RESUMEN

Esophageal cancer (EC) is a frequent malignant tumor in our world, and has a highly morbidity and mortality. It was reported that genetic factors play vital roles in its pathogenesis. Here, we performed a case - control study to evaluate the COL6A3 genetic variants and EC risk in a Chinese Han cohort. All subjects were genotyped with the Agena MassARRAY platform. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression after adjusting age and gender. We found that rs6720283 (G > A) allele had significantly enhanced EC risk (OR = 1.32, 95% CI = 1.11 alculate p = 0.002). Stratified analysis was performed by gender, age, alcohol drinking, BMI, TNM stage and lymph node metastasis, the results showed that rs7436, rs115510139 and rs6720283 were significantly associated with the risk of EC in different groups (all p < 0.05). Besides, no statistical significant was found between the COL6A3 gene polymorphisms and clinicopathological parameters such as TNM stage and lymph node metastasis among EC patients (p > 0.05). In conclusions, our study found that COL6A3 variants were associated with risk of EC in the Chinese population.

Asunto(s)

Pueblo Asiatico/genética , Colágeno Tipo VI/genética , Neoplasias Esofágicas/genética , Predisposición Genética a la Enfermedad , Anciano , Alelos , Estudios de Casos y Controles , China , Detección Precoz del Cáncer , Neoplasias Esofágicas/diagnóstico , Neoplasias Esofágicas/etnología , Femenino , Haplotipos , Humanos , Desequilibrio de Ligamiento , Masculino , Persona de Mediana Edad

RESUMEN

AIM: High-altitude pulmonary edema (HAPE), as a multifactorial disease, is caused by stress failure and involves both environmental and genetic factors. Study shows that IL-1 receptors can selectively decrease the oxygen arterial hypertension and influence the blood coagulation. So we evaluated whether genetic polymorphisms in IL1R1 and 1L1R2 genes are associated with the risk of HAPE in Chinese Han population. METHODS: Ten susceptible SNPs in the IL1R1 and IL1R2 genes were genotyped among 265 HAPE cases and 303 controls using the Agena MassARRAY platform. The associations of the SNP frequencies with HAPE were analyzed by chi-square (χ2 ) test/Fisher's test. The genetic models were used to evaluate associations. RESULTS: In the allele model, we found that rs2072472 was significantly associated with a 0.73-fold decreased risk of HAPE (OR = 0.73, 95% CI = 0.55-0.97, p = 0.033). In the genetic model analysis, the rs2072472 in IL1R2 gene was associated with a 0.32-fold decreased risk of HAPE in the codominant model, 0.67-fold decreased risk of HAPE in the dominant model, 0.36-fold decreasing the risk of HAPE in the recessive model, and 0.66-fold decreased risk of HAPE in the log-additive model, respectively. We found three candidate SNPs (rs11674595, rs4851527, and rs719250) in the IL1R2 gene have shown strong linkage, and none of the haplotypes was significantly associated with risk of HAPE. CONCLUSION: These findings suggested that IL1R2 polymorphisms may contribute to the protection of HAPE.

Asunto(s)

Mal de Altura/genética , Hipertensión Pulmonar/genética , Polimorfismo de Nucleótido Simple , Receptores Tipo II de Interleucina-1/genética , Adulto , Femenino , Humanos , Masculino

