Shanklin D. Radford

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D. Radford

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  • Presentation
    Placental hypervascularity does not cause perinatal brain injury
    ( 2011-04-27) Shanklin, D. Radford ; Shokouh-Amiri, M.
    Dizygotic twins at 38 weeks with separate placentas: twin A, a 2479 gram female, was healthy after vaginal delivery. Five minutes later when the amnion of twin B was ruptured artificially, the cord prolapsed and could not be repositioned. Some 25 minutes later a 2791 gram male was delivered by section. Brain injury was noted soon afterward and subsequent development was marked by severe cerebral palsy and mental retardation. Initial diagnosis of twin B's placenta was 'chorangiosis,' overlooking fresh thrombi blocking the umbilical vein and one umbilical artery. Subsequent assessment revealed the same change in twin A's placenta. Archival records had 18/500 (3.6%) stillborns and 17/418 (4.07%) newborns with central placental hypervascularity. Of 125 recent consult placentas there were 17/100 singleton and 11/25 (44%) twin placentas displaying this change. Of 229 section deliveries there were 0/42 stillborns and 5/187 newborns with this vascular pattern. Another set of 625 autopsies revealed none with both hypoxic encephalopathy and this placental finding. This structural change is the same often seen in placentas from high altitude such as in Denver. Cerebral palsy occurs less often in Colorado than in other American states, per epidemiological data.
  • Presentation
    Thyroid and adrenal factors in hyaline membrane disease
    ( 2011-04-10) Shanklin, D. Radford
    Pulmonary fibrosis implies antecedent lung injury which may or may not include inflammatory responses of the ordinary sort. The onset of breathing at mammalian birth is a different kind of lung injury, one occasioned by great physical stretch of the collapsed but moist fetal lung, and immediate exposure to over ten times the level of oxygen resident in the fetal organ. Access to a large archive, the perinatal mortality review from the Chicago Lying-In Hospital, has provided information very relevant to these questions, including the first regular documentation of the pulmonary lesion complex as related to clinical care: beginning in the late 1930s. The lesion complex is called hyaline membrane disease (HMD) from the condensation at the tissue:gas interface of protein exuded from the lung and its circulation.
  • Presentation
    Pulmonary oxygen toxicity is modulated by its paramagnetic property
    ( 2012-06-01) Shanklin, D. Radford
    Molecular interaction can be determined from biological experiments [MARM 2011, #415, p. 252]. Atomic attributes can be shown to be determinative in whole animal experiments under appropriatecircumstances [MARM 2012, #225, p. 169]. The dynamics of replenishing gas interchange in thedistal air spaces of the mammalian lung, and at the atmosphere-lung interface, are shown bydifferences in the extent of pulmonary lesions after the induction of respiratory distress and changesin the mix of the gases inhaled [Biol.Neonat. 20:140-158, 1972]. Such effects have significantbiological and pathogenetic consequences. Hyaline membrane disease (HMD) is a common andsometimes lethal disorder, especially in premature newborns [Clin.Med. 72:477-490, 1965;Int.J.Clin.Pharmacol. 5:20-25, 1971]. There is significant evidence the lesions can be induced by oxygen enrichment [New Eng.J.Med.277:833-837, 1967; Lab.Invest. 21:439-448, 1969]. Bilateral cervical vagotomy (BCV) is a standardmethod of inducing ventilatory distress which leads to HMD [J.Exp.Med. 66:397-404, 1937;Biol.Neonat. 6:340-360, 1964; Biol.Neonat. 11:61-86, 1967]. This model has relatively short median(2.50-7.22 hours) and mean (3.54-13.63 hours) post-BCV life spans [Lab.Invest. 21:439-448, 1969],making it difficult to identify subtle but important effects which might change the result. Thus, aslower model inducing ventilatory distress, previously studied, was again employed, thoracicrestraint (TR). In this model, quarter inch soft cloth adhesive tape is tightened around the lower ribcage of newborn rabbits, reducing the segmental thoracic circumference by 10%, and then placingthem [1] in a 480 ml clear plastic chamber with 100% oxygen running at 1.0L/min, or [2] in anidentical chamber resting on four adherent donut magnets with a varied field up to +1200 gauss. Parallel experiments were done using young adult female white mice to eliminate the effect ofventilatory distress induced by TR. Diatomic oxygen is the only gas in the inhalant mixtures noted which is inherently paramagnetic. Studies have considered the effects of magnetic fields on flame combustion which is a chemicalreaction involving oxygen [IEEE Trans.Mag. 21:2077-2079, 1985; IEEE Trans.Mag. 