Papers by Luis López-Rivera
<p>Incidence rates of RTIs in Peru by region, 1993–2008 per 100,000 inhabitants.</p
<p>*Note: The data for incidence rates by sex or age groups were standardized to the Peruvi... more <p>*Note: The data for incidence rates by sex or age groups were standardized to the Peruvian population of 2008.</p
<p>A) Males; B) Females; C) 18 Years and Older; D) Less than 18 Years.</p
<p>A) 18 years and older; B) Males; C) Less than 18 years; D) Females.</p
<p>A) Mortality; B) Fatality.</p
<p>Map of the regions of Peru.</p
<p>Fatality rate of RTIs in Peru by region, 1993–2008 per 100,000 RTI victims.</p
<p>Total Crude* and Adjusted** incidence of road traffic incidences in Peru, 1973–2008; ann... more <p>Total Crude* and Adjusted** incidence of road traffic incidences in Peru, 1973–2008; annual GDP per capita 1973–2008.</p
<p>*Notes: Variables tested in the adjusted models: (1) Total population, (2) Vehicle densi... more <p>*Notes: Variables tested in the adjusted models: (1) Total population, (2) Vehicle density, (3) Road density, (4) Allowance of imported used vehicles allowed. SOAT and the Zero Tolerance Plan were not associated with incidence, mortality or fatality in multivariable models.</p
<p>A) 18 years and older; B) Males; C) Less than 18 years; D) Females.</p
The Pediatric infectious disease journal, 2014
Vaccines against pandemic A/H1N1 influenza should provide protective immunity in children, becaus... more Vaccines against pandemic A/H1N1 influenza should provide protective immunity in children, because they are at greater risk of disease than adults. This study was conducted to identify the optimal dose of an MF59®-adjuvanted, egg-derived, A/H1N1 influenza vaccine for young children. Children 6-11 months (N = 144) and 12-35 months (N = 186) of age received vaccine formulations containing either 3.75 μg antigen with half the standard dose of MF59 or 7.5 μg antigen with a standard dose of MF59, or a nonadjuvanted formulation containing 15 μg antigen (children 12-35 months only). Participants were given 2 primary vaccine doses 3 weeks apart, followed by 1 booster dose of MF59-adjuvanted seasonal influenza vaccine 1 year later. Immunogenicity was assessed by hemagglutination inhibition and microneutralization assays. All vaccine formulations were highly immunogenic and met all 3 European licensure criteria after 2 doses. MF59-adjuvanted vaccines met all licensure criteria after 1 dose in...
Journal of the Autonomic Nervous System, 1994
The distribution of acetylcholinesterase (AChE)-positive nerve fibers and cells, as well as the e... more The distribution of acetylcholinesterase (AChE)-positive nerve fibers and cells, as well as the effects of acetylcholine (ACh) on ureteral smooth muscle and small resistance arteries were investigated in the equine ureter by means of histochemical, classic organ baths and myograph techniques. AChE-positive nerve fibers were widely distributed throughout the ureteral wall forming muscular, subepithelial and perivascular nerve plexuses, whose density was highest at the intravesical ureter. AChE-positive nerve cells were also identified grouped as adventitial or intramural ganglia. ACh increased concentration-dependently both the frequency of phasic contractile activity and basal tone of the isolated intravesical ureter, the pD2 values being 6.31 +/- 0.18 and 6.59 +/- 0.13, respectively. The ACh-induced motor effects in ureteral smooth muscle were blocked by atropine, giving pIC50 values of 8.58 +/- 0.08 and 9.68 +/- 0.05 for phasic activity and tone, respectively. Hexamethonium only inhibited ACh-evoked contractile activity at the highest concentration used. ACh elicited a potent endothelium-dependent relaxation of equine ureteral resistance arteries precontracted with 40 mM K-PSS, the pD2 value being 7.94 +/- 0.07. This relaxant response was abolished in the presence of the nitric oxide (NO) inhibitor, NG-nitro-L-arginine (L-NNA), the blockade being reversed by subsequent incubation with the NO exogenous substrate, L-arginine. The ACh-induced relaxation was competitively antagonized by atropine (pA2 = 10.05 +/- 0.18). The present results suggest the existence of a rich cholinergic innervation in the equine ureter which controls both ureteral smooth muscle and resistance arteries motor activity through the muscarinic effects of ACh. In addition, the ACh relaxant response in the ureteral resistance arteries seems to be mediated by NO.
