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Endocardite infeciosa é uma infeção da superfície interna do coração, geralmente as válvulas cardíacas. Os sintomas mais comuns são febre, pontos vermelhos de sangue na pele, sopro cardíaco, cansaço e anemia. Entre as possíveis complicações estão insuficiência valvular, insuficiência cardíaca, AVC e insuficiência renal.

A endocardite infeciosa é geralmente causada por uma infeção bacteriana ou, ainda que menos comum, por uma infeção fúngica. Entre os fatores de risco estão valvulopatias incluindo doenças reumáticas, cardiopatia congénita, próteses valvulares, hemodiálise, consumo de drogas intravenosas e pacemakers. As bactérias implicadas mais comuns são estreptococos ou estafilococos. O diagnóstico pode ser suspeito com base nos sintomas e confirmado com hemoculturas ou ecografia. Existe também uma forma de endocardite não infeciosa.

Os benefícios da administração de antibióticos a seguir a intervenções dentárias como forma de prevenção de endocardite não são ainda claros. Algumas orientações recomenda-nos para grupos de elevado risco. O tratamento geralmente consiste na administração de antibióticos por via intravenosa. A escolha dos antibióticos baseia-se nos resultados da hemocultura. Em alguns casos pode ser necessária cirurgia cardiovascular.

A doença afeta anualmente 5 em cada  pessoas. No entanto, a frequência varia conforme a região do mundo. A doença é mais frequente entre homens do que entre mulheres. O risco de morte entre pessoas infetadas é de cerca de 25%. Sem tratamento, a doença é quase sempre fatal.

Causas
Num indivíduo saudável, uma bacteremia (onde as bactérias entram na corrente sanguínea através de um pequeno corte ou ferida), normalmente, seria rapidamente eliminada, sem consequências adversas. Se uma válvula cardíaca é danificada ou coberta por um coágulo de sangue, a válvula proporciona um local para que as bactérias se instalem e uma infecção pode ser estabelecida, causando a endocardite infecciosa.

A infecção frequentemente produz vegetações, que são estruturas compostas de plaquetas, fibrina e microrganismos infecciosos. O aspecto da vegetação à ecocardiografia é de uma massa de material ecogênico, aderida a uma superfície endocárdica, geralmente anormal (valvas alteradas, locais de shunts, etc), e que apresenta uma mobilidade diferente da mobilidade da superfície à qual está aderida. Localiza-se geralmente na câmara para onde se dirige a regurgitação (face atrial na valva mitral e ventricular na valva aórtica) e tende a crescer nos folhetos das próteses biológicas e no anel das próteses mecânicas.
Nas valvas, ela pode se limitar às cúspides, mas pode invadir o anel ou as estruturas adjacentes, causando distúrbios de ritmo, comunicações entre as cavidades ou mesmo grandes abscessos. Ela pode acometer a valva mitral, a aórtica, a tricúspide ou a pulmonar e, com freqüência, lesando mais de uma. O acometimento pode ser por bactérias gram+, gram – ou por fungos. Atualmente, alterações valvares degenerativas e próteses, e não mais a doença reumática, representam as causas mais comuns de endocardite em países desenvolvidos.

Portanto, o conceito antigo de que a endocardite ocorria quase que exclusivamente em portadores de valvulopatias, já não se aplica e, cada vez mais, a endocardite é diagnosticada em pacientes com outros quadros.
Reumatismo crônico, que foi um fator de risco principal na época pré-antibióticos, é agora rara em países industrializados . Este grupo de pacientes em situação de risco, no entanto, foi substituído por um novo grupo de risco, que inclui usuários de drogas intravenosas(com os Estafilococos aureus despontando como causa crescente de endocardite), pessoas idosas com esclerose de válvula, pacientes com próteses intravasculares, aqueles expostos a doença nosocomiais e hemodiálise. No passado, a bacteremia causada por procedimentos dentários (na maioria dos casos por estreptococos viridans, que residem na cavidade oral) era clinicamente mais significativo do que realmente é hoje. No entanto, é importante que um dentista esteja ciente de quaisquer problemas do coração antes de iniciar o tratamento.
Outras condições que resultam em elevado número de bactérias que entram na corrente sanguínea incluem câncer colorretal (principalmente Streptococcus bovis), graves infecções do trato urinário e injeção de drogas (Staphylococcus aureus), sendo grande a incidência em usuários de drogas injetáveis, que tendem a ter suas válvulas cardíacas do lado direito infectadas. Com um grande número de bactérias, mesmo uma válvula cardíaca normal, podem ficar infectadas.

Embora tenha havido variações entre o estudos que foram revisados , Staphylococcus aureus  e Streptococcus  são responsável pela maioria dos casos de doença. Staphylococcus tende a prevalecer, identificando a flora da pele como uma importante fonte de infecção. Notamos também outras associações, como a Streptococcus bovis associada endocardite infecciosa (principalmente Streptococcus gallolyticus) em populações de idosos, e Streptococcus bovis foi frequentemente ligado ao sistema digestivo.

Fisiopatologia

O evento primario é a aderência das bactérias às válvulas danificadas. Este evento é concluído em poucos minutos durante a bacteremia transitória e envolve a válvula de tecido. A segunda etapa envolve a persistência e crescimento de bactérias dentro da lesão cardíaca, geralmente associada com a extensão e ao dano do tecido local. Disseminação de êmbolos sépticos vai tomando espaço em outros órgãos, como por exemplo o rim, baço e cérebro.

Lesões mecânicas
Qualquer escoriação do endotélio resulta em um contato direto entre o sangue e  os componentes subendoteliais do "hospedeiro", incluindo as proteínas extracelular da matriz, tromboplastina e o tecido, que desencadeiam coagulação do sangue. O coágulo que se forma sobre o endotélio danificado, contém grandes quantidades de fibrinogénio- fibrina, fibronectina, as proteínas do plasma e proteínas de plaquetas.
Patógenos associados à endocardite infecciosa avidamente ligam-se a estas estruturas e colonizam-se durante a bacteremia transitória. Por sua vez, as bactérias aderentes atraem e ativam monócitos do sangue para produzir mais tecido, assim como a citocina.  Citocinas e fatores pró-coagulantes contribuem para o alargamento dos coágulos infectados, denominado de vegetação. Este processo fornece um nicho para os micróbios. Lesões de válvulas mecânicas promovem a infecção por todos os agentes patogênicos classicamente associados com endocardite infecciosa, incluindo estafilococos, estreptococos, e enterococci.

Lesões inflamatórias
As células endoteliais respondem a inflamação local, através de várias moléculas, incluindo integrinas da família B1. Integrinas são proteínas de adesão, presentes na membrana que podem se conectar com o citoesqueleto. Integrinas da família B1 possuem fibronectina na superfície endotelial. Staphylococcus aureus e  alguns outros agentes patogênicos infecciosos estão associados a endocardite e transportam proteínas fibronectina de ligação em sua superfície. Assim, fibronectina vinculada sobre o endotélio apresenta uma superfície adesiva para circulação de estafilococos. Uma vez aderido, staph aureus consegue escapar das defesas do hospedeiro e agentes antibacterianos, e multiplicar-se, espalhando-se para órgãos distantes. Este comportamento é orquestrada por reguladores globais, como agr (gene acessório regulador) e SAR (Staphylococcal acessório regulador), que sente a densidade bacteriana e libera ou não a secreção de hemolisinas e toxinas a fim decompletar a invasão.

Staphylococcus aureus está associado à endocardite infecciosa em pacientes sem doença valvar previamente conhecido, e é freqüentemente responsável pela doença em usuários de drogas intravenosas. A válvula de inflamação pode surgir em situações clínicas complicadas, que são suscetíveis  a deposição local de fibronectina. Por exemplo, até 25% de pacientes com mais de 40 anos têm lesões degenerativas de válvula e inflamação local, que se assemelha a arterosclerose.  De forma similar, contínuas  injeções com materiais tóxicos usadas por usuários de drogas,  podem incentivar e promover a produção de citocinas, o que causa  lesões inflamatórias, especialmente nas válvulas do lado direito.

Características dos microorganismos
Os organismos mais frequentemente responsáveis por endocardite infecciosa são aqueles que possuem a maior capacidade de aderência a válvulas danificadas. Juntos, Staph aureus, Streptococcus spp e enterococos são responsáveis por mais de 80% de todos os casos da doença. Estes organismos têm adesinas de superfície que se apegam à vegetação. Estas adesinas são conhecidoas como MSCRAMMs ou componentes da superfície microbiana,  que reagem com matriz adesiva das moléculas. No caso do Staph aureus, o fibrinogênio ligado a proteínas, também chamado fator de aglutinação estão envolvidos na colonização da válvula e a infecção.

Persistência bacteriana in situ
Após a colonização da válvula, os microorganismos infecciosos em sua maioria sobrevivem e evitam as defesas do hospedeiro. Um acontecimento chave no processo é a maturação da vegetação, no qual o microrganismos tornam-se totalmente envolvidos. Tanto estafilococos e estreptococos pode desencadear a produção de monócitos no tecido local e induzir a agregação de plaquetas. Induzir a ativação de plaquetas bacterianas é uma faca de dois gumes pois, quando ativadas, as plaquetas liberam proteínas microbicidas, que matam as bactérias, alterando a sua membrana plasmática.

Microorganismos recuperados de pacientes com endocardite infecciosa  foram resistente indução de plaquetas, enquanto que as bactérias semelhantes de pacientes com outros tipos de infecção eram suscetíveis às plaquetas. Portanto, patógenos associados à endocardite infecciosa são resistentes a indução de plaquetas,  para tirar vantagem do efeito pró-coagulante.

