Quantitative analysis of the scientific literature is important for evaluating the evolution and state of science. To study how the density of biological literature has changed over the past two decades we visually inspected 1464 research articles related only to the biological sciences from ten scholarly journals (with average Impact Factors, IF, ranging from 3.8 to 32.1). By scoring the number of data items (tables and figures), density of composite figures (labeled panels per figure or PPF), as well as the number of authors, pages and references per research publication we calculated an Average Publishable Unit or APU for 1993, 2003, and 2013. The data show an overall increase in the average ± SD number of data items from 1993 to 2013 of approximately 7±3 to 14±11 and PPF ratio of 2±1 to 4±2 per article, suggesting that the APU has doubled in size over the past two decades. As expected, the increase in data items per article is mainly in the form of supplemental material, constituting 0 to 80% of the data items per publication in 2013, depending on the journal. The changes in the average number of pages (approx. 8±3 to 10±3), references (approx. 44±18 to 56±24) and authors (approx. 5±3 to 8±9) per article are also presented and discussed. The average number of data items, figure density and authors per publication are correlated with the journal’s average IF. The increasing APU size over time is important when considering the value of research articles for life scientists and publishers, as well as, the implications of these increasing trends in the mechanisms and economics of scientific communication.

Chronic social isolation could lead to a disruption in the Hypothalamic-Pituitary-Adrenal (HPA) axis, resulting in anxiety and depressive-like behaviors but cycling estrogens could modify these behaviors. The aim of this study was to determine if changes in ovarian hormones during the normal cycle could interact with social isolation to alter anxiety and depressive-like behaviors. In parallel, we examined the expression of glucocorticoid receptor (GR) and synaptic vesicle protein synaptophysin in the hippocampus and hypothalamus of Sprague Dawley normal cycling female rats. We assigned rats to either isolated or paired housing for 8 weeks. To assess anxiety and depressive-like behaviors, we used the open field test and forced swim test, respectively. Female rats were tested at either diestrus, estrus, or proestrus stage of the estrous cycle. After behaviors, rats were perfused and brains collected. Brain sections containing hippocampus and hypothalamus were analyzed using immunohistochemistry for synaptophysin and glucocorticoid receptor (GR) levels. We found an increase in depressive-like behaviors for isolated animals compared to paired housed rats, regardless of the estrous cycle stage. Interestingly, we found a decrease in anxiety behaviors in females in the estrus stage accompanied by a decrease in GR expression in hippocampal DG and CA3. However, no changes in synaptophysin were observed in any of the areas of studied. Our results support the beneficial effects of circulating ovarian hormones in anxiety, possibly by decreasing GR expression.

Substance use disorder (SUD) is a complex condition that involves the induction of molecular and physiological alterations by the use and abuse of illicit substances. The prevalence of illicit drug use has caused this disorder to grow exponentially over the past 5 years (National Institute of Drug Abuse, 2020). To date, there are several FDA-approved pharmacological treatments for substances that may cause dependency, such as heroin, morphine, alcohol, and nicotine, directed to the attenuation of drug craving, and increase time to relapse. Known as medication-assisted treatment, such FDA-approved pharmaceutical interventions can be used to increase the effectiveness of other substance abuse treatments, including the use of buprenorphine (commonly used in opioid use disorder, OUD).Buprenorphine works as a partial agonist that binds to the opioid receptors in the brain, allowing a partial activation of the receptor when it is activated with opioids, and thus reducing the rewarding effects (James & Williams, 2020). Another FDA-approved treatment for OUD is naloxone, a known opioid receptor antagonist that reduces activation and prevents other endogenous ligands to bind to that receptor (Becker & Chartoff, 2019;James & Williams, 2020). These types of pharmacological treatments are still not available for substances such as cocaine, methamphetamines, or cannabis which limit treatment options. The percentage cocaine users aged

Niemann‐Pick type C (NPC) disease is an autosomal recessive lysosomal storage disorder affecting mostly children, causing progressive neurological deterioration and death. NPC disease is caused by a mutation in either the NPC1 or NPC2 gene, leading to a loss of functional NPC1 or NPC2 protein. These proteins play a role in lipid egress from late endosomes and lysosomes, a deficiency in either results in intracellular accumulation of unesterified cholesterol and gangliosides. Storage is prominent in neurons, influencing cellular pathology, such as growth of ectopic dendrites on pyramidal neurons. This aberrant growth of dendrites following normal dendritogenesis has been documented in several lysosomal diseases characterized by ganglioside storage. Until recently, the visualization of this process depended on the Golgi method. New techniques, such as endogenous expression of fluorescent proteins, provide an in‐depth analysis of neuronal structure. We hypothesized that the accumulation of gangliosides in NPC disease will cause an initial enhancement of dendritogenesis along with ectopic dendrite growth followed by a subsequent degeneration of dendritic trees later in disease. Subsequently, we generated a transgenic Npc1 murine mouse model whose layer V cortical pyramidal neurons express yellow fluorescent protein (YFP) to investigate the dendritic abnormalities of NPC disease relative to lysosomal storage. Confocal imaging and Neurolucida Software are being used to image YFP+ pyramidal neurons, which will be analyzed for changes in dendritic size, complexity and pathological state.