Evidence-based Kernels: Fundamental Units of Behavioral Influence

This paper describes evidence-based kernels, fundamental units of behavioral influence that appear to underlie effective prevention and treatment for children, adults, and families. A kernel is a behavior–influence procedure shown through experimental analysis to affect a specific behavior and that is indivisible in the sense that removing any of its components would render it inert. Existing evidence shows that a variety of kernels can influence behavior in context, and some evidence suggests that frequent use or sufficient use of some kernels may produce longer lasting behavioral shifts. The analysis of kernels could contribute to an empirically based theory of behavioral influence, augment existing prevention or treatment efforts, facilitate the dissemination of effective prevention and treatment practices, clarify the active ingredients in existing interventions, and contribute to efficiently developing interventions that are more effective. Kernels involve one or more of the following mechanisms of behavior influence: reinforcement, altering antecedents, changing verbal relational responding, or changing physiological states directly. The paper describes 52 of these kernels, and details practical, theoretical, and research implications, including calling for a national database of kernels that influence human behavior

Intra-articular injection of synovial mesenchymal stem cells improves cartilage repair in a mouse injury model

Controversy remains whether articular cartilage has an endogenous stem/progenitor cell population, since its poor healing capacity after injury can lead to diseases such as osteoarthritis. In the joint environment there are mesenchymal stem/progenitor cells (MSCs) in the synovial membrane and synovial fluid that can differentiate into cartilage, but it is still under debate if these cells contribute to cartilage repair in vivo. In this study, we isolated a Sca-1 positive, chondrogenesis capable population of mouse synovial MSCs from C57BL6 and MRL/MpJ “super-healer” strains. Intra-articular injection of Sca-1 + GFP + synovial cells from C57BL6 or MRL/MpJ into C57BL6 mice following cartilage injury led to increased cartilage repair by 4 weeks after injury. GFP expression was detected in the injury site at 2 weeks, but not 4 weeks after injury. These results suggest that synovial stem/progenitor cells, regardless of strain background, have beneficial effects when injected into an injured joint. MSCs derived from MRL/MpJ mice did not promote an increased repair capacity compared to MSCs derived from non-healing C57BL6 controls; however, MRL/MpJ MSCs were observed within the defect area at the time points examined, while C57BL6 MSCs were not

Screening, early diagnosis, genetic markers, and predictors of diabetic nephropathy

peer reviewedKidney disease in diabetes greatly diminishes quality and quantity of life, and is very expensive. Focused attention to the early stages of diabetic nephropathy is urgently needed, to define better thérapies that may slow it down or even stop its progression, thus reducing its heavy burden. This chapter will address screening, early diagnosis, genetic markers, and predictors of diabetic nephropathy

Localization of ion-regulatory epithelia in embryos and hatchlings of two cephalopods

The tissue distribution and ontogeny of Na+/K+-ATPase has been examined as an indicator for ion-regulatory epithelia in whole animal sections of embryos and hatchlings of two cephalopod species: the squid Loligo vulgaris and the cuttlefish Sepia officinalis. This is the first report of the immunohistochemical localization of cephalopod Na+/K+-ATPase with the polyclonal antibody α (H-300) raised against the human α1-subunit of Na+/K+-ATPase. Na+/K+-ATPase immunoreactivity was observed in several tissues (gills, pancreatic appendages, nerves), exclusively located in baso-lateral membranes lining blood sinuses. Furthermore, large single cells in the gill of adult L. vulgaris specimens closely resembled Na+/K+-ATPase-rich cells described in fish. Immunohistochemical observations indicated that the amount and distribution of Na+/K+-ATPase in late cuttlefish embryos was similar to that found in juvenile and adult stages. The ion-regulatory epithelia (e.g., gills, excretory organs) of the squid embryos and paralarvae exhibited less differentiation than adults. Na+/K+-ATPase activities for whole animals were higher in hatchlings of S. officinalis (157.0 ± 32.4 µmol gFM−1 h−1) than in those of L. vulgaris (31.8 ± 3.3 µmol gFM−1 h−1). S. officinalis gills and pancreatic appendages achieved activities of 94.8 ± 18.5 and 421.8 ± 102.3 µmolATP gFM−1 h−1, respectively. High concentrations of Na+/K+-ATPase in late cephalopod embryos might be important in coping with the challenging abiotic conditions (low pH, high pCO2) that these organisms encounter inside their eggs. Our results also suggest a higher sensitivity of squid vs. cuttlefish embryos to environmental acid-base disturbances

Diseases of Renal Microcirculation: Diabetic Nephropathy

The prevalence of diabetes mellitus and its long-term vascular complications are increasing worldwide. Diabetic nephropathy is one of the main microvascular complications of diabetes and is characterized by the development of persistent macroalbuminuria (i.e., a urinary albumin excretion [UAE] >300 mg/24 h) or proteinuria (i.e., a urinary protein excretion >0.5 g/24 h). Characteristic glomerular changes of diabetic nephropathy include thickening of the glomerular basement membrane (GBM), mesangial expansion, and podocyte injury. Since type 1 and type 2 diabetic nephropathies share similar histologic characteristics as well as structural-functional relationships, one common classification is used to describe the pathologic classification of diabetic nephropathy for both type 1 and 2 diabetes. Although UAE should rather be considered as a continuous variable rather than using specific cutoff values, we describe the clinical course of diabetic nephropathy based on the classic approach using three stages based on urinary albumin excretion (i.e., normoalbuminuria, microalbuminuria, and macroalbuminuria). Diabetic nephropathy is a major independent risk factor for diabetes-related morbidity and mortality. However, a number of interventions are available that can reduce the risk of developing diabetic nephropathy and slow the progression hereof. Key treatment strategies that could reduce the incidence and progression of diabetic nephropathy include blood glucose control, blood pressure control, lipid-lowering therapy, and lifestyle interventions