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Tree mortality rates and the modes of tree death have recently been extensively investigated in the Amazon. However, efforts to describe these processes have not been well distributed across the basin. No study has yet investigated in depth tree mortality process in the unique low, open, bamboo-dominated forests of southwestern Amazonia, a region with a distinct climate and the epicenter of recent severe drought events. Here, we investigated the leading ways that trees die in the terra-firme forests of the southwestern Brazilian Amazon, to understand whether the dynamics of mortality differ from those recorded in other parts of the basin. Using data from six permanent plots located in southwestern Amazonia, we calculated the mortality rate for three main modes of tree death: standing, broken and uprooted. We thus identified the predominant mode of death over a 14 year period (2002–2016). We found that trees in the southwestern Amazon died mainly standing (325 trees, 0.8% year−1) and broken (362 trees, 0.8% year−1); significantly fewer trees died uprooted (156 trees, 0.4% year−1, equivalent to less than one in five of all trees dying). During the study period, the tree mode of death with the greatest proportion in the region alternated between standing and broken trees. Forest characteristics of the southwestern Amazon, like presence and high density of bamboo culms, and the fact that the region was subject to severe droughts in 2005 and 2010, may be affecting how trees die in southwestern Amazon. The presence of these factors makes the forest dynamics of the southwestern Amazon different from other regions of the Amazon basin.

Metachronous spinal dural arteriovenous fistulae (SDAVF) are two independent SDAVF, with the second lesion manifesting subsequently after treatment of the initial SDAVF. A 69-year-old male was found to have a new T6 metachronous SDAVF two years after successful treatment of a L1 SDAVF. The authors suggest that once successful treatment of a SDAVF is established, regular clinical and MRI follow-up every six months up to and possibly beyond two years should be considered. This may present an opportunity to prevent repeated insult to vulnerable patients via prompt identification and treatment of SDAVF, with an aim to improve prognosis in the event of recurrent, synchronous or metachronous lesions.

Background: Major depressive disorder is a pervasive and debilitating syndrome characterized by mood disturbances, anhedonia, and alterations in cognition. While the prevalence of major depressive disorder is twice as high for women as men, little is known about the molecular mechanisms that drive sex differences in depression susceptibility., Methods: We discovered that SLIT1, a secreted protein essential for axonal navigation and molecular guidance during development, is downregulated in the adult ventromedial prefrontal cortex (vmPFC) of women with depression compared with healthy control subjects, but not in men with depression. This sex-specific downregulation of Slit1 was also observed in the vmPFC of mice exposed to chronic variable stress. To identify a causal, sex-specific role for SLIT1 in depression-related behavioral abnormalities, we performed knockdown (KD) of Slit1 expression in the vmPFC of male and female mice., Results: When combined with stress exposure, vmPFC Slit1 KD reflected the human condition by inducing a sex-specific increase in anxiety- and depression-related behaviors. Furthermore, we found that vmPFC Slit1 KD decreased the dendritic arborization of vmPFC pyramidal neurons and decreased the excitability of the neurons in female mice, effects not observed in males. RNA sequencing analysis of the vmPFC after Slit1 KD in female mice revealed an augmented transcriptional stress signature., Conclusions: Together, our findings establish a crucial role for SLIT1 in regulating neurophysiological and transcriptional responses to stress within the female vmPFC and provide mechanistic insight into novel signaling pathways and molecular factors influencing sex differences in depression susceptibility., (Copyright © 2021 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Background: Global changes in gene expression underlying circuit and behavioral dysregulation associated with cocaine addiction remain incompletely understood. Here, we show how a history of cocaine self-administration (SA) reprograms transcriptome-wide responses throughout the brain's reward circuitry at baseline and in response to context and/or cocaine re-exposure after prolonged withdrawal (WD)., Methods: We assigned male mice to one of six groups: saline/cocaine SA + 24-hour WD or saline/cocaine SA + 30-day WD + an acute saline/cocaine challenge within the previous drug-paired context. RNA sequencing was conducted on six interconnected brain reward regions. Using pattern analysis of gene expression and factor analysis of behavior, we identified genes that are strongly associated with addiction-related behaviors and uniquely altered by a history of cocaine SA. We then identified potential upstream regulators of these genes., Results: We focused on three patterns of gene expression that reflect responses to 1) acute cocaine, 2) context re-exposure, and 3) drug + context re-exposure. These patterns revealed region-specific regulation of gene expression. Further analysis revealed that each of these gene expression patterns correlated with an addiction index-a composite score of several addiction-like behaviors during cocaine SA-in a region-specific manner. Cyclic adenosine monophosphate response element binding protein and nuclear receptor families were identified as key upstream regulators of genes associated with such behaviors., Conclusions: This comprehensive picture of transcriptome-wide regulation in the brain's reward circuitry by cocaine SA and prolonged WD provides new insight into the molecular basis of cocaine addiction, which will guide future studies of the key molecular pathways involved., (Copyright © 2018 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Drug addiction is a behavioral disorder characterized by dysregulated learning about drugs and associated cues that result in compulsive drug seeking and relapse. Learning about drug rewards and predictive cues is a complex process controlled by a computational network of neural connections interacting with transcriptional and molecular mechanisms within each cell to precisely guide behavior. The interplay between rapid, temporally specific neuronal activation, and longer-term changes in transcription is of critical importance in the expression of appropriate, or in the case of drug addiction, inappropriate behaviors. Thus, these factors and their interactions must be considered together, especially in the context of treatment. Understanding the complex interplay between epigenetic gene regulation and circuit connectivity will allow us to formulate novel therapies to normalize maladaptive reward behaviors, with a goal of modulating addictive behaviors, while leaving natural reward-associated behavior unaffected., (© 2017 Elsevier B.V. All rights reserved.)