ライフサイエンスコーパス: PTB

1 PTB cases were grouped as 1) Group 1- neonatal blood cul

2 PTB inhibits the induction and progression of periodonti

3 PTB rates were low and not significantly different with

4 PTB was released faster at pH 5.5 to 6.5 and consistentl

5 es.For the maternal genotype analysis, 1,165 PTBs and 3,830 term controls were evaluated.

6 hours after labor from 120 women (60 FTB, 60 PTB).

7 ia, Ohio, and New Jersey) (n = 1,940,213; 8% PTB).

8 on from 2000 through 2005 (n = 1,771,225; 8% PTB).

9 of PTBs nationally (corresponding to 15,808 PTBs) in 2010 could be attributed to PM2.5 (PM2.5 > 8.8

10 median age, 2.8 [min-max 0.8-8] years) and 9 PTB controls (median age, 3.7 [min-max 1.3-11.8] years).

11 adapter protein that possesses an SH2 and a PTB phosphotyrosine-binding motif.

12 n cervical cells of women destined to have a PTB.

13 s investigated by systemically administering PTB in the induction, progression, and recovery phases o

14 rs1800795 genotype CC is protective against PTB in women of European descent.

15 g that the CC genotype is protective against PTB.

16 rth also were positively associated with all PTB categories.

17 gestation was positively associated with all PTB outcomes, although magnitude varied by PTB category

18 4], LBW (ARR: 2.06; 95% CI: 1.03, 4.11), and PTB (ARR: 4.61; 95% CI: 2.31, 9.19) but not of stillbirt

19 ds ratio (OR) = 1.14, P = 3.1 x 10(-13)) and PTB (OR = 1.25, P = 5.8 x 10(-12)), and rs9271378[G] (MA

20 contribute to associations between PM2.5 and PTB.

21 portantly, the expression of hnRNP A1/A2 and PTB/nPTB is significantly altered in patients with front

22 modification for associations between EC and PTB by race/ethnicity and smoking status.

23 )/IL10(-)) in the blood and lung of EPTB and PTB subjects respectively.

24 to clearly differentiate LTBI from EPTB and PTB.

25 y measured BPA exposure during gestation and PTB.

26 itively and significantly related to LBW and PTB disparities, even after controlling for UV light ava

27 Data on LBW and PTB from 2007 (n = 2,825,620 births) were compared with

28 e predictions of the UVD hypothesis, LBW and PTB rate disparities were greatest in states with the hi

29 with lower risk of maternal anemia, LBW, and PTB.

30 sociation between the vaginal microbiota and PTB, demonstrate the benefits of high-resolution statist

31 H3K36me3-bound MRG15 and PTB regulate FGFR-2 splicing, which controls tumor growt

32 ption, creating a docking site for MRG15 and PTB.

33 cidate the association between rs1800975 and PTB.

34 ro studies suggested that binding of SH2 and PTB domains can enhance protein phosphorylation by prote

35 Simultaneously, the Anks1a PTB domain binds Sec23.

36 Adverse PM2.5-induced outcomes such as PTB and LBW are dependent upon the periods of maternal e

37 On assessing PTB by gestational week, we found that significant asthm

38 a LPS-induced model of infection-associated PTB, 101.10 prevented PTB, neonatal mortality, and fetal

39 edge, burden and costs of PM2.5-attributable PTB have not been estimated in the United States.

40 TB prevalence to quantify PM2.5-attributable PTB.

41 Attributable PTBs cost were estimated at $5.09 billion [sensitivity a

42 PHOSPHATE TRANSPORTER B (PTB) proteins are hypothesized to be the Na(+) /Pi sympo

43 tudies have assessed the association between PTB and a single nucleotide polymorphism (SNP), rs180079

44 Associations between PTB (n = 442,314) and air pollution exposures defined ac

45 Previously proposed associations between PTB and lower Lactobacillus and higher Gardnerella abund

46 We studied the relationships between PTB and exposure to different components of air pollutio

47 find that the CCM2 phosphotyrosine binding (PTB) domain displays a preference toward the third of th

48 y (PH) domain and a Phosphotyrosine Binding (PTB) domain.

