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The article presents an international perspectives on women's participation in the sciences and establishes an economic and socio-political context for stories of women pioneers in glaciology. These experiences of individual glaciologists reflects women's experience in higher education and sciences as a whole. The Renaissance marked a rebirth for female intellectuals but their subordinate social status persisted and access to education differed across national borders. It indicates that women who have sought advanced education and work in the sciences and mathematics have faced challenges in finding the appropriate training and admission to universities throughout history. Women continue to remain under-represented in math and physical sciences despite hard-won gains of the 20th century.

Background: Human-like H3N2 influenza viruses have repeatedly been transmitted to domestic pigs in different regions of the world, but it is still uncertain whether any of these variants could become established in pig populations. The fact that different subtypes of influenza viruses have been detected in pigs makes them an ideal candidate for the genesis of a possible reassortant virus with both human and avian origins. However, the determination of whether pigs can act as a "mixing vessel" for a possible future pandemic virus is still pending an answer. This prompted us to gather the epidemiological information and investigate the genetic evolution of swine influenza viruses in Jilin, China. Methods: Nasopharyngeal swabs were collected from pigs with respiratory illness in Jilin province, China from July 2007 to October 2008. All samples were screened for influenza A viruses. Three H3N2 swine influenza virus isolates were analyzed genetically and phylogenetically. Results: Influenza surveillance of pigs in Jilin province, China revealed that H3N2 influenza viruses were regularly detected from domestic pigs during 2007 to 2008. Phylogenetic analysis revealed that two distinguishable groups of H3N2 influenza viruses were present in pigs: the wholly contemporary human-like H3N2 viruses (represented by the Moscow/10/99-like sublineage) and double-reassortant viruses containing genes from contemporary human H3N2 viruses and avian H5 viruses, both co-circulating in pig populations. Conclusions: The present study reports for the first time the coexistence of wholly human-like H3N2 viruses and double-reassortant viruses that have emerged in pigs in Jilin, China. It provides updated information on the role of pigs in interspecies transmission and genetic reassortment of influenza viruses. [ABSTRACT FROM AUTHOR]

Neuronal plasticity deficits underliemanyof the neurobehavioral problems seen in fetal alcohol spectrum disorders (FASD). Recently,we showed that third trimester alcohol exposure leads to a persistent disruption in ocular dominance (OD) plasticity. For instance, a few days of monocular deprivation results in a robust reduction of cortical regions responsive to the deprived eye in normal animals, but not in ferrets exposed early to alcohol. This plasticity deficit can be reversed if alcohol-exposed animals are treated with a phosphodiesterase type 1 (PDE1) inhibitor during the period of monocular deprivation. PDE1 inhibition can increase cAMP and cGMP levels, activating transcription factors such as the cAMP response element binding protein (CREB) and the serum response factor (SRF). SRF is important for many plasticity processes such as LTP, LTD, spine motility, and axonal pathfinding. Here we attempt to rescue OD plasticity in alcohol-treated ferrets using a Sindbis viral vector to express a constitutively active form of SRF during the period of monocular deprivation. Using optical imaging of intrinsic signals and single-unit recordings, we observed that overexpression of a constitutively active form of SRF, but neither its dominant-negative nor GFP, restored OD plasticity in alcohol-treated animals. Surprisingly, this restoration was observed throughout the extent of the primary visual cortex and most cells infected by the virus were positive for GFAP rather than NeuN. This finding suggests that overexpression of SRF in astrocytes may reduce the deficits in neuronal plasticity seen in models of FASD. [ABSTRACT FROM AUTHOR]

The article discusses the study on the impact of global climate change on the spatial distributions of the basal melting and freezing at the Amery Ice Shelf in East Antartica. It examines the surface elevation and accumulation rate datasets of the ice velocity along with a column-averaged ice density model and hydrographic observations. It estimates the net melt over the ice-shelf base is which is higher than previous modeling and oceanographic estimates. It notes that the net basal melting accounts for about half of the total ice-shelf mass loss and from the iceberg discharge. It adds that the basal melting and freezing distribution map has provided a scientific basis for quantitative analysis of ice and ocean interaction at the ice-shelf and ocean interface.

