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Reported childhood adversity (CA) is associated with development of depression in adulthood and predicts a more severe course of illness. Although elevated serotonin 1A receptor (5-HT1AR) binding potential, especially in the raphe nuclei, has been shown to be a trait associated with major depression, we did not replicate this finding in an independent sample using the partial agonist positron emission tomography tracer [11C]CUMI-101. Evidence suggests that CA can induce long-lasting changes in expression of 5-HT1AR, and thus, a history of CA may explain the disparate findings.
Following up on our initial report, 28 unmedicated participants in a current depressive episode (bipolar n = 16, unipolar n = 12) and 19 non-depressed healthy volunteers (HVs) underwent [11C]CUMI-101 imaging to quantify 5-HT1AR binding potential. Participants in a depressive episode were stratified into mild/moderate and severe CA groups via the Childhood Trauma Questionnaire. We hypothesized higher hippocampal and raphe nuclei 5-HT1AR with severe CA compared with mild/moderate CA and HVs.
There was a group-by-region effect (p = 0.011) when considering HV, depressive episode mild/moderate CA, and depressive episode severe CA groups, driven by significantly higher hippocampal 5-HT1AR binding potential in participants in a depressive episode with severe CA relative to HVs (p = 0.019). Contrary to our hypothesis, no significant binding potential differences were detected in the raphe nuclei (p-values > 0.05).
With replication in larger samples, elevated hippocampal 5-HT1AR binding potential may serve as a promising biomarker through which to investigate the neurobiological link between CA and depression.
This practical manual provides a comprehensive yet concise guide to state-of-the-art molecular techniques and their applications. It starts with an overview of the essential principles of molecular techniques, followed by separate chapters detailing the use of these techniques in particular tissues and organs, and describing recommended treatment plans. Each chapter covers the tests available, their advantages, limitations, and use as diagnostic and prognostic tools, with key learning points at the end of each topic. Using both histologic and cytologic samples, it discusses how to interpret test results in a pathologic context and enables trainees and practising pathologists to gain an in-depth understanding of molecular diagnostic techniques and how to incorporate them into routine diagnostic practice. Aiding the daily practice of refining diagnosis, as well as offering a didactic approach, this book is an essential reference for practising pathologists and cytopathologists as well as trainees in pathology.
Clostridium difficile infection (CDI) in hospitalized patients is generally attributed to the current stay, but recent studies reveal high C. difficile colonization rates on admission.
To determine the rate of colonization with toxigenic C. difficile among intensive care unit patients upon admission as well as acquired during hospitalization, and the risk of subsequent CDI.
Prospective cohort study from April 15 through July 8, 2013. Adults admitted to an intensive care unit within 48 hours of admission to the Johns Hopkins Hospital, Baltimore, Maryland, were screened for colonization with toxigenic C. difficile. The primary outcome was risk of developing CDI.
Among 542 patients, 17 (3.1%) were colonized with toxigenic C. difficile on admission and an additional 3 patients were found to be colonized during hospitalization. Both colonization with toxigenic C. difficile on admission and colonization during hospitalization were associated with an increased risk for development of CDI (relative risk, 10.29 [95% CI, 2.24–47.40], P=.003; and 15.66 [4.01–61.08], P<.001, respectively). Using multivariable analysis, colonization on admission and colonization during hospitalization were independent predictors of CDI (relative risk, 8.62 [95% CI, 1.48–50.25], P=.017; and 10.93 [1.49–80.20], P=.019, respectively), while adjusting for potential confounders.
In intensive care unit patients, colonization with toxigenic C. difficile is an independent risk factor for development of subsequent CDI. Further studies are needed to identify populations with higher toxigenic C. difficile colonization rates possibly benefiting from screening or avoidance of agents known to promote CDI.
Infect. Control Hosp. Epidemiol. 2015;36(11):1324–1329
There has been a recent surge of interest in Clostridium difficile infection, which reflects an impressive increase in the number and severity of these infections. This review addresses some of the newer methods for detection of C. difficile infection at the bedside and in the laboratory. Particularly important are the new rapid diagnostic tests that detect toxigenic C. difficile using polymerase chain reaction and the combination tests that, either simultaneously or sequentially, screen for C. difficile and test for toxins A and B. It is expected that these new testing methods will largely supplant the enzyme immunoassays for toxins, which are used by most laboratories, departments, and divisions. The present goal is to combine clinical, laboratory, and animal research related to C. difficile that reflects issues that are considered to be major contemporary challenges. Among this work is the pursuit of studies of immune mechanisms to better control this disease.
Neurofibromatosis (NF) is a common neurocutaneous disorder that has an incidence of approximately 1 in 4000 (Mulvihill et al., 1990). Although NF has been postulated to have as many as eight different forms (Riccardi & Eichner, 1986), this classification system has not been widely adopted. Neurofibromatosis is a group of genetic disorders including NF type I (NF-I), NF type II (NF-II), and multiple schwannomatosis, each with distinctly different genetic mutations and pathologic bases. The NF-I gene is nearly ubiquitous in human tissues and so impacts virtually all organ systems. NF-I is particularly interesting to neurocognitive scientists because of its characteristic phenotypical abnormalities in development of form and function in brain. NF-II and multiple schwannomatosis are essentially disorders of cranial nerves, peripheral nerves, and meningeal tissues with no associated cognitive abnormalities and so these disorders will be excluded from this discussion.
The original term neurofibromatosis was derived at the turn of the last century but the disorder is also called von Recklinghausen's disease because the condition was described in the late 1800s clinically and scientifically by Friedrich Daniel von Recklinghausen (Cawthon et al., 1990; Crump, 1981; Viskochil et al., 1990). The molecular genetic basis of distinguishing clinical features of NF-I was localized to chromosome 17 in 1990 by two teams of investigators (Viskochil et al., 1990; Wallace et al., 1990).