bigbio/gad · Datasets at Hugging Face

id stringlengths 1 4	document_id stringlengths 1 4	text stringlengths 42 538	labels list
200	200	These data could partly explain the abnormal secretion of IL-10 occurring in schizophrenic patients in response to infections or different stressors and suggest a potential role of @GENE$ as a candidate gene for susceptibility to @DISEASE$.	[ "1" ]
201	201	Neither the genotypic frequencies for @GENE$ mutant alleles nor maternal tumor necrosis factor alpha plasma levels were increased in patients with @DISEASE$.	[ "1" ]
202	202	These findings suggest that the large size of a (@GENE$)(n) repeat in the HO-1 gene promoter may be associated with the development @DISEASE$ in Japanese male smokers.	[ "0" ]
203	203	These findings suggest that the change of C to G at position -9 of the @GENE$ gene is associated with the insulin resistance of @DISEASE$ due possibly to a potentiated hydrolysis of the PI3-kinase product.	[ "1" ]
204	204	The @GENE$ 2A13 and CYP 1A1 SNPs are associated with @DISEASE$ in a Caucasian population and may contribute to the understanding of the pathogenic mechanisms of uterine leiomyoma.	[ "0" ]
205	205	In @GENE$ 2 diabetic patients SNP3 is associated with triglyceride level, however there was no association between SNP3 and @DISEASE$.	[ "0" ]
206	206	In summary, our study shows that the 2756A-->G @DISEASE$ of @GENE$ in combination with MTHFR 677TT/1298AA and 677CT/1298AC can be associated with extremely high tHcy plasma levels.	[ "0" ]
207	207	The @GENE$ 5A-1171-6A genotype is an important determinant of @DISEASE$ pressure in this general population sample.	[ "0" ]
208	208	Therefore, the -786 @GENE$ genotype in NO synthase is a significant contributing factor for increasing the risk of @DISEASE$.	[ "0" ]
209	209	These findings support the view that polymorphic variants of the @GENE$ promoter region do not play a part in predisposing to BN, whereas they seem to predispose bulimic individuals to nutritional @DISEASE$ and increased harm avoidance.	[ "0" ]
210	210	We suggest that in @GENE$ gene polymorphisms the T allele at + 813 may decrease susceptibility to @DISEASE$.	[ "1" ]
211	211	Our results suggest that the C allele of the functional C748T polymorphism of @GENE$ may increase the risk of @DISEASE$.	[ "0" ]
212	212	Our data explain conflicting results in the literature regarding the sequence of @GENE$ but provide no support for a direct causal role for S100A2 in @DISEASE$.	[ "1" ]
213	213	It is unlikely that common variants in @GENE$ contribute significantly to @DISEASE$ susceptibility.	[ "0" ]
214	214	We conclude that BDNF and @GENE$ genes are not contributing significant risk effect among Finnish @DISEASE$ patients.	[ "0" ]
215	215	We conclude that polymorphism in the @GENE$ gene promoter does not play a relevant role in the @DISEASE$ of SLE in our population.	[ "0" ]
216	216	The 3'-UTR of the @GENE$ gene is involved in susceptibility to @DISEASE$.	[ "1" ]
217	217	Polymorphism of @GENE$ may contribute to development of BHR in @DISEASE$.	[ "1" ]
218	218	These results strongly suggest that the S89N polymorphism in the @GENE$ gene is associated with the development of @DISEASE$, via insulin sensitivity, in Japanese subjects.	[ "1" ]
219	219	Thus, the HERV-K(@GENE$) insertion is not associated with @DISEASE$ in Germans.	[ "0" ]
220	220	there is no allelic association between @DISEASE$ and @GENE$ gene polymorphisms.	[ "0" ]
221	221	These findings suggest an association between the genetic ability to produce low levels of @GENE$ and the susceptibility to develop chronic @DISEASE$ infection.	[ "1" ]
222	222	Overall, there was no significant association between this polymorphism and the risk of each @GENE$ @DISEASE$.	[ "0" ]
223	223	A significant association between @GENE$ Bam HI polymorphism and @DISEASE$ volume in patients with carotid atherothrombotic stroke confirms an important role of apoptosis in ischemic brain lesions formation that demands temporary antiapoptotic influence on patients with stroke.	[ "0" ]
224	224	the @GENE$ gene G395A allele carrier state may be associated with @DISEASE$ but not with coronary artery calcification in this Korean population.	[ "0" ]
225	225	A common variant of @GENE$, previously associated with a lower AHSG protein level, is thus more common among lean than @DISEASE$ and overweight men, supporting the results from Ahsg knock-out mice, namely, that AHSG modulates body mass.	[ "1" ]
226	226	Thus, TAP1 and @GENE$ genes polymorphism are not linked to @DISEASE$, since no association was found between a particular genotype and the disease.	[ "1" ]