Invasão e disseminação
Invasão tecidual e formação de abscessos são características principais da endocardite infecciosa. Ligado à superfície das adesinas, Staphylococcus aureus  produzem uma riqueza de exoenzimas que convertem tecidos do hospedeiro locais em nutrientes para o crescimento bacteriano e exotoxinas que são prejudiciais para o hospedeiro. A atuação desses fatores é controlado pelos reguladores globais e agr e sar e talvez sigB (sigma B) . sar e é ativado em infecções da vegetação.

Além disso, a inativação de agr por mutação ou por agentes bloqueadores diminui grandemente o formação de abscessos subcutâneos. Invasão e disseminação de outros patógenos associados a endocardite infecciosa, provavelmente, segue, cenários semelhantes. No entanto, uma vez que são menos destrutivo do que Staphylococcus aureus eles têm sido menos estudados.

Papel da transição bacteriana
Procedimentos médicocirúrgicos em locais ou materiais sem esterilização podem provocar bacteremia. Tais bacteremias geralmente são de curta duração (1-100 unidades formadoras de colónias por ml de sangue para menos de 10 minutos, no caso de uma extracção dentária). No entanto, eles podem promover a endocardite infecciosa em pacientes com lesão valvar pré-existentes. Bacteremia transitória surge espontaneamente durante a mastigação, escovação, e outras atividades normais, o que provavelmente explica por que a maioria dos casos de endocardite infecciosa não são por procedimentos médicos. Bacteremias espontâneas que surgem durante a mastigação podem explicar porque estreptococos orais são predominantes causa da doença. Assim, mesmo se a profilaxia antibiótica durante procedimentos odontológicos foram eficazes, só impede um número limitado de casos. Boa higiene dental é a melhor medida preventiva.

Papel de defesas do hospedeiro
A endocardite infecciosa é mais frequente devido a bactérias gram-positivas do que a gram-negativas bactérias. O C5b-C9 complexo de ataque da membrana, mata as bactérias gram-negativas por perfurarem sua membrana externa enquanto que as bactérias gram-positivas, , são resistentes à tal ataque. Algumas bactérias gram-negativas têm cápsulas espessas que ajudam a resistir morte induzida pelo complemento.

Um importante subgrupo de patógenos das bactérias gram-negativas associado à endocardite infecciosa inclui microorganismos do grupo HACEK assim como P aeruginosa em usuários de drogas intravenosas. Patogenios gram-positivos podem também resistir as defesas do hospedeiro celulares. Elas podem resistir a plaquetária induzida e responder aos anticorpos.

Fatores de risco
Sabemos que na maioria dos casos da doença, estão envolvidas as bactérias staphylococci e streptococci, logo, pacientes que apresentam infecções em suas próteses e apresentam ferimentos, como por exemplo os usuários de próteses com ferimentos na cavidade oral, podem desenvolver a doença. Deste modo, destacamos os seguintes fatores de risco:

Prolapso da válvula mitral;
Estenose aórtica senil;
Insuficiência mitral;
Pacientes com próteses dentárias;
Usuários de drogas intravenosas;
Pacientes com próteses intravasculares;
Pacientes expostos à doenças nosocomiais;
Pacientes que realizam hemodiálise

Antes da era dos antibióticos, a cardiopatia reumática crônica era considerado o fator de risco principal para a endocardite infecciosa. Hoje os fatores de risco são considerados em quatro categorias:

Endocardite Infecciosa das Válvulas Naturais
Está associado com doenças congênitas, assim como prolapso de válvula mitral. Apenas pacientes com refluxo de válvula possuem um risco maior de apresentar a doença. Estudos mostram que o prolapso de válvula mitral está associado a um baixo IMC, pressão arterial e de menor prevalência de Diabetes Mellitus. Com isso, pode-se pensar em uma variável cardiovascular protetiva.

Endocardite Infecciosa das Próteses Valvais
As próteses são a principal causa da estenose aórtica senil e do refluxo de válvula que é um fator de risco para a endocardite infecciosa. Muitos dos pacientes com próteses apresentam a patologia e mais da metade desses pacientes tem mais de 60 anos.

Endocardite Infecciosa em usuários de drogas intravenosas
Usuários de drogas injetáveis representam um grupo de risco, devido à doenças cardiovasculares já citadas acima. Os patógenos normalmente se originam da pele, devido ao contato com seringas, muitas vezes infectadas. Nos pacientes infectados pelo vírus HIV, existe uma chance ainda maior de mortalidade e de risco devido à endocardite infecciosa.

Endocardite Infecciosa Nosocomial
Está é uma categoria crescente. É muito frequente a presença de estafilococos e enterococos relacionados com os cateteres ou procedimentos médico-cirúrgicos, podendo desenvolver a patologia devido à infecção. A endocardite nosocomial é muito relevante devido à sua alta taxa de mortalidade.

Outro fator de risco importante da endocardite infecciosa é a hemodiálise. A doença é de duas a três vezes mais freqüente em pacientes em hemodiálise do que em pacientes de diálise peritoneal ou na população em geral. A maioria dos casos é devido ao Staphylococcus aureus.

Diagnóstico

Para que haja um diagnostico claro da endocardite infecciosa, é necessário que o cardiologista responsável pelo paciente com a suspeita da doença peça exames de sangue e de imagem. Assim, a "American Heart Association"criou uma diretriz, denominada Critérios de Duke:

Critérios de Duke
São necessários para o diagnóstico:

a) 2 critérios maiores ou

b) 1 critério maior e 3 menores ou

c) 5 critérios menores

Critérios maiores
Isolamento dos agentes típicos de Endocardite Infecciosa em duas hemoculturas distintas, sem foco primário: Streptococcus viridans, Streptococcus bovis, grupo HACEK, Staphylococcus aureus ou bacteremia por enterococo adquirido na comunidade;
Microorganismo compatível com endocardite infecciosa isolado em hemoculturas persistentemente positivas;
Única cultura ou sorologia positiva (IgG > 1:800) para Coxiella burnetii
Nova regurgitação valvar (aparecimento de sopro ou mudança de sopro pré-existente não é suficiente);
Ecocardiograma com evidências de endocardite (há 3 possíveis achados ecocardiográficos: massa intracardíaca oscilante ecogênica em sítio de lesão endocárdica, abscesso perivalvar e nova deiscência em valva prostética)

Critérios menores
Fator predisponente para doença (uso de drogas injetáveis ou doença cardiovascular predisponente)
Febre maior que 38oC
Fenômenos vasculares (exceto petéquias e outras hemorragias)
Fenômenos imunológicos (presença de fator reumatóide, glomerulonefrite, nódulo de Osler ou manchas de Roth)
Hemocultura positiva que não preencha critérios maiores ou evidência sorológica de infecção ativa (exclui-se hemocultura única positiva para estafilococo coagulase-negativo ou para microorganismo que raramente cause endocardite)

Condições cardiovasculares de risco para endocardite

Alto Risco

- Valvas protéticas

- Endocardite bacteriana prévia

- Doença congenita cianótica

- Shunts Sistêmico-pulmonares construídos cirurgicamente (Ex: Blalock-Taussig - correção de Tetralogia de Fallot)

- Ducto arterioso patente

- Regurgitação Aórtica

- Estenose Aórtica

- Regurgitação Mitral

- Dupla lesão mitral

- Comunicações interventriculares

- Coarctação da aorta

- Lesões intracardíacas reparadas cirurgicamente, que tenham anormalidade hemodinâmica residual

Risco Intermediário

- Prolapso da valva Mitral, com regurgitação

- Estenose mitral pura

- Doença valvar tricuspide

- Estenose pulmonar

- Hipertrofia Septal assimétrica

- Aorta bicuspide ou esclerose com calcificação aórtica, com anormalidades hemodinâmicas mínimas

- Doença valvar degenerativa do idoso

- Lesão intracardiaca com reparo cirurgico há menos de 6 meses, mesmo sem alterações hemodinamicas residuais.

Risco Baixo ou Nenhum
- Prolapso da valva Mitral, sem regurgitação

- Regurgitação valvar mínima (ex: escape mitral) sem anormalidade estrutural visivel ao ECO

- Defeitos do septo atrial isolados (fossa oval)

- Doença coronariana

- Placas ateroscleróticas

- Marca passos e desfibriladores automáticos implantados

- Cirurgia de revascularização miocardica prévia

- Correção cirúrgica com mais de 6 meses de lesão intra cardiaca, com mínima ou nenhuma alteração hemodinâmica residual.

- Passado de Doença de Kawasaki ou Doença Reumática sem comprometimento valvar.

Prevenção

O regime profilático eficaz no caso da endocardite infecciosa necessita de um equilíbrio, entre os riscos de efeitos colaterais provindos do tratamento e do desenvolvimento da doença.

Há grandes limitações referentes a essa temática devido aos estudos e experiências viáveis e realizadas em animais, estudos randomizados, onde há controle de placebo. Segundo estudos, a profilaxia é eficaz, porém evita um número fechado de casos.
Algo que contradiz, é que a principal causa não é por procedimentos cirúrgicos. O que corrobora ainda mais para a prevenção primária, que deve visar o foco na população da construção de hábitos de higiene bucal, por exemplo.

Como a endocardite infecciosa é uma condição associada a alta mortalidade e morbidade, a profilaxia deve seguir procedimento padrão em pacientes de risco, quando forem submetidos a procedimentos médicos, cirúrgicos ou dentários de risco para a doença.

A profilaxia é indicada para pacientes em condições de próteses valvulares, com antecedente de endocardite infecciosa, com cardiopatia congênita, valvopatia reumática, valvopatias adquiridas (doenças degenerativas, p. ex.); a regurgitação mitral; com miocardiopatia hipertrófica.

