- Windsbraut von TC Boyle, Edition Büchergilde
- Gold auf Lapislazuli. Die schönsten Liebesgedichte des Orients von Claudia Ott, CH Beck
- Die Kultur der Freiheit von Udo Di Fabio, CH Beck
- Pulverfaß am Hindukusch von Rob Johnson, Konrad Theiss Verlag
- Die afghanische Misere von Can Merey, Wiley-VCH Verlag
- Deutschland, jüdisch Heimatland von Michael Wolffsohn/Thomas Brechenmacher, Piper
- Irdische Mächte, göttliches Heil von Michael Burleigh, Deutsche Verlagsanstalt
- Der Ursprung des Menschen, von Yves Coppens, Hanser Verlag
- Jesus im Talmud von Peter Schäfer, Mohr Siebeck
- Überflieger: Warum manche Menschen erfolgreich sind - und andere nicht von Malcolm Gladwell, Campus
- Kultur um der Freiheit willen. Griechische Anfänge - Anfang Europas? von Christian Meier, Siedler
Samstag, 28. Februar 2009
Büchertisch
Freitag, 27. Februar 2009
Mit der Sensibilität des Herzens...
Frau Gutmann, Psychoonkologin, im Gespräch mit der Offenbach-Post...
Donnerstag, 26. Februar 2009
Fotografisches Kriegstagebuch - Alberichs grause Arbeit...
Am 16. März des Jahres 1917 zog der deutsche Stabsoffizier Armin Stäbler mit seinen Kameraden durch das Dörfchen Croisilles an der Somme. Das Foto, das Stäbler damals machte, zeigt einen wohlgeordneten Trupp, der sich gemächlich über die Dorfstraße auf die Kirche in der Ortsmitte zubewegt. Weit und breit ist kein Feind in Sicht. Am folgenden Tag fotografierte Stäbler sein Regiment nach getaner Arbeit. Jetzt stehen die deutschen Soldaten inmitten einer Trümmerlandschaft: Die Kirche ist vom Erdboden getilgt, sämtliche Häuser sind nahezu vollständig zerstört, kein Stein steht mehr auf dem anderen.
Mehr...
Mehr...
Mittwoch, 25. Februar 2009
...Ungeheuerlichkeiten...
...
WELT ONLINE: Es sind aber nicht nur die von ihnen beschriebenen normalen Bürger, die mit Unverständnis reagieren, sondern auch hochrangige Fußballfunktionäre wie der Kölner Manager Michael Meier, der eine eventuelle Sperre als „Ungeheuerlichkeit“ brandmarkt.
Martens: Sie sollten besser informiert sein und des differenzierter sehen. Das Prinzip der Dopingkontrollen als solches kann man nicht infrage stellen. Das wäre ungeheuerlich.
WELT ONLINE: Die Fußballbranche beruft sich darauf, dass nachweislich nicht gedopt wurde.
Martens: Darum geht es aber nicht. Man unterstellt ihnen nicht, dass sie gedopt haben. Wer jedoch nicht pünktlich erscheint, begeht einen Dopingverstoß. Es geht nicht ums Doping, es geht einzig und allein um die mögliche Verschleierung des Dopings. Laut Statuten müssen sie umgehend zur Dopingkontrolle erscheinen.
...
WELT ONLINE: Es sind aber nicht nur die von ihnen beschriebenen normalen Bürger, die mit Unverständnis reagieren, sondern auch hochrangige Fußballfunktionäre wie der Kölner Manager Michael Meier, der eine eventuelle Sperre als „Ungeheuerlichkeit“ brandmarkt.
Martens: Sie sollten besser informiert sein und des differenzierter sehen. Das Prinzip der Dopingkontrollen als solches kann man nicht infrage stellen. Das wäre ungeheuerlich.
WELT ONLINE: Die Fußballbranche beruft sich darauf, dass nachweislich nicht gedopt wurde.
Martens: Darum geht es aber nicht. Man unterstellt ihnen nicht, dass sie gedopt haben. Wer jedoch nicht pünktlich erscheint, begeht einen Dopingverstoß. Es geht nicht ums Doping, es geht einzig und allein um die mögliche Verschleierung des Dopings. Laut Statuten müssen sie umgehend zur Dopingkontrolle erscheinen.
...
Aschermittwoch
"Bedenke Mensch, daß du Staub bist und wieder zum Staub zurückkehren wirst", lassen sich die Kirchgänger am Aschermittwoch sagen und dabei Staub über den Kopf streuen bzw. in Kreuzform auf die Stirn zeichnen. Dabei besiegelt der Aschermittwoch nur, was in der Karnevalszeit in der Figur des Narren dargestellt wurde - die Nichtigkeit der Welt. Die Büttenredner hatten nichts anderes versucht, als die Eitelkeit der Großen bloßzustellen. Die Masken stellten die Laster und damit den Menschen auf seinen Abwegen dar.
Der Aschermittwoch berechnet sich von Ostern her. Zählt man unter Auslassung der Sonntage 40 Tage zurück, kommt man auf diesen Tag, der dann wie Karneval mit dem jeweiligen Ostertermin wechselt.
Der Aschenritus ist sehr alt, denn in der frühen Kirche wurden diejenigen, die eine schwere Sünde begangen hatten, am Beginn der Fastenzeit mit Asche bestreut und so in den Büßerstand aufgenommen. Sie konnten nicht mehr am Gottesdienst teilnehmen, bis sie am Gründonnerstag wieder in die Gemeinschaft aufgenommen wurden. Sie bekannten sich damit öffentlich als Sünder. Diese alte Form der Buße kam um die Jahrtausendwende zum Erliegen und wurde durch die in Irland entstandene Ohrenbeichte ersetzt. Während man diese neue Form des Bußsakramentes öfters empfangen kann, wurde die altkirchliche Form nur einmal im Leben gespendet.
Da der Aschermittwoch Fast- und zugleich Abstinenztag ist, d.h. auch der Verzehr von Fleisch verboten ist, kam es zur Herausbildung des Fischessens, das aber als Gegenmittel gegen den Alkoholkonsum und weniger als Ausdruck der Buße gesehen wird.
www.kath.de
Der Aschermittwoch berechnet sich von Ostern her. Zählt man unter Auslassung der Sonntage 40 Tage zurück, kommt man auf diesen Tag, der dann wie Karneval mit dem jeweiligen Ostertermin wechselt.
Der Aschenritus ist sehr alt, denn in der frühen Kirche wurden diejenigen, die eine schwere Sünde begangen hatten, am Beginn der Fastenzeit mit Asche bestreut und so in den Büßerstand aufgenommen. Sie konnten nicht mehr am Gottesdienst teilnehmen, bis sie am Gründonnerstag wieder in die Gemeinschaft aufgenommen wurden. Sie bekannten sich damit öffentlich als Sünder. Diese alte Form der Buße kam um die Jahrtausendwende zum Erliegen und wurde durch die in Irland entstandene Ohrenbeichte ersetzt. Während man diese neue Form des Bußsakramentes öfters empfangen kann, wurde die altkirchliche Form nur einmal im Leben gespendet.
Da der Aschermittwoch Fast- und zugleich Abstinenztag ist, d.h. auch der Verzehr von Fleisch verboten ist, kam es zur Herausbildung des Fischessens, das aber als Gegenmittel gegen den Alkoholkonsum und weniger als Ausdruck der Buße gesehen wird.
www.kath.de
Wie wird Bauchspeicheldrüsen-Krebs (das Pankreaskarzinom) diagnostiziert und behandelt?
Dienstag, 24. Februar 2009
Karneval und Fastnacht
Karneval heißt, dem Fleisch, lateinisch Carnis, Lebewohl sagen. Fastnacht ist im engeren Sinn der Karnevalsdienstag. Weil während der mit dem Aschermittwoch beginnenden vierzigtägigen Fastenzeit kein Fleisch gegessen werden durfte, begannen zuerst die Klöster, das Fleisch aufzuessen. Die Städte und Dörfer schlossen sich dem an. Die These, in der Fastnacht tauche altes germanisches Brauchtum wieder auf, erkennt die religiöse Bedeutung der Masken und des Narren nicht. Pfau, Fuchs, Bär und andere Tiere stehen für die sieben Laster. Der Narr ist der Dummkopf, der die Existenz Gottes leugnet. Das Narrenschiff, ohne Segel und Steuer, fährt die Insassen ins Verderben. Im Büttenredner hat sich die Funktion des Hofnarren erhalten, der den Politikern heute ihre Schwächen und Fehler vorhält.
Der rheinische Karneval ist in Gegnerschaft zur napoleonischen und preußischen Besatzung entstanden. Der Elferrat weist auf den elfköpfigen Jakobinerrat der französischen Revolution hin, der sich durch die Zahl von den 12 Aposteln unterscheiden wollte. Nachdem die Aufklärung dem Karneval sehr kritisch gegenüber gestanden hatte, lebte er 1823 mit der Romantik im Rheinland wieder auf. München übernahm die italienische Tradition der großen Bälle. Daß der Karneval in protestantischen Gebieten viel weniger bestimmend ist, hängt mit den Entwicklungen im Späten Mittelalter und in der Reformation zusammen. Es wurde nicht mehr die Grenze des Aschermittwoch eingehalten, eine Spaßgesellschaft feierte einfach bis weit in die Fastenzeit weiter. Eine religiöse Reformbewegung mußte diese Form des Karnevals ablehnen.
www.kath.de
Der rheinische Karneval ist in Gegnerschaft zur napoleonischen und preußischen Besatzung entstanden. Der Elferrat weist auf den elfköpfigen Jakobinerrat der französischen Revolution hin, der sich durch die Zahl von den 12 Aposteln unterscheiden wollte. Nachdem die Aufklärung dem Karneval sehr kritisch gegenüber gestanden hatte, lebte er 1823 mit der Romantik im Rheinland wieder auf. München übernahm die italienische Tradition der großen Bälle. Daß der Karneval in protestantischen Gebieten viel weniger bestimmend ist, hängt mit den Entwicklungen im Späten Mittelalter und in der Reformation zusammen. Es wurde nicht mehr die Grenze des Aschermittwoch eingehalten, eine Spaßgesellschaft feierte einfach bis weit in die Fastenzeit weiter. Eine religiöse Reformbewegung mußte diese Form des Karnevals ablehnen.
www.kath.de
Montag, 23. Februar 2009
„Blootwoosch, Kölsch un e lekker Mädche“
Rosenmontag
Der Rosenmontag ist eine verhältnismäßig junge Erfindung, 1823 wurde in Köln der erste Rosenmontagszug veranstaltet. Vorher waren der Dienstag als die "Nacht vor dem Beginn des Fastens" und der Sonntag mehr vom Straßenkarneval geprägt. Die Wagen, die bis heute häufig in Schiffsform gestaltet sind, gehen auf mittelalterliche Vorstellungen des Narrenschiffs zurück, das ohne Mast, Segel und Kompaß seine Insassen ins Verderben fährt. Deshalb wurde das Narrenschiff am Ende der Fastnacht an manchen Orten verbrannt.
www.kath.de
www.kath.de
Sonntag, 22. Februar 2009
Christ, we have lost a wing...
