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Neonatal hematology is a fast-growing field, and the majority of sick neonates will develop hematological problems. This is an essential guide to the pathogenesis, diagnosis and management of hematologic problems in the neonate. Guidance is practical, including blood test interpretation, advice on transfusions and reference ranges for hematological values. Chapters have been thoroughly revised according to the latest advances in the field for this updated third edition. Topics discussed include erythrocyte disorders, platelet disorders, leukocyte disorders, immunologic disorders and hemostatic disorders. Coverage of oncological issues has been expanded to two separate chapters on leukemia and solid tumors, making information more easily accessible. Approaches to identifying the cause of anemia in a neonate are explained, with detailed algorithms provided to aid clinicians in practice. Covering an important hematologic niche with an ever increasing amount of specialized knowledge, this book is a valuable resource for hematologists, neonatologists and pediatricians.
To characterize associations between exposures within and outside the medical workplace with healthcare personnel (HCP) SARS-CoV-2 infection, including the effect of various forms of respiratory protection.
Data collected via online survey from international participants.
1130 HCP (244 cases with laboratory-confirmed COVID-19, 886 controls healthy throughout the pandemic) from 67 countries not meeting pre-specified exclusion (healthy but not working, missing workplace exposure data, COVID symptoms without lab confirmation).
Respondents were queried regarding workplace exposures, respiratory protection, and extra-occupational activities. Odds ratios for HCP infection were calculated with multivariable logistic regression and sensitivity analyses controlling for confounders and known biases.
HCP infection was associated with non-aerosol-generating contact with COVID-19 patients (adjusted OR 1.4, 95% CI 1.04–1.9, p=0.03) and extra-occupational exposures including gatherings of ten or more, patronizing restaurants or bars, and public transportation (adjusted ORs ranging 3.1-16.2). Respirator use during aerosol-generating procedures (AGPs) was associated with lower odds of HCP infection (adjusted OR 0.4, 0.2 to 0.8, p=0.005), as was exposure to intensive care and dedicated COVID units, negative pressure rooms, and personal protective equipment (PPE) observers (adjusted ORs ranging 0.4-0.7).
COVID-19 transmission to HCP was associated with medical exposures currently considered lower-risk and multiple extra-occupational exposures, while exposures associated with proper use of appropriate PPE were protective. Closer scrutiny of infection control measures surrounding healthcare activities and medical settings considered lower risk, and continued awareness of the risks of public congregation, may reduce the incidence of HCP infection.
Bipolar disorder (BD) is a familial psychiatric disorder associated with frontotemporal and subcortical brain abnormalities. It is unclear whether such abnormalities are present in relatives without BD, and little is known about structural brain trajectories in those at risk.
Neuroimaging was conducted at baseline and at 2-year follow-up interval in 90 high-risk individuals with a first-degree BD relative (HR), and 56 participants with no family history of mental illness who could have non-BD diagnoses. All 146 subjects were aged 12–30 years at baseline. We examined longitudinal change in gray and white matter volume, cortical thickness, and surface area in the frontotemporal cortex and subcortical regions.
Compared to controls, HR participants showed accelerated cortical thinning and volume reduction in right lateralised frontal regions, including the inferior frontal gyrus, lateral orbitofrontal cortex, frontal pole and rostral middle frontal gyrus. Independent of time, the HR group had greater cortical thickness in the left caudal anterior cingulate cortex, larger volume in the right medial orbitofrontal cortex and greater area of right accumbens, compared to controls. This pattern was evident even in those without the new onset of psychopathology during the inter-scan interval.
This study suggests that differences previously observed in BD are developing prior to the onset of the disorder. The pattern of pathological acceleration of cortical thinning is likely consistent with a disturbance of molecular mechanisms responsible for normal cortical thinning. We also demonstrate that neuroanatomical differences in HR individuals may be progressive in some regions and stable in others.