RESUMEN

BACKGROUND: Malignant gliomas are the most common primary brain tumors. Various genetic factors play important roles in the development and prognosis of glioma. The present study focuses on the impact of MPHOSPH6, TNIP1 and several other genes (ACYP2, NAF1, TERC, TERT, OBFC1, ZNF208 and RTEL1) on telomere length and how this affects the prognosis of glioma. METHODS: Forty-three polymorphisms in nine genes from 605 glioma patients were selected. The association between genotype and survival outcome was analyzed using the Kaplan-Meier method, Cox regression analysis and the log-rank test. RESULTS: The 1-year overall survival (OS) rates of patients younger than 40 years of age was higher compared to those in patients older than 40 years of age. The 1-year OS rate of patients who underwent total resection was higher than that of patients whose gliomas were not completely resected. The 1-year OS rates of patients undergoing chemotherapy and of patients who did not undergo chemotherapy were 39.90% and 26.80%, respectively. Univariate analyses showed that ACYP2 rs12615793 and TERT rs2853676 loci affected progression-free survival in glioma patients; both ZNF208 rs8105767 and ACYP2 rs843720 affected the OS of patients with low-grade gliomas. Multivariate analyses suggested that MPHOSPH6 rs1056629 and rs1056654, and TERT rs2853676 loci were associated with good prognoses of patients with glioma or high-grade gliomas, whereas ZNF208 rs8105767 was associated with good prognosis of patients with low-grade glioma. CONCLUSIONS: Age, surgical resection and chemotherapy influenced the survival rates of glioma patients. TERT, MPHOSPH6, ACYP2 and ZNF208 genes were found to affect glioma prognosis.

Asunto(s)

Neoplasias Encefálicas/genética , Predisposición Genética a la Enfermedad/genética , Glioma/genética , Polimorfismo de Nucleótido Simple , Ácido Anhídrido Hidrolasas/genética , Neoplasias Encefálicas/patología , Neoplasias Encefálicas/terapia , Proteínas de Unión al ADN/genética , Frecuencia de los Genes , Genotipo , Glioma/patología , Glioma/terapia , Humanos , Estimación de Kaplan-Meier , Análisis Multivariante , Evaluación de Resultado en la Atención de Salud/métodos , Evaluación de Resultado en la Atención de Salud/estadística & datos numéricos , Pronóstico , Modelos de Riesgos Proporcionales

RESUMEN

BACKGROUND: Little is known about the contribution of ARHGAP22 polymorphism to diabetic retinopathy (DR) risk. We performed a case-control study to investigate the associations between ARHGAP22 and the risk of DR in a Chinese Han population. METHODS: A total of 341 patients with type 2 diabetes mellitus (T2DM) were selected. All patients underwent a complete eye examination. Based on this, the patients with T2DM were divided into two subgroups: 188 patients with DR and 153 patients without DR. Five single nucleotide polymorphism (SNPs) were selected and genotyped using the MassARRAY method (Sequenom, San Diego, CA, USA). The odds ratio (OR) and 95% confidence intervals (CIs) were calculated by unconditional logistic regression adjusted for age and sex. RESULTS: Two susceptibility SNPs in ARHGAP22 were found to be associated with an increased risk of DR both before and after the adjustment: rs10491034 under the dominant model (adjusted OR = 0.51, 95% CI = 0.27-0.95, p = 0.032) and additive model (adjusted OR = 0.47, 95% CI = 0.26-0.84, p = 0.0098) and rs3844492 under the codominant model (adjusted OR = 3.14, 95% CI = 1.10-9.01, p = 0.023) and recessive model (adjusted OR = 3.52, 95% CI = 1.26-9.85, p = 0.011). CONCLUSIONS: Our findings reveal a significant association between SNPs in the ARHGAP22 gene and DR risk in a Han Chinese population.

Asunto(s)

Diabetes Mellitus Tipo 2/complicaciones , Retinopatía Diabética/etiología , Retinopatía Diabética/genética , Proteínas Activadoras de GTPasa/genética , Predisposición Genética a la Enfermedad , Estudios de Casos y Controles , China , Diabetes Mellitus Tipo 2/genética , Diabetes Mellitus Tipo 2/fisiopatología , Retinopatía Diabética/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Polimorfismo de Nucleótido Simple

