An Analysis of Homicides in Oakland 2002, 2003 and 2004

The number of homicides committed in Oakland decreased substantially between 2003 and 2004. The decline has been attributed, in part, to the Oakland Police Department's Violence Reduction Plan launched in October 2003, greater collaboration between local and state law enforcement agencies, and increased community involvement in violence prevention activities.This report summarizes changes in specific characteristics of homicides over the past three years, such as victim and suspect demographic characteristics, locations of the crimes, the parole/probation status of victims and suspects, and the time of day and month that the homicides were committed. In addition to presenting annual data for 2002, 2003, and 2004, the tables and figures in this report show how characteristics of the homicides changed from year to year and over the three-year period

Exploring The Relationship Between Teacher Caring, Teacher Job Satisfaction, And Burnout In Alternative School Teachers

This study explores the relationship between teacher caring, teacher job satisfaction, and burnout in Kentucky alternative school teachers. The methodology was a cross-sectional, correlational web-based survey. Instrumentation included the Copenhagen Burnout Inventory (CBI), Teven’s Teacher Self-Report of Caring Survey, and the Teacher Job Satisfaction Scale (McCroskey’s Generalized Belief Measure). The independent variables were the three sub-dimensions of the CBI: Personal Burnout, Work Related Burnout, and Client Related Burnout. The dependent variables were Teacher Caring and Teacher Job Satisfaction. For context, teachers were asked about the size, location, and type of school they served, and the length of their teaching experience in regular and alternative schools. Descriptive analysis, ANOVA, and regression analyses were completed. Findings indicated that caring was not related to burnout, and that burnout and teacher job satisfaction have a weak negative relationship. This research might add to the sparse amount of literature related to teacher caring, teacher job satisfaction, and burnout in alternative schools. Keywords: burnout, caring, Copenhagen Burnout Inventory, job satisfactio

Wie hilfreich sind "ethische Richtlinien" am Einzelfall?: Eine vergleichende kasuistische Analyse der Deutschen Grundsätze, Britischen Guidelines und Schweizerischen Richtlinien zur Sterbebegleitung

Zusammenfassung: Entscheidungen der Therapiebegrenzung und in der Betreuung am Lebensende sind häufig komplex und von ethischen Problemen begleitet. Im Mittelpunkt der Untersuchung steht die entscheidende Frage, wie hilfreich existierende "Ethik-Richtlinien", die eine ethische Orientierung bei solchen Entscheidungen geben sollen, in der klinischen Praxis tatsächlich sind. Die Frage, welchen Nutzen "Ethik-Richtlinien" bei der Entscheidungsfindung haben oder haben können, wird hier exemplarisch an einem klinischen Fallbeispiel aus einer Ethik-Kooperationsstudie in der Intensivmedizin analysiert. Vergleichend werden hierzu "Ethik-Richtlinien" aus Deutschland, der Schweiz und aus Großbritannien herangezogen, die Gegenstand eines internationalen Projekts zur Analyse von Richtlinien waren. Die Möglichkeiten und Grenzen einer ethischen Orientierung an "Ethik-Richtlinien" bei Entscheidungsproblemen der Therapiebegrenzung und in der Betreuung am Lebensende werden anhand der Fallstudie diskutiert und illustriert. Abschließend werden Schlussfolgerungen für die Entwicklung ethischer Richtlinien für die klinische Praxis formulier

Endotelina-1 y -3 : efectos moduladores sobre el transportador neuronal de noradrenalina en el hipotálamo de rata. Receptores y vías intracelulares involucradas

