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1.
BMC Psychiatry ; 24(1): 353, 2024 May 10.
Article in English | MEDLINE | ID: mdl-38730300

ABSTRACT

BACKGROUND: The seven tiered behavioural and psychological symptoms of dementia (BPSD) model of service delivery has been used by inpatient units. The classification of each tier is broadly defined and not always agreed upon by clinicians. The case study uses novel approach by combining the BPSD classification criteria with clinical presentation to identify the clinical characteristics of the case and match these characteristics against the BPSD classification. This process was enhanced by using case specific measures such as the Neuropsychiatric Inventory (NPI) and Cohen Mansfield Agitation Inventory (CMAI) scales and key clinical data. CASE PRESENTATION: A case study of 76 year old male diagnosed with mixed Alzheimer's and Vascular dementia. The clinical presentation of the symptomatology was deemed to be extreme, thus fitting into the seventh tier (Extreme) of the BPSD model of service delivery. The case is considered to fit into the Extreme BPSD category given the high levels of aggression, which were consistently reflected in high scores on NPI and CMAI, as well as long length of inpatient stay (over 3 years). The average number of Pro re nata (PRN) psychotropics medications per month was 56 and seclusion episodes of 6 times per month, with each episode lasting on average 132 min shows severity of behaviours. His level of aggression had resulted in environmental damage and staff injuries. CONCLUSION: We recommend patient clinical characteristics, relevant hospital data and specific measures should be used to develop consensus around defining and classifying cases into Extreme BPSD.


Subject(s)
Aggression , Dementia, Vascular , Humans , Male , Aged , Aggression/psychology , Dementia, Vascular/psychology , Alzheimer Disease/psychology , Dementia/psychology , Behavioral Symptoms/diagnosis , Behavioral Symptoms/psychology , Behavioral Symptoms/etiology , Psychiatric Status Rating Scales
2.
Syst Rev ; 10(1): 275, 2021 10 25.
Article in English | MEDLINE | ID: mdl-34696804

ABSTRACT

BACKGROUND: Historically, eating disorders were not identified in older populations and it is only in more recent times that there is greater recognition of the existence of eating disorders among the elderly. This is despite the high level of morbidity and mortality associated with these disorders. Current guidelines focus on treatment of eating disorders within the adolescent and general adult age groups, without apparent concessions made for the older age group. The aim of this study was to review existing literature on the demographics and treatment of eating disorders in older people. METHODS/DESIGN: A systematic review of the literature was conducted using CINAHL, MEDLINE, EMBASE, PsycInfo, Scopus, and Web of Science to identify publications focusing on treatment of eating disorders in people over the age of 65 years, age of diagnosis, gender distribution, treatment setting, and treatment outcomes. RESULTS: A total of 35 articles (reporting on 39 cases) were relevant to our study, with 33 of the 35 articles being either case studies or case series. The mean age of participants was 73.2 years (range 66-94 years) with the majority (84.6%) being female. Most cases (84.6%) were diagnosed with anorexia nervosa, and 56.4% of all cases were reported as late onset (i.e., after age 40 years). The vast majority (94.8%) received treatment, of which 51.5% was hospital-based treatment. In case descriptions where improvement was reported, the majority described a multidimensional approach that included a combination of hospital admission, therapy and pharmacotherapy. Overall, 79.5% of cases who underwent treatment for an eating disorder improved, while 20.5% relapsed or died as a result of the complications from their eating disorder. There were significant inconsistencies and omissions in the way cases were described, thereby impacting on the interpretation of the results and potential conclusions. CONCLUSIONS: The information available on the treatment of eating disorders in people over the age of 65 years is limited. The quality of case reports to date makes it difficult to suggest specific assessment or treatment guidelines for this population.


Subject(s)
Anorexia Nervosa , Feeding and Eating Disorders , Adolescent , Adult , Aged , Aged, 80 and over , Anorexia Nervosa/therapy , Feeding and Eating Disorders/therapy , Female , Hospitalization , Humans , Treatment Outcome
4.
J Biol Chem ; 282(39): 28648-28658, 2007 Sep 28.
Article in English | MEDLINE | ID: mdl-17673465

ABSTRACT

Phosphoinositide (PI) 3-kinases play an important role in regulating the adhesive function of a variety of cell types through affinity modulation of integrins. Two type I PI 3-kinase isoforms (p110 beta and p110 gamma) have been implicated in G(i)-dependent integrin alpha(IIb)beta(3) regulation in platelets, however, the mechanisms by which they coordinate their signaling function remains unknown. By employing isoform-selective PI 3-kinase inhibitors and knock-out mouse models we have identified a unique mechanism of PI 3-kinase signaling co-operativity in platelets. We demonstrate that p110 beta is primarily responsible for G(i)-dependent phosphatidylinositol 3,4-bisphosphate (PI(3,4)P(2)) production in ADP-stimulated platelets and is linked to the activation of Rap1b and AKT. In contrast, defective integrin alpha(IIb)beta(3) activation in p110 gamma(-/-) platelets was not associated with alterations in the levels of PI(3,4)P(2) or active Rap1b/AKT. Analysis of the effects of active site pharmacological inhibitors confirmed that p110 gamma principally regulated integrin alpha(IIb)beta(3) activation through a non-catalytic signaling mechanism. Inhibition of the kinase function of PI 3-kinases, combined with deletion of p110 gamma, led to a major reduction in integrin alpha(IIb)beta(3) activation, resulting in a profound defect in platelet aggregation, hemostatic plug formation, and arterial thrombosis. These studies demonstrate a kinase-independent signaling function for p110 gamma in platelets. Moreover, they demonstrate that the combined catalytic and non-catalytic signaling function of p110 beta and p110 gamma is critical for P2Y(12)/G(i)-dependent integrin alpha(IIb)beta(3) regulation. These findings have potentially important implications for the rationale design of novel antiplatelet therapies targeting PI 3-kinase signaling pathways.


Subject(s)
Blood Platelets/enzymology , Phosphatidylinositol 3-Kinases/metabolism , Platelet Adhesiveness/physiology , Platelet Glycoprotein GPIIb-IIIa Complex/metabolism , Second Messenger Systems/physiology , Adenosine Diphosphate/metabolism , Adenosine Diphosphate/pharmacology , Animals , Blood Platelets/cytology , Enzyme Inhibitors/pharmacology , GTP-Binding Protein alpha Subunits, Gi-Go/metabolism , Isoenzymes/antagonists & inhibitors , Isoenzymes/genetics , Isoenzymes/metabolism , Membrane Proteins/agonists , Membrane Proteins/metabolism , Mice , Mice, Knockout , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol Phosphates/metabolism , Phosphoinositide-3 Kinase Inhibitors , Platelet Adhesiveness/drug effects , Proto-Oncogene Proteins c-akt/metabolism , Purinergic P2 Receptor Agonists , Receptors, Purinergic P2/metabolism , Receptors, Purinergic P2Y12 , Second Messenger Systems/drug effects , rap GTP-Binding Proteins/metabolism
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