227	227	Neither the @GENE$ 4G/5G polymorphism nor the PAI-1 antigen level is a strong risk factor for @DISEASE$.	[ "1" ]
228	228	Haplotype-based analysis of @GENE$ in patients with UP and BP @DISEASE$ and controls from northern Swedish descent provides preliminary evidence for protective association in both disorders and thus supports a central role for TPH2 in the pathogenesis of affective disorders.	[ "0" ]
229	229	The ecNOS gene a/b polymorphism and the NADH/NADPH oxidase @GENE$ gene C242T polymorphism were found to be significantly associated with the development of @DISEASE$ in Korean male patients less than 51 years old.	[ "1" ]
230	230	These data suggest that smokers with the @GENE$*6 genotype have a higher liability to @DISEASE$ on placebo and that they may be good candidates for bupropion treatment for smoking cessation.	[ "0" ]
231	231	Mutations in the @GENE$ receptor may predispose people to develop @DISEASE$ with gram-negative microorganisms.	[ "1" ]
232	232	Polymorphisms of @GENE$ gene were significantly association with human PFM, especially in female, suggesting the importance of DBP gene in the @DISEASE$ of human obesity.	[ "0" ]
233	233	These data imply the involvement of @GENE$ in chronic remodelling after conventional balloon angioplasty, and suggest that the 6A6A MMP3 genotype is a genetic susceptibility factor for @DISEASE$ after angioplasty without stenting.	[ "1" ]
234	234	The genetic predisposition at the HLA-DQB1 locus influences the severity of the mucosal @GENE$ in a dose-dependent manner, but not the clinical presentation, of @DISEASE$.	[ "0" ]
235	235	This study shows that the production of anti-@GENE$ autoantibodies in @DISEASE$ is associated with the DRB10301, DRB30101, DQA10501 and DQB10201 alleles which are in strong linkage disequilibrium.	[ "0" ]
236	236	SNP rs3744700 of @GENE$ gene is independently associated with the development of @DISEASE$ in Chinese Han population, and GG homozygote which is associated with increased expression of CXCL16 may have a promoting effect on CAD.	[ "1" ]
237	237	These findings provide direct evidence that CYP46 and @GENE$ polymorphisms synergically increase the risk for @DISEASE$ development, and influence on the rate of cognitive decline.	[ "1" ]
238	238	Our findings suggest that @GENE$ may be involved in the @DISEASE$ of micro- and macrovascular complications in type 1 diabetes, and that determination of MBL status might be used to identify patients at increased risk of developing these complications.	[ "0" ]
239	239	These results suggest that the @GENE$ @DISEASE$ genotype is associated with further suicide attempts among patients who have previously attempted suicide.	[ "0" ]
240	240	First, two thirds of @DISEASE$ manifesting in the first year of life can be explained by mutations in 4 genes only (NPHS1, @GENE$, WT1, or LAMB2).	[ "1" ]
241	241	In conclusion, @GENE$ gene promoter polymorphism could influence the radiological severity of rheumatoid arthritis and @DISEASE$ susceptibility, particularly in individuals lacking HLA-linked risk factors.	[ "0" ]
242	242	We conclude, that the -159T/C polymorphism in the @GENE$ monocyte receptor gene was not associated with progression of @DISEASE$ in this population nor did it influence the efficacy of pravastatin in the treatment of atherosclerosis.	[ "1" ]
243	243	This genotype-phenotype study indicates that in @GENE$-1 LQTS, mutations located in the transmembrane portion of the ion channel protein and the degree of ion channel @DISEASE$ caused by the mutations are important independent risk factors influencing the clinical course of this disorder.	[ "0" ]
244	244	The relatively low @DISEASE$ penetrance of this allele, along with the low population frequency, will limit the clinical applicability of germline testing for @GENE$*1100delC in North American kindreds.	[ "1" ]
245	245	The C/T polymorphism of the @GENE$ gene and circulating levels of hK2 are correlated and, in combination, are highly predictive for @DISEASE$.	[ "1" ]
246	246	Men who have the V allele of the @GENE$ gene have a twofold increase in the risk of prostate cancer development and an additional twofold increase in the risk of @DISEASE$ compared with men with the L/L genotype.	[ "0" ]
247	247	The @GENE$ allele frequency was higher among preeclamptic patients and the @DISEASE$ 1-1 phenotype was associated with more severe hypertension and proteinuria.	[ "0" ]
248	248	Thus, there is a significant association between the @GENE$-192R allele and @DISEASE$; the PON1-192R allele may play an important role in the genesis of coronary spasm, probably by attenuating the suppression of oxidative stress.	[ "1" ]
