Cell adhesion and culture medium dependent changes in the high frequency mechanical vibration induced proliferation, osteogenesis, and intracellular organization of human adipose stem cells.

High frequency (HF) mechanical vibration appears beneficial for in vitro osteogenesis of mesenchymal stem cells (MSCs). However, the current mechanobiological understanding of the method remains insufficient. We designed high-throughput stimulators to apply horizontal or vertical high magnitude HF (HMHF; 2.5 Gpeak, 100 Hz) vibration on human adipose stem cells (hASCs). We analyzed proliferation, alkaline phosphatase (ALP) activity, mineralization, and effects on the actin cytoskeleton and nuclei using immunocytochemical stainings. Proliferation was studied on a standard tissue culture plastic (sTCP) surface and on an adhesion supporting tissue culture plastic (asTCP) surface in basal (BM) and osteogenic (OM) culture medium conditions. We discovered that the improved cell adhesion was a prerequisite for vibration induced changes in the proliferation of hASCs. Similarly, the adhesion supporting surface enabled us to observe vibration initiated ALP activity and mineralization changes in OM condition. The horizontal vibration increased ALP activity, while vertical stimulation reduced ALP activity. However, mineralization was not enhanced by the HMHF vibration. We performed image-based analysis of actin and nuclei to obtain novel data of the intracellular-level responses to HF vibration in BM and OM conditions. Our quantitative results suggest that actin organizations were culture medium and stimulation direction dependent. Both stimulation directions decreased OM induced changes in nuclear size and elongation. Consequently, our findings of the nuclear deformations provide supportive evidence for the involvement of the nuclei in the mechanocoupling of HF vibration. Taken together, the results of this study enhanced the knowledge of the intracellular mechanisms of HF vibration induced osteogenesis of MSCs.

Priming of host resistance to protect cultured rainbow trout Oncorhynchus mykiss against eye flukes and parasite-induced cataracts.

In the present study, immunologically naive rainbow trout Oncorhynchus mykiss were experimentally exposed to a low-level Diplostomum spathaceum (Trematoda) infection to stimulate acquired resistance and, along with unexposed controls, were subsequently exposed to natural infection for 8 weeks. The priming of the host resistance, designed to simulate a procedure applicable in aquaculture, decreased the number of establishing parasites compared to untreated controls by the end of the experiment. This effect was slow and did not protect the fish against the parasite-induced cataracts. The results suggest that this type of priming of host resistance is probably inefficient in preventing the deleterious effects of D. spathaceum infection in aquaculture conditions.

Insulin resistance and lipid levels in adolescents with familial risk for psychosis.

OBJECTIVE: Type 2 diabetes and dyslipidemias co-occur frequently with schizophrenia. It is not known how common they are in adolescents with a familial risk for psychosis. METHOD: The Northern Finland 1986 Birth Cohort consists of 9432 children born alive in the two Northernmost provinces in Finland. At the age of 15/16 they participated in clinical examination including measurements of glucose, lipids and IR, and a questionnaire including items about their diet and physical activity. The Finnish Hospital Discharge Register was used to find out non-organic psychoses in parents during 1972-2000. This familial risk was found out in 54 boys and 68 girls. Their results were compared with other cohort members. RESULTS: No differences were observed in the cardiometabolic risk factors between the study groups. CONCLUSION: Our results suggest that familial risk for psychosis is not directly associated with disturbances of glucose and lipid metabolism among adolescents.

A follow-up EEG study in diabetic children.

498 electroencephalograms (EEGs) were recorded from 195 diabetic children during a follow-up study. The children were divided into stable and labile groups according to diabetes control. The labile group was further subdivided into hypoglycaemic, ketoacidotic and mixed groups. In general it was found that the labile children had significantly more abnormal findings in their EEGs than the stable children, as expected. This applied particularly to generalized discharges with spikes and sharp waves or focal findings, but not to cases with only a diffuse-slowing. Nonstatistical differences in EEG abnormality were seen between the hypoglycaemic and ketoacidotic group--an unexpected finding. During the follow-up the labile group more often had an increasing EEG abnormality than the stable group. For those children who had an EEG abnormality but without an increasing tendency, there was no difference in the EEGs between the labile and stable children. It was concluded tht some of the EEG abnormalities are acquired, and apparently produced by a metabolic disturbance caused by diabetes. However, other causes may be of genetic or perinatal origin, or perhaps a combination of different causes. Because of the multifactorial aetiology of the abnormalities, EEG cannot at present be recommended for routine testing of the effects of metabolic disturbance in diabetics.