In this thesis, we show that endothelin-1 and -3 (ET-1 and ET-3) behave as neuropeptides regulating the activity of the norepinephrine transporter (NET) in the anterior and posterior\nhypothalamus of normotensive rats. The regulation is complex and involves different ET receptor\nsubtypes, including the so called non-conventional or atypical receptors as well as multiple\nsignaling pathways.\nIn the anterior hypothalamus ET-1 reduces neuronal norepinephrine (NE) uptake by\ndecreasing the number of functional transporters without altering its affinity. The inhibitory effect\nof ET-1 is mediated by ETB receptors and involves different signaling pathways including NOS, PKA\nand PKC. These pathways induce the phosphorylation at serine a tyrosine sites which favor NET\ninteraction with syntaxin A1 leading to NET internalization and thereby decreasing the number of\nbinding site at the membrane surface of nerve terminals. Nevertheless, in the same hypothalamic\nregion, ET-3 increases neuronal NE uptake and thus NET activity by increasing the number of\ntransporters available at the neuronal membrane. This occurs as the result of NET mobilization\nfrom intracellular compartments to the membrane surface. ET-3 exerts its effect through the\nactivation of an atypical or non-conventional ET receptor which is coupled to a G protein. The\nactivation of atypical ET receptor / G protein involves different intracellular calcium-dependent\nmechanisms.\nIn the posterior hypothalamus both endothelins decrease NE uptake by reducing NET\nactivity as the result of diminished binging sites at the neuronal membrane. This is achieved\nbecause both endothelins favor NET internalization to intracellular compartments. ET-1 response\nis mediated by ETB receptors whereas that of ET-3 by the activation of an atypical or nonconventional\nET receptor coupled to a G protein. Regardless which receptor is activated, both\nendothelins activate the same intracellular pathways including neuronal NOS, PKA and PKC\nleading to the same response as that of ET-1 in the anterior hypothalamus.\nPresent findings together with previous studies from our laboratory strongly support that\nboth ET-1 and ET-3 behave as neuromodulators of noradrenergic transmission in the in the\nanterior and posterior hypothalamus of normotensive rats through the regulation of three major\nsteps: NET activity (as shown in the present thesis), neuronal NE release and tyrosine hydroxylase\nactivity and expression.\nIn the light of these results we propose that the regulation of cardiovascular physiology\ninduced by brain ETs is mediated by the decreased sympathoinhibition of the anterior\nhypothalamus and the increased sympathoexcitation of the anterior hypothalamus. Thus, our\nfindings may explain the net increase in the central sympathetic activity mediated by ETs\ndescribed by several authors.Fil: Hope, Sandra Ingrid. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Buenos Aires, ArgentinaEn el presente trabajo de tesis, demostramos que las endotelinas-1 y -3 (ET-1 y ET-3) se comportan como neuropéptidos moduladores de la actividad del transportador de noradrenalina\n(NET) en el hipotálamo anterior y posterior de ratas normotensas. La regulación del mismo por las\nETs es compleja e involucra diferentes subtipos de receptores de ETs, incluyendo los llamados no\nconvencionales o atípicos y múltiples vías de señalización.\nEn el hipotálamo anterior se observa que la ET-1 disminuye la captación neuronal de noradrenalina (NA) a expensas de la reducción de la actividad del NET debido a una disminución en los sitios de unión. Las modificaciones producidas en la actividad del NET son específicamente sobre la capacidad máxima de transporte de NA o sea número de transportadores funcionales sin alterar su afinidad. El efecto inhibitorio de la ET-1 es mediado por el receptor ETB e involucra\ndiferentes vías que incluyen la NOS neuronal, la PKA y la PKC. En general estas vías activan los sitios de fosforilación del transportador en los aminoácidos serina y tirosina interactuando entre\nSintaxina A1 y NET. Esto produce la regulación del transportador en la superficie neuronal\naumentando la internalización del NET, por lo tanto disminuye su número en la membrana de la terminal nerviosa. En esta misma región hipotalámica, la ET-3 incrementa la captación neuronal\nde NA por aumento de la actividad del NET debido a un incremento del número de transportadores expresados en la membrana de la neurona. Este efecto se basa en una movilización del NET desde los compartimentos intracelulares hacia la superficie de la membrana.\nEste neuropéptido ejercería su efecto a través de la activación de un receptor atípico o no convencional el cual está acoplado a una proteína G. La activación del complejo receptor\natípico/proteína G involucra diferentes mecanismos intracelulares Ca2+ dependientes.\nEn el hipotálamo posterior, ambos neuropéptidos disminuyen la captación neuronal de\nNA a expensas de la reducción de la actividad del NET como consecuencia de una disminución en\nlos sitios de unión. Este efecto es consecuencia de un incremento en la internalización del\ntransportador desde la superficie de la membrana neuronal hacia los depósitos intracelulares. En el caso de la ET-1 el efecto inhibitorio es mediado por el receptor ETB unido a proteína G y la ET-3 a través de la activación de un receptor atípico o no convencional el cual está acoplado a una\nproteína G. En ambas situaciones, independientemente del receptor que se active, el efecto inhibitorio de ambas ETs involucra diferentes vías intracelulares que incluyen a la NOS neuronal, PKA y PKC. Esto produciría el mismo efecto descripto previamente en el caso de la ET-1 en el hipotálamo anterior.\nSobre la base de los resultados obtenidos en la presente Tesis Doctoral sumado a los trabajos previos de nuestro grupo permiten demostrar contundentemente que tanto la ET-1 como la ET-3 se comportan como neuromoduladores de la transmisión noradrenérgica en el hipotálamo anterior como en el posterior, de animales normotensos, a través de la regulación de\ntres procesos importantes, la actividad del NET, la regulación de la liberación neuronal de NA y la\nactividad y expresión de la tirosina hidroxilasa. Por lo tanto, y a la luz de todos estos resultados,\npodemos inferir que los efectos producidos por las ETs a nivel central sobre la fisiología cardiovascular son consecuencia de la reducción en la simpatoinhibición a nivel del hipotálamo anterior y un incremento de la simpatoexitación del hipotálamo posterior. Todo esto daría respuesta al aumento de la actividad simpática central, producido por las ETs, que fuera\nobservado por diversos autores

