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• Mean and turbulent quantities of twin round jets presented at different Re. • Swirling strength analysis performed to study vortical structures of twin jets. • Turbulent/non-turbulent interface examined in jet's inner and outer shear layers. • Twin round and plane jets were compared. The aim of the current study is to delineate the effects of Reynolds number (Re = 5000–20,000) on the mean and turbulent properties as well as the turbulent structures of the flow issuing from twin round jets with nozzle spacing of 2.8 nozzle diameter (d). The measurements were performed using a high-resolution particle image velocimetry from the jet exit up to x/d = 40 to examine the merging, converging and combined regions of the twin jets. The results show that the velocity decay and jet spread rates, and the combined point location become Re -independent at Re > 10,000 while the merging points shift downstream as Re increases. Upstream of the merging point, the levels of Reynolds stresses and turbulent kinetic energy production are higher and vortical structures are more intense in the inner shear layers compared to the outer shear layers. At the merging point they equal each other and beyond this point the trends are opposite of those at the upstream. The flow analysis at turbulent/non-turbulent interface of the outer shear layer reveals that conditional streamwise velocity and spanwise vorticity are Re -independent while significantly larger transverse velocity is observed at the lowest Re. At the inner shear layer interface, on the other hand, the conditional properties do not show any dependence on Re. Two-point correlation functions exhibit the presence of larger structures in the outer shear layers due to more exposure to the ambient fluid compared to the inner shear layers. The size of the structures also decreased as Re increased indicating the effect of Re on large-scale engulfment. Joint and weighted joint probability density functions are presented to examine the flow behaviors in more details. [ABSTRACT FROM AUTHOR]

Aggression is an innate behavior that helps individuals succeed in environments with limited resources. Over the past few decades, neurobiologists have identified neural circuits that promote and modulate aggression; however, far less is known regarding the motivational processes that drive aggression. Recent research suggests that aggression can activate reward centers in the brain to promote positive valence. Here, we review major recent findings regarding neural circuits that regulate aggression, with an emphasis on those regions involved in the rewarding or reinforcing properties of aggressive behavior. [ABSTRACT FROM AUTHOR]

Inter-male aggression is an essential component of social behavior in organisms from insects to humans. However, when expressed inappropriately, aggression poses significant threats to the mental and physical health of both the aggressor and the target. Inappropriate aggression is a common feature of numerous neuropsychiatric disorders in humans and has been hypothesized to result from the atypical activation of reward circuitry in response to social targets. The lateral habenula (LHb) has recently been identified as a major node of the classical reward circuitry and inhibits the release of dopamine from the midbrain to signal negative valence. Here, we discuss the evidence linking LHb function to aggression and its valence, arguing that strong LHb outputs to the ventral tegmental area (VTA) and the dorsal raphe nucleus (DRN) are likely to play roles in aggression and its rewarding components. Future studies should aim to elucidate how various inputs and outputs of the LHb shape motivation and reward in the context of aggression. [ABSTRACT FROM AUTHOR]

Background: Despite 2.5 million infections and 169,000 deaths worldwide (as of April 20, 2020), no maternal deaths and only a few pregnant women afflicted with severe respiratory morbidity have been reported to be related to COVID-19 disease. Given the disproportionate burden of severe and fatal respiratory disease previously documented among pregnant women following other coronavirus-related outbreaks (SARS-CoV in 2003 and MERS-CoV in 2012) and influenza pandemics over the last century, the absence of reported maternal morbidity and mortality with COVID-19 disease is unexpected.Objective: To describe maternal and perinatal outcomes and death in a case series of pregnant women with COVID-19 disease.Study Design: We describe here a multiinstitution adjudicated case series from Iran that includes 9 pregnant women diagnosed with severe COVID-19 disease in their second or third trimester. All 9 pregnant women received a diagnosis of SARS-CoV-2 infection by reverse transcription polymerase chain reaction nucleic acid testing. Outcomes of these women were compared with their familial/household members with contact to the affected patient on or after their symptom onset. All data were reported at death or after a minimum of 14 days from date of admission with COVID-19 disease.Results: Among 9 pregnant women with severe COVID-19 disease, at the time of reporting, 7 of 9 died, 1 of 9 remains critically ill and ventilator dependent, and 1 of 9 recovered after prolonged hospitalization. We obtained self-verified familial/household cohort data in all 9 cases, and in each and every instance, maternal outcomes were more severe compared with outcomes of other high- and low-risk familial/household members (n=33 members for comparison).Conclusion: We report herein maternal deaths owing to COVID-19 disease. Until rigorously collected surveillance data emerge, it is prudent to be aware of the potential for maternal death among pregnant women diagnosed as having COVID-19 disease in their second or third trimester. [ABSTRACT FROM AUTHOR]