Há procedimentos, nos quais a profilaxia também é recomendada, como em tratamento e procedimentos dentários nos quais se espera sangramento da mucosa ou gengiva, cirurgia que envolve mucosas respiratórias ou intestinal, tonsilectomia e/ou adenoidectomia, cirurgia de próstata, de vias biliares ou histerectomia vaginal, escleroterapia de varizes esofagianas, dilatação do esôfago, dilatação uretral; parto vaginal na presença de infecção, incisão e drenagem de tecido infectado.

Tratamento

Endocardite aguda
É uma emergência infecciosa, inicia-se rapidamente a terapêutica antibiótica empírica

Utiliza-se geralmente vancomicina e ceftriaxona IV via infusões até que a identificação microbiana e susceptibilidade apresentem concentração inibitória mínima, assim torna possível a modificação da condução do tratamento, a terapia antimicrobiana, pois permitir atingir o microrganismo alvo específico.

Contextualiza-se que a utilização da gentamicina para tratar endocardite não é tão favorável quanto se pensava, devido a ausência de provas para apoiar a sua utilização, com uma exceção, quando há infecções provocadas por Enterococcus e variante estreptococos), neste caso há elevada taxa de complicações.

Endocardite subaguda
Neste caso, o estado hemodinâmico do paciente apresenta-se na maioria dos casos como estável. Há a administração de antibióticos, com duração longa, sendo de duas a seis semanas conforme a características da infecção e do microrganismo causador do desenvolvimento da doença, neste período procura-se identificar este microrganismo.

O organismo mais comum responsável pela endocardite infecciosa é Staphylococcus aureus, que apresenta alta resistência à penicilina, em sua maioria, sem necessária à substituição pela cefalotina, a alta resistência também com o fármaco oxacilina o que exige tratamento com vancomicina, que é administrada em casos de origem hospitalar por S. epidermidis.
A terapia anticoagulante não é recomendada, pois os anticoagulantes podem aumentar a probabilidade de culminar em hemorragia intracerebral, além de não previnem embolização na endocardite infecciosa, não sendo, portanto, usados rotineiramente no tratamento de endocardite. Porém, há pacientes que podem fazer uso de anticoagulante, devido a prótese valvar. Neste caso, o anticoagulante pode ser mantido, sendo necessário acompanhamento cuidadoso. Caso haja sinais de comprometimento do sistema nervoso central, é de caráter urgencial a suspensão da terapia anticoagulante.

Fora à endocardite aguda e subaguda, há a endocardite causada por várias infecções, como pelo Viridans estreptococos do grupo Streptococcus bovis que tem característica sensível à penicilina, sendo utilizada terapia com penicilina ou ceftriaxona juntamente com um aminoglicósidio durante a fase inicial do tratamento, cerca de duas semanas.

Já as cepas resistentes à penicilina de estreptococos do grupo viridans, nutricionalmente variante estreptococos como Granulicatella sp., Gemella sp. e Abiotrophia defectiva e enterococos são normalmente tratados com uma terapia de combinação, sendo penicilina e um aminoglicósidio durante quatro a seis semanas.

Tratamento cirúrgico
Essa intervenção reduz a incidência de mortalidade de pacientes com endocardite infecciosa que evoluem com ICC refratária, acometimento perivalvar com abscessos ou mesmo devido à doença não controlada, apesar do tratamento farmacológico à base de antibióticos adequados e em doses elevadas. Assim, os indivíduos que se encaixam neste perfil devem ser encaminhados para uma avaliação visando à cirurgia cardiovascular. Ressalta-se que indivíduos com próteses não é descartada a intervenção cirúrgica, sendo também necessário a avaliação para este procedimento.

A cura
Para ter sob controle, após o término da terapia antibiótica e/ou intervenção cirúrgica, faz-se preciso o controle com coleta de hemocultura (exame que investiga bactérias no sangue), tendo assim, o quadro sob controle de cura e detecção de reincidência.

Endocardite Infecciosa em Idosos
Com o aumento da população idosa, há o surgimento da prevalência e a maior disposição de aparecimento de diversas doenças, entre elas, podemos destacar a endocardite infecciosa, que atualmente torna-se mais prevalente em idosos comparados a adultos jovens. Idosos que são acometidos com essa doença observa-se que a mortalidade chega até 50% dos casos.

O autor Carvalho Filho (2003), relata que os fatores que propiciam a manifestação dessa doença nos indivíduos idosos são: "valvopatias, próteses valvares, implante de marcapasso, diabetes mellitus, neoplasias, infecções crônicas e manipulações de focos infecciosos com finalidade diagnóstica e/ou terapêutica".

O autor ainda relata, que quando observado esse tipo de paciente vulnerável a esses fatores de riscos, é de extrema importância submete-los a profilaxia antibiótica. O autor cita American Heart Association, essa associação recomenda o uso de fármacos em algumas situações especificas quando idosos estão acometidos a focos infecciosos. Quando o idoso for submetido a alguma manipulação dentária e do trato respiratório alto, em que o germe Streptococcus vividans é mais frequente, recomenda-se a utilização de amoxacilina na dose de 2,0 g via oral uma hora antes da manipulação.  Na ocorrência de manipulações urinárias e intestinais, em que o germe frequente é o Enterococcus faecalis, utiliza-se, na profilaxia, a ampicilina na dose de 2,0g via IM ou IV associada à gentamicina na dose de 1,5 mg por kg de peso (até o máximo de 120 mg) via IM, 30 minutos antes do procedimento e ampicilina 1,0g via IM ou IV seis horas após.

A maior ocorrência desta doença cardíaca em pacientes idosos dá-se principalmente no tratamento odontológico, que pode promover um alto risco a vida desses indivíduos. Mediante a esse cenário e os fármacos mencionados anteriormente, é de extrema relevância a prescrição de antimicrobianos objetivando prevenir bacteremias antes de procedimentos odontológicos que podem desencadear sangramento da mucosa.

Epidemiologia
Antigamente os estudos epidemiológicos envolvendo a endocardite infecciosa encontravam barreiras para serem concretizados, como a raridade da doença, a ausência da definição do caso e por não serem oficialmente registradas, fazendo com que os pesquisadores baseassem seus estudos em autópsias. Porém, em uma documentação epidemiológica entre 1993 e 2003 foi encontrado a descrição de 3.784 casos da doença. Nesses casos a média de idade encontrada variava entre 36 anos e 69 anos. Sabe-se que antigamente a faixa etária média para a doença era entre 30 – 40 anos, mas tem aumentado para 47-69 anos, devido o aumenta da longevidade e o tratamento médico, o que representa uma mudança nos dados, devido o aumento de pacientes idosos e contribuindo para a diminuição de casos relacionados à endocardite infecciosa por streptococcus oral, o índice médio da doença para indivíduos com idade inferior a 50 anos foi de 3,6 de 100.000 e variava de 5 a 15 de 100.000 por ano em indivíduos com idade acima dos 65 anos. Além disso a epidemiologia da doença é complexa devido às diferentes características clínicas da população estudada.

A endocardite infecciosa é letal caso não seja tratada com antibióticos, e o índice de mortalidade da doença antes da terapia com antibióticos alcançava 100%, e, atualmente, mesmo com a terapia antibiótica, a taxa permanece elevada em torno dos 25%. A taxa de mortalidade intrahospitalar chega a ser de 16% dos casos atendidos.  Apesar das melhorias na saúde e as formas de tratamento terem melhorado o diagnóstico e o prognóstico, a incidência da doença não diminui ao longo dos anos, devido a uma evolução progressiva dos fatores de risco. Cerca de 70% a 75% dos indivíduos com endocardite infecciosa tem história de cardiopatia.

A incidência da doença se dá na faixa de 11 a 50 casos por 1 milhão de habitantes por ano, sendo nos EUA 1,7 a 4,9 casos por 100.000 habitantes. A incidência entre homem - mulher também aparece nos estudos com uma relação média de dois casos para um, respectivamente.