249	249	These results provide strong evidence for pathogenic variant(s) in the 276-kb region harboring @GENE$ that influence intermediate AD phenotypes and risk for @DISEASE$.	[ "1" ]
250	250	The observed association suggests that individuals with @GENE$-251TT and interleukin-10-819TT, a combination presumably causing mild @DISEASE$, have a higher probability of the continuing Helicobacter pylori infection, especially among current smokers.	[ "0" ]
251	251	A frameshifting 2-base pair insertion at codon 99 of the @GENE$ gene produced typical @DISEASE$ and carrier findings (but no tapetallike reflex) in this family.	[ "1" ]
252	252	Through combination-analysis of the data about the A2M-I/D and the @GENE$-Ile1000Val variants, the A2M gene was suggested to be associated with @DISEASE$.	[ "1" ]
253	253	Thus, our findings provided no evidence for an association between the @GENE$ polymorphism and @DISEASE$-related or other personality traits.	[ "0" ]
254	254	Admission FVII and @GENE$ antigen levels, partially predicted by polymorphisms, are independent predictors of mortality and reinfarction in patients with @DISEASE$.	[ "0" ]
255	255	The microsatellite DNA polymorphism of @GENE$ gene may be associated with the genetic predisposition to develop nephropathy in Japanese patients with @DISEASE$.	[ "1" ]
256	256	These findings suggest that genetic polymorphisms in @GENE$ may play a role in controlling basal levels of total serum IgE, independent of @DISEASE$.	[ "0" ]
257	257	These results suggest an important role for @DISEASE$ and impaired @GENE$ activity in the etiology of ESCC and GCA.	[ "0" ]
258	258	Our findings have indicated that the individuals polymorphic for @GENE$ MspI either with GSTM1 null or with GSTT1 null genotypes revealed an increased risk for UADT @DISEASE$ than that ascribed to a single susceptible gene among the tobacco users in the pop	[ "0" ]
259	259	The @DISEASE$ of @GENE$ gene may be related to Uigur women breast cancer and bilateral breast cancer.	[ "0" ]
260	260	The @GENE$ gene a/b polymorphism and the NADH/NADPH oxidase p22 phox gene C242T polymorphism were found to be significantly associated with the development of @DISEASE$ in Korean male patients less than 51 years old.	[ "1" ]
261	261	Polymorphisms in the promoter region of the @GENE$ gene were not associated with the @DISEASE$ in the Caucasian T2DM patients.	[ "0" ]
262	262	@GENE$ deficiency is associated with @DISEASE$ in the German population and hence a likely risk factor for autoimmune disorders.	[ "1" ]
263	263	We conclude that the rare @GENE$ G allele may offer some protection against the development of sporadic @DISEASE$ in APOE epsilon4 noncarriers in Chinese.	[ "1" ]
264	264	These findings suggest that through regulation of @GENE$ trafficking, FATP1 might play a role in post-prandial lipid metabolism and development of @DISEASE$.	[ "0" ]
265	265	The albescent phenotype in @DISEASE$ appears to not be caused exclusively by a @GENE$/RDS gene mutation, and we suggest that the apolipoprotein E gene may play a role in the albescent phenotype.	[ "0" ]
266	266	The results indicate that specific polymorphisms in the CYP1B1, ESR1, and @GENE$ genes may play a role in progression of BBD to @DISEASE$ among Caucasian women.	[ "1" ]
267	267	The -30G-->A polymorphism of the beta-cell-specific promoter of GCK and the I27L polymorphism of @GENE$ seem to increase the risk of @DISEASE$ in Scandinavian women.	[ "1" ]
268	268	@GENE$ gene exon7 G894T polymorphism might relate to @DISEASE$ in Uygur population in Xinjiang province.	[ "0" ]
269	269	Our data indicate that @GENE$ does not contribute substantially to susceptibility to asthma, but it is possible that these polymorphisms influence @DISEASE$ activity and drug responses in individuals with asthma.	[ "0" ]
270	270	These data do not support an association of the @GENE$ and AT1R genotypes on @DISEASE$ in white patients with normal coronary arteries.	[ "0" ]
271	271	Our results suggest that the @GENE$ G870A SNP may contribute to genetic susceptibility to OPLs and involve in @DISEASE$ development.	[ "1" ]
272	272	We conclude that genetic variation in the TGF-beta1 gene neither influences the existence of @DISEASE$ nor the incidence of rejection upon @GENE$.	[ "0" ]
273	273	@GENE$ 94C>A and TPMT polymorphisms are associated with AZA-related @DISEASE$ in IBD patients.	[ "0" ]
274	274	These preliminary data suggest a modest positive association of caffeine and coffee @DISEASE$ with the OR for ovarian cancer that may be modified by @GENE$ genotype and exposures, such as cruciferous vegetable consumption, that influence CYP1A2 expression.	[ "0" ]
275	275	These results suggest, but do not prove, that @GENE$ participates in blood pressure control, and sequence substitutions at its gene locus confer an increased risk of @DISEASE$ to a substantial proportion of men.	[ "1" ]
276	276	There was no evidence of an association between the @GENE$ genotype and @DISEASE$ occurrence.	[ "1" ]
277	277	This study shows that genetic variation of the @GENE$ (M235T), but not the ACE (I/D), genotypes contributes to the presence of @DISEASE$ independently of blood pressure profile in a subset of the Spanish population with a high prevalence of cardiovascular disease.	[ "1" ]
278	278	The evidence suggests that @GENE$ mutations and polymorphisms are not a major cause of @DISEASE$ maldescent with or without associated undermasculinisation.	[ "0" ]
279	279	Our data suggest that the @GENE$ -374T/A polymorphism is one of the likely candidate determinants for the genetic variance of @DISEASE$ phenotype in coronary atherosclerosis.	[ "0" ]
280	280	We conclude that the C-->T substitution in exon 4 of the @GENE$ gene does not contribute to the predisposition to be affected by the @DISEASE$.	[ "1" ]
281	281	Our data suggest that neither the +36 TNFRSF1A SNP nor the +196 @GENE$ SNP is associated with RA severity in a population of Caucasian patients with @DISEASE$.	[ "1" ]
282	282	the Trp(64)Arg @DISEASE$ of @GENE$ has little or no influence on either body weight or body mass index in the general Japanese population.	[ "0" ]
283	283	Our results are consistent with previous reports and show that homozygotes of the less common A allele of MPO -463 polymorphism have @GENE$.6-fold lower risk of @DISEASE$.	[ "0" ]
284	284	The current findings indicate that the IL-17F H161R variant influences the risk of @DISEASE$ and is a natural @GENE$ antagonist, suggesting a potential role for IL-17F in the etiology of asthma.	[ "1" ]
285	285	Regulation of @GENE$ expression by the functional CCTTT-polymorphism does not modify @DISEASE$ pathogenesis.	[ "0" ]
286	286	As this R92P @DISEASE$ is present in two unaffected carriers it appears to be less penetrant than previously reported @GENE$ mutations involving cysteine residues in the extracellular domains.	[ "0" ]
287	287	We conclude that the @GENE$ gene may be a susceptibility gene for @DISEASE$.	[ "1" ]
288	288	AACT * @GENE$ allele may be associated with @DISEASE$ negatively in Shanghai area, and this effect only exists in non-ApoE * epsilon 4 AD.	[ "0" ]
289	289	The @GENE$ gene and Hemicentin-1 genes do not appear to be involved in a statistically significant fraction of dry @DISEASE$ cases in the Japanese population.	[ "1" ]
290	290	Thus, the @GENE$ haplotype, which is associated with elevated plasma sEPCR levels, is a candidate risk factor for @DISEASE$.	[ "0" ]
291	291	The NADH/@GENE$ oxidase p22 phox gene is a susceptibility locus for @DISEASE$ in men, and the stromelysin-1 and interleukin-6 genes are susceptibility loci in women.	[ "0" ]
292	292	The SLC22A4 and @GENE$ polymorphisms described as etiological in the Japanese study did not show a significant role in @DISEASE$ susceptibility in our population.	[ "1" ]
293	293	The results further strengthen the causative role of the @GENE$ gene in non-syndromic @DISEASE$ and add new insights into espin structure and function.	[ "0" ]
294	294	Our results suggest that latitude has a role in the influence of @GENE$ gene polymorphism on @DISEASE$ and confirm previous data showing its association with morningness-eveningness tendencies.	[ "0" ]
295	295	The association found between @GENE$ genotype and risk of MI suggests that TLR4 genetic variants could potentially affect the susceptibility to @DISEASE$ and that TLR4-mediated innate immunity is implicated in the pathogenesis of MI.	[ "1" ]
296	296	@GENE$ microsatellite polymorphism is significantly associated with the incidence and outcome of severe postoperative @DISEASE$.	[ "0" ]
297	297	Identification of SPINK1 mutations in 12.2% of patients with adult alcoholic and idiopathic chronic pancreatitis suggests an important role for @GENE$ as a predisposing factor in adult @DISEASE$.	[ "1" ]
298	298	RAS polymorphisms do not seem to play a role in the development of @DISEASE$ in the studied Tunisian @GENE$ 2 diabetic subjects.	[ "0" ]
299	299	These results suggest that APE1 Asp148Glu and @GENE$ Arg399Gln polymorphisms might modify the risk of @DISEASE$ attributable to cigarette smoking exposure.	[ "1" ]

