Comorbidity of attention deficit hyperactivity disorder and educational classification among in-patient populations of children and adolescents

This thesis is an ex post facto study of an in-patient population of 39 adolescents between the ages of twelve and eighteen at a New Jersey State Psychiatric Hospital for Adolescents and 74 pre-adolescents and adolescents between the ages of seven and fifteen at a Private Residential School in New Jersey. Of this population of N=113, n=48 were determined to have Attention Deficit Hyperactivity Disorder (ADHD) with an incidence rate of 42.5%. Significant co-morbidity of ADHD and Depression, Conduct Disorder/Oppositional Defiant Disorder, Psychotic Disorders, and Learning Disabilities were found. The incidence of co-morbidity of ADHD and Educational Classification was found to be significantly higher than the incidence researched among more diverse population groups as represented by the New Zealand (Anderson et. al., 1985) and Puerto Rico (Bird et. al., 1988) large population surveys. The ranked correlation between ADHD and Educational Classification was found to be r=.985 (P≥.01), and between ADHD, Classification and Other Behavioral Disorders was found to be r=.854 (P≥.01) This procedure supports the premise of utilizing Child Study Teams to provide data to plan globally and programmatically as well as to prepare individual education plans

Comparison of biofilm formation and migration of Streptococcus mutans on tooth roots and titanium miniscrews

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Micro-management: curbing chronic wound infection

Chronic wounds, including pressure ulcers, foot ulcers and venous leg ulcers have a detrimental impact on the health and well-being of an estimated 2% of people in the UK. Chronic wounds are normally colonised by bacteria and in some instances bacterial load increases sufficiently for infection to ensue. Once a chronic wound becomes infected it is difficult to resolve and a combination of continuous inflammation and bacterial proliferation makes these wounds difficult to manage. A state of prolonged inflammation can occur as a result of impaired homeostatic pathways which are exacerbated by bacterial growth. Chronic, infected wounds can persist for many months or even years, sometimes requiring surgical intervention in the form of regular debridement or amputation when other strategies such as antimicrobial treatments fail. The complex relationships between both oral microbiota and the host have been extensively characterised, including the shift from health to disease, and has allowed for the development of numerous control strategies. This knowledge combined with contemporary studies of chronic infected wounds can be used to develop an understanding of the relationship between the host and microorganism in the chronic wound environment. Such information has the potential to inform wound management including strategies to control infection and promote wound healing

Importance of heterogeneity in Porhyromonas gingivalis lipopolysaccharide lipid A in tissue specific inflammatory signaling

Lipopolysaccharide (LPS) of Porphyromonas gingivalis exists in at least two known forms, O-LPS and A-LPS. A-LPS shows heterogeneity in which two isoforms designated LPS1435/1449 and LPS1690 appear responsible for tissue specific immune signalingpathways activation and increased virulence. The modification of lipid A to tetra-acylated1435/1449 and/or penta-acylated1690 fatty acids indicates poor growth conditions and bioavailability of hemin. Hemin protects P. gingivalis from serum resistance and the lipid A serves as a site for its binding. The LPS1435/1449 and LPS1690 isoforms can produce opposite effects on the human Toll-like receptors (TLR) TLR 2 and TLR 4 activation. This enabless P. gingivalis to select the conditions for its entry, survival and that of its co-habiting species in the host, orchestrating its virulence to control innate immune pathway activation and biofilm dysbiosis. Thismini review describes a number of effects that LPS1435/1449 and LPS1690 can exert on the host tissues such as deregulation of the innate immune system, subversion of host cell autophagy, regulation of outer membrane vesicle production and adverse effects on pregnancy outcome. The ability to change its LPS1435/1449 and/or LPS1690 composition may enables P. gingivalis to paralyze local pro-inflammatory cytokine production, thereby gaining access to its primary location in periodontal tissue