A solar chimney power plant (SCPP) offers an efficient method of converting solar irradiation to electrical power. It can be combined with a nuclear power plant to improve its efficiency and minimize its environmental impact. Rather than dumping the waste heat rejected by a nuclear power plant to a wet cooling tower, a better solution may be to connect it to an SCPP. This is particularly true in arid regions. The SCPP can serve the function of a dry cooling tower and produce additional electrical power. In a solar chimney power plant, the energy of buoyant hot air is converted to electrical energy. SCPP includes a collector at ground level covered with a transparent roof. The sun heats the air inside the collector and the ground underneath. A tall chimney is placed at the center of the collector, with a turbine located at the base of the chimney. In this investigation, the surplus heat from the nuclear cycle is used to increase the temperature of the air in the collector and therefore produce more electricity in the solar chimney power plant. The efficiency of the nuclear plant will be lowered due to the higher temperature of the condenser, but the loss can be made up by the increased power of the solar chimney. Heat from the sun is always free once the solar plant has been constructed and is not normally considered in the efficiency calculation. Computational fluid dynamics (CFD) and thermal analysis have been performed to apply the available surplus heat from the nuclear cycle and to measure the available kinetic energy of air for the turbine of the solar chimney power plant system. The feasibility of the system is evaluated, and the thermal efficiency of the combined power plant has been computed. By applying this idea to a typical 1000 MW nuclear power plant with a nominal 35.3% thermal efficiency, its efficiency can be increased to 42.0%. The combined cycle as presented is advantageous in environments where water is scarce. The cooling tower is replaced by the solar chimney power plant utilizing the surplus heat from the available warm steam in the secondary loop of the reactor. [ABSTRACT FROM AUTHOR]

Aims Although approving new anticonvulsants was a major breakthrough in the field of epilepsy control, so far we have met limited success in almost one third of patients suffering from epilepsy and a definite and reliable method is yet to be found. Levosimendan demonstrated neuroprotective effects and reduced mortality in conditions in which seizure can be an etiology of death; however, the underlying neuroprotective mechanisms of levosimendan still eludes us. In the light of evidence suggesting levosimendan can be a K ATP channel opener and nitrergic pathway activator, levosimendan may exert antiseizure effects through K ATP channels and nitrergic pathway. Main methods In this study, the effects of levosimendan on seizure susceptibility was studied by PTZ-induced seizures model in mice. Key findings Administration of a single effective dose of levosimendan significantly increased seizures threshold and the nitrite level in the hippocampus and temporal cortex. Pretreatment with noneffective doses of glibenclamide (a K ATP channel blocker) and L-NAME (a non-selective NOS inhibitor) neutralize the anticonvulsant and nitrite elevating effects of levosimendan. While 7-NI (a neural NOS inhibitor) blocked the anticonvulsant effect of levosimendan, Aminoguanidine (an inducible NOS inhibitor) failed to affect the anticonvulsant effects of levosimendan. Cromakalim (a K ATP channel opener) or l -arginine (an NO precursor) augmented the anticonvulsant effects of a subeffective dose of levosimendan. Moreover, co-administration of noneffective doses of Glibenclamide and L-NAME demonstrated a synergistic effect in blocking the anticonvulsant effects of levosimendan. Significance Levosimendan has anticonvulsant effects possibly via K ATP /nNOS/NO pathway activation in the hippocampus and temporal cortex. [ABSTRACT FROM AUTHOR]