49 e N-terminal TBC1D1 phosphotyrosine-binding (PTB) domain has shown a replicated association with fami

50 re conserved in the phosphotyrosine-binding (PTB) domain of beta-amyloid precursor protein-binding Mi

51 re we show that the phosphotyrosine-binding (PTB) domain protein Ced-6, a well-established phagocytos

52 mology (PH) domain, phosphotyrosine-binding (PTB) domain, and leucine zipper motif (APPL)-positive en

53 Dab2, through its phosphotyrosine-binding (PTB) domain, inhibits platelet aggregation by competing

54 edominantly via its phosphotyrosine-binding (PTB) domain.

55 as well as the ShcD phosphotyrosine-binding (PTB) domain.

56 omology 2 (SH2) and phosphotyrosine-binding (PTB) domains.

57 s containing SH2 or phosphotyrosine-binding (PTB) domains.

58 The polypyrimidine tract binding (PTB) protein family of RBPs are important posttranscript

59 RM) domains of Polypyrimidine tract binding (PTB) protein, a major splicing regulator, interact with

60 um samples between women with preterm birth (PTB) and full-term birth (FTB) and correlate them with p

61 (PM2.5) during pregnancy with preterm birth (PTB) and low birth weight (LBW) but disagree over which

62 Racial/ethnic disparities in preterm birth (PTB) are well documented in the epidemiological literatu

63 of low birth weight (LBW) and preterm birth (PTB) between whites and blacks, because these outcomes a

64 Preterm birth (PTB) contributes significantly to infant mortality and m

65 Preterm birth (PTB) has been associated with exposure to air pollution,

66 Preterm birth (PTB) is a leading cause of neonatal death worldwide.

67 Preterm birth (PTB) is commonly accompanied by in utero fetal inflammat

68 Preterm birth (PTB) is the leading cause of neonatal morbidity and mort

69 Preterm birth (PTB) is the leading cause of neonatal morbidity and mort

70 Preterm birth (PTB) is the leading cause of neonatal mortality and morb

71 Preterm birth (PTB) is the leading cause of neonatal mortality, and sur

72 to understand disparities in preterm birth (PTB) prevalence between births of non-Hispanic black ind

73 Preterm birth (PTB) rates (11.4% in 2013) in the United States remain h

74 t air pollutants may increase preterm birth (PTB) risk, but critical exposure windows are uncertain.

75 consistently associated with preterm birth (PTB) to varying degrees, but roles of PM2.5 species have

76 Preterm birth (PTB), a leading cause of infant mortality and morbidity,

77 h potential for prediction of preterm birth (PTB), a problem affecting 15 million newborns annually.

78 emia, low birth weight (LBW), preterm birth (PTB), and stillbirth in rural Ethiopia.

79 on pregnancies complicated by preterm birth (PTB), IAI, and/or EONS.

80 f the role of inflammation in preterm birth (PTB), polymorphisms in and near the interleukin-6 gene (

81 lecular mechanisms regulating preterm birth (PTB)-associated cervical remodeling remain unclear.

82 TORC1 signaling is a cause of preterm birth (PTB).

83 me (APS) and a mouse model of preterm birth (PTB).

84 nk intrauterine infection and preterm birth (PTB).

85 been variably associated with preterm birth (PTB).

86 ing pregnancy and the risk of preterm birth (PTB).

87 ss are known risk factors for preterm birth (PTB); however, the mechanisms and pathways that influenc

88 ll for gestational age (SGA), preterm birth (PTB)].In an observational study in 987 newborns from 104

89 ith up to 40% of spontaneous preterm births (PTB).

90 embranes (pPROM) may lead to preterm births (PTBs).

91 g approach for photochemical tissue bonding (PTB).

92 The probe-to-bone (PTB) test is a commonly used clinical test for osteomyel

93 In addition, since both PTB and miR-221 are upregulated in liver and muscle of g

94 ferase reporter assays illustrated that both PTB and miR-221 bind AdipoR1-3'UTR and cooperatively inh

95 capability of N-phenacylthiazolium bromide (PTB), a glycated cross-link breaker, in the modulation o

96 el loaded with N-phenacylthiazolium bromide (PTB), which cleaves the crosslinks of advanced glycation

97 thin the framework of a project initiated by PTB, were investigated with respect to their isotopic co

98 ion of targeted events being co-regulated by PTB.

99 l PTB outcomes, although magnitude varied by PTB category [e.g., for a 1-mug/m3 increase, RD = 11.8 (

100 laparotomy, which is invasive, and can cause PTB in control animals.

