The effect of coeducational and same-sex cooperative learning groups on achievement

The purpose of this study was to explore the effects of coeducational and same sex cooperative learning groups on the achievement of first grade students. It is hypothesized that the academic performance of students in all subject areas while participating in a same-sex cooperative learning group will exceed their performance in the coeducational learning group. The subjects of this study were twenty-two first grade students from a southern New Jersey community. This study was divided into two experimental cycles – cycle A and cycle B. Cycle A included three weeks of coeducational cooperative learning groups and cycle B included three weeks of same-sex learning groups. After the two experimental cycles of this study were complete, the academic performance of males and females in the same-sex and coeducational cooperative learning groups was assessed. A t-test for non-independent samples was utilized which determines whether there was a significant difference between the means for the achievement of the males and females in the coeducational learning group and in the same-sex learning group. The t-test for nonindependent samples indicated a significance between the coeducational and same-sex learning groups

Does treatment of premature labor with terbutaline increase the risk of autism spectrum disorders?

Beta-adrenergic agents have been used in pregnant women for the treatment of premature labor and for the treatment of asthma. Concerns have been expressed that exposure to terbutaline, a beta-2 adrenergic agonist, may increase the risk of autism spectrum disorders (ASDs) in the offspring. This hypothesis deserves critical review, given the number of patients exposed to the drug in the last two decades. The results are important to both the obstetricians and patients who weigh the risks and benefits of interventions and to the pediatricians who counsel the families of affected children

Global Public Health Security

National public health institutes will play a key role in implementation of the revised International Health Regulations

Therapeutic Targeting of Replicative Immortality

One of the hallmarks of malignant cell populations is the ability to undergo continuous proliferation. This property allows clonal lineages to acquire sequential aberrations that can fuel increasingly autonomous growth, invasiveness, and therapeutic resistance. Innate cellular mechanisms have evolved to regulate replicative potential as a hedge against malignant progression. When activated in the absence of normal terminal differentiation cues, these mechanisms can result in a state of persistent cytostasis. This state, termed “senescence,” can be triggered by intrinsic cellular processes such as telomere dysfunction and oncogene expression, and by exogenous factors such as DNA damaging agents or oxidative environments. Despite differences in upstream signaling, senescence often involves convergent interdependent activation of tumor suppressors p53 and p16/pRB, but can be induced, albeit with reduced sensitivity, when these suppressors are compromised. Doses of conventional genotoxic drugs required to achieve cancer cell senescence are often much lower than doses required to achieve outright cell death. Additional therapies, such as those targeting cyclin dependent kinases or components of the PI3K signaling pathway, may induce senescence specifically in cancer cells by circumventing defects in tumor suppressor pathways or exploiting cancer cells’ heightened requirements for telomerase. Such treatments sufficient to induce cancer cell senescence could provide increased patient survival with fewer and less severe side effects than conventional cytotoxic regimens. This positive aspect is countered by important caveats regarding senescence reversibility, genomic instability, and paracrine effects that may increase heterogeneity and adaptive resistance of surviving cancer cells. Nevertheless, agents that effectively disrupt replicative immortality will likely be valuable components of new combinatorial approaches to cancer therapy

Rumors of disease in the global village: outbreak verification.

Emerging infectious diseases and the growth of information technology have produced new demands and possibilities for disease surveillance and response. Increasing numbers of outbreak reports must be assessed rapidly so that control efforts can be initiated and unsubstantiated reports can be identified to protect countries from unnecessary economic damage. The World Health Organization has set up a process for timely outbreak verification to convert large amounts of data into accurate information for suitable action. We describe the context and processes of outbreak verification and information dissemination

Surface plasmons of metallic surfaces perforated by nanoholes

Recent works dealt with the optical transmission on arrays of subwavelength holes perforated in a thick metallic film. We have performed simulations which quantitatively agree with experimental results and which unambiguously evidence that the extraordinary transmission is due to the excitation of a surface-plasmon-polariton (SPP) mode on the metallic film interfaces. We identify this SPP mode and show that its near-field possesses a hybrid character, gathering collective and localised effects which are both essential for the transmission.Comment: 16 pages, 4 figure

Therapeutic targeting of replicative immortality

One of the hallmarks of malignant cell populations is the ability to undergo continuous proliferation. This property allows clonal lineages to acquire sequential aberrations that can fuel increasingly autonomous growth, invasiveness, and therapeutic resistance. Innate cellular mechanisms have evolved to regulate replicative potential as a hedge against malignant progression. When activated in the absence of normal terminal differentiation cues, these mechanisms can result in a state of persistent cytostasis. This state, termed “senescence,” can be triggered by intrinsic cellular processes such as telomere dysfunction and oncogene expression, and by exogenous factors such as DNA damaging agents or oxidative environments. Despite differences in upstream signaling, senescence often involves convergent interdependent activation of tumor suppressors p53 and p16/pRB, but can be induced, albeit with reduced sensitivity, when these suppressors are compromised. Doses of conventional genotoxic drugs required to achieve cancer cell senescence are often much lower than doses required to achieve outright cell death. Additional therapies, such as those targeting cyclin dependent kinases or components of the PI3K signaling pathway, may induce senescence specifically in cancer cells by circumventing defects in tumor suppressor pathways or exploiting cancer cells’ heightened requirements for telomerase. Such treatments sufficient to induce cancer cell senescence could provide increased patient survival with fewer and less severe side effects than conventional cytotoxic regimens. This positive aspect is countered by important caveats regarding senescence reversibility, genomic instability, and paracrine effects that may increase heterogeneity and adaptive resistance of surviving cancer cells. Nevertheless, agents that effectively disrupt replicative immortality will likely be valuable components of new combinatorial approaches to cancer therapy