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J Nishioka

Publications and source records attributed to J Nishioka.

At least 19 recordsLinked to original sources
PubMed2001

Change in the concentrations of iron in different size fractions during a phytoplankton bloom in controlled ecosystem enclosures.

To observe micronutrient dynamics in the plankton ecosystem, controlled ecosystem enclosure (CEE) experiments were conducted in Saanich Inlet, B.C., Canada. Two CEEs (2.5 m in diameter, 16 m in length, one for Fe studies and the other for biological studies) were launched for the period 22 July to 5 August 1996 and enriched with 10 µM nitrate and 5.2 nM Fe (13% of total Fe) on day 1. Sampling from three integrated depths, intervals 0-4, 4-8 and 8-12 m, was performed on days 0, 1, 2, 3, 4, 5, 7, 9 and 11. Iron concentrations were measured for five size fractions: >25 µm particles, 2-25 µm particles, 0.2-2 µm particles, 0.2 µm-200 kDa small colloidal particles and <200 kDa soluble species. The sediment in the Fe enclosure was also collected on every sampling day after day 2 and its Fe was determined. Size-fractionated particulate organic carbon and total chlorophyll-a were also analyzed.The Fe in small colloidal particles (200 kDa-0.2 µm) comprised 78% of the traditionally defined dissolved phase (<0.2 µm) on day 1. Of all the size fractions of Fe, the small colloidal particulate fraction decreased most significantly during the phytoplankton bloom. In the dissolved fraction (<0.2 µm), the small colloidal particle fraction comprised 79% of the decrease. The decrease in concentration of Fe in small colloidal particles was larger than that of total Fe from day 1 to day 4. In contrast, the >25 µm Fe particles increased over the same period. These results suggest that Fe in small colloidal particles changed to >25 µm Fe particles during phytoplankton growth. A large amount of Fe was kept in the surface layer with the phytoplankton, and transported to the deep layer by phytoplankton sedimentation, at the end of the bloom. From these results, the small colloidal particulate Fe seems to be the most dynamic size fraction and a high percentage of Fe in small colloidal particles changed to large particles due to chemical/physical aggregation and/or physical adsorption to suspended particles such as phytoplankton cells.

Journal Article↗
PubMed2001

Enhanced absorption of insulin and (Asu(1,7))eel-calcitonin using novel azopolymer-coated pellets for colon-specific drug delivery.

The objective of this study was to estimate colon-specific delivery of insulin and (Asu(1,7))eel-calcitonin using novel azopolymer-coated pellets. In vitro drug-release experiments from the azopolymer-coated pellets containing fluorescein isothiocyanate dextran (MW 4400; FD-4) were carried out by the Japanese Pharmacopoeia (J.P.) XIII rotating basket method with some slight modifications. Little release of FD-4 from the pellets was observed in phosphate buffered saline. However, the release of FD-4 was markedly increased in the presence of rat cecal contents. The intestinal absorption of insulin and (Asu(1,7))eel-calcitonin after oral administration of the azopolymer-coated pellets containing these peptides with camostat mesilate was evaluated by measuring the hypoglycemic and hypocalcemic effects, respectively. A slight decrease in plasma glucose levels was observed following the oral administration of these pellets containing 12.5 IU of insulin compared with the same dose of insulin solution. Camostat mesilate, a protease inhibitor that is incorporated with insulin in these pellets, further decreased the plasma glucose levels in a dose-dependent manner. Similar results were also obtained with the oral administration of pellets containing (Asu(1,7))eel-calcitonin. These findings suggest that azopolymer-coated pellets may be useful carriers for the colon-specific delivery of peptides including insulin and (Asu(1,7))eel-calcitonin.