Assessing the discordance rate between local and central HER2 testing in women with locally determined HER2-negative breast cancer.

BackgroundThe importance of human epidermal growth factor receptor 2 (HER2) as a prognostic and predictive marker in invasive breast cancer is well established. Accurate assessment of HER2 status is essential to determine optimal treatment options.MethodsBreast cancer tumor tissue samples from the VIRGO observational cohort tissue substudy that were locally HER2-negative were retested centrally with both US Food and Drug Administration (FDA)-approved immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH) assays, using FDA-approved assay cutoffs; results were compared.ResultsOf the 552 unique patient samples centrally retested with local HER2-negative results recorded, tumor samples from 22 (4.0%) patients were determined to be HER2-positive (95% confidence interval [CI] = 2.5%-5.7%). Of these, 18 had been tested locally by only one testing methodology; 15 of 18 were HER2-positive after the central retesting, based on the testing methodology not performed locally. Compared with the 530 patients with centrally confirmed HER2-negative tumors, the 22 patients with centrally determined HER2-positive tumors were younger (median age 56.5 versus 60.0 years) and more likely to have ER/PR-negative tumors (27.3% versus 22.3%). These patients also had shorter median progression-free survival (6.4 months [95% CI = 3.8-15.9 months] versus 9.1 months [95% CI = 8.3-10.3 months]) and overall survival (25.9 months [95% CI = 13.8-not estimable] versus 27.9 months [95% CI = 25.0-32.9 months]).ConclusionsThis study highlights the limitations of employing just one HER2 testing methodology in current clinical practice. It identifies a cohort of patients who did not receive potentially efficacious therapy because their tumor HER2-positivity was not determined by the test initially used. Because of inherent limitations in testing methodologies, it is inadvisable to rely on a single test to rule out potential benefit from HER2-targeted therapy

Altered expression of Aquaporin-2 in one-kidney, one-clip hypertension

Aims: The aim of the present study was to evaluate the regulation of Aquaporin-2 (AQP2) water channel in the kidney of one-kidney, one-clip rats (Goldblatt-1 model). In addition, some mechanisms that underlie the role of AQP2 in the Goldblatt-1 model were evaluated. Main methods: Sprague-Dawley rats were divided in three groups: control two-kidney, no clip (C, 2 K-NC); nephrectomized one-kidney, no clip (N, 1 K-NC) and Goldblatt one-kidney, one-clip (G, 1 K-1C). AQP2 expression (by westernblot, real time PCR, immunohistochemistry and immunofluorescence), vasopressin V2 receptor expression (by real time PCR), cAMP concentration, NFkB and TonEBP (cytosol to nucleus ratio) were evaluated in the renal medulla. Key findings: AQP2 expression, V2 receptor expression and cAMP concentration were decreased in the renal medulla of 1 K-1C rats, NFkB translocation was favoured towards the nucleus suggesting its activation while TonEBP translocation was not altered in this model of hypertension. Significance: In this model of hypertension the decrease of AQP2 expression could be a mechanism that counteracts the high blood pressure promoting water excretion and this may be consequence of decreased vasopressin sensitivity and/or the increased activity of NFkB at renomedullary collecting duct level. Given that renovascular hypertension is among the most common causes of secondary hypertension, it is important to elucidate all the relevant mechanisms involved in the generation or in the compensation of the hypertensive state in order to improve the diagnoses and treatment of the patients.Fil: Albertoni Borghese, Maria Florencia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Hope, Sandra Ingrid. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiología Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Metabolismo del Fármaco. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Metabolismo del Fármaco; ArgentinaFil: Ortiz, Maria del Carmen. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Barchuk, Magalí. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Kessler, Camila. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; ArgentinaFil: Davio, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Vatta, Marcelo Sergio. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiología Humana; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Metabolismo del Fármaco. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Metabolismo del Fármaco; ArgentinaFil: Majowicz, Mónica Patricia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentin

Complete Genome Sequences of Paenibacillus Larvae Phages BN12, Dragolir, Kiel007, Leyra, Likha, Pagassa, PBL1c, and Tadhana

We present here the complete genomes of eight phages that infect Paenibacillus larvae, the causative agent of American foulbrood in honeybees. Phage PBL1c was originally isolated in 1984 from a P. larvae lysogen, while the remaining phages were isolated in 2014 from bee debris, honeycomb, and lysogens from three states in the USA

Prospective genomic surveillance of methicillin-resistant Staphylococcus aureus (MRSA) associated with bloodstream infection, England, 1 October 2012 to 30 September 2013.

BackgroundMandatory reporting of methicillin-resistant Staphylococcus aureus (MRSA) bloodstream infections (BSI) has occurred in England for over 15years. Epidemiological information is recorded, but routine collection of isolates for characterisation has not been routinely undertaken. Ongoing developments in whole-genome sequencing (WGS) have demonstrated its value in outbreak investigations and for determining the spread of antimicrobial resistance and bacterial population structure. Benefits of adding genomics to routine epidemiological MRSA surveillance are unknown.AimTo determine feasibility and potential utility of adding genomics to epidemiological surveillance of MRSA.MethodsWe conducted an epidemiological and genomic survey of MRSA BSI in England over a 1-year period (1 October 2012--30 September 2013).ResultsDuring the study period, 903 cases of MRSA BSI were reported; 425 isolates were available for sequencing of which, 276 (65%) were clonal complex (CC) 22. Addition of 64 MRSA genomes from published outbreak investigations showed that the study genomes could provide context for outbreak isolates and supported cluster identification. Comparison to other MRSA genome collections demonstrated variation in clonal diversity achieved through different sampling strategies and identified potentially high-risk clones e.g. USA300 and local expansion of CC5 MRSA in South West England.ConclusionsWe demonstrate the potential utility of combined epidemiological and genomic MRSA BSI surveillance to determine the national population structure of MRSA, contextualise previous MRSA outbreaks, and detect potentially high-risk lineages. These findings support the integration of epidemiological and genomic surveillance for MRSA BSI as a step towards a comprehensive surveillance programme in England.This work was supported by grants from the UK Clinical Research Collaboration Translational Infection Research Initiative, and the Medical Research Council (Grant Number G1000803) with contributions to the Grant from the Biotechnology and Biological Sciences Research Council, the National Institute for Health Research on behalf of the Department of Health, and the Chief Scientist Office of the Scottish Government Health Directorate (to Prof. Peacock); and the Wellcome Trust (to Prof. Parkhill [Grant 098051], Prof. Peacock). MST is a Wellcome Trust Clinical PhD Fellow at the University of Cambridge. MET is a Clinician Scientist Fellow, supported by the Academy of Medical Sciences and the Health Foundation, and by the National Institute for Health Research Cambridge Biomedical Research Centre. FC is supported by the Wellcome Trust (201344/Z/16/Z)