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Lin Xu

Publications and source records attributed to Lin Xu.

At least 145 records · Page 8Linked to original sources
PubMed2003

Up-regulation of secretory leukocyte protease inhibitor (SLPI) in the brain after ischemic stroke: adenoviral expression of SLPI protects brain from ischemic injury.

Secretory leukocyte protease inhibitor (SLPI) is a 12-kDa secreted protein initially identified from epithelial cells as an inhibitor of leukocyte serine proteases. In the present study, we described the identification of SLPI expression in ischemic cortex by suppression subtractive hybridization strategy. Our full-length rat SLPI cDNA shares 81% and 63% amino acid sequence identity with its mouse and human homologs, respectively, and with several polymorphisms to previous reported rat sequences. Northern blot analysis confirmed that SLPI mRNA was significantly induced in the ischemic brain tissue at 12 h (5.1-fold increase over sham controls, n = 4, p < 0.05), peaked at 2 days (26.1-fold increase, p < 0.001), and sustained up to 5 days (5.1-fold increase, p < 0.05). SLPI was localized in neurons and astrocytes in the peri-infarct zone from 24 to 72 h after middle cerebral artery occlusion by means of immunohistochemical and confocal microscopy analysis. Administration of a recombinant adenovirus overexpressing SLPI (Adv/SLPI) into the cortical tissue resulted in up to 58.4% reduction in ischemic lesion over controls at the site of Adv/SLPI expression (p < 0.01, n = 8) and significantly improved functional outcome (p < 0.01). These data suggest that the ischemia-induced expression of SLPI might play a neuroprotective role in focal stroke, possibly because of rapid inhibition of activated proteases and its suppression in inflammatory response.

Adenoviridae↗
PubMed2003

Inhibition of factor Xa reduces ischemic brain damage after thromboembolic stroke in rats.

BACKGROUND AND PURPOSE: Factor Xa (FXa) is a key coagulation protease and target for novel antithrombotic agents for prevention and treatment of diverse thromboembolic disorders. In the present study we describe the effect of a novel, potent, and selective FXa inhibitor, DPC602, on brain damage and neurobehavioral consequence in a rat thromboembolic model of stroke. METHODS: Thromboembolic stroke was induced in rats by placement of an autologous clot into the middle cerebral artery. RESULTS: Laser-Doppler monitoring of cerebral blood flow demonstrated that DPC602 (8 mg/kg, single IV/IP bolus pretreatment) markedly improved cerebral blood flow after thromboembolic stroke by 25% to 160% (n=6; P<0.001) at 1 to 6 hours. DPC602 demonstrated concentration- and time-dependent reductions in infarct size, with maximal effect (89% reduction; n=14; P<0.001) at the highest dose over controls. Neurological function was also significantly improved in DPC602-treated rats at days 1, 3, and 7 (n=13; P<0.01). DPC602 treatment did not cause cerebral hemorrhage, assessed by free hemoglobin in the ischemic brain tissues. CONCLUSIONS: These data suggest that anticoagulation with a selective FXa inhibitor might ameliorate the extent of ischemic brain damage and neurological deficits after a thromboembolic event. Enhanced clot dissolution and early reperfusion may account for the cerebrovascular-protective effect of the drug.

Animals↗
PubMed2003

Novel as1 and as2 defects in leaf adaxial-abaxial polarity reveal the requirement for ASYMMETRIC LEAVES1 and 2 and ERECTA functions in specifying leaf adaxial identity.

The shoot apical meristem (SAM) of seed plants is the site at which lateral organs are formed. Once organ primordia initiate from the SAM, they establish polarity along the adaxial-abaxial, proximodistal and mediolateral axes. Among these three axes, the adaxial-abaxial polarity is of primary importance in leaf patterning. In leaf development, once the adaxial-abaxial axis is established within leaf primordia, it provides cues for proper lamina growth and asymmetric development. It was reported previously that the Arabidopsis ASYMMETRIC LEAVES1 (AS1) and ASYMMETRIC LEAVES2 (AS2) genes are two key regulators of leaf polarity. In this work, we demonstrate a new function of the AS1 and AS2 genes in the establishment of adaxial-abaxial polarity by analyzing as1 and as2 alleles in the Landsberg erecta (Ler) genetic background. We provide genetic evidence that the Arabidopsis ERECTA (ER) gene is involved in the AS1-AS2 pathway to promote leaf adaxial fate. In addition, we show that AS1 and AS2 bind to each other, suggesting that AS1 and AS2 may form a complex that regulates the establishment of leaf polarity. We also report the effects on leaf polarity of overexpression of the AS1 or AS2 genes under the control of the cauliflower mosaic virus (CAMV) 35S promoter. Although plants with as1 and as2 mutations have very similar phenotypes, 35S::AS1/Ler and 35S::AS2/Ler transgenic plants showed dramatically different morphologies. A possible model of the AS1, AS2 and ER action in leaf polarity formation is discussed.

