Database : MEDLINE
Search on : pro-opiomelanocortin [Words]
References found : 6456 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 646 go to page                         

  1 / 6456 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29408859
[Au] Autor:Liu H; Wang J; Li L; Han C; He H; Xu H
[Ad] Address:Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, Sichuan, P.R. China.
[Ti] Title:Transcriptome analysis revealed the possible regulatory pathways initiating female geese broodiness within the hypothalamic-pituitary-gonadal axis.
[So] Source:PLoS One;13(2):e0191213, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Geese have the strongest tendency toward broodiness among all poultry. The mechanisms initiating broodiness within the goose hypothalamic-pituitary-gonadal axis (HPGA) are still unclear. Here, we reported the transcriptome differences between laying and initial nesting within the HPGA tissues of geese. We constructed a unigene database based on HPGA tissues and identified 128,148 unigenes, 100% of which have been annotated. By using Digital Gene Expression (DGE) sequencing, we screened 19, 110, 289, and 211 differentially expressed genes (DEGs) in the hypothalamus, pituitary gland, stroma ovarii, and follicles, respectively, between laying and nesting geese. Expression changes of hypocretin (HCRT) and pro-opiomelanocortin (POMC) in the hypothalamus of nesting geese may cause appetite reduction, which is possibly the first step and a prerequisite to initiate broodiness. In addition to prolactin (PRL), follicle-stimulating hormone (FSH) and luteinizing hormone (LH), genes including oxytocin-neurophysin (OXT), chordin-like protein 1 (CHRDL1) and growth hormone (GH), expressed in the pituitary gland, are new candidate molecules that may be involved in broodiness in geese. Heme oxygenase 1 (HMOX1) in the pituitary gland, the proto-oncogene c-Fos (FOS), heat shock protein 90-alpha (HSP90AA), and cyclin-dependent kinase 1 (CDK1) in the ovary that may consolidate and transduce signals regulating the HPGA during broodiness in geese.
[Mh] MeSH terms primary: Gonads/physiology
Hypothalamo-Hypophyseal System/physiology
Transcriptome
[Mh] MeSH terms secundary: Animals
Female
Geese
Gene Expression
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180207
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191213

  2 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29309431
[Au] Autor:Carmalt JL; Mortazavi S; McOnie RC; Allen AL; Unniappan S
[Ad] Address:Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
[Ti] Title:Profiles of pro-opiomelanocortin and encoded peptides, and their processing enzymes in equine pituitary pars intermedia dysfunction.
[So] Source:PLoS One;13(1):e0190796, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Equine pituitary pars intermedia dysfunction (PPID) is characterized by hyperplasia of the pars intermedia (PI) melanotrophs of the pituitary gland (PG), and increased production of proopiomelanocortin (POMC). POMC is cleaved by prohormone convertase 1 (PC1) to produce adrenocorticotropic hormone (ACTH), and further processing of ACTH by PC2 to produce alpha-melanocyte stimulating hormone (α-MSH) and corticotropin-like intermediate peptide (CLIP). High plasma ACTH concentrations in horses with PPID might be related to reduced conversion of ACTH to α-MSH by PCs. The hypothesis of this study was that PC1 and PC2 expression in the pituitary gland are altered in PPID, resulting in an abnormal relative abundance of POMC derived proteins. The objectives of this study were to identify the partial sequences of equine POMC, PC1, and PC2 mRNAs; and to determine whether the expression of POMC, PC1, and PC2 mRNAs in whole pituitary extracts, and POMC-protein in the cavernous sinus blood of horses are altered in PPID. We confirmed (RT-PCR and sequencing) that the partial sequences obtained match the corresponding regions of predicted equine POMC, PC1 and PC2 sequences. The expression (quantification by RT-qPCR) of POMC, PC1 and PC2 mRNAs were found upregulated in the pituitary of horses with PPID. Plasma (measured using RIA/ELISA) ACTH and α-MSH were elevated in PPID horses. These results indicate distinct differences in gene and protein expression of POMC and its intermediates, and processing enzymes in PPID. It provides evidence to support the notion that local, pituitary-specific inadequacies in prohormone processing likely contribute to equine PPID.
[Mh] MeSH terms primary: Peptides/metabolism
Pituitary Gland, Intermediate/metabolism
Pro-Opiomelanocortin/metabolism
[Mh] MeSH terms secundary: Adrenocorticotropic Hormone/blood
Amino Acid Sequence
Animals
Enzyme-Linked Immunosorbent Assay
Horses
Pituitary Gland, Intermediate/enzymology
Pro-Opiomelanocortin/blood
Pro-Opiomelanocortin/chemistry
Pro-Opiomelanocortin/genetics
Proprotein Convertase 1/genetics
Proprotein Convertase 1/metabolism
Proprotein Convertase 2/genetics
Proprotein Convertase 2/metabolism
RNA, Messenger/metabolism
Sequence Homology, Amino Acid
alpha-MSH/blood
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Peptides); 0 (RNA, Messenger); 581-05-5 (alpha-MSH); 66796-54-1 (Pro-Opiomelanocortin); 9002-60-2 (Adrenocorticotropic Hormone); EC 3.4.21.93 (Proprotein Convertase 1); EC 3.4.21.94 (Proprotein Convertase 2)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180109
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190796

