Religiosity and teen birth rate in the United States

<p>Abstract</p> <p>Background</p> <p>The children of teen mothers have been reported to have higher rates of several unfavorable mental health outcomes. Past research suggests several possible mechanisms for an association between religiosity and teen birth rate in communities.</p> <p>Methods</p> <p>The present study compiled publicly accessible data on birth rates, conservative religious beliefs, income, and abortion rates in the U.S., aggregated at the state level. Data on teen birth rates and abortion originated from the Center for Disease Control; on income, from the U.S. Bureau of the Census, and on religious beliefs, from the U.S. Religious Landscape Survey carried out by the Pew Forum on Religion and Public Life. We computed correlations and partial correlations.</p> <p>Results</p> <p>Increased religiosity in residents of states in the U.S. strongly predicted a higher teen birth rate, with r = 0.73 (p < 0.0005). Religiosity correlated negatively with median household income, with r = -0.66, and income correlated negatively with teen birth rate, with r = -0.63. But the correlation between religiosity and teen birth rate remained highly significant when income was controlled for via partial correlation: the partial correlation between religiosity and teen birth rate, controlling for income, was 0.53 (p < 0.0005). Abortion rate correlated negatively with religiosity, with r = -0.45, p = 0.002. However, the partial correlation between teen birth rate and religiosity remained high and significant when controlling for abortion rate (partial correlation = 0.68, p < 0.0005) and when controlling for both abortion rate and income (partial correlation = 0.54, p = 0.001).</p> <p>Conclusion</p> <p>With data aggregated at the state level, conservative religious beliefs strongly predict U.S. teen birth rates, in a relationship that does not appear to be the result of confounding by income or abortion rates. One possible explanation for this relationship is that teens in more religious communities may be less likely to use contraception.</p

Cactus pear: a natural product in cancer chemoprevention

BACKGROUND: Cancer chemoprevention is a new approach in cancer prevention, in which chemical agents are used to prevent cancer in normal and/or high-risk populations. Although chemoprevention has shown promise in some epithelial cancers, currently available preventive agents are limited and the agents are costly, generally with side effects. Natural products, such as grape seed, green tea, and certain herbs have demonstrated anti-cancer effects. To find a natural product that can be used in chemoprevention of cancer, we tested Arizona cactus fruit solution, the aqueous extracts of cactus pear, for its anti-cancer effects in cultured cells and in an animal model. METHOD: Aqueous extracts of cactus pear were used to treat immortalized ovarian and cervical epithelial cells, as well as ovarian, cervical, and bladder cancer cells. Aqueous extracts of cactus pear were used at six concentrations (0, 0.5, 1, 5, 10 or 25%) to treat cells for 1, 3, or 5 days. Growth inhibition, apoptosis induction, and cell cycle changes were analyzed in the cultured cells; the suppression of tumor growth in nude mice was evaluated and compared with the effect of a synthetic retinoid N-(4-hydroxyphernyl) retinamide (4-HPR), which is currently used as a chemoprevention agent. Immunohistochemistry staining of tissue samples from animal tumors was performed to examine the gene expression. RESULTS: Cells exposed to cactus pear extracts had a significant increase in apoptosis and growth inhibition in both immortalized epithelial cells and cancer cells in a dose- and time-dependent manner. It also affected cell cycle of cancer cells by increasing G1 and decreasing G2 and S phases. Both 4-HPR and cactus pear extracts significantly suppressed tumor growth in nude mice, increased annexin IV expression, and decreased VEGF expression. CONCLUSION: Arizona cactus pear extracts effectively inhibited cell growth in several different immortalized and cancer cell cultures, suppressed tumor growth in nude mice, and modulated expression of tumor-related genes. These effects were comparable with those caused by a synthetic retinoid currently used in chemoprevention trials. The mechanism of the anti-cancer effects of cactus pear extracts needs to be further studied

Phylostratigraphic tracking of cancer genes suggests a link to the emergence of multicellularity in metazoa