Bibliografia
 Andrade E.D., Passeri L.A., Mattos Filhos T.R. Prevenção da endocardite bacteriana - Novas recomendações da American Heart Association.
 Arq. Bras. Cardiol. vol.83 no.3 São Paulo Sept. 2004. Disponível em: http://dx.doi.org/10.1590/S0066-782X2004001500002
 Baddour et al. Diagnosis, Antimicrobial Therapy, and Management of Complications: A Statement for Healthcare Professionals From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association—Executive Summary: Endorsed by the Infectious Diseases Society of America. Circulation. 2005;111:3167-3184
 Barbosa M.M. Endocardite infecciosa: Perfil clínico em evolução. Arq Bras Cardiol, vol 83, nº3, setembro, 2004.
 Carvalho Filho, E.T. Medicina preventiva no idoso. Rev.bras.clín.ter: 29(1):8-18, jan. 2003
 Dajani AS, Tauber KA, Wilson W, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association JAMA. Circulation. 1997;96:358-66.
 Dajani, A.S.; Taubert, K.A.; Wilson, W.; et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA 1997; 277:1794-801.
 Grinberg M., Solimene M.C. Aspectos históricos da endocardit infecciosa. Rev Assoc Med Bras; 57(2):228-233, 2011.
 Gutierrez P., Calderaro D., Caramelli B. Endocardite Infecciosa. Rev Assoc Med Bras; 50(2): 109-26, 2004.
 Hoen B, Alla F, Selton-Suty C, et al. Changing profile of endocarditis, results of a 1 year survey in France. JAMA. 2002;288:75-82.
 Homma S, Grahame-Clarke C. Toward reducing embolic complications from endocarditis. Editorial comment. J Am Coll Cardiol. 2004;42:781-83.
 Lira, R. B.; Silva, S. C. Avaliação clínica da doença periodontal em pacientes com endocardite infecciosa. Rev Periodontia SOBRAPE, São Paulo, v. 11, n. 2, p. 31-35, mar. 2001.
 Moreillon P, Que Y. Infective endocarditis. 2004
 Remsey E S & Lytle B W – Repair of fungal aortic prosthetic valve endocarditis associated with periannular abscess. J Heart Valve Dis 1998; 7: 235-9
 Rocha C.A.S., Rocha M.S., Sprovieri S.R.S. O que há de novo na profilaxia da endocardite bacteriana. Deve-se mudar a conduta atual? Rev Bras Clin Med; 7:418-421, 2009.
 Rombaldi A.R. Endocardite Infecciosa na gravidez. Arq Bras Cardiol; 93 (6 supl. 1): e110-e178, 2009.
 Silva, V. M. F. Q. Endocardite infecciosa. Disponível em: http://www.fmt.am.gov.br/manual/endocardite.htm
 Silva, E.M.M; Gallo, A.K.G; Santos, D.M.; Barão, V.A.R.; Freitas Junior, A.C. Enfermidades do Paciente Idoso. Pesq Bras Odontoped Clin Integr, João Pessoa, v. 7, n. 1, p. 83-88, jan./abr. 2007
 Stamboulian, D. Carbone E. Recognition, management and prophylaxis of endocarditis. Drugs 1997; 54:730-44.

Patologia

redpajama_set_name: RedPajamaWikipedia


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text:
Spartanburg spotlights city supporters
The Spartanburg Area Chamber of Commerce used its annual meeting this week to shine a spotlight on the people and businesses working to move Spartanburg forward. The ceremony was presented by Spartanburg Regional Healthcare System.
"Spartanburg in 2018 is much different than it was five years ago, but the roots of today's successes were planted years ago," said Allen Smith, president and CEO of the Spartanburg Chamber, in a news release. "Spartanburg County is now home to more business and community growth than ever before, and record numbers of visitors come into the county for a host of reasons."
The following awards were presented during the chamber's annual meeting:
Ambassador of the Year: Maddi Currier, development associate at the Hope Center for Children
Young Professional of the Year: Landon Cohen, president of Light Transportation Co.
2017 Teachers of the Year: District 1, Joshua Fowler; District 2, Keri Belue; District 3, Kimberly Goode; District 4, Emily Montjoy; District 5, Laura Brockman; District 6, Janelle Courtney Dial; District 7, Vern Weygandt; Spartanburg Day School, Kim Ballenger; S.C. School for Deaf and Blind, John Preston Lewis
Duke Energy Citizenship and Service Award: Newt Hardie, founder of The Trees Coalition, was posthumously named the award winner for his work to fight kudzu across Spartanburg County.
Economic Futures Award: Auriga Polymers Inc. received the award for its 50 years of innovation in Spartanburg.
Elaine Harris Tourism Person of the Year: Patti Wetherford was posthumously named the award winner for her contributions to the tourism industry.
The James B. Thompson Small Business of the Year Award: Atlas Organics
Inclusion Advocate of the Year: Natasha Pitts, minority business development coordinator with the city of Spartanburg.
Minority Business Person of the Year: Charles Atchison, owner and founder of Atchison Transportation
The Chairman's Award: Spartanburg Mayor Junie White and Spartanburg County Council Chairman Jeff Horton
Neville Holcombe Distinguished Citizenship Award: U.S. Rep. Trey Gowdy

redpajama_set_name: RedPajamaCommonCrawl


text:
Cardiff Devils & EIHL chat
Those not coming back
Thread starter Devil_Abroad
Devil_Abroad
Thread starter #1
Pure speculation but I guess most believe that Reddick will be back. Indeed Todd stressed in public conversation to fans he will be a Devil for years to come
As for Crowder and Asselin it feels like they are retiring as if they're not coming back, no announcement elsewhere, and no announcement by the club then surely retirement it is for them both and this will be announced by the club once the new players are announced
This could also be the case for Strachan of course were it not for his age and his talent. If he is destined elsewhere then maybe both clubs have agreed not to disclose until Devils are ready to announce a replacement? Or maybe it's the same for Strachan as it was for Hotham every year? There is an agreement in place for him to return but he has until early August to seek other opportunities, maybe in Europe?
My hope is the latter and if so then we will have 2 returnees, 2 new forwards and 1 new D man
Again, I stress, pure speculation on my behalf
ASHIPP
The essential player of those names is Strachs. A player of such influence and experience - the real deal.Think everyone would love to see him return but we can live in hope.
Rumours suggest Reddick will return and Asselin/Crowder might retire. If that is the case, hope the Club uses the opportunity to bring in replacements who can demonstrate more consistency in games.
Ocko
The Hotham waiting until August agreement was never in place, he was always coming back every year. He didn't want to play anywhere else, he didn't want to play in the DEL despite offers. If he played in a better league he'd have to be in the gym every day, train harder etc. Plus we would never of waited until August to know if our number one D man was going elsewhere.
I'd be amazed if Strachan isn't coming back. He hasn't finished his MBA yet and won't until a few months into the season. He hasn't signed anywhere yet, so why not? Everyone is just assuming he isn't coming back and I haven't a clue why. He struggled to find a deal prior to coming to us, playing in the EIHL is hardly going to make the offers flood in either. He's either retiring or coming back for me.
I would be very suprised if Strachs hadn't received interest from other clubs before or after his season at the Devils - perhaps he simply hadn't received the right offer?
There are many examples of former NHL AND other players going to very good leagues after their time in the Elite League. Guy Lepine played for AHL Binghampton Senators. Craig Weller went on to play in the DEL and EBEL. Evan Mosey was selected by AHL Rockford IceHogs after one season over here to give examples of each.
Let's keep our fingers crossed Strachs will be returning.
Wannabe2
Ocko said:
That is so informative, and makes complete common sense, hopefully Strachan will return ( the real one that is ) as he is a huge asset to our team, and the Hotham explanation was one I never thought about, but was obviously the case. Cheers Ocko for that, so some great signings still to be released, how exciting is that, and it all kicks off shortly.
BostonBart22
Seems strange Hotham hasnt been picked up yet, he maybe taking time out after getting married maybe, or maybe waiting for a return to us around xmas.. just a thought..
Kevlar68
With Hotham Gone and Strach looking likely as not returning the recruitment for the replacements must be a nightmare. You wouldn't want to take a step back and finding 2 players of equal or better quality i would thought is going to be a true test.
Rich Best
I think Todd (or Lord?) has pretty admitted you can't replace hotham. You need all other D men to step up their points tally's to make up for the loss of assists and goals. Makes sense to me. I have been watching 25 years and hoth was the best.
Likes: Kevlar68
Nearest to the Hoth for me was Tyson Teplitsky.
Likes: Nathan George, DevilInside, ASHIPP and 3 others
Kevlar68 said:
Why is Strachan not looking likely?
SteveKing
I think it's really difficult (and probably not that smart) to compare individual players from one year to the next. The key is to build the best team. So for this year, Lordo is quite right that you can't replace Hotham straight up. That doesn't mean that our team will necessarily be worse. Hoth was one of our highest paid players so bringing in someone younger that has the potential to become the next Hoth but doesn't cost quite as much allows us to spend more money in other areas and hopefully the whole package ends up being better. From looking at our team for this year, I firmly believe that that will be the case.
Likes: Nathan George, jimmy snels, Bazza and 5 others
SteveKing said:
It must be the case, otherwise we are going backwards, and our club no longer goes backwards, those are past story's. We won't go backwards losing 1/2 players, they may be hard to replace, but they are all replaceable, all of them. History doesn't lie, they are all replaceable. Great feeling to know one goes out, and one comes in.
HAPPY HOCKEY DAYS
Likes: Chris and Kevlar68
TommyDevil13
I agree with Steve - it's important not to look at 'like for like' with Hotham's replacement. If he puts up 30 points (rather than 60 odd), but the extra salary can go towards more scoring depth in the forwards and/or a stronger D core generally, it will have been a shrewd move. After all, although we all know how magic Hoth is, if the ability to allocate salary to other positions results in 20 more goals scored, or 20 fewer goals conceded, over the course of the season, that might equate to 5-10 more wins overall. Ultimately, that is all that matters. The team doesn't need superstars if the collective unit keeps getting stronger as a whole.
Likes: Chris and ASHIPP
Wannabe2 said:
Alan Schuler...up with the both as well
Likes: SMJ
Very good player but never scored the goals.
jimmy snels
i thought tyson was actually the best D man id seen defensive wise. hotham was better going forward.
Kip Noble was pretty warm. Incredible skater.
Nott Simpson
Martin Lindman was an incredible D man who started his pro career with the Devils and then played in the DEL & SEL with distinction for many years
Likes: JD Bluebird&Devil and SMJ
Thread starter #19
Nott Simpson said:
Pretty good golfer too
I don't think he's coming back either ......just got a feeling he's not
The Inferno Dark
helensroose