RESUMEN

BACKGROUND: Glioblastoma (GBM) is a highly invasive, aggressive, and incurable brain tumor. Genetic factors play important roles in GBM risk. The aim of this study was to elucidate the influence of gene polymorphism on GBM susceptibility. MATERIAL AND METHODS: In this case-control study, we included 72 GBM patients and 320 healthy controls to analyze the association between 29 single-nucleotide polymorphisms and GBM cancer risk in the Chinese Han population. The single-nucleotide polymorphisms were determined by Sequenom MassARRAY RS1000 and statistical analysis was performed using SPSS software and SNPStats software. RESULTS: Using the χ(2) test, we found that rs2297440 and rs6010620 in RTEL1 increased risk of GBM. In the recessive model, we also found that the genotypes "CC" of rs2297440 and "GG" of rs6010620 in RTEL1 significantly increased GBM risk. The variant TT genotype of TREH rs17748 and the variant TT genotype of PHLDB1 rs498872 decreased GBM risk in the recessive model. We also found that the TREH rs17748 variant C allele showed an increased risk in males in the dominant model. CONCLUSIONS: Our results suggest a significant association between the RETL1, TREH, and PHLDB1 genes and GBM development in the Han Chinese population.

Asunto(s)

Neoplasias Encefálicas/genética , ADN Helicasas/genética , Predisposición Genética a la Enfermedad , Glioblastoma/genética , Péptidos y Proteínas de Señalización Intracelular/genética , Proteínas del Tejido Nervioso/genética , Polimorfismo de Nucleótido Simple , Trehalasa/genética , Estudios de Casos y Controles , China , Etnicidad/genética , Femenino , Humanos , Masculino , Factores de Riesgo

RESUMEN

Esophageal squamous cell carcinoma (ESCC) is one of most common and fatal forms of cancer worldwide. Recent studies have suggested that an aberrant microRNA (miRNA or miR) expression signature exists in ESCC. In the present study, in order to determine the involvement of miRNA in the development and progression of ESCC, the expression profiles of miRNA in 8 paired ESCC tissues and corresponding normal esophageal tissues were analyzed by miRNA microarray. A total of 43 differentially expressed miRNAs, including 27 downregulated and 16 upregulated miRNAs were found in the ESCC tissue samples. Among these miRNAs, we found that miR-1 was significantly downregulated. Subsequently, the expression of miR-1 was validated in 64 pairs of primary ESCC samples by RT-qPCR. The expression level of miR-1 was found to be frequently decreased, and significantly correlated with tumor invasion and an advanced clinical stage (P = 0.022 and P = 0.028, respectively). In addition, functional assays revealed that miR-1 inhibited cell proliferation, clonogenicity, cell invasion and migration. Bioinformatics analyses identified the major biological processes that were targeted by miR-1. These results suggest that miR-1 has a tumor-suppressive effect on the development and progression of ESCC. The findings of this study may contribute to the further understanding of the functions of miR-1 in ESCC.

Asunto(s)

Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patología , Movimiento Celular/genética , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/patología , Regulación Neoplásica de la Expresión Génica , MicroARNs/genética , Adulto , Anciano , Línea Celular Tumoral , Análisis por Conglomerados , Carcinoma de Células Escamosas de Esófago , Femenino , Perfilación de la Expresión Génica , Ontología de Genes , Humanos , Masculino , Persona de Mediana Edad , Clasificación del Tumor , Invasividad Neoplásica , Estadificación de Neoplasias , Carga Tumoral

