The Intratumor Bacterial and Fungal Microbiome Is Characterized by HPV,Smoking, and Alcohol Consumption in Head and Neck Squamous Cell Carcinoma

Head and neck squamous cell carcinoma (HNSCC) tumor phenotypes and clinical outcomes are significantly influenced by etiological agents, such as HPV infection, smoking, and alcohol consumption. Accordingly, the intratumor microbiome has been increasingly implicated in cancer progression and metastasis. However, few studies characterize the intratumor microbial landscape of HNSCC with respect to these etiological agents. In this study, we aimed to investigate the bacterial and fungal landscape of HNSCC in association with HPV infection, smoking, and alcohol consumption. RNA-sequencing data were extracted from The Cancer Genome Atlas (TCGA) regarding 449 tissue samples and 44 normal samples. Pathoscope 2.0 was used to extract the microbial reads. Microbe abundance was compared to clinical variables, oncogenic signatures, and immune-associated pathways. Our results demonstrated that a similar number of dysregulated microbes was overabundant in smokers and nonsmokers, while heavy drinkers were characterized by an underabundance of dysregulated microbes. Conversely, the majority of dysregulated microbes were overabundant in HPV+ tumor samples when compared to HPV- tumor samples. Moreover, we observed that many dysregulated microbes were associated with oncogenic and metastatic pathways, suggesting their roles in influencing carcinogenesis. These microbes provide insights regarding potential mechanisms for tumor pathogenesis and progression with respect to the three etiological agents.     

Bernard H. Fox (1917-2001).

Memorializes B. H. Fox, a research scientist internationally known for his work on the epidemiology and etiology of cancer. Fox was instrumental in establishing a new field of research best described as biopsychosocial cancer epidemiology. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Psychiatric disorders associated with risk for the development of eating disorders during adolescence and early adulthood.

Longitudinal data were used to investigate whether anxiety, depressive, disruptive, personality, or substance use disorders are associated with risk for the development of eating disorders during adolescence or early adulthood. Psychiatric disorders were assessed among 726 youths from a random community sample during adolescence and early adulthood. Depressive disorders during early adolescence were associated with elevated risk for the onset of eating disorders, dietary restriction, purging behavior, and recurrent weight fluctuations after preexisting eating problems and other psychiatric disorders were controlled statistically. Disruptive and personality disorders were independently associated with elevated risk for specific eating or weight problems. The present findings suggest that depressive disorders during early adolescence may contribute to the development of eating disorders during middle adolescence or early adulthood. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Etiological Contributions to Heavy Drinking From Late Adolescence to Young Adulthood.

The authors examined genetic and environmental contributions to stability and change in heavy drinking from late adolescence to young adulthood in a sample of 1,152 twin pairs. In men, heavy drinking was similarly heritable at ages 17 (h2 = .57) and 20 (h2 = .39), and its stability owed primarily to common genetic factors. In women, heavy drinking was less heritable than in men at ages 17 (h2 = .18) and 20 (h2 = .30) and its stability was primarily due to enduring shared environmental influences. P3 amplitude, an event-related brain potential marker of alcoholism risk, was less predictive of heavy drinking in women than in men, providing further support for the proposition that biological factors have less impact on heavy drinking in young adult women than in young adult men. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Introduction to the Special Section on Health and Cognitive Function.

Numerous factors related to health and diseases have been studied in relation to cognitive function. It has been shown that across the life span, systemic medical diseases can negatively impact cognitive function. Factors that influence the development of medical diseases, such as poor health habits, biological risk factors, hormones, genetic factors, exposure to environmental toxins, and certain treatments for disease, can also have an adverse effect on cognitive function. Conversely, factors such as high levels of education, good health habits, and some treatments for disease can be protective. Included in this special section are 6 empirical articles that examine the relation of health or disease to cognitive function. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Clinical adolescent psychology: What it is, and what it needs to be.

