SFTS were collected. Patients were divided into the non-SIRS and SIRS groups according to the presence of SIRS, then their clinical data were compared. Results A total of 290 patients diagnosed with SFTS were retrospectively enrolled, including 126(43.4%) patients with SIRS. Patients in the non-survivor group had more prevalence of SIRS than patients in the survivor group (P < 0.001), and SIRS (adjusted OR 2.885, 95% CI 1.226–6.786; P = 0.005) was shown as an independent risk factor for prognosis of patients with SFTS. Compared with patients without SIRS, patients with SIRS had lower WBC and neutrophils counts, and fibrinogen levels, but higher AST, LDH, amylase, lipase, CK, CK-MB, troponin I, APTT, thrombin time, D-dimer, CRP, IL-6, SAA levels, and viral load. The cumulative survival rate of patients with SIRS was significantly lower than that of patients without SIRS. Patients with SIRS also showed a higher incidence of bacterial or fungal infections than patients without SIRS. Conclusions SIRS is highly frequent in patients with SFTS, and it is associated with high mortality

ERK activation via A1542/3 limonoids attenuates erythroleukemia through transcriptional stimulation of cholesterol biosynthesis genes

Abstract Background Cholesterol plays vital roles in human physiology; abnormal levels have deleterious pathological consequences. In cancer, elevated or reduced expression of cholesterol biosynthesis is associated with good or poor prognosis, but the underlying mechanisms are largely unknown. The limonoid compounds A1542 and A1543 stimulate ERK/MAPK by direct binding, leading to leukemic cell death and suppression of leukemia in mouse models. In this study, we investigated the downstream consequences of these ERK/MAPK agonists in leukemic cells. Methods We employed RNAseq analysis combined with Q-RT-PCR, western blot and bioinformatics to identify and confirm genes whose expression was altered by A1542 and A1543 in leukemic cells. ShRNA lentiviruses were used to silence gene expression. Cell culture and an animal model (BALB/c) of erythroleukemia induced by Friend virus were utilized to validate effects of cholesterol on leukemia progression. Results RNAseq analysis of A1542-treated cells revealed the induction of all 18 genes implicated in cholesterol biosynthesis. Expression of these cholesterol genes was blocked by cedrelone, an ERK inhibitor. The cholesterol inhibitor lovastatin diminished ERK/MAPK activation by A1542, thereby reducing leukemic cell death induced by this ERK1/2 agonist. Growth inhibition by cholesterol was observed both at the intracellular level, and when orally administrated into a leukemic mouse model. Both HDL and LDL also suppressed leukemogenesis, implicating these lipids as important prognostic markers for leukemia progression. Mechanistically, knockdown experiments revealed that the activation of SREBP1/2 by A1542-A1543 was responsible for induction of only a sub-set of cholesterol biosynthesis genes. Induction of other regulatory factors by A1542-A1543 including EGR1, AP1 (FOS + JUN) LDLR, IER2 and others may cooperate with SREBP1/2 to induce cholesterol genes. Indeed, pharmacological inhibition of AP1 significantly inhibited cholesterol gene expression induced by A1542. In addition to leukemia, high expression of cholesterol biosynthesis genes was found to correlate with better prognosis in renal cancer. Conclusions This study demonstrates that ERK1/2 agonists suppress leukemia and possibly other types of cancer through transcriptional stimulation of cholesterol biosynthesis genes

FLI1 induces erythroleukemia through opposing effects on UBASH3A and UBASH3B expression

