Familiengründung in Deutschland

Background

Based on the declining birth rates in Germany, one might assume that there are a growing number of people who would like to have children but are unable to. However, studies conducted over the past few years have shown that in fact the number of people who choose not to have children is on in the rise.

Methods

This report gives an overview of the current demographic situation and presents the results of a longitudinal study.

Results

Starting a family is a relatively stabile objective in life. However, only a minority of respondents currently wanted to have a child, while two thirds did not wish to have one at present. Women have children earlier than men. The ideal number of children is generally higher than the actual number. Pregnancies are often planned, but they are not always realised.

Conclusions

Since a large number of individuals and couples in Germany postpone the realisation of their desire to have a child, it can be assumed that this voluntary childlessness may result in involuntary childlessness. Education about fertility as a valuable resource should thus be promoted.     

Einzelreferate und Buchbesprechungen

Ohne Zusammenfassung     

Suramin induces and enhances apoptosis in a model of hyperoxia-induced oligodendrocyte injury

Recent evidence suggests oxygen as a powerful trigger for cell death in the immature white matter, leading to periventricular leukomalacia (PVL) as a cause of adverse neurological outcome in survivors of preterm birth. This oligodendrocyte (OL) death is associated with oxidative stress, upregulation of apoptotic signaling factors (i.e., Fas, caspase-3) and decreased amounts of neurotrophins. In search of neuroprotective strategies we investigated whether the polysulfonated urea derivative suramin, recently identified as a potent inhibitor of Fas signaling, affords neuroprotection in an in vitro model of hyperoxia-induced injury to immature oligodendrocytes. Immature OLs (OLN-93) were subjected to 80% hyperoxia (48 h) in the presence or absence of suramin (0, 30, 60, 120 microM). Cell death was assessed by flow cytometry (Annexin V, caspase-3 activity assay) and immunohistochemistry for activated caspase-3. Immunoblotting for the death receptor Fas, cleaved caspase-8 and the phosphorylated isoform of the serine-threonin kinase Akt (pAkt) was performed. Suramin lead to OL apoptosis and potentiated hyperoxia-induced injury in a dose-dependent manner. Immunoblotting revealed increased Fas and caspase-8 expression by suramin treatment. This effect was significantly enhanced when suramin was combined with hyperoxia. Furthermore, pAkt levels decreased following suramin exposure, indicating interference with neurotrophin-dependent growth factor signaling. These data indicate that suramin causes apoptotic cell death and aggravates hyperoxia-induced cell death in immature OLs. Its mechanism of action includes an increase of previously described hyperoxia-induced expression of pro-apoptotic factors and deprivation of growth factor dependent signaling components.     

Two types of mitochondrial crystals in diseased human skeletal muscle fibers

Mitochondrial crystalline inclusions, frequently found in mitochondrial myopathies, were analyzed by crystallographic techniques and computer-aided image processing. It could be shown that these structures were real crystals. There are two distinct types of crystal, which can be distinguished by shape, size, and pattern. So-called type I crystals are usually present in the intracristal space, whereas the type II crystals are preferentially located in the intermembrane space between outer and inner mitochondrial membranes. The unit cell dimensions were found to be 38 x 34 x 8 nm for the type I crystals and 20 x 17 x 8 nm for the type II crystals. These results strongly suggest that the crystals are composed of macromolecules, presumably proteins. Arguments are presented that indicate that type I crystals occur only in type 1 muscle fibers and type II crystals in type 2 muscle fibers.     

血清胸苷激酶1检测对恶性肿瘤诊断及疗效评估的意义

目的探讨血清胸苷激酶1（TK1）作为肿瘤细胞增殖标志物对恶性肿瘤诊断及疗效评估的意义。方法应用免疫印迹-增强化学发光法检测恶性肿瘤组（53例）治疗前后、体格检查组（49例）以及健康对照组（18名）的血清TK1水平。治疗前与治疗后比较用配对t检验,治疗前和后分别与健康对照组、体格检查组比较采用两独立样本均数比较t检验。结果恶性肿瘤组治疗前STK1为0．3—11．3（2．4±2．0）pmol／L;恶性肿瘤组治疗后STK1为0．3～5．0（0．9±0．8）pmol／L;体格检查组STK1为0．1～2．1（0．8±0．3）pmol／L;健康对照组STK1为0．5～1．2（0．7±0．2）pmol／L。恶性肿瘤组治疗前与治疗后之间STK1水平差异有统计学意义（t=5．257,P〈0．0001）。恶性肿瘤组治疗前与健康对照组和体格检查组STK1水平比较,差异均有统计学意义（t=3．568和5．460,P=0．001和〈0．0001）,而恶性肿瘤组治疗后与健康对照组和体格检查组STK1水平比较,差异均无统计学意义（t=1．056和0．715,P均〉0．05）。结论血清TK1检测细胞增殖有较高的特异性和灵敏度,对临床监测恶性肿瘤疗效和在体格检查中进行恶性肿瘤风险筛查具有重要意义。     

Imaging proliferation in lung tumors with PET: 18F-FLT versus 18F-FDG.

Recently, the thymidine analog 3'-deoxy-3'-(18)F-fluorothymidine (FLT) was suggested for imaging tumoral proliferation. In this prospective study, we examined whether (18)F-FLT better determines proliferative activity in newly diagnosed lung nodules than does (18)F-FDG. METHODS: Twenty-six patients with pulmonary nodules on chest CT were examined with PET and the tracers (18)F-FDG and (18)F-FLT. Tumoral uptake was determined by calculation of standardized uptake value (SUV). Within 2 wk, patients underwent resective surgery or had core biopsy. Proliferative activity was estimated by counting nuclei stained with the Ki-67-specific monoclonal antibody MIB-1 per total number of nuclei in representative tissue specimens. The correlation between the percentage of proliferating cells and the SUVs for (18)F-FLT and (18)F-FDG was determined using linear regression analysis. RESULTS: Eighteen patients had malignant tumors (13 with non-small cell lung cancer [NSCLC], 1 with small cell lung cancer, and 4 with pulmonary metastases from extrapulmonary tumors); 8 had benign lesions. In all visible lesions, mean (18)F-FDG uptake was 4.1 (median, 4.4; SD, 3.0; range, 1.0-10.6), and mean (18)F-FLT uptake was 1.8 (median, 1.2; SD, 2.0; range, 0.8-6.4). Statistical analysis revealed a significantly higher uptake of (18)F-FDG than of (18)F-FLT (Mann-Whitney U test, P < 0.05). (18)F-FLT SUV correlated better with proliferation index (P < 0.0001; r = 0.92) than did (18)F-FDG SUV (P < 0.001; r = 0.59). With the exception of 1 carcinoma in situ, all malignant tumors showed increased (18)F-FDG PET uptake. (18)F-FLT PET was false-negative in the carcinoma in situ, in another NSCLC with a low proliferation index, and in a patient with lung metastases from colorectal cancer. Increased (18)F-FLT uptake was related exclusively to malignant tumors. By contrast, (18)F-FDG PET was false-positive in 4 of 8 patients with benign lesions. CONCLUSION: (18)F-FLT uptake correlates better with proliferation of lung tumors than does uptake of (18)F-FDG and might be more useful as a selective biomarker for tumor proliferation.