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I am beyond excited to be creating these lovely hand-crafted flowers with an upcoming Private Class for Shelley! How fun it will be to see the combinations of designs the ladies will create. Like a snowflake, two will not be the same - with our Designer Series Paper - the double sided images will give freedom to our creativity!
WOW what lovely, big blossom! Here the petals of three sizes become one this flower (there are 10 different die-cuts to create amazing looking flowers in ONE die!). To create a lovely 6" full Spring paper-flower - I can take this one packet of FREE Sale~A~Bration Best Year Ever Designer Series Paper to make a full bouquet of Spring, trendy and cool flowers!
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Maria Butina, the accused Russian Spy who allegedly worked with a Russian oligarch to influence the 2016 election, may be close to negotiating a plea deal that could shed light on allegations the National Rifle Association (NRA) funneled Russian money to Republican candidates.
U.S. District Judge Tanya Chutkan, sitting in Washington, ruled today (Dec 6) that Butina is entiled to a public defender. The move is being interpreted as a prelude to a plea deal, according to Courthouse News Service.
Butina has been in solitary confinement at the Alexandria Detention Center in Virginia since July when she was indicted by a grand jury on charges of conspiracy and acting as a foreign agent.
The fetching Russian allegedly wooed top Republicans and NRA officials into a dalliance with Russian oligarchs and the Kremlin's intelligence apparatus. The relationship may have included a massive influx of cash. The NRA spent $30 million on Trump's election.
The Senate Intelligence Committee has asked the NRA to turn over records and other documents. The goal is to shed light on its relationship with Russian interests including the details behind a 2015 Kremlin trip by NRA officials, according to The Daily Beast. .
Maria Butina, 30, and her mentor, Russian oligarch Alexander Torshin is deputy governor of Russia's central bank and has close ties to Russian President Vladimir Putin.
Butina maintains that she was trying to build support for her gun advocacy group in Russia. She was also taking college courses toward a master's degree and was in the country on a student status.
Prosecutors fueled suggestions a plea deal is in the works by canceling a Dec. 18 status hearing and apparently withdraw subpoenas seeking Butina's records from American University, in Washington, D.C. where she attended classes.
Robert Driscoll, the private lawyer who has represented Butina and defense attorney Alfred Carry reportedly held a conference call with Chutkan and Asst. U.S. Attorneys Erik Kenreson and Thomas Saunders, according to CNS.
Chutkan sealed the conference transcript and gave Butina's attorneys until Dec. 10 to submit arguments why it should remain sealed.
McClatchy, a Midwestern news service, reported in January that special counsel Robert Mueller was investigating whether the NRA was a conduit for Russian money to support Trump's campaign.
Former NRA President David Keene, incoming president Peter Brownell, Milwaukee Sheriff David Clarke and NRA donors Jim Gregory, Arnold Goldschlager and Hilary Goldschlager made the trip, according to The Daily Beast.
The FBI, the CIA, the National Security Agency, Justice Department, the Treasury Department's Financial Crimes Enforcement Network and representatives of the director of national intelligence, are reportedly investigating if money may have moved from the Kremlin to covertly help Trump win, the two sources told McClatchy.
Specifically, Butina was indicted July 17 by a grand jury on charges of conspiracy to act and failing to register as an agent of a foreign government. She pleaded not guilty. Her attorney said Butina was merely networking to develop relationships with Americans, according to The Washington Post.
Among Butina's 4,588 Facebook connections are NRA officials, gun lobbyists, a Justice Department staffer, a congressional aide, the top organizer of the National Prayer Breakfast and an executive with the Outdoor Channel.
She peppered her page with glamour photos as well as poses with a variety of guns.
Check out her images below and follow IM on Twitter for the latest updates on this breaking story.


text:
What Else for January 22, 2020
Taylor Swift shares behind the scenes footage in Miss Americana trailer ahead of Sundance premiere
Show Your Work: On Brand With Brad – and with Beyoncé?
Daniel Craig and Rami Malek cover Entertainment Weekly to promote No Time To Die
Bella & Abel are still together
Posted by Lainey at December 29, 2015 19:07:18 December 29, 2015 19:07:18
On Sunday E! reported exclusively that Bella Hadid and The Weeknd were "taking a break". The two did not spend Christmas together. And he was apparently flirting with some girls at a show in Miami. The next day, however, the two were seen together, in Miami, hanging out on DJ Khaled's boat. So either the break is over or there was no break to begin with, although it's probably only a matter of time? For starters, Bella's only 19 years old. And while 2015 was all about the rise of Gigi, 2016 might be all about Bella's ascent alongside Gigi's continued domination.
As for Abel…
He released two new songs last week, Low Life and Pass Dat. Both, as usual, are about his well-documented lifestyle. All those lyrics about being kicked out of the Ritz because he trashed it too many times? Definitely not fiction if he's talking about how he is at home. And a lot of that happened before Beauty Behind The Madness became Spotify's most streamed album of the year. Fame doesn't usually miss an opportunity to turn bad into worse.
KDNPIX, FameFlynet
Tags: Bella Hadid , The Weeknd
The Weeknd and Greta Gerwig support Timothee Chalamet at New York premiere of The King
Timothee Chalamet returns to TIFF after making out with Lily-Rose Depp on a yacht in Capri
Gigi Hadid reportedly introduced Tyler Cameron to Taylor Swift after the VMAs
Bella Hadid and The Weeknd have reportedly broken up again
Top Reads on LaineyGossip


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text:
Q: How do I stop Windows 10 going to sleep after locking with Win+L key I've got a Dell XPS 13 (9360) with Windows 10 Home.
Steps to reproduce:

*

*Open power options (Win-X, O)

*Click change plan settings next to the current plan ("Dell" in my case)

*Set both "on battery" and "plugged in" change "Put the computer to sleep" to something high or "Never" (I have 15 mins for battery, 1 hour for plugged in, tried "Never" for both too)

*Click save changes

*Open screen saver settings (Win-S, Change screen saver)

*Ensure screen saver is off (None)

*Ensure "On resume, display logon screen" is off

*Click OK

*Lock computer with Win-L

*Wait...

Expected behaviour:

*

*Screen switches off after a short delay (~30 secs).

*Computer stays on, crunching whatever data you've left it to do.

Actual behaviour:

*

*Screen switches off after a short delay (~30 secs).

*Computer goes to sleep after a further ~15 seconds.

I would've thought this was a simple problem, but I've spent over two hours Googling etc for a solution. The closest I could find to my problem was this, which is similar but not the same, and the solution doesn't work for me:

*

*Windows 10 Sleeps Before Set Time

A: I also found this about letting Console Lock been seen - and changed. This allowed my power options to change it to 0 minutes, and then allowed screensaver to actually start.
HKEY_LOCAL_MACHINE\SYSTEM\CurrentControlSet\Control\Power\PowerSettings\7516b95f-f776-4464-8c53-06167f40cc99\8EC4B3A5-6868-48c2-BE75-4F3044BE88A7

Change Attributes DWORD to:

*

*1 = Hide "Console lock display off timeout"

*2 = Show "Console lock display off timeout"

Source: https://www.eightforums.com/tutorials/8267-power-options-add-console-lock-display-off-timeout.html

A: After running PowerCfg /q and reviewing this page, I believe I have determined the solution to this problem.
There appear to be many power settings that just don't show up in my advanced power options window.  One is Sleep → System unattended sleep timeout.
To make it visible, I opened regedit.exe and found this key:
HKEY_LOCAL_MACHINE\SYSTEM\CurrentControlSet\Control\Power\PowerSettings\238C9FA8-0AAD-41ED-83F4-97BE242C8F20\7bc4a2f9-d8fc-4469-b07b-33eb785aaca0

Set its Attributes DWORD value to 2.  This will make it show up in your advanced settings.  Go there and configure it to be zero minutes if you don't want it to sleep when you lock your screen.

A: Thanks, very helpful.
I found this official link about this on Microsoft Docs which I thought might be helpful:
Sleep unattended idle timeout, Windows Vista with Service Pack 1 (SP1), Windows Server 2008 R2, and later versions of Windows.
Specifies the duration of inactivity before the system automatically enters sleep after waking from sleep in an unattended state.
For example, if the system wakes from sleep because of a timed event or a wake on LAN (WoL) event, the sleep unattended idle timeout value will be used instead of the sleep idle timeout value.
Aliases and setting visibility
Windows Provisioning: UnattendTimeout
PowerCfg: UnattendTimeout
GUID: 7bc4a2f9-d8fc-4469-b07b-33eb785aaca0
Hidden setting: Yes <-- Unhidden with:
Computer\HKEY_LOCAL_MACHINE\SYSTEM\CurrentControlSet\Control\Power\PowerSettings\238C9FA8-0AAD-41ED-83F4-97BE242C8F20\7bc4a2f9-d8fc-4469-b07b-33eb785aaca0\Attributes = 2
Values
The value denotes the number of seconds.
Minimum value: 0 (Never idle to sleep)
Maximum value: Maximum integer

A: We had the same issue with a bunch of XPS 9370s, the laptop went into standby after the screen was locked. We have one laptop where the issue did not occure and exportet it's power scheme. By importing it to the other XPSes were able to make them have as expected - but by now we have no clue why.
You can findn the exported power scheme here: https://www.dropbox.com/s/mvajdkh14358471/dell.pwr?dl=0
Import it with an elevated prompt: powercfg /import 'fullpathtofile'

A: Control Panel => Hardware and Sound => Power Options has these settings:
HDD
    Turn off hard disk after:
Wireless Adapter Settings
    Power Saving Mode:
Sleep
    Sleep after:
    System unattended sleep timeout:
    Hibernate after:

It seems like "System unattended sleep timeout" can be changed from GUI too in Windows 10.

A: Make sure your mouse and keyboard are not connected to the USB ports of your monitor.  If your monitor goes to sleep, your mouse and keyboard will not function and make it seem like your computer went to sleep.

