Mortality and causes of death among asylum seekers in the Netherlands, 2002-2005.

BACKGROUND: The world's growing population of asylum seekers faces different health risks from the populations of their host countries because of risk factors before and after migration. There is a current lack of insight into their health status. METHODS: A unique notification system was designed to monitor mortality in Dutch asylum seeker centres (2002-2005). RESULTS: Standardised for age and sex, overall mortality among asylum seekers shows no difference from the Dutch population. However, it differs between subpopulations by sex, age and region of origin and by cause of death. Mortality among asylum seekers is higher than among the Dutch reference population at younger ages and lower at ages above 40. The most common causes of death among asylum seekers are cancer, cardiovascular diseases and external causes. Increased mortality was found from infectious diseases (males, standardised mortality ratio (SMR)=5.44 (95% CI 3.22 to 8.59); females, SMR=7.53 (95% CI 4.22 to 12.43)), external causes (males, SMR=1.95 (95% CI 0.52 to 2.46); females SMR=1.60 (95% CI 0.87 to 2.68)) and congenital anomalies in females (SMR 2.42; 95% CI 1.16 to 4.45). Considerable differences were found between regions of origin. Maternal mortality was increased (rate ratio 10.08; 95% CI 8.02 to 12.83) as a result of deaths among African women. CONCLUSION: Certain subgroups of asylum seekers (classified by age, sex and region of origin) are at increased risk of certain causes of death compared with the host population. Policies and services for asylum seekers should address both causes for which asylum seekers are at increased risk and causes with large absolute mortality, taking into account differences between subgroups.

Cell proliferation kinetics of six xenografted human cervix carcinomas: comparison of autoradiography and bromodeoxyuridine labelling methods.

Cell kinetic and histologic parameters of six xenografted tumours with volume doubling times ranging from 6 to 43 d were investigated in order to obtain kinetic information on a panel of tumours to be used in radiobiological studies. The six tumours covered a range of histologies and their DNA indices varied from 2.7 to 1.4. The length of the cell cycle (Tc), potential doubling time (Tpot) and labelling index (LI) were determined by continuous labelling with [3H]TdR and autoradiography in three tumours, Tc varied from 30 to 40 h. Determinations of the length of the S phase (Ts) were found to be less reliable by this method. Data on Ts and LI were also determined in all six tumours using bromodeoxyuridine (Brd) labelling and the single sample method: values of Tpot were slightly longer than those obtained via the autoradiographic method. In addition, multiple samples were taken after BrdU labelling. Tc was determined by fitting the data obtained from mid-S, mid-G2 and mid-G1 windows to curves described by a damped oscillator. Data obtained via the mid-S window were found to be most reliable. Generally, cell cycle times obtained by the BrdU method were longer than those observed with the autoradiographic method. Differences between the two methods could be explained by inaccuracies in the determination of Ts, LI and Tc and differences in the experimental approach. We consider the BrdU labelling method to be a suitable alternative for the time-consuming autoradiography, if data on Ts or Tpot are sufficient. Due to difficulties in the reproducibility of the immunofluorescence staining and asynchronization of cells approximately 10 h after labelling, the method of windows analysis was affected by similar problems to those observed in interpretation of percentage labelled mitosis (PLM) curves. However, the method may serve as an alternative to determine cell cycle times in vitro and, if improved technically, in vivo. Careful comparison of the data obtained from mid-S, mid-G1 and mid-G2 windows may increase the reliability of the determination of cell kinetic parameters.

The relationship between radiosensitivity and cell kinetic effects after low- and high-dose-rate irradiation in five human tumors in nude mice.

Radiation-induced synchronization of cells in the radiosensitive G2 phase can, theoretically, be applied to individual tailoring of fractionation schemes, possibly rendering radiotherapy more effective. For that purpose, cell cycle perturbations were studied in five xenografts by flow cytometry. A dose-dependent increase of cells in G2 phase was noticed in all five tumor cell lines after high-dose-rate irradiation, and in four tumor cell lines after low-dose-rate irradiation. The timing of maximum accumulation was not related to dose, but coincided with the cell cycle time of the respective tumors. Furthermore, the increase in the number of cells in G2 phase correlated with the radiosensitivity of the tumors as assessed by measurements of regrowth delays. The observed synchronization provides a basis for further investigations on the relevance of radiation-induced cell cycle synchrony to the effectiveness of fractionated radiotherapy.

Cell cycle traverse in NHIK-3025 carcinoma of the uterine cervix after low-dose-rate irradiation.

Theoretically, fractionation schemes could be tailored to the individual pattern of radiation-induced synchronization of cells in the radiosensitive G2 phase, leading to more effective radiotherapy. Using a human cervical carcinoma xenografted to nude mice, the effects of low-dose-rate irradiation on the cell cycle distribution were studied. Flow cytometric analysis demonstrated that cells accumulated in G2 + M phase 35 h after a total dose of 10 Gy of 137Cs irradiation. This accumulation time corresponded closely to the cell cycle time (Tc) (31 h) of this tumor, as determined by autoradiography. Further experiments are planned to determine the potential of fractionation schemes adjusted to the Tc-related accumulation in G2 in improving the effectiveness of radiotherapy.

Relationship between cell kinetics and radiation-induced arrest of proliferating cells in G2: relevance to efficacy of radiotherapy.

Monitoring the radiation-induced G2-arrest with flow cytometry disclosed the relationship between the pattern of accumulation in G2 and the cell kinetics (Tc), as assessed with semi-continuous labelling. A close relationship between these two parameters was observed in a murine mammary tumour after high dose-rate irradiation and in human cervix tumours (xenografted and in patients) after low dose-rate irradiation. In inoperable tumours of the oral cavity, a G2-arrest, observed in the first two weeks of fractionated therapy, was found to predict a local cure. Consequently, it was concluded that the cells accumulated in G2 were not doomed cells. This process of radiation-induced synchronization might be exploited in fractionation schemes of which treatment intervals are adjusted to the Tc-related timing of the radiation-induced G2-arrest.

Impaired energy metabolism in platelets from patients with Wiskott-Aldrich syndrome.

The platelet function defect seen in patients with Wiskott-Aldrich syndrome (WAS) has been ascribed to abnormal mitochondrial energy generation. The present study reveals a reduced energy content and low adenylate energy charge in platelets from two WAS-patients. Energy consumption in the resting platelets is slightly beyond the normal range, especially when ATP-resynthesis is primarily glycolytic. When platelets are stimulated with thrombin, the increase in energy consumption is 40-60% lower than in controls, both when energy is produced in glycolysis as when the mitochondria supply most of the energy. Analysis of the electron transport chain reveals no abnormalities. In contrast, the balance between glycolytic and mitochondrial ATP resynthesis is disturbed with a lowered contribution of oxidative ATP production. No such abnormalities are found in two WAS-carriers with the exception of a slight impairment in energy consumption during stimulation with thrombin. Thus, the platelet malfunction in WAS may be caused by a defect in the regulation of energy generation.