bigbio/gad · Datasets at Hugging Face

id stringlengths 1 4	document_id stringlengths 1 4	text stringlengths 42 538	labels list
300	300	In conclusion, these results indicated that these two variations in the @GENE$-1alpha gene might not contribute to the risk of @DISEASE$ and type 2 diabetes in the Chinese population studied here.	[ "0" ]
301	301	There was a significantly higher frequency of the a allele of intron 4 in both nondiabetic and diabetic hemodialysis patients, so the polymorphism of intron 4 of the @GENE$ gene may have a wide influence on the progression of @DISEASE$.	[ "1" ]
302	302	We conclude that the investigated @GENE$ gene variants do not significantly influence @DISEASE$ as assessed by the KSP in the present population.	[ "0" ]
303	303	Our results demonstrate that the @GENE$1 allele, previously reported as a marker for CYP3A5 expression in human kidney, is associated with increased risk for BEN, while CYP3A41B and CYP2D6 genotypes do not significantly modify the risk for the @DISEASE$.	[ "0" ]
304	304	We found a greater risk of developing @DISEASE$ among individuals carrying the exon-8 insertion allele in the @GENE$ gene, independent of sex, age, physical activity, and sedentary lifestyle, which may partly explain some discrepancies found in the literature.	[ "1" ]
305	305	The @GENE$ gene may be involved in the development of @DISEASE$ by influencing the ability of individuals to use environmental support.	[ "1" ]
306	306	G421C polymorphism in the regulatory region of @GENE$ gene is correlated with @DISEASE$.	[ "0" ]
307	307	Polymorphisms of the tPA or @GENE$ genes probably do not significantly influence the risk of anerial @DISEASE$ thrombosis, or pregnancy morbidity in patients with aPL.	[ "0" ]
308	308	The results showed that @GENE$ @DISEASE$ on exon 2, exon 3 and exon 4 found in Chinese population contributes partly to early onset PD.	[ "0" ]
309	309	These data, if confirmed in larger studies, may begin to explain the differences in @DISEASE$ incidence by ethnicity, suggest a role for levels of @GENE$ expression in generation of SIDS susceptibility, and provide an important tool for identifying at-risk individuals and estimating the risk of recurrence.	[ "1" ]
310	310	We conclude that the presence of the Glu298Asp @GENE$ gene variant could be a marker of increased risk of developing @DISEASE$.	[ "1" ]
311	311	no evidence of an association between any of the three polymorphisms or @GENE$ haplotypes and @DISEASE$ was observed.	[ "0" ]
312	312	The A allele in the @GENE$/-607 gene promoter region may be involved in the development of @DISEASE$ in the Korean population.	[ "0" ]
313	313	These results suggest that the @GENE$ promoter polymorphism has no effect on risk and course of @DISEASE$ in the three cancer entities that were analyzed.	[ "0" ]
314	314	Our results indicate that co-existence of a @DISEASE$ in either the @GENE$ or CD14 gene, and in NOD2/CARD15 is associated with an increased susceptibility to developing CD compared to UC, and to developing either CD or UC compared to healthy individuals.	[ "0" ]
315	315	Our results suggest that MAO-A, COMT, @GENE$, DRD2, and DRD4 gene variants are not involved in susceptibility toward different time courses in @DISEASE$.	[ "1" ]
316	316	These findings suggest that @GENE$ genotype may be an important factor in tumorigenesis of @DISEASE$ and cancers related to hereditary nonpolyposis CRC among individuals with mismatch repair defects.	[ "1" ]
317	317	The N34S @DISEASE$ of @GENE$ appears not to be a distinct genetic risk factor in patients with sporadic pancreatic cancer.	[ "0" ]
318	318	The frequency of the 500 C>G polymorphism in the 3'@GENE$ in the CDKN2A gene was not significantly higher in @DISEASE$ compared to healthy controls.	[ "0" ]
319	319	Due to skewed X-chromosome inactivation, elderly women in populations with prevalent @GENE$ mutations are at risk of @DISEASE$.	[ "1" ]
320	320	Our results suggest that @GENE$ genotype may be a useful prognostic marker for @DISEASE$, however further specifically designed studies are needed to assess its value in this respect.	[ "1" ]
321	321	No association was demonstrated for @DISEASE$ and this particular @GENE$ polymorphism.	[ "1" ]
322	322	@GENE$ genotypes and haplotypes impact @DISEASE$-1 disease progression independently of CD4+ lymphocyte count and plasma HIV-1 RNA load, suggesting that the fundamental role of CX3CR1 in the alteration of disease progression might be the recruitment of immunomodulatory cells responsible for the control of HIV-1.	[ "1" ]
323	323	Our data do not support the involvement of 5-HT(1B/1D) and @GENE$) receptor gene polymorphisms in migraine with aura, yet do suggest a possible role for a locus at or near the hSERT gene in the susceptibility to @DISEASE$.	[ "1" ]