Administration, Oral↗
PubMed2001

Mitotic checkpoint protein hsMAD2 as a marker predicting liver metastasis of human gastric cancers.

hsMAD2, the human homologue of mitotic arrest deficient 2 (MAD2), is a key component of the mitotic checkpoint system. Recently, mutations and decreased expression of mitotic checkpoint genes including hsMAD2 have been reported in cancer cell lines with defective mitotic checkpoint. However, the genetic alterations in the genomic hsMAD2 gene have not been determined in gastric cancers. Moreover, the biological implications of the overexpressed hsMAD2 in primary cancers are unknown. In this study, we analyzed 32 primary gastric cancers with polymerase chain reaction (PCR) amplification of all exons, including flanking intronic sequences, of the genomic hsMAD2 gene followed by direct DNA sequencing. We also measured the hsMAD2 protein levels in cancer and normal tissues by semi-quantitative immunoblotting. No mutations were found in the coding sequences, although three single nucleotide polymorphisms (SNPs) were identified in the noncoding sequences in 13 of 32 patients. These SNPs were not associated with either hsMAD2 expression or disease progression. The semi-quantitative western blot analysis showed hsMAD2 was significantly overexpressed in gastric cancer tissues compared with corresponding normal tissues (P < 0.001). The calculated ratio of the hsMAD2 protein in cancer tissue (C) to that in corresponding normal tissue (N) (C / N ratio) was significantly higher in patients with well differentiated adenocarcinoma (P = 0.0274) or with synchronous liver metastasis (P = 0.0025). A C / N ratio greater than 3 was observed more frequently in patients with synchronous liver metastasis. Therefore, C / N ratio > 3 may be clinically important as a predictive indicator for metachronous liver metastasis of gastric cancers.

Adenocarcinoma↗
PubMed2001

[Plasma levels of soluble fibrin in patients with disseminated intravascular coagulation].

Soluble fibrin(SF) is formed in the early-activated state of blood coagulation and quantitative measurement of SF shows high potential as a parameter for the diagnosis of suspected disseminated intravascular coagulation(DIC). The aim of the present study is to evaluate the usefulness of a newly developed SF test utilizing SF specific monoclonal antibody(F405). Among hemopoietic and non-hemopoietic tumor patients, 249 patients with suspected DIC were collected. The SF level showed a good correlation with the DIC score and the SF levels in DIC patients were significantly higher than those in s-DIC and pre-DIC patients. Receiver operating characteristic(ROC) analysis also showed that the specificity and sensitivity of the SF assay were higher than those of thrombin-antithrombin complex(TAT). In conclusion, these results indicate that the SF assay is a highly precise method for the diagnosis and screening of DIC stages.

Disseminated Intravascular Coagulation↗
PubMed2000

Plasma levels of activated protein C-protein C inhibitor complex in patients with hypercoagulable states.

Plasma levels of activated protein C (APC)-protein C inhibitor (PCI) were significantly increased in patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), acute myocardial infarction (AMI), pulmonary embolism (PE), or deep vein thrombosis (DVT) and in patients undergoing hemodialysis (HD). Plasma levels of APC-alpha(1)-antitrypsin (AT) complex were significantly increased in patients with DIC and in those with TTP. Plasma levels of PCI were significantly decreased in patients with DIC, non-DIC, or TTP and in those undergoing HD. In the pre-DIC stage, the plasma levels of APC-PCI complex were significantly increased but not those of APC-alpha(1)-AT complex. These data suggest that measurements of APC-PCI complex and APC-alpha(1)-AT complex may be useful for the diagnosis of DIC. After treatment of DIC, the plasma levels of APC-PCI complex and APC-alpha(1)-AT complex were significantly decreased, but not those of PCI. Plasma levels of thrombin-antithrombin complex (TAT), plasmin-alpha(2)-plasmin complex (PPIC), D-dimer, and soluble fibrin monomer (SFM) were markedly increased in patients with DIC or pre-DIC and were moderately increased in patients with non-DIC, TTP, AMI, PE, or DVT and in those undergoing HD. The receiving operating characteristic (ROC) analysis showed that SFM and the APC-PCT complex are useful markers for diagnosis of DIC. The specificity of plasma TAT and PPIC levels was low. The positive rate of APC-PCI complex was higher than 90% with DIC, TTP, AMI, PE, and it was higher than 60% with DVT and HD. Since the APC-PCI complex was elevated not only in patients with venous thrombosis but also in those with arterial thrombosis, components of the protein C pathway might be useful markers for the diagnosis of arterial thrombosis.

Antithrombin III↗
PubMed2000

Detection of methylthioadenosine phosphorylase (MTAP) and p16 gene deletion in T cell acute lymphoblastic leukemia by real-time quantitative PCR assay.