RESUMEN

Colorectal cancer (CRC) is a common malignant tumor that is influenced by an interaction between genetic and environmental factors. Currently, the inherited factors of CRC are unclear. Our study selected 19 tag single nucleotide polymorphisms (tSNPs) to investigate whether they were associated with CRC in the Han population. In this Han Chinese case-control study, we genotyped 203 CRC cases and 296 controls using Sequenom MassARRAY technology and analyzed their associations with CRC using χ(2) tests, SNPStats software, and SHEsis software. Based on χ(2) tests, PLCE1 -rs2077218, rs11187877 (p = 0.049) and C11orf92-C11orf93-rs3802842 (p = 0.023) correlate with CRC risk. In the genetic model analyses, we found the genotype "CC" of rs3802842 in C11orf92-C11orf93 may significantly increase CRC risk in the recessive model (p = 0.0071), whereas "GT" of rs17109928 in NOC3L may decrease the risk in the over-dominant model (p = 0.0091). Using SHEsis software, we found PLCE1 and NOC3L are strongly linked, and the "GCCATTCTGTC" haplotype may increase the risk of CRC (p = 0.049). We found three genes (PLCE1, C11orf92-C11orf93, and NOC3L) are associated with CRC susceptibility. In combination with previous reports, our results suggest that these genes may be associated with CRC in the Han population.

Asunto(s)

Pueblo Asiatico/genética , Factores de Transcripción con Cremalleras de Leucina de Carácter Básico/genética , Neoplasias Colorrectales/genética , Predisposición Genética a la Enfermedad/genética , Proteínas de Neoplasias/genética , Proteínas Nucleares/genética , Fosfoinositido Fosfolipasa C/genética , Estudios de Casos y Controles , Femenino , Genotipo , Humanos , Masculino , Espectrometría de Masas , Persona de Mediana Edad , Polimorfismo de Nucleótido Simple/genética , ARN , Factores de Riesgo

RESUMEN

Glioblastoma (GBM) is the highest-grade glioma in astrocytoma. Patients often have poor prognosis due to therapeutic resistance and tumor recurrence. Identification of the genetic factors of GBM could be important contribution to early prevention of this disease. We genotyped 17 tag single-nucleotide polymorphisms (tSNPs) from nine genes in this study, including 72 cases and 302 controls. SNP genotyping was conducted using Sequenom MassARRAY RS1000. Statistical analysis of the association between tSNPs and GBM was performed using the χ (2) test and SNPStats software. The rs3829382 in FLT3 was associated with increased odds of developing GBM using the χ (2) test. When we analyzed tSNPs under different inheritance models, we found rs9642393 in EGFR increased odds of developing GBM in the dominant model. After stratification by gender, we found that rs12645561 in NEIL3 and rs2291427 in ALOX5 were associated with developing GBM. Polymorphisms within FLT3, EGFR, NEIL3, and ALOX5 may contribute to the occurrence of GBM in the Han Chinese population. However, the functional significance of these polymorphisms needs further investigation.

Asunto(s)

Araquidonato 5-Lipooxigenasa/genética , Receptores ErbB/genética , Predisposición Genética a la Enfermedad/genética , Glioblastoma/genética , N-Glicosil Hidrolasas/genética , Polimorfismo de Nucleótido Simple/genética , Tirosina Quinasa 3 Similar a fms/genética , Adulto , Pueblo Asiatico/genética , Neoplasias Encefálicas/etiología , Neoplasias Encefálicas/genética , Femenino , Genotipo , Glioblastoma/etiología , Humanos , Masculino , Persona de Mediana Edad

RESUMEN

To investigate the effect of serum leptin level and leptin receptor (Lepr) genetic mutation on chronic bronchitis, we measured the serum leptin levels of 236 patients with chronic bronchitis and 107 healthy controls by ELISA, the genotype distribution of Lepr gene containing Gln223Arg polymorphic sites by the polymerase chain reaction-restriction fragment length polymorphism (RFLP) method, the levels of inflammatory markers in serum, and the concentration of neutrophils. We found that the GG genotype distribution and G gene frequency of Lepr gene Gln223Arg site of the patient group were higher than that in the control group. The serum high-sensitivity C-reactive protein and neutrophil granulocyte levels of the patient group were higher than those of the control group. But the leptin concentrations of those with GG genotype were lower than those with AA+AG genotype (P < .05). The mutation of Lepr gene Gln223Arg site may not directly influence the leptin level but could possibly advance the disease through inhibiting the biological effect of leptin.