Fehlerprävention in der Chirurgie lautete der Titel der Fortbildung in Berlin...
Daniel Scheidegger, Universitätsspital Basel, hielt einen beeindruckenden Vortrag - er begann mit dem Original-Dialog zweier Piloten vor dem Absturz - nichts deutet auf eine Katastrophe hin, und dann summieren sich kleine Fehler bis man nur noch hört "Christ, we have lost a wing..."
Markus Büchler, Chirurgische Universitätsklinik Heidelberg, hielt einen überzeugenden und authentischen Vortrag zum Thema "Mortalitäts- und Morbitätskonferenz"...Vorbilder gesucht? Er ist ein Vorbild!
Mehr...
Daniel Scheidegger, Universitätsspital Basel, hielt einen beeindruckenden Vortrag - er begann mit dem Original-Dialog zweier Piloten vor dem Absturz - nichts deutet auf eine Katastrophe hin, und dann summieren sich kleine Fehler bis man nur noch hört "Christ, we have lost a wing..."
Markus Büchler, Chirurgische Universitätsklinik Heidelberg, hielt einen überzeugenden und authentischen Vortrag zum Thema "Mortalitäts- und Morbitätskonferenz"...Vorbilder gesucht? Er ist ein Vorbild!
Mehr...
Revierderby
Schalke - BVB 1 : 1
Versunken im Mittelmaß - und Fans randalieren...in den 50iger Jahren wurden die Fans vom Bahnhof zum Stadion von berittener Polizei begleitet...gestern erzählte mir Thomas, daß beim Pokalspiel Kickers-Eintracht "jeder" einen "eigenen" Polizisten als Begleitung hatte...
Versunken im Mittelmaß - und Fans randalieren...in den 50iger Jahren wurden die Fans vom Bahnhof zum Stadion von berittener Polizei begleitet...gestern erzählte mir Thomas, daß beim Pokalspiel Kickers-Eintracht "jeder" einen "eigenen" Polizisten als Begleitung hatte...
Samstag, 21. Februar 2009
Freitag, 20. Februar 2009
Von den Folgen der Wirtschaftskrise für unsere Gesundheit...
Health, Medical Care, and Economic Crisis
Ralph Catalano, Ph.D.
NEJM Volume 360:749-751 February 19, 2009 Number 8
On December 1, 2008, the National Bureau of Economic Research declared that the U.S. economy had been in recession since December 2007. The number of Americans seeking unemployment compensation has reached levels unmatched since 1983, when we were suffering the worst recession since the Great Depression. Intuition suggests that the fear or experience of job loss, coupled with the declining value of homes and investments, makes many of us anxious, causes us to reduce discretionary spending (including that on medical care), and distracts us from taking preventive measures. Many physicians may therefore assume that our economic crisis will increase the burden of illness on our society. But does a contracting economy actually affect the health of a population? And if so, how?
A few months ago, when the current recession was still called an economic downturn, reports in the lay press highlighted research suggesting that a troubled economy often results in improved health in the population. In reality, researchers' findings on this score have been decidedly mixed — and have left much room for speculation about cause and effect, action and reaction, and the complex factors at play.
Most researchers agree that involuntary job loss increases the risk of psychiatric disorder and its somatic sequelae. Much research has found a strong correlation between job loss and clinical and subclinical depression, anxiety, substance abuse, and antisocial behavior. Longitudinal panel studies have suggested that job loss tends to precede the onset of psychiatric disorders, although selection bias clearly contributes to the correlation.1
Research has also shown that there are strong associations between involuntary job loss and somatic illness.2 Although prospective research has suggested that when the two are associated, the job loss typically precedes the illness, such research remains sparser than that focused on psychiatric outcomes. Critics argue that selection bias confounds the findings, because severe illness in persons of working age typically has precursors, including absenteeism and health insurance claims, that employers notice. Workers who take multiple sick days or begin to file more insurance claims than usual become targets for layoff when the demand for labor wanes. Nevertheless, job loss might be considered the proximal cause of illness in such cases, because persons with similar distal risks who remain employed are less likely to become seriously ill.
Research on the effect of a contracting economy on persons other than those who lose their jobs remains more controversial. Much of this work mimics research on environmental exposure to an ambient pathogen, in that researchers estimate a measurable response to some economic indicator. This "ecologic" work has not demonstrated a clear association between a failing economy and nearly any outcome except psychiatric disorders and accidental injuries: the rates of the former increase during bad economic times, whereas the rates of the latter decrease.
Some research has addressed the question of whether merely residing in an area with a contracting labor market contributes to the likelihood of illness. This work has often yielded results consistent with research on consumer behavior, but it has ambiguous implications for population health. Actual or feared loss of income, for example, may cause households to reduce consumption and substitute cheaper goods for costlier ones. The effects may include a reduction in risky behavior, such as driving or alcohol use, and therefore a reduction in accidental injuries. Income loss may also lead some people to consume fewer calories and thereby to avoid obesity. Others, however, may substitute inexpensive, less nutritious food for more healthful alternatives.
As this summary implies, countervailing mechanisms make the net effect of economic contraction on a population's health difficult to estimate. The results of research into less-studied mechanisms reinforce this ambiguity; it is not always easy to discern the causes underlying observed associations, and some associations seem to contradict others. For example, workers with a history of absenteeism due to health problems must compete with people without such a history when the demand for labor declines, and they reportedly respond to this competition in two ways that affect health. Those whose absenteeism stems from risk-taking behavior — alcohol abuse, for example — may try harder to control their problem behavior and thereby achieve better health. Workers with a chronic disease, for their part, may try to work when ill, and their health may suffer for it.
A contracting economy can drive wages down to levels at which people with compensable disabilities stop competing for jobs and accept disability insurance payments. The incidence of disabling illness therefore appears to increase with economic contraction, when it may merely be that people with marginal disabilities have decided to seek diagnosis and assistance.
People who believe they have lost jobs or income for reasons unrelated to their performance understandably feel frustrated. Some "treat" this frustration with alcohol, and others may take it out through aggression against people who cause them anxiety. Researchers often invoke this frustration–aggression mechanism to explain, for example, the relatively high levels of violence among job-losers. Some people may act out their aggression by calling attention to the behavioral or physical deficits of others, which might explain why the use of police power to coerce people perceived as dangerous or disabled into psychiatric treatment reportedly increases when the economy contracts.3
The literature also includes studies, not yet replicated, showing that a contracting economy affects health by distracting or impeding us from adherence to preventive measures. Researchers report, for example, that the incidence of sudden infant death syndrome increases among black families during times of economic contraction.4 Among women with newly detected breast tumors, the ratio of local tumors to those that are more advanced reportedly decreases during bad economic times, suggesting that women may be impeded from undergoing screening.5 Other research suggests that economic decline induces autonomic adaptations with implications for health, though it is not always clear what the mechanisms might be. For example, the male-to-female ratio of fetal deaths reportedly rises, whereas that of live births reportedly falls, during economic crises.
Despite the complexities involved in estimating the sum of illness induced and averted by a contracting economy, some researchers claim that historical data suggest we can typically expect a net reduction in illness during bad economic times. Others look at the same history and find no pattern justifying strong expectations.
The implications of our current recession for medical care providers may be less ambiguous, however. Since we appear to be at the outset of a contraction matched only by the Great Depression and the recession of 1982–1983, the historical data provide little statistical purchase for forecasting our lot. But we can look to the relatively well understood effect of economic contraction on psychological services for an indication of what might happen to the use of medical care during the recession. At the onset of bad economic times, the demand for psychiatric services declines, with fewer visits for "maintenance" but eventually more for acute episodes. "Coerced" treatment increases as society's tolerance for people with behavioral problems drops. Generalizing from psychiatry, I expect that medical care providers will first see a small decrease in demand as copayments become more onerous, more patients lose their insurance, and some people take fewer risks and perhaps become healthier. People who seek care will be more likely to have insurance and may feel that their employment status and social standing are threatened by society's lower tolerance for their physical or behavioral deviance. As time passes, however, I would expect to see increased demand for services from people who "deferred maintenance" because of costs and therefore become ill.
These predictions raise questions that are worth considering. How can we reduce the suffering of job-losers and their family members who will become ill but not seek help at the onset of illness? How can we encourage them to seek care? How can we finance their care if they seek it? Surely, we can devise a plan for those made sick, directly or indirectly, by the failure to regulate our economy. After all, we seem to be at no loss for the cleverness and resources to rescue those who capitalized on that negligence.
References
Murphy GC, Athanasou JA. The effect of unemployment on mental health. J Occup Organ Psychol 1999;72:83-99.
Dooley D, Fielding J, Levi L. Health and unemployment. Annu Rev Public Health 1996;17:449-465. [CrossRef][ISI][Medline]
Catalano R, Snowden L, Shumway M, Kessell E. Unemployment and civil commitment: a test of the intolerance hypothesis. Aggress Behav 2007;33:272-280. [CrossRef][ISI][Medline]
Bruckner TA. Economic antecedents of prone infant sleep placement among black mothers. Ann Epidemiol 2008;18:678-681. [CrossRef][ISI][Medline]
Catalano RA, Satariano WA, Ciemins EL. Unemployment and the detection of early stage breast tumors among African Americans and non-Hispanic whites. Ann Epidemiol 2003;13:8-15. [CrossRef][ISI][Medline]
Ralph Catalano, Ph.D.