A: can also try powercfg /a in cmd, if it's in s0 profile, then the computer is 'connected standby' enabled, disable it to switch back to tranditional standby mode
i have a lot dell new laptops (7410) with hardware firmware enables 'connected standby', after i disabled it, they run as per the power option config

redpajama_set_name: RedPajamaStackExchange


Performance update we are pleased to announce that the Flying Irish Dance Troupe will be performing again this year.
All proceeds to benefit the Westford & District Pipes and Drums and the Lowell Mason's Association. Please come out and support these two fine groups.
Tickets on sale now see link on right of page.


text:
Doxa Increases Its Eagle Ford Shale Oil & Gas Interests In South Texas And Updates Operations
VANCOUVER, BRITISH COLUMBIA - Doxa Energy Ltd. - TSX Venture Exchange DXA. - ("Doxa" or the "Company"), announced today that it has more than doubled its net holdings within the oil & gas condensate windows of the Eagle Ford Shale trend of South Texas.
Eagle Ford Shale Additions and Update
The Company's recent Eagle Ford Shale interest acquisitions, when combined with the original Peeler Project acreage (see Doxa news, May 25, 2010), gives Doxa working interests ranging from 14% to 20% under 4,832 gross acres. The new properties are situated in Atascosa, McMullen and Zavala Counties. The Company also reports that it is in negotiations to acquire additional significant participation interests throughout the Eagle Ford Shale trend, and once finalized, it will outline details on the result of this effort. The Eagle Ford Shale is a prolific new oil & gas play that is transforming a wide swath of South Texas in to one of the most active resource plays in the US.
Doxa announced that the new acquisitions include a 15% working interest (11.25% net revenue interest) in the 640 acre Epley project in McMullen County, Texas, operated by San Isidro Development Company. Drilling operations on the initial horizontal well (the "Epley No. 1H") have been commenced and will be targeting the gas condensate window of the Eagle Ford Shale formation below 11,000'.
As previously reported in connection with the Peeler Project, Doxa expects drilling operations to commence on the initial horizontal well targeting the Eagle Ford Shale in third quarter, 2010. Based on projected well spacing as reported by EOG Resources on its contiguous Eagle Ford Shale project, Doxa is estimating that as many as 14 wells will be completed on the Peeler Project (based on 140 acre spacing). On this basis Doxa expects that over 35 gross wells could ultimately be drilled on acreage under which it now owns interests. The Company also believes that activity and reserve estimates recently disclosed by EOG and other operators on projects proximate to its acquired acreage continue to de-risk the play and support the prospective per well recovery estimates set out in the Graham Report for the Peeler Project.
Update on Other Projects
Additionally, Doxa is also pleased to report that it has agreed to sell a portion of a 1,032 acre lease block it previously acquired in the Edwards trend that it does not consider to be strategic. Profit from the sale net to the Company is expected to be approximately US$414,327 with closing scheduled to occur this month. The Company expects to drill an Edwards formation test on the retained portion of the acreage block later this year.
Finally, Doxa announced that it participated for a 6.25% working interest in the drilling of the Vitera No. 1 in Wharton County, Texas. The Vitera No. 1, which was drilled to total depth at 15,534', targeted various Wilcox formation objectives which did not develop as expected, and the well is scheduled to be plugged and abandoned as a dry hole. The Company does not expect to participate in additional drilling operations on this prospect at this time.
Option Grant
The Company advises that that it has granted incentive stock options to certain officers and consultants entitling them to purchase up to 269,000 common shares of the capital stock in the Company at a price of $0.38 per share until June 11, 2015. The above is subject to regulatory approval.
For further information contact: Scott Parsons Director or Paul McKenzie Director 604.642.2625 or visit www.doxaenergy.com
Neither TSX Venture Exchange nor its Regulation Services providers (as that term is defined in the policies of the TSX Venture Exchange) accepts responsibility for the adequacy or accuracy of this release.
Statements in this press release other than purely historical information, including statements relating to the Company's future plans, objectives or expected results, constitute forward-looking statements. Forward-looking statements are based on numerous assumptions and are subject to the risks and uncertainties inherent in the Company's business, including risks inherent in oil and gas exploration and development, and uncertainties in connection with anticipated commodity prices for oil and natural gas, growth of worldwide market demand, exploration capital requirements, length of asset life and availability of qualified personnel, among others As a result, actual results may vary materially from those described in the forward-looking statements.
You can view the Next News Releases item: Mon Jul 19, 2010, Doxa Announces Completion Of Horizontal Drilling Operations In The Eagle Ford Shale, South Texas
You can view the Previous News Releases item: Tue May 25, 2010, Doxa Closes Qualifying Transaction


Popularity - 183 views, 1.6 views per day, 118 days on eBay. Very high amount of views. 2 sold, 3 available.
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Seller - 4,273+ items sold. 0% negative feedback. Great seller with very good positive feedback and over 50 ratings.
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text:
How the Camelot myth was born: Reflections on JFK's public execution
No full investigation of JFK's murder ever happened. And whether Oswald acted alone isn't the big question
By Bob Hennelly
November 27, 2017 9:59AM (UTC)
John F. Kennedy rides in the motorcade in Dallas, Texas., Nov. 22, 1963. (AP)
This article originally appeared on Insider NJ. Published with permission.
This month it is 54 years since President John F. Kennedy's public execution. I was in the third grade at the Richard E. Byrd School in Glen Rock, New Jersey, when I found out he had been assassinated. As an Irish Catholic kid in a household obsessed with JFK, I had followed the ups and and downs of his 1960 primary campaign. I attribute my lifelong interest in politics and my career in journalism to that early engagement in our nation's narrative.
A case can be made that the first crack in the public's confidence in the news media, a crack candidate Donald Trump masterfully exploited, can be traced back to those bloody days in Dallas when Kennedy was killed and Lee Harvey Oswald's murder was also televised. Within days of the back-to-back murders, the black-and-white movie newsreels proclaimed for the nation, with Dragnet-type theme music underneath, that the assassin had been caught and killed by a man who "took the law into his own hands."
Even today, opinion polls show a majority of Americans still aren't buying it. For decades, the corporate news media has marched in lockstep endorsement of the government's official "lone gunman" theory of the case, even though we now have evidence the theory was conceived in the immediate aftermath of JFK's murder.
For me now, at age 62, this anniversary also marks just how our society has positively evolved with the diminishing ability of male power to preserve its privilege. Decades of coverups have been blown apart in just a few news cycles.
And there is a viral purge of powerful men, a forest of towering giants in the media, government, the arts and business, all clear-cut by allegations of sexual misconduct on the job. In case after case, men at the pinnacle of their personal power have used their position to try and get sexual gratification from women that the org chart said were subordinates.
Why, this tsunami of rightful female rage has enough velocity to resurface President Clinton's asymmetrical sexual predations. Yet you don't get a Bill Clinton without a Jack Kennedy.
In all the hagiography around our 35th president, we have yet to reconcile his sexual addiction, which has been documented even by National Geographic. Since forever there's been this notion that our "great men" are entitled to great appetites. How else would we know them? What's the point of being in charge if you can't dominate and exploit everything in your dominion?
In retrospect, it is easy to understand how the national security state, as presided over by FBI Director J. Edgar Hoover, who had his own closet issues, and the Kennedy brain trust, had a mutual interest in seeing to it that there was never a real homicide investigation into JFK's death. The Kennedy brand and the covert national security apparatus would not have survived it.
For me, this has always been the critical inflection point that is lost in all the cacophony over whether or not Oswald acted alone. To go down that rabbit hole is to miss the really big takeaway from JFK's murder and the creation of the official mythopoetic narrative of his life and death.
It served to burnish the JFK legacy and concealed the extent of the national security state's covert actions, right as things were starting to cook in Southeast Asia.
Think about it. By keeping the lid on the depth and breadth of our national security state it was possible for it to go on and stage COINTELPRO, the extra-legal targeting of Black Panthers, student radicals and other dissident Americans. Not long after JFK's murder, the FBI still had the cover it needed to anonymously write a letter to Martin Luther King Jr to try and convince the civil rights leader to kill himself.
Surely, a truly independent investigation into JFK's murder, without a predetermined outcome, would have revealed all the FBI knew about JFK's womanizing and about Oswald's movements before the assassination. No doubt that would have prompted the public to ask why, if they knew so much about Oswald before the JFK murder, they managed to lose track of him.
For the Kennedys, anything short of the Camelot epitaph would have been problematic for the family brand. For Hoover and the folks at the CIA, the intellectual exercise of asking who might have had a motive for killing JFK would also have meant exposing the numerous extralegal political assassinations the U.S. had supported all over the world.
In the latest reporting on the partial release of the long-awaited national security JFK files, the news media reported as "breaking news" that just 48 hours after the killing, FBI Director Edgar J. Hoover decreed there would be only one narrative advanced — that Lee Harvey Oswald was the lone gunmen.
But that data point hanging out there without context is just more faux news. Back in 1994, at the height of the dust-up over Oliver Stone's movie JFK, Jerry Polikoff and I wrote a cover story for the Village Voice entitled "How Time-Life, the New York Times, and CBS Killed the Conspiracy Theory."
Through the happy circumstance of my lawyer wife, Debbie, working for Riker Danzig — where former Attorney General Nicholas Katzenbach was working in the early 1990s — I was able to interview him about what went on in the immediate aftermath of JFK's murder. As No. 2 at the Department of Justice under Attorney General Robert F. Kennedy, it fell to Katzenbach to step up and run things because his boss was too distraught to lead the agency. According to Katzenbach, it was RFK who dismissed getting to the bottom of who killed his older brother.
As we wrote back in the Village Voice in 1994:
J. Edgar Hoover, supreme patriarch of the FBI and all-powerful with a distraught Robert Kennedy out of the way, knew just how to exploit the opportunity. Deputy Attorney General Nicholas Katzenbach recalls that Robert Kennedy, attorney general at the time, was so despondent he didn't even see the point of an investigation. "What the hell's the difference? He's gone," Katzenbach remembers RFK saying before handing over the reins.
Just three days after the assassination an internal Justice Department memo from Katzenbach to Bill Moyers, then a top aide to Lyndon Johnson, spelled out the Justice Department's strategy, a strategy that would prevail to a shocking degree right through the end of the decade:
"1. The public must be satisfied that Oswald was the assassin; that he did not have confederates who are still at large; and that the evidence was such that he would have been convicted at trial.
"2. Speculation about Oswald's motivation ought to be cut off, and we should have some basis for rebutting thought that this was a Communist conspiracy or (as the Iron Curtain press is saying) a right-wing conspiracy to blame it on the Communists. Unfortunately the facts on Oswald seem about too pat – too obvious (Marxist, Cuba, Russian wife, etc.). The Dallas police have put out statements on the Communist conspiracy theory, and it was they who were in charge when he was shot and thus silenced."
Katzenbach, whose memo sets out the Warren report results a year before the commission reached them, suggests that a "Presidential Commission of unimpeachable personnel" be appointed to examine evidence and reach conclusions. In closing he writes, "I think, however, that a statement that all the facts will be made public property in an orderly and responsible way should be made now. We need something to head off public speculation or Congressional hearings of the wrong sort."
Fifty-four years later, the national security state is still holding on to JFK material and redacted much of what they have released.
The Senate's Church committee report, issued in 1976, confirmed that while investigating the murder "top FBI officials were continually concerned with protecting the Bureau's reputation." Even Katzenbach in our interview conceded that Hoover would never "let the agency be embarrassed by any information on the bureau itself. He just would never show it. But how would you know it? What could you do?"
Back in 1994, we obtained an FBI memo that documented how easy it was for Hoover to get the the "free press" under control. On Nov. 25, 1963, the White House learned that The Washington Post planned an editorial calling for the convening of a presidential commission to investigate the assassination. Though Lyndon Johnson planned to do just that, the strategy was to get the FBI report out first. The memo states that Katzenbach called Washington Post editor Russell Wiggins and told him that "the Department of Justice seriously hoped that the Washington Post would not encourage any specific means" by which the facts should be made available to the public.
The memo also describes a conversation an FBI agent had with Al Friendly, the Post's managing editor, discouraging publication of the editorial and suggesting that it would "merely 'muddy the waters' and would create further confusion and hysteria." The editorial never appeared. Later that day, Hoover triumphantly boasted in another FBI memo that "I called Mr. Walter Jenkins at the White House and advised him that we had killed the editorial in the Post."
Back in 1994, we wrote in the Village Voice: "The FBI had the electronic media wired as well. A December 11, 1963, teletype from the FBI office in New York to J. Edgar Hoover indicates that NBC had given the bureau assurances that it would 'televise only those items which are in consonance with bureau report [on the assassination].'"
For the national security state, the priority had always been to control the narrative at any price. A truly open inquiry into the JFK murder was too fraught with potential unknowns and potential problematic disclosures. Give the people a hero and a bedtime story and let destiny sort out the rest. The corporate news media, back in 1963, were entirely agents of that national security state. Thus the Camelot myth was born.
Bob Hennelly
Bob Hennelly has written and reported for the Village Voice, Pacifica Radio, WNYC, CBS MoneyWatch and other outlets. He is now a reporter for the Chief-Leader, covering public unions and the civil service in New York City. Follow him on Twitter: @stucknation
MORE FROM Bob Hennelly
Bill Clinton Conspiracy Conspiracy Theory Donald Trump Fbi J. Edgar Hoover Jfk Assassination John F. Kennedy Lee Harvey Oswald Lyndon B. Johnson Robert F. Kennedy