Asunto(s)

Bronquitis Crónica/genética , Polimorfismo Genético/genética , Receptores de Leptina/genética , Anciano , Bronquitis Crónica/sangre , Estudios de Casos y Controles , Femenino , Humanos , Leptina/sangre , Masculino , Persona de Mediana Edad

RESUMEN

Emerging evidence suggests the involvement of altered microRNA (miRNA) regulation in heart failure pathogenesis. We established a rat volume-overload heart failure model, and examined miRNA expression in normal rats and in the heart failure model, both with and without treatment with bisoprolol. Using miRNA microarrays, we identified 46 differentially expressed miRNAs in the rat heart failure model compared with normal rats. We also identified 18 differentially expressed miRNAs following treatment of normal rats with bisoprolol. Treatment with bisoprolol reversed, to varying degrees, the expression of 10 of the 46 miRNAs whose expression was differentially expressed in the heart failure model. Bioinformatic category analysis of the predicted target genes of these 10 miRNAs suggested that several encode ion-binding proteins. Our results showed that bisoprolol intervention can significantly improve cardiac function and decrease myocardial reconstruction in chronic heart failure. These data suggest that the expression of many miRNAs changes during heart failure, and that bisoprolol may exert its cardioprotective effects in part by reversing the differential expression of some of these genes.

Asunto(s)

Bisoprolol/farmacología , Regulación de la Expresión Génica/efectos de los fármacos , Insuficiencia Cardíaca/patología , Corazón/efectos de los fármacos , MicroARNs/metabolismo , Antagonistas de Receptores Adrenérgicos beta 1/farmacología , Animales , Volumen Cardíaco , Biología Computacional , Modelos Animales de Enfermedad , Ecocardiografía , Perfilación de la Expresión Génica , Iones/química , Masculino , Modelos Estadísticos , Miocardio/metabolismo , Análisis de Secuencia por Matrices de Oligonucleótidos , ARN/metabolismo , Ratas , Ratas Sprague-Dawley , Factores de Tiempo

RESUMEN

Common variants of multiple genes play a role in glioma onset. However, research related to astrocytoma, the most common primary brain neoplasm, is rare. In this study, we chose 21 tagging SNPs (tSNPs), previously reported to be associated with glioma risk in a Chinese case-control study from Xi'an, China, and identified their contributions to astrocytoma susceptibility. We found an association with astrocytoma susceptibility for two tSNPs (rs6010620 and rs2853676) in two different genes: regulator of telomere elongation helicase 1 (RTEL1) and telomerase reverse transcriptase (TERT), respectively. We confirmed our results using recessive, dominant, and additive models. In the recessive model, we found two tSNPs (rs2297440 and rs6010620) associated with increased astrocytoma risk. In the dominant model, we found that rs2853676 was associated with increased astrocytoma risk. In the additive model, all three tSNPs (rs2297440, rs2853676, and rs6010620) were associated with increased astrocytoma risk. Our results demonstrate, for the first time, the potential roles of RTEL1 and TERT in astrocytoma development.

Asunto(s)

Astrocitoma/genética , Neoplasias Encefálicas/genética , ADN Helicasas/genética , Predisposición Genética a la Enfermedad/genética , Polimorfismo de Nucleótido Simple , Telomerasa/genética , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Pueblo Asiatico/genética , Astrocitoma/etnología , Neoplasias Encefálicas/etnología , Estudios de Casos y Controles , Niño , Preescolar , China , Femenino , Frecuencia de los Genes , Predisposición Genética a la Enfermedad/etnología , Genotipo , Humanos , Lactante , Masculino , Persona de Mediana Edad , Oportunidad Relativa , Factores de Riesgo , Adulto Joven

