Background Previous studies have shown that poor family environments are related to more sleep problems; however, little is known about how family irregularity in early life affects the development of sleep problems over childhood using objective sleep measures. The current study tests the hypothesis that early family irregularity contributes to the development of sleep problems. Methods This population‐based study comprises 5,443 children from the Generation R Study. Family irregularity was measured with seven maternal‐reported questions on family routines when children were 2 and 4 years old. Mothers reported on sleep problems at child age 3, 6, and 10 years, whereas children completed questionnaires on sleep problems at age 10. Additionally, we used tri‐axial wrist accelerometers for five nights in 851 children (mean age 11.7 years) to assess sleep objectively. Results Family irregularity was associated with more mother‐ and child‐reported sleep problems at ages 3, 6, and 10 years as well as with a shorter sleep duration and later objective sleep onset, but not with sleep efficiency or waking time. The association between family irregularity and multi‐informant subjective sleep problems at age 10 years was mediated by mother‐reported child psychopathology at age 6 years. Conclusions Our findings show a long‐term robust association of preschool family irregularity with more sleep problems during childhood as well as shorter sleep duration and later sleep onset as measured objectively with actigraphy. In part, these sleep problems were associated with family irregularity by way of child psychopathology. These findings suggest that interventions improving preschool family irregularity, which are targeted to reduce child psychopathology, may also impact the development of sleep problems beneficially.

The aim of this study was to investigate expression of cyclin D1, bcl-2, p53, Ki-67 and HER-2 proteins in 14 cases of non-small cell lung cancer and to establish their correlation to classical clinico-pathological findings, and alleged prognostic value to estimate biological potential of tumor. Retrospective pilot study of the surgically treated non-small cell lung cancer biopsy specimen, paraffin embedded, used immunohistochemical method to demonstrate expression of cyclin D1, bcl-2, p53, Ki-67 and HER-2. Protein quantification was performed by the semi-quantitative method. Achieved results were correlated with classical clinico-pathological parameters, like tumor size, histological type, differentiation level, presence of vascular invasion and metastasis in regional lymph nodes. Out of 14 cases of non-small cell lung cancer, squamous cell carcinoma was found in 7 patients, giant cell carcinoma in 3, adenocarcinoma in 2, and 1 case of pleomorphic and mucoepidermoid carcinoma. Expression of cyclin D1 was not found, while expression of HER-2 and bcl-2 protein was established in one cases each. p53 expression was noted in 8 cases (57,1%). Statistically positive significant correlation (p<0,05) was found among: presence of lymphovascular invasion to tumor tissue and appearance of nodal metastasis; proliferation Ki-67 index and level of tumor differentiation, i.e. size of tumor. Other investigated parameters showed no significant statistically dependence. p53 expression was not correlated to any of the investigated parameters what might imply the possibility that there is an independent pathway of this protein expression. Negative expression of bcl-2 protein points out to possibility that it is not included into process of tumor apoptosis, as well as that proteins cyclin D1 and HER-2 are not included into processes of the tumor genesis. Since the proliferative activity of the tumor, measured by the expression of Ki-67, is correlated to the gradus and size of the tumor mass, Ki-67 protein can be of a prognostic value to determine biological potential of non-small cell lung cancer.

Retrospective study was conducted in surgical intensive care unit (ICU) in Clinical Hospital Center Zagreb in 2005. The aim of study was to create guidelines for empirical antibiotic therapy of sepsis in ICU for unknown causative agent based on antimicrobial susceptibility of causative bacteria. Thirty-two patients with severe sepsis were included in study and from medical records their clinical and microbiological data were analyzed. Antimicrobial susceptibility of the strains isolated from the blood-culture was tested by disk diffusion method according to CLSI (Clinical Laboratory Standard Institution). We used APACHE II score to predict the severity of illness. Mann-Whitney test and chi2 test were used to test statistical significance difference between results. Acinetobacter baumannii and Pseudomonas aeruginosa were the predominant causative agent. Acinetobacter baumannii was displaying excellent susceptibility to ampicillin+sulbactam and carbapenems, whereas Pseudomonas aeruginosa was showed good susceptibility on ceftazidim and carbapenems. Methicillin-resistant Staphylococcus aureus (MRSA), third predominant causative agent exhibiting good susceptibility to vancomycin and linezolide. The recommended therapy is empirical antibiotic therapy and should cover all important pathogens.