Methylthioadenosine phosphorylase (MTAP) deficiency in tumors can be therapeutically exploited for selective therapy. Many tumors lacking MTAP have been found to homozygously delete the chromosome 9p region containing the p16 tumor suppressor gene. Several methods have been used to detect chromosome 9p deletions in primary tumors. However, the accurate diagnosis of chromosome 9p deletions has been hampered by the presence of contaminating normal cells. In search of an accurate and sensitive diagnostic method, we have developed the real-time polymerase chain reaction assay using the TaqMan chemistry for quantitative detection of MTAP and p16 gene deletions. The assay's feasibility was tested with peripheral blood leukocytes (PBL) from 29 patients with adult T cell leukemia (ATL) previously analyzed with Southern blot analysis and validated on 39 PBL or bone marrow samples from childhood T cell acute lymphoblastic leukemia (T-ALL). Homozygous deletions of MTAP and p16 genes were detected respectively in six (20.7%) and eight (27.6%) of 29 ATL samples and in 15 (38.5%) and 23 (59%) of 39 T-ALL samples. The results correlated well with those of Southern blot analysis. It is of significance that the newly developed method can successfully detect homozygous deletions of these genes in samples containing as low as 33% blast cells. This rapid and sensitive method may be useful in searching for candidates for selective therapy targeting MTAP deficiency.

Adult↗
PubMed2000

Increased hemostatic molecular markers in patients undergoing anticoagulant therapy.

We evaluated several molecular markers of hemostasis in 92 patients with hypercoagulable states treated with anticoagulant therapy. In all patients, the average values of the international normalized ratio (INR) were 1.70 +/- 0.50; this increase in INR was not, however, significant in patients under thrombotest (TT) monitoring. There were no thrombotic or severe bleeding complications in these patients during a period of 27 months. Plasma levels of thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex (PPIC), D-dimer, and soluble fibrin monomer (sFM) were slightly increased, suggesting that anticoagulant therapy was not completely effective in our Japanese patients based on the values of the TT. The INR was negatively correlated with TT, protein C, and protein S and particularly with TT between 10 and 80%. The range of TT was not correlated with the plasma level of TAT, PPIC, D-dimer, or sFM, but the range of INR was correlated with the plasma level of TAT, D-dimer, and sFM. The percentage of TAT, D-dimer, and sFM within normal range was significantly lower in patients with high INR. These findings show that INR is better than TT for the monitoring of warfarin therapy and that the therapeutic values of INR during the anticoagulant therapy should be > 1.7 in Japanese patients.

Adult↗
PubMed2000

Bovine protein C inhibitor has a unique reactive site and can transiently inhibit plasmin.

Protein C inhibitor (PCI) regulates the anticoagulant protein C pathway by neutralizing activated protein C and thrombin-thrombomodulin complex in the human hemostatic system. In this study, we cloned a full-length bovine PCI cDNA encoding a putative 19-residue signal peptide and a 385-residue mature protein; this showed 70.6%, 70.6%, 57.5% and 59.6% amino acid sequence homology with the human, rhesus monkey, rat and mouse PCIs, respectively. Bovine PCI mRNA (2.1 kb in size) was expressed strongly in the liver, and moderately in the kidney and testis, but not in other tissues tested. Bovine PCI has a putative reactive site peptide bond, Lys-Ser, that is different from the reactive site sequence (Arg-Ser) of other species' PCI. We found that bovine PCI transiently inhibits bovine plasmin, but not human plasmin. Western blot analysis showed that the reactive site of bovine PCI is cleaved during the course of complex formation with bovine plasmin; degraded PCI is released from the complex gradually concomitant with the recovery of plasmin activity. These findings suggest that bovine PCI plays a role not only in the protein C pathway but also in the fibrinolytic activity of bovine hemostatic system.

Amino Acid Sequence↗
PubMed1999

Transcriptional regulation of the CDK inhibitor p16INK4a gene by a novel pRb-associated repressor, RBAR1.

p16, also known as INK4a, CDKN2, or MTS1, plays an important role in the control of the cell cycle progression, and retinoblastoma protein (pRb) is suggested to be involved in the transcriptional regulation of p16. However, it is not fully understood how pRb regulates transcription of the p16 gene. Nuclear proteins prepared only from the pRb-nonfunctional human tumor cells were found to bind to the 5'-flanking sequence of the p16 gene in the presence of Zn2+ by electrophoretic mobility shift assay (EMSA). EMSA using mutagenized 5'-flanking sequences as competitors suggested that the sequence at position -97 to -87 relative to first ATG of the p16 gene was critical for protein binding. Transient reporter assay indicated that the sequence identified by EMSA acted as a silencer element in the pRb-nonfunctional tumor cells, showing the presence of a transcriptional repressor associated with functional pRb (RBAR1).