101 1-CCM2 interaction by destabilizing the CCM2 PTB domain and that a KRIT1 mutation also disrupts this

102 the 2.75 A co-crystal structure of the CCM2 PTB domain with a peptide corresponding to KRIT1(NPX(Y/F

103 We classified PTB into four categories (20-27, 28-31, 32-34, and 35-36

104 an RNA-protein complex minimally comprising PTB, MBNL and their cognate RNA-binding sites.

105 f the tissue area achieved with conventional PTB.

106 We converted PTB odds ratio (OR), identified in a previous meta-analy

107 Core PTB proteins are present at the plasma membrane of the l

108 Moreover, levels of core PTB mRNAs of M. polymorpha and the streptophyte alga Col

109 The expression of M. polymorpha core PTB proteins in the Saccharomyces cerevisiae pho2 mutant

110 in culture-negative but clinically diagnosed PTB was 37.8% and 83.8%, respectively.

111 t MTB/RIF is an effective tool in diagnosing PTB but will be more cost-effective for sputum-negative

112 xpectedly found that invoking the documented PTB-REST-miR-124 loop generates only immature neurons.

113 mmation is an etiological factor that drives PTB, and oxidative stress is associated with PTB.

114 stabilization pathway, but also by enhanced PTB-dependent, cap-independent translation.

115 lifornia spanning 2005 to 2010 and estimated PTBs and other adverse birth outcomes for infants borne

116 and neighborhood-level variables (16.1% for PTB) explained a greater proportion of the black-white d

117 20, 213) and RD = 145 (95% CI: -50, 341) for PTB during weeks 28-31 and 32-34, respectively.

118 Overall, individual (17.5% for PTB) and neighborhood-level variables (16.1% for PTB) ex

119 birth outcomes than air pollution (5.7% for PTB).

120 ons estimated the odds ratio and 95% CIs for PTB on the basis of the interaction of maternal asthma a

121 have identified an underlying mechanism for PTB and a potential therapeutic strategy for treating th

122 We reviewed all published papers for PTB phenotype and SNP rs1800795 genotype.

123 Stool holds promise for PTB diagnosis in HIV-infected children.

124 Adjusted odds ratios for PTB in association with interquartile range (IQR) increa

125 with asthma may experience a higher risk for PTB after exposure to traffic-related pollutants such as

126 rapeutic target in women who are at risk for PTB and associated complications in the affected offspri

127 ominantly Caucasian (n = 39) at low risk for PTB, the second predominantly African American and at hi

128 gs were investigated to predict the risk for PTB.

129 e significantly enriched in target sites for PTB, Tra2beta and STAR proteins.

130 D3 on response to antimicrobial therapy for PTB and to evaluate the influence of single-nucleotide p

131 roach to developing effective tocolytics for PTB management.

132 that even apparently curative treatment for PTB may not eradicate all of the MTB bacteria in most pa

133 and 95% confidence intervals (CIs) for four PTB categories were estimated for each exposure using li

134 53 staining was comparable in membranes from PTB and term birth pregnancies, whereas only <30% and <4

135 TORC1 signaling is also a signature of human PTB.

136 We identified PTB sequences in streptophyte genomes.

137 serum PGE2 and PD, CAL, and GCF TNF-alpha in PTB, periodontitis may cause an overall increase of labo

138 od to decompose racial/ethnic disparities in PTB.

139 ethod identifies novel genes dysregulated in PTB and provides a generalized framework to identify GWA

140 llutants were associated with an increase in PTB.

141 an important driver of neonatal morbidity in PTB and identify 101.10 as a safe and effective candidat

142 eta, IL-6, IL-8, and PGF2alpha, resulting in PTB and marked neonatal mortality.

143 ing discrete periods of pregnancy results in PTB and LBW.

144 treatment in vitro but was less apparent in PTBs.

145 kers, and concentrations were higher than in PTBs (P < 0.05).

146 y well-characterized host factors, including PTB, La, and DDX3, which have been shown to play a role

147 nd a poor outcome composite (POC), including PTB (<37 gestational weeks) and LBW (<2,500 g).

148 intravaginal LPS administration could induce PTB by stimulating an inflammatory response of the utero

149 against spontaneous and inflammation-induced PTB in p53d/d females.

