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  • Myofibroblast and endothelial cell proliferation during murine myocardial infarct repair. 14633615

    Granulation tissue formation is a critical step in infarct repair, however, the kinetics of cell replication and the molecules that regulate this process are poorly understood. In uninjured mouse hearts and at 2 days post-infarction, very little DNA synthesis (measured by incorporation of a BrdU pulse) was detected in any cell type. Four days after permanent coronary occlusion, the rates of myofibroblast (smooth muscle alpha-actin and BrdU double-positive) and endothelial cell (CD31 and BrdU double-positive) proliferation were 15.4 +/- 1.1% and 2.9 +/- 0.5%, respectively. Most proliferating cells were located at the interface of the infarct and viable tissue. By 1 week, fibroblast and endothelial cell proliferation declined to 4.1 +/- 0.6% and 0.7 +/- 0.1%, respectively. In the 2-week infarct, the remaining necrosis had been phagocytosed, and fibroblast and endothelial cell proliferation were less than 0.5%. Although leukocytes were abundant throughout infarct repair, no significant proliferation was detected at any time in cells expressing CD45 or mac-3. Infarct size at 4 days was 38 +/- 5% of the left ventricle and contracted to 20 +/- 4% by 4 weeks. After 4 days, the chamber dilated to four times that of the control hearts and remained so for the duration of the time course. The vascular density (per mm(2)) declined from 3643 +/- 82 in control hearts to 2716 +/- 197 at 1 week and 1010 +/- 47 at 4 weeks post-myocardial infarction (MI). The average percent area occupied by vessels did not change significantly between the groups but the area/vessel ( micro m(2)) increased from 14.1 +/- 0.3 in control hearts to 16.9 +/- 1.9 at 1 week and 38.7 +/- 7.9 at 4 weeks post-MI. These data indicate that mitogens for fibroblasts and endothelial cells peak within 4 days of infarction in the mouse heart. This provides the basis for identifying the responsible molecules and developing strategies to alter wound repair and improve cardiac function.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Phlorizin induces lipolysis and alters meal patterns in both early- and late-lactation dairy cows. 17369222

    Phlorizin is known to increase whole-body glucose demand, but it has also stimulated lipolysis in past studies in ruminants. Increased lipolysis complicates studies of dry matter intake (DMI) regulation by hepatic oxidation by providing the liver with additional oxidative substrate. Therefore, to assess whether increased glucose demand selectively increases DMI for cows in negative energy balance, phlorizin was administered to early- and late-lactation cows. Six Holstein cows in early lactation (19 +/- 6 DIM, 50.0 +/- 1.8 kg/d of milk, mean +/- SD) and 6 Holstein cows in late lactation (228 +/- 18 DIM, 30.6 +/- 1.9 kg/d of milk) were randomly assigned to treatment sequence in a crossover design. Periods were 14 d with 7-d adaptation periods and 7 d of treatment. Phlorizin (4 g/d) and propylene glycol (carrier and control) were administered subcutaneously every 6 h throughout the treatment periods. Feeding behavior and DMI data were collected for the final 4 d of each treatment period; blood samples and total urine output were collected on d 4 of each treatment period. Phlorizin caused urinary loss of glucose at 333 g/d in early-lactation cows and 532 g/d in late-lactation cows. Phlorizin increased plasma nonesterified fatty acid concentrations similarly in early- and late-lactation cows, but did not significantly alter plasma insulin concentrations. Treatment with phlorizin tended to decrease meal size, but also decreased intermeal interval, resulting in no effect on DMI. The effects of phlorizin on lipolysis, feeding behavior, and DMI are not dependent on relative energy balance.
    Document Type:
    Reference
    Product Catalog Number:
    GL-32K
    Product Catalog Name:
    Glucagon RIA

  • Phosphoprotein phosphatase inhibitor-2. Identification as a species of molecular weight 31,000 in rabbit muscle, liver, and other tissues. 2987219

    Specific antibodies, raised to purified rabbit skeletal muscle inhibitor-2, were used to analyze for the presence of inhibitor-2 in extracts of rabbit skeletal, cardiac, and diaphragm muscles, liver, kidney, brain, and lung. Direct analyses of the extracts by "Western blotting" revealed several immunoreactive species, apparent molecular weights in the range 26,000-136,000, as well as species with the electrophoretic mobility of inhibitor-2, apparent molecular weight 31,000. When supernatants from boiled extracts were similarly analyzed, most of the immunoreactive material was lost and the species corresponding to inhibitor-2 became prominent. Liver and muscle were studied in more detail; immunoprecipitates from either boiled or unboiled extracts were analyzed by Western blotting. The dominant polypeptide now was the species of apparent molecular weight 31,000, corresponding to inhibitor-2. Higher molecular weight species (115,000 in muscle and 136,000 in liver) were also detectable. The amount of inhibitor-2 detected in immunoprecipitates was not greatly different whether unboiled or boiled tissue extracts were used. In addition, extraction of the precipitates by boiling released material that inhibited purified type 1 protein phosphatase. The results suggest that inhibitor-2 is widely distributed in rabbit tissues and is found predominantly as a form of apparent molecular weight 31,000. In particular, the study provides direct demonstration of a species in rabbit liver with similar properties to rabbit muscle inhibitor-2.
    Document Type:
    Reference
    Product Catalog Number:
    14-162