Cyclin-Dependent Kinase Inhibitor p16↗
PubMed1999

Hemostatic markers in Japanese patients undergoing anticoagulant therapy under thrombo-test monitoring.

The objective of this study was to evaluate several molecular markers of hemostasis in 84 patients with hypercoagulable state, treated with warfarin under thrombo-test (TT) monitoring; TT was expressed as percent of control (TT%). In all patients, the average values of international normalized ratio (INR) of prothrombin time (PT;PT-INR) was 1.68+/-0.49; this increase in PT-INR was not, however, significant in patients under TT% monitoring. There were no thrombotic or severe bleeding complications in these patients during a period of 2 years. Plasma levels of thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex (PPIC), D-dimer, and soluble fibrin monomer (sFM) were slightly increased, suggesting that anticoagulant therapy was not completely effective in our Japanese patients based on the values of TT%. Activated partial thromboplastin time, PT-INR, TT% and protein C activity were significantly correlated with the dose of warfarin; fibrinogen, activated thromboplastin, TAT, PPIC, D-dimer, sFM, protein S and thrombomodulin were not significantly correlated with the dose of warfarin. The PT-INR was negatively correlated with TT%, protein C and protein S, and the correlation between PT-INR and TT-INR was better than that between PT-INR and TT%. The range of TT% was not correlated with the plasma levels of TAT, PPIC, D-dimer or sFM, but the range of PT-INR was correlated with the plasma level of TAT, D-dimer and sFM. The percentage of TAT, D-dimer and sFM within normal range was significantly low in patients with high PT-INR. These finding showed that PT-INR is better than TT% for monitoring the anticoagulant therapy with warfarin, and that TT should be expressed as INR. The values of PT-INR should be more than 1.7 during the anticoagulant therapy with warfarin in Japanese patients with high risk of thrombosis.

Adult↗
PubMed1999

Association of oestrogen receptor gene polymorphisms with age at onset of rheumatoid arthritis.

OBJECTIVE: In view of the possible role of oestrogens in the pathogenesis of rheumatoid arthritis (RA), this study investigated the association between oestrogen receptor (OR) gene polymorphisms and RA. METHODS: Pvu II and Xba I restriction fragment length polymorphisms of the OR gene were analysed in 70 male and 240 female patients with RA, and in 300 male and 350 female controls. The absence or presence of restriction sites were represented as P, p (Pvu II) or X, x (Xba I). The distribution of OR genotypes was compared between the RA and control subjects by sex. RA patients were divided into subgroups according to their OR genotypes, then the age at onset, seropositivity, and rheumatoid nodule positivity were compared between the subgroups. RESULTS: The OR genotype frequency of distribution did not have significant differences between the male RA and male controls nor between the female RA and female controls. In women with RA, there was a significant difference of age at onset between the subgroups (uncorrected p = 0.047, corrected p = 0.94). Female patients with the OR genotype PPxx (homozygote of Px) tended to have developed RA at a younger age, whereas those with PPXX and ppxx (lack of Px haplotype) developed RA at an older age. In men with RA, there was no association between the OR genotype and age at onset. In seropositivity and rheumatoid nodule positivity, there was no significant difference between subgroups for either sex. CONCLUSIONS: Some variants of the OR gene are related to the onset of RA in women in certain age periods, suggesting the role of the interaction between the OR gene and serum concentrations of oestrogen at the onset of the disease.

Adult↗
PubMed1998

Molecular cloning, tissue distribution and androgen regulation of rat protein C inhibitor.