A modern, two bedroom mid terrace home situated within the popular West End area of the Cathedral City of Lincoln. The property has recently been fully refurbished and briefly comprises of a Lounge, Kitchen, First Floor Landing, Two Bedrooms and a Bathroom. Externally, the property has allocated off road parking immediately to the front of the property. The property is well positioned for nearby amenities and a wider range of amenities and facilities in the City centre itself and would ideally suit a first time buyer or buy to let investor. NO CHAIN!


text:
Posted on July 14, 2020 November 10, 2020 by intricateminglings
Central London Footways: a transport network for London's Covid-19 recovery
By Emma Griffin and David Harrison
In 1854, nine years before the arrival of the Underground, 400,000 people walked into the City of London every day. These walks weren't the final leg of a journey from a mainline station, or within the centre: they were the entire commute.
Londoners still love to walk, of course (two thirds of all trips are walked in the Square mile). But we walk much shorter distances than our predecessors. Currently only 5% of commuter travel to the City is on foot. The average walk-all-the-way trip across London is less than 1km, according to TfL's Strategic Walking Analysis.
This has got to change and fast. Walking more and further is critical to tackle our health, pollution and climate crises. It is also critical to avoid contagion and relieve pressure on roads and public transport as we recover from the coronavirus pandemic.
In September, London Living Streets and Urban Good, with funding from Transport for London, will launch Central London Footways: a printed and online map and information resource that will prompt Londoners and visitors to walk longer distances on everyday journeys. Check out the routes below and at https://footways.london.
The map illustrates a network of routes, devised by London Living Streets, that connects London's mainline train stations, popular destinations and green spaces with the city's most welcoming, appealing and accessible streets. This is about getting people from A to B, but in the most enjoyable and healthy way possible.
For journeys under 30 minutes, the walking journey is just a few minutes longer, or about the same time, as a journey on a train or taxi. It takes just 20 minutes to walk from Euston to the British Museum, compared to 17 minutes via the tube and 18 minutes in a cab. A walk from Waterloo to British Museum is slightly longer at 28 minutes, but this is only 10 minutes slower than the Underground or eight minutes slower than a taxi.
And any minutes lost are easily made up for in terms of health and wellbeing. A 20-minute walk burns 80 calories, adds 2,400 steps to the pedometer, clears the mind, promotes creative thoughts, reduces depression, helps digestion, lowers blood pressure and generally makes us feel fantastic. Walking has been described as a superpower.
A walk from Waterloo to the British Museum also gives Londoners and visitors the best experience of the city, passing some pretty amazing places including Somerset House, Royal Opera House, Covent Garden and Camden's new transformation of the public space at Princes Circus.
Given all these perks, it is a pity that more than 3,000 people took the tube between Waterloo and Tottenham Court Road, near the British Museum, every day before the Covid-19 lockdown.
This is all about to change as a result of the changes TfL and boroughs are making in order to find more space for people walking and cycling as we emerge from the coronavirus lockdown. TfL, as part of its Streetspace for London plans, is widening pavements and councils including Camden, the City, Hackney, Islington, Lambeth, Southwark and Westminster are creating low-traffic corridors by closing residential streets to through-traffic. Footways will make sure Londoners make the most of these transformations.
Footways is the culmination of 18 months of work by London Living Streets who have walked the streets with residents, businesses, cultural organisations, councillors and officers to find the most efficient and attractive network. The work is supported by London's inner London boroughs and a number of other organisations listed here.
The Footways map and design concept is by Urban Good and will be distributed for free from September.
In the meantime, take a look at the routes on Google My Maps, share your thoughts, let us know if you'd like free printed copies and start using them on journeys within and to central London.
2 Replies to "Central London Footways: a transport network for London's Covid-19 recovery"
Why is so hard to find the actual map?
intricateminglings says:
Hi Philip, the map is being published on 16th September. Until then, it is available on Googlemaps. See bottom of the post. Sign up on footways.london to order a free copy. Thanks.
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text:
New Release Review - Difret
True story of an incident that led to the outlawing of child bride abductions in Ethiopia.
Review by Eric Hillis
Directed by: Zeresenay Mehari
Starring: Meron Getnet, Tizita Hagere, Rahel Teshome
Detailing a precedent setting case that led to the criminalising of the abduction of young girls for forced marriages in Ethiopia, Difret is a story worth telling in the current climate of religious fundamentalism and its negative impact on women. Despite its good intentions, Zeresenay Mehari's film is a misfire, thanks to a heavy handed, didactic screenplay and a lack of credible dialogue.
14-year-old Hirut (Hagere) is on her way home from school in rural Ethiopia when a group of armed men on horseback abduct her, taking her to another village where she is raped by an older man who intends to make her his bride. During an escape attempt, Hirut shoots her would be spouse dead and is arrested by the local police. An Ethiopian tradition, the abduction of young girls for marriage is perfectly legal (the film is set in the late '90s), and as a result of her self defence killing, Hirut faces execution for her crime.
Enter women's rights activist Meaza (the striking Getnet), who runs a non-profit organisation in the country's capital city Addis Ababa devoted to providing free aid to women who find themselves in need of such help. Facing hostility from the local authorities and the male populace of the rural village, Meaza takes Hirut into her care leading up to the trial. Witnesses willing to back up Hirut's claim of self defence are non-existent, and Meaza faces the greatest legal battle of her career.
Difret features a 'Presented by Angelina Jolie' credit, guaranteeing it a wider audience outside Ethiopia than that afforded to the rest of the African nation's cinematic output. Jolie came on board as executive producer following the film's completion, but it's all too clear that the film was always intended for international audiences. This is to the film's detriment, as presuming non-Ethiopians will have little familiarity with the country's more dubious traditions, every little detail is crudely spelled out through scene after scene of clunky dialogue. Only the conversations between Meaza and Hirut feel realistic; the rest of the movie plays like a series of lectures on Ethiopia's tribal customs and legal practices.
With an over-written script that rarely allows for nuance, ambiguity or visual storytelling, Difret is a plodding African cousin to Spielberg's Lincoln; a shame, as in Meron Getnet and Tizita Hagere it features two engaging stars who deserve a much better international platform for their talents.
Labels: By Eric Hillis, New Releases


