11 research outputs found

    Survivorship and Growth of Seedlings and Saplings in Urban Forests

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    Research in 1993, 2003, and 2013 showed high rates of tree mortality and low rates of recruitment (new trees) in Portland, Oregon’s Forest Park. To determine if the lack of young trees was an urban phenomenon, we added three control sites in the Mount Hood National Forest in 2013. Last summer, seedlings and saplings were measured at all sites in Forest Park, the Ancient Forest Preserve, and at the control sites. Seedlings are trees less than 2 meters tall, and saplings are trees greater than 2 meters tall but having a dbh of less than 10cm. The 2018 data was compared to that collected in 2013. We measured dbh (diameter at breast height) of saplings and the basal area for seedlings, as well as the tree height and the height of the lowest living branch. In 2018, the control sites had significantly more live trees, more coniferous trees, more shade tolerant trees, and more seedlings and saplings. We also found that the seedlings and saplings in 2018 had a greater diameter at the control sites than the urban sites. We found significantly more dead trees in 2018 than 2013 in Forest Park

    Soil Characteristics in Relation to Urban Tree Mortality

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    Research in 1993, 2003, and 2013 showed high rates of tree mortality and low rates of recruitment (new trees) in Portland, Oregon’s Forest Park. Three control sites in the Mount Hood National Forest were added in 2013; research from 2018 showed the control sites had significantly more live trees, and more seedlings and saplings than the urban sites. For the last three summers, we have been studying the soil at our sites to elucidate possible causes for the observed low rates of recruitment. Data from 2017, 2018, and 2019 have shown the control sites have significantly deeper O horizons, higher rates of soil respiration, and lower levels of electroconductivity (EC) than the urban sites. We believe changes to the soil may be related to the lack of recruitment in urban forests

    Primary Intraocular Lens Implantation in the Setting of Penetrating Ocular Trauma

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    Purpose: To evaluate the clinical outcome of patients who underwent lensectomy and intraocular lens (IOL) implantation at the time of primary repair of a penetrating ocular injury. Methods: A review of 14 patients who sustained cataracts and lens rupture in the setting of a corneal laceration to determine anatomic and visual outcome, in addition to complications related to the primary IOL. Results: The IOL remained anatomically stable in all 14 patients with no complications encountered at implantation or after surgery. Final visual acuity in 9 of the 14 patients was 20/40 or better. Six patients underwent pars plana vitrectomy for removal of an intraocular foreign body. Conclusion: Intraocular lens implantation at the time of lensectomy and primary repair of a corneal laceration allows good visual rehabilitation with restoration of binocular function and serves as an alternative to contact lens correction in select patients

    Regulation of Atrial Natriuretic Peptide Secretion by Cholinergic and Pacap Neurons of the Gastric Antrum

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    Atrial natriuretic peptide (ANP) released from enterochromaffin cells helps regulate antral somatostatin secretion, but the mechanisms regulating ANP secretion are not known. We superfused rat antral segments with selective neural agonists/antagonists to identify the neural pathways regulating ANP secretion. The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) stimulated ANP secretion; the effect was abolished by hexamethonium but doubled by atropine. Atropine\u27s effect implied that DMPP activated concomitantly cholinergic neurons that inhibit and noncholinergic neurons that stimulate ANP secretion, the latter effect predominating. Methacholine inhibited ANP secretion. Neither bombesin nor vasoactive intestinal polypeptide stimulated ANP secretion, whereas pituitary adenylate cyclase-activating polypeptide (PACAP)-27, PACAP-38, and maxadilan [PACAP type 1 (PAC1) agonist] each stimulated ANP secretion. The PAC1 antagonist M65 1) abolished PACAP-27/38-stimulated ANP secretion; 2) inhibited basal ANP secretion by 28 ± 5%, implying that endogenous PACAP stimulates ANP secretion; and 3) converted the ANP response to DMPP from 109 ± 21% above to 40 ± 5% below basal, unmasking the cholinergic component and indicating that DMPP activated PACAP neurons that stimulate ANP secretion. Combined atropine and M65 restored DMPP-stimulated ANP secretion to basal levels. ANP secretion in the antrum is thus regulated by intramural cholinergic and PACAP neurons; cholinergic neurons inhibit and PACAP neurons stimulate ANP secretion
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