Synaptic vesicle glycoprotein 2 enables viable aneuploidy following centrosome amplification.

Amplified centrosome number causes genomic instability, most severely through division into more than two aneuploid daughter cells (multipolar mitosis). Several mechanisms that suppress multipolar division have been uncovered, yet mechanisms that favor viable multipolar division are poorly understood. To uncover factors that promote viability in cells with frequent centrosome amplification and multipolar division, we conducted an unbiased genetic screen.

Guard cell apoplastic photosynthate accumulation corresponds to a phloem-loading mechanism.

Apoplastic phloem loaders have an apoplastic step in the movement of the translocated sugar, prototypically sucrose, from the mesophyll to the companion cell-sieve tube element complex. In these plants, leaf apoplastic sucrose becomes concentrated in the guard cell wall to nominally 150 mM by transpiration during the photoperiod. This concentration of external sucrose is sufficient to diminish stomatal aperture size in an isolated system and to regulate expression of certain genes.

Guard-cell apoplastic sucrose concentration--a link between leaf photosynthesis and stomatal aperture size in the apoplastic phloem loader Vicia faba L.

In broad bean (Vicia faba L.), an apoplastic phloem loader, the sucrose concentration increases up to approximately 2 mM in the leaf apoplast and up to approximately 150 mM in the guard-cell apoplast during the photoperiod. This high concentration in the guard-cell apoplast results from transpiration and is sufficient osmotically to reduce stomatal aperture size by up to 3 microm or approximately 25% of the maximum aperture size.

Dyspepsia and its overlap with irritable bowel syndrome.

Patients with functional dyspepsia and the irritable bowel syndrome are commonly seen in both primary care and gastroenterology subspecialty settings. Although functional dyspepsia and the irritable bowel syndrome can occur separately, recent research suggests that they often appear together as an overlap syndrome and thus may represent different portions of a unifying spectrum of disease. Despite their widespread prevalence, the pathogenesis of these disorders is not well established but may include impaired gastric emptying, gastric dysrhythmias, hypersensitivity (to acid exposure and to stretch), and Helicobacter pylori infection.

Impaired fatty acid oxidation as a cause of liver disease associated with hyperemesis gravidarum.

Hyperemesis gravidarum (HG) is the most severe form of illness within the spectrum of nausea and vomiting of pregnancy. Liver disease, usually consisting of mild serum transaminase elevation, occurs in almost 50% of patients with HG. While multiple risk factors have been proposed, the etiology and underlying mechanism of maternal liver disease associated with HG remains unclear.

Requirements for activation of the signal-transduction network that leads to regulatory phosphorylation of leaf guard-cell phosphoenolpyruvate carboxylase during fusicoccin-stimulated stomatal opening.

Leaves regulate gas exchange through control of stomata in the epidermis. Stomatal aperture increases when the flanking guard cells accumulate K+ or other osmolytes. K+ accumulation is stoichiometric with H+ extrusion, which is compensated for by phosphoenolpyruvate carboxylase (PEPC, EC 4.