Whether unintentional or by design, built, social, and perceived environments influence the human experience. Behavior is not solely the product of a rational motivated actor, operating independently from his or her environment; rather, it is also a function of edifices, neighborhoods, and public spaces, as well as the inhabitants, community norms, and the social capital they generate. Likewise, addictive behaviors have as much to do with the environmental contexts surrounding individuals as with their unique biological factors, specific brain mechanisms, and psychogenic causes. Any attempt to address addiction at either individual or population levels would benefit from careful consideration of the social and contextual influences on cognitions, opportunities, motivations, and behaviors. Interventions informed by this understanding are more likely to be efficacious than those solely targeted toward individual biology, motivations, or attitudes. In this chapter, we discuss the relationship between physical and social environments (PSE), health, and the behavior of humans. We then focus on the influential role of the PSE on the consumption of alcohol, tobacco, and other substances; food, eating behaviors, and addictions contributing to the current obesity epidemic; and a selection of other behavioral addictions. The chapter closes by discussing methodological considerations and implications for professional practice.
A non-GMO trait called Inzen™ was recently commercialized in grain sorghum to combat weedy grasses, allowing the use of nicosulfuron POST in the crop. Inzen™ grain sorghum carries a double mutation in the acetolactate synthase (ALS) gene Val560Ile and Trp574Leu, which potentially results in cross-resistance to a wide assortment of ALS-inhibiting herbicides. To evaluate the scope of cross-resistance to Weed Science Society of America Group 2 herbicides in addition to nicosulfuron, tests were conducted in 2016 and 2017 at the Lon Mann Cotton Research Station near Marianna, AR, the Arkansas Agricultural Research and Extension Center in Fayetteville, AR, and in 2016 at the Pine Tree Research Station near Colt, AR. The tests included ALS-inhibiting herbicides from all five families: sulfonylureas, imidazolinones, pyrimidinylthiobenzoics, triazolinones, and triazolopyrimidines. Treatments were made PRE or POST to grain sorghum at a 1× rate for crops in which each herbicide is labeled. Grain sorghum planted in the PRE trial were Inzen™ and a conventional cultivar. Visible estimates of injury and sorghum heights were recorded at 2 and 4 wk after herbicide application, and yield data were collected at crop maturity. In the PRE trial, no visible injury, sorghum height reduction, or yield loss were observed in plots containing the Inzen™ cultivar. Applications made POST to the Inzen™ grain sorghum caused visible injury, sorghum height reduction, and yield loss of 20%, 13%, and 35%, respectively, only in plots where bispyribac-Na was applied. There was no impact on the crop from other POST-applied ALS-inhibiting herbicides. These results demonstrate that the Inzen™ trait confers cross-resistance to most ALS-inhibiting herbicides and could offer promising new alternatives for weed control and protection from carryover of residual ALS-inhibiting herbicides in grain sorghum.
Cohorting patients who are colonized or infected with multidrug-resistant organisms (MDROs) protects uncolonized patients from acquiring MDROs in healthcare settings. The potential for cross transmission within the cohort and the possibility of colonized patients acquiring secondary isolates with additional antibiotic resistance traits is often neglected. We searched for evidence of cross transmission of KPC+ Klebsiella pneumoniae (KPC-Kp) colonization among cohorted patients in a long-term acute-care hospital (LTACH), and we evaluated the impact of secondary acquisitions on resistance potential.
Genomic epidemiological investigation.
A high-prevalence LTACH during a bundled intervention that included cohorting KPC-Kp–positive patients.
Whole-genome sequencing (WGS) and location data were analyzed to identify potential cases of cross transmission between cohorted patients.
Secondary KPC-Kp isolates from 19 of 28 admission-positive patients were more closely related to another patient’s isolate than to their own admission isolate. Of these 19 cases, 14 showed strong genomic evidence for cross transmission (<10 single nucleotide variants or SNVs), and most of these patients occupied shared cohort floors (12 patients) or rooms (4 patients) at the same time. Of the 14 patients with strong genomic evidence of acquisition, 12 acquired antibiotic resistance genes not found in their primary isolates.
