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The CA provided some valuable insights into how to improve the financial services of FFIs to the population by adapting the existing services. The results of this research show that the VBP particularly can improve its credit services by offering individual loans, as this kind of lending scheme was strongly preferred by the sample population. This approach would also reduce the administration time of the credit procedure, i.e. TCs.115 It could also go hand in hand with the increasing introduction of physical collateral instead of group liability, as farmers showed that they are able and willing to use their land use certificates Red Books ; as collateral. However, without an effective land market for trading Red Books, it will probably be risky for the credit institutes to rely more on land use certificates as collateral. Nevertheless, VBP and VBARD together already have enormous outreach. At this stage, implementing a consolidation policy and establishing financially sustainable structures would deserve priority over boosting credit outreach further by implementing new structures. An important element for inducing innovation in the microfinance industry is to nurture conditions for greater competition between different suppliers. As long as no effective competition exists in the rural financial market in Northern Vietnam, there is little incentive for the institutes to improve their products. The only competition exists between the VBP and the VBARD. This research has shown that poor households are able and willing to save. Over 80% of the households demand a formal savings scheme. The supply of savings services offers firstly the possibility to create financially sustainable structures within the existing institutes, and secondly to boost the outreach of the formal financial sector. When offering savings services to the rural population, especially to the poor, close physical proximity to customers is seen as a key factor. This proximity could be achieved by creating decentralized profit centers. Credit officers would collect and pay out savings as well as performing all credit activities. Thus, the deposit collection could be done within the village. The local savings collection by the credit officer would also influence very positively the credit business. The credit officer has access to a much broader range of information to.
Small ventricular septal defect arterial O2 saturation 90%, hemoglobin 123 g L ; . PPH was a diagnosis of exclusion and required the demonstrated absence of a variety of cardiopulmonary and systemic diseases, as previously described.4 None of the patients had familial PAH. Patients had a right heart catheterization and a 6-minute walk at baseline and after 3 months of treatment. Two 6-minute walks were performed before entering the study to avoid confounding training effects. The 6-minute walks were performed randomly during working hours, but the catheterizations always were performed early in the morning, before the morning dose of sildenafil. Patients 3, 4, and 5 had cardiac MRI at baseline and after 3 months of treatment. Patients 1 and 2 could not be studied because of claustrophobia and a pacemaker, respectively. MRI studies were performed on a 1.5 T Siemens Sonata unit using a body phase-array coil. The right ventricle was imaged using 8- to 9-mm contiguous, single-slice, breath-hold cine, true-FISP sequences in the short-axis plane.
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Yang et al uretic peptide binding sites in the rat central nervous system and adrenal gland. J Ncurosci 1986; 6: 2004-2011 Kurihara M, Saavedra JM, Shigematsu K: Localization and characterization of atria! natriuretic peptide binding sites in discrete areas of rat brain and pituitary gland by quantitative autoradiography. Brain Res 1987; 4O8: 31-39 Sved AF, Imaizuma T, Talman WT, Reis DJ: Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesion. Hypertension 1985; 7: 262-267 McKitrick DJ, Calaresu FR: Cardiovascular responses to microinjection of ANF into dorsal medulla of rats. J Physiol 1988; 255: R182-R187 13. Ermirio R, Ruggeri P, Cogo CE, Molinari C, Calaresu FR: Neuronal and cardiovascular responses to ANF microinjected into the solitary nucleus. J Physiol 1989; 256: R577-R582 14. Parinos G, Watson C: The Rat Brain in Stereotwdc Coordinates. New York, Academic Press, 1986 15. Catelli JM, Sved AF: Enhanced pressor response to GABA in the nucleus tractus solitarii of the spontaneously hypertensive rat. Eur J Pharmacol 1988; 151: 243-248 Mukoyama M, Nakao K, Yamada T, Itoh H, Sugawara A, Satio Y, Arai H, Hosoda K, Shirakami G, Morri N, Shiono S, Imura H: A monoclonal antibody against N-terminus of ar-atrial natriuretic polypeptide a-ANP ; : A useful tool for preferential detection of naturally circulating ANP. Biochem Biophys Res Commun 1988; 151: 1277-1284 Itoh H, Nakao K, Mukoyama M, Yamada T, Hosoda K, Shirakami G, Morri N, Sugawara A, Saito Y, Shiono S, Arai H, Yoshida I, Imura H: Chronic blockade of endogenous atria! natriuretic polypeptide ANP ; by monoclonal antibody against ANP accelerates the development of hypertension in spontaneously hypertensive and deoxycorticosterone acetate-salthypertensive rats. Clin Invest 1989; 84: 145-154 Lindmark R, Thoren-Tolling K, Sjoquist J: Binding of immunoglobulins of protein A and