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This document presents statistical data on the status of women in full-time teaching positions in 164 college and university art departments. This status can best be summarized by the relationship, "the higher, the fewer." The percentage of women at various faculty ranks decreases steadily from instructor to full professor. Necessarily, the opposite is true for men. The data do not provide an answer to why "the higher, the fewer" relationship holds so pervasively. However, they do indicate that in those departments that have Ph.D.'s on their faculties, the percentage of women with Ph.D.'s exceeds the percentage of men by almost 25%. Hence, although women are concentrated at the lower ranks, they may be more highly trained on the average than their male colleagues. (Author/HS)

Selective inhibition of disease-related proteins underpins the majority of successful drug–target interactions. However, development of effective antagonists is often hampered by targets that are not druggable using conventional approaches. Here, we apply engineered zinc-finger protein transcription factors (ZFP TFs) to the endogenous phospholamban (PLN) gene, which encodes a well validated but recalcitrant drug target in heart failure. We show that potent repression of PLN expression can be achieved with specificity that approaches single-gene regulation. Moreover, ZFP-driven repression of PLN increases calcium reuptake kinetics and improves contractile function of cardiac muscle both in vitro and in an animal model of heart failure. These results support the development of the PLN repressor as therapy for heart failure, and provide evidence that delivery of engineered ZFP TFs to native organs can drive therapeutically relevant levels of gene repression in vivo. Given the adaptability of designed ZFPs for binding diverse DNA sequences and the ubiquity of potential targets (promoter proximal DNA), our findings suggest that engineered ZFP repressors represent a powerful tool for the therapeutic inhibition of disease-related genes, therefore, offering the potential for therapeutic intervention in heart failure and other poorly treated human diseases.

We hypothesize that the inositol 1,4,5-trisphosphate receptor (InsP3R) signaling pathway is crucial for the development of cardiac arrhythmia caused by paclitaxel treatment. Paclitaxel, a well established drug used for cancer chemotherapy, constrains tumor growth through a microtubule stabilizing mechanism. However, use of paclitaxel is limited by serious side effects including bradycardia, which cannot be explained by its effect on microtubules. Recently, a new binding partner of paclitaxel was described - neuronal calcium sensor-1 (NCS-1), a protein that modulates the function of the InsP3R and that we found to be expressed in cardiomoycytes. After treating neonatal ventricular cardiomyocytes from rats with a therapeutic dose of paclitaxel for several hours, NCS-1 levels were markedly elevated. The same effect was also detectable in vivo, in hearts extracted from adult mice chronically injected with paclitaxel. Using live cell imaging, we observed an increase in the peak of the intracellular calcium signal and a significant decrease in the spontaneous calcium oscillation frequency in paclitaxel treated cardiomyocytes compared to control. The changes could not be explained by the function of ryanodine receptors (RyR) because there is no functional interaction between NCS-1 and RyR, as previously shown in bilayer experiments, and no paclitaxel-dependent change in RyR expression. However, co-immunoprecipitation confirmed a direct interaction between NCS-1 and InsP3R type 2, the predominant isoform in cardiomyocytes. To test whether this interaction is functionally relevant, we stimulated cardiomyocytes with endothelin, an activator of the InsP3 signaling cascade and found a difference in calcium transients between paclitaxel-treated and untreated cardiomyocytes. NCS-1 knockdown in cardiomyocytes by shRNA validated our findings. Taken together, our results suggest that paclitaxel-induced cardiac arrhythmia in patients is mediated by the interaction of NCS-1 and the InsP3R. This gives us a new understanding of the pathomechanism and provides a new approach for reducing the side effects of paclitaxel treatment and optimizing cancer chemotherapy.

For women, achieving success in the art world—as artists or art historians—is difficult. As creative individuals in a male-dominated field, women in art share problems and aspirations with professional women in society as a whole. An inquiry into the value of women's studies in art and art history sheds light upon many problems inherent in the past and present politics of the art world, both within and outside of the university.1

The College Art Association Committee on the Status of Women (formerly the Women's Caucus of the C.A.A.) sent out a questionnaire to seek data on women faculty members in American colleges and universities, based on information published in their catalogues. 164 questionnaires were returned. Barbara Ehrlich White of the Dept. of Fine Arts, Tufts, University has prepared a statistical analysis of this information with the assistance of Leon S. White, a specialist in Operations Research at M.LT.The 164 departments came from institutions located in 29 states. 129 depart-ments offer art history and studio, 20 art history only, II studio only, 4 art education only.

The restoration of succinoxidase and succinic ferricyanide reductase in acetone-extracted electron-transport particles from beef heart mitochondria has been studied. In the succinoxidase system, coenzyme Q 10 and analogs with long isoprenoid chains require addition of accessory lipid material in order to be fully effective, whereas short-chain analogs are more effective without accessory lipids. The action of the accessory lipids is related to a positioning effect on the Q analogs, and it appears that no additional electron carrier function other than coenzyme Q is involved.

Behavioral and electrophysiological experiments were made to examine the hypothesis that G-proteins modulate the voltage-dependent calcium channel in the marine ciliate Paramecium calkinsi. It was found that guanosine-5’-O-(3-thiotriphosphate) (GTP-γ-S), an analogue of GTP that binds to and activates G-proteins, increased the duration of backward swimming behavior in reversibly permeabilized Paramecium in an irreversible and concentration-dependent manner. At 1 μmol 1−1 GTP-γ-S, the duration of backward swimming behavior was increased fivefold. Other nucleotides and related compounds did not have a significant effect on the backward swimming behavior. To evaluate whether the behavioral effects were due to ion channel modulation, the calcium action potential in intact Paramecium was monitored before and after guanine nucleotide injection. Within 5 min after the injection of GTP-γ-S or GTP into the cell, the duration of the calcium action potential was prolonged at least threefold. Like the behavioral response, the GTP-y-S effect on the calcium action potential duration was irreversible, whereas the effect of GTP began to decay after 6 min. GDP-β-S, which binds to and inactivates G-proteins, markedly reduced the calcium action potential within 5 min after injection. These results support the hypothesis that the voltage-dependent calcium channels present in Paramecium are modulated by GTP-binding proteins.