Acquisition of secondary KPC-Kp isolates carrying distinct antibiotic resistance genes was detected in nearly half of cohorted patients. These results highlight the importance of healthcare provider adherence to infection prevention protocols within cohort locations, and they indicate the need for future studies to assess whether multiple-strain acquisition increases risk of adverse patient outcomes.
This chapter provides a wide-ranging review of the clinical pharmacology of drugs for the treatment of schizophrenia and psychosis other than clozapine. These are dopamine receptor antagonists and dopamine partial agonists (as per the new Neuroscience-based Nomenclature (NbN) classification). This chapter covers their pharmacodynamics, pharmacokinetics, adverse effects, the latest evidence regarding their ‘antipsychotic’ mechanism of action, their use in the acute and maintenance treatment of schizophrenia, other therapeutic indications and some controversies that surround their use.
Dopamine receptor antagonists and dopamine partial agonists are commonly referred to as antipsychotics. As a clinical shorthand the term ‘antipsychotic’ is likely to remain in use.
According to the stress inoculation hypothesis, successfully navigating life stressors may improve one's ability to cope with subsequent stressors, thereby increasing psychiatric resilience.
Among individuals with no baseline history of post-traumatic stress disorder (PTSD) and/or major depressive disorder (MDD), to determine whether a history of a stressful life event protected participants against the development of PTSD and/or MDD after a natural disaster.
Analyses utilised data from a multiwave, prospective cohort study of adult Chilean primary care attendees (years 2003–2011; n = 1160). At baseline, participants completed the Composite International Diagnostic Interview (CIDI), a comprehensive psychiatric diagnostic instrument, and the List of Threatening Experiences, a 12-item questionnaire that measures major stressful life events. During the study (2010), the sixth most powerful earthquake on record struck Chile. One year later (2011), the CIDI was re-administered to assess post-disaster PTSD and/or MDD.
Marginal structural logistic regressions indicated that for every one-unit increase in the number of pre-disaster stressors, the odds of developing post-disaster PTSD or MDD increased (OR = 1.21, 95% CI 1.08–1.37, and OR = 1.16, 95% CI 1.06–1.27 respectively). When categorising pre-disaster stressors, individuals with four or more stressors (compared with no stressors) had higher odds of developing post-disaster PTSD (OR = 2.77, 95% CI 1.52–5.04), and a dose–response relationship between pre-disaster stressors and post-disaster MDD was found.
In contrast to the stress inoculation hypothesis, results indicated that experiencing multiple stressors increased the vulnerability to developing PTSD and/or MDD after a natural disaster. Increased knowledge regarding the individual variations of these disorders is essential to inform targeted mental health interventions after a natural disaster, especially in under-studied populations.
Unit cohesion may protect service member mental health by mitigating effects of combat exposure; however, questions remain about the origins of potential stress-buffering effects. We examined buffering effects associated with two forms of unit cohesion (peer-oriented horizontal cohesion and subordinate-leader vertical cohesion) defined as either individual-level or aggregated unit-level variables.
Longitudinal survey data from US Army soldiers who deployed to Afghanistan in 2012 were analyzed using mixed-effects regression. Models evaluated individual- and unit-level interaction effects of combat exposure and cohesion during deployment on symptoms of post-traumatic stress disorder (PTSD), depression, and suicidal ideation reported at 3 months post-deployment (model n's = 6684 to 6826). Given the small effective sample size (k = 89), the significance of unit-level interactions was evaluated at a 90% confidence level.
At the individual-level, buffering effects of horizontal cohesion were found for PTSD symptoms [B = −0.11, 95% CI (−0.18 to −0.04), p < 0.01] and depressive symptoms [B = −0.06, 95% CI (−0.10 to −0.01), p < 0.05]; while a buffering effect of vertical cohesion was observed for PTSD symptoms only [B = −0.03, 95% CI (−0.06 to −0.0001), p < 0.05]. At the unit-level, buffering effects of horizontal (but not vertical) cohesion were observed for PTSD symptoms [B = −0.91, 90% CI (−1.70 to −0.11), p = 0.06], depressive symptoms [B = −0.83, 90% CI (−1.24 to −0.41), p < 0.01], and suicidal ideation [B = −0.32, 90% CI (−0.62 to −0.01), p = 0.08].