immunoglobulin levels in mammalian sera. Immunol Methods 1983; 62: 1-13 Yang RH, Jin H, Chen YF, Wyss JM, Oparil S: Blockade of endogenous anterior hypothalamic atrial natriuretic peptide with monoclonal antibody lowers blood pressure in spontaneously hypertensive rats. Clin Invest 1990, 86: 1985-1990 Jin H, Yang RH, Chen YF, Jackson RM, Itoh H, Mukoyama M, Nakao K, Imura H, Oparil S: Atrial natriuretic peptide in acute hypoxia-inducted pulmonary hypertension in rats. JAppl Physiol 1991; 71: 807-814 Ruskoaho H, Leppaluoto J: Immunoreactive atrial natriuretic peptide in ventricles, atria, hypothalamus, and plasma of genetically hypertensive rats. Ore Res 1988; 62: 384-394 Kuchel O, Debinski W, Thibault G, Cantin M, Genest J: Ganglionic, spinal cord and hypothalamic atrial natriuretic factor Its distribution, origin and possible role in spontaneously hypertensive rats. Hypertens 1988; 6 suppl ; : 279-281 23. Imada T, Takayanagi R, Inagami T: Changes in the content of atrial natriuretic factor with the progression of hypertension in spontaneously hypertensive rats. Biochem Biophys Res Commun 1985; 133: 759-765 Takayanagi R, Imada T, Grammer RT, Misono KS, Naruse M, Inagami T: Atrial natriuretic factor in spontaneously hypertensive rats: Concentration changes with the progression of hypertension and elevated formation of cyclic GMP. Hypertens 1986; 4 suppl ; : 303-307 25. Morri N, Kawauwa N, Itoh H, Sugawara A, Sakamoto M, Yamada T, Shiono S, Kihera M, Mano M, Yamori Y, Imura H: Increased tissue level of atrial natriuretic polypeptide in the hypothalamus and septum of spontaneously hypertensive rats. Hypertens 1988; 4 suppl ; : 3O9-312 26. Takayanagi R, Grammer RT, Inagama T: Regional increase of cyclic GMP by atrial natriuretic factor in rat brain: Markedly elevated response in spontaneously hypertensive rats. Life Sci 1986: 39: 573-580 Squadrito F, Frisina N, Buemi M, Sturniolo R, Autolitano A, Magri V, Squadrito G, Caputi AP: A comparison of synthetic human and rat ANP administered intracerebroventricularly in.
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Table. Examples of Gene Variants That Have Been Associated With Multiple Sclerosis Phenotype.
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Patris M, Bouchard J-M, Bougerol T, et al. Citalopram versus fluoxetine; a doubleblind, controlled, multicentre, phase III trial in patients with unipolar major depression treated in general practice. Int Clin Psychopharmacol. 1996; 11: 129-136.
Unadjusted and adjusted for contraindications ; data feedback will be provided. The unadjusted denominator will include all patients with prior myocardial infarction. The adjusted denominator will exclude patients with: History of Class IV congestive ; heart failure Bradycardia, defined as heart rate less than 50 bpm without beta-blocker therapy History of second or third degree AV block without permanent pacemaker Physician documentation indicating that treatment was considered and hydroxychloroquine.
I was finally diagnosed with Addison's in 1980, at the age of 40, after eight months of to-ing and fro-ing to various specialists. I was told I was anorexic, I was in need of tranquilizers because I was turning 40 - endless excuses for a problem they could not solve. By this time I had lost about 10 kilos, as I was not eating properly. I just could not force food down, and I guess was becoming anaemic due to this. When I started vomiting in the morning my husband decided enough was enough, and we went to see a Dr Tambyah at Mt. Elizabeth Hospital in Singapore. At this stage I was barely able to walk six or seven metres without having to sit down and rest. Dr Tambyah looked at me, looked at my notes and said: "I think I know what's wrong with you". I was admitted to the hospital, a 24 hour urine sample was taken, and next day he came and told me I had Addison's. I was started on Cortisone Acetate and Florinef immediately, and within a day began to feel so much better. I was given a CT scan to see if there was any calcification of the adrenal glands, but nothing showed up so they said the glands had atrophied. I at present taking hydrocortisone 10 mg BD and Florinef 0.1mg 1 tablet in the morning and 1 2 tablet in the evening. I take my afternoon dose of hydrocortisone later than advised, and it does not present a problem for me with regard to sleeping. I find if I schedule it earlier in the afternoon, I inclined to forget it sometimes, so it's easier to leave the pills on the table and take them with my evening meal.
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Frequently associated with a bronchodilator response, but generally with preservation of the PaC02 until the development of severe airway ob struction. The symptoms noted by enrollees in the Registry were similar to those associated with nonarAT deficiency emphysema, but also included symptoms more commonly associated with asthma and or chronic bronchitis. However, despite the fact that the Registry is the largest of its kind dealing with arAT deficiency, there are certain methodologic aspects of the Registry that temper how its results may be generalized to the general population with ax-AT deficiency. Recause the Registry is not popu lation based, the assembled cohort is not a represen tative sample of all individuals with this disorder. More specifically, because of the methods of recruit and hydroxyurea.