Background: Phylostratigraphy is a method used to correlate the evolutionary origin of founder genes (that is, functional founder protein domains) of gene families with particular macroevolutionary transitions. It is based on a model of genome evolution that suggests that the origin of complex phenotypic innovations will be accompanied by the emergence of such founder genes, the descendants of which can still be traced in extant organisms. The origin of multicellularity can be considered to be a macroevolutionary transition, for which new gene functions would have been required. Cancer should be tightly connected to multicellular life since it can be viewed as a malfunction of interaction between cells in a multicellular organism. A phylostratigraphic tracking of the origin of cancer genes should, therefore, also provide insights into the origin of multicellularity. Results: We find two strong peaks of the emergence of cancer related protein domains, one at the time of the origin of the first cell and the other around the time of the evolution of the multicellular metazoan organisms. These peaks correlate with two major classes of cancer genes, the 'caretakers', which are involved in general functions that support genome stability and the 'gatekeepers', which are involved in cellular signalling and growth processes. Interestingly, this phylogenetic succession mirrors the ontogenetic succession of tumour progression, where mutations in caretakers are thought to precede mutations in gatekeepers. Conclusions: A link between multicellularity and formation of cancer has often been predicted. However, this has not so far been explicitly tested. Although we find that a significant number of protein domains involved in cancer predate the origin of multicellularity, the second peak of cancer protein domain emergence is, indeed, connected to a phylogenetic level where multicellular animals have emerged. The fact that we can find a strong and consistent signal for this second peak in the phylostratigraphic map implies that a complex multi-level selection process has driven the transition to multicellularity

Articular cartilage and changes in Arthritis: Cell biology of osteoarthritis

The reaction patterns of chondrocytes in osteoarthritis can be summarized in five categories: (1) proliferation and cell death (apoptosis); changes in (2) synthetic activity and (3) degradation; (4) phenotypic modulation of the articular chondrocytes; and (5) formation of osteophytes. In osteoarthritis, the primary responses are reinitiation of synthesis of cartilage macromolecules, the initiation of synthesis of types IIA and III procollagens as markers of a more primitive phenotype, and synthesis of active proteolytic enzymes. Reversion to a fibroblast-like phenotype, known as 'dedifferentiation', does not appear to be an important component. Proliferation plays a role in forming characteristic chondrocyte clusters near the surface, while apoptosis probably occurs primarily in the calcified cartilage

The chrondoprotective actions of a natural product are associated with the activation of IGF-1 production by human chondrocytes despite the presence of IL-1β

BACKGROUND: Cartilage loss is a hallmark of arthritis and follows activation of catabolic processes concomitant with a disruption of anabolic pathways like insulin-like growth factor 1 (IGF-1). We hypothesized that two natural products of South American origin, would limit cartilage degradation by respectively suppressing catabolism and activating local IGF-1 anabolic pathways. One extract, derived from cat's claw (Uncaria guianensis, vincaria(®)), is a well-described inhibitor of NF-κB. The other extract, derived from the vegetable Lepidium meyenii (RNI 249), possessed an uncertain mechanism of action but with defined ethnomedical applications for fertility and vitality. METHODS: Human cartilage samples were procured from surgical specimens with consent, and were evaluated either as explants or as primary chondrocytes prepared after enzymatic digestion of cartilage matrix. Assessments included IGF-1 gene expression, IGF-1 production (ELISA), cartilage matrix degradation and nitric oxide (NO) production, under basal conditions and in the presence of IL-1β. RESULTS: RNI 249 enhanced basal IGF-1 mRNA levels in human chondrocytes by 2.7 fold, an effect that was further enhanced to 3.8 fold by co-administration with vincaria. Enhanced basal IGF-1 production by RNI 249 alone and together with vincaria, was confirmed in both explants and in primary chondrocytes (P <0.05). As expected, IL-1β exposure completely silenced IGF-1 production by chondrocytes. However, in the presence of IL-1β both RNI 249 and vincaria protected IGF-1 production in an additive manner (P <0.01) with the combination restoring chondrocyte IGF-1 production to normal levels. Cartilage NO production was dramatically enhanced by IL-1β. Both vincaria and RNI 249 partially attenuated NO production in an additive manner (p < 0.05). IL-1β – induced degradation of cartilage matrix was quantified as glycosaminoglycan release. Individually RNI 249 or vincaria, prevented this catabolic action of IL-1β. CONCLUSION: The identification of agents that activate the autocrine production of IGF-1 in cartilage, even in the face of suppressive pro-inflammatory, catabolic cytokines like IL-1β, represents a novel therapeutic approach to cartilage biology. Chondroprotection associated with prevention of the catabolic events and the potential for sustained anabolic activity with this natural product suggests that it holds significant promise in the treatment of debilitating joint diseases

Methods for assessing the regenerative responses of neural tissue

In order to establish novel therapeutic paradigms and advance the field of regenerative medicine, methods for their effective implementation as well as rigorous assessment of outcomes are critical. This is especially evident and challenging in the context of treating complex and devastating neurodegenerative disorders, such as Parkinson’s disease, multiple sclerosis, and ischemic stroke. Stem cell-based approaches offer great promise in addressing these conditions. Here, we demonstrate an approach for identifying factors that mobilize endogenous neural stem cells in the repair and recovery of the central nervous system of rodents, involving site-specific administration of growth factors that activate particular signal transduction pathways, and that allows for the assessment of outcome utilizing magnetic resonance imaging and immunohistochemistry