Moreover, knockdown of MALAT1 expression enhances blood-brain tumor barrier permeability via miR-140, which may provide a double benefit of MALAT1 suppression by increasing the delivery of chemotherapy agents into the GBM tissues. On the other hand, there also exist some cell culture and animal studies showing that MALAT1 acts as a tumor suppressor in GBMs by suppression of ERK/MAPK and MMP2 signaling and by repression of miR-155 with subsequent increase of FBXW7. Whether protective or detrimental, MALAT1 seems to be an important component of GBM pathogenesis and hence; novels studies are needed in versatile models, including many different primary GBM cultures, orthotopic and xenogreft in vivo models and transgenic mice. To study the influence of the PGC-1β gene on chicken adipocyte proliferation and differentiation, we constructed RNA interference (RNAi) vectors that target the PGC-1β gene and transfected these vectors into adipocytes. Oil Red O staining and a CCK-8 cell kit were used to determine cell triglyceride accumulation status and cell proliferation after transfection, respectively. The mRNA abundances of PGC-1β and adipocyte-differentiation-related genes (PPARγ, C/EBPα, SREBP-1c, FAS, and A-FABP) were detected by real-time PCR. The results showed that the mRNA and protein abundances of PGC-1β in PGC-1β-shRNA transfected adipocytes were significantly lower than those in the control. Interference decreased cell differentiation, but did not depress the cell proliferation. PGC-1β interference impeded the triglyceride accumulation, the mRNA expression levels of nuclear receptors PPARγ and SREBP-1c, and fatty acid synthetase (FAS), and both proteins PPARγ and SREBP-1c, and the fatty acids transporting protein A-FABP. Generally, PGC-1β modulated the cell differentiation and triglyceride accumulation in chicken adipocytes. Many studies implicate altered cyclic nucleotide signaling in the pathophysiology of major depressive disorder (MDD), bipolar disorder (BPD), and schizophrenia (SCZ). As such, we explored how phosphodiesterases 2A (PDE2A) and 10A (PDE10A)-enzymes that break down cyclic nucleotides-may be altered in brains of these patients. Using autoradiographic in situ hybridization on postmortem brain tissue from the Stanley Foundation Neuropathology Consortium, we measured expression of PDE2 and PDE10 mRNA in multiple brain regions implicated in psychiatric pathophysiology, including cingulate cortex, orbital frontal cortex (OFC), superior temporal gyrus, hippocampus, parahippocampal cortex, amygdala, and the striatum. We also assessed how PDE2A and PDE10A expression changes in these brain regions across development using the Allen Institute for Brain Science Brainspan database. Compared to controls, patients with SCZ, MDD and BPD all showed reduced PDE2A mRNA in the amygdala. In contrast, PDE2A expression changes in frontal cortical regions were only significant in patients with SCZ, while those in caudal entorhinal cortex, hippocampus, and the striatum were most pronounced in patients with BPD. PDE10A expression was only detected in striatum and did not differ by disease group; however, all groups showed significantly less PDE10A mRNA expression in ventral versus dorsal striatum. Across development, PDE2A mRNA increased in these brain regions; whereas, PDE10A mRNA expression decreased in all regions except striatum. Thus, PDE2A mRNA expression changes in both a disorder- and brain region-specific manner, potentially implicating PDE2A as a novel diagnostic and/or patient-selection biomarker or therapeutic target. OBJECTIVE Emotion dysregulation has been suggested to be a potent risk factor for multiple psychiatric conditions. Altered amygdala-prefrontal cortex (PFC) connectivity has been consistently linked to emotion dysregulation. Recent data indicate that amygdala-PFC functional connectivity undergoes a prolonged period of development, with amygdala reactivity during early childhood potentially shaping this unfolding process. Little is known about the relationships between amygdala-PFC functional connectivity, amygdala reactivity, and emotion regulation during early childhood. This information is likely critical for understanding early emotion dysregulation as a transdiagnostic risk factor for psychopathology. The current study examined the relationships between amygdala functional connectivity, amygdala reactivity, and emotion regulation in preschoolers. METHOD Sixty-six medication naïve 4- to 6-year-olds participated in a study where resting-state functional magnetic resonance imaging (rs-fcMRI) and parent-reported child emotion regulation ability data were collected. fMRI data collected during a face viewing task was also available for 24 children. RESULTS Right amygdala-medial PFC (mPFC) functional connectivity was positively associated with child emotion regulation ability and negatively associated with child negative affect and right amygdala reactivity to facial expressions of emotion. Right amygdala-mPFC functional connectivity also statistically mediated the relationship between heightened right amygdala reactivity and elevated child negative affect. CONCLUSION Study findings suggest that amygdala-mPFC functional connectivity during early childhood, and its relationships with amygdala reactivity and emotion regulation during this highly sensitive developmental period, may play an important role in early emotional development. These results inform the neurodevelopmental biology of emotion regulation and its potential relationship with risk for psychopathology. Glyphosate-based herbicides are among the most produced and widely-used herbicides. Studies have shown that commercial formulations and adjuvants may be more toxic to non-target organisms than the active ingredients alone, but the mechanisms