324	324	With the results obtained in this study a possible contribution of the @GENE$ gene in @DISEASE$ etiopathogenesis cannot be ruled out.	[ "1" ]
325	325	In conclusion, an initial dosing regimen for tacrolimus based on knowledge of the @GENE$ genotype and subsequently guided by concentration measurements has the potential to increase the proportion of patients achieving target @DISEASE$ concentrations early after transplantation.	[ "0" ]
326	326	Mutations in exon 11 of @GENE$ gene exist in the patients with @DISEASE$, and the mutations may be pathological.	[ "1" ]
327	327	Variants in @GENE$ are unlikely to be a major risk factor for the most common form of human NTDs, lumbosacral @DISEASE$.	[ "0" ]
328	328	The current results taken together suggest that, aside from other known causes of lung cancer, such as tobacco smoke, the existence of polymorphisms in the @GENE$ gene and, specifically, the presence of the G2677T @DISEASE$ can be crucial in conferring susceptibility to lung cancer.	[ "0" ]
329	329	The results of this study using detailed objective markers of @DISEASE$ disease do not support the hypothesis that impaired folate metabolism as reflected by the @GENE$ genotype is involved in the development of atopic disease.	[ "0" ]
330	330	The association of the F279 loss of function variant with the reduced risk of CVD supports the concept that @GENE$) plays a proatherogenic and causative role in @DISEASE$.	[ "1" ]
331	331	The @GENE$ -102 variant allele appears to be associated with an improved @DISEASE$-free survival in all patients, and more dramatically in subjects who received adjuvant radiation therapy.	[ "0" ]
332	332	The present study does not support that the investigated @GENE$ variants have a major influence on susceptibility to @DISEASE$ or related neurobiological traits.	[ "1" ]
333	333	Our results indicate that genetic variants in STAT3, independent of @DISEASE$ treatment, are determinants of FEV1 in both adults and children with asthma, and suggest that STAT3 may participate in inflammatory pathways that have an @GENE$ on level of lung function.	[ "0" ]
334	334	Our data support @GENE$/CP2/LSF as a candidate gene/risk factor for AD and provide justification for future studies to investigate the role of this gene in @DISEASE$.	[ "1" ]
335	335	These results suggest that @GENE$ promoter genotype may be involved in @DISEASE$.	[ "0" ]
336	336	The @GENE$ gene is significantly associated with RA susceptibility, suggesting the possibility that PD-1 may contribute to the pathogenesis of @DISEASE$.	[ "1" ]
337	337	Functional variants in both @GENE$ and TAS2R38 correlate with alcohol @DISEASE$ in African-American families.	[ "0" ]
338	338	Therefore, @GENE$ splicing mutations may be associated with a small proportion of @DISEASE$ cases.	[ "1" ]
339	339	Our data suggest that the @GENE$ gene determines susceptibility to @DISEASE$.	[ "1" ]
340	340	Although the sample size is relatively small, these findings suggest that a codon 31 polymorphism in @GENE$ may be associated with the development of @DISEASE$.	[ "0" ]
341	341	These findings support involvement of @GENE$ in the regulation of @DISEASE$ pressure.	[ "0" ]
342	342	The 584C/T polymorphism of the @GENE$ gene was associated with @DISEASE$ independently of HDL-C levels and thus may be involved in the pathogenesis of AMI.	[ "1" ]
343	343	These results indicate that mutations in NLGN3 and NLGN4 genes are responsible for at most a small fraction of autism cases and additional screenings in other @DISEASE$ populations are needed to better determine the frequency with which mutations in NLGN3 and @GENE$ occur in autism.	[ "1" ]
344	344	Through combination-analysis of the data about the @GENE$-I/D and the A2M-Ile1000Val variants, the A2M gene was suggested to be associated with @DISEASE$.	[ "1" ]
345	345	Our results support the hypothesis that @GENE$ genotype affects etiology and outcome of a variety of childhood @DISEASE$.	[ "0" ]
346	346	Our data suggest that -607 A/C (rs1946518) and -137 G/C (rs187238) polymorphisms within the @GENE$-promoter region do not play a major role in @DISEASE$ predisposition.	[ "1" ]
347	347	We conclude that sequence variation in the BACE1 or @GENE$ gene is not a significant risk factor for AD; however, a combination of a specific BACE1 allele and APOE epsilon 4 may increase the risk for @DISEASE$ over and above that attributed to APOE epsilon 4 alone.	[ "1" ]
348	348	We conclude that in the population studied here there is no association between @GENE$-K and @DISEASE$, or that if such a relationship exists it is precluded by another, as yet unknown factor.	[ "1" ]
