1,993 publications from this institution
This commentary highlights the importance of regular physical activity to the nation’s health and discusses some of the major challenges and opportunities currently facing the field.
National and international organizations recommend creation of environments that support physical activity where people live, work, play, study, and travel
We assessed the relationship between young children's movement skills and their physical activity in early adolescence. Balance, agility, eye-hand coordination, and skinfold thicknesses in 207 Mexican American and Anglo American children (104 boys, 103 girls) were measured at ages 4, 5, and 6 years. Habitual physical activity was assessed at the age of 12 years by two interviewer-administered 7-day recalls. Ethnic differences in movement skills were not found. Young girls were better at jumping and balancing, and young boys were better at catching. Tracking of skills was low, and children's early childhood skills were not related to their physical activity 6 years later. Further studies involving additional movement skills and other populations are recommended to determine if enhanced movement skills in children promote subsequent physical activity.
Nuclear factor-κB (NF-κB) transcription factors and their signaling pathways have come to the forefront of the cancer field as mechanistic links connecting chronic inflammation and oncogenesis (1). These master transcription factors integrate multiple stimuli and co-ordinate innate and adaptive immune responses involved in acute and chronic inflammation (2). Epidemiological studies which pointed out that chronic inflammation and persistent infections greatly increase the risk of cancers of stomach, colon, and liver first suggested a link between inflammation, the innate immune response, and cancer (3). NF-κB was suggested as the molecular culprit that bridges these pathophysiological states and responses (1). However, establishing the association between NF-κB signaling and oncogenesis has been a challenging task because NF-κB and its activating machinery are rarely mutated in cancer cells in the same way as classical oncogenes (like Ras) or tumor-suppressor genes (like p53). Nonetheless, much evidence has been gathered, both through correlative studies and through direct experimentation, that NF-κB signaling does indeed contribute to cancer development and progression, mainly in inflammation-associated cancers, but also in cancers where underlying chronic inflammation plays little or no role (for example, breast and prostate cancers). The list of human cancers that were found to exhibit constitutive NF-κB activation is long (see Table 29.1). Experimental evidence providing causality for NF-κB signaling in oncogenesis has accumulated over the past several years (4), and will be detailed in this chapter.
IKKalpha is specifically required for formation of cornea and conjunctiva. This function may be exerted through an effect on NF-kappaB activity.
A plethora of experimental and epidemiological evidence supports a critical role for inflammation and adaptive immunity in the onset of cancer and in shaping its response to therapy. These data are particularly robust for gastrointestinal (GI) cancers, such as those affecting the GI tract, liver, and pancreas, on which this review is focused. We propose a unifying hypothesis according to which intestinal barrier disruption is the origin of tumor-promoting inflammation that acts in conjunction with tissue-specific cancer-initiating mutations. The gut microbiota and its products impact tissue-resident and recruited myeloid cells that promote tumorigenesis through secretion of growth- and survival-promoting cytokines that act on epithelial cells, as well as fibrogenic and immunosuppressive cytokines that interfere with the proper function of adaptive antitumor immunity. Understanding these relationships should improve our ability to prevent cancer development and stimulate the immune system to eliminate existing malignancies.
