The Contributing Factors to Adolescent Depression

Objective: This paper reviews individual, familial, peer, and societal factors influencing adolescent depression in developed countries. Background: Depression usually onsets at adolescence and contributes to high DALYs. Since depression is treatable, efforts should be made to reduce its prevalence and effect. Methods: The research consisted of looking at literature relevant to the topic and age group and conducting interviews with experts who know about and have worked with adolescent depression. Discussion: Adolescents begins at the onset of puberty, allowing different biological factors such as genetics, stress of puberty, and cognitive changes to increase vulnerability to depression. Adolescents who had substance abuse problems and/or held stronger neuroticism personality trait were more susceptibility to depression. Unhealthy familial relations and peer relations was also linked to depression risk. Negative life event often predated depression onset. Living with a parent who had depression increased chances of depression for their offspring. The performance-driven society puts pressure on adolescents that when unable to cope or extrinsically motivated can increase risk of depression. There could be possible risks with social media in centralizing one depression definition, increasing comparing behaviors lowering self-esteem, and difficulty distinguishing true reality. Stigma and lack of adolescent-focused care can prevent adolescents from seeking and getting the help that they need. Conclusion: The paper looked at a few factors that influence depression. Different factors interact changing depression vulnerability. Possible next steps are looking at these factors and how to decrease the risk to improve adolescent depression prevalence

From qd to LR, or, how were the qd and LR algorithms discovered?

Perhaps, the most astonishing idea in eigenvalue computation is Rutishauser's idea of applying the LR transform to a matrix for generating a sequence of similar matrices that become more and more triangular. The same idea is the foundation of the ubiquitous QR algorithm. It is well known that this idea originated in Rutishauser's qd algorithm, which precedes the LR algorithm and can be understood as applying LR to a tridiagonal matrix. But how did Rutishauser discover qd and when did he find the qd-LR connection? We checked some of the early sources and have come up with an explanatio

