Langerhans cells (LC) are cell types found in the skin and gingiva. LC have immunological functions as phagocytic cells and as antigen-presenting cells for T and B lymphocytes. Sections from biopsies of the gingiva in cases of periodontal disease were found to have increased numbers of LC. These biopsies also contained intragingival bacteria. Serial sections of frozen specimens of human gingiva were prepared for staining. Hematoxylin and eosin were used for tissue survey, the Gram stain for assessment of bacterial invasion, anti-Leu-6 monoclonal antibody associated with peroxidase technique (PAP) to identify LC, antibacterial sera to Bacteroides gingivalis and Actinobacillus actinomycetemcomitans associated with peroxidase to specifically identify these two common periodontopathogenic bacteria. Additional positive identification of bacteria was performed by preparing the same histological section containing gram-stained particles for scanning electron microscope and transmission electron microscope LC confirmation. The results suggest that the increased number of LC seen in diseased sites of oral epithelium containing intragingival microorganisms may be one of the host immune mechanisms to penetration by bacteria.

Background: The past 30 years have witnessed growing scientific interest regarding the impact of mindfulness-based interventions (MBIs) on cognitive functions. Several theories propose that habitually exercising mindfulness skills can improve cognitive abilities, but no comprehensive quantitative reviews of the effect of MBIs on global and unique cognitive domains exist to date. Method: This systematic review thus examined the effects of MBI on global cognitive ability (GCA) and 16 specific cognitive domains. MBI randomized controlled trials (RCTs) that administered cognitive tests pre- and post-treatment were included. Open-trials, non-randomized MBIs, and case-control studies were excluded. Keywords included “mindful*,” AND “executive attention (EA),” OR “working memory (WM).” Robust variance estimation and moderator analyses were conducted. Results: Ninety-five RCTs (n = 7,408) met eligibility criteria. MBI (vs. waitlist or no-treatment) had small-to-moderate significant effects on GCA, WM accuracy, inhibition accuracy and latency, EA, sustained attention accuracy, processing speed, and subjective attentional control (SAC) (g = 0.24 – 0.52). Likewise, MBI (vs. active control) had small-to-moderate positive effects on GCA, orienting, EA, WM accuracy, sustained attention (indexed by intra-individual coefficient of variation), and SAC (average g = 0.17 – 0.41). Age, gender, study quality, treatment duration, publication year, retention, statistical analysis, and country, moderated some treatment effects. Publication bias analyses showed that reliable treatment effects were restricted to EA, WM accuracy, inhibition accuracy, sustained attention, and SAC, depending on the control group. Conclusion: MBIs confer notable neuropsychological benefits and dose-response effects on some specific (vs. global) cognitive domains. Limitations, theoretical, and applied implications are discussed. (Note: This paper has not been peer reviewed. Please do not copy or cite without author's permission.)

The impaired disengagement hypothesis (Koster, De Lissnyder, Derakshan, & De Raedt, 2011) posits that executive dysfunction can predict future heightened depression and anxiety due to chronic poor attentional control and repetitive negative thinking across prolonged durations. Simultaneously, scar theories (Ottaviani et al., 2016) assert that increased psychopathology may forecast subsequent executive functioning (EF) deficits because of wear-and-tear of psychophysiological systems over protracted timescales. However, most work on EF-psychopathology relations have been cross-sectional, which precludes causal inferences. Thus, this study aimed to test the within-person relations between EF, depression and anxiety. Older adult participants (n = 856) averaged 81.59 years of age (SD = 7.10, range = 70–110, 58.53% females, 76.87% Whites). Assessments were conducted across four waves, each spaced approximately 2 years apart over a span of 8 years. EF was assessed using six behavioral measures (animal fluency, controlled oral word association test, backward counting, serial 7s subtraction, backward digit span, symbol digit modalities test). Depression and anxiety symptoms were measured with the Neuropsychiatric Inventory. Bivariate dual latent change score (BCS) and random-intercept cross-lagged panel models (RI-CLPM) were conducted to minimize measurement error as well as adjust for autoregressive effects, regression to the mean, and between-person variances. Within persons, RI-CLPMs revealed that prior greater depression symptoms forecasted lower subsequent EF, but not vice versa (d = -0.29 vs. -0.03). BCS models showed that within-person rise in depression symptoms at a time-lag predicted EF decrements at the next time-lag, but not the opposite (d = -0.20 vs. 0.14). Further, significant, small-to-moderate, negative between-person relations between EF and depression or anxiety severity were observed (d = -0.42 to -0.26). Neither within-person cross-lagged relations (d = -0.09–-0.06) nor change-to-future change associations (d = -0.04–0.04) were found between anxiety and EF. Prospective, within-person findings offer some evidence for developmental scar theories as opposed to vulnerability models. We discussed theoretical and clinical implications, such as potentially reducing the risk of future executive dysfunction-related neuropsychiatric disorders by targeting depression symptoms.

Background: Scar models propose that elevated psychiatric disorder severity predisposes people to future decreased executive function (EF) through heightened inflammation. However, most prior research on this topic has been cross-sectional. We thus investigated if increased Time 1 (T1) common psychiatric disorder severity predicted Time 3 (T3) EF decrement via Time 2 (T2) inflammation in two unique samples. Methods: Community- dwelling adults participated in Study 1 (n = 614) and Study 2 (n = 945). Both studies measured T1 common psychiatric disorder severity (Composite International Diagnostic Interview–Short Form major depressive disorder, generalized anxiety disorder, and panic disorder severity scales), T2 inflammation (interleukin-6, C-reactive protein, and fibrinogen blood concentration), and T3 EF (Brief Test of Adult Cognition by Telephone). Structural equation modeling was conducted. Results: Greater T1 diagnostic severity predicted higher T2 inflammation (after 2 months in Study 1: Cohen’s d = 0.84; following 9 years in Study 2: d = 0.82). Moreover, higher T2 inflammation predicted lower T3 EF (after 18 months in Study 1: d = -1.30; following 9 years in Study 2: d = -1.18), with large effect sizes. Further, the mediation paths were significantly moderate-to-large in Study 1 (d = 0.76) and Study 2 (d = 0.69). Socio-demographic, lifestyle, medication use, and physical health variables did not moderate these mediation models. Conclusions: Inflammation may be a mechanism explaining the T1 common psychiatric disorder severity–T3 EF relation. Treatments that target inflammation and/or anxiety or depressive disorders may prevent some individuals from experiencing EF decline.