Arabidopsis↗
PubMed2003

Long-term effect of stent placement in 115 patients with Budd-Chiari syndrome.

AIM: To report the long-term effect of stent placement in 115 patients with Budd-Chiari syndrome (BCS). METHODS: One hundred and fifteen patients with BCS were treated by percutaneous stent placement. One hundred and two patients had IVC stent placement, 30 patients had HV stent placement, 17 of them underwent both IVC stent and HV stent. All the procedures were performed with guidance of ultrasound. RESULTS: The successful rates in placing IVC stent and HV stent were 94% (96/102) and 87% (26/30), respectively. Ninety-seven patients with 112 stents (90 IVC stents, 22 HV stents) were followed up. 96.7% (87/90) IVC stents and 90.9% (20/22) HV stents remained patent during follow up periods (mean 49 months, 45 months, respectively). Five of 112 stents in the 97 patients developed occlusion. Absence of anticoagulants after the procedure and types of obstruction (segmental and occlusive) before the procedure were related to a higher incidence of stent occlusion. CONCLUSION: Patients with BCS caused by short length obstruction can be treated by IVC stent placement, HV stent placement or both IVC and HV stent placement depending on the sites of obstruction. The long-term effect is satisfactory. Anticoagulants are strongly recommended after the procedure especially for BCS patients caused by segmental occlusion.

Adolescent↗
PubMed2003

Generation of cytotoxic T cell against HBcAg using retrovirally transduced dendritic cells.

AIM: Cytotoxic T lymphocytes (CTLs) play an important role in resolving HBV infection. In the present study, we attempted to evaluate the efficiency of bone marrow-derived dendritic cells (DCs) transduced with recombinant retroviral vector bearing hepatitis B virus (HBV) core gene and the capability of generating CTLs against HBcAg by genetically modified DCs in vivo. METHODS: A retroviral vector containing HBV core gene was constructed. Replicating DC progenitor of C57BL/6 mice was transduced by retroviral vector and continually cultured in the presence of recombinant mouse granulocyte-macrophage colony-stimulating factor (rmGM-CSF) and interleukin-4(IL-4) for 6 days. LPS was added and cultured for additional two days. The efficiency of gene transfer was determined by PCR, Western blot and FACS. Transduced DCs immunized C57BL/6 mice subcutaneously 2 times at an one-week interval. Intracellular IFN-gamma and IL-4 of immunized mice lymphocytes were analyzed. Generation of CTLs in lymphocytes stimulated with mitomycin C-treated EL4-C cell which stably expresses HBcAg was determined by LDH release assays. RESULTS: Recombinant retroviral expression vector (pLCSN) was positively detected by PCR as well as enzyme digestion with EcoRI and BamH I. Retroviruses were generated by pLCSN transfection packing cell and the virus titer was 3 x 10(5) CFU/ml. Indirect immunofluorescence and FACS showed that HBV core gene was expressed in murine fibroblasts. Transduced bone marrow cells had capability of differentiating into DCs in vitro in the presence of rmGM-CSF and rmIL-4. The result of PCR showed that HBV core gene was integrated into the genome of transduced DCs. Western blot analysis showed that HBV core gene was expressed in DCs. The transduction rate was 28 % determined by FACS. Retroviral transduction had no influence on DCs expressions of CD80 and MHC class II. HBcAg specific CTLs and Th1 type immune responses could be generated in the mice by using transduced DCs as antigen presenting cells (APCs). CONCLUSION: Retroviral transduction of myeloid DCs progenitors expresses efficiently HBcAg, and genetically modified DCs evoke a higher CTLs response than HBcAg in vivo.

Animals↗
PubMed2003

[Expression of HBcAg in eukaryotic cells by retroviral vector mediated gene transfer].

BACKGROUND: To construct recombinant retroviral vector expressing HBcAg in eukaryotic cells. METHODS: The HBV core gene fragment was amplified by using PCR from pADR which contains complement nucleotide sequence of HBV subtype adr and cloned into retroviral expression plasmid pLXSN, then transfected into packing cell (PT67) with lipofec AMINE. After 2-3 weeks selection with G418, large colonies were isolated and transferred to individual plates. Virus-containing medium was collected and used to infect NIH3T3, EL4 and mouse bone marrow derived dendritic cells(DC). DNA was extracted from infected cells and tested by PCR. Indirect immunofluorescence and FACS were used to detect the expression of HBcAg. Cell mediated immunity of immunized C57BL/6 mice with transduced DC was analyzed. RESULTS: The insertion of HBV core gene fragment in the recombinant retroviral plasmid was confirmed by PCR as well as enzyme digestion with EcoR1 and BamH2. The viral titer reached 3 x 10(5) CFU/ml. The result of PCR showed that the HBV core gene had been integrated into the genome of infected NIH3T3 cells. Indirect immunofluorescence and FACS analysis showed that HBcAg had been expressed in these cells. HBcAg specific CTL responses could be generated in mice immunized with retrovirus transduced DC. CONCLUSIONS: HBV core gene had been integrated into eukaryotic cells with retroviral vector and target gene had been expressed efficiently. These results may have some impact on gene therapy of chronic hepatitis B.