200

These data could partly explain the abnormal secretion of IL-10 occurring in schizophrenic patients in response to infections or different stressors and suggest a potential role of @GENE$ as a candidate gene for susceptibility to @DISEASE$.

[ "1" ]

201

Neither the genotypic frequencies for @GENE$ mutant alleles nor maternal tumor necrosis factor alpha plasma levels were increased in patients with @DISEASE$.

[ "1" ]

202

These findings suggest that the large size of a (@GENE$)(n) repeat in the HO-1 gene promoter may be associated with the development @DISEASE$ in Japanese male smokers.

[ "0" ]

203

These findings suggest that the change of C to G at position -9 of the @GENE$ gene is associated with the insulin resistance of @DISEASE$ due possibly to a potentiated hydrolysis of the PI3-kinase product.

[ "1" ]

204

The @GENE$ 2A13 and CYP 1A1 SNPs are associated with @DISEASE$ in a Caucasian population and may contribute to the understanding of the pathogenic mechanisms of uterine leiomyoma.

[ "0" ]

205

In @GENE$ 2 diabetic patients SNP3 is associated with triglyceride level, however there was no association between SNP3 and @DISEASE$.

[ "0" ]

206

In summary, our study shows that the 2756A-->G @DISEASE$ of @GENE$ in combination with MTHFR 677TT/1298AA and 677CT/1298AC can be associated with extremely high tHcy plasma levels.

[ "0" ]

207

The @GENE$ 5A-1171-6A genotype is an important determinant of @DISEASE$ pressure in this general population sample.

[ "0" ]

208

Therefore, the -786 @GENE$ genotype in NO synthase is a significant contributing factor for increasing the risk of @DISEASE$.

[ "0" ]

209

These findings support the view that polymorphic variants of the @GENE$ promoter region do not play a part in predisposing to BN, whereas they seem to predispose bulimic individuals to nutritional @DISEASE$ and increased harm avoidance.

[ "0" ]

210

We suggest that in @GENE$ gene polymorphisms the T allele at + 813 may decrease susceptibility to @DISEASE$.

[ "1" ]

211

Our results suggest that the C allele of the functional C748T polymorphism of @GENE$ may increase the risk of @DISEASE$.

[ "0" ]

212

Our data explain conflicting results in the literature regarding the sequence of @GENE$ but provide no support for a direct causal role for S100A2 in @DISEASE$.

[ "1" ]

213

It is unlikely that common variants in @GENE$ contribute significantly to @DISEASE$ susceptibility.

[ "0" ]

214

We conclude that BDNF and @GENE$ genes are not contributing significant risk effect among Finnish @DISEASE$ patients.

[ "0" ]

215

We conclude that polymorphism in the @GENE$ gene promoter does not play a relevant role in the @DISEASE$ of SLE in our population.

[ "0" ]

216

The 3'-UTR of the @GENE$ gene is involved in susceptibility to @DISEASE$.

[ "1" ]

217

Polymorphism of @GENE$ may contribute to development of BHR in @DISEASE$.

[ "1" ]

218

These results strongly suggest that the S89N polymorphism in the @GENE$ gene is associated with the development of @DISEASE$, via insulin sensitivity, in Japanese subjects.

[ "1" ]

219

Thus, the HERV-K(@GENE$) insertion is not associated with @DISEASE$ in Germans.

[ "0" ]

220

there is no allelic association between @DISEASE$ and @GENE$ gene polymorphisms.

[ "0" ]

221

These findings suggest an association between the genetic ability to produce low levels of @GENE$ and the susceptibility to develop chronic @DISEASE$ infection.

[ "1" ]

222

Overall, there was no significant association between this polymorphism and the risk of each @GENE$ @DISEASE$.

[ "0" ]

223

A significant association between @GENE$ Bam HI polymorphism and @DISEASE$ volume in patients with carotid atherothrombotic stroke confirms an important role of apoptosis in ischemic brain lesions formation that demands temporary antiapoptotic influence on patients with stroke.

