Reduced lymphocyte response to mitogens in patients with Bancroftian filariasis

Peripheral blood lymphocytes from patients with acute and chronic Wuchereria bancrofti infections responded poorly to concanavalin A, phytohaemagglutinin and pokeweed mitogen when cultured in heat-inactivated pooled normal serum. The lymphocyte response to mitogens in carriers of microfilariae (mff) were normal. The suppression of transformation to mitogens was not reversible by the removal of plastic adherent cells. Incubation with mitogens and the adult filarial worm antigen (BmA) did not alter the mitogen response either in control subjects or in filarial patients. The possible mechanism of immunosuppression is discussed.     

Multiscale neural signatures of major depressive,anxiety, and stress-related disorders

The extent of shared and distinct neural mechanisms underlying major depressive disorder (MDD), anxiety, and stress-related disorders is still unclear. We compared the neural signatures of these disorders in 5,405 UK Biobank patients and 21,727 healthy controls. We found the greatest case–control differences in resting-state functional connectivity and cortical thickness in MDD, followed by anxiety and stress-related disorders. Neural signatures for MDD and anxiety disorders were highly concordant, whereas stress-related disorders showed a distinct pattern. Controlling for cross-disorder genetic risk somewhat decreased the similarity between functional neural signatures of stress-related disorders and both MDD and anxiety disorders. Among cases and healthy controls, reduced within-network and increased between-network frontoparietal and default mode connectivity were associated with poorer cognitive performance (processing speed, attention, associative learning, and fluid intelligence). These results provide evidence for distinct neural circuit function impairments in MDD and anxiety disorders compared to stress disorders, yet cognitive impairment appears unrelated to diagnosis and varies with circuit function.

Major depressive disorder (MDD) and anxiety disorders (i.e., generalized anxiety disorder and panic disorder without agoraphobia) are highly comorbid psychiatric disorders (1–3), with shared epidemiologic, developmental, and genetic features (4, 5), and are among the leading causes of disability worldwide (6). Depression and anxiety are often triggered by stressful life events, thus sharing the etiology of stress-related disorders that are defined by occurrence of a severe stressor or trauma (7). More specifically, posttraumatic stress disorder (PTSD) is characterized by hyperarousal states during recurring flashbacks to the stressful event, while stress adjustment disorder is characterized by depressive symptoms in response to a severe stressor (7). Unlike MDD and anxiety disorders, which are recurrent or chronic, stress adjustment disorder resolves within 6 mo after termination of the stressor. While considerable neurobiological research has been conducted at a disorder-specific level, few studies have investigated a broad spectrum of MDD, anxiety, and stress disorders to examine shared and distinct neural correlates.Task-based functional MRI (fMRI) findings point to disrupted emotional processing and executive dysfunction, exemplified by disrupted cognitive control (8, 9), across a variety of disorders, including but not limited to MDD and anxiety disorders. Similarly, gray matter reductions have been shown in the insular and anterior cingulate cortices across mood, anxiety, and other disorders (10, 11). Many of these similarities in brain structure have been shown to be partially attributable to similarities in common variant architectures (12), encouraging the consideration of genetic risk measures in studies of intermediate imaging phenotypes for psychiatric illness. Polygenic liability for psychiatric disorders can be quantified using polygenic risk scores (PRSs), which are predictive of disease progression (13) and often transdiagnostically informative (14, 15). Therefore, parsing transdiagnostic phenotypes that capture the shared and distinct genetic, neurobiological, and cognitive basis of symptoms presenting across disorders could have utility in improving psychiatric nosology (16).Inferior prefrontal and insular cortex, the inferior parietal lobule, and the putamen are hypoactivated in task-based fMRI paradigms across MDD, anxiety disorders, and stress-related disorders (17), implicating inhibitory control and salience processing as shared neural phenotypes underlying these disorders. Impairments in executive functions such as inhibitory control over emotional reactivity and negative mood may capture a transdiagnostic dimension of psychopathology (18, 19). Executive function is also impaired by anxiety, which reduces cognitive flexibility, working memory (20), and attentional control (21). While some evidence also supports executive dysfunction in PTSD (22, 23), psychological theories of posttraumatic stress typically emphasize the effects of the traumatic event on memory (24, 25). Executive dysfunction may be linked to both dysregulated mood in MDD and heightened emotional reactivity in anxiety disorders (26) and thus provides a promising transdiagnostic treatment target.Here we leveraged multimodal data from the UK Biobank to determine unique and shared features of brain structure and function in MDD, anxiety disorders (ANX), and stress-related disorders (STR), as well as the relationship of such neuroimaging measures to several aspects of cognitive function across these disorders. The UK Biobank includes midlife and older adults and is thus also suitable for investigating cognition in the context of aging with and without MDD, anxiety, and stress-related disorders. We selected trail making performance (27), digit–symbol substitution (28), fluid intelligence (29), and paired associate learning (PAL) (30) to measure key domains of cognitive function, expecting executive function and processing speed impairments in MDD and anxiety disorders and memory deficits in stress-related disorders. We used second-order statistical comparisons to investigate genetic and environmental contributions to disorder similarity. We expected to find default mode and frontostriatal connectivity differences in MDD (31) and anxiety disorders (32, 33), resulting in shared neural signatures. We also hypothesized reduced cortical thickness of the frontoparietal regions in both MDD and anxiety disorders (34–36) and a separate neural signature of stress-related disorders focused on the hippocampal regions (37). Given varying degrees of shared genetic liability for our selected disorders and our interest in disentangling their overlapping vs. discrete neural signatures, we anticipated that controlling for disease-specific PRS would impact the correlation of cross-disorder neural signatures, providing insight into nature vs. nurture components of these intermediate phenotypes. Finally, we expected connectivity of frontoparietal (FPN), attention, and default mode networks (DMN) to underlie cognitive performance across disorders.     