349	349	This observation provides evidence that @GENE$ may have a role in determining the genetic susceptibility to and @DISEASE$ of ulcerative colitis.	[ "0" ]
350	350	Our data are consistent with the hypothesis that @GENE$ is involved in the @DISEASE$ of human atherosclerosis and myocardial infarction.	[ "0" ]
351	351	The Lys412Glu polymorphism of the @GENE$ gene in a hypertensive candidate chromosomal region is associated with @DISEASE$ in Han Chinese.	[ "0" ]
352	352	We did not confirm the previously reported association of this MHC2TA polymorphism with @DISEASE$ in our @GENE$ population despite its ethnic similarities with the Swedish population in which it was first described.	[ "0" ]
353	353	@GENE$ GGN and CAG allele combinations are strongly associated with @DISEASE$ indices in older adults, particularly in women.	[ "0" ]
354	354	We conclude that the @GENE$ @DISEASE$ in the reported XY female occurred de novo and is associated with sex reversal.	[ "0" ]
355	355	These preliminary data indicate that genetic polymorphisms in @GENE$ might play an important role in human prostate @DISEASE$.	[ "0" ]
356	356	The RFLPs of the @GENE$ gene may constitute a @DISEASE$ modifying factor through sex hormone production.	[ "0" ]
357	357	The present study demonstrated that genetic variations of @GENE$ are significantly associated with @DISEASE$ in the Korean population.	[ "0" ]
358	358	Statistical analysis indicated that there is no association of this @GENE$ variant and @DISEASE$ and hence the gene does not appear to play a genetically significant role in disease susceptibility.	[ "1" ]
359	359	Our data suggest that variants in the @GENE$ gene are unlikely to contribute to the predisposition for the lean or @DISEASE$ state.	[ "1" ]
360	360	These results strongly argue against a major role of @GENE$ polymorphisms in the pathogenesis of @DISEASE$.	[ "1" ]
361	361	In this study of @DISEASE$ patients, @GENE$ was not related to polymorphisms in the KCNJ11 gene.	[ "0" ]
362	362	We found several mutations in @GENE$ gene associated with @DISEASE$, the definite role of these mutations in URAT1 activity needs to be further studied.	[ "0" ]
363	363	We conclude that the presence of CTG-->@GENE$ (Leu-->Val) substitution in codon 125 in CD31 is not associated with protection from severe @DISEASE$, and we suggest that selective forces other than malaria may maintain this high-frequency polymorphism.	[ "0" ]
364	364	These findings suggest that the @GENE$ gene plays a role as one of the modifying factors for @DISEASE$.	[ "1" ]
365	365	Polymorphisms in the oxidative stress-related genes (CYP1A1, GSTM1, GSTT1, @GENE$, MnSOD) do not seem to be risk factors for @DISEASE$.	[ "1" ]
366	366	Our data provide strong evidence that the @GENE$ gene is a susceptibility factor for @DISEASE$, especially in females, and influences individual systolic blood pressure in the Chinese Han population.	[ "0" ]
367	367	@GENE$ polymorphism is not associated with genesis of @DISEASE$, but may be a risk factor for the progression of IgA nephropathy in Japanese.	[ "1" ]
368	368	Genetic variations in @GENE$ may define a high-risk subgroup of @DISEASE$ where the component of chronic bronchitis is predominant.	[ "1" ]
369	369	The results suggest that the presence of alleles HLA-G0104, @GENE$07/06, HCMV sequences and the fetal inheritance of maternal G*0104, should be considered as conditioning factors for the development of @DISEASE$.	[ "1" ]
370	370	Our data indicate that @GENE$ does not contribute substantially to susceptibility to @DISEASE$, but it is possible that these polymorphisms influence disease activity and drug responses in individuals with asthma.	[ "1" ]
371	371	The His645Asp polymorphism of the histamine metabolising enzyme @GENE$ is related to severity of @DISEASE$.	[ "1" ]
372	372	The T(-786)C promoter polymorphism and its interaction with exon 7 Glu298Asp affect endothelium-dependent @DISEASE$ in mild-to-moderate @GENE$ patients and NT Caucasian subjects.	[ "0" ]
373	373	The @GENE$ A6986G polymorphism may be specifically associated with a decreased risk of low-grade or early @DISEASE$.	[ "0" ]
374	374	We conclude that 1) the genetic analyses of @GENE$ and SP-A locus should be performed separately for black and white populations and 2) SP-A alleles/genotypes and SP-B variant may contribute to the etiology of RDS and/or may serve as markers for @DISEASE$ subgroups.	[ "0" ]
375	375	SNPs in @GENE$ and WIT1 genes are significantly associated with FSGS, suggesting that variants in these genes may mediate @DISEASE$ by altering WT1 function.	[ "0" ]
376	376	In conclusion, our @DISEASE$ suggests that the @GENE$ gene, especially together with APOE 4, may contribute to the development of AD.	[ "0" ]