NEJM Volume 360:749-751 February 19, 2009 Number 8
On December 1, 2008, the National Bureau of Economic Research declared that the U.S. economy had been in recession since December 2007. The number of Americans seeking unemployment compensation has reached levels unmatched since 1983, when we were suffering the worst recession since the Great Depression. Intuition suggests that the fear or experience of job loss, coupled with the declining value of homes and investments, makes many of us anxious, causes us to reduce discretionary spending (including that on medical care), and distracts us from taking preventive measures. Many physicians may therefore assume that our economic crisis will increase the burden of illness on our society. But does a contracting economy actually affect the health of a population? And if so, how?
A few months ago, when the current recession was still called an economic downturn, reports in the lay press highlighted research suggesting that a troubled economy often results in improved health in the population. In reality, researchers' findings on this score have been decidedly mixed — and have left much room for speculation about cause and effect, action and reaction, and the complex factors at play.
Most researchers agree that involuntary job loss increases the risk of psychiatric disorder and its somatic sequelae. Much research has found a strong correlation between job loss and clinical and subclinical depression, anxiety, substance abuse, and antisocial behavior. Longitudinal panel studies have suggested that job loss tends to precede the onset of psychiatric disorders, although selection bias clearly contributes to the correlation.1
Research has also shown that there are strong associations between involuntary job loss and somatic illness.2 Although prospective research has suggested that when the two are associated, the job loss typically precedes the illness, such research remains sparser than that focused on psychiatric outcomes. Critics argue that selection bias confounds the findings, because severe illness in persons of working age typically has precursors, including absenteeism and health insurance claims, that employers notice. Workers who take multiple sick days or begin to file more insurance claims than usual become targets for layoff when the demand for labor wanes. Nevertheless, job loss might be considered the proximal cause of illness in such cases, because persons with similar distal risks who remain employed are less likely to become seriously ill.
Research on the effect of a contracting economy on persons other than those who lose their jobs remains more controversial. Much of this work mimics research on environmental exposure to an ambient pathogen, in that researchers estimate a measurable response to some economic indicator. This "ecologic" work has not demonstrated a clear association between a failing economy and nearly any outcome except psychiatric disorders and accidental injuries: the rates of the former increase during bad economic times, whereas the rates of the latter decrease.
Some research has addressed the question of whether merely residing in an area with a contracting labor market contributes to the likelihood of illness. This work has often yielded results consistent with research on consumer behavior, but it has ambiguous implications for population health. Actual or feared loss of income, for example, may cause households to reduce consumption and substitute cheaper goods for costlier ones. The effects may include a reduction in risky behavior, such as driving or alcohol use, and therefore a reduction in accidental injuries. Income loss may also lead some people to consume fewer calories and thereby to avoid obesity. Others, however, may substitute inexpensive, less nutritious food for more healthful alternatives.
As this summary implies, countervailing mechanisms make the net effect of economic contraction on a population's health difficult to estimate. The results of research into less-studied mechanisms reinforce this ambiguity; it is not always easy to discern the causes underlying observed associations, and some associations seem to contradict others. For example, workers with a history of absenteeism due to health problems must compete with people without such a history when the demand for labor declines, and they reportedly respond to this competition in two ways that affect health. Those whose absenteeism stems from risk-taking behavior — alcohol abuse, for example — may try harder to control their problem behavior and thereby achieve better health. Workers with a chronic disease, for their part, may try to work when ill, and their health may suffer for it.
A contracting economy can drive wages down to levels at which people with compensable disabilities stop competing for jobs and accept disability insurance payments. The incidence of disabling illness therefore appears to increase with economic contraction, when it may merely be that people with marginal disabilities have decided to seek diagnosis and assistance.
People who believe they have lost jobs or income for reasons unrelated to their performance understandably feel frustrated. Some "treat" this frustration with alcohol, and others may take it out through aggression against people who cause them anxiety. Researchers often invoke this frustration–aggression mechanism to explain, for example, the relatively high levels of violence among job-losers. Some people may act out their aggression by calling attention to the behavioral or physical deficits of others, which might explain why the use of police power to coerce people perceived as dangerous or disabled into psychiatric treatment reportedly increases when the economy contracts.3
The literature also includes studies, not yet replicated, showing that a contracting economy affects health by distracting or impeding us from adherence to preventive measures. Researchers report, for example, that the incidence of sudden infant death syndrome increases among black families during times of economic contraction.4 Among women with newly detected breast tumors, the ratio of local tumors to those that are more advanced reportedly decreases during bad economic times, suggesting that women may be impeded from undergoing screening.5 Other research suggests that economic decline induces autonomic adaptations with implications for health, though it is not always clear what the mechanisms might be. For example, the male-to-female ratio of fetal deaths reportedly rises, whereas that of live births reportedly falls, during economic crises.
Despite the complexities involved in estimating the sum of illness induced and averted by a contracting economy, some researchers claim that historical data suggest we can typically expect a net reduction in illness during bad economic times. Others look at the same history and find no pattern justifying strong expectations.
The implications of our current recession for medical care providers may be less ambiguous, however. Since we appear to be at the outset of a contraction matched only by the Great Depression and the recession of 1982–1983, the historical data provide little statistical purchase for forecasting our lot. But we can look to the relatively well understood effect of economic contraction on psychological services for an indication of what might happen to the use of medical care during the recession. At the onset of bad economic times, the demand for psychiatric services declines, with fewer visits for "maintenance" but eventually more for acute episodes. "Coerced" treatment increases as society's tolerance for people with behavioral problems drops. Generalizing from psychiatry, I expect that medical care providers will first see a small decrease in demand as copayments become more onerous, more patients lose their insurance, and some people take fewer risks and perhaps become healthier. People who seek care will be more likely to have insurance and may feel that their employment status and social standing are threatened by society's lower tolerance for their physical or behavioral deviance. As time passes, however, I would expect to see increased demand for services from people who "deferred maintenance" because of costs and therefore become ill.
These predictions raise questions that are worth considering. How can we reduce the suffering of job-losers and their family members who will become ill but not seek help at the onset of illness? How can we encourage them to seek care? How can we finance their care if they seek it? Surely, we can devise a plan for those made sick, directly or indirectly, by the failure to regulate our economy. After all, we seem to be at no loss for the cleverness and resources to rescue those who capitalized on that negligence.
References
Murphy GC, Athanasou JA. The effect of unemployment on mental health. J Occup Organ Psychol 1999;72:83-99.
Dooley D, Fielding J, Levi L. Health and unemployment. Annu Rev Public Health 1996;17:449-465. [CrossRef][ISI][Medline]
Catalano R, Snowden L, Shumway M, Kessell E. Unemployment and civil commitment: a test of the intolerance hypothesis. Aggress Behav 2007;33:272-280. [CrossRef][ISI][Medline]
Bruckner TA. Economic antecedents of prone infant sleep placement among black mothers. Ann Epidemiol 2008;18:678-681. [CrossRef][ISI][Medline]
Catalano RA, Satariano WA, Ciemins EL. Unemployment and the detection of early stage breast tumors among African Americans and non-Hispanic whites. Ann Epidemiol 2003;13:8-15. [CrossRef][ISI][Medline]
Donnerstag, 19. Februar 2009
A chicken sandwich leading to intensive care
Cite this as: BMJ 2009;338:b200
Case report
R Som, foundation year 2 doctor, R Wynne-Simmons, foundation year 2 doctor, J Islam, specialty trainee in medicine, S Lawman, consultant nephrologist
1 Sussex Kidney Unit, Royal Sussex County Hospital, Brighton BN2 5BE
Correspondence to: R Som rsom@doctors.org.uk
Case study
A 28 year old man presented to the accident and emergency department with central abdominal pain that had lasted just over a day and was "cramping" in nature. He had had bloody diarrhoea for three days, with increasing frequency and amount of blood. He had eaten a chicken sandwich purchased from a canteen the day before the onset of symptoms. There was no history of recent foreign travel or any important medical history.
On examination he was found to be warm and well perfused, and his abdomen was soft, with mild generalised tenderness. On admission his full blood count, renal function and liver function tests were all within normal range.
Three days after admission he had persistent bloody diarrhoea; his haemoglobin concentration had dropped by 40 g/l to 126 g/l. Colonoscopy and biopsies showed acute indeterminate colitis. His white cell count was 23.3x109/l, neutrophils 19.1x106/l, platelets 49x109/l, international normalised ratio 1.0, APTT (activated partial thromboplastin time)1.0, C reactive protein 256 mg/l, urea 19.7 mmol/l, creatinine 530 µmol/l, potassium 4.8 mmol/l, serum lactate dehydrogenase 3452 U/l. He quickly became anuric.
Questions
1 What is the diagnosis?
2 What would you expect to find on culture of stool?
3 What would you expect to see on a blood film?
4 What is the differential diagnosis?
5 What two therapeutic procedures might this patient have?
Answers
Short answers
1 Haemolytic uraemic syndrome—diarrhoea positive.
2 Escherichia coli O157:H7.
3 Blood film would show signs of haemolysis—schistocytes, spherocytes, and reticulocytosis.
4 Thrombotic thrombocytopenic purpura.
5 Plasma exchange and dialysis.
Outcome
The diagnosis of haemolytic uraemic syndrome was supported by a stool culture positive for Escherichia coli O157:H7, a blood film showing fragmented blood cells, a full blood count showing low platelets, and raised lactate dehydrogenase. He may have contracted E coli O157:H7 from the sandwich (though this is impossible to confirm). He needed haemodialysis and a total of 11 plasma exchanges. Renal biopsy showed glomerular intravascular thrombosis in keeping with haemolytic uraemic syndrome and acute tubular necrosis. One week after the diagnosis was made his condition deteriorated; he had several tonic-clonic seizures needing admission to the intensive care unit. After three weeks his clinical condition improved, and he was finally discharged home after a month with normal renal function.
