Elderly gynaecological cancer patients at risk for poor end of life care: a population-based study from the Swedish Register of Palliative Care.

Introduction: Poorer end-of-life (EOL) care for elderly cancer patients has been reported. We assessed the impact of age on 13 indicators for the quality of EOL care as well as adherence to 6 national quality indicators in gynaecological cancer patients.Methods: Age-dependent differences in 13 palliative care quality indicators were studied in gynaecological cancer patients registered in the population-based Swedish Register of Palliative Care. Association between the patient's age and each quality indicator was analyzed by logistic regression, adjusted for place of death where appropriate. Adherence to six national quality indicators determined by the Swedish National Board of Health and Welfare was estimated in all patients.Results: We included 3940 patients with the following age distribution: 1.6% were 18-39 years of age, 12.3% 40-59 years, 37.2% 60-74 years, 28.9% 75-84 years and 20% were ≥85 years. Age-dependent differences in implementation rate were present for some of the 13 quality indicators. Compared to elderly cancer patients, younger patients were more likely to be cared for by a specialized palliative care service, more often informed about imminent death as well as assessed for pain. For most national quality indicators, the goal level was not met. Only for the 'on demand prescription for pain', the goal level was reached.Conclusions: EOL care did not meet national quality indicators in this population-based data from Sweden, in particular in the elderly population. Elderly gynaecological cancer patients are at high risk of poorer EOL care without the involvement of specialized palliative care services. Palliative care services need to be implemented across all institutions of EOL care to ensure good and equal care.

Increasing the number of patients receiving information about transition to end-of-life care: the effect of a half-day physician and nurse training.

INTRODUCTION: Honest prognostication and information for patients are important parts of end-of-life care. This study examined whether an educational intervention could increase the proportion of patients who received information about the transition to end-of-life (ITEOL care). METHOD: Two municipalities (in charge of nursing homes) and two hospitals were randomised to receive an interactive half-day course about ITEOL for physicians and nurses. The proportion of patients who received ITEOL was measured with data from the Swedish Register of Palliative Care (SRPC). Patients were only included if they died an expected death and maintained their ability to express their will until days or hours before their death. Four hospitals and four municipalities were assigned controls, matched by hospital size, population and proportion of patients receiving ITEOL at baseline. RESULTS: The proportion of patients in the intervention group who received ITEOL increased from 35.1% (during a 6-month period before the intervention) to 42% (during a 6-month period after the intervention). The proportion in the control group increased from 30.4% to 33.7%. The effect of the intervention was significant (p=0.005) in a multivariable model adjusted for time, age, gender and cause of death. CONCLUSION: More patients at end-of-life received ITEOL after an educative half-day intervention directed to physicians and nurses.

Long-term lithium treatment in bipolar disorder is associated with longer leukocyte telomeres.

Telomere shortening is a hallmark of aging and has been associated with oxidative stress, inflammation and chronic somatic, as well as psychiatric disorders, including schizophrenia and depression. Additionally, antidepressants have been found to protect against telomere shortening. However, pharmacological telomere studies are lacking in bipolar disorder (BD). Therefore, the objective of this study was to explore telomere length (TL) in patients with BD in the context of lithium treatment. We determined TL by quantitative real-time PCR using peripheral blood leukocytes. Participants were outpatients diagnosed with BD type 1 or 2 (n=256) and healthy controls (n=139). Retrospective case-control and case-case study designs were applied. Lithium response (LiR) was scored using the Alda-Scale. Lithium-treated BD patients overall, as well as those on lithium monotherapy, had 35% longer telomeres compared with controls (P<0.0005, partial η(2)=0.13). TL correlated positively with lithium treatment duration of >30 months (P=0.031, R(2)=0.13) and was negatively associated with increasing number of depressive episodes (P<0.007). BD patients responding well to lithium treatment had longer telomeres than those not responding well. This is the first study to report a positive effect of long-term lithium treatment on TL. Importantly, longer TL was also associated with a better LiR in BD patients. These data suggest that lithium exerts a protective effect against telomere shortening especially when therapeutically efficacious. We hypothesize that induction of telomerase activity may be involved in LiR in BD.

Amphetamines for improving recovery after stroke.