Background: Fetal alcohol spectrum disorders (FASD) are the leading cause of mental retardation in the western world and children with FASD present altered somatosensory, auditory and visual processing. There is growing evidence that some of these sensory processing problems may be related to altered cortical maps caused by impaired developmental neuronal plasticity. Methodology/Principal Findings: Here we show that the primary visual cortex of ferrets exposed to alcohol during the third trimester equivalent of human gestation have decreased CREB phosphorylation and poor orientation selectivity revealed by western blotting, optical imaging of intrinsic signals and single-unit extracellular recording techniques. Treating animals several days after the period of alcohol exposure with a phosphodiesterase type 1 inhibitor (Vinpocetine) increased CREB phosphorylation and restored orientation selectivity columns and neuronal orientation tuning. Conclusions/Significance: These findings suggest that CREB function is important for the maturation of orientation selectivity and that plasticity enhancement by vinpocetine may play a role in the treatment of sensory problems in FASD. [ABSTRACT FROM AUTHOR]

Investigates the gene expression patterns of human breast cancers. Suppression of protein tyrosine kinases; Gene profiling of the mammary gland; Induction of calcium-signaling pathways in mammary models of cancer.

BackgroundThe 2020 Chinese guidelines for ultrasound malignancy risk stratification of thyroid nodules: the C-TIRADS (C-TIRADS for short) put forward a method for stratifying the malignancy risk of thyroid nodules, but there are few studies about its value in differentiating benign and malignant thyroid nodules.ObjectiveTo compare the value of ultrasound-based thyroid nodule malignancy risk stratification in differentiating malignant and benign thyroid nodule between C-TIRADS and 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: the American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer (ATA guidelines for short) .MethodsA total of 336 inpatients who underwent surgery and ultrasound examination in Bozhou People's Hospital from January 2019 to May 2021 were selected as participants. Four ultrasonologists with a title higher than attending physician were equally randomized into groups A and B for evaluating ultrasonic examination results according to ultrasound-based thyroid nodule malignancy risk stratification in C-TIRADS and ATA guidelines, respectively. The accuracies of ultrasound-based thyroid nodule malignancy stratification in the two guidelines in differentiating malignant and benign thyroid nodules were assessed using intraoperative or postoperative pathological findings (gold standard for diagnosis) , and were further analyzed using ROC analysis.ResultsAccording to intraoperative or postoperative pathological findings, the participants had 367 thyroid nodules in total, including 253 benign nodules and 114 malignant nodules. The nodules were classified as follows according to the TI-RADS in the C-TIRADS by ultrasonologists in group A: (1) 253 benign nodules: 2 were in TI-RADS 5 category, 23, 30, and 80 were in categories 4c, 4b, and 4a, respectively, 103 were in 3 category, and 15 were in 2 category; (2) 114 malignant nodules: 24 were in TI-RADS 5 category, 59 were in 4c category, 22 were in 4b category, 6 were in 4a category and 3 were in 3 category. And the classification of nodules according to the ATA guideline by ultrasonologists in group B was: (1) 253 benign nodules: 13, 53, 47, 118 were high, intermediate, low, and very low suspicion pattern for malignancy, respectively, and 22 were benign pattern; (2) 114 malignant nodules: 76, 24, 8, 6 were high, intermediate, low, and very low suspicion pattern for malignancy, respectively. ROC analysis showed that, AUCs of ultrasound-based thyroid nodule malignancy risk stratification in differentiating malignant and benign thyroid nodules between C-TIRADS and ATA guidelines were 0.890〔95%CI (0.815, 0.918) 〕and 0.780〔95%CI (0.750, 0.876) 〕, with significant difference (Z=13.62, P

Cisplatin is an established chemotherapeutic drug for treatment of solid-organ cancers and is the primary drug used in the treatment of head and neck cancer; however, cisplatin-induced nephrotoxicity largely limits its clinical use. Inhibition of sphingosine kinase 2 (SphK2) has been demonstrated to alleviate various kidney diseases. Therefore, we hypothesized that inhibition of SphK2 could also protect against cisplatin-induced nephrotoxicity. Results from the present study showed that the SphK2 inhibitor ABC294640 or knockdown of SphK2 by siRNA blocked the cisplatin-induced increase of cellular injury markers (neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and cleaved caspase-3) by Western blot analysis in HK-2 cells, a human renal tubular cell line. In addition, SphK2 inhibition blocked cisplatin-induced activation of NF-κB by Western blot analysis and immunostaining analysis. Furthermore, SphK2 inhibition suppressed cisplatin-induced increases of proinflammatory markers (NLR family pyrin domain containing 3, interleukin-1β, and interleukin-6). Genetic deletion of the SphK2 gene in mice further confirmed that inhibition of SphK2 protected against cisplatin-induced kidney damage in vivo. Compared with wild-type mice, SphK2 knockout mice exhibited less renal dysfunction and reduced promotion of kidney injury markers, inflammatory factors, tubular morphology damage, and fibrotic staining. At the same time, the SphK2 inhibitor ABC294640 failed to interfere with the activity of cisplatin or radiation in two cell culture models of head and neck cancer. It is concluded that inhibition of Sphk2 protects against cisplatin-induced kidney injury. SphK2 may be used as a potential therapeutic target for the prevention or treatment of cisplatininduced kidney injury. NEW & NOTEWORTHY The present study provides new findings that sphingosine kinase 2 (SphK2) is highly expressed in renal tubules, cisplatin treatment increases the expression of SphK2 in proximal tubular cells and kidneys, and inhibition of SphK2 alleviates cisplatin-induced kidney injury by suppressing the activation of NF-κB, production of inflammatory factors, and apoptosis. SphK2 may serve as a potential therapeutic target for the prevention or treatment of cisplatin-induced nephrotoxicity. [ABSTRACT FROM AUTHOR]