You're an unprincipled man, Hud.
Hud is directed by Martin Ritt and adapted to screenplay by Irving Ravetch and Harriet Frank Jr., from the Larry McMurty novel Horsemen, Pass By. It stars Paul Newman, Melvyn Douglas, Patricia Neal and Brandon de Wilde. Music is by Elmer Bernstein and cinematography by James Wong Howe.
Hud Bannon (Newman) doesn't care for much outside of himself, life is to be enjoyed by drinking, fighting, bedding women and basically anything as long as he avoids responsibility for it. This greatly upsets his father, Homer (Douglas), a very principled man who is tormented... read the rest.


text:
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redpajama_set_name: RedPajamaGithub


text:
Sometimes I update with reasonable regularity, then I'll go months with no sign of life. Sorry about that.
There has been so much going on for the past year in my film world/life that it's often hard to keep up. Between the ever-increasing volume of preservation and restoration work (not to mention all the filmmaker and lab interactions, inspections, inventory, and collection management that goes with it, and even further not to mention the horrendous amount of email I feel like I'm always drowning in), plus the huge amount of stuff I have going on with Los Angeles Filmforum's very exciting Alternative Projections project, it's been hard for me to make time to post things here.
But I do definitely want to continue to be able to share the bizarre or interesting projects, findings, discoveries, etc. that I feel are a big part of my work, so I'll try update things a bit more regularly here. I just have to cultivate it as a habitual activity.
Above is a still from the incredible The Death of the Gorilla (1966), by the inimitable Peter Mays. This is what you might call a local classic, in that it's known to the L.A. avant-garde community, and is a crucial part of L.A. avant-garde history, but it's been shamefully left out of a lot of larger histories of experimental film. This film is a masterwork and should be a classic (whatever that means). It's also now newly restored, and is showing in the 2011 edition of Views From the Avant-Garde at New York Film Festival, as well as other locales, and I hope you get a chance to check it out.
Peter made this film by shooting 100ft. camera rolls of 16mm 7255 Ektachrome Commercial off of his television. He would run the film entirely through the camera with a certain color gel in front of the lens, and shoot fragmented bursts of primarily low-budget horror, sci-fi, and exotica stuff, with some King Kong and other recognizable features thrown into the mix. Upon reaching the end of the roll, he would rewind the entire roll, then do another full pass in-camera, shooting again off the television, this time with a different color gel. He sometimes did 6-8 full passes with 6-8 different colors in this manner. He got roll after roll of amazing, kaleidoscopic material this way. Immediately after getting his very best roll yet, he produced a total dud, which is how he knew the shooting was done. He then VERY extensively edited the material into a rough psychedelic narrative, and also created a similarly kaleidoscopic collage soundtrack to go with the image. The end result is 16 minutes of mind-blowing psychedelic genius, with all superimpositions produced in-camera, no exception.
Actually, you may have already seen some images from this film without realizing it. Strips from the film make up the entire cover of Taschen's Art Cinema coffee table book.
The preservation didn't actually take a ton of time. But it was an interesting experience, and unique in a couple of ways.
Peter had actually undertaken his own project to preserve and make available his work a few years prior, culminating in an incredibly elaborate and resourcefully executed DVD set of his work, from his earliest shorts to his most recent Flash animations. With a lot of films in his filmography, and some of them confusing due to variant versions, incompleteness, and other issues, he and I agreed that the best way to start working on anything of his was to go title-by-title, with The Death of the Gorilla seeming an obvious place to start, it being his most well-known film.
Peter had attempted to get the original 16mm mag track for the film transferred a few years back, to no success. The audio house had told him it couldn't be done effectively, and instead he made a new optical track positive from his track negative, and used that as the audio source for his digital transfer and DVD.
Acetate mag stock does have a tendency to deteriorate more readily and alarmingly than picture, something to do with the metal oxide "aggravating" the acetate base it's on. Most mag stocks switched to much more stable polyester in the 1970s/'80s.
When I got the mag track from Peter, it was pretty stinky with vinegar syndrome, and fairly warped and starting to curl. But it wasn't as bad as some really nasty mags I'd encountered, and I was pretty confident it could be transferred. Nick Bergh at Endpoint Audio really knows how to handle deteriorating mag well, and I gave it to him, which eventually yielded a very nice transfer. At Audio Mechanics, we checked the mag against an existing transfer of the optical track, and it was superior, though not by a huge margin, as the source for the track's audio was recorded ambiently off of television with a mic, and was pretty lo-fi to begin with. But the mag still sounded a bit better.
In the meantime, the original picture had its own issues. 7255 Ektachrome Commercial stock doesn't have nearly the color stability problems of its successor, the dreaded 7252 ECO (covered elsewhere in this blog), and Peter's original still has great looking color and contrast. It was also undamaged – no tears, perf damage, anything like that.
Normally, an element like this would be printed on a wetgate printer, the liquid in the gate helping to fill in scratches and blemishes on the source element, so the newly made element is as scratch-free and clean as possible. But we couldn't print Peter's original this way for two reasons. First, the head and tail titles were hand-painted (and beautifully, I might add – see end of this post). More problematic were the splices – Peter had originally edited the film with tape splices, which have held firm, but separated slightly over time, leaving a sliver of a gap in between pretty much all of them (and there are many many hundreds of splices in the original). If printed as-is, these slivers of splice gaps would be visible throughout the movie as punctuating white horizontal bars, occurring annoyingly and constantly throughout the film, especially since the framelines shift a bit over the course of the movie. To compensate for this, Peter, in his incredible focus and diligence, actually blackened out the splice gaps with a black marker, OVER the tape splices. So any attempt to clean or wet-print this original would wash away not only the hand-painted titles, but ALL of the "corrections" to the splice gaps. Yikes.
Also, because the adhesive from the tape splices had oozed somewhat over the years, every opposite lap of film from any given tape splice had dirt and adhesive residue stuck to it, on both sides of the film, constantly, throughout its entire length. Yikes again.
What to do? Well, the solution was painfully clear. I had to hand clean the entire thing, a foot at a time, all the way through, on both base and emulsion sides of the roll. Which I did. I hand-cleaned every single instance of that adhesive gunk and the dirt sticking to the adhesive gunk, through 600+ feet of the original for this film, on both sides. It took a while, but not as long as I thought it would.
In the meantime, another unique aspect of the project presented itself, which was very helpful. Extremely presciently, Peter had cut together a short, 50ft. roll of original outtakes from the film which represented a lot of the film's various looks. He did this specifically to be used as a test roll, so the lab could print the short test roll and experiment with exposures and timing, rather than print the full original a bunch of times. VERY helpful.
So while cleaning the original, I sent this test roll to the lab – Colorlab in this case. The wonderful and brilliant timer there, Chris Hughes, and the great Julia Nicoll got the test roll printed to internegative, then timed to print. Peter and I had decided pretty early on that the film should absolutely be printed as a "one light". In other words, there would be no timing light changes for the entirety of the film – one "best" light setting would be used for the whole thing. The reasoning for this was twofold – Peter had originally printed it this way in the 1960s, and the nature of the film's concept and making suggested this approach made the most sense. In other words, all of the superimpositions and color effects should be treated equally on a neutral grounding, not diversely modified from sequence to sequence or anything like that.
Additionally, Peter and I agreed the lab should try to make the new print look as much like the original as possible. Normally one might be matching a screening print of a film rather than the original, because perhaps there's a certain amount of color correction or other exposure modification that would have taken place in the film's printing. But in this case, we agreed that matching the original again fit the film's concept and execution, and also allowed for a very fine, subtle, high quality mirroring of the original as an object, rather than trying to artificially match a Kodachrome print, which would be a lot less subtle, a lot more contrasty, and miss the film's fine detail somewhat.
The test came back from Colorlab looking great, and needed only a tiny correction (1 point lighter, 1 point less blue). It looked beautiful. In the meantime, I had finished hand-cleaning the original, and shipped it to Colorlab for them to do another dry cleaning pass and then print it according to the results gotten from the test. Also in the meantime, the sound work had been finished and a new digital sound master, new mag track, and new optical track negative were created. Colorlab produced a new internegative and a first answer print with sound that hit the film exactly on the money. It looked fantastic. Peter saw it and was absolutely thrilled. I compared it to the 1960s Kodachrome print, which, though also beautiful, was not as good as the new one, which had a lot more range of color and subtlety of detail, closer to the original.
The new print premiered at Rotterdam 2011 in a pair of restored L.A. experimental film programs I put together, and I hope Rob Todd doesn't mind me quoting him as calling the film "a maximalist monsterpiece".
To conclude this really long post, I thought I'd share a few more stills from the film:
And here are some pictures showing the film's beautifully hand-painted main titles:
Author Mark TPosted on September 22, 2011 July 22, 2017 Categories film preservation
2 thoughts on "The Death of the Gorilla (1966) by Peter Mays"
filipa c says:
Dear Mark,
I am writing on behalf of Oporto, an independent screening space in Lisbon. We are really interested on the Mark Langdon films that you have worked with.
Could you please contact us at filipaevcordeiro@gmail.com
Here is our website link, for your reference http://oportolisboa.blogspot.com/
Filipa Cordeiro
(on behalf of Oporto)
I meant Chris Langdon, of course, that was a typing mistake 🙂
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