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In April 2005, the Nuclear Decommissioning Authority NDA ; was formed with the mission to deal with the UK's nuclear legacy facilities to time and cost, safely and with respect for the environment. This goal is ambitious and requires that training and education provision in nuclear topics is expanded and broadened. To appeal to this requirement, Lancaster designed and launched a postgraduate scheme in October 2004 which anticipated the postgraduate needs of engineers working in or aspiring to work in the decommissioning sector. This course built upon our experience with the Safety Engineering MSc. and followed a similar format in order to balance the needs of the workplace and the individual student
Normally, people breathe through their noses. The nose acts as an air filter. It controls the temperature and humidity of the air before it reaches the lungs. When you exercise, your body needs more air and you breathe faster. You start breathing through your mouth. Air that comes through your mouth has not been filtered, warmed, or moistened by your nose. This means the air that gets to your airways is cooler and drier than usual. If you have asthma, your extra-sensitive airways react to the cool, dry air. The muscles around the airways twitch and squeeze tighter. Tighter airways mean there is less space for the air to pass through. This makes you wheeze, cough and feel short of breath.
To describe the population ascending Monte Aconcagua information by questionnaires was obtained from 919 returning mountaineers between January 3 and 31, 2001, at Laguna de los Horcones 2900 m ; . AMS is defined as a score 4 of the Lake Louise self report questionnaire, which was filled out in retrospect for the day when subjects had felt worst. Climbers came from Europe: 54%, South America: 27%, North America: 14%, Asia and Oceania: 5%. 15 % were women. Further characteristics are: Age years ; : 30: 27%; 3039: and 50: 13%. BMI kg m 2 ; 20: 8%; 21-23: Training h week ; : 04: 29%; 10: Days spent above 3000 m per year: 04: 28% and 20: 28%. Previous highest altitude m ; : 4000: 8%; 4001-6000: took analgesics, 16% acetazolamide, 3% sleeping pills and 1% corticosteroids. 51% abstained from any drugs. The summit was reached by 60%. The prevalence of AMS individuals taking acetazolamide and corticosteroids excluded ; was 39 % 95% CI: 35-43% ; . Conclusions: There is a large variability regarding previous mountaineering experience, a low percentage of women, and a rather high success rate on Aconcagua. The prevalence of AMS is comparable to data reported in the literature for studies using similar definitions of AMS.
VAGINAL OXYGEN AND CARBON DIOXIDE DURING MENSES Schlievert consulted with the group regarding the historical knowledge of human vaginal gas tensions, design of the studies, and development of the manuscript. He did not receive compensation for the work associated with this study. REFERENCES 1. Beller FK and Schweppe KW. Review on the biology of menstrual blood. In: The Biology of the Fluids of the Female Genital Tract, edited by Beller FK and Schumacker GFB. North-Holland, NY: Elseiver, 1979. 2. Bergdoll MS. Toxic shock syndrome. J Venom Anim Toxins 3: 6 21, Berkley SF, Hightower AW, Broome CV, and Reingold AL. The relationship of tampon characteristics to menstrual toxic shock syndrome. J Med Assoc 258: 917920, 1987. Bonventre PF, Linnemann C, Weckback LS, Staneck JL, Buncher R, Vigdorth E, Ritz H, Archer D, and Smith B. Antibody responses to toxic-shock-syndrome TSS ; toxin by patients with TSS and by healthy staphylococcal carriers. J Infect Dis 150: 662 666, Bonventre PF, Thompson MR, Adinolfi LE, Gillis ZA, and Parsonnet J. Neutralization of toxic shock syndrome toxin-1 by monoclonal antibodies in vitro and in vivo. Infect Immun 56: 135141, 1988. Brackstad OG, Assbakk K, and Maeland JA. Detection of Staphylococcus aureus by polymerase chain reaction amplification of the nuc gene. J Clin Microbiol 62: 1654 1660, Brown WJ. Variations in the vaginal bacterial flora: a preliminary report. Ann Intern Med 96: 931934, 1982. Casewell MW and Hill RL. The carrier state: methicillin-resistant Staphylococcus aureus. J Antimicrob Chemother 18m Suppl A: 112, 1986. 9. Chapin K and Musgnug M. Evaluation of three rapid methods for the direct identification of Staphylococcus aureus from positive blood cultures. J Clin Microbiol 41: 4224 4327, Chow AW, Bartlett KH, Percival-Smith R, and Morrison BJ. Vaginal colonization with Staphylococcus aureus, positive for toxic-shock marker protein, and Escherichia coli in healthy women. J Infect Dis 150: 80 84, Czerwinski BS. Variation in feminine hygiene practices as a function of age. J Obstet Gynecol Neonatal Nurs 29: 625 633, Davis CC, Kremer MJ, Schlievert PM, and Squier CA. Penetration of toxic shock syndrome toxin-1 across porcine vaginal mucosa ex vivo: permeability characteristics, toxin distribution and tissue damage. J Obstet Gynecol 189: 17851791, 2003. Davis JP, Chesney PJ, Wand PJ, and LaVenture M. Toxic-shock syndrome: epidemiologic features, recurrence, risk factors, and prevention. N Engl J Med 303: 1429 1435, Dickgiesser N, Brombacher A, and Wiest W. Toxic shock syndrome toxin-1 producing strains of Staphylococcus aureus in vaginal smears. Geburtshilfe Frauenheilkd 47: 104 106, Korn AP, Hessol NA, Padian NS, Bolan GA, Donegan E, Landers DV, and Schacter J. Risk factors for plasma cell endometritis among women with cervical Neisseria gonorrhoeae, cervical Chlamydia trachomatis, or bacterial vaginosis. J Obstet Gynecol 178: 987990, 1998. Lanes SF and Rothman KJ. Tampon absorbency, composition and oxygen content and risk of toxic shock syndrome. J Clin Epidemiol 43: 1379 1385, Lansdell LW, Taplin D, and Aldrich TE. Recovery of Staphylococcus aureus from multiple body sites in menstruating women. J Clin Microbiol 20: 307310, 1984. Lee-Wong AC and Downs SA. Investigation by improved syringe method of effect of tampons on production in vitro of toxic shock syndrome toxin 1 by Staphylococcus aureus. J Clin Microbiol 27: 2482 2487, Linnemann CCJ, Staneck JL, Hornstein S, Barden TP, Rauh JL, Boneventre PF, Buncher R, and Benting A. The epidemiology of genital colonization with Staphylococcus aureus. Ann Intern Med 96: 940 944, Lowy FD. Staphylococcus aureus infections. N Engl J Med 339: 520 532, Magid MO and Geiger J. The intravaginal tampon in menstrual hygiene: a clinical study. Med Record 155: 316 318, Mayer KH and Anderson DJ. Heterosexual HIV transmission. Infect Agents Dis 4: 273284, 1995.
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As shown in figure 4, the decrease in total CO2 sensitivity Sp + Sc ; combined with a diminished apnoeic threshold imply that the ventilatory response curves to CO2 intersect at a PET, CO2 of about 5 kPa. At a PET, CO2 below this value acetazolamide stimulates ventilation during moderate hypoxaemia in anaesthetized cats.
Oelz O, Maggiorini M, Brtsch P. Prevention and treatment of AMS and HAPE. In: Abstract book of the international congress of mountain medicine "Franois-Xavier Bagnoud.' Interlaken, Switzerland: AKM Congress ' Service Basel, 1997; 23. Wilson I. Failure of acetazolamide to prevent acute mountain sickness. Postgrad Med J 1985; 61: 472. Ramsay LE. Prophylaxis of acute mountain sickness. Lancet 1977; i: 540-1. Ried LD, Carter KA, Ellsworth A. Acetazolamide or dexamethasone for prevention of acute mountain sickness: a meta-analysis. J Wilderness Med 1994; 5: 34-48. Jadad AR, Moore RA, Carroll D, Jenkinson C, Reynolds DJM, Gavaghan DJ, et al. Assessing the quality of reports of randomized clinical trials: is blinding necessary? Control Clin Trials 1996; 17: 1-12. Morris JA, Gardner MJ. Calculating confidence intervals for relative risk, odds ratios, and standardised ratios and rates. In: Gardner MJ, Altman DG, eds. Statistics with confidence. London: BMJ Publishing, 1995. Yusuf S, Peto R, Lewis J, Collins R, Sleight P. Beta blockade during and after myocardial infarction: an overview of the randomized trials. Progr Cardiovasc Res 1985; 27: 335-71. McQuay HJ, Moore RA. Using numerical results from systematic reviews in clinical practice. Ann Intern Med 1997; 126: 712-20. Cook RJ, Sackett DL. The number needed to treat: a clinically useful measure of treatment effect. BMJ 1995; 310: 452-4. Bradwell AR, Dykes PW, Coote JH, Forster PJ, Milles JJ. Effect of acetazolamide on exercise performance and muscle mass at high altitude. Lancet 1986; i: 1001-5. Bradwell AR, Coote JH. The BMRES 1984 Medical Research Expedition to the Himalayas. Postgrad Med J 1987; 63: 165-7. Morrissey SC, Keohane K, Coote JH. The effect of acetazolamide on breath holding at high altitude. Postgrad Med J 1987; 63: 189-90. Bartsch P, Maggiorini M, Ritter M, Noti C, Vock P, Oelz O. Prevention of high-altitude pulmonary edema by nifedipine. N Engl J Med 1991; 325: 1284-9. Kronenberg RS, Cain SM. Effect of acetazolamide on physiologic and subjective responses of men to 14000 feet. School of Aviation Medicine Technical Report 1967; 67: 1-10. Goerre S, Wenk M, Bartsch P, Luscher TF, Niroomand F, Hohenhaus E, et al. Endothelin-1 in pulmonary hypertension associated with high-altitude exposure. Circulation 1995; 91: 359-64. Kronenberg RS, Cain SM. Effect of acetazolamide and hypoxia on cerebrospinal fluid bicarbonate. J Appl Physiol 1968; 24: 17-20. Aoki VS, Robinson SM. Body hydration and the incidence and severity of acute mountain sickness. J Appl Physiol 1971; 31: 363-7. Bernhard WN, Miller Schalick L, Gittelsohn A. Dexamethasone for prophylaxis against acute mountain sickness during rapid ascent to 5334 m. J Wilderness Med 1994; 5: 331-8. Bernhard WN, Miller L, Delaney PA, Bernhard TM, Barnas GM. Acetazolamide plus low dose dexamethasone is better than acetazolamide alone to ameliorate symptoms of acute mountain sickness. Aviat Space Environ Med 1998; 69: 883-6. Bradwell AR, Burnett D, Davies F. Acetazolamide in control of acute mountain sickness. Lancet 1981; i: 180-3. Brookfield DSK, Liston WA, Brown GV. Use of spironolactone in the prevention of acute mountain sickness on Kilimanjaro. East Afr Med J 1977; 54: 690-1. Burki NK, Khan SA, Hameed MA. The effects of acetazolamide on the ventilatory response to high altitude hypoxia. Chest 1992; 101: 736-41. Burtscher M, Likar R, Nachbauer W, Philadelphy M. Aspirin for prophylaxis against headache at high altitudes: randomised, double blind, placebo controlled trial. BMJ 1998; 316: 1057-8. Cain SM, Dunn JE. Low dose of acetazolamide to aid accomodation of men to altitude. J Appl Physiol 1966; 21: 1195-200. Carson RP, Evans