Forty-five prepubertal children treated with hGH for short stature took part in the study. Twenty-three were GH deficient, aged 3-14.2 yr. Eight patients, aged 10.5-15 yr, were treated with hGH for Turner's syndrome, and 14 patients, aged 3-9 yr, were treated for intrauterine growth retardation IUGR ; . GH deficiency was defined as at least 2 subnormal GH responses to 2 separate provocative tests peak GH, lo pg L ; . All patients except 1 had partial isolated idiopathic GH deficiency. The patient who had complete GH deficiency in a context of panhypopituitarism received Tq and hydrocortisone replacement therapy beginning 2 months before hGH treatment. hGH was given by daily SC injection [Saizen, Serono Milan, Italy.
The study drug formulations or known immunosuppression were also exclusion criteria. The study was performed in accordance with the Declaration of Helsinki and all applicable amendments. All patients gave written informed consent prior to enrollment, and the study was reviewed and approved by the recognized ethics review committee at each individual center and ibandronate
~: Ag-Ab not added. No DNP added, demonstrated by the addition of 2 mg corticosteroid to the bottom compartment. Only 40% inhibition of chemotaxis occurred, in contrast to 99% inhibition when the same amount was added directly to the cell suspension in the upper compartment Text-fig. 1. ; . Furthermore, the addition of 1.25 mg hydrocortisone to the lower compartment resulted in no inhibition of chemotaxis, although a comparable amount added directly to the cell suspension in the upper compartment would result in 92 % inhibition of chemotaxis Text-fig. 1. ; . I t likely that inhibition of chemotaxis after addition of steroid to the lower compartment was due to diffusion into the cell suspension of the upper compartment. In addition, it was found that the inhibitory effects of hydrocortisone were, to a large extent, irreversible, since washing the PMN's failed to result in significant restoration of the chemotactic capacity of these cells. The restriction of the inhibitory effect to certain corticosteroids was demonstrated by the finding that another steroid, estrone, at a concentration in the cell.
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There is no accepted normal range for cortisol concentrations in the preterm infant. Clinically well preterm infants may have quite low cortisol concentrations without evidence of harm.36 However, lower cortisol concentrations and or decreased response to adrenal stimulation have been documented in sicker infants, in those receiving vasopressor support or mechanical ventilation, and in those developing BPD or dying.69, 12, 13 These lower values are contrary to the expectation that the seriously ill should have higher cortisol concentrations than well individuals and may be similar to the relative adrenal insufficiency documented in other critically ill patients, which manifests as cardiovascular instability and increased mortality.13 The decreased mortality rate in hydrocortisone-treated infants born after chorioamnionitis may be analogous to the decreased mortality reported in adults with septic shock and adrenal insufficiency treated with hydrocortisone.4 Hydrocortisone-treated infants in this study also showed higher blood pressure without an increase in hypertension. We found that infants developing BPD had decreased cortisol response to ACTH stimulation after the treatment period, which is consistent with several previous studies showing decreased basal and or stimulated cortisol values early in life in such infants6, 12, 14, 20, and with the hypothesis that decreased adrenal function promotes the development of BPD in intubated extremely low birth weight infants. In 1 previous study, Ng et al38 reported that although lower cortisol values in the first week of life correlated with a longer duration of oxygen therapy, by the second week the reverse was true: higher cortisol values correlated with longer duration of oxygen therapy, perhaps indicating a stress response to continuing illness. The infants in our study were smaller and sicker, and all were intubated at study entry. These more immature infants might be at risk for a longer period of developmental adrenal immaturity. In our study, we also included the presence or absence of histologic chorioamnionitis in the analyses. Because chorioamnionitis increases both inflammation and cortisol concentrations in the fetus and newborn, 15, 18, 20, not including this factor in the analysis may mask differences between groups. Hydrocortisone treatment resulted in serum concentrations similar to values previously documented in other patient populations under stress.14 However, a few infants had substantially elevated cortisol concentrations, and those who experienced spontaneous gastrointestinal perforation had significantly higher values than those who did not, both before and during therapy, suggesting that cortisol concentrations should be monitored in infants being treated with hydrocortisone. Patient enrollment in this study was stopped because of a significant increase in apparently spontaneous perforation of the gastrointestinal tract in hydrocortisone-treated infants. Differentiating this entity from NEC can be difficult; however, there was no difference in NEC-associated perforation between groups. Spontaneous gastrointestinal perforation occurred less often in this placebo group 2% ; than has and ifex.
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Since the stool and urine samples are analysed on the day of the survey, it should not take long to collate the results and produce a short report that describes the prevalence and intensity of infection in each school and each area. WHO recommendations should then be used to decide on appropriate action Tables 1 and 2 ; . Schistosomiasis and STH have slightly different cut-offs for action; crucially, however, where the two infections co-exist they are treated at the same time.
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