Daily Eastern News: October 2, 2007

https://thekeep.eiu.edu/den_2007_oct/1001/thumbnail.jp

Daily Eastern News: October 2, 2007

https://thekeep.eiu.edu/den_2007_oct/1001/thumbnail.jp

Osalise või täieliku NCAM valgu puudulikkusega hiirte fenotüüp

Väitekirja elektrooniline versioon ei sisalda publikatsioone.Sünaptiline plastilisus on aju plastilisuse üks oluline osa, mis võimaldab ajul pidevalt luua ja eemaldada rakkudevahelisi kontakte. Aju plastilisus, mis hõlmab närvikoe erinevaid morfoloogilisi muutusi, on oluline faktor nii kognitiivsetele võimetele nagu õppimine, mälu, aistingud ja teadvus kui ka meeleoluseisunditele. Neuronaalsete rakkude adhesioonimolekul (NCAM) ja tema polüsialüülitud vorm (PSA-NCAM) on valgud, mis on üheks peamisteks sünaptilise plastilisuse kujundajateks. Eelnevad uuringud kinnitavad, et NCAM molekulid on võimelised seostuma nii omavahel kui ka teiste erinevate rakupinna valkudega. Sel moel osaleb NCAM/PSA-NCAM erinevate signaalradade käivitamises ja regulatsioonis. Üheks olulisemaks NCAMi interaktsioonipartneriks on fibroblastide kasvufaktori retseptor 1 (FGFR1). Käesoleva uurimistöö eesmärgiks oli selgitada, kuidas osaline (NCAM+/-) või täielik (NCAM-/-) NCAM/PSA-NCAMi puudumine hiirtel mõjutab nende loomade fenotüüpi; vaadeldi, kas NCAM-/- hiirte ärevuskäitumine võib olla mõjutatud nende halvenenud kognitiivsetest võimetest. Selgitamaks, milline signaalrada vastutab kognitiivsete ja milline depressioonisarnase käitumise eest, uuriti nendel hiirtel NCAM-vahendatud signaalradu, peamisi interaktsioonipartnereid ning serotonergilist süsteemi. Antud töö tulemused kinnitasid, et NCAM-/- hiirtel esines depressioonisarnane käitumine ning olid vähenenud kognitiivsed võimed. NCAM+/- hiirtel esines samuti depressioonisarnane käitumine, kuid nende kognitiivsed võimed ei olnud kontrollhiirtega võrreldes muutunud. Selgus ka, et NCAM-/- hiirte käitumine ärevuskatsetes on mõjutatud nende halvenenud kognitiivsetest võimetest. Leiti, et nii NCAM+/- kui NCAM-/- hiirtel esinesid muutused FGFR1 aktivatsioonis, kuid erinevalt NCAM-/- hiirtest ei kaasnenud NCAM+/- hiirtel FGFR1 aktivatsiooni langusega kaltsium-kalmoduliinist sõltuvate kinaaside II ja IV (CaMKII ja IV) ning transkriptsioonifaktori CREB aktivatsiooni muutust, mis võibki olla nende loomade käitumusliku fenotüübi põhjus. Ühtlasi leiti, et NCAM puudulikkus mõjutab serotoniini transporteri ekspressiooni ning oletatavalt just vähenenud serotoniini transporteri ekspressioon võib olla nendel loomadel ilmnenud depressioonisarnase käitumise põhjuseks.Synaptic plasticity is one of the main factors responsible for brain plasticity. For sense and consciousness, emotional behaviour and for cognitive processes, such as learning and memory, continuous activity-induced remodelling of neuronal circuits is required. Neural cell adhesion molecule (NCAM) and its polysialyted form (PSA-NCAM) are the most significant key players in synaptic plasticity, providing stable connections between cells and at the same time, remodelling synaptic networks. It has been shown that NCAM is capable of binding to a number of proteins on the cell surface including the NCAM molecule itself on the opposing cell surface. Thus, many downstream signal pathways are dependent on NCAM/PSA-NCAM-mediated cellular signalling. One of the major interaction partners of NCAM is fibroblast growth factor receptor 1 (FGFR1). The aim of this study was to explore the effect of partial (NCAM+/-) or complete (NCAM-/-) deficiency in NCAM/PSA-NCAM on the behavioural phenotype of mice and to illuminate how disrupted cognitive abilities influence NCAM-/- mice in anxiety tests. The intracellular pathway responsible for the cognitive dysfunction in the mice and those pathways implicated in the reduced ability of the mice to cope with stress were investigated by examining the main NCAM pathways and NCAM interaction partners and also alterations in the serotonergic system. The data show that NCAM-/- mice demonstrate a depression-like behaviour with altered cognitive functions. NCAM+/- mice demonstrate a depression-like behaviour without alterations in cognitive functions. The data also show that the impaired cognition of NCAM-/- mice affect their behaviour in anxiety tests. We found that both NCAM+/- and NCAM-/- mice showed reduced phosphorylation of the FGFR1 but in contrast to NCAM-/- mice, the observed behavioural phenotype in NCAM+/- mice was not associated with alterations in the basal levels of the transcription factor CREB or phosphorylated Ca2+-calmodulin-dependent protein kinase II and IV (CaMKII and CaMKIV).We also found that reduced levels of NCAM/PSA-NCAM led to alterations in the expression of the serotonin transporter. Thus, the observed depression-like phenotype in NCAM+/- or NCAM-/- mice may be caused by a reduction in expression of the serotonin transporter

Decision making processes in people with symptoms of acute myocardial infarction: qualitative study

Objective To identify, the themes that influence decision making processes used by patients with symptoms of acute myocardial infarction. Design Qualitative study using semistructured interviews. Setting Two district hospitals in North Yorkshire. Participants 22 patients admitted to hospital with confirmed second, third, or fourth acute myocardial infarction. Main outcome measure Patients' perceptions of their experience between the onset of symptoms and the decision to seek medical help. Results Six main themes that influence the decision making process were identified: appraisal of In symptoms, perceived risk, previous experience, psychological and emotional factors, use of the NHS, and context of the event. Conclusions Knowledge of symptoms may not be enough to promote prompt action in the event of an acute myocardial infarction. Cognitive and emotional processes, individual beliefs and values, and the influence of the context of the event should also be considered in individual interventions designed to reduce delay in the event of symptoms of acute myocardial infarction