150 e model of intrauterine inflammation-induced PTB to determine whether Nrf2 is a modifier of susceptib

151 riggers spontaneous and inflammation-induced PTB.

152 ive laparotomy model of inflammation-induced PTB.

153 intrauterine LPS injection reliably induces PTB in the mouse and mimics the local inflammatory and i

154 r receptor-bound protein 2) and the isolated PTB domain of Shc (SHC adaptor protein) to the EGF recep

155 ShcA generally uses its PTB domain to engage activated receptor tyrosine kinases

156 onger binds phosphotyrosine residues via its PTB domain.

157 ional RNA-binding proteins, such as hnRNP L, PTB/nPTB and hnRNP A1/A2.

158 educed the rate of alpha-GalCer-induced late PTB and improved neonatal survival.

159 lactosylceramide (alpha-GalCer) induced late PTB and neonatal mortality.

160 ice that underwent alpha-GalCer-induced late PTB had bradycardia and died shortly after delivery.

161 t iNKT cell activation in vivo leads to late PTB by initiating innate and adaptive immune responses a

162 The overall proportion of LBW, PTB, and stillbirth were 9.1%, 13.6%, and 4.5%, respecti

163 then used the RR estimates and county-level PTB prevalence to quantify PM2.5-attributable PTB.

164 ng to KRIT1(NPX(Y/F)3), revealing a Dab-like PTB fold for CCM2 and its interaction with KRIT1(NPX(Y/F

165 the uteroplacental tissues, while minimizing PTB in control animals.

166 Both Mint1 PTB domain and Mso1p induce vesicle aggregation/clusteri

167 ity of hPDLCs were noted with 0.05 to 0.1 mM PTB treatment at 24 hours.

168 ise in [Ca(2+)]i Finally, ChQ prevents mouse PTBs induced by bacterial endotoxin LPS or progesterone

169 sensitivities obtained for culture-negative PTB (82.4%) and EPTB (75.0%) in HIV-positive patients si

170 tropolymerization of poly(toluidine blue O) (PTB) and glucose oxidase (GOx) with an electroanalytical

171 ay provide new insight into the aetiology of PTB and improve our ability to predict and prevent PTB.

172 stimated PM2.5 attributable fraction (AF) of PTB was highest in urban counties, with highest AFs in t

173 ere we conduct genome-wide G x E analyses of PTB in 1,733 African-American women (698 mothers of PTB;

174 (LEP) was estimated using a meta-analysis of PTB-associated IQ loss, and well-established relationshi

175 anked candidate SNPs from a meta-analysis of PTB-GWAS to coding genes and developed a PPI network enr

176 t MBNL-binding sites increase the binding of PTB to its own sites.

177 We aimed to estimate burden of PTB in the United States and economic costs attributable

178 time points during pregnancy on 130 cases of PTB and 352 randomly assigned controls.

179 Clinical classifications of PTB were defined as "spontaneous," which was preceded by

180 When examining clinical classifications of PTB, urinary BPA late in pregnancy was significantly ass

181 tribute substantially to burden and costs of PTB in the United States, and considerable health and ec

182 Depletion of PTB or miR-221 increased, while overexpression of these

183 From 355 cases with final diagnosis of PTB, 263 (71.8%) had definite diagnosis and 92 cases had

184 ns of that model and show that disruption of PTB-dependent particle assembly inhibits rescue in trans

185 During myogenesis, downregulation of PTB and miR-221 robustly induced AdipoR1 translation, pr

186 Few robust genetic factors of PTB have been identified.

187 Uterine contraction is a central feature of PTB, so gaining new insights into the mechanisms of this

188 rvous system, the function and importance of PTB protein 2 (Ptbp2) as a key alternative splicing regu

189 ionality requires sequential inactivation of PTB and the PTB paralog nPTB in HAFs.

190 inhibitor rapamycin reduced the incidence of PTB in the p53d/d mice.

191 essential for more successful management of PTB.

192 ine LPS injection is a useful novel model of PTB for future studies and concords with the principles

193 1,733 African-American women (698 mothers of PTB; 1,035 of term birth) from the Boston Birth Cohort.

194 Odds of PTB were significantly higher among women with asthma fo

195 obiota contributes to the pathophysiology of PTB, but conflicting results in recent years have raised

196 The predicted differences in probability of PTB between black and white infants was 0.056 (95% CI: 0

197 a CB1 antagonist greatly reduced the rate of PTB inFaah(-/-)females exposed to LPS.

