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1.
Alzheimer Dis Assoc Disord ; 33(2): 124-128, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31094709

RESUMO

PURPOSE: The aim of this study was to evaluate the relationship between olfactory function and hippocampal volume in patients with mild cognitive impairment (MCI). METHODS: We enrolled a total of 31 MCI patients and 9 normal control subjects. All participants underwent 3.0 T-magnetic resonance imaging scanning. The scan results were processed using GE ADW4.6 processing software and V0xar 3D workstation to acquire the hippocampal volume. The University of Pennsylvania Smell Identification Test (UPSIT) was used to evaluate the olfactory function of MCI patients. The correlations of UPSIT score with hippocampal volume and hippocampal head volume were evaluated by Pearson correlation coefficient analysis. RESULTS: MCI patients had significantly smaller left (2.78±0.50 vs. 3.19±0.31 cm(3)) and right (2.97±0.42 vs. 3.31±0.25 cm(3)) hippocampal volumes compared with normal controls (P<0.05). In addition, patients with olfactory dysfunction had smaller volumes of the hippocampus (left hippocampal volume, 2.57±0.39 vs. 3.23±0.40 cm(3); right hippocampal volume, 2.86±0.43 vs. 3.22±0.30 cm(3)) and hippocampal head (left hippocampal head volume, 1.18±0.16 vs. 1.53±0.25 cm(3); right hippocampal head volume, 1.25±0.22 vs. 1.54±0.22 cm(3)) compared with those with normal olfactory function (P<0.05). No significant difference in the hippocampal body volume and hippocampal tail volume was found between MCI patients with olfactory loss and those with normal olfactory function. The UPSIT score was significantly positively correlated with left hippocampal volume (r=0.55, P<0.05), right hippocampal volume (r=0.42, P<0.05), left hippocampal head volume (r=0.53, P<0.05), and right hippocampal head volume (r=0.45, P<0.05). CONCLUSIONS: Olfactory function correlates well with hippocampal volume among patients with MCI.


Assuntos
Disfunção Cognitiva/fisiopatologia , Hipocampo/fisiopatologia , Processamento de Imagem Assistida por Computador , Transtornos do Olfato , Idoso , Estudos de Casos e Controles , China , Feminino , Humanos , Imagem por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Olfato/fisiologia
2.
J Cell Mol Med ; 23(1): 47-58, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30394676

RESUMO

Alzheimer's disease (AD) is a complex neurodegenerative disease and the most common cause of dementia among the elderly. There has been increasing recognition of sex differences in AD prevalence, clinical manifestation, disease course and prognosis. However, there have been few studies on the molecular mechanism underlying these differences. To address this issue, we carried out global gene expression and integrative network analyses based on expression profiles (GSE84422) across 17 cortical regions of 125 individuals with AD. There were few genes that were differentially expressed across the 17 regions between the two sexes, with only four (encoding glutamate metabotropic receptor 2, oestrogen-related receptor beta, kinesin family member 26B, and aspartoacylase) that were differentially expressed in three regions. A pan-cortical brain region co-expression network analysis identified pathways and genes (eg, glycogen synthase kinase 3ß) that were significantly associated with clinical characteristics of AD (such as neurofibrillary score) in males only. Similarity analyses between region-specific networks indicated that male patients exhibited greater variability, especially in the superior parietal lobule, dorsolateral prefrontal cortex and occipital visual cortex. A network module analysis revealed an association between clinical traits and crosstalk of sex-specific modules. An examination of temporal and spatial patterns of sex differences in AD showed that molecular networks were more conserved in females than in males in different cortical regions and at different AD stages. These findings provide insight into critical molecular pathways governing sex differences in AD pathology.