  • Antagonistic Smad transcription factors control the dauer/non-dauer switch in C. elegans. 20081192

    The C. elegans daf-8 gene encodes an R-Smad that is expressed in a subset of head neurons, the intestine, gonadal distal tip cells and the excretory cell. We found that DAF-8, which inhibits the DAF-3 Co-Smad, is associated with DAF-3 and the DAF-14 Smad in vivo and in vitro. Overexpression of daf-8 conferred a dauer-defective phenotype and suppressed constitutive dauer formation in daf-8 and daf-14 mutants. In contrast to mammalian systems described thus far, active DAF-3 drives a feedback regulatory loop that represses transcription of daf-7 (a TGFbeta ligand) and daf-8 by directly binding to their regulatory regions. Hence, DAF-8 and DAF-3 are mutually antagonistic. The feedback repression may reinforce the developmental switch by allowing DAF-3 to freely activate dauer transcription in target tissues, unless sufficiently inhibited by DAF-8 and DAF-14. In the adult, DAF-8 downregulates lag-2 expression in the distal tip cells, thus promoting germ line meiosis. This function does not involve DAF-3, thereby avoiding the feedback loop that functions in the dauer switch.
    Document Type:
    Reference
    Product Catalog Number:
    06-570
    Product Catalog Name:
    Anti-phospho-Histone H3 (Ser10) Antibody, Mitosis Marker

  • Combined efficacy of nisin and pediocin with sodium lactate, citric acid, phytic acid, and potassium sorbate and EDTA in reducing the Listeria monocytogenes population of ... 16013374

    The inability of chlorine to completely inactivate human bacterial pathogens on whole and fresh-cut produce suggests a need for other antimicrobial washing treatments. Nisin (50 microg/ml) and pediocin (100 AU/ml) individually or in combination with sodium lactate (2%), potassium sorbate (0.02%), phytic acid (0.02%), and citric acid (10 mM) were tested as possible sanitizer treatments for reducing the population of Listeria monocytogenes on cabbage, broccoli, and mung bean sprouts. Cabbage, broccoli, and mung bean sprouts were inoculated with a five-strain cocktail of L. monocytogenes at 4.61, 4.34, and 4.67 log CFU/g, respectively. Inoculated produce was left at room temperature (25 degrees C) for up to 4 h before antimicrobial treatment. Washing treatments were applied to inoculated produce for 1 min, and surviving bacterial populations were determined. When tested alone, all compounds resulted in 2.20- to 4.35-log reductions of L. monocytogenes on mung bean, cabbage, and broccoli, respectively. The combination treatments nisin-phytic acid and nisin-pediocin-phytic acid caused significant (P < 0.05) reductions of L. monocytogenes on cabbage and broccoli but not on mung bean sprouts. Pediocin treatment alone or in combination with any of the organic acid tested was more effective in reducing L. monocytogenes populations than the nisin treatment alone. Although none of the combination treatments completely eliminated the pathogen on the produce, the results suggest that some of the treatments evaluated in this study can be used to improve the microbial safety of fresh-cut cabbage, broccoli, and mung bean sprouts.
    Document Type:
    Reference
    Product Catalog Number:
    04-409

  • Phenotypic diversity and expression of GABAergic inhibitory interneurons during postnatal development in lumbar spinal cord of glutamic acid decarboxylase 67-green fluore ... 19560523

    The synthesis enzyme glutamic acid decarboxylase (GAD65 or GAD67) identifies neurons as GABAergic. Recent studies have characterized the physiological properties of spinal cord GABAergic interneurons using lines of GAD67-green fluorescent protein (GFP) transgenic mice. A more complete characterization of their phenotype is required to better understand the role of this population of inhibitory neurons in spinal cord function. Here, we characterize the distribution of lumbar spinal cord GAD67-GFP neurons at postnatal days (P) 0, 7, and 14, and adult based on their co-expression with GABA and determine the molecular phenotype of GAD67-GFP neurons at P14 based on the expression of various neuropeptides, calcium binding proteins, and other markers. At all ages greater than 67% of GFP(+) neurons were also GABA(+). With increasing age; (i) GFP(+) and GABA(+) cell numbers declined, (ii) ventral horn GFP(+) and GABA(+) neurons vanished, and (iii) somatic labeling was reduced while terminal labeling increased. At P14, vasoactive intestinal peptide and bombesin were expressed in approximately 63% and approximately 35% of GFP(+) cells, respectively. Somatostatin was found in a small number of neurons, whereas calcitonin gene-related peptide never co-localized with GFP. Moderate co-expression was found for all the Ca(2+) binding proteins examined. Notably, most laminae I-II parvalbumin(+) neurons were also GFP(+). Neurogranin, a protein kinase C substrate, was found in approximately 1/2 of GFP(+) cells. Lastly, while only 7% of GFP(+) cells contain nitric oxide synthase (NOS), these cells represent a large fraction of all NOS(+) cells. We conclude that GAD67-GFP neurons represent the majority of spinal GABAergic neurons and that mouse dorsal horn GAD67-GFP(+) neurons comprise a phenotypically diverse population.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple