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Radical oxygen species and hypoxia reoxygenation REFERENCES 1. Al-Mehdi AB, Zhao G, Dodia C, Tozawa K, Costa K, Muzykantov V, Ross C, Blecha F, Dinauer M and Fisher AB. Endothelial NADPH oxidase as the source of oxidants in lungs exposed to ischemia or high K + . Circ Res 83: 730-737, 1998. Annas A, Brittebo E and Hellman B. Evaluation of benzo a ; pyrene-induced DNA damage in human endothelial cells using alkaline single cell gel electrophoresis. Mutat Res 471: 145-155, 2000. Armstrong JS and Jones DP. Glutathione depletion enforces the mitochondrial permeability transition and causes cell death in Bcl-2 overexpressing HL60 cells. Faseb J 16: 1263-1265, 2002. Bonne C, Muller A and Villain M. Free radicals in retinal ischemia. Gen Pharmacol 30: 275-280, 1998. Bouloumie A, Bauersachs J, Linz W, Scholkens BA, Wiemer G, Fleming I and Busse R. Endothelial dysfunction coincides with an enhanced nitric oxide synthase expression and superoxide anion production. Hypertension 30: 934-941, 1997. Boveris A. Mitochondrial production of superoxide radical and hydrogen peroxide. Adv Exp Med Biol 78: 67-82, 1977. Caraceni P, Ryu HS, van Thiel DH and Borle AB. Source of oxygen free radicals produced by rat hepatocytes during postanoxic reoxygenation. Biochim Biophys Acta 1268: 249-254, 1995. Chandel NS, Maltepe E, Goldwasser E, Mathieu CE, Simon MC and Schumacker PT. Mitochondrial reactive oxygen species trigger hypoxia-induced transcription. Proc Natl Acad Sci U S A 95: 11715-11720, 1998. Chen Q, Vazquez EJ, Moghaddas S, Hoppel CL and Lesnefsky EJ. Production of reactive oxygen species by mitochondria: central role of complex III. J Biol Chem 278: 36027-36031, 2003. Corda S, Laplace C, Vicaut E and Duranteau J. Rapid reactive oxygen species production by mitochondria in endothelial cells exposed to tumor necrosis factor-alpha is mediated by ceramide. J Respir Cell Mol Biol 24: 762-768, 2001. Eddy LJ, Stewart JR, Jones HP, Engerson TD, McCord JM and Downey JM. Free radical-producing enzyme, xanthine oxidase, is undetectable in human hearts. J Physiol 253: H709-711, 1987. 12. Genova ML, Ventura B, Giuliano G, Bovina C, Formiggini G, Parenti Castelli G and Lenaz G. The site of production of superoxide radical in mitochondrial Complex I is not a bound ubisemiquinone but presumably iron-sulfur cluster N2. FEBS Lett 505: 364-368, 2001. Gierse JK, Hauser SD, Creely DP, Koboldt C, Rangwala SH, Isakson PC and Seibert K. Expression and selective inhibition of the constitutive and inducible forms of human cyclo-oxygenase. Biochem J 305 Pt 2 ; : 479-484, 1995. 14. Gottlieb RA. Cytochrome P450: major player in reperfusion injury. Arch Biochem Biophys 420: 262-267, 2003. Granger DN, Hollwarth ME and Parks DA. Ischemia-reperfusion injury: role of oxygen-derived free radicals. Acta Physiol Scand Suppl 548: 47-63, 1986. Granger DN and Korthuis RJ. Physiologic mechanisms of postischemic tissue injury. Annu Rev Physiol 57: 311-332, 1995. Griendling KK, Minieri CA, Ollerenshaw JD and Alexander RW. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Circ Res 74: 1141-1148, 1994. Hensley K, Pye QN, Maidt ML, Stewart CA, Robinson KA, Jaffrey F and Floyd RA. Interaction of alpha-phenyl-N-tert-butyl nitrone and alternative electron acceptors with complex I indicates a substrate reduction site upstream from the rotenone binding site. J Neurochem 71: 2549-2557, 1998.
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Threshold above which the prostatic concentration must rise in order to stimulate prostatic cell number 28 ; . Finatseride treatment in rats has been shown to reduce the intraprostatic DHT concentration to near castrate levels but raises the testosterone concentration to the same value as intraprostatic DHT concentrations in intact rats 6, 9 ; . The effect on the prostate of finasteride and other 5 -reductase inhibitors is a high degree of cell atrophy with minimal evidence of cell loss. Finxsteride administration does not result in upregulation of TRPM-2 mRNA in the prostates of treated rats 6, 7, 16 ; , although there was an increase in TRPM-2 protein using another 5 -reductase inhibitor 3 ; . Inhibition of apoptosis occurs at an intraprostatic testosterone concentration 10 ng g tissue ; approximately half that seen with finasteride treatment and a DHT concentration half that of a normal intact rat. On the other hand, the concentration of testosterone in the prostate needed to maximally stimulate secretory activity is greater than the intraprostatic testosterone concentration in rats treated with finasteride. Our results offer an explanation for the inability of 5 -reductase inhibitors to decrease the prostate weight to the same extent as castration. In summary, DHT appears to be more potent than testosterone at stimulating prostate epithelial cell function as measured by ductal mass, but the two androgens were equipotent at preventing prostate cell death after castration. Our study provides an explanation for the inability of 5 -reductase inhibition to reduce prostate weight to the same extent as castration. In order to understand the molecular mechanisms that might explain our observations, detailed studies will be needed to examine the effect of testosterone and DHT on specific genes in the prostate and flagyl.
Dear Madam, In relation to the above article, [Modern Medicine, March 2005] current evidence indicates that breast feeding does not protect against atopic dermatitis in the general population. Reference Hoare C et al. Health Technol Assess 2000: 4 97 16 Yours sincerely, DR JF BOURKE Consultant Dermatologist South InfirmaryVictoria Hospital Cork.
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For pediatric patients 5 feet tall 35 kg 75 lbs. ; , follow Seizures Pediatric ; protocol. RECOGNITION Seizure: A sudden episode of unresponsiveness, characterized by mild to severe involuntary contractions of skeletal muscles. Postictal: Third phase of a convulsive seizure. Convulsions stop, and the patient may be drowsy or remain unconscious for hours. TREATMENT 1. 2. 3. Unless unable to rule out trauma, stabilize neck and spine with cervical collar and spineboard as soon as possible. Perform initial assessment while protecting the airway with an appropriate airway. Protect patient from sustaining any injuries. Position on left side unless contraindicated ; , and remove secretions if needed. Administer OXYGEN with the highest concentration device tolerated; assist ventilation's as necessary. If signs of ventilatory problems arise, follow the Airway Management and Respiratory Support protocol. Obtain history from family and or bystanders including medications. Determine, if possible, any previous history of seizure activity. Assess the patient; determine the level of consciousness with the AVPU method or Glascow Coma Scale. If electronic glucose meter is available, determine blood glucose bG ; concentration If the bG concentration is 60 mg dl or if the patient has signs and or symptoms of hypoglycemia regardless of the availability of bG measurement, and the patient's mental status is "alert" A or becomes alert to "verbal" V stimuli, then administer an ORAL GLUCOSE product as indicated below: 10.1 Administer ORAL GLUCOSE with approximately 15 grams of GLUCOSE e.g. Glucola, Glutose 15TM, InstaGlucose ; . 10.2 Do not administer ORAL GLUCOSE product to a patient who is vomiting, nauseated, or not fully awake.
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FIG. 2. A, Mean seminal vesicle weights in adult rats treated in utero with increasing doses of the Bo-reductase inhibitor finasteride. Asterisks represent doses of finasteride that are significantly different from control values P C 0.05 ; . B, Mean vas deferens weights in adult rats treated in utero with increasing doses of the 5cY-reductase inhibitor finasteride. Asterisks represent doses of finasteride that are significantly different from control values P 0.05 ; . Note that there is no significant difference in weight with the increasing doses. C, Mean epididymal weights in adult rats treated in utero with increasing doses of the 5o-reductase inhibitor finasteride. Asterisks represent doses of finasteride that are significantly different from control values P 0.05 ; . Note that there is no persistent significant difference in weight with the increasing doses.
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Patients with 5-reductase-2 deficiency syndrome have decreased circulating and prostatic DHT concentration due to decreased conversion of testosterone to DHT. In the affected male adults, the prostate is nonpalpable on rectal examination 61, 78 ; and is found to be rudimentary on transrectal ultrasound and MRI visualization 69 ; . Prostatic volumes are approximately a tenth of those of age-matched controls see Figure 3 ; . Histological analysis of prostate biopsy from these patients reveals fibrous connective tissue, smooth muscle, and no identifiable epithelial tissue, suggesting atrophic epithelium or lack of epithelial differentiation 69 ; . Plasma PSA is low or undetectable in these patients. Administration of DHT results in enlargement of the prostate Figure 3 ; , and an elevation of plasma PSA levels 66, 79, 80 ; . These findings provide clinical evidence that prostate differentiation and growth as well as circulating PSA level is mediated largely by DHT. However, the mere presence of a prostate in these individuals supports the notion that other growth factors are also involved in its organogenesis. Further supportive evidence is provided by animal studies using 5-reductase-2 inhibitors and gene knockout. Administration of a 5-reductase-2 inhibitor, finasteride, in rats 81, 82 ; and monkeys 83 ; impairs male sexual differentiation and prostate development. The prostate in mice with genetic disruption of either 5-reductase-2 or 5-reductase-2 plus 5-reductase-1 gene is small, but it is puzzling that these knockout animals have normal external genitalia in male offspring 84.
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PHO5 promoter necessitates a longer induction time e.g. 48 h ; , which is longer than the 1216 h needed when the CUP1 promoter is used. Finally, the importance of the strategy with the ubiquitinfusion protein system has been stressed above. The kinetic studies showed that both the type 1 and type 2 isoenzymes of 5-R are highly expressed and fully active in S. cere isiae. The type 2 isoenzyme has a higher affinity for testosterone but a lower capacity for conversion than type 1. It has already been reported that the two rat isoforms have different sensitivities to finasteride [28], and this observation has been confirmed in the present study with the enzymes produced in yeast : the Ki for fknasteride was found to be higher for type 1 14.66 nM ; than for type 2 2.7 nM ; . Finally, the two isoforms expressed in yeast have the same pH optima as the respective native enzymes, i.e. a wide pH range from 6 to 7.5 ; for type 1, and a narrow pH optimum at 5.5 for type 2. The fractionation studies indicate that the two isoenzymes may have different intracellular localizations. It was found that the highest enzymic activity of type 2 was present in the 20 000 g pellet. Even if a complete resolution of the major yeast organelles by subcellular fractionation was not established as firmly as for mammalian cells, the 20 000 g fraction seems to contain most of the cellular membranes derived from the endoplasmic reticulum [8]. A preferential localization in the perinuclear ergastoplasm has been described for the type 2 isoenzyme in human androgensensitive tissue [30, 31]. In the present study the activity of the type 1 isoform was observed in the 1000 g and 2500 g pellets two fractions known to contain the cell nuclei ; . The perinuclear or nuclear localization of the type 1 isoenzyme might facilitate the formation of DHT, and its subsequent binding to nuclear androgen receptors [32], before the rapid inactivation of DHT to less potent androgens such as 3-diol by the action of the cytoplasmic enzyme 3-hydroxysteroid dehydrogenase ; [33]. It is probably premature to extrapolate to mammalian tissues the different localizations of the two 5-R isoenzymes found in the yeast cellular fractions ; if this occurs also in mammals, different intracellular physiological role s ; of the two enzymes could be postulated. The association of the 5-R type 1 with the enriched nuclear fraction in yeast partly conflicts with the results by Ordman et al. [26], who found the highest activity of type 1 isoenzyme produced in yeast cells in the 12 000 g fraction. The discrepancy is probably explained by the difference in the homogenization procedure adopted ; in fact, homogenization of the yeast spheroplasts with a Teflon homogenizer, reported by Ordman et al., might have damaged the nuclei and altered the sedimentation properties of the organelles. In the present study, homogenization was obtained by slight sonication, which prevents nuclear damage. The present data on the preferential nuclear association of 5R type 1 find support in studies performed in mammals, even if a final agreement on the cellular compartmentalization of the native 5-R isoenzymes in rat and human tissues is not yet available [1, 31, 3441]. We thank Dr. David W. Russell Southwestern Medical Center, Dallas, TX, U.S.A. ; for the full-length cDNAs for rat 5-reductase types 1 and 2 and for helpful revision of the manuscript. This work was supported by AIRC, MURST, CNR Projects ACRO 95.00395.PF39, FATMA 95.00868.PF41, AGING 95.01020.PF40, and Bilateral project 94.02374.CT04.
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Induced relaxation of arteriolar smooth muscle. Thus both systolic and diastolic blood pressure display a minor decrease. Determinants of Fetal Oxygenation Fetus develops in an environment of low oxygen tension relative to the mother. The maternal uterine blood vessels and the fetal umbilical blood vessels run in parallel and oxygen is exchanged passively. Consequently fetal oxygen pressure can never exceed the maternal venous oxygen pressure. Therefore mechanisms used to exchange fetal oxygenation are : a ; Fetal Hb, which has high affinity for oxygen relative to adult Hb. b ; Increased perfusion rate of some fetal organs as compared to adult organs. Fetal oxygen delivery can be impaired by respiratory, cardiovascular and hematological problems in the fetus. Even with these adoptive measures small medication in maternal Po2 seen in acute asthma episode can lead to poor uteroplacental perfusion. Obviously these scenarios can be detrimental to the well being of the fetus. Effects of Asthma on Pregnancy Controlled studies that have evaluated outcomes of pregnancy in asthmatic compared with non-asthmatic women have suggested that maternal asthma increases the risk of perinatal mortality, pre-eclampsia, complicated labour, low birth weight infants and preterm births compared with non asthmatic women 8, 9 ; . An increasing hypothesis regarding adverse fetal outcome is that there may be abnormal levels of the placental enzyme, which may lead to reduce fetal growth in asthmatic mothers. The enzyme 11b hydroxy steroid dehydrogenase type 2 presents excess maternal cortisol from reaching the fetus by metabolizing cortisol to its inactive form cortisone. Studies have demonstrated reduced enzyme activity in neonates with intrauterine growth retardation 10 ; Mechanism postulated to explain the possible increased perinatal risk have included: 1. Hypoxia and other physiological consequences of poorly controlled asthma 2. Medications used to treat asthma 3. Pathogenic or demographic factors associated with asthma but actually could not by the disease or its treatment In pregnant women uncontrolled asthma has been associated with respiratory symptoms, emergency department visit, hospitalization, respiratory failure, preeclampsia or death8. 34.
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CHCs were first funded by the federal government as part of the Johnson Administration's War on Poverty in the mid-1960s. By the early 1970s, about 100 neighborhood health centers were established under the Economic Opportunity Act EOA ; . These centers provide accessible, affordable personal health care services to low-income families, the underserved and the underprivileged. The Public Health Service began funding neighborhood health centers in 1969. Currently, the CHC federal grant program is authorized under section 330 of the Health Centers Consolidation Act of 1996.1 CHCs provide comprehensive, coordinated, culturally appropriate health care services, including prenatal care, obstetrics, chronic disease management, preventive services and inpatient care. To be classified as a CHC and to be eligible for federal funding, a center must meet the following criteria.
Patient 3 An obese male patient, aged 32 years, was referred for infertility evaluation. The couple had been trying to achieve pregnancy for 6 months. He had been on finasteride 1 mg day for more than 1 year. There were no abnormalities in his physical exam. His first seminal analysis presented total concentration of 970, 000 spermatozoa ml with 30% motility and 16% normally shaped spermatozoa ml.8 A second exam showed a total concentration of 360 thousand spermatozoa ml with 20% motility and 15% of normal shape. Finasteridee treatment was interrupted, and after 3 months a seminal analysis showed a total concentration of 10 million spermatozoa ml with 60% motility and 22% of normal shape.8 Another seminal analysis was done 3 months later and showed total concentration of 7.2 million spermatozoa ml with 50% motility and 22% of normal shape.
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Ence from placebo increased over time, and the percent of subjects rated by the investigator as hav ing improved hair growth also increased through out the study. By month 12, 52% of subjects in the finasteride group were rated as improved com pared with 3 1 % of those in the placebo group Fig 3 ; . Further improvements in investigator assessments were seen through the second year open extension portion of the study data not shown ; . Global photographic assessment Analysis of global photographs demonstrated.
Based on the observations that androgens are necessary for the development of prostate cancer and that men with a congenital deficiency of the 5--reductase type 2 enzyme do not develop prostate cancer, a 7-year randomised, controlled trial with the drug finasteride was undertaken with 18 882 men who were 55 years, had a normal prostate on digital rectal examination and a PSA of 3 ng ml. The study was ended 15 months prematurely because the end-point had been reached and continuing the trial would not have changed the outcome. Men who received finasteride, which inhibits conversion of testosterone to dihydrotestosterone DHT ; by targeting the 5--reductase type 2 enzyme, had a prostate cancer prevalence reduction of 24.8% 24.4% to 18.4%. However, the prevalence of Gleason 7-10 tumours was higher in the finasteride arm 6.4% versus 5.1% ; although 98% of the tumours were clinically localised. 204 ; . Klein et al 2005 ; 205 ; have questioned the validity of the conclusion in relation to the rate of clinically-significant prostate cancer detection in this trial. They present a model of risk and benefit that estimates the potential influence of histological artefact due to finasteride-induced effect on prostatic epithelial appearances ; in the assignment of excess risk for high-grade disease and possible overdetection bias introduced by finasteride-induced volume reduction in prostates for the treated patients 205 ; . A further industry-sponsored study, the REDUCE Reduction by DUtasteride in prostate cancer Events ; trial is in progress. In this randomised, controlled study involving 8 000 men with PSA values between 2 and 10 ng ml dutasteride, which inhibits both isoforms of the 5--reductase enzyme, is being used in the treatment arm. All patients in this trial are being biopsied at least twice during the study unlike the finasteride study in which prostatic biopsies were recommended if the annual PSA adjusted for the effect of finasteride ; exceeded 4 ng ml the digital rectal examination was abnormal. Recent research suggests that inhibition of the irreversible action of 5-reductase to convert testosterone to the more transcriptionally active dihydrotestosterone may have untoward effects in relation to prostate cancer. Dihydrotestosterone in turn is hydroxylated to 3-diol and 3-Adiol which do not bind to the androgen receptor but have a strong affinity for oestrogen receptors, the result of which is thought to have a direct effect on prostate development and homeostasis 206 ; . The binding of 3-Adiol to oestrogen receptor beta ER ; induces expression of the cell adhesion molecule E-cadherin, loss of which is associated with a more aggressive phenotype in prostate cancer cells 38.
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