Protein C inhibitor (PCI) is the plasma serine protease inhibitor of activated protein C, the active enzyme of the anticoagulant protein C pathway. Recently, PCI was also detected in human seminal plasma and reproductive organs (testis, seminal vesicle and prostate) suggesting that PCI may also play an important role in the reproductive system. In this study, we cloned the full length of rat PCI cDNA, and determined its amino acid sequence and tissue distribution. We also evaluated the effect of androgen on PCI mRNA expression in seminal vesicles and testes. The isolated 2074-bp rat PCI cDNA was composed of a 47-bp 5'-non-coding region, a 1218-bp coding region of a 406-amino acid precursor protein, a stop codon and a 806-bp 3'-non-coding region. The deduced amino acid sequence of rat PCI showed 85.7%, 64.1% and 62.2% homology with that of mouse, rhesus monkey and human PCIs, respectively. Northern blot analysis showed that the rat PCI mRNA is expressed strongly in the seminal vesicle, moderately in the testis, but not in the liver. PCI mRNA expression in seminal vesicles and testes was found to increase during the process of development, suggesting that it is under androgen control. Subsequently, we examined the effect of castration and/or treatment with 17beta-estradiol or testosterone on PCI mRNA expression in the mature rat seminal vesicles. The PCI mRNA expression in seminal vesicles was significantly decreased after castration or 17beta-estradiol treatment. Testosterone itself did not affect PCI mRNA expression, but treatment in castrated rats significantly enhanced its mRNA expression. These findings suggest that the PCI gene expression in rat seminal vesicles is regulated by androgen.

Amino Acid Sequence↗
PubMed1998

Regulation of the human protein C inhibitor gene expression in HepG2 cells: role of Sp1 and AP2.

Protein C inhibitor (PCI) is the plasma inhibitor of activated protein C, which is the main protease of the anticoagulant protein C pathway. In this study the transcriptional regulation of human PCI gene in the human hepatoma cell line, HepG2, was characterized by evaluating the transient expression of a luciferase reporter gene. The 5' flanking region (residues -1587 to +2) of the PCI gene showed an adequate transcriptional activity, the maximum transcriptional activity being in a region between residues -452 and -94, which contains an Sp1-binding site, two AP2-binding sites and an inverted AP2-binding site. Transient expression assays with various deletion mutants and site-directed mutants showed that the Sp1-binding site (residues -302 to -294) has a potent promoter activity and that the upstream AP2-binding site (residues -350 to -343) has a potent enhancer activity; no activity was detected in the inverted (residues -413 to -404) and downstream (residues -136 to -127) AP2-binding sites. In addition, a region of the PCI gene (residues -452 to -414) containing the STATx-binding site, the A-activator (AA)-binding site, and the interferon alpha (IFN-alpha) response element, and another region of the PCI gene (residues -176 to -147) containing the GATA-1 and the IFN-gamma response element showed potent silencer activities. Gel mobility-shift assays with various DNA fragments indicated that the Sp1-binding site, the upstream AP2-binding site, the AA-binding site and the IFN-gamma response element interact with nuclear protein(s) of HepG2 cells. These findings suggest that the Sp1-binding site is the promoter, the AP2-binding site (residues -350 to -343) the enhancer, and both the AA-binding site and the IFN-gamma response element are the silencers of human PCI gene expression in HepG2 cells.

Base Sequence↗
PubMed1998

Protein C inhibitor secreted from activated platelets efficiently inhibits activated protein C on phosphatidylethanolamine of platelet membrane and microvesicles.

Protein C inhibitor (PCI) was detected in human platelets (2.9 ng/10(9) cells) and megakaryocytic cells (1.5 ng/10(6) cells). PCI mRNA was also detected in both platelets and megakaryocytic cells using nested polymerase chain reaction. PCI was found to be located in the alpha-granules of resting platelets. Approximately 30% of the total amount of PCI in platelets was released after stimulation with ADP, collagen, adrenalin, thrombin, or thrombin receptor-activating peptide. Secreted PCI was detected on the surface of activated platelets and phospholipid microvesicles. PCI secreted from thrombin receptor-activating peptide-stimulated platelets inhibited activated protein C (APC) efficiently. PCI significantly inhibited APC in the presence of phospholipid vesicles prepared using rabbit brain cephalin (RBC) or a mixture of 40% phosphatidylethanolamine (PE), 20% phosphatidylserine (PS), and 40% phosphatidylcholine (PC) with a second order rate constant of 1.0 x 10(6) M-1.min-1. Of these phospholipids, PE was critical for this inhibition. The dissociation constants of the binding of APC or PCI to solid phase phospholipids showed that APC binds more preferably to PE than to RBC or PS, and PCI to PE or RBC than to PS or PC. PCI binding to solid phase phospholipids depended on the presence of PE. RBC- or PE-bound PCI inhibited APC significantly but only weakly the gamma-carboxyglutamic acid domainless APC. The gamma-carboxyglutamic acid fragment of protein C suppressed the PCI-mediated inhibition of APC on solid phase RBC or PE. Most of the APC.PCI complex formed on solid phase RBC or PE was released into the soluble phase. These findings suggest that PCI secreted from activated platelets binds preferably to PE of platelet membrane and microvesicles and that it inhibits phospholipid-bound APC efficiently.