377	377	The effect of air pollution from traffic on childhood @DISEASE$ appears to be modified by @GENE$ and TNF variants, supporting a role of genes controlling the antioxidative system and inflammatory response in allergy.	[ "0" ]
378	378	These results suggest that @GENE$ genetic polymorphism may not be associated with development of advanced @DISEASE$ in Korean women.	[ "1" ]
379	379	The -30G-->A polymorphism of the beta-@GENE$-specific promoter of GCK and the I27L polymorphism of HNF1A seem to increase the risk of @DISEASE$ in Scandinavian women.	[ "0" ]
380	380	In conclusion, the data provide evidence that a low frequency sequence variation in the @GENE$ gene could play a role in the etiology of @DISEASE$.	[ "1" ]
381	381	The polymorphism of @GENE$) locus allele in ADAM33 gene is associated with the susceptibility to @DISEASE$ in South China Han population.	[ "0" ]
382	382	We conclude that @GENE$-589T, but not TNF-alpha-3082 or Fcalpha RIbeta*G, is a risk factor for the development of atopy, @DISEASE$, and rhinitis by 12 mo of age.	[ "1" ]
383	383	Our results lead us to postulate that the @GENE$'87 bp and the LRP exon 3 C alleles of the LRP gene (or another locus that might be in linkage disequilibrium with these LRP polymorphic sites) could modify cerebrovascular LRP function or expression in noncapillary cerebral vessels, leading to an increased cerebrovascular @DISEASE$.	[ "0" ]
384	384	These results suggest that the @GENE$ gene contributes to @DISEASE$ susceptibility and may be involved in regulating IgE levels in atopic asthma.	[ "1" ]
385	385	These findings indicated that the polymorphism of CD14 but not @GENE$ Asp299Gly mutation was associated with Chinese patients with @DISEASE$, and the CD14 gene may contribute to the predisposition to colorectal cancer.	[ "1" ]
386	386	G61C @DISEASE$ of the @GENE$ gene, together with other environmental factors and/or genetic factors, could predispose to chronic pancreatitis, by interfering with the normal organization of keratin filaments.	[ "0" ]
387	387	The Arg194Trp and Arg399Gln polymorphisms of the @GENE$ gene may not be associated with @DISEASE$ in Polish population.	[ "1" ]
388	388	These results provide, for the first time, evidence supporting the association of @GENE$ with @DISEASE$ in postmenopausal women.	[ "0" ]
389	389	, this study argues against the use of the @GENE$ SNP309 as a prognostic marker in @DISEASE$.	[ "0" ]
390	390	The frequency of allele TNF2 in @DISEASE$ patients was significantly higher than in controls (chi 2 = 11.69, @GENE$.001), suggesting an association of this allele with higher risk of pulmonary tuberculosis or a disturbed immune response.	[ "0" ]
391	391	1) the @GENE$ promoter polymorphism contributes to variation in HLA and HDL(2) in the three ethnic groups; 2) WA men had higher HLA than BA and JA men, related to ethnic differences in central @DISEASE$ but not LIPC allele frequency; and 3) the higher HLA in WA men did not contribute to the ethnic differences in HDL, as the differences in HDL were made up entirely of differences in HDL(3) and not HDL(2).	[ "1" ]
392	392	Our results suggest that the @GENE$ epsilon 4 allele is the only known genetic risk factor for late-onset, sporadic @DISEASE$.	[ "1" ]
393	393	These results call in question the hypothesis that either @GENE$ or CNTF can be used as molecular markers for @DISEASE$ or late onset depression in the elderly.	[ "1" ]
394	394	Our results do not support earlier reports of an association between allele 1 in the 3'UTR of the @GENE$ gene and @DISEASE$.	[ "1" ]
395	395	Overall, our data show that in Spain a minority of adult-onset high-pressure POAG patients carry heterozygous @DISEASE$-causing mutations in the @GENE$ gene and that OPTN is not involved in either OHT or POAG.	[ "0" ]
396	396	These findings in a large, well characterized @DISEASE$ population, reveal that, while FLAP is an important enzyme in cys-LTs biosynthesis, polymorphisms in the @GENE$ gene are not likely to be functionally associated with the asthma phenotype.	[ "1" ]
397	397	Chinese individuals >or=50 years of age carrying the AG genotype of @GENE$ may be at an increased risk of developing @DISEASE$, and the GG genotype of NFKBIA may be considered as a prognostic factor for Swedish CRC patients.	[ "1" ]
398	398	In Japanese @DISEASE$, the +49A allele of @GENE$ increased in the presence of SSc with the anti-RNP antibody.	[ "1" ]
399	399	This study suggests a putative role of the @GENE$ gene polymorphism at position 49 of exon 1 for @DISEASE$ in the Korean population, although the detailed mechanisms remained to be elucidated.	[ "1" ]

