Breast cancer, psychological distress and life events among young women

Since 1983, studies have suggested an interaction between the severe life events, psychological distress and the etiology of Cancer. However, these associations are still under dispute

Comparative analysis of neural transcriptomes and functional implication of unannotated intronic expression

<p>Abstract</p> <p>Background</p> <p>The transcriptome and its regulation bridge the genome and the phenome. Recent RNA-seq studies unveiled complex transcriptomes with previously unknown transcripts and functions. To investigate the characteristics of neural transcriptomes and possible functions of previously unknown transcripts, we analyzed and compared nine recent RNA-seq datasets corresponding to tissues/organs ranging from stem cell, embryonic brain cortex to adult whole brain.</p> <p>Results</p> <p>We found that the neural and stem cell transcriptomes share global similarity in both gene and chromosomal expression, but are quite different from those of liver or muscle. We also found an unusually high level of unannotated expression in mouse embryonic brains. The intronic unannotated expression was found to be strongly associated with genes annotated for neurogenesis, axon guidance, negative regulation of transcription, and neural transmission. These functions are the hallmarks of the late embryonic stage cortex, and crucial for synaptogenesis and neural circuit formation.</p> <p>Conclusions</p> <p>Our results revealed unique global and local landscapes of neural transcriptomes. It also suggested potential functional roles for previously unknown transcripts actively expressed in the developing brain cortex. Our findings provide new insights into potentially novel genes, gene functions and regulatory mechanisms in early brain development.</p

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

BMP signaling and microtubule organization regulate synaptic strength

The strength of synaptic transmission between a neuron and multiple postsynaptic partners can vary considerably. We have studied synaptic heterogeneity using the glutamatergic Drosophila neuromuscular junction (NMJ), which contains multiple synaptic connections of varying strengths between a motor axon and muscle fiber. In larval NMJs, there is a gradient of synaptic transmission from weak proximal to strong distal boutons. We imaged synaptic transmission with the postsynaptically targeted fluorescent calcium sensor SynapCam, to investigate the molecular pathways that determine synaptic strength and set up this gradient. We discovered that mutations in the Bone Morphogenetic Protein (BMP) signaling pathway disrupt production of strong distal boutons. We find that strong connections contain unbundled microtubules in the boutons, suggesting a role for microtubule organization in transmission strength. The spastin mutation, which disorganizes microtubules, disrupted the transmission gradient, supporting this interpretation. We propose that the BMP pathway, shown previously to function in the homeostatic regulation of synaptic growth, also boosts synaptic transmission in a spatially selective manner that depends on the microtubule system

A Modified Technique for Nipple-Areola Complex Reconstruction

2This book, written by leading international experts, deals exclusively with reconstruction techniques for the Nipple-Areolar Complex (NAC). The first chapters present the history of the Nipple-Areolar Complex reconstruction and the anatomy of this part of the body. After discussing the abnormalities of the Nipple-Areolar Complex and how to prevent Nipple-Areolar Complex disorders, the book provides extensive documentation on techniques for correcting nipple hypertrophy, nipple inversion, and for increasing nipple projection. Readers will also find helpful information of malposition and tumors of the Nipple-Areolar Complex, as well as complications that can arise during the various surgical techniques. The book offers an invaluable guide for residents and fellow, practicing and highly experienced plastic surgeons, general surgeons, and those in cosmetic surgical subspecialites.nonenoneParodi, Pier Camillo; Almesberger, DariaParodi, Pier Camillo; Almesberger, Dari

Resting-state EEG source localization and functional connectivity in schizophrenia-like psychosis of epilepsy

BACKGROUND: It is unclear whether, like in schizophrenia, psychosis-related disruption in connectivity between certain regions, as an index of intrinsic functional disintegration, occurs in schizophrenia-like psychosis of epilepsy (SLPE). In this study, we sought to determine abnormal patterns of resting-state EEG oscillations and functional connectivity in patients with SLPE, compared with nonpsychotic epilepsy patients, and to assess correlations with psychopathological deficits. METHODOLOGY/PRINCIPAL FINDINGS: Resting EEG was recorded in 21 patients with focal epilepsy and SLPE and in 21 clinically-matched non-psychotic epilepsy controls. Source current density and functional connectivity were determined using eLORETA software. For connectivity analysis, a novel nonlinear connectivity measure called "lagged phase synchronization" was used. We found increased theta oscillations in regions involved in the default mode network (DMN), namely the medial and lateral parietal cortex bilaterally in the psychotic patients relative to their nonpsychotic counterparts. In addition, patients with psychosis had increased beta temporo-prefrontal connectivity in the hemisphere with predominant seizure focus. This functional connectivity in temporo-prefrontal circuits correlated with positive symptoms. Additionally, there was increased interhemispheric phase synchronization between the auditory cortex of the affected temporal lobe and the Broca's area correlating with auditory hallucination scores. CONCLUSIONS/SIGNIFICANCE: In addition to dysfunction of parietal regions that are part of the DMN, resting-state disrupted connectivity of the medial temporal cortex with prefrontal areas that are either involved in the DMN or implicated in psychopathological dysfunction may be critical to schizophrenia-like psychosis, especially in individuals with temporal lobe epilepsy. This suggests that DMN deficits might be a core neurobiological feature of the disorder, and that abnormalities in theta oscillations and beta phase synchronization represent the underlying neural activity