The Impact of Authentic and Diverse Racial Representation in Children's Literature

This study examines the impact of authentic and diverse racial representation in children's literature on students. This study examines the current lack of representation of Black, Indigenous, and People of Color (BIPOC) students in classroom literature and misrepresentation and stereotyping in children's literature. It also examines how some teachers lack the knowledge and experience to address racial representation and diversity in their classrooms. This study uses data from a teacher interview to analyze their experience and understanding of how using literature that has authentic and diverse racial representation has affected their students. The research provides evidence that using children's literature that includes authentic and diverse racial representation in the classroom can increase students' motivation and engage them in higher-order thinking skills to help improve their academic performance. Understanding the positive impact that diverse representation in children's literature can have on students can bring awareness to current and future teachers about analyzing and evaluating the effectiveness of the literature in their classrooms

Monoaminergic and histaminergic strategies and treatments in brain diseases

The monoaminergic systems are the target of several drugs for the treatment of mood, motor and cognitive disorders as well as neurological conditions. In most cases, advances have occurred through serendipity, except for Parkinson's disease where the pathophysiology led almost immediately to the introduction of dopamine restoring agents. Extensive neuropharmacological studies first showed that the primary target of antipsychotics, antidepressants, and anxiolytic drugs were specific components of the monoaminergic systems. Later, some dramatic side effects associated with older medicines were shown to disappear with new chemical compounds targeting the origin of the therapeutic benefit more specifically. The increased knowledge regarding the function and interaction of the monoaminergic systems in the brain resulting from in vivo neurochemical and neurophysiological studies indicated new monoaminergic targets that could achieve the efficacy of the older medicines with fewer side-effects. Yet, this accumulated knowledge regarding monoamines did not produce valuable strategies for diseases where no monoaminergic drug has been shown to be effective. Here, we emphasize the new therapeutic and monoaminergic-based strategies for the treatment of psychiatric diseases. We will consider three main groups of diseases, based on the evidence of monoamines involvement (schizophrenia, depression, obesity), the identification of monoamines in the diseases processes (Parkinson's disease, addiction) and the prospect of the involvement of monoaminergic mechanisms (epilepsy, Alzheimer's disease, stroke). In most cases, the clinically available monoaminergic drugs induce widespread modifications of amine tone or excitability through neurobiological networks and exemplify the overlap between therapeutic approaches to psychiatric and neurological conditions. More recent developments that have resulted in improved drug specificity and responses will be discussed in this review.peer-reviewe

Effect of Berberine on Cell Survival in the Developing Rat Brain Damaged by MK-801

Berberine is an isoquinoline alkaloid isolated from goldenthread, Coptidis Rhizoma and shown to have many biological and pharmacological effects. We previously reported that berberine promotes cell survival and differentiation of neural stem cells. To examine whether berberine has survival promoting effect on damaged neuronal cells, we generated a cellular model under oxidative stress and an neonatal animal model of degenerating brain disease by injecting MK-801. MK801, a noncompetitive antagonist of N-methyl-d-aspartate (NMDA) receptors, acts as a neurotoxin in developing rats by inhibiting NMDA receptors and induce neuronal cell death. We found that the survival rate of the SH-SY5Y cells under oxidative stress was increased by 287% and 344%, when treated with 1.5 and 3.0µg/ml berberine, respectively. In the developing rats injected by MK801, we observed that TUNEL positive apoptotic cells were outspread in entire brain. The cell death was decreased more than 3 fold in the brains of the MK-801-induced neurodegenerative animal model when berberine was treated to the model animals. This suggests that berberine promotes activity dependent cell survival mediated by NMDA receptor because berberine is known to activate neurons by blocking K+ current or lowering the threshold of the action potential. Taken together, berberine has neuroprotective effect on damaged neurons and neurodegenerating brains of neonatal animal model induced by MK-801 administration

Effects of vatinoxan on cardiorespiratory function and gastrointestinal motility during constant-rate medetomidine infusion in standing horses

Background Medetomidine suppresses cardiovascular function and reduces gastrointestinal motility in horses mainly through peripheral alpha(2)-adrenoceptors. Vatinoxan, a peripheral alpha(2)-antagonist, has been shown experimentally to alleviate the adverse effects of some alpha(2)-agonists in horses. However, vatinoxan has not been investigated during constant-rate infusion (CRI) of medetomidine in standing horses. Objectives To evaluate effects of vatinoxan on cardiovascular function, gastrointestinal motility and on sedation level during CRI of medetomidine. Study design Experimental, randomised, blinded, cross-over study. Methods Six healthy horses were given medetomidine hydrochloride, 7 mu g/kg i.v., without (MED) and with (MED+V) vatinoxan hydrochloride, 140 mu g/kg i.v., followed by CRI of medetomidine at 3.5 mu g/kg/h for 60 min. Cardiorespiratory variables were recorded and borborygmi and sedation levels were scored for 120 min. Plasma drug concentrations were measured. The data were analysed using repeated measures ANCOVA and paired t-tests as appropriate. Results Initially heart rate (HR) was significantly lower and mean arterial blood pressure (MAP) significantly higher with MED compared with MED+V. For example at 10 min HR (mean +/- s.d.) was 26 +/- 2 and 31 +/- 5 beats/minute (P = 0.04) and MAP 129 +/- 15 and 103 +/- 13 mmHg (PPeer reviewe

The role of hypothalamic H1 receptor antagonism in antipsychotic-induced weight gain

Treatment with second generation antipsychotics (SGAs), notably olanzapine and clozapine, causes severe obesity side effects. Antagonism of histamine H1 receptors has been identified as a main cause of SGA-induced obesity, but the molecular mechanisms associated with this antagonism in different stages of SGA-induced weight gain remain unclear. This review aims to explore the potential role of hypothalamic histamine H1 receptors in different stages of SGA-induced weight gain/obesity and the molecular pathways related to SGA-induced antagonism of these receptors. Initial data have demonstrated the importance of hypothalamic H1 receptors in both short- and long-term SGA-induced obesity. Blocking hypothalamic H1 receptors by SGAs activates AMP-activated protein kinase (AMPK), a well-known feeding regulator. During short-term treatment, hypothalamic H1 receptor antagonism by SGAs may activate the AMPK—carnitine palmitoyltransferase 1 signaling to rapidly increase caloric intake and result in weight gain. During long-term SGA treatment, hypothalamic H1 receptor antagonism can reduce thermogenesis, possibly by inhibiting the sympathetic outflows to the brainstem rostral raphe pallidus and rostral ventrolateral medulla, therefore decreasing brown adipose tissue thermogenesis. Additionally, blocking of hypothalamic H1 receptors by SGAs may also contribute to fat accumulation by decreasing lipolysis but increasing lipogenesis in white adipose tissue. In summary, antagonism of hypothalamic H1 receptors by SGAs may time-dependently affect the hypothalamus-brainstem circuits to cause weight gain by stimulating appetite and fat accumulation but reducing energy expenditure. The H1 receptor and its downstream signaling molecules could be valuable targets for the design of new compounds for treating SGA-induced weight gain/obesity