Abstract Background FLI1 is an oncogenic transcription factor that promotes diverse malignancies through mechanisms that are not fully understood. Herein, FLI1 is shown to regulate the expression of Ubiquitin Associated and SH3 Domain Containing A/B (UBASH3A/B) genes. UBASH3B and UBASH3A are found to act as an oncogene and tumor suppressor, respectively, and their combined effect determines erythroleukemia progression downstream of FLI1. Methods Promoter analysis combined with luciferase assays and chromatin immunoprecipitation (ChIP) analysis were applied on the UBASH3A/B promoters. RNAseq analysis combined with bioinformatic was used to determine the effect of knocking-down UBASH3A and UBASH3B in leukemic cells. Downstream targets of UBASH3A/B were inhibited in leukemic cells either via lentivirus-shRNAs or small molecule inhibitors. Western blotting and RT-qPCR were used to determine transcription levels, MTT assays to assess proliferation rate, and flow cytometry to examine apoptotic index. Results Knockdown of FLI1 in erythroleukemic cells identified the UBASH3A/B genes as potential downstream targets. Herein, we show that FLI1 directly binds to the UBASH3B promoter, leading to its activation and leukemic cell proliferation. In contrast, FLI1 indirectly inhibits UBASH3A transcription via GATA2, thereby antagonizing leukemic growth. These results suggest oncogenic and tumor suppressor roles for UBASH3B and UBASH3A in erythroleukemia, respectively. Mechanistically, we show that UBASH3B indirectly inhibits AP1 (FOS and JUN) expression, and that its loss leads to inhibition of apoptosis and acceleration of proliferation. UBASH3B also positively regulates the SYK gene expression and its inhibition suppresses leukemia progression. High expression of UBASH3B in diverse tumors was associated with worse prognosis. In contrast, UBASH3A knockdown in erythroleukemic cells increased proliferation; and this was associated with a dramatic induction of the HSP70 gene, HSPA1B. Accordingly, knockdown of HSPA1B in erythroleukemia cells significantly accelerated leukemic cell proliferation. Accordingly, overexpression of UBASH3A in different cancers was predominantly associated with good prognosis. These results suggest for the first time that UBASH3A plays a tumor suppressor role in part through activation of HSPA1B. Conclusions FLI1 promotes erythroleukemia progression in part by modulating expression of the oncogenic UBASH3B and tumor suppressor UBASH3A

Lovastatin inhibits erythroleukemia progression through KLF2-mediated suppression of MAPK/ERK signaling

Abstract Background Lovastatin, an HMG-CoA inhibitor and an effective cholesterol lowering drug, exhibits anti-neoplastic activity towards several types of cancer, although the underlying mechanism is still not fully understood. Herein, we investigated mechanism of growth inhibition of leukemic cells by lovastatin. Methods RNAseq analysis was used to explore the effect of lovastatin on gene expression in leukemic cells. An animal model of leukemia was used to test the effect of this statin in vivo. FAM83A and DDIT4 expression was knocked-downed in leukemia cells via lentivirus-shRNA. Western blotting, RT-qPCR, cell cycle analysis and apoptosis assays were used to determine the effect of lovastatin-induced growth suppression in leukemic cells in vitro. Results Lovastatin treatment strongly inhibited cancer progression in a mouse model of erythroleukemia induced by Friend virus. In tissue culture, lovastatin inhibited cell proliferation through induction of G1 phase cell cycle arrest and apoptosis. Interestingly, lovastatin induced most known genes associated with cholesterol biosynthesis in leukemic cells. Moreover, it suppressed ERK1/2 phosphorylation by downregulating FAM83A and DDIT4, two mediators of MAP-Kinase signaling. RNAseq analysis of lovastatin treated leukemic cells revealed a strong induction of the tumor suppressor gene KLF2. Accordingly, lentivirus-mediated knockdown of KLF2 antagonized leukemia cell suppression induced by lovastatin, associated with higher ERK1/2 phosphorylation compared to control. We further show that KLF2 induction by lovastatin is responsible for lower expression of the FAM83A and DDIT4 oncogenes, involved in the activation of ERK1/2. KLF2 activation by lovastatin also activated a subset of cholesterol biosynthesis genes that may further contribute to leukemia suppression. Conclusions These results implicate KLF2-mediated FAM83A/DDIT4/MAPK suppression and activation of cholesterol biosynthesis as the mechanism of leukemia cell growth inhibition by lovastatin