Long answers
1 Diagnosis
Haemolytic uraemic syndrome is a form of thrombotic microangiopathy first described by Gasser et al,1 characterised by the triad of acute renal failure, haemolytic anaemia, and thrombocytopenia.2 It primarily affects children3 but can occur in adults.4 5
Haemolytic uraemic syndrome is classified as either diarrhoea positive or diarrhoea negative, depending on whether the patient has a diarrhoeal prodrome. The history taking should aim to establish whether the diarrhoea is infective or secondary to inflammatory bowel disease or other forms of colitis, which are important differentials as the diarrhoea may be bloody. In diarrhoea positive haemolytic uraemic syndrome, the diarrhoea is nearly always secondary to infection; therefore a careful travel and diet history is necessary. Abdominal pain should also cause the clinician to consider causes of acute abdomen as differentials.6
The pathophysiology of haemolytic uraemic syndrome is poorly understood. Damage to endothelial cells leads to an increase in proinflammatory and prothrombotic factors.7 Aggregation of platelets causes consumptive thrombocytopenia8 and the formation of microthrombi that are deposited in renal vasculature. These mechanisms reduce platelet count and cause renal failure. This microangiopathology is then responsible for mechanical haemolysis of red blood cells and the subsequent fall in haemoglobin concentration. Thus systemic symptoms may occur because of anaemia, and oliguria and hypertension can result because of rapid decline in renal function.
In diarrhoea negative haemolytic uraemic syndrome the triggers include antibodies, viruses (HIV, for example) and drugs,9 and the history taking and examination should focus on these. This form of the syndrome is less common.8
The diagnosis of haemolytic uraemic syndrome can be made only when haemolytic anaemia, thrombocytopenia, and renal failure are all confirmed.6
Investigations in haemolytic uraemic syndrome SerologyAnaemia secondary to haemolysis
Thrombocytopenia
Raised lactase dehydrogenase—confirms haemolysis
Blood film—schistocytes, spherocytes, and reticulocytosis
Urea and creatinine—when both are raised, acute renal failure is indicated
Serum concentrations of complement—possible familial cause24 25
Serum concentrations of drugs—immunosuppressants, for example26 27
MicrobiologicalStool cultures—screen for E coli O157:H7, but also other causes of infective diarrhoea
Blood cultures—screen for E coli O157:H7
HistologicalRenal biopsy—confirms the diagnosis and indicates the prognosis28 29
ImagingRenal ultrasound—check size of kidneys and exclude urinary outflow obstruction as the cause of renal failure
2 Findings on culture of stool
Escherichia coli O157:H7 releases Shiga toxins, triggering endothelial damage that leads to haemolytic uraemic syndrome; it is the commonest cause of the syndrome.6 8 10 The bacterium can be grown from stool and blood cultures.
E coli O157:H7 is transmitted through eating undercooked food, particularly meat. Beef,11 venison, and unpasteurised milk11 have been implicated. The faeco-oral route is another potential mode of transmission.11
3 Expected findings on blood film
On a blood film, schistocytes, spherocytes, and reticulocytosis indicate haemolysis. At a microscopic level, the haemolysis is essentially secondary to mechanical shearing by vessels narrowed by platelet aggregation. Lactate dehydrogenase is released when erythrocytes break down, and therefore a raised serum concentration confirms haemolysis.
4 Main differential diagnosis
A common difficulty is differentiating between haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura (TTP).4 Some clinicians say that the two are on a spectrum of the same disease; others claim that they are two distinct conditions with similar clinical manifestations.5 Those who say they are distinct conditions cite the differing pathophysiology: endothelial damage in haemolytic uraemic syndrome, and the autoimmune process of ADAMTS13 inhibition in TTP.12 13 14
The pathophysiology of secondary TTP is poorly understood, and much work recently has highlighted the importance of von Willebrand factor in haemolytic uraemic syndrome, thus blurring its boundary with TTP.4 5 13
Clinically, there is much overlap. The classic description of TTP is a pentad of microangiopathic haemolytic anaemia, thrombocytopenia, acute renal failure, neurological sequelae, and fever,15 though there are no particular pathognomonic features. Neurological symptoms are thought to be more common in TTP and renal failure more marked in haemolytic uraemic syndrome.16 Renal failure is an essential criterion in the diagnosis of haemolytic uraemic syndrome. This helps to distinguish the two conditions, as does the presence of diarrhoeal prodrome in haemolytic uraemic syndrome.
5 Therapeutic procedures
Few clear guidelines exist for treating haemolytic uraemic syndrome—as management is often at the discretion of the doctor, treatment stratagems vary.17 Fluid balance and electrolyte abnormalities caused by acute renal failure need to be managed, and dialysis is often indicated.
Plasmapheresis has been shown to improve survival and prognosis18 19 and is preferred to plasma infusion because it treats fluid overload20 (large volumes of plasma are needed for therapeutic effects) and because it is an extracorporeal form of treatment.21 22 This is true in both forms of haemolytic uraemic syndrome. Plasmapheresis is contraindicated when the syndrome is secondary to S pneumoniae, as antibodies to Thomsen-Freidenreich antigen circulate in adult plasma.21
The use of antibiotics in haemolytic uraemic syndrome remains controversial. Although E coli O157:H7 has been shown to be vulnerable to certain antibiotics22 there is strong evidence that using antibiotics can worsen haemolytic uraemic syndrome22 and can trigger the syndrome by enhancing release of Shiga toxins.22 23
Cite this as: BMJ 2009;338:b200
References
Gasser C, Gautier E, Steck A, Siebenmann RE, Oechslin R. Hemolytic-uremic syndrome: bilateral necrosis of the renal cortex in acute acquired hemolytic anemia. Schweiz Med Wochenschr 1955;85:905-9.[Medline]
Neild GH. Haemolytic-uraemic syndrome in practice. Lancet 1994;343:398-401.[CrossRef][ISI][Medline]
Corrigan JJ Jr, Boineau FG. Hemolytic-uremic syndrome. Pediatr Rev 2001;22:365-9.[Free Full Text]
Gerth J, Busch M, Oyen F, Schneppenheim R, Keller T, Budde U, et al. Thrombotic microangiopathy in a 17-year-old patient: TTP, HUS or a bit of both? Clin Nephrol 2007;68:405-11.[ISI][Medline]
Desch K, Motto D. Is there a shared pathophysiology for thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome? J Am Soc Nephrol 2007;18(9):2457-60. Epub 2007 Aug 8.[Abstract/Free Full Text]
Razzaq S. Hemolytic uremic syndrome: an emerging health risk. Am Fam Physician 2006;74:991-6.[ISI][Medline]
Andreoli SP. The pathophysiology of the hemolytic uremic syndrome. Curr Opin Nephrol Hypertens 1999;8:459-64.[CrossRef][ISI][Medline]
Shapiro W. Hemolytic uremic syndrome. e-Medicine January 2007. http://emedicine.medscape.com.proxy.ub.uni-frankfurt.de/article/779218-overview
Liu J, Hutzler M, Li C, Pechet L. Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS): the new thinking. J Thromb Thrombolysis 2001;11:261-72.[CrossRef][ISI][Medline]
Banatvala N, Griffin PM, Greene KD, Barrett TJ, Bibb WF, Green JH, et al. The United States national prospective hemolytic uremic syndrome study: microbiologic, serologic, clinical, and epidemiologic findings. J Infect Dis 2001;183:1063-70.[CrossRef][ISI][Medline]
Health Protection Agency. E coli O157:H7. February 2008. www.hpa.org.uk/web/HPAwebFile/HPAweb_C/1194947412547
Moake JL. Moschcowitz, multimers, and metalloprotease. N Engl J Med 1998;339:1629-31.[Free Full Text]
Furlan M, Robles R, Galbusera M, Remuzzi G, Kyrle PA, Brenner B, et al. Von Willebrand factor-cleaving protease in thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome. N Engl J Med 1998;339:1578-84.[Abstract/Free Full Text]
Tsai HM, Lian EC. Antibodies to von Willebrand factor-cleaving protease in acute thrombotic thrombocytopenic purpura. N Engl J Med 1998;339:1585-94.[Abstract/Free Full Text]
Rust R. Thrombotic thrombocytopenic purpura. e-Medicine June 2006. http://emedicine.medscape.com.proxy.ub.uni-frankfurt.de/article/1178534-overview
Bahloul M, Dammak H, Kallel H, Khlaf-Bouaziz N, Ben Hamida C, Chaari A, et al. Thrombotic microangiopathies. Incidence, pathogenesis, diagnosis, treatment and prognosis. J Mal Vasc 2007;32:75-82.[ISI][Medline]
George JN. How I treat patients with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Blood 2000;96:1223-9.[Abstract/Free Full Text]
Lara PN Jr, Coe TL, Zhou H, Fernando L, Holland PV, Wun T. Improved survival with plasma exchange in patients with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Am J Med 1999;107:573-9.[CrossRef][ISI][Medline]
Hayward CP, Sutton DM, Carter WH Jr, Campbell ED, Scott JG, Francombe WH, et al. Treatment outcomes in patients with adult thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Arch Intern Med 1994;154:982-7.[CrossRef][ISI][Medline]
Coppo P, Bussel A, Charrier S, Adrie C, Galicier L, Boulanger E, et al. High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome. Medicine (Baltimore) 2003;82:27-38.[CrossRef][Medline]
Parmar MS. Hemolytic uremic syndrome. e-Medicine December 2008. http://emedicine.medscape.com.proxy.ub.uni-frankfurt.de/article/201181-overview
Panos GZ, Betsi GI, Falagas ME. Systematic review: are antibiotics detrimental or beneficial for the treatment of patients with Escherichia coli O157:H7 infection? Aliment Pharmacol Ther 2006;24:731-42.[CrossRef][ISI][Medline]
Walterspiel JN, Ashkenazi S, Morrow AL, Cleary TG. Effect of subinhibitory concentrations of antibiotics on extracellular Shiga-like toxin. Infection 1992;20:25-9.[CrossRef][ISI][Medline]
Pickering MC, Cook HT. Translational mini-review series on complement factor H: renal diseases associated with complement factor H: novel insights from humans and animals. Clin Exp Immunol 2008;151:210-30.[ISI][Medline]
Atkinson JP, Goodship TH. Complement factor H and the hemolytic uremic syndrome. J Exp Med 2007;204:1245-8.[Abstract/Free Full Text]
Abraham KA, Little MA, Dorman AM, Walshe JJ. Hemolytic-uremic syndrome in association with both cyclosporine and tacrolimus. Transpl Int 2000;13:443-7.[CrossRef][ISI][Medline]
Wen YK, Chen ML. Rescue treatment for cyclosporine-associated hemolytic-uremic syndrome with intravenous immunoglobulin. Clin Nephrol 2006;66:58-62.[ISI][Medline]
Morel-Maroger L, Kanfer A, Solez K, Sraer JD, Richet G. Prognostic importance of vascular lesions in acute renal failure with microangiopathic hemolytic anemia (hemolytic-uremic syndrome): clinicopathologic study in 20 adults. Kidney Int 1979;15:548-58.[ISI][Medline]
Matsumae T, Takebayashi S, Naito S. The clinico-pathological characteristics and outcome in hemolytic-uremic syndrome of adults. Clin Nephrol 1996;45:153-62.[ISI][Medline]
Case report
R Som, foundation year 2 doctor, R Wynne-Simmons, foundation year 2 doctor, J Islam, specialty trainee in medicine, S Lawman, consultant nephrologist
1 Sussex Kidney Unit, Royal Sussex County Hospital, Brighton BN2 5BE
Correspondence to: R Som rsom@doctors.org.uk
Case study
A 28 year old man presented to the accident and emergency department with central abdominal pain that had lasted just over a day and was "cramping" in nature. He had had bloody diarrhoea for three days, with increasing frequency and amount of blood. He had eaten a chicken sandwich purchased from a canteen the day before the onset of symptoms. There was no history of recent foreign travel or any important medical history.