300

In conclusion, these results indicated that these two variations in the @GENE$-1alpha gene might not contribute to the risk of @DISEASE$ and type 2 diabetes in the Chinese population studied here.

[ "0" ]

301

There was a significantly higher frequency of the a allele of intron 4 in both nondiabetic and diabetic hemodialysis patients, so the polymorphism of intron 4 of the @GENE$ gene may have a wide influence on the progression of @DISEASE$.

[ "1" ]

302

We conclude that the investigated @GENE$ gene variants do not significantly influence @DISEASE$ as assessed by the KSP in the present population.

[ "0" ]

303

Our results demonstrate that the @GENE$*1 allele, previously reported as a marker for CYP3A5 expression in human kidney, is associated with increased risk for BEN, while CYP3A4*1B and CYP2D6 genotypes do not significantly modify the risk for the @DISEASE$.

[ "0" ]

304

We found a greater risk of developing @DISEASE$ among individuals carrying the exon-8 insertion allele in the @GENE$ gene, independent of sex, age, physical activity, and sedentary lifestyle, which may partly explain some discrepancies found in the literature.

[ "1" ]

305

The @GENE$ gene may be involved in the development of @DISEASE$ by influencing the ability of individuals to use environmental support.

[ "1" ]

306

G421C polymorphism in the regulatory region of @GENE$ gene is correlated with @DISEASE$.

[ "0" ]

307

Polymorphisms of the tPA or @GENE$ genes probably do not significantly influence the risk of anerial @DISEASE$ thrombosis, or pregnancy morbidity in patients with aPL.

[ "0" ]

308

The results showed that @GENE$ @DISEASE$ on exon 2, exon 3 and exon 4 found in Chinese population contributes partly to early onset PD.

[ "0" ]

309

These data, if confirmed in larger studies, may begin to explain the differences in @DISEASE$ incidence by ethnicity, suggest a role for levels of @GENE$ expression in generation of SIDS susceptibility, and provide an important tool for identifying at-risk individuals and estimating the risk of recurrence.

[ "1" ]

310

We conclude that the presence of the Glu298Asp @GENE$ gene variant could be a marker of increased risk of developing @DISEASE$.

[ "1" ]

311

no evidence of an association between any of the three polymorphisms or @GENE$ haplotypes and @DISEASE$ was observed.

[ "0" ]

312

The A allele in the @GENE$/-607 gene promoter region may be involved in the development of @DISEASE$ in the Korean population.

[ "0" ]

313

These results suggest that the @GENE$ promoter polymorphism has no effect on risk and course of @DISEASE$ in the three cancer entities that were analyzed.

[ "0" ]

314

Our results indicate that co-existence of a @DISEASE$ in either the @GENE$ or CD14 gene, and in NOD2/CARD15 is associated with an increased susceptibility to developing CD compared to UC, and to developing either CD or UC compared to healthy individuals.

[ "0" ]

315

Our results suggest that MAO-A, COMT, @GENE$, DRD2, and DRD4 gene variants are not involved in susceptibility toward different time courses in @DISEASE$.

[ "1" ]

316

These findings suggest that @GENE$ genotype may be an important factor in tumorigenesis of @DISEASE$ and cancers related to hereditary nonpolyposis CRC among individuals with mismatch repair defects.

[ "1" ]

317

The N34S @DISEASE$ of @GENE$ appears not to be a distinct genetic risk factor in patients with sporadic pancreatic cancer.

[ "0" ]

318

The frequency of the 500 C>G polymorphism in the 3'@GENE$ in the CDKN2A gene was not significantly higher in @DISEASE$ compared to healthy controls.

[ "0" ]

319

Due to skewed X-chromosome inactivation, elderly women in populations with prevalent @GENE$ mutations are at risk of @DISEASE$.

[ "1" ]

320

Our results suggest that @GENE$ genotype may be a useful prognostic marker for @DISEASE$, however further specifically designed studies are needed to assess its value in this respect.

[ "1" ]

321

No association was demonstrated for @DISEASE$ and this particular @GENE$ polymorphism.

[ "1" ]

322

@GENE$ genotypes and haplotypes impact @DISEASE$-1 disease progression independently of CD4+ lymphocyte count and plasma HIV-1 RNA load, suggesting that the fundamental role of CX3CR1 in the alteration of disease progression might be the recruitment of immunomodulatory cells responsible for the control of HIV-1.