WO, Shields JL, Hannon JP. Symptomatology, pathophysiology, and treatment of acute mountain sickness. Federation Proc 1969; 28: 1085-91. Ellsworth AJ, Larson EB, Strickland D. A randomized trial of dexamethasone and acetazolamide for acute mountain sickness prophylaxis. J Med 1987; 83: 1024-30. Ellsworth AJ, Meyer EF, Larson EB. Acetazolamide or dexamethasone use versus placebo to prevent acute mountain sickness on Mount Rainier. West J Med 1991; 154: 289-93. Forwand SA, Landowne M, Follansbee JB, Hansen JE. Effect of acetazolamide on acute mountain sickness. N Engl J Med 1968; 279: 839-45. Greene MK, Kerr AM, McIntosh IB, Prescott RJ. Acetazolamide in prevention of acute mountain sickness: a double-blind controlled cross-over study. BMJ 1981; 283: 811-3. Hackett PH, Roach RC, Wood RA, Foutch RG, Meehan RT, Rennie D, et al. Dexamethasone for prevention and treatment of acute mountain sickness. Aviat Space Environ Med 1988; 59: 950-4. Hohenhaus E, Niroomand F, Goerre S, Vock P, Oelz O, Bartsch P. Nifedipine does not prevent acute mountain sickness. J Respir Crit Care Med 1994; 150: 857-60. Jain SC, Singh MV, Sharma VM, Rawal SB, Tyagi AK. Amelioration of acute mountain sickness: comparative study of acetazolamide and spironolactone. Int J Biometeorol 1986; 30: 293-300. Jobe JB, Shukitt-Hale B, Banderet LE, Rock PB. Effects of dexamethasone and high terrestrial altitude on cognitive performance and affect. Aviat Space Environ Med 1991; 62: 727-32. Johnson TS, Rock PB, Fulco CS, Trad LA, Spark RF, Maher JT. Prevention of acute mountain sickness by dexamethasone. N Engl J Med 1984; 310: 683-6. Larson EB, Roach RC, Schoene RB, Hornbein TF. Acute mountain sickness and acetazolamide. Clinical efficacy and effect on ventilation. JAMA 1982; 248: 328-32. Montgomery AB, Luce JM, Michael P, Mills J. Effects of dexamethasone on the incidence of acute mountain sickness at two intermediate altitudes. JAMA 1989; 261: 734-6. Nicholson AN, Smith PA, Stone BM, Bradwell AR, Coote JH. Altitude insomnia: studies during an expedition to the himalayas. Sleep 1988; 11: 354-61. Roach RC, Larson EB, Hornbein TF, Houston CS, Bartlett S, Hardesty J, et al. Acute mountain sickness, antacids, and ventilation during rapid, active ascent of Mount Rainier. Aviat Space Environ Med 1983; 54: 397-401. Rock PB, Johnson TS, Cymerman A, Burse RL, Falk LJ, Fulco CS. Effect of dexamethasone on symptoms of acute mountain sickness at Pikes Peak, Colorado 4300m ; . Aviat Space Environ Med 1987; 58: 668-72. Rock PB, Johnson TS, Larson RF, Fulco CS, Trad L, Cymerman A. Dexamethasone as prophylaxis for acute mountain sickness: Effect of dose level. Chest 1989; 95: 568-73. Roncin JP, Schwartz F, D Arbigny P. EGb 761 in control of acute mountain sickness and vascular reactivity to cold exposure. Aviat Space Environ Med 1996; 67: 445-52. Utz G, Schlierf G, Barth P, Linhart P, Wollenweber J. Prevention of acute mountain sickness using acetazolamide. Mnch Med Wochenschr 1970; 112: 1122-4. Whons RNW, Colpitts M, Clement T, Karusa A, Blackett WB, Foutch R, et al. Phenytoin and acute mountain sickness on Mount Everest. J Med 1986; 80: 32-6. Zell SC, Goodman PH. Acetazolamide and dexamethasone in the prevention of acute mountain sickness. West J Med 1988; 148: 541-5. Hackett PH, Rennie D. Rales, peripheral edema, retinal hemorrhage and acute mountain sickness. J Med 1979; 67: 214-8. Houston CS. High altitude illness--disease with protean manifestation. JAMA 1976; 236: 2193-5. Coates G, Gray GW, Mansell A, Nahmias C, Powles A, Sutton J, et al. Changes in lung volume, lung density, and distribution of ventilation during hypobaric decompression. J Appl Physiol 1979; 46: 752-5 and acidophilus.
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Fig. 5. Effect of HCl injection and acetazolamide injection on sodium efflux and ammonia excretion rate in Scyliorhtma and acitretin.
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May contribute to the higher control R values obtained with 99nTc-ECD 2.07 0.24 compared to 1.79 0.13 ; 26 ; . The time to reach the steady state is the same for these two tracers and will not contribute to the difference 26 ; . All three tracers measure the familiar increase of CBF by acetazolamide 12, 21, 27, ; . In comparison the highest CBF increase + 54.9% ; is measured by [I23I]IMP, which has previ ously been reported 19 ; and has been partly attributed to a pH effect. Alkaline urine, which results from a carbonic anhydrase inhibitor such as acetazolamide ApCO2 0; ApO2 + 20; ABP -8 ; 21 ; , leads to reabsorption and an increase of the serum levels of basic drugs, with subsequent higher concentra tions in the central nervous system compartment 29, 30 ; . N-Isopropyl-Y-iodoamphetamine as a basic compound is, there fore, more susceptible to possible drug interactions in partic ular, those with marked influences on systemic and urine pH ; than are 99mTc-HMPAO and 99mTc-ECD, explaining the sig nificantly enhanced CBF effect with [I23I]IMP and acetazol amide. could, thus, be the more sensitive tracer to assess cerebrovascular reserve through acetazolamide intervention. The underestimation of acetazolamide-induced CBF in creases, which would normally have been expected with 99mTcHMPAO due to high flow, was not obvious in this study 41% compared to 35% ; 26.31 ; but was indicated with 99mTc-ECD 34.3% ; 32 ; . The first-pass extraction rate is flow-dependent for 99mTc-ECD and 99mTc-HMPAO, and back-flux affects 99mTc-HMPAO retention more than it does 99mTc-ECD reten tion. Therefore, the question arises of whether a certain degree 1900 and actimmune
6.46, 2.15 to 19.40, number needed to treat 7 ; , 18% for ginkgo 1, 0.52 to 1.90 ; , and 7% for combined ginkgo and acetazolamide 2.95, 1.30 to 6.70 ; . Conclusions When compared with placebo, ginkgo is not effective at preventing acute mountain sickness. Acetazolamide 250 mg twice daily afforded robust protection against symptoms of acute mountain sickness.
Trials of a new treatment called Glial-cell-line-derived Neurotrophic Factor GDNF ; for Parkinson's Disease are underway to determine if it is toxic in humans. Monkeys with Parkinson's treated with this agent showed a reduction in Parkinsonian symptoms, and had higher dopamine levels in their brains. It is thought that this might be useful in slowing the progression of Parkinson's, and perhaps may promote partial recovery. Unfortunately it has to be given through a device that injects the medication directly into the fluid cavities inside the brain the ventricles ; . Another recent development in the treatment of Parkinson's is the drug GPI 1046, a socalled neuroimmunophilin. This drug has effects on both the immune system as well as nerve tissue. So far it has only been used in experimental models of Parkinson's in mice and rats. It has been reported that cyclic menstrual hormone changes can profoundly affect PS symptoms and the amount of medication needed in premenopausal women, although there have not been any reported problems of post menopausal women who are taking estrogens having interactions with PS medications. It has also been reported that Acetazolamide Diamox ; , a diuretic or "water pill" ; type of medication might help to control these fluctuations in premenopausal women, although this remains to be confirmed in large numbers of women with PS. In menopausal women, hormone replacement therapy with estrogen appears to be associated with a better clinical course of Parkinson's when it is started in postmenopausal women with a short duration of disease who are not yet on Ldopa. The studies indicating that hormonal replacement therapy might be beneficial are still in the preliminary stages in 1998, and there are still no guidelines as to what doses might be beneficial, or how long the benefit lasts. While there is much research going on related to PS, another interesting area of research is that to try to improve the balance or walking of those with PS. One such area is the development of "virtual reality glasses." The internet web site for this is at the University of Washington, Therapeutic Virtual Reality Projects: : hitl.washington projects medicine parkinsons and adalimumab.
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By increasing the probability of NMDA channel opening, as suggested by Huettner and Bean 1988 ; . The requirement for coexposure to NMDA also suggests that the tectal NMDA channel has a relatively limited open time in untreated animals, perhaps owing to the rapid clearing of glutamate from the synaptic cleft, and that the exogenously applied NMDA significantly increases the NMDA channel activity.
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Alimohammadi, H. and Silver, W.L. 2001 ; The effects of acetazolamide on trigeminal sensitivity to nicotine and carbon dioxide [abstract]. Chem. Senses, 26, 1046. Berkes, E.A. 2002 ; Carbonic anhydrase expression in allergic rhinitis. J. Allergy Clin. Immunol., 109, S263. Brown, D., Garcia-Segura, L.M. and Orci, L. 1984 ; Carbonic anhydrase is present in olfactory receptor cells. Histochemistry, 80, 307309. Bryant, B.P. 2000 ; The roles of carbonic anhydrase in gustation, olfaction and chemical irritation. In Chegwidden, W.R., Carter, N.D. and Edwards, Y.H. eds ; , The Carbonic Anhydrases: New Horizons. Birkhauser Verlag, Basel, vol. 90, pp. 365374. Cain W.S. 1987 ; A functional index of human sensory irritation. Indoor Air '87: Proceedings of the 4th International Conference on Indoor Air Quality and Climate. Institute for water, soil, and air hygiene, Berlin, pp. 661665. Caterina M.J., Leffler, A., Malmberg, A.B., Martin, W.J., Trafton, J., Petersen-Zeitz, K.R., Koltzenburg, M., Basbaum, A.I. and Julius, D. 2000 ; Impaired nociception and pain sensation in mice lacking the capsaicin receptor. Science, 288, 30613. Cavaliere, F., Masieri, S., Nori, S. and Magalini, S.I. 1996 ; Carbonic anhydrase in human nasal epithelium: localization and effect of the inhibition by dichlorphenamide. Am. J. Rhinol., 10, 113117 and adriamycin!
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Just as your transplanted kidney should begin to make urine right away, your transplanted pancreas will begin making insulin. You will most likely have normal blood glucose levels soon after surgery. However, many transplant centers use a continuous infusion of insulin through an IV for the first few days after transplant. This does not mean that the pancreas is not working, but that it is being spared from working too hard in the early days after transplant. Giving IV insulin during this time is associated with fewer postoperative complications. Some patients may need to take insulin for a short time after SPK transplant. To make.