On examination he was found to be warm and well perfused, and his abdomen was soft, with mild generalised tenderness. On admission his full blood count, renal function and liver function tests were all within normal range.
Three days after admission he had persistent bloody diarrhoea; his haemoglobin concentration had dropped by 40 g/l to 126 g/l. Colonoscopy and biopsies showed acute indeterminate colitis. His white cell count was 23.3x109/l, neutrophils 19.1x106/l, platelets 49x109/l, international normalised ratio 1.0, APTT (activated partial thromboplastin time)1.0, C reactive protein 256 mg/l, urea 19.7 mmol/l, creatinine 530 µmol/l, potassium 4.8 mmol/l, serum lactate dehydrogenase 3452 U/l. He quickly became anuric.
Questions
1 What is the diagnosis?
2 What would you expect to find on culture of stool?
3 What would you expect to see on a blood film?
4 What is the differential diagnosis?
5 What two therapeutic procedures might this patient have?
Answers
Short answers
1 Haemolytic uraemic syndrome—diarrhoea positive.
2 Escherichia coli O157:H7.
3 Blood film would show signs of haemolysis—schistocytes, spherocytes, and reticulocytosis.
4 Thrombotic thrombocytopenic purpura.
5 Plasma exchange and dialysis.
Outcome
The diagnosis of haemolytic uraemic syndrome was supported by a stool culture positive for Escherichia coli O157:H7, a blood film showing fragmented blood cells, a full blood count showing low platelets, and raised lactate dehydrogenase. He may have contracted E coli O157:H7 from the sandwich (though this is impossible to confirm). He needed haemodialysis and a total of 11 plasma exchanges. Renal biopsy showed glomerular intravascular thrombosis in keeping with haemolytic uraemic syndrome and acute tubular necrosis. One week after the diagnosis was made his condition deteriorated; he had several tonic-clonic seizures needing admission to the intensive care unit. After three weeks his clinical condition improved, and he was finally discharged home after a month with normal renal function.
Long answers
1 Diagnosis
Haemolytic uraemic syndrome is a form of thrombotic microangiopathy first described by Gasser et al,1 characterised by the triad of acute renal failure, haemolytic anaemia, and thrombocytopenia.2 It primarily affects children3 but can occur in adults.4 5
Haemolytic uraemic syndrome is classified as either diarrhoea positive or diarrhoea negative, depending on whether the patient has a diarrhoeal prodrome. The history taking should aim to establish whether the diarrhoea is infective or secondary to inflammatory bowel disease or other forms of colitis, which are important differentials as the diarrhoea may be bloody. In diarrhoea positive haemolytic uraemic syndrome, the diarrhoea is nearly always secondary to infection; therefore a careful travel and diet history is necessary. Abdominal pain should also cause the clinician to consider causes of acute abdomen as differentials.6
The pathophysiology of haemolytic uraemic syndrome is poorly understood. Damage to endothelial cells leads to an increase in proinflammatory and prothrombotic factors.7 Aggregation of platelets causes consumptive thrombocytopenia8 and the formation of microthrombi that are deposited in renal vasculature. These mechanisms reduce platelet count and cause renal failure. This microangiopathology is then responsible for mechanical haemolysis of red blood cells and the subsequent fall in haemoglobin concentration. Thus systemic symptoms may occur because of anaemia, and oliguria and hypertension can result because of rapid decline in renal function.
In diarrhoea negative haemolytic uraemic syndrome the triggers include antibodies, viruses (HIV, for example) and drugs,9 and the history taking and examination should focus on these. This form of the syndrome is less common.8
The diagnosis of haemolytic uraemic syndrome can be made only when haemolytic anaemia, thrombocytopenia, and renal failure are all confirmed.6
Investigations in haemolytic uraemic syndrome SerologyAnaemia secondary to haemolysis
Thrombocytopenia
Raised lactase dehydrogenase—confirms haemolysis
Blood film—schistocytes, spherocytes, and reticulocytosis
Urea and creatinine—when both are raised, acute renal failure is indicated
Serum concentrations of complement—possible familial cause24 25
Serum concentrations of drugs—immunosuppressants, for example26 27
MicrobiologicalStool cultures—screen for E coli O157:H7, but also other causes of infective diarrhoea
Blood cultures—screen for E coli O157:H7
HistologicalRenal biopsy—confirms the diagnosis and indicates the prognosis28 29
ImagingRenal ultrasound—check size of kidneys and exclude urinary outflow obstruction as the cause of renal failure
2 Findings on culture of stool
Escherichia coli O157:H7 releases Shiga toxins, triggering endothelial damage that leads to haemolytic uraemic syndrome; it is the commonest cause of the syndrome.6 8 10 The bacterium can be grown from stool and blood cultures.
E coli O157:H7 is transmitted through eating undercooked food, particularly meat. Beef,11 venison, and unpasteurised milk11 have been implicated. The faeco-oral route is another potential mode of transmission.11
3 Expected findings on blood film
On a blood film, schistocytes, spherocytes, and reticulocytosis indicate haemolysis. At a microscopic level, the haemolysis is essentially secondary to mechanical shearing by vessels narrowed by platelet aggregation. Lactate dehydrogenase is released when erythrocytes break down, and therefore a raised serum concentration confirms haemolysis.
4 Main differential diagnosis
A common difficulty is differentiating between haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura (TTP).4 Some clinicians say that the two are on a spectrum of the same disease; others claim that they are two distinct conditions with similar clinical manifestations.5 Those who say they are distinct conditions cite the differing pathophysiology: endothelial damage in haemolytic uraemic syndrome, and the autoimmune process of ADAMTS13 inhibition in TTP.12 13 14
The pathophysiology of secondary TTP is poorly understood, and much work recently has highlighted the importance of von Willebrand factor in haemolytic uraemic syndrome, thus blurring its boundary with TTP.4 5 13
Clinically, there is much overlap. The classic description of TTP is a pentad of microangiopathic haemolytic anaemia, thrombocytopenia, acute renal failure, neurological sequelae, and fever,15 though there are no particular pathognomonic features. Neurological symptoms are thought to be more common in TTP and renal failure more marked in haemolytic uraemic syndrome.16 Renal failure is an essential criterion in the diagnosis of haemolytic uraemic syndrome. This helps to distinguish the two conditions, as does the presence of diarrhoeal prodrome in haemolytic uraemic syndrome.
5 Therapeutic procedures
Few clear guidelines exist for treating haemolytic uraemic syndrome—as management is often at the discretion of the doctor, treatment stratagems vary.17 Fluid balance and electrolyte abnormalities caused by acute renal failure need to be managed, and dialysis is often indicated.