Assuntos
Doença de Alzheimer/genética , Encéfalo/metabolismo , Perfilação da Expressão Gênica/métodos , Redes Reguladoras de Genes , Doença de Alzheimer/patologia , Feminino , Humanos , Masculino , Lobo Occipital/metabolismo , Córtex Pré-Frontal/metabolismo , Fatores Sexuais , Córtex Visual/metabolismo
3.
Brain Inj ; 27(10): 1190-8, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23895636

RESUMO

PRIMARY OBJECTIVE: Following stroke, hypothermia is reported to reduce both cellular and extracellular damage. This study aimed to examine the effects of focal mild hypothermia on proteins associated with both extracellular (matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of MMP-9 (TIMP-1)) and cellular damage (Tau-1 and ß-amyloid precursor protein (ß-APP)) to characterize the protective effects of hypothermia. METHODS AND PROCEDURES: Male Wistar rats received ischaemic damage using a transient, focal ischaemia/reperfusion model. Afterwards, one group (HT) received 6 hours of focal mild hypothermia (33 °C) applied to the head, while another remained at normal temperature (NT). The brains were collected at 6, 12, 24, 48 and 72 hours after hypothermia to measure infarct volume ratio and to detect cells immunopositive for MMP-9, TIMP-1, Tau-1 and ß-APP, while neurological deficits were examined separately after 2 weeks. MAIN OUTCOMES AND RESULTS: Focal mild hypothermia had no effect on infarct volume ratio but expression of MMP-9, TIMP-1 Tau-1 and ß-APP was decreased. Furthermore, neurological function in the HT group was better than in the NT group. CONCLUSIONS: Focal mild hypothermia has protective effects on cerebral ischaemia-reperfusion injury characterized by decreased expression of MMP-9, TIMP-1, Tau-1 and ß-APP, along with improvement of neurological function despite no changes in infarct volume.


Assuntos
Precursor de Proteína beta-Amiloide/metabolismo , Encéfalo/metabolismo , Infarto Cerebral/metabolismo , Infarto Cerebral/terapia , Hipotermia Induzida , Metaloproteinase 9 da Matriz/metabolismo , Fragmentos de Peptídeos/metabolismo , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/terapia , Inibidor Tecidual de Metaloproteinase-1/metabolismo , Proteínas tau/metabolismo , Análise de Variância , Animais , Infarto Cerebral/patologia , Regulação para Baixo , Imuno-Histoquímica , Masculino , Ratos , Ratos Wistar , Recuperação de Função Fisiológica
4.
PLoS One ; 7(6): e37858, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22701584

RESUMO

Associations between interleukin 6 (IL-6) polymorphisms and Alzheimer's disease (AD) remain controversial and ambiguous. The aim of this meta-analysis is to explore more precise estimations for the relationship between IL-6-174 G/C and -572 C/G polymorphisms and risk for AD. Electronic searches for all publications in databases PubMed and EMBASE were conducted on the associations between IL-6 polymorphisms and risk for AD until January 2012. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated using fixed and random effects models. Twenty-seven studies were included with a total of 19,135 individuals, involving 6,632 AD patients and 12,503 controls. For IL-6-174 G/C polymorphism, the combined results showed significant differences in recessive model (CC vs. CG+GG: OR = 0.65, 95%CI = 0.52-0.82). As regards IL-6-572 C/G polymorphism, significant associations were shown in dominant model (CG+GG vs. CC: OR= 0.73, 95% CI = 0.62-0.86) and in additive model (GG vs. CC, OR= 0.66, 95% CI = 0.46-0.96). In conclusion, genotype CC of IL-6-174 G/C and genotype GG plus GC of IL-6-572 C/G could decrease the risk of AD.


Assuntos
Doença de Alzheimer/genética , Predisposição Genética para Doença/genética , Interleucina-6/genética , Polimorfismo de Nucleotídeo Único/genética , Estudos de Associação Genética , Humanos , Padrões de Herança/genética , Razão de Chances
5.
J Neuroimmunol ; 244(1-2): 94-6, 2012 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-22329905

