PubMed Health⌕ Search

Biomedical subjects

Lihua Wang

Publications and source records attributed to Lihua Wang.

At least 19 recordsLinked to original sources
PubMed2007

Large-scale genome-wide linkage analysis for loci linked to BMD at different skeletal sites in extreme selected sibships.

UNLABELLED: Few genome-wide linkage studies of osteoporosis have been conducted in the Asian population. We performed a genome-wide scan involving 3093 adult siblings with at least one sib-pair extremely concordant or discordant for hip BMD. Our results indicated four genome-wide significant QTLs for BMD. In comparison with 12 previous reported linkage studies, we reveal novel linkage regions that have reaching global significance. INTRODUCTION: The genetic basis for osteoporosis has been firmly established, but efforts to identify genes associated with this complex trait have been incomplete, especially in Asian populations. The purpose of this study was to identify quantitative trait loci (QTLs) for BMD in a Chinese population. MATERIALS AND METHODS: We performed a genome-wide scan involving 3093 siblings 25-64 years of age from 941 families, with at least one sib-pair extreme concordant or discordant for total hip BMD from a large community-based cohort (n = 23,327) in Anhui, China. Linkage analysis was performed on BMD residuals adjusted for age, height, weight, occupation, cigarette smoking, physical activity, and alcohol consumption using the revised Haseman-Elston regression-based linkage model. RESULTS: Our results revealed significant QTLs on chromosome 7p21.2 for femoral neck BMD (LOD = 3.68) and on chromosome 2q24.3 for total hip BMD (LOD = 3.65). Suggestive linkage regions were found to overlap among different skeletal sites on chromosomes 2q, 7p, and 16q. Sex-specific linkage analysis further revealed a significant QTL for lumbar spine BMD on chromosome 13q21.1 (LOD = 3.62) in women only. When performing multivariate linkage analysis by combining BMDs at four skeletal sites (i.e., whole body, total hip, femoral neck, and lumbar spine BMD), an additional significant QTL was found at chromosome 5q21.2 (LOD = 4.56). None of these significant QTLs found in our study overlapped with major QTLs reported by other studies. CONCLUSIONS: This study reveals four novel QTLs in a Chinese population and suggests that BMD at different skeletal sites may also share common genetic determinants.

Asian People↗
PubMed2006

Stimulation of colonic mucosal growth associated with oxidized redox status in rats.

Limited data in animal models suggest that colonic mucosa undergoes adaptive growth following massive small bowel resection (SBR). In vitro data suggest that intestinal cell growth is regulated by reactive oxygen species and redox couples [e.g., glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) redox]. We investigated the effects of SBR and alterations in redox on colonic growth indexes in rats after either small bowel transection (TX) or 80% midjejunoileal resection (RX). Rats were pair fed +/- blockade of endogenous GSH synthesis with buthionine sulfoximine (BSO). Indexes of colonic growth, proliferation, and apoptosis and GSH/GSSG and Cys/CySS redox potentials (E(h)) were determined. RX significantly increased colonic crypt depth, number of cells per crypt, and epithelial cell proliferation [crypt cell bromodeoxyuridine (BrdU) incorporation]. Administration of BSO markedly decreased colonic mucosal GSH, GSSG, and Cys concentrations in both TX and RX groups, with a resultant oxidation of GSH/GSSG and Cys/CySS E(h). BSO did not alter colonic crypt cell apoptosis but significantly increased all colonic mucosal growth indexes (crypt depth, cells/crypt, and BrdU incorporation) in both TX and RX groups in a time- and dose-dependent manner. BSO significantly decreased plasma GSH and GSSG, oxidized GSH/GSSG E(h), and increased plasma Cys and CySS concentrations. Collectively, these data provide in vivo evidence indicating that oxidized colonic mucosal redox status stimulates colonic mucosal growth in rats. The data also suggest that GSH is required to maintain normal colonic and plasma Cys/CySS homeostasis in these animal models.

Animals↗
PubMed2006

Increased flexibility enhances misincorporation: temperature effects on nucleotide incorporation opposite a bulky carcinogen-DNA adduct by a Y-family DNA polymerase.