Plasmapheresis has been shown to improve survival and prognosis18 19 and is preferred to plasma infusion because it treats fluid overload20 (large volumes of plasma are needed for therapeutic effects) and because it is an extracorporeal form of treatment.21 22 This is true in both forms of haemolytic uraemic syndrome. Plasmapheresis is contraindicated when the syndrome is secondary to S pneumoniae, as antibodies to Thomsen-Freidenreich antigen circulate in adult plasma.21
The use of antibiotics in haemolytic uraemic syndrome remains controversial. Although E coli O157:H7 has been shown to be vulnerable to certain antibiotics22 there is strong evidence that using antibiotics can worsen haemolytic uraemic syndrome22 and can trigger the syndrome by enhancing release of Shiga toxins.22 23
Cite this as: BMJ 2009;338:b200
References
Gasser C, Gautier E, Steck A, Siebenmann RE, Oechslin R. Hemolytic-uremic syndrome: bilateral necrosis of the renal cortex in acute acquired hemolytic anemia. Schweiz Med Wochenschr 1955;85:905-9.[Medline]
Neild GH. Haemolytic-uraemic syndrome in practice. Lancet 1994;343:398-401.[CrossRef][ISI][Medline]
Corrigan JJ Jr, Boineau FG. Hemolytic-uremic syndrome. Pediatr Rev 2001;22:365-9.[Free Full Text]
Gerth J, Busch M, Oyen F, Schneppenheim R, Keller T, Budde U, et al. Thrombotic microangiopathy in a 17-year-old patient: TTP, HUS or a bit of both? Clin Nephrol 2007;68:405-11.[ISI][Medline]
Desch K, Motto D. Is there a shared pathophysiology for thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome? J Am Soc Nephrol 2007;18(9):2457-60. Epub 2007 Aug 8.[Abstract/Free Full Text]
Razzaq S. Hemolytic uremic syndrome: an emerging health risk. Am Fam Physician 2006;74:991-6.[ISI][Medline]
Andreoli SP. The pathophysiology of the hemolytic uremic syndrome. Curr Opin Nephrol Hypertens 1999;8:459-64.[CrossRef][ISI][Medline]
Shapiro W. Hemolytic uremic syndrome. e-Medicine January 2007. http://emedicine.medscape.com.proxy.ub.uni-frankfurt.de/article/779218-overview
Liu J, Hutzler M, Li C, Pechet L. Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS): the new thinking. J Thromb Thrombolysis 2001;11:261-72.[CrossRef][ISI][Medline]
Banatvala N, Griffin PM, Greene KD, Barrett TJ, Bibb WF, Green JH, et al. The United States national prospective hemolytic uremic syndrome study: microbiologic, serologic, clinical, and epidemiologic findings. J Infect Dis 2001;183:1063-70.[CrossRef][ISI][Medline]
Health Protection Agency. E coli O157:H7. February 2008. www.hpa.org.uk/web/HPAwebFile/HPAweb_C/1194947412547
Moake JL. Moschcowitz, multimers, and metalloprotease. N Engl J Med 1998;339:1629-31.[Free Full Text]
Furlan M, Robles R, Galbusera M, Remuzzi G, Kyrle PA, Brenner B, et al. Von Willebrand factor-cleaving protease in thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome. N Engl J Med 1998;339:1578-84.[Abstract/Free Full Text]
Tsai HM, Lian EC. Antibodies to von Willebrand factor-cleaving protease in acute thrombotic thrombocytopenic purpura. N Engl J Med 1998;339:1585-94.[Abstract/Free Full Text]
Rust R. Thrombotic thrombocytopenic purpura. e-Medicine June 2006. http://emedicine.medscape.com.proxy.ub.uni-frankfurt.de/article/1178534-overview
Bahloul M, Dammak H, Kallel H, Khlaf-Bouaziz N, Ben Hamida C, Chaari A, et al. Thrombotic microangiopathies. Incidence, pathogenesis, diagnosis, treatment and prognosis. J Mal Vasc 2007;32:75-82.[ISI][Medline]
George JN. How I treat patients with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Blood 2000;96:1223-9.[Abstract/Free Full Text]
Lara PN Jr, Coe TL, Zhou H, Fernando L, Holland PV, Wun T. Improved survival with plasma exchange in patients with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Am J Med 1999;107:573-9.[CrossRef][ISI][Medline]
Hayward CP, Sutton DM, Carter WH Jr, Campbell ED, Scott JG, Francombe WH, et al. Treatment outcomes in patients with adult thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Arch Intern Med 1994;154:982-7.[CrossRef][ISI][Medline]
Coppo P, Bussel A, Charrier S, Adrie C, Galicier L, Boulanger E, et al. High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome. Medicine (Baltimore) 2003;82:27-38.[CrossRef][Medline]
Parmar MS. Hemolytic uremic syndrome. e-Medicine December 2008. http://emedicine.medscape.com.proxy.ub.uni-frankfurt.de/article/201181-overview
Panos GZ, Betsi GI, Falagas ME. Systematic review: are antibiotics detrimental or beneficial for the treatment of patients with Escherichia coli O157:H7 infection? Aliment Pharmacol Ther 2006;24:731-42.[CrossRef][ISI][Medline]
Walterspiel JN, Ashkenazi S, Morrow AL, Cleary TG. Effect of subinhibitory concentrations of antibiotics on extracellular Shiga-like toxin. Infection 1992;20:25-9.[CrossRef][ISI][Medline]
Pickering MC, Cook HT. Translational mini-review series on complement factor H: renal diseases associated with complement factor H: novel insights from humans and animals. Clin Exp Immunol 2008;151:210-30.[ISI][Medline]
Atkinson JP, Goodship TH. Complement factor H and the hemolytic uremic syndrome. J Exp Med 2007;204:1245-8.[Abstract/Free Full Text]
Abraham KA, Little MA, Dorman AM, Walshe JJ. Hemolytic-uremic syndrome in association with both cyclosporine and tacrolimus. Transpl Int 2000;13:443-7.[CrossRef][ISI][Medline]
Wen YK, Chen ML. Rescue treatment for cyclosporine-associated hemolytic-uremic syndrome with intravenous immunoglobulin. Clin Nephrol 2006;66:58-62.[ISI][Medline]
Morel-Maroger L, Kanfer A, Solez K, Sraer JD, Richet G. Prognostic importance of vascular lesions in acute renal failure with microangiopathic hemolytic anemia (hemolytic-uremic syndrome): clinicopathologic study in 20 adults. Kidney Int 1979;15:548-58.[ISI][Medline]
Matsumae T, Takebayashi S, Naito S. The clinico-pathological characteristics and outcome in hemolytic-uremic syndrome of adults. Clin Nephrol 1996;45:153-62.[ISI][Medline]
Mittwoch, 18. Februar 2009
Dienstag, 17. Februar 2009
Demonstrations of Physical Signs in Clinical Surgery
Chris Barrett, specialist registrar in neurosurgery, Newcastle General Hospital, Newcastle upon Tyne
chris.barrett@nuth.nhs.uk
Hamilton Bailey’s classic text is well known to most surgeons, many editions having been published around the world over the years. It is essentially a textbook of clinical surgical examination that emphasises a logical approach to history taking, examination, and investigation. It is also memorable for a number of striking illustrations and the author’s incisive (and often witty) thoughts.
Bailey was a surgeon from another era. He had a strong family background in medicine, but his early career was colourful, to say the least. At the outbreak of the first world war, while still only a medical student, he joined the Red Cross and was despatched with the British Expeditionary Force to the western front. He was then captured, and while working as a prisoner of war on the railways he was accused of being involved in the sabotage of a German troop train. Bailey was reprieved; one of his French co-accused was not so lucky.
Later in the war he served as a naval surgeon aboard HMS Iron Duke during the battle of Jutland. This was undoubtedly an important experience for Bailey and informed both his strongly practical approach and his interest in military surgery, which lasted his whole career.
After the war Bailey was appointed to posts in Birmingham and then London. In addition to a busy clinical practice he embarked on a prolific writing career, with an emphasis on surgical education. Many of his publications have undergone many incarnations and are still in use today, such as Bailey & Love’s Short Practice of Surgery and Emergency Surgery. However, it is perhaps Physical Signs that has generated the most affection.
As always, Bailey takes an extremely well structured and logical approach. He begins by considering basic clinical signs and then moves from head to toe (lower limb) in separate chapters, discussing the localised pathology and specialised examination pertinent to each area. Many illustrations, photographic and diagrammatic, help to enliven his accurate, measured prose. He also includes, as footnotes, short biographical references on the eponymous syndromes and notes on the Greek and Latin etymology of medical terms. Often neglected in more recent publications, interesting details such as anatomists who later became bishops or the fact that the word atheroma has its origins in the ancient Greek for porridge are unforgettable.
Overall, what is striking is the breadth of Bailey’s learning and erudition. He was a general surgeon in the traditional sense, able to turn his hand to the diagnosis of surgical pathology in any part of the body and including orthopaedics, paediatrics, and neurosurgery. Though not without humour or a sense of the absurd, his writing is underlined by a strong respect for patients and for the art and science of medicine. Undoubtedly the emphasis on clinical aspects of surgery is Bailey’s fundamental message. "The history, and physical methods of examination, must always remain the main channels by which a diagnosis is made."
Cite this as: BMJ 2009;338:a2992
Demonstrations of Physical Signs in Clinical Surgery
By Hamilton Bailey
First published 1927
chris.barrett@nuth.nhs.uk
Hamilton Bailey’s classic text is well known to most surgeons, many editions having been published around the world over the years. It is essentially a textbook of clinical surgical examination that emphasises a logical approach to history taking, examination, and investigation. It is also memorable for a number of striking illustrations and the author’s incisive (and often witty) thoughts.
Bailey was a surgeon from another era. He had a strong family background in medicine, but his early career was colourful, to say the least. At the outbreak of the first world war, while still only a medical student, he joined the Red Cross and was despatched with the British Expeditionary Force to the western front. He was then captured, and while working as a prisoner of war on the railways he was accused of being involved in the sabotage of a German troop train. Bailey was reprieved; one of his French co-accused was not so lucky.
Later in the war he served as a naval surgeon aboard HMS Iron Duke during the battle of Jutland. This was undoubtedly an important experience for Bailey and informed both his strongly practical approach and his interest in military surgery, which lasted his whole career.
After the war Bailey was appointed to posts in Birmingham and then London. In addition to a busy clinical practice he embarked on a prolific writing career, with an emphasis on surgical education. Many of his publications have undergone many incarnations and are still in use today, such as Bailey & Love’s Short Practice of Surgery and Emergency Surgery. However, it is perhaps Physical Signs that has generated the most affection.
As always, Bailey takes an extremely well structured and logical approach. He begins by considering basic clinical signs and then moves from head to toe (lower limb) in separate chapters, discussing the localised pathology and specialised examination pertinent to each area. Many illustrations, photographic and diagrammatic, help to enliven his accurate, measured prose. He also includes, as footnotes, short biographical references on the eponymous syndromes and notes on the Greek and Latin etymology of medical terms. Often neglected in more recent publications, interesting details such as anatomists who later became bishops or the fact that the word atheroma has its origins in the ancient Greek for porridge are unforgettable.
Overall, what is striking is the breadth of Bailey’s learning and erudition. He was a general surgeon in the traditional sense, able to turn his hand to the diagnosis of surgical pathology in any part of the body and including orthopaedics, paediatrics, and neurosurgery. Though not without humour or a sense of the absurd, his writing is underlined by a strong respect for patients and for the art and science of medicine. Undoubtedly the emphasis on clinical aspects of surgery is Bailey’s fundamental message. "The history, and physical methods of examination, must always remain the main channels by which a diagnosis is made."