RESUMO

Osteopontin (OPN) and interleukin-23 (IL-23) are pro-inflammatory cytokines proposed to play central roles to the development of multiple sclerosis (MS). The aim of this study was to evaluate levels of OPN, IL-23 and other inflammatory cytokines and investigate their relationships in serum and cerebrospinal fluid (CSF) in patients with MS. Fifty one MS patients and 48 patients with non-inflammatory neurological diseases (NIND) were recruited from clinic. The levels of OPN, IL-23, IL-17, IL-6, and tumor necrosis factor-alpha (TNF-alpha) in serum and CSF were determined in each participant. Compared with NIND group, MS patients had significantly elevated levels of OPN, IL-23, IL-17 and TNF-alpha in CSF, and elevated levels of IL-23, IL-17 and TNF-alpha in serum (All P<0.001). In MS patients, OPN and IL-23 were positively correlated with IL-17 (r=0.302, P=0.019; r=0.417, P=0.001, respectively); and IL-23 was positively correlated with EDSS (r=0.329, P=0.019). Both OPN and IL-23 may play pivotal role in development of MS and might be specific markers and therapeutic targets for MS.


Assuntos
Interleucina-23/sangue , Interleucina-23/líquido cefalorraquidiano , Esclerose Múltipla/sangue , Esclerose Múltipla/líquido cefalorraquidiano , Osteopontina/sangue , Osteopontina/líquido cefalorraquidiano , Adulto , Citocinas/sangue , Citocinas/líquido cefalorraquidiano , Feminino , Humanos , Interleucina-1beta/sangue , Masculino , Pessoa de Meia-Idade , Doenças do Sistema Nervoso/sangue , Doenças do Sistema Nervoso/líquido cefalorraquidiano , Adulto Jovem
6.
J Biochem Mol Toxicol ; 24(4): 235-41, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20806394

RESUMO

The prion protein peptide PrP106-126 induces cell apoptosis through mechanisms involving production of intracellular reactive oxygen species. The present study investigated the effects of edaravone, a potent free radical scavenger in clinical use, on cell cytotoxicity induced by PrP106-126. Results showed that PrP106-126 decreased PC12 cell viability in a dose- and time-dependent manner. Edaravone significantly antagonized the cytotoxic effects of PrP106-126. Mechanistically, PrP106-126 decreased PC 12 intracellular glutathione (GSH) concentrations, decreased superoxide dismutase (SOD) enzyme activity, increased concentrations of the oxidation end product malondialdehyde (MDA), depolarized the mitochondrial membrane, and increased caspase-3 activity. Edaravone alone did not affect GSH, SOD, or MDA but did effectively reverse all of the intracellular prooxidant effects induced by PrP106-126 and inhibit induced apoptosis in PC12 cells. In conclusion, edaravone may be a viable candidate for the treatment of oxidative stress-induced neurodegenerative disease.


Assuntos
Antipirina/análogos & derivados , Depuradores de Radicais Livres/farmacologia , Proteínas PrPC/metabolismo , Animais , Antipirina/farmacologia , Caspase 3/metabolismo , Morte Celular/efeitos dos fármacos , Edaravone , Glutationa/genética , Glutationa/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Malondialdeído/metabolismo , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Membranas Mitocondriais/metabolismo , Células PC12 , Proteínas PrPC/genética , Ratos , Superóxido Dismutase/metabolismo
7.
Neurol Res ; 32(8): 835-40, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20426902

RESUMO

OBJECTIVES: We investigated the relationship between glial cell line-derived neurotrophic factor (GDNF), nestin, and the activation of endogenous neural stem cells (NSCs) following cerebral infarction in humans. METHODS: Post-mortem brain specimens from patients who died following cerebral infarction were examined. RESULTS: Compared with the controls, the number of nestin-positive cells was increased at 4·5-10 hours in the subgranular zone of the hippocampus dentate gyrus and at 24-72 hours in the subventricular zone, reaching maximum levels at 120-144 hours. Cell numbers decreased at 216-326 hours, but remained elevated compared with controls. Similar results were found when examining the expression of GDNF following ischemia. Furthermore, the expression of nestin and GDNF showed a statistically significant positive correlation over time. CONCLUSIONS: Our results indicate that, as in other mammals, proliferation of endogenous neural stem cells in the subventricular zone and subgranular zone of the hippocampus dentate gyrus of humans is activated by cerebral infarction and may be related to increases in GDNF expression.