BACKGROUND: Animal research shows that treatment with amphetamines improves recovery after focal cerebral ischaemia. If the effects are similar in humans, amphetamine treatment could have a major impact on recovery from stroke. OBJECTIVES: To assess the effects of amphetamine treatment in patients with stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched January 2006), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 1, 2006), MEDLINE (1966 to January 2006), EMBASE (1980 to January 2006), CINAHL (1982 to January 2006), CINAHL (1982 to January 2006), Science Citation Index (1992 to March 2005) and registers of ongoing trials. We also checked the reference lists of all relevant articles and reviews, and contacted researchers in the field. SELECTION CRITERIA: Randomized unconfounded trials comparing amphetamine with placebo. DATA COLLECTION AND ANALYSIS: Two review authors independently selected trials for inclusion and assessed trial quality; one extracted the data. MAIN RESULTS: Ten studies involving 287 patients were included, but not all trials contributed data to each outcome examined in this review. The quality of the trials varied but was generally high. Based on three trials (106 patients) there was no evidence that amphetamine treatment reduced death or dependence (Peto's odds ratio (Peto OR) 1.5, 95% confidence interval (CI) 0.6 to 3.3). Imbalances at baseline with more serious stroke allocated to amphetamine may account for the trend for more deaths at the end of follow up among amphetamine-allocated patients (Peto OR 2.8, 95% CI 0.9 to 8.6). Based on two trials (73 patients) systolic (weighted mean difference (WMD) 8.4 mm Hg, 95% CI 1.6 to 15.2) and diastolic (WMD 4.9 mm Hg, 95% CI 1.1 to 8.8) blood pressure, as well as heart rate, increased (WMD 10.6 bpm, 95% CI 3.3 to 17.8) in amphetamine-allocated patients. Based on six studies (176 patients) there was evidence of a better relative change from baseline to last follow up in motor function (WMD -6.1 points; 95% CI -10.4 to -1.9) Different results with different analysis approaches emphasize caution in the interpretation of the results. AUTHORS' CONCLUSIONS: At present, too few patients have been studied to draw any definite conclusions about the effects of amphetamine treatment on recovery from stroke. The suggested benefits on motor function and the non-significant trend towards increased risk of death could be related to imbalances in prognostic variables or other bias in the studies. Further research is therefore justified.

Amphetamines for improving recovery after stroke.

BACKGROUND: Experimental animal research shows that treatment with amphetamines improves recovery after focal cerebral ischaemia. If the effect were similar in humans, amphetamine treatment could have a major impact on recovery from stroke. OBJECTIVES: The objective of this review was to assess the effects of amphetamine treatment in patients with stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched November 2002). In addition, we searched the Cochrane Controlled Trials Register (Cochrane Library, Issue 4 2002), MEDLINE (1966-September 2002), EMBASE (1980-November 2002), and Science Citation Index (1992-December 2002). The reference lists of all relevant articles and reviews were checked, and we contacted researchers in the field to identify further published and unpublished studies. SELECTION CRITERIA: Randomized unconfounded trials comparing amphetamine with placebo. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected trials for inclusion, assessed trial quality and extracted the data. MAIN RESULTS: Seven studies involving 172 patients were included. The quality of the trials varied but was generally high. Based on two trials (85 patients) there was no evidence that amphetamine treatment reduced death or dependence (Peto's odds ratio, [Peto OR] 1.54; 95% Confidence Interval [CI] 0.64 to 3.73). In these two trials, there were imbalances at baseline, with more serious strokes allocated to amphetamine. This imbalance may account for the trend for more deaths at the end of follow-up among amphetamine allocated patients (Peto OR 3.33; 95% CI 0.99 to 11.24). Based on 4 studies (95 patients) there was evidence of a better relative change in motor function according to the Fugl-Meyer motor scale (Weighted Mean Difference, [WMD] -8.17 points; 95% CI -13.58 to -2.76) and based on 1 study (21 patients) there was evidence of a better change in language function as assessed by the Porch Index of Communicative Ability score (WMD -7.51 points; 95% CI -14.42 to -0.60) in amphetamine allocated patients. REVIEWER'S CONCLUSIONS: At present, too few patients have been studied to draw any definite conclusions about the effects of amphetamine treatment on recovery from stroke. The suggested benefits on motor and language function, and the non-significant trend towards increased risk of death, could be related to imbalances in prognostic variables or other bias in studies. Further research in this area is therefore justified.

Determination of RN(-) phenotype in pigs at slaughter-line using visual and near-infrared spectroscopy.