[ "1" ]

323

Our data do not support the involvement of 5-HT(1B/1D) and @GENE$) receptor gene polymorphisms in migraine with aura, yet do suggest a possible role for a locus at or near the hSERT gene in the susceptibility to @DISEASE$.

[ "1" ]

324

With the results obtained in this study a possible contribution of the @GENE$ gene in @DISEASE$ etiopathogenesis cannot be ruled out.

[ "1" ]

325

In conclusion, an initial dosing regimen for tacrolimus based on knowledge of the @GENE$ genotype and subsequently guided by concentration measurements has the potential to increase the proportion of patients achieving target @DISEASE$ concentrations early after transplantation.

[ "0" ]

326

Mutations in exon 11 of @GENE$ gene exist in the patients with @DISEASE$, and the mutations may be pathological.

[ "1" ]

327

Variants in @GENE$ are unlikely to be a major risk factor for the most common form of human NTDs, lumbosacral @DISEASE$.

[ "0" ]

328

The current results taken together suggest that, aside from other known causes of lung cancer, such as tobacco smoke, the existence of polymorphisms in the @GENE$ gene and, specifically, the presence of the G2677T @DISEASE$ can be crucial in conferring susceptibility to lung cancer.

[ "0" ]

329

The results of this study using detailed objective markers of @DISEASE$ disease do not support the hypothesis that impaired folate metabolism as reflected by the @GENE$ genotype is involved in the development of atopic disease.

[ "0" ]

330

The association of the F279 loss of function variant with the reduced risk of CVD supports the concept that @GENE$) plays a proatherogenic and causative role in @DISEASE$.

[ "1" ]

331

The @GENE$ -102 variant allele appears to be associated with an improved @DISEASE$-free survival in all patients, and more dramatically in subjects who received adjuvant radiation therapy.

[ "0" ]

332

The present study does not support that the investigated @GENE$ variants have a major influence on susceptibility to @DISEASE$ or related neurobiological traits.

[ "1" ]

333

Our results indicate that genetic variants in STAT3, independent of @DISEASE$ treatment, are determinants of FEV1 in both adults and children with asthma, and suggest that STAT3 may participate in inflammatory pathways that have an @GENE$ on level of lung function.

[ "0" ]

334

Our data support @GENE$/CP2/LSF as a candidate gene/risk factor for AD and provide justification for future studies to investigate the role of this gene in @DISEASE$.

[ "1" ]

335

These results suggest that @GENE$ promoter genotype may be involved in @DISEASE$.

[ "0" ]

336

The @GENE$ gene is significantly associated with RA susceptibility, suggesting the possibility that PD-1 may contribute to the pathogenesis of @DISEASE$.

[ "1" ]

337

Functional variants in both @GENE$ and TAS2R38 correlate with alcohol @DISEASE$ in African-American families.

[ "0" ]

338

Therefore, @GENE$ splicing mutations may be associated with a small proportion of @DISEASE$ cases.

[ "1" ]

339

Our data suggest that the @GENE$ gene determines susceptibility to @DISEASE$.

[ "1" ]

340

Although the sample size is relatively small, these findings suggest that a codon 31 polymorphism in @GENE$ may be associated with the development of @DISEASE$.

[ "0" ]

341

These findings support involvement of @GENE$ in the regulation of @DISEASE$ pressure.

[ "0" ]

342

The 584C/T polymorphism of the @GENE$ gene was associated with @DISEASE$ independently of HDL-C levels and thus may be involved in the pathogenesis of AMI.

[ "1" ]

343

These results indicate that mutations in NLGN3 and NLGN4 genes are responsible for at most a small fraction of autism cases and additional screenings in other @DISEASE$ populations are needed to better determine the frequency with which mutations in NLGN3 and @GENE$ occur in autism.

[ "1" ]

344

Through combination-analysis of the data about the @GENE$-I/D and the A2M-Ile1000Val variants, the A2M gene was suggested to be associated with @DISEASE$.

[ "1" ]

345

Our results support the hypothesis that @GENE$ genotype affects etiology and outcome of a variety of childhood @DISEASE$.

[ "0" ]

346

Our data suggest that -607 A/C (rs1946518) and -137 G/C (rs187238) polymorphisms within the @GENE$-promoter region do not play a major role in @DISEASE$ predisposition.

[ "1" ]

347

We conclude that sequence variation in the BACE1 or @GENE$ gene is not a significant risk factor for AD; however, a combination of a specific BACE1 allele and APOE epsilon 4 may increase the risk for @DISEASE$ over and above that attributed to APOE epsilon 4 alone.

[ "1" ]

348

We conclude that in the population studied here there is no association between @GENE$-K and @DISEASE$, or that if such a relationship exists it is precluded by another, as yet unknown factor.