Policies and interventions that enhance horizontal cohesion may protect combat-exposed units against post-deployment mental health problems. Efforts to support individual soldiers who report low levels of horizontal or vertical cohesion may also yield mental health benefits.
The search for mechanisms in personality disorders (PDs) is of growing importance, because PDs are prevalent, costly, and challenging to treat. Unfortunately, there is a dearth of compelling mechanistic research on PDs and psychopathology more broadly, due to equivocal definitions of a “mechanism” and study designs that are atheoretical and/or ill-suited for causal inferences.This chapter defines mechanisms as elements of possible causal sequence, which not only increase the probability of observed outcomes but also reveal how the outcomes occur. In addition, the authors argue that it is not always necessary to break down a mechanism to its most elemental physical parts; rather, it is important to consider how mechanisms act as complex, interacting components of a causal chain, with a focus on those that could serve as viable targets for prevention and intervention. Considering this broader definition of a “mechanism,” it is crucial that PD researchers ground their work in testable theories, such as those considering dimensional, transdiagnostic precursors to PDs. In this chapter, the authors also address various design and statistical considerations in PD mechanistic research and highlight promising developments in identifying mechanisms of PDs across multiple levels of measurement (e.g., biological, contextual, environmental) and across the lifespan.
This rejoinder addresses commentaries by Markon and Bornovalova and colleagues. Markon highlighted challenges associated with determining cause and effect in mechanistic research. He theorized that “weak emergence” may account, in part, for the complex development of personality pathology. Bornovalova and colleagues addressed transactional relations between various phenomena that may influence development of personality pathology over time. In this rejoinder, the authors build upon these commentaries to further highlight challenges associated with identifying true mechanisms in psychopathology. They hypothesize that dynamical systems models, which conceptualize people as systems open to incalculable environmental influences, may provide an alternative approach through which researchers can examine complex mechanisms more accurately. Although such models are nascent in clinical research, particularly in the context of personality disorders, these approaches may provide more nuanced interpretations of mechanisms and may ultimately enrich our understanding of processes underlying the emergence of personality disorders.
Introduction: The Emergency Departments (ED) is a gateway to the health care system for many psychiatric patients. As a consequence of hospital administrative factors and overcrowding, admitted psychiatric patients are often boarded in the ED while waiting for an inpatient bed. There is currently a lack of evidence to quantify the effect that ED boarding has on psychiatric patients. The primary objective of this study is to determine whether a patient's length of stay is related to longer ED boarding time. Methods: This study is a retrospective cohort using data from an administrative source, which was obtained from patient records captured in the Sunrise Clinical Manager EMR used across Calgary, Alberta EDs from 2014-2018. A hierarchical Bayesian regression analysis was used to model the several patient-level and hospital-level factors. The mean and variance was defined by the exposure of interest, namely hours in the Emergency Department after admission to psychiatry unit expressed as a continuous variable. An interaction between this exposure and patient-level confounders was used to model the changing effect of a patient's severity in the ED on their boarding time. Results: The median boarding time for patients in our study was 6.6 hours (standard deviation 17.3), while the average was 13.6 hours. Patients who were boarded for greater than 6 hours more frequently required an antipsychotic (37% vs 11%; SMD 0.651), sedative (52% vs 29%; SMD 0.483) or restraints (18% vs. 14%; SMD 0.102). In crude analysis there was no difference in median length of stay for patients that were boarding more than 6 hours compared to those boarded for less than 6 hours (8 days vs 9 days; SMD 0.012).The rate ratio for length of stay is 1.05 with 95% posterior interval 1.04 - 1.06 for each 24 hour increase in boarding time. This means that for each 1 day worth of boarding time, the length of stay (in days) increases 1.05 times (or 0.05 days/day boarding time). Conclusion: Boarding time is associated with a small but absolute increase in length of stay for psychiatric patients. Decreasing boarding time could have ripple effects for ED efficiency and overall patient outcomes.