The Y-family DNA polymerase Dpo4, from the thermophilic crenarchaeon Sulfolobus solfataricus P2, offers a valuable opportunity to investigate the effect of conformational flexibility on the bypass of bulky lesions because of its ability to function efficiently at a wide range of temperatures. Combined molecular modeling and experimental kinetic studies have been carried out for 10S-(+)-trans-anti-[BP]-N2-dG ((+)-ta-[BP]G), a lesion derived from the covalent reaction of a benzo[a]pyrene metabolite with guanine in DNA, at 55 degrees C and results compared with an earlier study at 37 degrees C (Perlow-Poehnelt, R. A., Likhterov, I., Scicchitano, D. A., Geacintov, N. E., and Broyde, S. (2004) J. Biol. Chem. 279, 36951-36961). The experimental results show that there is more overall nucleotide insertion opposite (+)-ta-[BP]G due to particularly enhanced mismatch incorporation at 55 degrees C compared with 37 degrees C. The molecular dynamics simulations suggest that mismatched nucleotide insertion opposite (+)-ta-[BP]G is increased at 55 degrees C compared with 37 degrees C because the higher temperature shifts the preference of the damaged base from the anti to the syn conformation, with the carcinogen on the more open major groove side. The mismatched dNTP structures are less distorted when the damaged base is syn than when it is anti, at the higher temperature. However, with the normal partner dCTP, the anti conformation with close to Watson-Crick alignment remains more favorable. The molecular dynamics simulations are consistent with the kcat values for nucleotide incorporation opposite the lesion studied, providing structural interpretation of the experimental observations. The observed temperature effect suggests that conformational flexibility plays a role in nucleotide incorporation and bypass fidelity opposite (+)-ta-[BP]G by Dpo4.

Base Pair Mismatch↗
PubMed2006

The investigation of 137Cs and 90Sr background radiation levels in soil and plant around Tianwan NPP, China.

(137)Cs and (90)Sr background levels in soil and plant around Tianwan Nuclear Power Plant (NPP) are reported. Eighty-four soil samples and 44 plant samples were collected from March 2000 to April 2002. The samples were analyzed by gamma spectrometry and radiochemical separation procedure to quantify (137)Cs and (90)Sr radioactivities. The concentrations (Bqkg(-1) dry weight) have been observed in the range of 0.6-1.6 for (90)Sr and 1.4-6.9 for (137)Cs in soils, their average values are 1.0+/-0.3 and 4.6+/-1.6, respectively, which are relatively lower than the reported values in neighboring countries. The mean concentrations (in Bqkg(-1) fresh weight except for tea and grass which is expressed in Bqkg(-1) dry weight) of (137)Cs and (90)Sr are 0.1+/-0.03 and 7.7+/-4.1 in pine needle, 0.27+/-0.05 and 3.0+/-1.1 in tea, 0.65+/-0.19 and 2.1+/-0.3 in grass, 0.033+/-0.021 and 0.084+/-0.045 in wheat, 0.019+/-0.01 and 0.23+/-0.06 in China cabbage, and 0.009+/-0.007 and 0.024+/-0.084 in rice, respectively. The pine needle and tea can be regarded as indicator species for (90)Sr and (137)Cs. The soil-to-plant transfer factor (TF) values of (90)Sr and (137)Cs are, respectively, 0.022 and 0.031 for rice, 0.066 and 3.83 for China cabbage, 0.0088 and 0.089 for wheat, and 0.037 and 0.56 for grass.

Cesium Radioisotopes↗
PubMed2006

Sequence and organization of the Trichoplusia ni ascovirus 2c (Ascoviridae) genome.

The complete Trichoplusia ni ascovirus 2c (TnAV-2c) genome sequence was determined. The circular genome contains 174,059 bp with 165 open reading frames (ORFs) of greater than 180 bp and two major homologous regions (hrs). The genome is quite A+T rich at 64.6%. Fifty-four ORFs had homologues in other insect viruses, such as ascoviruses, iridoviruses, baculoviruses and entomopoxviruses; 30 ORFs showed low identities with those from different parasitic protozoa and 12 ORFs were unique to TnAV-2c. TnAV-2c has 15 ORFs that could be grouped into six gene families. Three major conserved repeating sequences were identified and were interspersed in two regions. BLAST analyses revealed that there were 16 enzymes involved in gene transcription, DNA replication, and nucleotide metabolism. TnAV-2c has 12 and 25 ORFs sharing high identities with ascovirus and iridovirus homologues, respectively. The codon usage bias appears to be more similar to Spodoptera frugiperda ascovirus 1a than to iridoviruses.