  3 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29457782
[Au] Autor:Kim GH; Shi G; Somlo DR; Haataja L; Song S; Long Q; Nillni EA; Low MJ; Arvan P; Myers MG; Qi L
[Ad] Address:Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
[Ti] Title:Hypothalamic ER-associated degradation regulates POMC maturation, feeding, and age-associated obesity.
[So] Source:J Clin Invest;128(3):1125-1140, 2018 Mar 01.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pro-opiomelanocortin (POMC) neurons function as key regulators of metabolism and physiology by releasing prohormone-derived neuropeptides with distinct biological activities. However, our understanding of early events in prohormone maturation in the ER remains incomplete. Highlighting the significance of this gap in knowledge, a single POMC cysteine-to-phenylalanine mutation at position 28 (POMC-C28F) is defective for ER processing and causes early onset obesity in a dominant-negative manner in humans through an unclear mechanism. Here, we report a pathologically important role of Sel1L-Hrd1, the protein complex of ER-associated degradation (ERAD), within POMC neurons. Mice with POMC neuron-specific Sel1L deficiency developed age-associated obesity due, at least in part, to the ER retention of POMC that led to hyperphagia. The Sel1L-Hrd1 complex targets a fraction of nascent POMC molecules for ubiquitination and proteasomal degradation, preventing accumulation of misfolded and aggregated POMC, thereby ensuring that another fraction of POMC can undergo normal posttranslational processing and trafficking for secretion. Moreover, we found that the disease-associated POMC-C28F mutant evades ERAD and becomes aggregated due to the presence of a highly reactive unpaired cysteine thiol at position 50. Thus, this study not only identifies ERAD as an important mechanism regulating POMC maturation within the ER, but also provides insights into the pathogenesis of monogenic obesity associated with defective prohormone folding.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  4 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29483626
[Au] Autor:Ogawa K; Suga H; Ozone C; Sakakibara M; Yamada T; Kano M; Mitsumoto K; Kasai T; Kodani Y; Nagasaki H; Yamamoto N; Hagiwara D; Goto M; Banno R; Sugimura Y; Arima H
[Ad] Address:Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
[Ti] Title:Vasopressin-secreting neurons derived from human embryonic stem cells through specific induction of dorsal hypothalamic progenitors.
[So] Source:Sci Rep;8(1):3615, 2018 Feb 26.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Arginine-vasopressin (AVP) neurons exist in the hypothalamus, a major region of the diencephalon, and play an essential role in water balance. Here, we established the differentiation method for AVP-secreting neurons from human embryonic stem cells (hESCs) by recapitulating in vitro the in vivo embryonic developmental processes of AVP neurons. At first, the differentiation efficiency was improved. That was achieved through the optimization of the culture condition for obtaining dorsal hypothalamic progenitors. Secondly, the induced AVP neurons were identified by immunohistochemistry and these neurons secreted AVP after potassium chloride stimulation. Additionally, other hypothalamic neuropeptides were also detected, such as oxytocin, corticotropin-releasing hormone, thyrotropin-releasing hormone, pro-opiomelanocortin, agouti-related peptide, orexin, and melanin-concentrating hormone. This is the first report describing the generation of secretory AVP neurons derived from hESCs. This method will be applicable to research using disease models and, potentially, for regenerative medicine of the hypothalamus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-22053-x