[ "1" ]

349

This observation provides evidence that @GENE$ may have a role in determining the genetic susceptibility to and @DISEASE$ of ulcerative colitis.

[ "0" ]

350

Our data are consistent with the hypothesis that @GENE$ is involved in the @DISEASE$ of human atherosclerosis and myocardial infarction.

[ "0" ]

351

The Lys412Glu polymorphism of the @GENE$ gene in a hypertensive candidate chromosomal region is associated with @DISEASE$ in Han Chinese.

[ "0" ]

352

We did not confirm the previously reported association of this MHC2TA polymorphism with @DISEASE$ in our @GENE$ population despite its ethnic similarities with the Swedish population in which it was first described.

[ "0" ]

353

@GENE$ GGN and CAG allele combinations are strongly associated with @DISEASE$ indices in older adults, particularly in women.

[ "0" ]

354

We conclude that the @GENE$ @DISEASE$ in the reported XY female occurred de novo and is associated with sex reversal.

[ "0" ]

355

These preliminary data indicate that genetic polymorphisms in @GENE$ might play an important role in human prostate @DISEASE$.

[ "0" ]

356

The RFLPs of the @GENE$ gene may constitute a @DISEASE$ modifying factor through sex hormone production.

[ "0" ]

357

The present study demonstrated that genetic variations of @GENE$ are significantly associated with @DISEASE$ in the Korean population.

[ "0" ]

358

Statistical analysis indicated that there is no association of this @GENE$ variant and @DISEASE$ and hence the gene does not appear to play a genetically significant role in disease susceptibility.

[ "1" ]

359

Our data suggest that variants in the @GENE$ gene are unlikely to contribute to the predisposition for the lean or @DISEASE$ state.

[ "1" ]

360

These results strongly argue against a major role of @GENE$ polymorphisms in the pathogenesis of @DISEASE$.

[ "1" ]

361

In this study of @DISEASE$ patients, @GENE$ was not related to polymorphisms in the KCNJ11 gene.

[ "0" ]

362

We found several mutations in @GENE$ gene associated with @DISEASE$, the definite role of these mutations in URAT1 activity needs to be further studied.

[ "0" ]

363

We conclude that the presence of CTG-->@GENE$ (Leu-->Val) substitution in codon 125 in CD31 is not associated with protection from severe @DISEASE$, and we suggest that selective forces other than malaria may maintain this high-frequency polymorphism.

[ "0" ]

364

These findings suggest that the @GENE$ gene plays a role as one of the modifying factors for @DISEASE$.

[ "1" ]

365

Polymorphisms in the oxidative stress-related genes (CYP1A1, GSTM1, GSTT1, @GENE$, MnSOD) do not seem to be risk factors for @DISEASE$.

[ "1" ]

366

Our data provide strong evidence that the @GENE$ gene is a susceptibility factor for @DISEASE$, especially in females, and influences individual systolic blood pressure in the Chinese Han population.

[ "0" ]

367

@GENE$ polymorphism is not associated with genesis of @DISEASE$, but may be a risk factor for the progression of IgA nephropathy in Japanese.

[ "1" ]

368

Genetic variations in @GENE$ may define a high-risk subgroup of @DISEASE$ where the component of chronic bronchitis is predominant.

[ "1" ]

369

The results suggest that the presence of alleles HLA-G*0104, @GENE$*07/06, HCMV sequences and the fetal inheritance of maternal G*0104, should be considered as conditioning factors for the development of @DISEASE$.

[ "1" ]

370

Our data indicate that @GENE$ does not contribute substantially to susceptibility to @DISEASE$, but it is possible that these polymorphisms influence disease activity and drug responses in individuals with asthma.

[ "1" ]

371

The His645Asp polymorphism of the histamine metabolising enzyme @GENE$ is related to severity of @DISEASE$.

[ "1" ]

372

The T(-786)C promoter polymorphism and its interaction with exon 7 Glu298Asp affect endothelium-dependent @DISEASE$ in mild-to-moderate @GENE$ patients and NT Caucasian subjects.

[ "0" ]

373

The @GENE$ A6986G polymorphism may be specifically associated with a decreased risk of low-grade or early @DISEASE$.

[ "0" ]

374

We conclude that 1) the genetic analyses of @GENE$ and SP-A locus should be performed separately for black and white populations and 2) SP-A alleles/genotypes and SP-B variant may contribute to the etiology of RDS and/or may serve as markers for @DISEASE$ subgroups.

[ "0" ]

375

SNPs in @GENE$ and WIT1 genes are significantly associated with FSGS, suggesting that variants in these genes may mediate @DISEASE$ by altering WT1 function.

[ "0" ]

376

In conclusion, our @DISEASE$ suggests that the @GENE$ gene, especially together with APOE 4, may contribute to the development of AD.