Assuntos
Isquemia Encefálica/metabolismo , Isquemia Encefálica/patologia , Fator Neurotrófico Derivado de Linhagem de Célula Glial/biossíntese , Proteínas de Filamentos Intermediários/biossíntese , Proteínas do Tecido Nervoso/biossíntese , Células-Tronco Neurais/metabolismo , Células-Tronco Neurais/patologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Regulação da Expressão Gênica , Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética , Humanos , Proteínas de Filamentos Intermediários/genética , Masculino , Pessoa de Meia-Idade , Proteínas do Tecido Nervoso/genética , Nestina , Regulação para Cima/genética
8.
Neurosci Lett ; 475(3): 132-5, 2010 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-20347937

RESUMO

In animal models, endoplasmic reticulum (ER) stress and apoptosis take place around cerebral infarction areas during ischemia, which presumably protect tissues from necroses-induced injury as well as promote cells toward death. We examined whether these pathological changes, especially temporal occurrence, were present in patients who suffered from cerebral ischemia. The studies by immunohistochemistry show that ER chaperone glucose-regulated protein (GRP78) and caspase-9 elevate around infarction areas. The experiments by terminal deoxynucleotidy transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick-end labeling (TUNEL) illustrate that TUNEL-positive cells are higher around infarction tissues than controls. Moreover, GRP78, caspase-9 and TUNEL cells emerge one after another during ischemia. In conclusion, ER stress, apoptosis initiation and DNA fragment develop sequentially in ischemic human brain. ER stress during excessive ischemia stimulates apoptotic cell death beyond activating a defense for nerve cells being away from injury.


Assuntos
Apoptose , Infarto Encefálico/patologia , Isquemia Encefálica/complicações , Encéfalo/patologia , Retículo Endoplasmático/patologia , Encéfalo/metabolismo , Infarto Encefálico/etiologia , Infarto Encefálico/metabolismo , Isquemia Encefálica/metabolismo , Isquemia Encefálica/patologia , Caspase 9/metabolismo , Retículo Endoplasmático/metabolismo , Proteínas de Choque Térmico/metabolismo , Humanos , Marcação In Situ das Extremidades Cortadas , Pessoa de Meia-Idade
9.
Zhonghua Yi Xue Za Zhi ; 88(47): 3337-41, 2008 Dec 23.
Artigo em Chinês | MEDLINE | ID: mdl-19257964

RESUMO

OBJECTIVE: To investigate the relationship of basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) and proliferation of endogenous neural stem cells (NSCs) after human cerebral infarction. METHODS: Paraffin-embedded brain tissues of 22 human fatal cases of CI from the brain tissues around subventricular zone and subgranular layer zone were stained with HE and immunohistochemistry stain. The endogenous neural stem cells were marked by nestin. The expression changes of EGF, bFGF and nestin in the perihematomal tissues were analysed with the SPSS 13.0 system. RESULTS: (1) Compared with the controls, the number of nestin-positive cells increased at 24 - 72 h (14 +/- 6)/HP in the ipsilateral SVZ and began to rise at 4.5 - 10 h (11 +/- 5)/HP in the ipsilateral SGZ, reached maximum at 120 - 144 h ((38 +/- 7)/HP in the SVZ, (54 +/- 17)/HP in the SGZ, and decreased markedly at 216 - 336 h, but it was still elevated compared with the controls (P < 0.05). (2) The number of bFGF-positive cells increased at 4.5 - 10 h (8.1 +/- 2.9)/HP in the SVZ, (19.0 +/- 8.2)/HP in the SGZ, reached maximum at 24 - 70 h (15.6 +/- 3.5)/HP in the SVZ, (32.0 +/- 5.7)/HP in the SGZ and decreased at 72 - 96 h, but it was still elevated compared with the controls (P < 0.05). (3) The number of EGF-positive cells increased at 4.5 - 10 h (4.3 +/- 1.6)/HP in the SVZ, (7.0 +/- 3.7)/HP in the SGZ, reached maximum at 120 - 144 h (27.0 +/- 1.4)/HP in the SVZ, (51.5 +/- 4.9)/HP in the SGZ and decreased at 216 - 336 h, but it was still elevated compared with the controls (P < 0.05). CONCLUSIONS: Perhaps the increased expression of EGF and bFGF after CI was a reaction of endogenous reparation and it correlated with the proliferation and endogenous of neural stem cells in human.