The specific characteristics of meat from the Hampshire breed of pig, including high glycogen content and low ultimate pH and technological yield, have been associated with the dominant RN gene. In Sweden, purebred Hampshire or Hampshire x Yorkshire is often used as terminal sire in the three-way crosses used for pig meat production. For the industry producing cured and cooked hams there is a need to detect the RN(-) carriers of the pigs early post mortem in order to select non-carriers for ham production. In the present study, the possibility of separating RN(-) carriers from non-carriers using a combination of visual and near-infrared (NIR) spectroscopic measurements in reflectance mode through a fibre-optic probe has been studied on commercial pigs in a slaughterhouse. The NIR measurements were performed 30 min post-mortem. Sixty-three animals were considered to be carriers and 33 animals non-carriers based on their glycolytic potential in M. semimembranosus (above 200 µmol/g for RN(-)rn(+) and below 180 µmol/g for rn(+)rn(+)). By using NIR together with classification with neural networks, RN(-) carriers could be separated from non-carriers. None of the carriers and only four non-carriers of the RN gene were misclassified as carriers of the RN gene. The ultimate pH could be predicted using linear partial least squares regression with a correlation coefficient of 0.57 and an accuracy of 0.074 root mean square error of prediction.

New concepts for drug therapy after stroke. Can we enhance recovery?

Neurologic functions improve in most patients days and weeks after onset of a stroke. This can not be explained by recovery of the early salvageable ischemia zone. The most likely mechanism is relearning, a process in which healthy brain takes over functions lost with the infarct. Experimental studies indicate that this recovery can be modulated by pharmacological agents. NMDA antagonists and GABA agonists found to reduce infarct size in stroke models may have a harmful effect on relearning and neurologic recovery. This should be considered when clinical trial protocols are designed.

Two-Dimensional Visualization of Fluorescence Lifetimes by use of a Picosecond Laser and a Streak Camera.

Two-dimensional distributions of the effective lifetime of the fluorescence emission induced by short-pulsed laser radiation are obtained from two-dimensional images recorded with a streak camera and a charge-coupled device by means of a separation algorithm method (SAM). In theory, the best response with respect to noise is obtained for lifetimes corresponding to a range of pixels of 5-50 in the CCD, that is, 5-50 ps at the fastest streak speed. In experiments the SAM is compared with pure time-resolved measurements, and it is used for two-dimensional lifetime evaluation. The laser-pulse duration is 25 ps, and the lower limit of the lifetime resolution as used in the experiments is estimated to be 200-250 ps. The results demonstrate the possibility of performing pattern recognition independently of the relative distribution of emission intensity between regions of different fluorescence lifetimes. The technique is demonstrated for static objects but can in principle be extended to nonstationary objects if two detectors are used.

The blood-brain barrier in adrenaline-induced hypertension. Circadian variations and modification by beta-adrenoreceptor antagonists.

Rats were subjected to adrenaline-induced acute hypertension during either the day or night. Albumin leakage into the brain was studied with Evans blue and 125I labeled serum albumin. The leakage was significantly lower during the night than during the day (P less than 0.001). d,1-propranolol had a protective effect (P less than 0.001) during the day and a slight reduction of the radioactivity (P less than 0.05 in some parts of the brain) was obtained by metoprolol (10 mg/kg) but not by butoxamine (10 mg/kg). None of the drugs reduced the tracer leakage during the night. The results suggest that the degree of alertness is of importance for the function of the blood-brain barrier in acute hypertension. However, the present experimental situation does not allow a separation of the effect of alertness per se and dark/light cycles. The changed vulnerability during the night could be related to enhanced neuronal activity, altered beta-adrenoreceptor sensitivity or to hormonal factors.

Blood-brain barrier to albumin in awake rats in acute hypertension induced by adrenaline, noradrenaline or angiotensin.

Acute hypertension was induced by adrenaline, noradrenaline or angiotensin in awake unrestrained rats with chronic indwelling catheters in a jugular vein and in the aorta. The leakage of 125IHSA (human serum albumin) into the brains from rats given adrenaline was significantly larger than in the brains from rats given noradrenaline or angiotensin. It is likely that the enhanced vulnerability of the blood-brain barrier to an adrenaline-induced increase in blood pressure is due to the beta-adrenergic stimulating effect of adrenaline.