RESUMEN

Recent advances in human genetic studies have opened new avenues for the identification of susceptibility genes for many complex genetic disorders, especially in the field of rare cancers such as glioma. Glioma is one of the least understood human tumors and the etiology for glioma is barely known. Hundreds of single-nucleotide polymorphisms (SNPs) are found to be related to the risk of glioma in previous studies. This study is committed to investigate the role of heredity in this disorder. To examine and validate how common variants contribute to glioma susceptibility in the Han Chinese population, we evaluated 12 tagging SNPs in a case-control study in the Chinese Han population from Xi'an city of China (301 cases and 302 controls). Overall, two protective alleles and one risk allele for glioma were found by genetic model analyses. In dominant model, the allele "T" of rs6947203 in the RPA3 gene acts as a protective allele [odds ratio (OR), 0.59; 95% confidence interval (CI), 0.22-0.90; p=0.014]. In recessive model, the allele "C" of rs1042522 in the TP53 gene acts as a risk allele (OR, 1.65; 95% CI, 1.05-2.59; p=0.0314). In additive model, the allele "G" of rs4140805 in the RPA3 gene (OR, 0.73; 95% CI, 0.53-0.99; p=0.0437) and the allele "T" of rs6947203 in the RPA3 gene (OR, 0.62; 95% CI, 0.42-0.92; p=0.0177) both act as protective alleles. We also observed a haplotype of "CC" in the TP53 gene with an increased risk of 34% of developing glioma (p=0.0306). Our results, combined with previous studies, ascertain the potential role of the TP53 gene to glioma onset.

Asunto(s)

Pueblo Asiatico/genética , Neoplasias Encefálicas/genética , Proteínas de Unión al ADN/genética , Genes p53 , Glioma/genética , Adulto , Estudios de Casos y Controles , Femenino , Predisposición Genética a la Enfermedad , Genotipo , Humanos , Masculino , Polimorfismo de Nucleótido Simple , Factores de Riesgo , Encuestas y Cuestionarios

RESUMEN

N-Myc downstream-regulated gene 4 (NDRG4) plays important roles in cellular differentiation and neurite formation. It is required for cell cycle progression and survival in established glioblastoma cell lines and cancer stem cell-enriched cells. The aim of this study was to evaluate the correlation of NDRG4 expression with the clinicopathological features and prognosis in patients with gliomas. Immunohistochemistry and Western blot analysis were used to investigate the expression of NDRG4 protein, respectively, in 128 patients with gliomas. Immunohistochemistry showed that NDRG4 expression was significantly reduced in glioma relative to nonneoplastic brain tissues (P = 0.008), and that its expression decreased with increasing glioma grade. These results were in line with the results of Western blot analysis. In addition, a non-parametric analysis revealed that the reduced NDRG4 expression was significantly correlated with a low Karnofsky performance score (P = 0.01), frequent intra-tumor necrosis (P = 0.03), and poor overall survival (P = 0.01). Furthermore, multivariate analysis showed that NDRG4 expression (P = 0.03) and intra-tumor necrosis (P = 0.03) were two important independent prognostic factors identified by the Cox proportional hazard model. Our results provide convincing evidence for the first time that the expression of NDRG4 is downregulated in human gliomas. The glioma patients with lower NDRG4 expression have a poor prognosis.

Asunto(s)

Neoplasias Encefálicas/metabolismo , Regulación hacia Abajo , Glioma/metabolismo , Proteínas Musculares/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Adolescente , Adulto , Anciano , Neoplasias Encefálicas/mortalidad , Neoplasias Encefálicas/patología , Niño , Femenino , Glioma/mortalidad , Glioma/patología , Humanos , Inmunohistoquímica , Masculino , Persona de Mediana Edad , Pronóstico , Tasa de Supervivencia