Association of Metabolic Syndrome With Incident Dementia: Role of Number and Age at Measurement of Components in a 28-Year Follow-up of the Whitehall II Cohort Study

OBJECTIVEPrevious research suggests an inconsistent association between Metabolic syndrome (MetS) and incident dementia. We examined the role of number of MetS components and age at their assessment for incident dementia.RESEARCH DESIGN AND METHODSMetS components (fasting glucose, triglycerides, waist circumference, blood pressure, and HDL cholesterol) on 7,265, 6,660, and 3,608 participants at <60, 60 to <70, and ≥70 years of age were used to examine associations with incident dementia using cause-specific Cox regression.RESULTSAnalyses of MetS measured at <60, 60 to <70, and ≥70 years involved 393 (5.4%), 497 (7.5%), and 284 (7.9%) dementia cases over a median follow-up of 20.8, 10.4, and 4.2 years, respectively. Every additional MetS component before 60 (hazard ratio [HR] 1.13 [95% CI 1.05, 1.23]) and 60 to <70 (HR 1.08 [95% CI 1.00, 1.16]) but not ≥70 years (HR 1.04 [95% CI 0.96, 1.13]) was associated with higher dementia risk. MetS defined conventionally (≥3 components) before 60 years (HR 1.23 [95% CI 0.96, 1.57]), between 60 and 70 years (HR 1.14 [95% CI 0.91, 1.42]), or >70 years of age (HR 1.10 [95% CI 0.86, 1.40]) was not associated with incident dementia. Multistate models showed higher risk of dementia in those with ≥1 (HR 1.99 [95% CI 1.08, 3.66]) and ≥2 MetS components (HR 1.69 [95% CI 1.12, 2.56]) before 60 years of age, even when they remained free of cardiovascular disease over the follow-up.CONCLUSIONSRisk of incident dementia increases with every additional MetS component present in midlife rather than after accumulation of three components; only part of this risk is mediated by cardiovascular disease.     

Polymeric Surfactants: Recent Advancement in Their Synthesis,Properties, and Industrial Applications

Polymeric surfactants are a special class of the polymers that have amphiphilic characteristics of surfactants. In selective solvents, polymeric surfactants exhibit interesting association processes and develop self-assembled structures. Their capacity to create micellar aggregates with stimuli-responsive behavior in aqueous solutions, enables the creation of smart materials for many applications. The only restrictions to the creation of polymeric surfactants with complicated structures using current synthetic methods are the researchers' interests and creativity. The chemical structure of the polymer and its aqueous solution characteristics (viscosity and surface tension) should be demonstrated as having a distinct and commonly accepted connection. Unavailability of systematic and updated review on these important molecules demands a comprehensive compilation and consistent discussion on key physical aspects, characterization, synthetic techniques, and their useful applications like enhanced recovery of oil, antimicrobial potential, water treatment, pharmaceutical, etc.