Animals↗
PubMed1998

Intramedullary fibular graft for supracondylar fracture of the femur following total knee arthroplasty.

We describe a successful treatment, intramedullary fibular grafting, for a patient with a supracondylar fracture of the femur following total knee arthroplasty in which the fracture region was comminuted and a segmental large bone defect was present. Free autogenous fibular was inserted into the medullary cavity from the intercondylar region and fixed to the proximal fragment of the femur with augmented fixation using a small plate and screws. Our procedure makes it easy to perform large segmental bone grafting and internal fixation at the same time for such a condition.

Aged↗
PubMed1998

Protein C anticoagulant system in patients with interstitial lung disease.

Excessive procoagulant activity in the alveolar space may play a relevant role in the pathogenesis of pulmonary fibrosis. Hypercoagulability results from the disruption of the balance between the procoagulant and anticoagulant factors. The aim of this study was to assess the levels of molecular markers of the anticoagulant protein C (PC) pathway in the bronchoalveolar lavage fluid (BALF) and plasma of 11 patients with idiopathic pulmonary fibrosis (IPF), 14 with sarcoidosis and 16 with collagen vascular disease (CVD)-associated interstitial lung disease (CVD-ILD). Six healthy nonsmoking volunteers served as control subjects. BALF concentrations of the marker of clotting activation, thrombin- antithrombin III complex (TAT), in patients with sarcoidosis and CVD-ILD were significantly greater than those in control subjects. PC levels in BALF were markedly higher in patients with IPF (610 +/- 150 ng/ml), sarcoidosis (680 +/- 170 ng/ml), and CVD-ILD (1,580 +/- 600 ng/ml) than in control subjects (230 +/- 140 ng/ml). BALF concentrations of activated PC-PC inhibitor (APC-PCI) complex were significantly decreased in IPF (0.46 +/- 0.16 ng/ml), sarcoidosis (0. 43 +/- 0.11 ng/ml), and CVD-ILD (0.50 +/- 0.15 ng/ml) patients as compared with control subjects (1.08 +/- 0.23 ng/ml). APC-PCI/PC ratios were significantly lower in patients with IPF (2.70 +/- 1.74 ng/microg), sarcoidosis (1.94 +/- 0.82 ng/microg), and CVD-ILD (1.89 +/- 0.68 ng/microg) than in control subjects (15.91 +/- 8.45 ng/microg). Plasma levels of APC- PCI and the APC-PCI/PC ratio were also significantly decreased in patients with CVD-ILD as compared with control subjects. Overall, these findings suggest that decreased PC activation with increased procoagulant activity occurs in patients with ILD.

Antithrombin III↗
PubMed1998

Estrogen receptor gene polymorphism and generalized osteoarthritis.

OBJECTIVE: Generalized osteoarthritis (OA) is a common disease, more often affecting women than men. Although genetic factors are known to be the major risk factor, the genes related to its development are as yet undetermined. We investigated the association between estrogen receptor gene polymorphisms and generalized OA. METHODS: Pvu II and Xba I restriction fragment length polymorphisms (RFLP) of estrogen receptor gene were analyzed in 65 Japanese patients with generalized OA and in 318 healthy control women. The RFLP were represented as Pp(Pvu II) and Xx(Xba I), with capital and small letters signifying the absence and the presence of restriction sites, respectively. RESULTS: Estrogen receptor genotype PpXx, with the combination of the Pvu II and Xba I RFLP, is a significant risk factor for the disease subset (odds ratio 1.86, 95% confidence interval 1.03-3.24; p = 0.039). The association of this genotype was more obvious in patients with severe radiographic changes and in younger patients. CONCLUSION: Some variant of the estrogen receptor gene is a genetic marker for generalized OA. How this genotype affects development of the disease remains to be elucidated.

Age Factors↗