Clinical studies suggest that heightened peripheral inflammation contributes to the pathogenesis of stress-related disorders, including major depressive disorder. However, the molecular mechanisms within peripheral immune cells that mediate enhanced stress vulnerability are not well known. Because microRNAs (miRs) are important regulators of immune response, we sought to examine their role in mediating inflammatory and behavioral responses to repeated social defeat stress (RSDS), a mouse model of stress vulnerability that produces susceptible and resilient phenotypes. We isolated Ly6chigh monocytes via fluorescence-activated cell sorting in the blood of susceptible and resilient mice following RSDS and profiled miR expression via quantitative real-time polymerase chain reaction. Bone marrow chimeric mice were generated to confirm a causal role of the miR-106b∼25 cluster in bone marrow–derived leukocytes in mediating stress resilience versus susceptibility. We found that RSDS produces an increase in circulating Ly6chigh inflammatory monocytes in both susceptible and resilient mice. We next investigated whether intrinsic leukocyte posttranscriptional mechanisms contribute to individual differences in stress response and the resilient phenotype. Of the miRs profiled in our panel, eight were significantly regulated by RSDS within Ly6chigh monocytes, including miR-25-3p, a member of the miR-106b∼25 cluster. Selective knockout of the miR-106b∼25 cluster in peripheral leukocytes promoted behavioral resilience to RSDS. Our results identify the miR-106b∼25 cluster as a key regulator of stress-induced inflammation and depression that may represent a novel therapeutic target for drug development. [ABSTRACT FROM AUTHOR]

Abstract Background Homeostatic plasticity in mesolimbic dopamine (DA) neurons plays an essential role in mediating resilience to social stress. Recent evidence implicates an association between stress resilience and projections from the locus coeruleus (LC) to the ventral tegmental area (VTA) (LC→VTA) DA system. However, the precise circuitry and molecular mechanisms of the homeostatic plasticity in mesolimbic DA neurons mediated by the LC→VTA circuitry, and its role in conferring resilience to social defeat stress, have not been described. Methods In a well-established chronic social defeat stress model of depression, using projection-specific electrophysiological recordings and optogenetic, pharmacological, and molecular profiling techniques, we investigated the functional role and molecular basis of an LC→VTA circuit in conferring resilience to social defeat stress. Results We found that LC neurons projecting to the VTA exhibit enhanced firing activity in resilient, but not susceptible, mice. Optogenetically mimicking this firing adaptation in susceptible mice reverses their depression-related behaviors, and induces reversal of cellular hyperactivity and homeostatic plasticity in VTA DA neurons projecting to the nucleus accumbens. Circuit-specific molecular profiling studies reveal that α 1 - and β 3 -adrenergic receptors are highly expressed in VTA→nucleus accumbens DA neurons. Pharmacologically activating these receptors induces similar proresilient effects at the ion channel and cellular and behavioral levels, whereas antagonizing these receptors blocks the proresilient effect of optogenetic activation of LC→VTA circuit neurons in susceptible mice. Conclusions These findings reveal a key role of the LC→VTA circuit in mediating homeostatic plasticity in stress resilience and reveal α 1 - and β 3 -adrenergic receptors as new molecular targets for therapeutically promoting resilience. [ABSTRACT FROM AUTHOR]

Ataxia telangiectasia (AT) is an autosomal recessive disorder with an estimated prevalence of 1/40,000 to 1/100,000 in reported populations. There is a 25% possibility for having an affected child when parents are carriers for the ATM gene mutation. There is no cure available for this disease and prenatal testing is strongly recommended for prevention of this disease. Although the preferred method is the direct mutation analysis of the ATM gene, the large size of the ATM gene with 63 exons and the large number of possible mutations in patients considerably limit efficiency of mutation analysis as a diagnostic choice. Indirect method is a better tool when parents are not carriers of founder mutation and pass different mutations to their children. Indirect molecular diagnosis using ATM-related molecular markers facilitates prenatal diagnosis of AT children. In this study, four molecular markers: D11S2179, D11S1787, D11S535, D11S1343 are genotyped in 19 unrelated families from different regions of Iran. Those markers are amplified using extracted sequence primers from the Gene Bank with their described PCR conditions. Amplified products were separated using denaturing PAGE gels, and data were analyzed to detect their pattern of inheritance in each family. In all families, segregation of alleles was according to Mendelian inheritance, and affected chromosomes were distinguishable from unaffected ones. All carriers and affected patients were diagnosed accurately. Thus, this method is effectively useful in prenatal diagnosis of AT. [Copyright &y& Elsevier]