[ "0" ]

224

the @GENE$ gene G395A allele carrier state may be associated with @DISEASE$ but not with coronary artery calcification in this Korean population.

[ "0" ]

225

A common variant of @GENE$, previously associated with a lower AHSG protein level, is thus more common among lean than @DISEASE$ and overweight men, supporting the results from Ahsg knock-out mice, namely, that AHSG modulates body mass.

[ "1" ]

226

Thus, TAP1 and @GENE$ genes polymorphism are not linked to @DISEASE$, since no association was found between a particular genotype and the disease.

[ "1" ]

227

Neither the @GENE$ 4G/5G polymorphism nor the PAI-1 antigen level is a strong risk factor for @DISEASE$.

[ "1" ]

228

Haplotype-based analysis of @GENE$ in patients with UP and BP @DISEASE$ and controls from northern Swedish descent provides preliminary evidence for protective association in both disorders and thus supports a central role for TPH2 in the pathogenesis of affective disorders.

[ "0" ]

229

The ecNOS gene a/b polymorphism and the NADH/NADPH oxidase @GENE$ gene C242T polymorphism were found to be significantly associated with the development of @DISEASE$ in Korean male patients less than 51 years old.

[ "1" ]

230

These data suggest that smokers with the @GENE$*6 genotype have a higher liability to @DISEASE$ on placebo and that they may be good candidates for bupropion treatment for smoking cessation.

[ "0" ]

231

Mutations in the @GENE$ receptor may predispose people to develop @DISEASE$ with gram-negative microorganisms.

[ "1" ]

232

Polymorphisms of @GENE$ gene were significantly association with human PFM, especially in female, suggesting the importance of DBP gene in the @DISEASE$ of human obesity.

[ "0" ]

233

These data imply the involvement of @GENE$ in chronic remodelling after conventional balloon angioplasty, and suggest that the 6A6A MMP3 genotype is a genetic susceptibility factor for @DISEASE$ after angioplasty without stenting.

[ "1" ]

234

The genetic predisposition at the HLA-DQB1 locus influences the severity of the mucosal @GENE$ in a dose-dependent manner, but not the clinical presentation, of @DISEASE$.

[ "0" ]

235

This study shows that the production of anti-@GENE$ autoantibodies in @DISEASE$ is associated with the DRB1*0301, DRB3*0101, DQA1*0501 and DQB1*0201 alleles which are in strong linkage disequilibrium.

[ "0" ]

236

SNP rs3744700 of @GENE$ gene is independently associated with the development of @DISEASE$ in Chinese Han population, and GG homozygote which is associated with increased expression of CXCL16 may have a promoting effect on CAD.

[ "1" ]

237

These findings provide direct evidence that CYP46 and @GENE$ polymorphisms synergically increase the risk for @DISEASE$ development, and influence on the rate of cognitive decline.

[ "1" ]

238

Our findings suggest that @GENE$ may be involved in the @DISEASE$ of micro- and macrovascular complications in type 1 diabetes, and that determination of MBL status might be used to identify patients at increased risk of developing these complications.

[ "0" ]

239

These results suggest that the @GENE$ @DISEASE$ genotype is associated with further suicide attempts among patients who have previously attempted suicide.

[ "0" ]

240

First, two thirds of @DISEASE$ manifesting in the first year of life can be explained by mutations in 4 genes only (NPHS1, @GENE$, WT1, or LAMB2).

[ "1" ]

241

In conclusion, @GENE$ gene promoter polymorphism could influence the radiological severity of rheumatoid arthritis and @DISEASE$ susceptibility, particularly in individuals lacking HLA-linked risk factors.

[ "0" ]

242

We conclude, that the -159T/C polymorphism in the @GENE$ monocyte receptor gene was not associated with progression of @DISEASE$ in this population nor did it influence the efficacy of pravastatin in the treatment of atherosclerosis.

[ "1" ]

243

This genotype-phenotype study indicates that in @GENE$-1 LQTS, mutations located in the transmembrane portion of the ion channel protein and the degree of ion channel @DISEASE$ caused by the mutations are important independent risk factors influencing the clinical course of this disorder.

[ "0" ]

244

The relatively low @DISEASE$ penetrance of this allele, along with the low population frequency, will limit the clinical applicability of germline testing for @GENE$*1100delC in North American kindreds.

[ "1" ]

245

The C/T polymorphism of the @GENE$ gene and circulating levels of hK2 are correlated and, in combination, are highly predictive for @DISEASE$.

[ "1" ]

246

Men who have the V allele of the @GENE$ gene have a twofold increase in the risk of prostate cancer development and an additional twofold increase in the risk of @DISEASE$ compared with men with the L/L genotype.

