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Feeding or pentagastrin in dogs, probably because of a decreased mucosal blood flow. More recently, Hasebe et al. 1998 ; showed with isolated mouse whole stomach that the use of N -nitro-L-arginine decreased the acid secretion induced by pentagastrin or vagal electrical stimulation. The present results, however, clearly showed that endogenous NO exerts a negative influence on the acid secretory response induced by gastric distention. Because L-NAME is known to cause gastric hypoperfusion Alumets et al., 1982; Bredt et al., 1990; Esplugues et al., 1996 ; , it is unlikely that the enhanced acid secretion observed under the blockade of NO production is attributable to an increase in the mucosal blood flow. It should also be noted in this study that the enhancement by L-NAME of the distention-induced acid response was almost totally attenuated by vagotomy and capsaicin pretreatment, again confirming that gastric distention requires both sensory and vagus nerves for eliciting stimulation of acid secretion. Because NO-containing neurons have been identified in the central nervous system as well as in the gastrointestinal mucosa Bredt et al., 1990 ; and because NO plays a role as a neuromodulator in some nonadrenergic noncholinergic neurons in the gut Sanders and Ward, 1992; Moncada et al., 1993 ; , it is possible that NO decreases vagally mediated acid secretion by suppressing neuronal activity of the vagus nerves. On the other hand, it is known that vagally induced acid secretion is in part mediated by endogenous histamine release from enterochromaffin-like ECL ; cells Richardson, 1978; Sandvik et al., 1987 ; . We found that gastric distention also caused a release of histamine in the mucosa via a mechanism that depends on both vagus nerves and NO. Salvemini et al. 1991 ; reported that exogenous NO inhibited the release of histamine in rat mast cells, mediated via a guanylate and vicoprofen. 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There have been no direct comparisons of glatiramer, interferon--1a, and interferon--1b. Direct comparisons of these drugs in well-designed trials are obviously necessary before conclusions may be drawn about their relative advantages and disadvantages. The potential advantages of combining these agents need to be evaluated. Glatiramer acetate and interferon--1b, both of which cause immunomodulatory changes in T helper-1 cell lines, have been studied in combination in one study.Their action was found to be additive.42 Based on available evidence, any of the three agents could be chosen for initial therapy for RRMS. If the initial choice fails, then one of the other agents can be selected. A treatment algorithm for MS is presented in Exhibit 3.43 and xalatan.
Falciparum malaria kills over 1 million individuals in subSaharan Africa each year, and the development of an effective malaria vaccine remains a public health priority. Plasmodium falciparum is inoculated by mosquitoes into the human bloodstream as a motile sporozoite that requires development within hepatocytes prior to infecting erythrocytes. Although severe disease occurs during the erythrocytic phase of infection, a protective vaccine could limit parasite growth at any stage of development. Because cytotoxic T lymphocytes CTLs ; and gamma interferon IFN- ; can kill liver-stage malaria parasites in animal models 26, 28, 31, ; , human vaccines designed to control the liver-stage of P. falciparum have focused on eliciting similar responses. Liver-stage antigen 1 LSA-1 ; 15 ; , a 200-kDa antigen that accumulates as flocculent material in the parasitophorous vacuole of infected hepatocytes 17 ; , is a leading candidate for inclusion in a P. falciparum vaccine. LSA-1 contains several B- and T-cell epitopes that are immunogenic during the course of natural infection 12 ; , and it stimulates CTLs and IFN- in naturally exposed individuals 12, 16 ; . A specific LSA-1 peptide that associates with HLA-B53 elicits CTL responses 16 ; , and HLA-B53 has been associated with naturally acquired resistance to severe malaria in some but not all studies 9, 16 ; . Human residents of areas where malaria is holoendemic develop naturally acquired resistance to malarial infection, and this resistance serves as a model for vaccine development. Because P. falciparum can cause frequent infections, and ongoing infection can bias measurements of immune responses 23 ; , cross-sectional studies have a limited ability to define responses that predict protection. Therefore, we conducted a prospective study, defining the reappearance of parasitemia after eradication therapy in a cohort of naturally exposed volunteers, to examine the protective role of naturally acquired anti-LSA-1 responses. Understanding the relationship be * Corresponding author. Present address: Room 2028, Immunology, Building 40, Walter Reed Army Institute of Research, 14th & Dahlia St., Washington, DC 20307-5100. Phone: 202 ; 782-1234 or 202 ; 7820200. Fax: 202 ; 782-0748. E-mail: duffyp wrsmtp-ccmail.army l. Present address: Hospital of the University of Pennsylvania, Department of Pathology and Laboratory Medicine, Philadelphia, PA 19104. 3424.

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