Cite this as: BMJ 2009;338:a2992
Demonstrations of Physical Signs in Clinical Surgery
By Hamilton Bailey
First published 1927
Montag, 16. Februar 2009
Demokratische Fotografie
„i had this notion of what i called a democratic way of looking around: that nothing was more important or less important." william eggleston
Der amerikanische Künstler William Eggleston (*1939, Memphis, USA) gilt als einer der stilbildenden Fotografen des 20. Jahrhunderts.
Jetzt ist ihm eine Retrospektive im Haus der Kunst, München, gewidmet.
Mehr...
Der amerikanische Künstler William Eggleston (*1939, Memphis, USA) gilt als einer der stilbildenden Fotografen des 20. Jahrhunderts.
Jetzt ist ihm eine Retrospektive im Haus der Kunst, München, gewidmet.
Mehr...
Im Mittelmaß versunken...
BVB - Cottbus 1 : 1...
Cottbus? Da war doch was...ich erinnere mich dunkel...
Cottbus? Da war doch was...ich erinnere mich dunkel...
Sonntag, 15. Februar 2009
Esskultur...
- Iss (frische) Lebensmittel
- Nicht zu viel
- Vor allem Pflanzen, besonders Blätter
- Iss wie ein Allesfresser
- Zahle mehr, iss weniger
- Iss immer an einem Tisch
- Versuche, nicht alleine zu essen
- Koche und, wenn es dir möglich ist, lege einen Garten an
- Vermeide Nahrungsmittel mit Inhaltsstoffen die a) dir nicht vertraut sind, b) unaussprechbar sind, c) mehr als fünf an der Zahl sind oder d) Glucose-Fructose-Sirup enthalten
- Vermeide Nahrungsmittel mit gesundheitsbezogenen Behauptungen
- Lass den Supermarkt so oft wie möglich links liegen
Michael Pollan im Interview "Unsere Esskultur beruht auf Missbrauch"
Frankfurter Allgemeine Sonntagszeitung 15. Februar 2009 Nr 7 Seite 52
Wo Hass aufbricht, stimmt etwas nicht...
Der Philosoph Robert Spaemann im Interview der Frankfurter Allgemeinen Sonntagszeitung , 15. Februar 2009 Nr 7 Seite 4
...Sie haben gesagt, der Papst vertraue auf die Macht der Liebe. Die Folge sind Zorn, Hass, Furor.
Ja. Impugnabant me gratis, heißt es in einem Psalm. Sie haben mich wegen nichts, sie haben mich grundlos verfolgt. Wo Hass aufbricht, da stimmt etwas nicht. Und bloß, weil der Papst etwas tut, was im Evangelium als Kennzeichen des guten Hirten verstanden wird, nämlich dass er 99 Schafe im Schafstall läßt und dem einen nachgeht, um das auch wieder zurückzuholen, das wird ihm jetzt vorgeworfen. Da kann er nur sagen: Ich tue, was Jesus gesagt hat, was der gute Hirte tun soll.
...Sie haben gesagt, der Papst vertraue auf die Macht der Liebe. Die Folge sind Zorn, Hass, Furor.
Ja. Impugnabant me gratis, heißt es in einem Psalm. Sie haben mich wegen nichts, sie haben mich grundlos verfolgt. Wo Hass aufbricht, da stimmt etwas nicht. Und bloß, weil der Papst etwas tut, was im Evangelium als Kennzeichen des guten Hirten verstanden wird, nämlich dass er 99 Schafe im Schafstall läßt und dem einen nachgeht, um das auch wieder zurückzuholen, das wird ihm jetzt vorgeworfen. Da kann er nur sagen: Ich tue, was Jesus gesagt hat, was der gute Hirte tun soll.
Samstag, 14. Februar 2009
Valentinstag
Harschgefrorener Schnee
Eisblau und kalt ein
weiter Himmel...
Gen Westen weißverpackte
Wälder,
im Morgenlicht vor
dunkler Wolkenwand
der Träumer geht
auf Reisen
Und findet dich
im Abendlicht
des Sommers...
Walter Frank
Eisblau und kalt ein
weiter Himmel...
Gen Westen weißverpackte
Wälder,
im Morgenlicht vor
dunkler Wolkenwand
der Träumer geht
auf Reisen
Und findet dich
im Abendlicht
des Sommers...
Walter Frank
Freitag, 13. Februar 2009
DRG-System revisited - außer Spesen nichts gewesen...
Prof. Jürgen Stausberg kommentiert zürückhaltend aber eindeutig...
Was sollte das DRG-System leisten?
1. Verbesserung von Qualität und Wirtschaftlichkeit im Gesundheitswesen
2. Transparenz
3. Verbesserung der Behandlungsqualität
Punkte 1 und 2 sind nicht erreicht, im Gegenteil, die Kosten im Gesundheitswesen steigen und von Transparenz kann schon gar keine Rede mehr sein bei der groteskten Dokumentationsmaschinerie und Bürokratie.
Ob eine verbesserte Behandlungsqualität auf die DRGs zurückzuführen ist, muß mehr als bezweifelt werden.
Konsequenz - DRGs abschaffen...
Mehr...
Was sollte das DRG-System leisten?
1. Verbesserung von Qualität und Wirtschaftlichkeit im Gesundheitswesen
2. Transparenz
3. Verbesserung der Behandlungsqualität
Punkte 1 und 2 sind nicht erreicht, im Gegenteil, die Kosten im Gesundheitswesen steigen und von Transparenz kann schon gar keine Rede mehr sein bei der groteskten Dokumentationsmaschinerie und Bürokratie.
Ob eine verbesserte Behandlungsqualität auf die DRGs zurückzuführen ist, muß mehr als bezweifelt werden.
Konsequenz - DRGs abschaffen...
Mehr...
Donnerstag, 12. Februar 2009
Doping und kein Ende...
Dr. med. Stefan Feiler hat einen sehr informativen Artikel über "Doping im Sport" geschrieben.
Mal Hand aufs Herz. Wer von Ihnen kennt denn Marc Blume? Noch nie gehört?Und wer kennt Namen wie Ben Johnson, Marion Jones, Tim Montgomery, Dwain Chambers oder Linford Christie? Schon mal gehört? Na bitte.
Sportler wie der deutsche Sprinter Marc Blume, für die Ehrlichkeit und Fairness noch einen gewissen Stellenwert haben, wurden in der Vergangenheit seitens des Publikums und Medien nicht selten als „Olympiatouristen“ belächelt. Wesentlich mehr Publikums- und Medienaufmerksamkeit bekamen da schon die oben genannten fünf überführten Dopingsünder.
Kaum ein interessierter „Konsument“ von Olympischen Spielen oder anderen Wettkämpfen glaubt Umfragen zufolge heute noch an den sauberen Sport gemäß dem Motto „Dabeisein ist alles“. Zumindest nicht im Hochleistungsbereich.
Die Dopingmisere allein der Schachfigur Sportler/in zuzuschreiben wäre aber zu billig. Doping ist ein gesellschaftliches Problem.
Mehr... im Archiv Sport und Herausforderungen
Mal Hand aufs Herz. Wer von Ihnen kennt denn Marc Blume? Noch nie gehört?Und wer kennt Namen wie Ben Johnson, Marion Jones, Tim Montgomery, Dwain Chambers oder Linford Christie? Schon mal gehört? Na bitte.
Sportler wie der deutsche Sprinter Marc Blume, für die Ehrlichkeit und Fairness noch einen gewissen Stellenwert haben, wurden in der Vergangenheit seitens des Publikums und Medien nicht selten als „Olympiatouristen“ belächelt. Wesentlich mehr Publikums- und Medienaufmerksamkeit bekamen da schon die oben genannten fünf überführten Dopingsünder.
Kaum ein interessierter „Konsument“ von Olympischen Spielen oder anderen Wettkämpfen glaubt Umfragen zufolge heute noch an den sauberen Sport gemäß dem Motto „Dabeisein ist alles“. Zumindest nicht im Hochleistungsbereich.
Die Dopingmisere allein der Schachfigur Sportler/in zuzuschreiben wäre aber zu billig. Doping ist ein gesellschaftliches Problem.
Mehr... im Archiv Sport und Herausforderungen
Mittwoch, 11. Februar 2009
Kommunikation...
"Dass in der inneren und äußeren Kommunikation des Vatikans etwas grundlegend verbessert werden muss, dass pfeifen doch die Spatzen von den Dächern."
Der Mainzer Bischof, Karl Kardinal Lehmann
Der Mainzer Bischof, Karl Kardinal Lehmann
Dienstag, 10. Februar 2009
Ärzte, Patienten und die Pharmaindustrie...
Fiona Godlee, editor, BMJ
fgodlee@bmj.com
In the Royal College of Physicians’ report on relations between industry, academia, and the NHS (doi:10.1136/bmj.b442) Iain Chalmers is quoted as saying, "I do not blame industry for trying to get away with anything that is normally considered to be its primary purpose, which is to make profits and look after its shareholders’ interests. It is our profession that has colluded in all of this and been prepared to go along with it—we are the people to blame because we need not have stood for it."
By "all of this" I assume Chalmers means the many ways in which drugs are promoted in the guise of science, education, and information: the misreporting of industry funded research, the use of ghost writers and key opinion leaders, the provision of free courses and conferences. His words echo Suzanne Fletcher’s in the BMJ last year (2008;337:a1023, doi:10.1136/bmj.a1023). For these practices to flourish, doctors have had to at least acquiesce, if not actively take part, as researchers, guest authors, paid opinion leaders, and recipients of gifts and hospitality.
As our cover image shows, it takes two to tango. It’s time for the profession to take a lead. This means saying no to gifts and hospitality, ensuring that research and clinical collaborations are transparent and unbiased in their design and reporting, refusing to be a guest or ghost author, declining the role of paid opinion leader, paying our way for information and education, and refusing industry support unless it is entirely transparent and in patients’ or the public’s best interests.