23:2752-2754,1987; J.Appl.Phys. 69:2734-2736, 1991; Combus.Flame 93:207-214, 1993]; oxygenation incapillaries [Int.J.Math. Anal. 4:1697-1706, 2010]; and also on organic photochemical reactions[Acc.Chem.Res. 13:369-377, 1980], which, taken together, indicate magnetic influences on the flowand orientation of oxygen as gas and in solution. Two principal objective results from theseexperiments demonstrate an effect of the magnetic field on the whole animal and on the extent oflung injury. The newborn rabbit survival in pure 100% oxygen was 58.56 ± 3.19 hours versus 82.89± 4.91 hours in magnetized oxygen ( p <0.0001); the difference in gross lung injury was 47.46 ± 6.51per cent versus 99.57 ± 0.43 per cent respectively (p<0.0001). The adult female mice in pure 100%mean survival was 53.71 ± 5.40 hours versus 64.57 ± 2.93 hours in magnetized oxygen (p≈0.015);the respective percentages of lung injury were 61.67 ± 10.91 and 55.75 ± 10.45 (n.s.). But, when theresult is considered on the basis of rate of lung injury per hour, magnetized oxygen is much slower. The rates for newborn rabbits were, (magnetized oxygen) 1.3728%/hour and (plain oxygen),1.7969%/hour, a ratio of 1.3088, or 24.6% slower. In mice the rates were 0.8634%/hour and1.2617%/hour respectively, a ratio of 1.462, or 31.5% slower. A variable magnetic field added to whole animal models of pulmonary oxygen toxicity changes theoutcome in two overt ways: [1] survival is enhanced, but despite this, [2] the rate of formation oflung injury is reduced by 24% in newborn rabbits and by 31% in young adult female white mice. Thus, the toxic effect of oxygen is reduced systemically and in the lung by low strength magneticfield effects on inhaled paramagnetic 100% oxygen.
  • Presentation
    Argon and the pathophysiology of pulmonary oxygen toxicity
    ( 2011-05-23) Shanklin, D. Radford
    Molecular interaction can be determined from biological experiments. In the case of dynamics at the atmosphere-lung interface the physicochemical and atomic attributes of inhalant gases has significant biological and pathogenetic consequences. Hyaline membrane disease (HMD) is a common and sometimes lethal disorder, especially in premature newborns. Current therapy includes artificial ventilation and increased oxygen in the inspired air, despite evidence the lesions can be induced by oxygen enrichment [Lab.Invest. 21 439, 19691. Bilateral cervical vagotomy (BCV) is a standard method of inducing ventilatory distress which leads to HMD [J Exp.Med. 66:397, 1937; Biol.Neonat. 6:340, 1964; Biol. Neonat. 1 1 :6 I. 19671. The lungs of post-vagotomy newborn rabbits show the lesions of HMD in extent directly proportionate to the percentage of oxygen in polybaric (0.2 - 3.0 Atm.Abs) mixtures with nitrogen. Avery [Pediatrics 32:801, 19631 found that lesions of HMD did not form at very low levels of oxygen (3-4% in nitrogen] in various newborn animals. suggesting that inhalant hypoxia was not a pathogenetic factorper se. The observation of lung injury proportionate to oxygen percentage indicates the physiological axiom of gas effects by their partial pressure is an artefact of sea level gas dynamics. The toxic effect of oxygen can be viewed as nitrogen lack. Some lung injury does occur when only 3 and 7 per cent oxygen in nitrogen is used, suggesting rather a specific oxygen effect. When nitrogen is replaced by hydrogen, helium. neon, argon, or sulfur hexafluoride, the extent of lesions often increases, indicating again a fundamental oxygen-nitrogen interaction. Low level studies with hydrogen and argon are especially instructive with and without BCV: (1) extremely long survival without BCV in oxygen-argon at 3% and 7 %; (2) significant but less enhancement of survival in 3% oxygen-hydrogen; (3) no distinction in survival after BCV for 3% oxygen in nitrogen or hydrogen; (4) a pattern of lesion formation in the alternative gas mixtures which suggests nitrogen has a partially protective effect along with its stochastic competition for a conlmon oxygen-nitrogen receptor or transmembrane port; and (5) generally, the mammalian lung is well adapted by evolution to current atmospheric composition but at the price of more inhaled oxygen than is required for cellular function [Perspect.Biol.Med. 13:80, 19691, allowing for toxic effects. The distinctions amongst these gases in the biologic sense are due to differences in their mass, moiloatomic or diatomic structure: possibly viscosity in air passageway flow, inherent energy state, and at low levcls, in the electron saturation of the outer atomic shell. Unbuffered oxygen enrichment of air for ventilatory support is fundamentally injurious; hydrogen has obvious risks in a clinical setting but argon, which is abundant, non-flammable, and relatively non-toxic, may be the diluent gas of choice for ventilatory support.