[ "0" ]

377

The effect of air pollution from traffic on childhood @DISEASE$ appears to be modified by @GENE$ and TNF variants, supporting a role of genes controlling the antioxidative system and inflammatory response in allergy.

[ "0" ]

378

These results suggest that @GENE$ genetic polymorphism may not be associated with development of advanced @DISEASE$ in Korean women.

[ "1" ]

379

The -30G-->A polymorphism of the beta-@GENE$-specific promoter of GCK and the I27L polymorphism of HNF1A seem to increase the risk of @DISEASE$ in Scandinavian women.

[ "0" ]

380

In conclusion, the data provide evidence that a low frequency sequence variation in the @GENE$ gene could play a role in the etiology of @DISEASE$.

[ "1" ]

381

The polymorphism of @GENE$) locus allele in ADAM33 gene is associated with the susceptibility to @DISEASE$ in South China Han population.

[ "0" ]

382

We conclude that @GENE$-589*T, but not TNF-alpha-308*2 or Fcalpha RIbeta*G, is a risk factor for the development of atopy, @DISEASE$, and rhinitis by 12 mo of age.

[ "1" ]

383

Our results lead us to postulate that the @GENE$'87 bp and the LRP exon 3 C alleles of the LRP gene (or another locus that might be in linkage disequilibrium with these LRP polymorphic sites) could modify cerebrovascular LRP function or expression in noncapillary cerebral vessels, leading to an increased cerebrovascular @DISEASE$.

[ "0" ]

384

These results suggest that the @GENE$ gene contributes to @DISEASE$ susceptibility and may be involved in regulating IgE levels in atopic asthma.

[ "1" ]

385

These findings indicated that the polymorphism of CD14 but not @GENE$ Asp299Gly mutation was associated with Chinese patients with @DISEASE$, and the CD14 gene may contribute to the predisposition to colorectal cancer.

[ "1" ]

386

G61C @DISEASE$ of the @GENE$ gene, together with other environmental factors and/or genetic factors, could predispose to chronic pancreatitis, by interfering with the normal organization of keratin filaments.

[ "0" ]

387

The Arg194Trp and Arg399Gln polymorphisms of the @GENE$ gene may not be associated with @DISEASE$ in Polish population.

[ "1" ]

388

These results provide, for the first time, evidence supporting the association of @GENE$ with @DISEASE$ in postmenopausal women.

[ "0" ]

389

, this study argues against the use of the @GENE$ SNP309 as a prognostic marker in @DISEASE$.

[ "0" ]

390

The frequency of allele TNF2 in @DISEASE$ patients was significantly higher than in controls (chi 2 = 11.69, @GENE$.001), suggesting an association of this allele with higher risk of pulmonary tuberculosis or a disturbed immune response.

[ "0" ]

391

1) the @GENE$ promoter polymorphism contributes to variation in HLA and HDL(2) in the three ethnic groups; 2) WA men had higher HLA than BA and JA men, related to ethnic differences in central @DISEASE$ but not LIPC allele frequency; and 3) the higher HLA in WA men did not contribute to the ethnic differences in HDL, as the differences in HDL were made up entirely of differences in HDL(3) and not HDL(2).

[ "1" ]

392

Our results suggest that the @GENE$ epsilon 4 allele is the only known genetic risk factor for late-onset, sporadic @DISEASE$.

[ "1" ]

393

These results call in question the hypothesis that either @GENE$ or CNTF can be used as molecular markers for @DISEASE$ or late onset depression in the elderly.

[ "1" ]

394

Our results do not support earlier reports of an association between allele 1 in the 3'UTR of the @GENE$ gene and @DISEASE$.

[ "1" ]

395

Overall, our data show that in Spain a minority of adult-onset high-pressure POAG patients carry heterozygous @DISEASE$-causing mutations in the @GENE$ gene and that OPTN is not involved in either OHT or POAG.

[ "0" ]

396

These findings in a large, well characterized @DISEASE$ population, reveal that, while FLAP is an important enzyme in cys-LTs biosynthesis, polymorphisms in the @GENE$ gene are not likely to be functionally associated with the asthma phenotype.

[ "1" ]

397

Chinese individuals >or=50 years of age carrying the AG genotype of @GENE$ may be at an increased risk of developing @DISEASE$, and the GG genotype of NFKBIA may be considered as a prognostic factor for Swedish CRC patients.

[ "1" ]

398

In Japanese @DISEASE$, the +49A allele of @GENE$ increased in the presence of SSc with the anti-RNP antibody.

[ "1" ]

399

This study suggests a putative role of the @GENE$ gene polymorphism at position 49 of exon 1 for @DISEASE$ in the Korean population, although the detailed mechanisms remained to be elucidated.

[ "1" ]