[ "0" ]

247

The @GENE$ allele frequency was higher among preeclamptic patients and the @DISEASE$ 1-1 phenotype was associated with more severe hypertension and proteinuria.

[ "0" ]

248

Thus, there is a significant association between the @GENE$-192R allele and @DISEASE$; the PON1-192R allele may play an important role in the genesis of coronary spasm, probably by attenuating the suppression of oxidative stress.

[ "1" ]

249

These results provide strong evidence for pathogenic variant(s) in the 276-kb region harboring @GENE$ that influence intermediate AD phenotypes and risk for @DISEASE$.

[ "1" ]

250

The observed association suggests that individuals with @GENE$-251TT and interleukin-10-819TT, a combination presumably causing mild @DISEASE$, have a higher probability of the continuing Helicobacter pylori infection, especially among current smokers.

[ "0" ]

251

A frameshifting 2-base pair insertion at codon 99 of the @GENE$ gene produced typical @DISEASE$ and carrier findings (but no tapetallike reflex) in this family.

[ "1" ]

252

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

[ "1" ]

253

Thus, our findings provided no evidence for an association between the @GENE$ polymorphism and @DISEASE$-related or other personality traits.

[ "0" ]

254

Admission FVII and @GENE$ antigen levels, partially predicted by polymorphisms, are independent predictors of mortality and reinfarction in patients with @DISEASE$.

[ "0" ]

255

The microsatellite DNA polymorphism of @GENE$ gene may be associated with the genetic predisposition to develop nephropathy in Japanese patients with @DISEASE$.

[ "1" ]

256

These findings suggest that genetic polymorphisms in @GENE$ may play a role in controlling basal levels of total serum IgE, independent of @DISEASE$.

[ "0" ]

257

These results suggest an important role for @DISEASE$ and impaired @GENE$ activity in the etiology of ESCC and GCA.

[ "0" ]

258

Our findings have indicated that the individuals polymorphic for @GENE$ MspI either with GSTM1 null or with GSTT1 null genotypes revealed an increased risk for UADT @DISEASE$ than that ascribed to a single susceptible gene among the tobacco users in the pop

[ "0" ]

259

The @DISEASE$ of @GENE$ gene may be related to Uigur women breast cancer and bilateral breast cancer.

[ "0" ]

260

The @GENE$ gene a/b polymorphism and the NADH/NADPH oxidase p22 phox gene C242T polymorphism were found to be significantly associated with the development of @DISEASE$ in Korean male patients less than 51 years old.

[ "1" ]

261

Polymorphisms in the promoter region of the @GENE$ gene were not associated with the @DISEASE$ in the Caucasian T2DM patients.

[ "0" ]

262

@GENE$ deficiency is associated with @DISEASE$ in the German population and hence a likely risk factor for autoimmune disorders.

[ "1" ]

263

We conclude that the rare @GENE$ G allele may offer some protection against the development of sporadic @DISEASE$ in APOE epsilon4 noncarriers in Chinese.

[ "1" ]

264

These findings suggest that through regulation of @GENE$ trafficking, FATP1 might play a role in post-prandial lipid metabolism and development of @DISEASE$.

[ "0" ]

265

The albescent phenotype in @DISEASE$ appears to not be caused exclusively by a @GENE$/RDS gene mutation, and we suggest that the apolipoprotein E gene may play a role in the albescent phenotype.

[ "0" ]

266

The results indicate that specific polymorphisms in the CYP1B1, ESR1, and @GENE$ genes may play a role in progression of BBD to @DISEASE$ among Caucasian women.

[ "1" ]

267

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

[ "1" ]

268

@GENE$ gene exon7 G894T polymorphism might relate to @DISEASE$ in Uygur population in Xinjiang province.

[ "0" ]

269

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

[ "0" ]

270

These data do not support an association of the @GENE$ and AT1R genotypes on @DISEASE$ in white patients with normal coronary arteries.

[ "0" ]

271

Our results suggest that the @GENE$ G870A SNP may contribute to genetic susceptibility to OPLs and involve in @DISEASE$ development.

[ "1" ]

272

We conclude that genetic variation in the TGF-beta1 gene neither influences the existence of @DISEASE$ nor the incidence of rejection upon @GENE$.

[ "0" ]

273

@GENE$ 94C>A and TPMT polymorphisms are associated with AZA-related @DISEASE$ in IBD patients.

[ "0" ]

274

These preliminary data suggest a modest positive association of caffeine and coffee @DISEASE$ with the OR for ovarian cancer that may be modified by @GENE$ genotype and exposures, such as cruciferous vegetable consumption, that influence CYP1A2 expression.