Commentary by Joanna C. Jen, MD, PhD The participation of the cerebellum in various feedback circuits involving sensorimotor pathways ensures smooth and precise voluntary and involuntary movement. The superior cerebellar peduncle carries efferent cerebellar projections to the red nucleus and thalamus, as well as the reticular formation. Ascending fibers project to the cortex, from which corticopontine fibers originate to descend to the pontine nuclei, with postsynaptic pontocerebellar fibers carried by the middle cerebellar peduncle, thus closing an important feedback loop between the cerebellum and the cortex. Another feedback loop consists of projections from the red nucleus to the inferior olive, which projects to the cerebellum, which in turn projects back to the red nucleus, thereby indirectly modulating descending rubrospinal and reticulospinal tracts. It is well known that disruption at different levels of these circuits can lead to ataxia. Demyelinating lesions in multiple sclerosis can cause paroxysmal ataxia presumably from ephaptic transmission of demyelinated axons ; , yet reports of ischemic subcortical lesions causing episodic ataxia have been rare. The report from Matsui et al. describes a patient with a left midbrain infarct who, 6 weeks later, developed paroxysmal right arm ataxia and dysarthria with increasing frequency. The authors observed left parietal hypoperfusion by SPECT, which the authors correlated with frequent spells and that improved but did not normalize ; when the patient became free of symptoms after taking phenytoin. The authors hypothesized that sprouting and ephaptic transmission underlies paroxysmal ataxia in this case. The case study raises interesting hypotheses of CNS injury and repair, but the exact mechanisms require further elucidation and confirmation. Many questions remain unanswered. Did sprouting recur? If so, where did it occur? What triggers paroxysmal ataxia and why should it respond to phenytoin? Diaschisis in the setting of subcortical infarcts is often asymptomatic, and whether parietal hypometabolism accounts for paroxysmal ataxia is speculative; the technique does not allow for temporal resolution for the brief spells in this patient. Phenytoin, which blocks voltagegated sodium channels, is not known to inhibit sprouting. Whether there may be a reorganization of ion channels zone of ischemic injury to account for altered cell excitability and response to phenytoin brings to mind potentially overlapping mechanisms with congenital episodic ataxia and multiple sclerosis. Two subtypes of episodic ataxia, EA1 and EA2, have been shown to result from defects in ion channels abundantly expressed in the cerebellum. There have been anecdotal reports of responsiveness to anti-epileptics in EA1-associated epilepsy caused by heterozygous mutations in a neuronal voltage-gated potassium channel. The brief and recurrent nature of the patient's symptoms in this report is more similar to EA1 than EA2. EA1 symptoms are generally not responsive to medications. EA2 can be dramatically responsive to acetazolamide, 1 and a recent report described three EA2 patients who responded to 4-aminopyridine 4-AP ; , a blocker of potassium channel.2 Of note, acetazolamide has been reported to be effective in treating paroxysmal symptoms in multiple sclerosis3 presumed to arise from ephatic transmission of partially demyelinated axons.4 Since demyelination affects the distribution of potassium channels, it may be interesting to look into how MS patients with paroxysmal symptoms may respond 4-AP and aggrenox.
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That the transmembrane potential at the mouth of the pore is reduced by 2.5% from Vm, but this reduction diminishes to 0.1% at only 30 away from the center of the pore. Thus, the shunting effect is unlikely to explain the observed rise in threshold. Hence, both continuum and singlechannel considerations suggest that increases in electroporation thresholds are not a result of the increase in membrane conductivity. More likely reasons for the decrease in membrane susceptibility to electroporation are stabilizing lipid-monomer and lipid-dimer interactions. Stabilizing lipid-dimer interactions have been found in molecular dynamics simulations, particularly between the tryptophan side chains of the gD and the surrounding lipids Woolf and Roux, 1994 ; . Such interactions may cause gD to alter the mechanical properties of the membrane, and this was tested on GUVs in the present study. Such vesicles are also a well-characterized system, and have been used to evaluate the effects of various membrane constituents on their mechanical properties Evans and Needham, 1986 ; . Being primarily hydrophobic and incorporating into the fatty acid region of the bilayer, gD was shown in the present study to have effects similar to cholesterol, which increases both the area expansivity modulus and electroporation threshold of the membrane Needham and Nunn, 1990; Evans and Needham, 1986; Needham and Hochmuth, 1989 ; . The gD-induced increases of both K and lysis tension Fig. 5 ; indicate an increase in the mechanical stability of the POPC membrane. A number of electroporation models predict that increases in the mechanical stability of the membrane will increase membrane electroporation thresholds Maldarelli and Stebe, 1992; Dimitrov, 1984; Needham and Hochmuth, 1989 ; . In particular, the electromechanical model of Needham and Hochmuth 1989 ; predicts a relationship between area expansivity modulus and the electroporation threshold at zero membrane tension that takes the form and acidophilus.
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