  5 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29352321
[Au] Autor:Jacobi CLJ; Stein C
[Ad] Address:Klinik für Anästhesiologie und operative Intensivmedizin, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany.
[Ti] Title:Inflammatory-linked changes in CpG island methylation of three opioid peptide genes in a rat model for pain.
[So] Source:PLoS One;13(1):e0191698, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Expression of the opioid peptide genes proopiomelanocortin (Pomc), proenkephalin (Penk), and prodynorphin (Pdyn), in immune cells plays a key role in endogenous pain control. In a rat model of painful unilateral paw inflammation, we isolated cells from popliteal lymph nodes and evaluated the role of CpG island C5-methylation on the transcriptional activation of those genes. Using methylated DNA immunoprecipitation, we sorted gDNA into methylated (me) and non-me fractions and then determined the CpG island methylation status of each fraction via quantitative Real Time-PCR (qRT-PCR). In silico analysis by MethPrimer software identified one CpG island in Pdyn and three each in Pomc and Penk. No substantial changes in C5-methylation of any gene were observed. In conclusion, the CpG island methylation status does not seem to be a key regulator of opioid gene activation in immune cells during peripheral tissue inflammation.
[Mh] MeSH terms primary: CpG Islands
DNA Methylation
Enkephalins/genetics
Inflammation/genetics
Pain/genetics
Pro-Opiomelanocortin/genetics
Protein Precursors/genetics
[Mh] MeSH terms secundary: Animals
Disease Models, Animal
Gene Expression Regulation
Inflammation/metabolism
Male
Pain/metabolism
Rats
Rats, Wistar
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Enkephalins); 0 (Protein Precursors); 0 (proenkephalin); 66796-54-1 (Pro-Opiomelanocortin); 93443-35-7 (preproenkephalin)
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[Js] Journal subset:IM
[Da] Date of entry for processing:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191698

  6 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29207922
[Au] Autor:Daniels S; Pratt M; Zhou Y; Leri F
[Ad] Address:1 University of Guelph, Guelph, Canada.
[Ti] Title:Effect of steady-state methadone on high fructose corn syrup consumption in rats.
[So] Source:J Psychopharmacol;32(2):215-222, 2018 Feb.
[Is] ISSN:1461-7285
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Patients undergoing methadone maintenance treatment self-report enhanced preferences for, and excessive consumption of, foods rich in sugar. However, it is unclear whether these are direct pharmacological effects of methadone or the consequences of metabolic dysfunctions induced by addiction to illicit opiates. Hence, the current study in drug-naïve male Sprague-Dawley rats explored the effects of steady-state methadone delivered by osmotic mini-pumps (13 days; 0, 10, 30 mg/kg/day) on consumption of rat chow and a palatable, sweet, liquid high fructose corn syrup solution. Six days after the removal of the pumps, mRNA expression of genes involved in responses to stress and rewards were quantified: pro-opiomelanocortin in the hypothalamus, mu-opioid receptor in the nucleus accumbens, and dopamine D2 receptor in the dorsal striatum. Taste reactivity and locomotion tests were also performed throughout the study. It was found that methadone increased caloric intake from high fructose corn syrup and reduced caloric intake from chow, effects that could not be directly ascribed to changes in high fructose corn syrup taste reactivity or motor functions. However, the changes in caloric intake displayed significant tolerance, and mRNA expression analysis suggested that methadone attenuated the effect of high fructose corn syrup on pro-opiomelanocortin mRNA, and possibly on dopamine D2 receptor mRNA. These findings in rats suggest that the pharmacological effect of methadone, administered to achieve steady-state maintenance, may not be the primary cause of dietary alterations reported by patients maintained on methadone.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:In-Data-Review
[do] DOI:10.1177/0269881117742116