Journal of the Autonomic Nervous System, 1991
The distribution of cholinergic nerve fibres, as well as the characterization of the muscarinic r... more The distribution of cholinergic nerve fibres, as well as the characterization of the muscarinic receptors responsible for the contraction, were determined in the detrusor smooth muscle of the sheep. The results obtained demonstrated a rich presence of acetylcholinesterase (AChE)-positive fibres distributed throughout the bladder body forming dense neuromuscular, subepithelial and perivascular plexuses. Furthermore, intramural ganglia containing AChE-positive cell bodies were identified. However, acetylcholine and carbachol induced a dose-dependent contraction of detrusor smooth muscle. The effect observed with carbachol was competitively antagonized by atropine (pA2: 8.94), pirenzepine (pA2: 7.38), AF-DX 116 (pA2: 7.35), 4-DAMP (pA2: 9.26) and hexahydroxiladifenidol (HHSiD) (pA2: 8.49). The pA2 value for pirenzepine is intermediate between M1- and M2-receptors which suggests that this antagonist does not act on M1- or M2-receptors, but that it does on M3-receptors. The pA2 value for AF-DX 116 is consistent with the presence of M2-receptors in this tissue. Moreover, the pA2 values obtained for both 4-DAMP and HHSiD are in agreement with the presence of M3-receptors, due to the lack of effect of pirenzepine on M1-muscarinic receptors. These results indicate the existence of a rich parasympathetic innervation in the sheep detrusor muscle and suggest that its contraction could be mediated by the stimulation of muscarinic receptors belonging to both M3- and M2-subtypes.
Neurourology and Urodynamics, 2006
The Journal of Urology, 2004
The current in vitro study was performed to investigate intracellular mechanisms underlying prost... more The current in vitro study was performed to investigate intracellular mechanisms underlying prostaglandin E1 (PGE1) elicited vasodilation in isolated penile resistance arteries and evaluate whether there may be interactions with the nitric oxide (NO)/cyclic guanosine 3&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;,5&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-monophosphate (cGMP) pathway. Second or third order branches of the horse deep intracavernous penile artery were mounted in microvascular myographs. The vasodilator effects of PGE1 and cyclic adenosine 3&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;,5&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-monophosphate (cAMP) elevating agents were evaluated in the absence and the presence of inhibitors of the adenylate cyclase/cAMP and the NO/cGMP pathways. PGE1, the adenylate cyclase activator forskolin, and the phosphodiesterase types 3 and 4 inhibitors milrinone and rolipram, respectively, dose dependently relaxed penile resistance arteries with rolipram being the most potent of the 4 relaxant agents. Threshold concentrations of rolipram markedly enhanced PGE1 elicited relaxations. The inhibition of cAMP dependent protein kinase decreased relaxant responses to PGE1, forskolin and rolipram. Neither mechanical endothelial cell removal nor the blockade of NO synthase or guanylate cyclase altered PGE1 relaxant responses. However, combined treatment with blockers of cAMP dependent protein kinase and cGMP dependent protein kinase unmasked an inhibitory effect of the latter on relaxations induced by PGE1 and forskolin. These results provide evidence for cAMP involvement in PGE1 elicited vasodilation of penile resistance arteries. They underline the importance of the adenylate cyclase/cAMP pathway in the relaxation of penile erectile tissue. Moreover, cAMP elevating agents seem to cross-activate cGMP dependent protein kinase, thus, interacting downstream with the NO/cGMP cascade.
The Journal of Urology, 2006
We investigated the role of the vascular endothelium and the L-arginine/nitric oxide pathway in t... more We investigated the role of the vascular endothelium and the L-arginine/nitric oxide pathway in the vasorelaxant effect of the phosphodiesterase type 5 inhibitor sildenafil in penile resistance arteries. Second or third order branches of the horse deep intracavernous penile artery were mounted in microvascular myographs. The vasodilator effects of sildenafil and the NO donor SNAP (S-nitrosoacetyl-D,L-penicillamine) were evaluated in the absence and presence of the endothelium and inhibitors of the NO/cGMP (cyclic guanosine 3&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;,5&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-monophosphate) pathway. In phenylephrine precontracted, endothelium intact arteries sildenafil elicited potent relaxations that were markedly decreased by the blockade of soluble guanylate cyclase with ODQ (1H-[1,2,4]oxadiazolo[4-3a]quinoxalin-1-one). Endothelium removal and the inhibition of NO synthase with N(G)-nitro-L-arginine (L-NOARG) caused pronounced inhibition of sildenafil elicited relaxations but not of SNAP induced responses. Combined treatment with the cyclooxygenase blocker indomethacin and L-NOARG caused significantly greater inhibition of sildenafil relaxations than that produced by L-NOARG alone. Inhibitors of the cGMP (PKG) and the cAMP (cyclic adenosine 3&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;,5&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-monophosphate) dependent protein kinases Rp-8-Br-PET-cGMPS (beta-phenyl-1, N2-etheno-8-bromoguanosine-3&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;,5&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-cyclic monophosphorothioate, Rp-isomer) and Rp-8-CPT-cAMPS (Rp-8-CPT-cAMPS (8-(4-chlorophenylthio)…
Journal of Geophysical Research, 2009
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Papers by Luis López-Rivera