Assuntos
Infarto Cerebral/metabolismo , Fator de Crescimento Epidérmico/metabolismo , Células-Tronco Multipotentes/citologia , Neurônios/citologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Diferenciação Celular , Proliferação de Células , Células Cultivadas , Feminino , Fator 2 de Crescimento de Fibroblastos/metabolismo , Humanos , Masculino , Pessoa de Meia-Idade , Células-Tronco Multipotentes/metabolismo , Neurônios/metabolismo
10.
Nan Fang Yi Ke Da Xue Xue Bao ; 27(12): 1830-3, 2007 Dec.
Artigo em Chinês | MEDLINE | ID: mdl-18158995

RESUMO

OBJECTIVE: To establish a method for fingerprinting of Fuzhisan (FZS, a traditional Chinese medicinal preparation) using high-performance liquid chromatography with ultraviolet and evaporative light scattering detector (HPLC-UV/ELSD) to allow simultaneous determination of 5 major constituents in the preparation. METHODS: HPLC-UV/ELSD analysis was performed on water AlltechC18 column (5 microm, 4.6 mm x 250 mm) with a mixture of acetonitrile (A) and 0.1% acetice acid water (B) as the mobile phase. The solvent A gradient for elution was 0, 12%; 25, 20%; 30, 20%; 75, 30%; 105, 40%; 120, 80%; 130, 12%, with the flow rate of 1.0 ml/min; and the column temperature at 30 degrees . The detective wavelength was 335 nm, drift tube temperature was 80 degrees , pressure of nebulizer gas was 25 psi. The similarities between the HPLC-UV/ELSD fingerprints of the 12 extracts were calculated using similarity evaluation software. RESULTS: The fingerprint of FZS was established and the 5 major constituents were identified. The complementarity between the fingerprints of UV and ELSD was analyzed, showing good correlation between 12 batches of FZS. CONCLUSION: The method for fingerprinting can simultaneously characterize the main chemical constituents in FZS and allows stable, effective and comprehensive quality control and evaluation of FZS for a single sample.


Assuntos
Cromatografia Líquida de Alta Pressão/métodos , Medicamentos de Ervas Chinesas/química , Espalhamento de Radiação , Medicamentos de Ervas Chinesas/normas , Luz , Controle de Qualidade , Raios Ultravioleta
11.
Zhonghua Yi Xue Za Zhi ; 87(27): 1904-7, 2007 Jul 17.
Artigo em Chinês | MEDLINE | ID: mdl-17923014