Inactive endosialidase-based detection of bacterial and oncofetal polysialic acid

Polysialic acid is a carbohydrate polymer which consist of N-acetylneuraminic acid units joined by alpha2,8-linkages. It is developmentally regulated and has an important role during normal neuronal development. In adults, it participates in complex neurological processes, such as memory, neural plasticity, tumor cell growth and metastasis. Polysialic acid also constitutes the capsule of some meningitis and sepsis-causing bacteria, such as Escherichia coli K1, group B meningococci, Mannheimia haemolytica A2 and Moraxella nonliquefaciens. Polysialic acid is poorly immunogenic; therefore high affinity antibodies against it are difficult to prepare, thus specific and fast detection methods are needed. Endosialidase is an enzyme derived from the E. coli K1 bacteriophage, which specifically recognizes and degrades polysialic acid. In this study, a novel detection method for polysialic acid was developed based on a fusion protein of inactive endosialidase and the green fluorescent protein. It utilizes the ability of the mutant, inactive endosialidase to bind but not cleave polysialic acid. Sequencing of the endosialidase gene revealed that amino acid substitutions near the active site of the enzyme differentiate the active and inactive forms of the enzyme. The fusion protein was applied for the detection of polysialic acid in bacteria and neuroblastoma. The results indicate that the fusion protein is a fast, sensitive and specific reagent for the detection of polysialic acid. The use of an inactive enzyme as a specific molecular tool for the detection of its substrate represents an approach which could potentially find wide applicability in the specific detection of diverse macromolecules.Siirretty Doriast

Social Saliency: Visual Psychophysics and Single-Neuron Recordings in Humans

My thesis studies how people pay attention to other people and the environment. How does the brain figure out what is important and what are the neural mechanisms underlying attention? What is special about salient social cues compared to salient non-social cues? In Chapter I, I review social cues that attract attention, with an emphasis on the neurobiology of these social cues. I also review neurological and psychiatric links: the relationship between saliency, the amygdala and autism. The first empirical chapter then begins by noting that people constantly move in the environment. In Chapter II, I study the spatial cues that attract attention during locomotion using a cued speeded discrimination task. I found that when the motion was expansive, attention was attracted towards the singular point of the optic flow (the focus of expansion, FOE) in a sustained fashion. The more ecologically valid the motion features became (e.g., temporal expansion of each object, spatial depth structure implied by distribution of the size of the objects), the stronger the attentional effects. However, compared to inanimate objects and cues, people preferentially attend to animals and faces, a process in which the amygdala is thought to play an important role. To directly compare social cues and non-social cues in the same experiment and investigate the neural structures processing social cues, in Chapter III, I employ a change detection task and test four rare patients with bilateral amygdala lesions. All four amygdala patients showed a normal pattern of reliably faster and more accurate detection of animate stimuli, suggesting that advantageous processing of social cues can be preserved even without the amygdala, a key structure of the “social brain”. People not only attend to faces, but also pay attention to others’ facial emotions and analyze faces in great detail. Humans have a dedicated system for processing faces and the amygdala has long been associated with a key role in recognizing facial emotions. In Chapter IV, I study the neural mechanisms of emotion perception and find that single neurons in the human amygdala are selective for subjective judgment of others’ emotions. Lastly, people typically pay special attention to faces and people, but people with autism spectrum disorders (ASD) might not. To further study social attention and explore possible deficits of social attention in autism, in Chapter V, I employ a visual search task and show that people with ASD have reduced attention, especially social attention, to target-congruent objects in the search array. This deficit cannot be explained by low-level visual properties of the stimuli and is independent of the amygdala, but it is dependent on task demands. Overall, through visual psychophysics with concurrent eye-tracking, my thesis found and analyzed socially salient cues and compared social vs. non-social cues and healthy vs. clinical populations. Neural mechanisms underlying social saliency were elucidated through electrophysiology and lesion studies. I finally propose further research questions based on the findings in my thesis and introduce my follow-up studies and preliminary results beyond the scope of this thesis in the very last section, Future Directions