Growth and biochemical characteristics of a detachment variant of CHO cells.

A variant subline of Chinese hamster cells (line CHO) was isolated that had increased resistance to detachment from the substratum. Comparisons between parental and variant cells of the complex carbohydrates liberated during trypsin detachment showed that the variant cells synthesized little or no hyaluronic acid. These cells also had reduced amounts of other complex carbohydrates in the cell periphery. However, parental and variant cells did not differ in morphology, growth control, or cyclic AMP concentration. Profound changes in the physical nature of the cell periphery, in themselves, evidently are insufficient to cause changes in many aspects of cell behavior.     

Oxygen consumption following exercise of moderate intensity and duration.

To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age = 27.6 (SD 3.8) years, VO2max = 46.1 (SD 8.5) ml min-1 kg-1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO2max, 40 min at 60% VO2max, 20 min at 70% VO2max, and 40 min at 70% VO2max). O2 uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO2 rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P < 0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO2 returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO2max) or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.     

Age-Related Modulation of the Effects of Obesity on Gene Expression Profiles of Mouse Bone Marrow and Epididymal Adipocytes

This study aimed to characterize and compare the effects of obesity on gene expression profiles in two distinct adipose depots, epididymal and bone marrow, at two different ages in mice. Alterations in gene expression were analyzed in adipocytes isolated from diet-induced obese (DIO) C57BL/6J male mice at 6 and 14 months of age and from leptin deficient mice (ob/ob) at 6 months of age using microarrays. DIO affected gene expression in both depots at 6 and 14 months, but more genes were altered in epididymal than bone marrow adipocytes at each age and younger mice displayed more changes than older animals. In epididymal adipocytes a total of 2789 (9.6%) genes were differentially expressed at 6-months with DIO, whereas 952 (3.3%) were affected at 14-months. In bone marrow adipocytes, 347 (1.2%) genes were differentially expressed at 6-months with DIO, whereas only 189 (0.66%) were changed at 14-months. 133 genes were altered by DIO in both fat depots at 6-months, and 37 genes at 14-months. Only four genes were altered in both depots at both ages with DIO. Bone marrow adipocytes are less responsive to DIO than epididymal adipocytes and the response of both depots to DIO declines with age. This loss of responsiveness with age is likely due to age-associated changes in expression of genes related to adipogenesis, inflammation and mitochondrial function that are similar to and obscure the changes commonly associated with DIO. Patterns of gene expression were generally similar in epididymal adipocytes from ob/ob and DIO mice; however, several genes were differentially expressed in bone marrow adipocytes from ob/ob and DIO mice, perhaps reflecting the importance of leptin signaling for bone metabolism. In conclusion, obesity affects age-associated alterations in gene expression in both epididymal and bone marrow adipocytes regardless of diet or genetic background.     

Revisiting recent etiological theories of functions

Arguably, the most widely endorsed account of normative functions in philosophy of biology is an etiological theory that holds that the function of current traits is fixed by the past selection history of other traits of that type. The earlier formulations of this “selected-effects” theory had trouble accommodating vestigial traits. In order to remedy these difficulties, the influential recent selection or modern history selected-effects theory was introduced. This paper expands upon and strengthens the argument that this theory has trouble stemming from recent “no variation” cases. In addition, several influential arguments for the necessity of including a selection requirement in a theory of normative biological functions are contested. It is suggested that accounting for biological functions in certain areas of biology (such as physiology and the neurosciences) does not require adverting to selection.     

Growth hormone pulsatility profile characteristics following acute heavy resistance exercise.

This investigation examined the hypothesis that acute heavy resistance exercise (AHRE) would increase overnight concentrations of circulating human growth hormone (hGH). Ten men (22 +/- 1 yr, 177 +/- 2 cm, 79 +/- 3 kg, 11 +/- 1% body fat) underwent two overnight blood draws sampled every 10 min from 1700 to 0600: a control and an AHRE condition. The AHRE was conducted from 1500 to 1700 and was a high-volume, multiset exercise bout. Three different immunoassays measured hGH concentrations: the Nichols immunoradiometric assay (Nichols IRMA), National Institute of Diabetes and Digestive and Kidney Diseases radioimmunoassay (NIDDK RIA), and the Diagnostic Systems Laboratory immunofunctional assay (DSL IFA). The Pulsar peak detection system was used to evaluate the pulsatility profile characteristics of hGH. Maximum hGH was lower in the exercise (10.7 microg/l) vs. the control (15.4 microg/l) condition. Mean pulse amplitude was lower in the exercise vs. control condition when measured by the Nichols IRMA and the DSL IFA. A differential pattern of release was also observed after exercise in which hGH was lower in the first half of sleep but higher in the second half. We conclude that AHRE does influence the temporal pattern of overnight hGH pulsatility. Additionally, because of the unique molecular basis of the DSL IFA, this influence does have biological relevance because functionally intact molecules are affected.     

Rat embryo fibroblasts transformed by c-Jun display highly metastatic and angiogenic activities in vivo and deregulate gene expression of both angiogenic and antiangiogenic factors.

The comparative tumorigenicity in rats and nude mice of cell lines derived from FR3T3 and transformed by either c-jun, ras, SV40 lt, or bovine papilloma virus type 1 (BPV1) oncogenes was investigated. c-Jun-transformed cells were as tumorigenic and metastatic as Ras-transformed cells. Latencies were short, and numerous pulmonary metastases were observed in all injected animals. In contrast, tumors induced by s.c. injection of SV40-transformed cells developed slower, and none of the animals who received injections i.v. presented with metastases. BPV1-transformed cells had an intermediate tumorigenic and metastatic activity. Microvessels present in the different tumors were revealed by immunostaining with Griffonia (Bandeiraea) Simplicifolia lectin 1. Tumors obtained with c-Jun-transformed cells exhibited more neovascularization than those induced by the other oncogenes. By comparison to FR3T3 cells or SV40- or BPV1-transformed cells, c-Jun-transformed fibroblasts repress the antiangiogenic thrombospondin-1 and SPARC genes, whereas we found that they express higher levels of gene expression of the angiogenic vascular endothelial growth factor. Finally, as compared with cells before passage in animals, thrombospondin-1, SPARC, and VEGF gene expression was also deregulated in cell lines isolated from primary tumors induced by BPV1-transformants. Our results indicate that the high transforming potential of c-Jun, evidenced as soon as transformation is established in vitro, correlates with deregulation of gene expression of both angiogenic and antiangiogenic factors leading to rapid neovascularization of tumors.