198 We estimated risk differences (RD) of PTB (reported per 106 pregnancies) associated with chang

199 us crispatus was associated with low risk of PTB in both cohorts, while Lactobacillus iners was not,

200 een domestic or commuting PA and the risk of PTB.

201 ria based on the results to rank the risk of PTB.

202 icantly associated with an increased risk of PTB.

203 antly associated with an increase of risk of PTB.

204 cy was inversely associated with the risk of PTB.

205 significant beneficial effect on the risk of PTB.

206 pregnancy, the pooled relative risk (RR) of PTB was 0.83 [95% confidence interval (CI) = 0.74-0.93]

207 division of labour between the four RRMs of PTB.

208 that should be controlled for in studies of PTB.

209 We conducted a study of PTB compared with term birth in two cohorts of pregnant

210 les and within the clinical subcategories of PTB.

211 reterm myometrium to identify subnetworks of PTB-SNP associated genes coordinately expressed with lab

212 been presented clinically with suspicion of PTB.

213 to the timing of exposure and the timing of PTB.

214 An estimated 3.32% of PTBs nationally (corresponding to 15,808 PTBs) in 2010 c

215 tients with nontuberculous mycobacteria, old PTB scar, and immune reconstitution syndrome.

216 us, evidence of effects of PM2.5 exposure on PTB, even if small in magnitude, is cause for concern.

217 maternal pre-pregnancy overweight/obesity on PTB risk, with rs11161721 (PG x E=1.8 x 10(-8); empirica

218 as significantly higher in LTBI than EPTB or PTB subjects.

219 rtions of participants with culture-positive PTB initiated on appropriate TB treatment within 30 days

220 m), 159 (12.4%) of whom had culture-positive PTB.

221 as markers of senescence phenotype in pPROM, PTBs, and term births.

222 ntaneous preterm labor (PTL), which precedes PTB.

223 In the last 6 weeks of pregnancy, PTB risk associated with particulate matter with aerodyn

224 In hospitalized patients with presumptive PTB in a low-burden setting, NAAT can reduce AII and is

225 Among the 318 admissions with presumptive PTB, 20 (6.3%) were culture-positive for Mycobacterium t

226 d improve our ability to predict and prevent PTB.

227 ratrol have therapeutic potential to prevent PTB.

228 f infection-associated PTB, 101.10 prevented PTB, neonatal mortality, and fetal brain inflammation.

229 by the polypyrimidine tract binding protein PTB to convert mouse embryonic fibroblasts (MEFs) into f

230 es for polypyrimidine tract-binding protein (PTB) and additional negative regulatory elements consist

231 rotein polypyrimidine tract-binding protein (PTB) in posttranscriptional regulation of AdipoR1 during

232 tes of polypyrimidine tract-binding protein (PTB), heterogeneous nuclear ribonucleoprotein (hnRNP) F/

233 or the polypyrimidine tract-binding protein (PTB), which also provides a new evidence to support the

234 o polypyrimidine tract RNA-binding proteins (PTBs), one near-ubiquitously expressed (Ptbp1) and anoth

235 uish subjects with latent (LTBI), pulmonary (PTB) or extrapulmonary (EPTB) tuberculosis remains uncle

236 second RRM domain of the splicing regulator PTB.

237 s of the adapter proteins outside of the SH2/PTB domains are important for stabilizing the binding of

238 ar signaling pathways downstream of the ShcA PTB domain, which both positively and negatively regulat

239 essful development of improved and shortened PTB-treatment strategies.

240 Specifically, PTB misexpression changes AS of PHYTOCHROME INTERACTING

241 h increased odds of delivering a spontaneous PTB.

242 embranes in women with pPROM and spontaneous PTB with intact membranes (<34 weeks) and the inducibili

243 vaginal LPS administration did not stimulate PTB.

244 Patients who had suspected PTB were enrolled into the study.

245 fferent specimens in children with suspected PTB.

246 Systemic PTB administration significantly reduced periodontal bon

247 for cases of culture-positive pulmonary TB (PTB; 91.3%) and extrapulmonary TB (EPTB; 92.3%), and the

248 mutation occurs in a location of the TBC1D1 PTB domain that is predicted to have a function in a put

249 ative exons in transfected cells showed that PTB binding sites were critical for splicing of a casset

250 The PTB phenotype was defined as gestational age (GA) < 37 w

251 uires sequential inactivation of PTB and the PTB paralog nPTB in HAFs.