[ "0" ]

275

These results suggest, but do not prove, that @GENE$ participates in blood pressure control, and sequence substitutions at its gene locus confer an increased risk of @DISEASE$ to a substantial proportion of men.

[ "1" ]

276

There was no evidence of an association between the @GENE$ genotype and @DISEASE$ occurrence.

[ "1" ]

277

This study shows that genetic variation of the @GENE$ (M235T), but not the ACE (I/D), genotypes contributes to the presence of @DISEASE$ independently of blood pressure profile in a subset of the Spanish population with a high prevalence of cardiovascular disease.

[ "1" ]

278

The evidence suggests that @GENE$ mutations and polymorphisms are not a major cause of @DISEASE$ maldescent with or without associated undermasculinisation.

[ "0" ]

279

Our data suggest that the @GENE$ -374T/A polymorphism is one of the likely candidate determinants for the genetic variance of @DISEASE$ phenotype in coronary atherosclerosis.

[ "0" ]

280

We conclude that the C-->T substitution in exon 4 of the @GENE$ gene does not contribute to the predisposition to be affected by the @DISEASE$.

[ "1" ]

281

Our data suggest that neither the +36 TNFRSF1A SNP nor the +196 @GENE$ SNP is associated with RA severity in a population of Caucasian patients with @DISEASE$.

[ "1" ]

282

the Trp(64)Arg @DISEASE$ of @GENE$ has little or no influence on either body weight or body mass index in the general Japanese population.

[ "0" ]

283

Our results are consistent with previous reports and show that homozygotes of the less common A allele of MPO -463 polymorphism have @GENE$.6-fold lower risk of @DISEASE$.

[ "0" ]

284

The current findings indicate that the IL-17F H161R variant influences the risk of @DISEASE$ and is a natural @GENE$ antagonist, suggesting a potential role for IL-17F in the etiology of asthma.

[ "1" ]

285

Regulation of @GENE$ expression by the functional CCTTT-polymorphism does not modify @DISEASE$ pathogenesis.

[ "0" ]

286

As this R92P @DISEASE$ is present in two unaffected carriers it appears to be less penetrant than previously reported @GENE$ mutations involving cysteine residues in the extracellular domains.

[ "0" ]

287

We conclude that the @GENE$ gene may be a susceptibility gene for @DISEASE$.

[ "1" ]

288

AACT * @GENE$ allele may be associated with @DISEASE$ negatively in Shanghai area, and this effect only exists in non-ApoE * epsilon 4 AD.

[ "0" ]

289

The @GENE$ gene and Hemicentin-1 genes do not appear to be involved in a statistically significant fraction of dry @DISEASE$ cases in the Japanese population.

[ "1" ]

290

Thus, the @GENE$ haplotype, which is associated with elevated plasma sEPCR levels, is a candidate risk factor for @DISEASE$.

[ "0" ]

291

The NADH/@GENE$ oxidase p22 phox gene is a susceptibility locus for @DISEASE$ in men, and the stromelysin-1 and interleukin-6 genes are susceptibility loci in women.

[ "0" ]

292

The SLC22A4 and @GENE$ polymorphisms described as etiological in the Japanese study did not show a significant role in @DISEASE$ susceptibility in our population.

[ "1" ]

293

The results further strengthen the causative role of the @GENE$ gene in non-syndromic @DISEASE$ and add new insights into espin structure and function.

[ "0" ]

294

Our results suggest that latitude has a role in the influence of @GENE$ gene polymorphism on @DISEASE$ and confirm previous data showing its association with morningness-eveningness tendencies.

[ "0" ]

295

The association found between @GENE$ genotype and risk of MI suggests that TLR4 genetic variants could potentially affect the susceptibility to @DISEASE$ and that TLR4-mediated innate immunity is implicated in the pathogenesis of MI.

[ "1" ]

296

@GENE$ microsatellite polymorphism is significantly associated with the incidence and outcome of severe postoperative @DISEASE$.

[ "0" ]

297

Identification of SPINK1 mutations in 12.2% of patients with adult alcoholic and idiopathic chronic pancreatitis suggests an important role for @GENE$ as a predisposing factor in adult @DISEASE$.

[ "1" ]

298

RAS polymorphisms do not seem to play a role in the development of @DISEASE$ in the studied Tunisian @GENE$ 2 diabetic subjects.

[ "0" ]

299

These results suggest that APE1 Asp148Glu and @GENE$ Arg399Gln polymorphisms might modify the risk of @DISEASE$ attributable to cigarette smoking exposure.

[ "1" ]