To compensate for increases in photon flux density (PFD), photosynthetic organisms possess mechanisms for reversibly modulating their photosynthetic apparatus to minimize photodamage. The photoacclimation response in Chlamydomonas reinhardtii was assessed following a 10‐fold increase in PFD over 24 h. In addition to a 50% reduction in the amount of chlorophyll and light‐harvesting complexes (LHC) per cell, the expression of genes encoding polypeptides of the light‐harvesting antenna were also affected. The abundance of Lhcb (a LHCII gene), Lhcb4 (a CP29‐like gene), and Lhca (a LHCI gene) transcripts were reduced by 65 to 80%, within 1–2 h; however, the RNA levels of all three genes recovered to their low‐light (LL) concentrations within 6–8 h. To determine the role of transcript turnover in this transient decline in abundance, the stability of all transcripts was measured. Although there was no change in the Lhcb or Lhca transcript turnover time, the Lhcb4 mRNA stability decreased 2.5‐fold immediately following high‐light (HL) stress. The Lhcb transcript abundance, on the other hand, was primarily dictated by the rate of transcription as determined using an arylsulphatase reporter gene system. Transcription from the Lhcb promoter was initially repressed in HL but recovered to the LL rate after 6–9 h. Interestingly, the LHCII and CP29 transcripts recovered to their prestress levels before there were significant reductions in the abundance of their corresponding polypeptides. Although there are short‐term alterations in transcription and transcript stability, the long‐term acclimation of the light‐harvesting antennae to HL occurs primarily at the translational level.

No abstract

The cornerstone of treatment for early-stage non-small cell lung cancer (NSCLC) has long been surgical resection. Over the past few years, there has been a paradigm shift to provide adjuvant platinum-based chemotherapy for patients with completely resected stage II-IIIA NSCLC founded on large randomized clinical trials demonstrating longer overall survival with this treatment. Reassuringly, the National Cancer Institute of Canada Cancer Therapeutics Group JBR.10 trial recently reported a continued survival advantage for patients treated with adjuvant chemotherapy after >9 years of median follow-up. In contrast, the gains from using this approach for stage IB disease are less clear, although data from an unplanned subgroup analysis suggest benefit for patients with tumors >4 cm. Herein, we review the evidence supporting adjuvant therapy in early-stage NSCLC patients before discussing key mitigating factors in providing treatment, such as stage of disease and the impact of the new seventh edition of the tumor-node-metastasis classification system. Criteria such as patient age and performance status, as well as the value of appropriate chemotherapy selection, are highlighted as measures to help guide management. The role of postoperative radiotherapy and the future landscape of early-stage NSCLC research are also explored; namely, therapeutic strategies exploiting pharmacogenomic and gene-expression profiling, in an attempt to personalize care, and the integration of novel targeted therapies into adjuvant clinical trials. The Oncologist 2010;15:862-872

We report six sibs with arthrogryposis multiplex congenita and a Pena-Shokeir phenotype, born to a healthy woman who was discovered to have asymptomatic myasthenia gravis (MG). This is the first report of anti-acetylcholine receptor (AChR) antibodies causing fetal akinesia/hypokinesia sequence in the offspring of an asymptomatic mother.

This study showed the presence of more than one biomarker was a stronger long-term predictor of incident dementia than any biomarker alone. After adjusting for the risk of dying, amyloid deposition and WMLs were stronger predictors of dementia than HIP volume. The risk of dying during follow-up was associated with both neurodegeneration and amyloid deposition, especially in individuals with MCI.

The role of cyclic adenosine monophosphate (cAMP) is poorly understood in the regulation of normal and abnormal hepatic cell growth. In this study, we examined the regulation of intracellular cAMP levels and its effect on nuclear cAMP responsive elements (CREs) in a rat model of hepatocellular carcinoma (HCC). Tumorigenic liver cells were cultured from an in vivo model of HCC and the role of cAMP in cell mitogenesis determined. These data demonstrated agents that elevate intracellular cAMP ([cAMP]i) levels caused significant dose-dependent inhibition of serum-stimulated mitogenesis in HCC cells. Cells were next analyzed for transcription factor expression and activity following increased [cAMP]i. These data demonstrated time- and dose-dependent increases in CRE binding protein (pCREB) activity, a maximal response occurring after 10-20 min before returning to basal levels within 60 min. In contrast, increased [cAMP]i levels led to sustained inducible cAMP early repressor (ICER) II/IIgamma mRNA and protein induction. To understand these data in relation to the in vivo setting, HCC tumors were analyzed and compared to pair-matched normal liver (NL) samples. These studies demonstrated significantly elevated Gsalpha-protein expression in HCC versus NL in the absence of significant changes in basal cAMP levels. Analysis of total and active CREB demonstrated significantly increased total CREB/pCREB in HCC versus NL. Further analysis of CRE expression demonstrated significantly increased expression of ICER mRNA and protein in HCC versus sham operated (Sh). These data demonstrate cAMP, while capable of stimulating promitogenic CREB activation inhibits cell mitogenesis in HCC possibly via ICER induction.

Informants described the complexity of the nature and dynamics of gender violence, strongly informed by Nicaragua's fairly progressive laws. The participants described holistic, fully integrated services as the intended functioning of the system. These services were often thwarted by gaps-fragmentation and lack of resources-and were additionally hampered by substantial individual and structural economical obstacles.

Background Individuals in treatment for alcohol use disorder (AUD) display deficits across a broad range of cognitive processes. Disruptions in affective processing are understudied, but may be particularly important for interpersonal functioning and post-treatment adaptation. In particular, the role of sex in AUD-associated emotion processing deficits remains largely unaddressed and was a focus of the current investigation. Methods Fifty-six treatment seekers with AUD and 54 healthy community controls (N = 110) were administered an emotional face discrimination task. Non-affective tasks included a sex-discrimination task and two brief measures of executive functioning. Two measures of interpersonal function were included. Results Emotion processing deficits were evident among women with AUD relative to other groups. This sex-contingent relationship was not observed in measures of executive function, sex-discrimination or interpersonal problems, although individuals with AUD performed more poorly on these measures. Conclusions Results were consistent with extant literatures examining cognitive, affective and interpersonal functioning among individuals with AUD, and provided novel evidence of vulnerability to alcohol-associated deficits in emotion processing among women. While similar sex-contingent effects were not apparent among other measures, results support modest interrelationships, specifically including the import of emotion processing to interpersonal functioning in AUD. These data offer guidance for further systematic investigation and highlight important considerations for future relapse-prevention and recovery-facilitation efforts.