This commentary on the special section on clinical adolescent psychology (G. Holmbeck & P. Kendall, 2002) reviews and critiques the conceptual and empirical articles that this compilation comprises. As articulated in the conceptual contributions to this collection, two fundamental principles should guide research on the etiology, prevention, and treatment of psychological disorder and dysfunction during adolescence: First, drawing on the field of developmental psychopathology, the study of clinical adolescent psychology should focus on the trajectories of disorder that precede, characterize, and follow adolescence. Second, drawing on the literature on normative adolescent development, the study of clinical adolescent psychology must proceed with an explicit recognition of the unique biological, cognitive, psychosocial, and contextual features that define adolescence as a developmental period. Although the study of clinical adolescent psychology, as evidenced by this collection of articles, is appropriately grounded in the broader enterprise of developmental psychopathology, less progress has been made with respect to die integration of the study of clinical phenomena in adolescence with the study of normative adolescent development. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A factor analysis of the Beck Inventory of Depression.

Afactor analysis of the Beck Inventory of Depression, based on the responses of 254 significantly depressed hospital patients, has yielded 3 interpretable factors. The largest factor was that of affective depression referred to here as a factor of "guilty depression." The 2 remaining factors were interpreted as "retarded depression" and "somatic disturbance." These 3 factors showed some correspondence to the factors found by other investigators. The suggestion is made that the etiology of various depressed states may be associated with different levels of mental functioning. The need for additional factor analytic studies, which include behavioral and physiological measures, is noted. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Social psychological correlates of mental illness and mental health.

If there is ever to be a single comprehensive theory and/or research program concerned with the etiology of mental illness, the widely diversified empirical and theoretical findings will have to be meaningfully integrated. The present paper critically reviews theories and research from the environmental-demographic level and the interpersonal level. The large number of phenotypical relationships reported have led only to vaguely formulated and speculative interpretations suggesting the need for a reformulation which will suggest genotypes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Invited review: Abomasal damage in veal calves

Within all cattle production systems, veal calves are the most severely affected by abomasal damage, with current prevalence at slaughter ranging from 70 to 93% of all animals affected. Although most damage is found in the pyloric region of the abomasum, fundic lesions are also found. Despite past research into the etiology of abomasal damage and the many risk factors that have been proposed, consensus on the causal factors of abomasal damage in veal calves has not yet been reached. The aim of this review was to integrate and analyze available information on the etiology of, and possible risk factors for, abomasal damage in veal calves. We describe various proposed pathways through which risk factors may contribute to damage formation and conclude that the etiology of abomasal damage is most likely multifactorial, with diet being a main contributor. Pyloric lesions, the most common type of damage in veal calves, are likely the result of large and infrequent milk and solid feed meals, whereas fundic lesions may be caused by stress, although the evidence for this is inconclusive. Providing calves with multiple smaller milk and solid feed meals (or ad libitum provision) may decrease abomasal damage. In future research, ulcers, erosions, and scars as well as fundic and pyloric lesions should be recorded separately, because etiologies of these may differ. Further research is required to understand the exact pathway(s) by which milk replacer causes abomasal damage in veal calves; that is, whether low abomasal pH, overloading, or composition are important. Further research is also required to elucidate whether rapid intake of milk replacer and solid feed, which is influenced by restricted amounts fed, inter-calf competition, and calf breed, increases abomasal damage. Research is also needed into the effect of medication and nutrient deficiencies other than iron. The types of experimental designs that can be used for future research could be enhanced if a means to assess abomasal damage antemortem is developed. We conclude that it is unlikely that abomasal or ruminal hairballs, iron deficiency, water provision, and various infections and diseases are significant contributors to abomasal damage in veal calves.     

Social dominance mediates the association of testosterone and neurobehavioral disinhibition with risk for substance use disorder.

This investigation determined the influence of testosterone and neurobehavioral disinhibition (ND) on risk for substance use disorder (SUD). Testosterone level during puberty was hypothesized to promote social dominance associated with norm-violating behavior that, in turn, predisposes individuals to use of illicit drugs and, subsequently, SUD. Using a prospective paradigm, the authors recruited 179 boys (mean age=11.62 years, SD=0.88) and followed up when participants were ages 12-14, 16, 19, and 22. Results indicated that social dominance/norm-violating behavior (SD/NVB) at age 16 mediated the association between testosterone level (ages 12-14) and SUD (age 22). In addition, SD/NVB mediated the association between ND and SUD. These findings suggest that development of SUD is influenced by androgen-dependent and neurobehavioral processes via a social motivational style characterized by SD/NVB. (PsycINFO Database Record (c) 2010 APA, all rights reserved)