of action of these chemicals remain unclear. The aim of this study was to investigate the in vitro effects of glyphosate, a commercial formulation and adjuvant alone using primary culture of hemocytes from the European abalone Haliotis tuberculata, a commonly farmed shellfish. Glyphosate was found to have negligible effects on viability, phagocytic activities and lysosome stability even with very high doses (i.e. 100 mg L-1). By contrast, greater effects on viability were observed for the commercial formulation and adjuvant alone, with EC50 values of 41.42 mg L-1 and 1.85 mg L-1, respectively. These results demonstrate that the toxic sublethal effects (i.e. phagocytic activity and destabilization of lysosomal membranes) of formulated glyphosate came from adjuvants and suggest they may be related to cell and organelle membrane destabilization. BACKGROUND Patients with outflow tract ventricular tachycardia (OTVT) with normal echocardiogram are labeled as idiopathic VT (IVT). However, a subset of these patients is subsequently diagnosed with underlying cardiac sarcoidosis (CS). OBJECTIVE Whether electrocardiogram (ECG) abnormalities in sinus rhythm (SR) can differentiate underlying CS from IVT. METHODS We retrospectively analyzed the SR-ECGs of 42 patients with OTVT/premature ventricular complexes (PVC) and normal echocardiography. All underwent advanced imaging with cardiac magnetic resonance (CMR)/18FDG PET-CT for screening of CS. Twenty-two patients had significant abnormalities in cardiac imaging and subsequently had biopsy-proven CS (Cases). Twenty patients had normal imaging and were categorized as IVT (Controls). SR-ECGs of all patients were analyzed by 2 independent, blinded observers. RESULTS Baseline characteristics were comparable. Among the ECG features analyzed – fascicular (FB) or bundle branch block (BBB) was seen in 9/22 Cases vs. 1/20 controls (p = 0.01). Among patients without FB or BBB, fragmented QRS (fQRS) was present in 9/13 cases but in none of the controls (p  less then  0.001). Low voltage QRS was more often seen among cases as compared to controls (10/22 vs. 3/20 p = 0.03). A stepwise algorithm based on these 3 sets of ECG findings helped to diagnose CS among patients presenting with OTVT/PVC with sensitivity of 91%, specificity of 75%, a PPV of 80%, and a NPV of 88%. CONCLUSIONS In patients presenting with OTVT/PVC FB/BBB, fQRS, and low QRS voltage on the baseline ECG were more often observed among patients with underlying CS as compared to true IVT. These findings may help to distinguish underlying CS among Cases presenting with OTVT/PVC. The cell behaviors associated with gastrulation in sea urchins have been well described. More recently, considerable progress has been made in elucidating gene regulatory networks (GRNs) that underlie the specification of early embryonic territories in this experimental model. This review integrates information from these two avenues of work. I discuss the principal cell movements that take place during sea urchin gastrulation, with an emphasis on molecular effectors of the movements, and summarize our current understanding of the gene regulatory circuitry upstream of those effectors. A case is made that GRN biology can provide a causal explanation of gastrulation, although additional analysis is needed at several levels of biological organization in order to provide a deeper understanding of this complex morphogenetic process. Gonadally intact female rats display sexual behaviors only during a portion of the estrus cycle. In standard experimental setups, the on- and offset of sexual behavior is gradual. However, in naturalistic settings, it is almost instantaneous. We assessed the changes in sociosexual behaviors at the beginning and end of behavioral estrus in ovariectomized females treated with ovarian hormones. Rats were housed in a seminatural environment, in groups of three males and four females. We scored female and male behavior during the 8 min preceding and following the first and last lordosis of behavioral estrus. Immediately before the first lordosis, there was a sharp increase in female paracopulatory behaviors whereas the end of estrus was marked by a sudden decrease in these behaviors. There was no systematic change in other female behavior patterns. These data suggest that the display of female paracopulatory behaviors plays a key role. Both during transition into and out of behavioral estrus, most behavioral changes occurred within one minute. The rapid changes must be unrelated to ovarian hormone fluctuations in these ovariectomized females. Perhaps they can be explained in terms of hormone-induced, dynamic (chaotic) changes in the function of critical structures within the brain. Viviparous reproduction is characterized by maternal retention of developing offspring within the reproductive tract during gestation, culminating in live birth. In some cases, a mother will provide nutrition beyond that present in the yolk; this is known as matrotrophic viviparity. While this phenomenon is best associated with mammals, it is observed in insects such as the viviparous cockroach, Diploptera punctata. Female D. punctata carry developing embryos in the brood sac, a reproductive organ that acts as both a uterus and a placenta by protecting and providing a nutritive secretion to the intrauterine developing progeny. While the basic physiology of D. punctata pregnancy has been characterized, little is known about the molecular mechanisms underlying this phenomenon. This study combines RNA-seq analysis, RNA interference, and other assays to characterize molecular and physiological changes associated with D. punctata reproduction. A comparison of four stages of the female reproductive cycle revealed unique gene expression profiles corresponding to each stage.