252 d two Pi uptake mechanisms - mediated by the PTB and PHT1 proteins, respectively - from their strepto

253 Pooled sensitivity and specificity for the PTB test was 0.87 (95% confidence interval [CI], .75-.93

254 eration in the mouse model of APS and in the PTB model.

255 ieved through independent mutagenesis of the PTB domain and the CH1 tyrosine residues, and successive

256 to systematically review the accuracy of the PTB test to diagnose diabetic foot OM.

257 Here we report that the PTB adaptor Anks1a is specifically localized to the ER o

258 We conclude that the PTB test can accurately rule in diabetic foot OM in the

259 rminal domains of ICAP-1alpha, unmasking the PTB domain, thereby permitting ICAP-1alpha binding onto

260 enol A (BPA), is understudied with regard to PTB.

261 a and air pollutant exposures in relation to PTB risk.

262 ther Nrf2 is a modifier of susceptibility to PTB and prematurity-related morbidity and mortality in t

263 actions that may determine susceptibility to PTB.

264 oid lipid mediator, were more susceptible to PTB upon lipopolysaccharide (LPS) challenge.

265 d 277,643 controls), pulmonary tuberculosis (PTB) and M. tuberculosis infection.

266 in the treatment of pulmonary tuberculosis (PTB) are variously limited by small sample sizes, inadeq

267 ldren with suspected pulmonary tuberculosis (PTB) detected 8/17 (47%) culture-confirmed tuberculosis

268 ith culture-positive pulmonary tuberculosis (PTB) initiated on appropriate TB treatment within 30 day

269 agnosis of pediatric pulmonary tuberculosis (PTB) using Xpert MTB/RIF (Mycobacterium tuberculosis/rif

270 approaches to treat pulmonary tuberculosis (PTB).

271 tients infected with pulmonary tuberculosis (PTB).

272 nts with presumptive pulmonary tuberculosis (PTB).

273 pinal cord); and (2) pulmonary tuberculosis (PTB).

274 (HIV) infection and pulmonary tuberculosis (PTB).

275 riodontal ligament cells (hPDLCs) undergoing PTB treatment were evaluated in vitro.

276 ubstantial biological value in understanding PTB.

277 with FAS pre-mRNA under conditions in which PTB represses FAS exon 6 splicing.

278 onducted a clinical trial in 390 adults with PTB in Ulaanbaatar, Mongolia, who were randomized to rec

279 rs9271378[G] (MAF = 32.5%), associated with PTB (OR = 0.78, P = 2.5 x 10(-12))--both located between

280 EC was positively associated with PTB after 27 and before 35 weeks of gestation.

281 appeared to be more strongly associated with PTB than exposures during other time periods.

282 TWIST1, genes not previously associated with PTB, both of which regulate processes clearly relevant t

283 SO4 exposure were positively associated with PTB, though magnitude varied across gestational weeks.

284 to identify genetic variants associated with PTB.

285 gnancy was not significantly associated with PTB.

286 PTB, and oxidative stress is associated with PTB.

287 remature cervical remodeling associated with PTB.

288 d; there was no significant association with PTB (OR 0.98, 95% CI 0.72 - 1.33).

289 ginalis explained the genus association with PTB.

290 es and developed a PPI network enriched with PTB-SNP carrying genes.

291 xperimental periodontitis plus hydrogel with PTB (group PP).

292 a direct protein-to-protein interaction with PTB, and RNA binding by MBNL promotes this interaction,

293 n-based, pH-responsive hydrogels loaded with PTB can retard the initiation of and facilitate the reco

294 A chitosan-based hydrogel loaded with PTB was fabricated, and the in vitro release profile was

295 portion of adult, HIV-negative patients with PTB after a standard 6-month treatment plus 1 year follo

296 eplicated association of these variants with PTB in samples of European ancestry from Russia and Croa

297 Women with PTB demonstrated worse periodontal parameters and signif

298 Women with PTB exhibited significantly more periodontitis, worse pe

299 s with GCF levels of TNF-alpha in women with PTB.

300 rimental periodontitis plus hydrogel without PTB (group PH); and 4) experimental periodontitis plus h