Animals↗
PubMed2006

Sequence-specific detection of femtomolar DNA via a chronocoulometric DNA sensor (CDS): effects of nanoparticle-mediated amplification and nanoscale control of DNA assembly at electrodes.

We herein report a novel nanoparticle-based electrochemical DNA detection approach. This DNA sensor is based on a "sandwich" detection strategy, which involves capture probe DNA immobilized on gold electrodes and reporter probe DNA labeled with gold nanoparticles that flank the target DNA sequence. Electrochemical signals are generated by chronocoulometric interrogation of [Ru(NH(3))(6)](3+) that quantitatively binds to surface-confined capture probe DNA via electrostatic interactions. We demonstrated that the incorporation of a gold nanoparticle in this sensor design significantly enhanced the sensitivity and the selectivity. Nanoscale control of the self-assembly process of DNA probes at gold electrodes further increased the sensor performance. As a result of these two combined effects, this DNA sensor could detect as low as femtomolar (zeptomoles) DNA targets and exhibited excellent selectivity against even a single-base mismatch. In addition, this novel DNA sensor showed fairly good reproducibility, stability, and reusability.

DNA↗
PubMed2006

Mutagenic nucleotide incorporation and hindered translocation by a food carcinogen C8-dG adduct in Sulfolobus solfataricus P2 DNA polymerase IV (Dpo4): modeling and dynamics studies.

Bulky carcinogen-DNA adducts commonly cause replicative polymerases to stall, leading to a switch to bypass polymerases. We have investigated nucleotide incorporation opposite the major adduct of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in the DinB family polymerase, Dpo4, using molecular modeling and molecular dynamics (MD) simulations. PhIP, the most prevalent heterocyclic aromatic amine formed by cooking of proteinaceous food, is mutagenic in mammalian cells and is implicated in mammary and colon tumors. Our results show that the dG-C8-PhIP adduct can be accommodated in the spacious major groove Dpo4 open pocket, with Dpo4 capable of incorporating dCTP, dTTP or dATP opposite the adduct reasonably well. However, the PhIP ring system on the minor groove side would seriously disturb the active site, regardless of the presence and identity of dNTP. Furthermore, the simulations indicate that dATP and dTTP are better incorporated in the damaged system than in their respective mismatched but unmodified controls, suggesting that the PhIP adduct enhances incorporation of these mismatches. Finally, bulky C8-dG adducts, situated in the major groove, are likely to impede translocation in this polymerase (Rechkoblit et al. (2006), PLoS Biol., 4, e11). However, N2-dG adducts, which can reside on the minor groove side, appear to cause less hindrance when in this position.

Binding Sites↗
PubMed2006

Epimorphin(-/-) mice have increased intestinal growth, decreased susceptibility to dextran sodium sulfate colitis, and impaired spermatogenesis.

Dynamic and reciprocal epithelial-mesenchymal interactions are critical for the normal morphogenesis and maintenance of epithelia. Epimorphin has been identified as a unique molecule expressed by mesenchymal cells and myofibroblasts and has putative morphogenetic effects in multiple epithelial tissues, including intestine, skin, mammary gland, lung, gallbladder, and liver. To define the in vivo role of epimorphin, we created epimorphin-null mice by targeted inactivation of the epimorphin gene. Male epimorphin-/- mice are sterile due to abnormal testicular development and impaired spermatogenesis. Intestinal growth is increased in epimorphin-/- mice due to augmented crypt cell proliferation and crypt fission during the neonatal (suckling) period, mediated at least in part by changes in bone morphogenetic protein (Bmp) and Wnt/beta-catenin signaling pathways. Colonic mucosal injury and colitis induced by dextran sodium sulfate (DSS) are ameliorated in epimorphin-/- mice, probably due to the increased proliferative capacity of the epimorphin-/- colon. These in vivo findings support the notion that epimorphin is a key stromal regulator of epithelial cell proliferation and growth in the intestine. In addition, our studies demonstrate a novel and critical role for epimorphin in regulating testicular development and growth as well as spermatogenesis.

Animals↗
PubMed2006

BALT development and augmentation of hyperoxic lung injury in mice deficient in NQO1 and NQO2.

NAD(P)H/NRH:quinone oxidoreductases (NQO1 and NQO2) protect against oxidative stress and neoplasia. Cross-breeding of NQO1-/- with NQO2-/- mice generated double-knockout (DKO) mice. DKO mice were born normal yet showed myelogenous hyperplasia as observed in single-knockout mice. DKO mice also showed bronchial-associated lymphoid tissue (BALT) that increased in number and size with age. BALT was absent in wild-type and single-knockout mice. Further analysis demonstrated infiltration of neutrophils and macrophages in BALT and significant increases in the serum cytokines TNFalpha, IL-6, and IL-1beta and increased expression of iNOS and higher nitric oxide in lung macrophages. The development of BALT in DKO mice presumably led to the release of cytokines and higher lung macrophage activation, because histologically spleen, thymus, and blood cultures and urine analysis showed absence of infection. Additionally, the DKO mice upon exposure to hyperoxia demonstrated severe intra-alveolar edema and perivascular inflammation and massive infiltration with neutrophils, compared with wild-type mice. These results suggest that NQO1 and NQO2 combined protect mice against lung inflammation, BALT, and hyperoxic lung injury.

Animals↗
PubMed2006

A new anti conformation for N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (AAF-dG) allows Watson-Crick pairing in the Sulfolobus solfataricus P2 DNA polymerase IV (Dpo4).

Primer extension studies have shown that the Y-family DNA polymerase IV (Dpo4) from Sulfolobus solfataricus P2 can preferentially insert C opposite N-(deoxyguanosin-8-yl)-2-acetylaminofluorene (AAF-dG) [F. Boudsocq, S. Iwai, F. Hanaoka and R. Woodgate (2001) Nucleic Acids Res., 29, 4607-4616]. Our goal is to elucidate on a structural level how AAF-dG can be harbored in the Dpo4 active site opposite an incoming dCTP, using molecular modeling and molecular dynamics simulations, since AAF-dG prefers the syn glycosidic torsion. Both anti and syn conformations of the templating AAF-dG in a Dpo4 ternary complex were investigated. All four dNTPs were studied. We found that an anti glycosidic torsion with C1'-exo deoxyribose conformation allows AAF-dG to be Watson-Crick hydrogen-bonded with dCTP with modest polymerase perturbation, but other nucleotides are more distorting. The AAF is situated in the Dpo4 major groove open pocket with fluorenyl rings 3'- and acetyl 5'-directed along the modified strand, irrespective of dNTP. With AAF-dG syn, the fluorenyl rings are in the small minor groove pocket and the active site region is highly distorted. The anti-AAF-dG conformation with C1'-exo sugar pucker can explain the preferential incorporation of dC by Dpo4. Possible relevance of our new major groove structure for AAF-dG to other polymerases, lesion repair and solution conformations are discussed.

2-Acetylaminofluorene↗
PubMed2006

Activation of focal adhesion kinase by hepatitis B virus HBx protein: multiple functions in viral replication.

The hepatitis B virus (HBV) X protein (HBx) is a multifunctional regulator of cellular signal transduction and transcription pathways and has a critical role in HBV replication. Much of the cytoplasmic signal transduction activity associated with HBx expression and its stimulation of viral replication is attributable to HBx-induced activation of calcium signaling pathways involving Pyk2 and Src tyrosine kinases. To further characterize upstream signal transduction pathways that are required for HBx activity, including activation of Src and mitogen-activated protein kinase (MAPK) cascades, we determined whether focal adhesion kinase (FAK), a known regulator of Src family kinases and the other member of the Pyk2/FAK kinase family, is activated by HBx. We report that HBx activates FAK and that FAK activation is important for multiple HBx functions. Dominant inhibiting forms of FAK blocked HBx activation of Src kinases and downstream signal transduction, HBx stimulation of NF-kappaB and AP-1-dependent transcription, and HBV DNA replication. We also demonstrate that HBx-induced activation of FAK is dependent on cellular calcium signaling, which is modulated by HBx. Moreover, prolonged expression of HBx increases both FAK activity and its level of expression. FAK activation may play a role in cellular transformation and cancer progression. HBx stimulation of FAK activity and abundance may also be relevant as a potential cofactor in HBV-associated hepatocellular carcinoma.

Animals↗
PubMed2006

A regulatory role for the C5a anaphylatoxin in type 2 immunity in asthma.

Complement component 5 (C5) has been described as either promoting or protecting against airway hyperresponsiveness (AHR) in experimental allergic asthma, suggesting pleomorphic effects of C5. Here we report that local pharmacological targeting of the C5a receptor (C5aR) prior to initial allergen sensitization in murine models of inhalation tolerance or allergic asthma resulted in either induction or marked enhancement of Th2-polarized immune responses, airway inflammation, and AHR. Importantly, C5aR-deficient mice exhibited a similar, increased allergic phenotype. Pulmonary allergen exposure in C5aR-targeted mice resulted in increased sensitization and accumulation of CD4+ CD69+ T cells associated with a marked increase in pulmonary myeloid, but not plasmacytoid, DC numbers. Pulmonary DCs from C5aR-targeted mice produced large amounts of CC chemokine ligand 17 (CCL17) and CCL22 ex vivo, suggesting a negative impact of C5aR signaling on pulmonary homing of Th2 cells. In contrast, C5aR targeting in sensitized mice led to suppressed airway inflammation and AHR but was still associated with enhanced production of Th2 effector cytokines. These data suggest a dual role for C5a in allergic asthma, i.e., protection from the development of maladaptive type 2 immune responses during allergen sensitization at the DC/T cell interface but enhancement of airway inflammation and AHR in an established inflammatory environment.

Allergens↗
PubMed2006

[A clinical analysis of intractable spontaneous epistaxis with 289 cases reviewed].

OBJECTIVE: To explore the clinical characteristics and the prevention strategy of intractable spontaneous epistaxis. METHOD: Two hundred and eighty-nine patients with intractable spontaneous epistaxis were retrospectively analyzed. RESULT: Intractable spontaneous epistaxis was characterized by the onset season, age, sex, and the associated disease. Nasal septums were the most common sites of bleeding. Recurrent epistaxis was mainly associated with the failure of locating the bleeding sites. CONCLUSION: Control of elevated blood pressure is essential for the prevention of intractable spontaneous epistaxis. Once epistaxis occurs, the importance of the first treatment for the haemostasis should be emphasized. For the uncontrollable epistaxis, multiple interventions are necessary.

Adolescent↗
PubMed2005

Electrochemical interrogation of DNA monolayers on gold surfaces.

In this report, we systematically investigated DNA immobilization at gold surfaces with electrochemical techniques. Comparative cyclic voltammetric and chronocoulometric studies suggested that DNA monolayers immobilized at gold surfaces were not homogeneous. Nonspecific Au-DNA interactions existed even with the treatment of mercaptohexanol, which was known to competitively remove loosely bound DNA at gold surfaces. While both thiolated and nonthiolated DNA formed monolayers on gold surfaces, their hybridization abilities were distinctly different. In contrast to thiolated DNA probes, nonthiolated DNA probes immobilized at gold surfaces were essentially nonhybridizable. The experimental results presented here might be useful for the design of high-performance electrochemical DNA sensors.

DNA↗
PubMed2005

Targeted intestinal overexpression of the immediate early gene tis7 in transgenic mice increases triglyceride absorption and adiposity.

Following loss of functional small bowel surface area due to surgical resection, the remnant gut undergoes an adaptive response characterized by increased crypt cell proliferation and enhanced villus height and crypt depth, resulting in augmented intestinal nutrient absorptive capacity. Previous studies showed that expression of the immediate early gene tis7 is markedly up-regulated in intestinal enterocytes during the adaptive response. To study its role in the enterocyte, transgenic mice were generated that specifically overexpress TIS7 in the gut. Nucleotides -596 to +21 of the rat liver fatty acid-binding protein promoter were used to direct abundant overexpression of TIS7 into small intestinal upper crypt and villus enterocytes. TIS7 transgenic mice had increased total body adiposity and decreased lean muscle mass compared with normal littermates. Oxygen consumption levels, body weight, surface area, and small bowel weight were decreased. On a high fat diet, transgenic mice exhibited a more rapid and proportionately greater gain in body weight with persistently elevated total body adiposity and increased hepatic fat accumulation. Bolus fat feeding resulted in a greater increase in serum triglyceride levels and an accelerated appearance of enterocytic, lamina propria, and hepatic fat. Changes in fat homeostasis were linked to increased expression of genes involved in enterocytic triglyceride metabolism and changes in growth with decreased insulin-like growth factor-1 expression. Thus, TIS7 overexpression in the intestine altered growth, metabolic rate, adiposity, and intestinal triglyceride absorption. These results suggest that TIS7 is a unique mediator of nutrient absorptive and metabolic adaptation following gut resection.

Adipose Tissue↗
PubMed2005

Formylpeptide receptor FPR and the rapid growth of malignant human gliomas.

BACKGROUND: The formylpeptide receptor (FPR) is a G-protein-coupled receptor (GPCR) that mediates chemotaxis of phagocytic leukocytes induced by bacterial peptide N-formyl-methionyl-leucyl-phenylalanine (fMLF). We previously showed that selected human glioma cell lines also express functional FPR. We therefore investigated the relationship between FPR expression and the biologic behavior of glioma cells. METHODS: Expression and function of FPR in the human glioblastoma cell line U-87 were examined by reverse transcription-polymerase chain reaction (RT-PCR) and chemotaxis assays, respectively. FPR protein expression was detected in specimens from 33 human primary gliomas by immunohistochemistry. FPR short interfering (si) RNA was used to block FPR expression in U-87 cells. Cell proliferation was assessed by measuring DNA synthesis. Xenograft tumor formation and growth were measured in nude mice. Endogenous FPR agonist activity released by necrotic tumor cells was assessed by measuring FPR activation in an FPR-transfected basophil leukemia cell line and live U-87 cells. Vascular endothelial growth factor (VEGF) mRNA was assessed by RT-PCR, and VEGF protein was assessed by enzyme-linked immunosorbent assay. All statistical tests were two-sided. RESULTS: FPR was selectively expressed by the highly malignant human glioblastoma cell line U-87 and most primary grade IV glioblastomas multiforme and grade III anaplastic astrocytomas. U-87 cells responded to the FPR agonist fMLF by chemotaxis (i.e., increased motility), increased cell proliferation, and increased production of VEGF protein. FPR siRNA substantially reduced the tumorigenicity of U-87 cells in nude mice (38 days after implantation, mean tumor volume from wild-type U-87 cells = 842 mm3, 95% confidence interval [CI] = 721 to 963 mm3; and from FPR-siRNA transfected U-87 cells = 225 mm3, 95% CI = 194 to 256 mm3; P = .001). Necrotic glioblastoma cells released a factor(s) that activated FPR in live U-87 cells. CONCLUSIONS: FPR is expressed by highly malignant human glioma cells and appears to mediate motility, growth, and angiogenesis of human glioblastoma by interacting with host-derived agonists. Thus, FPR may represent a molecular target for the development of novel antiglioma therapeutics.

Animals↗
PubMed2005

Cytochrome P450 gene polymorphisms and risk of low birth weight.

This study investigated the association between polymorphisms in cytochrome P450 genes (CYP1A1MspI, CYP1A1HincII, and CYP2E1) and low birth weight. Between July 1999 and June 2002, we conducted a study using infant-parents triads in Anqing, China. The analyses included the families of 248 normal birth weight, full-term infants, and 248 low-birth-weight infants. Genotyping was performed for the polymorphisms of cytochrome P450 genes using standard techniques. We used log-linear modeling to analyze the association of CYP1A1 and CYP2E1 gene polymorphisms with the risk of low birth weight. In the analysis of children's genotypes, the relative risk was 1.92 (95% confidence interval: 1.05, 3.52, p=0.034) for CYP1A1MspI C/C6235 compared with CYP1A1 MspI T/T6235. In the analysis of mothers' genotypes, an association was also seen for maternal CYP1A1MspI C/C6235 compared with CYP1A1MspI T/T6235 (relative risk: 1.68, 95% confidence interval: 1.06, 2.68, p=0.029). We did not observe a joint effect between mother's and children's genotypes. Analysis of control triads suggests Mendelian transmissions of the variant alleles of CYP1A1MspI, CYP1A1HincII, and CYP2E1. In conclusion, both infant and maternal CYP1A1MspI C/C6235 genotypes were associated with increased risk of low birth weight in our study population. This suggests a possible role for human cytochrome P450 variability in the etiology of low birth weight.

Alleles↗