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Reports on a method by which human and bovine capillary endothelial cells were switched from growth to apoptosis. Methods used; Results; Cell shape found to govern whether individual cells grow or die; Local geometric control of cell growth and viability; Mechanism for developmental regulation within the tissue microenvironment.

Studies a tripeptide containing alternating imidazole and pyrrole carboxamides and with specific binding abilities to six-base pair 5'-(A,T)GCGC(A,T)-3' sites in the minor groove of DNA. Binding patterns of peptides; Antiparallel orientation in minor groove; Recognition of a specific guanine amino group in the GCGC core through a hydrogen bond.

Dip-pen nanolithography was used to construct arrays of proteins with 100- to 350-nanometer features. These nanoarrays exhibit almost no detectable nonspecific binding of proteins to their passivated portions even in complex mixtures of proteins, and therefore provide the opportunity to study a variety of surface-mediated biological recognition processes. For example, reactions involving the protein features and antigens in complex solutions can be screened easily by atomic force microscopy. As further proof-of-concept, these arrays were used to study cellular adhesion at the submicrometer scale. [ABSTRACT FROM AUTHOR]

Focuses on a method that uses the process of selective withdrawal of one fluid through a second immiscible fluid to coat small particles with polymer films. Withdrawal of fluid through a tube with its orifice slightly above a water-oil interface; Major feature of spout collapse; Utilization of confocal and optical microscopies.

Introduction: The circadian clock is a transcriptional oscillator that is thought to couple internal energetic processes with the solar cycle. Circadian oscillation in activity of nicotinamide phosphoribo-syltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD+) bio-synthesis, feeds back to regulate activity of the deacetylase SIRT1 and transcription of genes encoding core clock components. Despite evidence that NAD+-dependent enzymes are important in fasting and oxidative metabolism, it is not known how the circadian cycle might affect this process. We investi-gated the role of clock control of NAD+ in mitochondrial dynamics and energy production. Methods: We monitored the response to fasting in liver of wild-type and circadian mutant mice. Quantitative analyses of NAD+ biosynthesis, lipid and glucose oxidation, and acetylation of mitochon-drial proteins were performed across the circadian cycle in circadian mutant mice and in cell-based systems. Proteins displaying increased acetylation in Bmall mutant liver were identified by mass spectrometry, and SIRT3 activity was evaluated using label-free self-assembled monolayer and matrix desorption ionization (SAMDI) mass spectrometry in liver lysate from Bmall and Sirt3 knockout mice. The role of NAD+ deficiency in SIRT3 activity, mito-chondrial protein acetylation, lipid oxidation, and oxygen consumption was evaluated after intraperitoneal administration of the NAD+ precursor NMN to raise NAD+ levels in Bmall mutant and wild-type mice. Results: Lipid oxidation and mitochondrial protein acetylation exhibited circadian oscillations that corresponded with the clock-driven NAD+ cycle in mouse liver. Rhythmic NAD* and oxidative cycles were self-sustained in fasted mice and in C2C12 myotubes, demonstrating clock control of mitochondrial function even when nutrient state remained constant. Transcription of gly-colytic genes was antiphasic to lipid oxidation rhythms, and glycolytic gene expression and lactate production were increased in Bmall-/- fibroblasts, whereas the converse occurred in Cryl-/-,Cry2-/- mutants. Lack of Bmall in liver led to decreased SIRT3 activity and increased mitochondrial protein acetylation, resulting in reduced function of oxidative enzymes. Finally, NAD+ supplementation with NMN restored protein deacetylation of SIRT3 targets and enhanced mitochondrial function in circadian mutant mice. Discussion: Mitochondria are central to energy homeostasis in eukaryotes, and our results show that the circadian clock generates oscillations in mito-chondrial oxidative capacity through rhythmic regulation of NAD+ biosyn-thesis. The clock thereby facilitates oxidative rhythms that correspond with the fasting-feeding cycle to maximize energy production during rest. Use of NAD+ as a central node in coupling circadian and metabolic cycles provides a rapid and reversible mechanism to augment mitochondrial oxidative func-tion at the appropriate time in the light-dark cycle. [ABSTRACT FROM AUTHOR]