  7 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29412826
[Au] Autor:Al-Najim W; Roux CWL; Docherty NG
[Ad] Address:Diabetes Complications Research Centre, Conway Institute, School of Medicine and Medical Sciences, University College Dublin, Ireland; Investigative Science, Imperial College London, UK.
[Ti] Title:Integrated insights into the role of alpha-melanocyte stimulatory hormone in the control of food intake and glycaemia.
[So] Source:Peptides;100:243-248, 2018 Feb.
[Is] ISSN:1873-5169
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Identifying peptide hormones with multipotent actions on both weight and glycaemia can have a significant impact on therapeutic options in the treatment of obesity and diabetes. This has been exemplified by recent advances involving pharmacological exploitation of glucagon-like peptide 1 biology. Herein, we summarise evidence supporting the potential candidacy in this light of alpha-melanocyte stimulatory hormone, an endogenous peptide hormone and a breakdown product of the neuropeptide pro-opiomelanocortin. We reference its well described central actions in the control of food intake and moreover highlight new data pointing to an important role for this peptide hormone in the periphery, in relation to glycaemic control.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180207
[Lr] Last revision date:180207
[St] Status:In-Data-Review

  8 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29293568
[Au] Autor:Do K; Laing BT; Landry T; Bunner W; Mersaud N; Matsubara T; Li P; Yuan Y; Lu Q; Huang H
[Ad] Address:Department of Kinesiology, East Carolina University, Greenville, North Carolina, United States of America.
[Ti] Title:The effects of exercise on hypothalamic neurodegeneration of Alzheimer's disease mouse model.
[So] Source:PLoS One;13(1):e0190205, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Alzheimer's disease is a neurodegenerative disorder that affects the central nervous system. In this study, we characterized and examined the early metabolic changes in the triple transgenic mouse AD model (3xtg-AD), and their relationship with the hypothalamus, a key regulator of metabolism in the central nervous system. We observed that the 3xtg-AD model exhibited significantly higher oxygen consumption as well as food intake before reported amyloid plaque formation, indicating that metabolic abnormalities occurred at early onset in the 3xtg-AD model compared with their counterparts. Analysis of gene expression in the hypothalamus indicated increased mRNA expression of inflammation- and apoptosis-related genes, as well as decreased gene expression of Agouti-related protein (AgRP) and Melanocortin 4 receptor (MC4R) at 12 weeks of age. Immunofluorescence analysis revealed that pro-opiomelanocortin (POMC) and NPY-expressing neurons decreased at 24 weeks in the 3xtg-AD model. Four weeks of voluntary exercise were sufficient to reverse the gene expression of inflammation and apoptotic markers in the hypothalamus, six weeks of exercise improved glucose metabolism, moreover, 8 weeks of voluntary exercise training attenuated apoptosis and augmented POMC and NPY-expressing neuronal populations in the hypothalamus compared to the control group. Our results indicated that early onset of metabolic abnormalities may contribute to the pathology of AD, which is associated with increased inflammation as well as decreased neuronal population and key neuropeptides in the hypothalamus. Furthermore, early intervention by voluntary exercise normalized hypothalamic inflammation and neurodegeneration as well as glucose metabolism in the 3xtg-AD model. The data, taken as a whole, suggests a hypothalamic-mediated mechanism where exercise prevents the progression of dementia and of Alzheimer's disease.
[Mh] MeSH terms primary: Alzheimer Disease/pathology
Disease Models, Animal
Hypothalamus/pathology
Physical Conditioning, Animal
[Mh] MeSH terms secundary: Animals
Biomarkers/metabolism
Gene Expression Regulation
Glucose/metabolism
Hypothalamus/metabolism
In Situ Nick-End Labeling
Mice
Mice, Transgenic
Mitochondria/metabolism
Pro-Opiomelanocortin/metabolism
Real-Time Polymerase Chain Reaction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Biomarkers); 66796-54-1 (Pro-Opiomelanocortin); IY9XDZ35W2 (Glucose)
[Em] Entry month:1802
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[Js] Journal subset:IM
[Da] Date of entry for processing:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190205