The fetal liver (FL) serves as a predominant site for expansion of functional hematopoietic stem cells (HSCs) during mouse embryogenesis. However, the mechanisms for HSC development in FL remain poorly understood. In this study, we demonstrate that deletion of activating transcription factor 4 (ATF4) significantly impaired hematopoietic development and reduced HSC self-renewal in FL. In contrast, generation of the first HSC population in the aorta-gonad-mesonephros region was not affected. The migration activity of ATF4-/- HSCs was moderately reduced. Interestingly, the HSC-supporting ability of both endothelial and stromal cells in FL was significantly compromised in the absence of ATF4. Gene profiling using RNA-seq revealed down regulated expression of a panel of cytokines in ATF4-/- stromal cells, including angiopoietin-like protein 3 (Angptl3) and vascular endothelial growth factor A (VEGFA). Addition of Angptl3, but not VEGFA, partially rescued the repopulating defect of ATF4-/- HSCsin the culture. Furthermore, chromatin immunoprecipitation assay in conjunction with silencing RNA-mediated silencing and complementary DNA over expression showed transcriptional control of Angptl3 by ATF4. To summarize, ATF4 plays a pivotal role in functional expansion and repopulating efficiency of HSCs in developing FL, and it acts through upregulating transcription of cytokines such as Angptl3 in the microenvironment. [ABSTRACT FROM AUTHOR]

In this study both adult male and female antennal sensilla of Trogoderma granarium Everts, 1896 and Trogoderma variabile Ballion, 1878 (Coleoptera: Dermestidae) were observed by scanning electron microscope. The antennae of both species were found to consist of a scape, a pedicel and a flagellum with 9 subsegments, i.e., flagellomeres. Four categories of antennal sensilla including 10 types were found in these 2 species. The sensilla were designated, sensilla chaetica I, sensilla chaetica II, sensilla chaetica III, sensilla basiconica I, sensilla basiconica II, sensilla basiconica III, sensilla basiconica IV, sensilla basiconica V, sensilla coeloconica and Böhm bristles. The characteristics and distribution of these antennal sensilla were described, and relevant differences between the male and the female were compared. Finally, the probable functions and their applications in taxonomy were briefly discussed. These findings provide an improved understanding of the morphology of the antennae in these 2 species and can help to distinguish them clearly. Besides, these results also will support investigations into adaptions of these Trogoderma species to storage environments. [ABSTRACT FROM AUTHOR]

In mouse mid-gestational embryos, definitive hematopoietic stem progenitor cells are derived directly from a very small proportion of the arterial endothelium. However, the physiological mechanisms restraining excessive endothelial-hematopoietic transition remain elusive. We show here that genetic deletion of Smad4 from the endothelium stage (using Tie2-Cre), but not from embryonic hematopoietic cells (using Vav-Cre), leads to a strikingly augmented emergence of intra-arterial hematopoietic clusters and an enhanced in vitro generation of hematopoietic progenitors, with no increase in the proliferation and survival of hematopoietic cluster cells. This finding indicates a temporally restricted negative effect of Smad4 on the endothelial to hematopoietic progenitor transition. Furthermore, the absence of endothelial Smad4 causes an increased expression of subaortic bone morphogenetic protein 4 and an activation of aortic extracellular signal-regulated kinase, thereby resulting in the excessive generation of blood cells. Collectively, our data for the first time identify a physiological suppressor that functions specifically during the transition of endothelial cells to hematopoietic progenitors and further suggest that endothelial Smad4 is a crucial modulator of the subaortic microenvironment that controls the hematopoietic fate of the aortic endothelium. [ABSTRACT FROM AUTHOR]