RESUMEN

INTRODUCTION: Glioma is one of the most aggressive human tumors; however, little is known about its genetic risk factors. The role of heredity is likely to be explained by combinations of common low-risk variants. Previous studies have indicated that more than 100 single nucleotide polymorphisms (SNPs) are associated with the risk of glioma. METHODS: To further investigate how and to what extent these SNPs contribute to glioma susceptibility in a Chinese population, we analyzed 43 SNPs of 226 glioma patients and 254 normal people in order to evaluate the associations between SNPs and the risk of glioma. RESULTS: Overall, we found three protective alleles for glioma in patients: the allele "G" of rs1801275 in the IL4R gene by allele model (odds ratio [OR], 0.71; 95% confidence interval [CI], 0.50-0.99; P=0.04) and dominant model (OR, 0.67; 95% CI, 0.46-0.99; P=0.04) analysis respectively, the allele "T" of rs17748 in the TREH gene by recessive model (OR, 0.48; 95% CI, 0.23-1.01; P=0.05) analysis, and the allele "G" of rs6470745 in CCDC26 gene by recessive model (OR, 0.48; 95% CI, 0.26-0.89; P=0.02) analysis. CONCLUSION: This study provides evidence for three glioma susceptibility genes - TREH, IL4R and CCDC26 - in a Chinese population; this may shed light on molecular markers of glioma susceptibility and could therefore be used as a diagnostic and prognostic marker for glioma patients in clinical study.

Asunto(s)

Glioma/genética , Subunidad alfa del Receptor de Interleucina-4/genética , Péptidos y Proteínas de Señalización Intracelular/genética , Trehalasa/genética , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Pueblo Asiatico/genética , Niño , Preescolar , China , Femenino , Predisposición Genética a la Enfermedad , Humanos , Masculino , Persona de Mediana Edad , Modelos Genéticos , Polimorfismo de Nucleótido Simple , ARN Largo no Codificante , Adulto Joven

RESUMEN

AIM: We have carried out a bibliometric analysis on the development of ametropia literature to determine its growth rule and tendency, and to provide the basis for the problems related to ametropia research. METHODS: Literatures that contained the descriptors of ametropia in title or paper published before Nov. 10, 2010 in PubMed databases (www.ncbi.nlm.nih.gov/Pubmed) were selected. As bibliometric indicators of ametropia, biomedical journals referring to ophthalmology by ISSN were calculated. The principal bibliometric indicators: Price's and Bradford's laws were applied on the increase or dispersion of scientific literature, the participation index of languages and the journals. By means of manual coding, literatures were classified according to documents study and statistical analysis. RESULTS: The literatures cited in ametropia, astigmatism, myopia and hypermetropia had accumulated to 26475, which consists of Review (n=1560), Randomized Controlled Trial (n=776), Practice Guideline (n=10), Meta-Analysis (n=23), Letter (n=1222), Editorial (n=328), Clinical Trial (n=1726) and Others (n=20830), and Humans (n=23073), Animals(n=1434) and others (n=1968). 1136 literatures were included in PubMed Central, 22384 in MEDLINE and 2955 in others. The ametropia literatures rose every 5 years which of the ametropia-year cumulated amount of the literatures had three periods: before 1900, slowly increasing from 1901 to 1950, rapidly rising from 1951 to 2010 (increased approximate exponentiation exponent). Sixty kinds of languages listed in PubMed databases, of which English is dominant for aborting to ametropia research documents before 2010 (77.32%, 20471/26475). The document languages of top eight account for 95.58% (English, German, French, Japanese, Russian, Italian, Spanish, Chinese), and others for 4.42% (1171/26475). The SCI database includes 48 ophthalmologic journals and the impact factor of 39 journals is ≥1 on Thomson-Reuters in 2010. Of 48 ophthalmologic journals, there were 14785 documents (55.85%) of ametropia, astigmatism, myopia, and hypermetropia. Others were without exception. CONCLUSION: The bibliometric analysis results show that ametropia literature are increased progressively, approximate exponentiation exponent during 1951-2010. In addition, ametropia research has become more popular since nearly half century.