  9 / 6456 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 29391540
[Au] Autor:Kinyua AW; Ko CM; Doan KV; Yang DJ; Huynh MKQ; Moh SH; Choi YH; Kim KW
[Ad] Address:Departments of Pharmacology and Global Medical Science, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea.
[Ti] Title:4-hydroxy-3-methoxycinnamic acid regulates orexigenic peptides and hepatic glucose homeostasis through phosphorylation of FoxO1.
[So] Source:Exp Mol Med;50(2):e437, 2018 Feb 02.
[Is] ISSN:2092-6413
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:4-hydroxy-3-methoxycinnamic acid (ferulic acid, FA) is known to have numerous beneficial health effects, including anti-obesity and anti-hyperglycemic properties. However, the molecular networks that modulate the beneficial FA-induced metabolic effects have not been well elucidated. In this study, we explored the molecular mechanisms mediating the beneficial metabolic effects of FA. In mice, FA protected against high-fat diet-induced weight gain, reduced food intake and exhibited an overall improved metabolic phenotype. The food intake suppression by FA was accompanied by a specific reduction in hypothalamic orexigenic neuropeptides, including agouti-related protein and neuropeptide Y, with no significant changes in the anorexigenic peptides pro-opiomelanocortin and cocaine and amphetamine-regulated transcript. FA treatment also inhibited fat accumulation in the liver and white adipose tissue and suppressed the expression of gluconeogenic genes, including phosphoenolpyruvate carboxylase and glucose-6-phosphatase. Furthermore, we show that FA phosphorylated and inactivated the transcription factor FoxO1, which positively regulates the expression of gluconeogenic and orexigenic genes, providing evidence that FA might exert its beneficial metabolic effects through inhibition of FoxO1 function in the periphery and the hypothalamus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180206
[Lr] Last revision date:180206
[St] Status:In-Data-Review
[do] DOI:10.1038/emm.2017.253

  10 / 6456 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 29397535
[Au] Autor:Romanova IV; Derkach KV; Mikhrina AL; Sukhov IB; Mikhailova EV; Shpakov AO
[Ad] Address:I.M. Sechenov Institute of Evolutionary Physiology and Biochemistry of Russian Academy of Sciences, Saint Petersburg, Russia. irinaromanova@mail.ru.
[Ti] Title:The Leptin, Dopamine and Serotonin Receptors in Hypothalamic POMC-Neurons of Normal and Obese Rodents.
[So] Source:Neurochem Res;, 2018 Feb 03.
[Is] ISSN:1573-6903
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The pro-opiomelanocortin (POMC)-expressing neurons of the hypothalamic arcuate nucleus (ARC) are involved in the control of food intake and metabolic processes. It is assumed that, in addition to leptin, the activity of these neurons is regulated by serotonin and dopamine, but only subtype 2C serotonin receptors (5-HT R) was identified earlier on the POMC-neurons. The aim of this work was a comparative study of the localization and number of leptin receptors (LepR), types 1 and 2 dopamine receptors (D R, D R), 5-HT R and 5-HT R on the POMC-neurons and the expression of the genes encoding them in the ARC of the normal and diet-induced obese (DIO) rodents and the agouti mice (A /a) with the melanocortin obesity. As shown by immunohistochemistry (IHC), all the studied receptors were located on the POMC-immunopositive neurons, and their IHC-content was in agreement with the expression of their genes. In DIO rats the number of D R and D R in the POMC-neurons and their expression in the ARC were reduced. In DIO mice the number of D R and D R did not change, while the number of LepR and 5-HT R was increased, although to a small extent. In the POMC-neurons of agouti mice the number of LepR, D R, 5-HT R and 5-HT R was increased, and the D R number was reduced. Thus, our data demonstrates for the first time the localization of different types of the serotonin and dopamine receptors on the POMC-neurons and a specific pattern of the changes of their number and expression in the DIO and melanocortin obesity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180204
[Lr] Last revision date:180204
[St] Status:Publisher
[do] DOI:10.1007/s11064-018-2485-z


page 1 of 646 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information