Library Researchers 2015-07-05T06:05:45Z Letters to the Editor : Challenges of forensic science Letters to the Editor : Challenges of forensic science Shanklin, D. Radford Letters: Challenges Of Forensic Science. Published August 6, 2012 Author Posting. © The Author, 2012. The definitive version was published in Chemical & Engineering News 90 (2012): 3-4. 2012-07-09T00:00:00Z On the pulmonary toxicity of oxygen. 5. Electronic structure and the paramagnetic property of oxygen On the pulmonary toxicity of oxygen. 5. Electronic structure and the paramagnetic property of oxygen Shanklin, D. Radford Oxygen uptake by the pulmonary circulation is a chemical reaction. The physicochemical attributesof oxygen are critical when studying pulmonary oxygen toxicity. Extent of lung injury depends onthe percentage of oxygen in an oxygen:nitrogen mix in polybaric circumstances (Shanklin, 1969). Further change in extent of lesion follows when other gases are used in the inhalant mix instead of nitrogen (Shanklin and Lester, 1972), with oxygen at 21-100% of the mix. Comparative subatmospheric oxygen levels down to 3% in hydrogen, helium, nitrogen, argon, or sulfurhexafluoride, were run with and without ventilatory distress by the Farber (1937) model, bilateralcervical vagotomy (BCV). This yielded coherent results indicating a need to consider molecular characteristics at the atomic level. Molecular mass and size, gas viscosity, and thermal conductivity yielded no obvious correlates to lung injury. Saturation of the outer electron shells of the diluents fit the empiric data, prospectively an interaction between oxygen and nitrogen from their electronegativity and closely approximate molecular mass, size, and shape. The lesion is essentially eliminated at 7% oxygen in nitrogen. At 3% oxygen, the least lesion is found with N2, H2, and SF6,all gases with incomplete outer electron shells, allowing for transient, possibly polarized, covalent bonding with oxygen as the significant minority component in the mix. Argon and helium do not interfere with oxygen. With 3% oxygen in argon without BCV, the experiments ran so long (>70hours) they were terminated once the point had been made. 3% oxygen in argon after BCV yielded a mean survival more than twice that of BCV in air, indicating a remarkable degree of nitrogen interference with oxygen in the respiratory medium of terrestrial animal life. Argon displayed other advantages for the lung compared to nitrogen. Hydrogen, nitrogen, and oxygen are diatomic molecules, a feature which does relate to the extent of lung injury, but only oxygen is paramagnetic. Magnetic effects on lesion formation were tested: [1] with ventilatory distress induced in newbornrabbits, and [2] in young adult female white mice exposed to 100% oxygen without addedmechanical distress. A noninvasive model for ventilatory distress, thoracic restraint (TR), withlonger mean survivals of 40-50 hours, was employed rather than the Farber model. Parallel runs with TR, one subset receiving 100% oxygen in a plastic chamber resting on six strong ring magnetswith measured fields up to +1200 gauss, the other plain 100% oxygen, were performed. Bothsubsets developed moderate metabolic acidosis with average weight losses circa 25%, but over different time courses, 82.89 ± 4.91 hours in magnetized oxygen, 55.4 per cent longer than the 53.34 ± 9.82 hours in plain oxygen ( p <0.001). The longer survival in magnetized oxygen meant extensive lung injury (99.57 ± 0.42% pleural surface, versus 83.86 ± 14.03%), but the rate of lesionformation was 30.89 per cent faster in plain oxygen (1.5722% per hour) than in magnetized oxygen(1.2012% per hour), a difference significant at p <0.001. The effect of oxygen without mechanical ventilatory distress was examined in female adult whitemice exposed to oxygen or magnetized oxygen. Similar survivals and weight losses were achieved. The rate of lung lesion formation was different, 1.2617% per hour in plain oxygen, 46.13 per centfaster than 0.8634% per hour in magnetized oxygen. A variable magnetic field, with animals moving and breathing in chambers flooded with oxygen, has both systemic and pulmonary effectswhich alter the rate of lesion formation due to oxygen toxicity. Paramagnetic oxygen in a magneticfield influences the effect of oxygen toxicity on the lung but at these strengths of field it does notovercome significant mechanical disturbance. Author Posting. © The Author(s), 2012. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Experimental and Molecular Pathology 93 (2012): 365-377, doi:10.1016/j.yexmp.2012.08.007. 2012-06-01T00:00:00Z Pulmonary oxygen toxicity is modulated by its paramagnetic property Pulmonary oxygen toxicity is modulated by its paramagnetic property 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. Author Posting. © The Author, 2012. Paper presented at the 43rd Middle Atlantic Regional Meeting, American Chemical Society, University of Maryland, Baltimore County, Baltimore, MD, May 31- June 2, 2012 2012-06-01T00:00:00Z On the pulmonary toxicity of oxygen. 4. The thyroid arena On the pulmonary toxicity of oxygen. 4. The thyroid arena Shanklin, D. Radford Normally developed thyroid function is critical to the transition from fetal to neonatal life with the onset of independent thermoregulation, the most conspicuous of the many ways in which thyroid secretions act throughout the body. A role for thyroid secretions in growth and maturation of the lungs as part of the preparation for the onset of breathing has been recognized for some time but how this contributes to tissue and cell processes and defenses under the duress of respiratory distress has not been well examined. Extensive archival autopsy material was searched for thyroid and adrenal weights, first by gestational age, and then for changes during the first hours after birth as ratios to body weight. After a gestational age of 22 weeks the fetal thyroid and adrenal glands at autopsy in those with hyaline membrane disease are persistently half the size of those in "normal" infants dying with other disorders. When the thyroid is examined shortly after birth it reveals a post natal loss of mass per body weight of similar orders of magnitude which does not occur in the control group. A clinical sample of premature infants with (12) and without (14) hyaline membrane disease was tested for T4, TSH, TBG, and total serum protein. The results also demonstrate a special subset with lower birth weights at the same gestational age, and lower serum T4 and total serum protein. Ventilatory distress in newborn rabbits was induced by bilateral cervical vagotomy at 24 hours post natal following earlier injection of thyroxine (T4) or thyroid stimulating hormone (TSH) and comparisons were made with untreated animals and by dose. Early life thyroidectomy was performed followed by exposure to either air or 100% oxygen. A final experiment in air was vagotomy after thyroidectomy. Composite analysis of these methods indicates that thyroid factors are both operative and important in the newborn animal with ventilatory distress. This work and the archival data indicate those infants destined to develop hyaline membrane disease through respiratory distress are a distinct developmental and clinical subset with the point of departure from otherwise normal development and maturation in the second or early third trimester. This interval is known to be a period of marked variation in the overview indicators of fetal progress through gestational time. The initiating factor or circumstance which then separates this special subset from normal future development is placed by these observations firmly into the period when human fetal TSH dramatically rises 7-fold (17.5-25.5 weeks) followed by a lesser 3 to 4 fold increase in T4 which is extended into the early third trimester. The earlier part of this interval is characterized by the thyrotrophic action of chorionic gonadotropin (hCG). The possibility that abnormalities in the intrauterine environment secondary to maternal infection play a role within this time frame is indicated by the demonstration that interleukin-2 (IL-2) induces an anterior pituitary release of TSH. Since IL-2 has this property and is not an acute phase cytokine, some form of chronic infection or an immunopathic process seems more likely as a possible active factor in pathogenesis. Author Posting. © The Author(s), 2011. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Experimental and Molecular Pathology 92 (2012): 140-154, doi:10.1016/j.yexmp.2011.11.006. 2011-11-01T00:00:00Z