RESUMO

OBJECTIVE: To observe the expression of heme oxygenase-1 (HO-1) and Bcl-2, an apoptosis-modulating protein, in the neurons surrounding the hematoma in human being. METHODS: Specimens of cerebral cortex tissue 1 - 3 cm around the hemorrhagic focus with the size of 2.0 cm x 1.5 cm x 0.3 cm were collected during autopsy from 39 patients, 17 males and 22 females, aged 62.8 (36 - 84), who died from intracerebral hemorrhage 2 - 10 h, 17 - 30 h, 36 - 96 h, 120 - 216 h, or 240 - 408 h before. Specimens of brain tissue of the same size at the opposite side were collected as controls. Immunohistochemistry was used to examine the expression of HO-1 and Bcl-2 protein. RESULTS: (1) Expression of HO-1 could be detected in the specimens of the 2 h group, increased in the specimens of the 2 - 10 h group [(5.1 +/- 2.0)/HP], reached the peak in the 17 - 30 h group [(11.3 +/- 0.9)/HP], then began to decrease in the specimens of the 240 - 408 h group [(6.4 +/- 0.6)/HP] (F = 42.80, P < 0.001). The HO-1 expression of the control group remained negative at any time-point. (2) Expression of Bcl-2 could be detected in the specimens of the 2 - 10 h group [(4.2 +/- 1.7)/HP], was increased in the 17 - 30 h group [(6.6 +/- 0.5)/HP], reached the peak in the 36 approximately 96 h group [(8.9 +/- 1.1)/HP], then began to decrease, and was (4.7 +/- 0.6)/HP in the 240 approximately 408 h group (F = 29.59, P < 0.001). The Bcl-2 expression remained negative at any time point in the control group. (3) The expressions of HO-1 was positively correlated with the expression of Bcl-2 (r = 0.66, P < 0.001). CONCLUSIONS: Over-expression of HO-1 and Bcl-2 in the neurons provide a potential protection or destruction mechanism after intracerebral hemorrhage in human.


Assuntos
Hemorragia Cerebral/complicações , Hematoma/metabolismo , Heme Oxigenase-1/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Adulto , Idoso , Idoso de 80 Anos ou mais , Autopsia , Córtex Cerebral/metabolismo , Feminino , Hematoma/complicações , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Neurônios/metabolismo
12.
Zhonghua Yi Xue Za Zhi ; 86(13): 906-10, 2006 Apr 04.
Artigo em Chinês | MEDLINE | ID: mdl-16759517

RESUMO

OBJECTIVE: To examined the effect of local mild hypothermia on the expression of aquaporin-4 (AQP-4) following intracerebral hemorrhage (ICH) in rats and clarified the mechanism of hypothermia on brain edema formation following ICH. METHODS: Two hundreds and forty male Wistar rats were randomly divided into two groups: the intracerebral hemorrhage (ICH) group, in which autologous arterial blood were stereotaxically injected into right caudate nucleus; the local mild hypothermia (ICH + H) group, in which the rats were given 4 h local mild hypothermia after the injection of blood. Each group was divided into 6 subgroups: control, 6 h, 24 h, 72 h, 5 d and 7 d after operation; Brain water content was determined by dry-wet weight method and the permeability of BBB was measured by Evans-Blue extravasation. RT-PCR and Western blot were respectively used to evaluate AQP-4 mRNA and protein expression. RESULTS: In ICH group, compared with control, ICH significantly increased BWC, the permeability of BBB and the expression of AQP-4 mRNA, all began at 6 h and peaked at 72 h (P < 0.01), the increased protein expression of AQP-4 began at 24 h and also peaked at 72 h (P < 0.01). AQP-4 expression positively correlated, both at the mRNA and the protein level, with the permeability of BBB (r = 0.78 and r = 0.76 respectively). In ICH + H group, compared with ICH group, the elevation of BWC, BBB permeability and AQP-4 protein expression were strongly attenuated at all time point by hypothermia treatment (P < 0.01), while AQP-4 mRNA levels demonstrated a modest attenuation from 48 h. At 72 h, AQP-4 mRNA optical density (A) decreased from 1.25 +/- 0.03 (ICH group) to 1.04 +/- 0.02 (P < 0.01), AQP-4 protein expression (A) decreased from 0.77 +/- 0.08 (ICH group) to 0.25 +/- 0.04 (P < 0.01). CONCLUSIONS: This study indicates that BBB breakdown can increase the expression of AQP-4; local mild hypothermia can significantly reduce brain edema formation after ICH by suppressing the elevation of AQP-4 protein expression; Inhibition of BBB breakdown and the elevation of AQP-4 protein expression with local mild hypothermia appear to contribute to brain protection in this model.


Assuntos
Aquaporina 4/genética , Hemorragia Cerebral/fisiopatologia , Hipotermia Induzida , Animais , Aquaporina 4/metabolismo , Barreira Hematoencefálica/fisiopatologia , Western Blotting , Masculino , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Distribuição Aleatória , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa
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