• Consecutive crashes are primary crashes and immediately caused secondary crashes. • Traffic hazards transmit through vehicular interactions for consecutive crashes. • Two-level logistic model outperforms random-effects and random parameter models. • Factors for consecutive crashes are investigated. A consecutive crash consists of a primary crash and one or more secondary crashes that occur subsequently in a short period of time within a certain distance. It often affects a relatively large area of road space and the traffic disruption created can be difficult for traffic managers to control and resolve. This study identifies the factors delineating a primary crash that results in secondary crashes within a minute from a regular crash that does not result in any secondary crashes. Random-effects, random-parameter and two-level binary logistic regression models are applied to data collected on 8779 crashes on the freeway network of the Guizhou Province, China in 2018, of which 299 are consecutive crashes. According to the AIC values, the two-level logistic model outperforms the other two models. Rear-end primary crashes have a significant random effect varying across road segments on the occurrence of consecutive crashes. Various crash types (rear-end, roll-over and side-swipe), tunnel crash and foggy weather are positively associated with the possibility to cause subsequent consecutive crashes, whereas single-vehicle crash, truck involvement and the time periods with poorer natural lighting are less likely to incur consecutive crashes. Recommendations are provided to minimize the possibility of the occurrence of consecutive crashes on a freeway. [ABSTRACT FROM AUTHOR]

Objective: To investigate the changes in cyclophilin A (CyPA) signal pathway in rat myocardial tissue after cardiopulmonary resuscitation (CPR)., Methods: Sixty-eight healthy male Sprague-Dawley (SD) rats were randomly divided into sham operation group (n = 8), instantaneous CPR after cardiac arrest (CA), immediate CPR after CA (CRP), and 15, 30, 60 and 120 minutes after CPR groups, respectively, with 10 rats in each group. Asphyxia was simulated by occlusion of the tracheal tube at the end of exhalation. Mechanical ventilation, compression and epinephrine injection were given for restoration of spontaneous circulation (ROSC) in order to reproduce cardiopulmonary resuscitation after cardiac arrest (CA-CPR) models in rats. Hemodynamic changes were recorded at different time points. The blood was collected from abdominal aorta, and myocardial tissue was also harvested. The serum CyPA and CD147 levels were determined by enzyme-linked immunosorbent assay (ELISA). The protein positive cells and mRNA expression of CyPA and CD147 in myocardial tissue of the rats were determined by immunohistochemical and real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR ). The protein expressions of matrix metalloproteinases (MMP-2, MMP-9) and myeloperoxidase (MPO) in rat myocardial tissue were determined by Western Blot. The neutrophil infiltration in rat myocardial tissue was assessed by hematoxylin and eosin (HE) staining., Results: The heart rate of rat was lowered to 0 with arterial pressure lowered immediately after CA. Arterial pressure was elevated to normal range immediately after CPR. Heart rate was restored at about 30 minutes later, and the dose of epinephrine was 50-60 µg, and ROSC time was 1-4 minutes. Compared with those of the sham group, serum CyPA and CD147 levels were gradually increased along with elongation of ROCS time within 120 minutes, and peaked at 120 minutes, CyPA was increased from (786.11 ± 3.93) µL to (2001.80 ± 10.61) µg/L, and CD147 was increased from (2.94 ± 0.02) µg/L to (5.99 ± 0.023) µg/L (P < 0.05 or P < 0.01). CyPA and CD147 mRNA expressions (A value) in rat myocardial tissue were gradually increased, and peaked at 120 minutes. Relative expression of CyPA at 120 minutes was 2.42 ± 0.05 when it was 1 in the control, and relative expression of CD147 at 120 minutes was 1.88 ± 0.10 (both P < 0.01). The immunohistochemical results under light microscope showed that the brown positive cells were gradually increased, which indicated that the expressions of CyPA and CD147 were increased. Expressions of MMP-2, MMP-9 and MPO (gray value) in myocardial tissue were also gradually increased, peaking at 120 minutes, and MMP-2 was increased from 0.396 ± 0.021 to 0.879 ± 0.020, MMP-9 was increased from 0.372 ± 0.009 to 0.819 ± 0.012, and MPO was increased from 0.176 ± 0.005 to 0.829 ± 0.018 (P < 0.05 or P < 0.01). No obvious neutrophil infiltration in myocardial tissue was found with HE staining., Conclusion: Expressions of CyPA and CD147 were up-regulated in serum and myocardial tissue after CPR in rats, which may be the markers of inflammatory reaction.