GISHGenomic in situ hybridization reveals cryptic genetic differences between maize and its putative wild progenitor Zea mays subsp. parviglumis.

The aim of this paper is to test with genomic in situ hybridization the genomic affinities between maize and its putative progenitor Zea mays subsp. parviglumis. Blocking procedures were applied for the purpose of improving discrimination among chromosome regions. Unlabeled genomic DNA from Z. mays subsp. parviglumis as a blocking agent and labeled genomic DNA from maize were hybridized on maize chromosomes. On the other hand, mitotic metaphases from Z. mays subsp. parviglumis were blocked with unlabeled genomic DNA of maize and hybridized with labeled genomic DNA from Z. mays subsp. parviglumis. Both experiments showed that either maize or Z. mays subsp. parviglumis chromosomes have their own unique sequences. This means an unexpected degree of divergence if Z. mays subsp. parviglumis is the only progenitor of maize, a result that is discussed in relation to our previous genomic in situ hybridization observations and to the different scenarios proposed about the origin of maize.     

Melanin content and MC1R function independently affect UVR-induced DNA damage in cultured human melanocytes

Malignant transformation of melanocytes leads to melanoma, the most fatal form of skin cancer. Ultraviolet radiation (UVR)-induced DNA photoproducts play an important role in melanomagenesis. Cutaneous melanin content represents a major photoprotective mechanism against UVR-induced DNA damage, and generally correlates inversely with the risk of skin cancer, including melanoma. Melanoma risk is also determined by susceptibility genes, one of which is the melanocortin 1 receptor (MC1R) gene. Certain MC1R alleles are strongly associated with melanoma. We hereby present experimental evidence for the role of two melanoma risk factors, constitutive pigmentation, as assessed by total melanin, eumelanin and pheomelanin contents, and MC1R genotype and function, in determining the induction and repair of DNA photoproducts in cultured human melanocytes after irradiation with increasing doses of UVR. We found that total melanin and eumelanin contents (MC and EC) correlated inversely with the extent of UVR-induced growth arrest, apoptosis and induction of cyclobutane pyrimidine dimers (CPD), but not with hydrogen peroxide release in melanocytes expressing functional MC1R. In comparison, melanocytes with loss-of-function MC1R, regardless of their MC or EC, sustained more UVR-induced apoptosis and CPD, and exhibited reduced CPD repair. Therefore, MC, mainly EC, and MC1R function are independent determinants of UVR-induced DNA damage in melanocytes.     

Yohimbine increases plasma insulin concentrations of dogs

Recent evidence suggests that catecholamines inhibit insulin release by stimulating alpha 2-adrenoreceptors in beta-cells of the pancreatic islets. In the present study, iv injections of 0.1 and 0.3 mg/kg of yohimbine, an alpha 2-adrenoreceptor antagonist, resulted in increased plasma insulin and decreased plasma glucose concentrations in the dog. The use of alpha 2-adrenoreceptor antagonists may be of value in non-insulin-dependent diabetic patients by counteracting the inhibitory influence of endogenous catecholamines.     

Unconjugated bilirubin inhibits VCAM-1-mediated transendothelial leukocyte migration

During lymphocyte migration, engagement of VCAM-1 stimulates the generation of endothelial cell-derived reactive oxygen species (ROS) and activation of matrix metalloproteinases, facilitating endothelial retraction. Because bilirubin is a potent antioxidant, we examined the hypothesis that this bile pigment inhibits VCAM-1-dependent cellular events. The migration of isolated murine splenic lymphocytes across monolayers of murine endothelial cell lines (which constitutively express VCAM-1) is significantly inhibited by physiological concentrations of bilirubin, in the absence of an effect on lymphocyte adhesion. Bilirubin administration also suppresses VCAM-1-stimulated ROS generation and reduces endothelial cell matrix metalloproteinase activity. In a murine asthma model characterized by VCAM-1-dependent airway inflammation, treatment of C57BL6/J mice with i.p. bilirubin decreases the total leukocyte count in the lung parenchyma and lavage fluid, through specific inhibition of eosinophil and lymphocyte infiltration. Blood eosinophil counts were increased in bilirubin-treated animals, while VCAM-1 expression in the capillary endothelium and cytokine levels in both lung lavage and supernatants from cultured lymph node lymphocytes were unchanged, suggesting that bilirubin inhibits leukocyte migration. Conclusion: bilirubin blocks VCAM-1-dependent lymphocyte migration in vitro and ameliorates VCAM-1-mediated airway inflammation in vivo, apparently through the suppression of cellular ROS production. These findings support a potential role for bilirubin as an endogenous immunomodulatory agent.     

Single and dual task gait training in people with Parkinson's Disease: A protocol for a randomised controlled trial

Background  

Difficulty performing more than one task at a time (dual tasking) is a common and disabling problem experienced by people with Parkinson disease (PD). If asked to perform another task when walking, people with PD often take shorter steps or walk more slowly. Currently there is uncertainty about whether clinicians should teach people with PD to avoid dual tasking or whether they should encourage them to practice dual tasking with the hope that practice will lead to enhanced performance. This study will address this issue by comparing single to dual task gait training.     

Reactions between diglycolaldehyde dithioacetals and some nucleophiles

The homogeneous, neutral polysaccharide isolated from the crude polysaccharide of the fruit pulp from bael (Aegle marmelos) contains arabinose, galactose, and glucose in the molar ratios of 2:3:14. The linkages among the different monosaccharide residues were established through methylation analysis and Smith-degradation studies of the polysaccharide. The anomeric configurations of the different glycosyl groups were determined by study of the chromium trioxide oxidation of the acetylated polysaccharide. Results of these experiments have been discussed in order to assess the structure of the neutral polysaccharide.     

Cholinergic location of delta-opioid receptors in canine atria and SA node

Delta-opioid receptors (DORs) are associated with ischemic preconditioning and vagal transmission in the sinoatrial (SA) node and atria. Although functional studies suggested that DORs are prejunctional on parasympathetic nerve terminals, their precise location remains unconfirmed. DORs were colocalized in tissue slices and synaptosomes from the canine right atrium and SA node along with cholinergic and adrenergic markers, vesicular acetylcholine transporter (VAChT), and tyrosine hydroxylase (TH). Synapsin I immunofluorescence verified the neural character of tissue structures and isolated synaptosomes. Acetylcholine and norepinephrine measurements suggested the presence of both cholinergic and adrenergic synaptosomes. Fluorescent analysis of VAChT and TH signals indicated that >80% of the synapsin-positive synaptosomes were of cholinergic origin and <8% were adrenergic. DORs colocalized 75-85% with synapsin in tissue slices from both atria and SA node. The colocalization was equally strong (85%) for nodal synaptosomes but less so for atrial synaptosomes (57%). Colocalization between DOR and VAChT was 75-85% regardless of the source. Overlap between DOR and TH was uniformly low, ranging from 8% to 17%. Western blots with synaptosomal extracts confirmed two DOR-positive bands at molecular masses corresponding to those reported for DOR monomers and dimers. The abundance of DOR was greater in nodal synaptosomes than in atrial synaptosomes, largely attributable to a greater abundance of monomers in the SA node. The abundant nodal and atrial DORs predominantly associated with cholinergic nerve terminals support the hypothesis that prejunctional DORs regulate vagal transmission locally within the heart.