Will the RCP report make a difference, as its instigator Ian Gilmore hopes (doi:10.1136/bmj.b439)? Our editorialist Joe Collier thinks not (doi:10.1136/bmj.b443). He calls the report "flawed" and a missed opportunity. But I am more hopeful. It seems to me that we may have reached a turning point. Trust in the industry has fallen so low among large swathes of the profession and the public that industry itself now sees that corrective action is critical for business. If its undoubted contribution to health and the economy are to be properly acknowledged and built upon, it too has to take a lead and change its approach.
We have commissioned five commentaries on the relationship between industry, doctors, and patients. Scott Gottlieb calls for less but better regulation (doi:10.1136/bmj.b234). Gordon Coutts, a company chief executive, praises joint working initiatives such as "find and treat" strategies for patients at high risk (doi:10.1136/bmj.b232). Richard Tiner, an industry spokesman, believes that current regulation provides robust controls (doi:10.1136/bmj.b252). Harlan Krumholz and Joseph Ross call for explicit standards of conduct including greater transparency, an end to industry funding of continuing medical education, tighter regulation for industry funded research, and an end to payment and intimidation of clinical opinion leaders (doi:10.1136/bmj.b211). Finally, former journal editor Marcia Angell says there should be no relationship because the missions of industry and health care are so fundamentally different (doi:10.1136/bmj.b222). Which view is most in line with yours? You can vote and give us your comments on bmj.com.
Cite this as: BMJ 2009;338:b463
fgodlee@bmj.com
In the Royal College of Physicians’ report on relations between industry, academia, and the NHS (doi:10.1136/bmj.b442) Iain Chalmers is quoted as saying, "I do not blame industry for trying to get away with anything that is normally considered to be its primary purpose, which is to make profits and look after its shareholders’ interests. It is our profession that has colluded in all of this and been prepared to go along with it—we are the people to blame because we need not have stood for it."
By "all of this" I assume Chalmers means the many ways in which drugs are promoted in the guise of science, education, and information: the misreporting of industry funded research, the use of ghost writers and key opinion leaders, the provision of free courses and conferences. His words echo Suzanne Fletcher’s in the BMJ last year (2008;337:a1023, doi:10.1136/bmj.a1023). For these practices to flourish, doctors have had to at least acquiesce, if not actively take part, as researchers, guest authors, paid opinion leaders, and recipients of gifts and hospitality.
As our cover image shows, it takes two to tango. It’s time for the profession to take a lead. This means saying no to gifts and hospitality, ensuring that research and clinical collaborations are transparent and unbiased in their design and reporting, refusing to be a guest or ghost author, declining the role of paid opinion leader, paying our way for information and education, and refusing industry support unless it is entirely transparent and in patients’ or the public’s best interests.
Will the RCP report make a difference, as its instigator Ian Gilmore hopes (doi:10.1136/bmj.b439)? Our editorialist Joe Collier thinks not (doi:10.1136/bmj.b443). He calls the report "flawed" and a missed opportunity. But I am more hopeful. It seems to me that we may have reached a turning point. Trust in the industry has fallen so low among large swathes of the profession and the public that industry itself now sees that corrective action is critical for business. If its undoubted contribution to health and the economy are to be properly acknowledged and built upon, it too has to take a lead and change its approach.
We have commissioned five commentaries on the relationship between industry, doctors, and patients. Scott Gottlieb calls for less but better regulation (doi:10.1136/bmj.b234). Gordon Coutts, a company chief executive, praises joint working initiatives such as "find and treat" strategies for patients at high risk (doi:10.1136/bmj.b232). Richard Tiner, an industry spokesman, believes that current regulation provides robust controls (doi:10.1136/bmj.b252). Harlan Krumholz and Joseph Ross call for explicit standards of conduct including greater transparency, an end to industry funding of continuing medical education, tighter regulation for industry funded research, and an end to payment and intimidation of clinical opinion leaders (doi:10.1136/bmj.b211). Finally, former journal editor Marcia Angell says there should be no relationship because the missions of industry and health care are so fundamentally different (doi:10.1136/bmj.b222). Which view is most in line with yours? You can vote and give us your comments on bmj.com.
Cite this as: BMJ 2009;338:b463
Sonntag, 8. Februar 2009
Bayern - BVB
Bayern - BVB 3 : 1...
Der Bayern-Sturm schießt die Borussen ab...zwei Tore in den letzten Minuten!
Der Bayern-Sturm schießt die Borussen ab...zwei Tore in den letzten Minuten!
Samstag, 7. Februar 2009
Frauen und Lungenkrebs...
Am heutigen 3. Frankfurter Lungenkrebs sprach Frau Prof. Jäger über den Lungenkrebs bei Frauen.
Ausgehend von der Beobachtung einer besseren Prognose bei vielen soliden Tumore bei Frauen, kann man dies auch bei an Lungenkrebs erkrankten Frauen nachweisen. Verantwortlich dafür sind ua folgende Faktoren
1. Frauen nehmen häufiger an Screening-Untersuchungen und klinischen Studien teil
2. Frauen verarbeiten eine Krebsdiagnose besser als Männer
3. Männer begehen häufiger Selbstmord bei einer Krebserkrankung als Frauen
4. Nach der Menopause haben Frauen mit einem NSCLC (Nichtkleinzelliges Lungenkarzinom) ein besseres Überleben als Männer
5. Die Expression von Östrogenrezeptoren im Tumorgewebe scheint dabei eine Rolle zu spielen
Frau Prof. Jäger sprach in ihrer Zusammenfassung davon, daß Frauen auf der einen Seite eher ein tabakassoziiertes NSCLC bekommen als Männer (dh es reicht ein geringerer Tabakkonsum), auf der anderen Seite sprechen Frauen auf neoadjuvante und palliative Therapien besser an.
Ausgehend von der Beobachtung einer besseren Prognose bei vielen soliden Tumore bei Frauen, kann man dies auch bei an Lungenkrebs erkrankten Frauen nachweisen. Verantwortlich dafür sind ua folgende Faktoren
1. Frauen nehmen häufiger an Screening-Untersuchungen und klinischen Studien teil
2. Frauen verarbeiten eine Krebsdiagnose besser als Männer
3. Männer begehen häufiger Selbstmord bei einer Krebserkrankung als Frauen
4. Nach der Menopause haben Frauen mit einem NSCLC (Nichtkleinzelliges Lungenkarzinom) ein besseres Überleben als Männer
5. Die Expression von Östrogenrezeptoren im Tumorgewebe scheint dabei eine Rolle zu spielen
Frau Prof. Jäger sprach in ihrer Zusammenfassung davon, daß Frauen auf der einen Seite eher ein tabakassoziiertes NSCLC bekommen als Männer (dh es reicht ein geringerer Tabakkonsum), auf der anderen Seite sprechen Frauen auf neoadjuvante und palliative Therapien besser an.
Tag der offenen Tür...
...im Haus des Lebenslangen Lernens - Campus Dreieich...
Schön, das Engagement unserer Krankenpflegeschülerinnen und -schüler zu sehen!
Ein paar Impressionen gibt es hier zu sehen...
Schön, das Engagement unserer Krankenpflegeschülerinnen und -schüler zu sehen!
Ein paar Impressionen gibt es hier zu sehen...
Mittwoch, 4. Februar 2009
Dienstag, 3. Februar 2009
"In der Wirtschaft gibt es...
...keine Ethik und Moral. Die Finanzkrise ist eine Chance, dies zu verändern."
Bischof Lehmann
Bischof Lehmann
Montag, 2. Februar 2009
Glücklich werden...
1. Schlafen Sie genug!
2. Treffen Sie sich mit Ihren Freunden! Das sind - neben Sex - die glücklichsten Stunden überhaupt.
3. Passen Sie auf, mit wem Sie sich vergleichen!
4. Erinnern Sie sich!
5. Denken Sie nach!
Daniel Kahneman im Interview "Geld macht glücklicher als Ehe"
Frankfurter Allgemeine Sonntagszeitung 1. Februar 2009 Nr 5 Seite 40
2. Treffen Sie sich mit Ihren Freunden! Das sind - neben Sex - die glücklichsten Stunden überhaupt.
3. Passen Sie auf, mit wem Sie sich vergleichen!
4. Erinnern Sie sich!
5. Denken Sie nach!
Daniel Kahneman im Interview "Geld macht glücklicher als Ehe"
Frankfurter Allgemeine Sonntagszeitung 1. Februar 2009 Nr 5 Seite 40
Sonntag, 1. Februar 2009
"Die zehn Millionen sind...
...ja nicht der tatsächliche Marktwert, der Junge ist ja viel mehr wert."
Bayern Münchens Manager Uli Hoeneß über Lukas Podolski, der für zehn Millionen Euro "Ablöse" zum 1. FC Köln zurückkehrt.
Offenbach Post Samstag, 31. Januar 2009, Rubrik Spruch des Tages
Bayern Münchens Manager Uli Hoeneß über Lukas Podolski, der für zehn Millionen Euro "Ablöse" zum 1. FC Köln zurückkehrt.
Offenbach Post Samstag, 31. Januar 2009, Rubrik Spruch des Tages
John Updike - Requiem
It came to me the other day:
Were you to die, no one would say,
"Oh, what a shame! So young, so full
Of promise - depths unplumbable!"
Instead a shrug an tearless eyes
Will greet my overdue demise!
The wide response will be, I know,
"I thought he died a while ago."
For life's a shabby subterfuge,
And death is real, and dark, and huge.
The shock of it will register
Nowhere but where it will occur.
Frankfurter Allgemeine Zeitung Samstag, 31. Januar 2009 Nr 26 Seite 31
Were you to die, no one would say,
"Oh, what a shame! So young, so full
Of promise - depths unplumbable!"
Instead a shrug an tearless eyes
Will greet my overdue demise!
The wide response will be, I know,
"I thought he died a while ago."
For life's a shabby subterfuge,
And death is real, and dark, and huge.
The shock of it will register
Nowhere but where it will occur.
Frankfurter Allgemeine Zeitung Samstag, 31. Januar 2009 Nr 26 Seite 31
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