3T3 Cells↗
PubMed2003

[Construction and identification of recombinant adenovirus vector containing thioredoxin reductase gene].

AIM: To construct recombinant adenovirus vector containing human thioredoxin reductase (TR) gene and to explore the correlation between antioxidant activity of TR and the degenerative neuropathy. METHODS: Full length TR cDNA was obtained from recombinant plasmid pGEM-TR via digestion with Apa I and Not I and was cloned into pShuttle vector and pShuttle-TR was recut with I-Ceu I and PI-Sce I. Fragment containing TR gene and CMV promoter was inserted into E1 and E3 deficient adeno-X virus DNA, and then the recombinant adenovirus vector was transfected into HEK 293 cells through lipofectamine and identified by PCR. The TR expression on and in cell lysate of CV1 cells infected with recombinant adenovirus was by immuno fluorescence assay and Western blot analysis. RESULTS: After replication of recombinant adenovirus Adeno-TR, the virus titer was about 4.4x10(11) pfu/L. The TR expression on CV1 cells was proved by fluorescent microscopy. Western blot analysis showed a band with relative molecular mass (M(r)) of 55,000. CONCLUSION: A recombinant adenovirus vector has been successfully constructed and TR is expressed on CV1 cells. This result lays the foundation for further study on function of TR and its correlation with degenerative neuropathy.

Adenoviridae↗
PubMed2002

Recombinant adenoviral expression of dominant negative IkappaBalpha protects brain from cerebral ischemic injury.

Transcription factor NF-kappaB is associated with inflammatory response and cell survival. Under inactive condition, NF-kappaB is sequestered in the cytoplasm by an anchor protein, inhibitor of NF-kappaB (IkappaB). NF-kappaB was shown to be activated during ischemic brain injury. In the present study we have investigated the role of NF-kappaB in ischemic brain injury using a recombinant adenovirus expressing a dominant negative form of IkappaB (Adv/IkappaBdn) to specifically inhibit NF-kappaB activation. Our data demonstrated that cortical injection of Adv/IkappaBdn significantly reduced ischemic brain injury following permanent occlusion of the middle cerebral artery (MCAO) in rats, showing 55% reduction (p<0.01, n=8) in total ischemic lesion or 80% reduction (p<0.001) in the cortical area with Adv/IkappaBdn expression. Similarly, Adv/IkappaBdn expression significantly decreased neurological deficits (37% reduction over controls, p<0.01, n=8). These data provide further evidence for the role of NF-kappaB/IkappaB in ischemic brain injury and suggest that inhibition of NF-kappaB is neuroprotective in focal stroke.

Adenoviridae↗
PubMed2002

An ACTH- and ATP-regulated background K+ channel in adrenocortical cells is TREK-1.

Bovine adrenal zona fasciculata (AZF) cells express a background K(+) channel (I(AC)) that sets the resting potential and acts pivotally in ACTH-stimulated cortisol secretion. We have cloned a bTREK-1 (KCNK2) tandem-pore K(+) channel cDNA from AZF cells with properties that identify it as the native I(AC). The bTREK-1 cDNA is expressed robustly in AZF cells and includes transcripts of 4.9, 3.6, and 2.8 kb. In patch clamp recordings made from transiently transfected cells, bTREK-1 displayed distinctive properties of I(AC) in AZF cells. Specifically, bTREK-1 currents were outwardly rectifying with a large instantaneous and smaller time-dependent component. Similar to I(AC), bTREK-1 increased spontaneously in amplitude over many minutes of whole cell recording and was blocked potently by Ca(2+) antagonists including penfluridol and mibefradil and by 8-(4-chlorophenylthio)-cAMP. Unitary TREK-1 and I(AC) currents were nearly identical in amplitude. The native I(AC) current, in turn, displayed properties that together are specific to TREK-1 K(+) channels. These include activation by intracellular acidification, enhancement by the neuroprotective agent riluzole, and outward rectification. bTREK-1 current differed from native K(+) current only in its lack of ATP dependence. In contrast to I(AC), the current density of bTREK-1 in human embryonic kidney-293 cells was not increased by raising pipette ATP from 0.1 to 5 mm. Further, the enhancement of I(AC) current in AZF cells by low pH and riluzole was facilitated by, and dependent on, ATP at millimolar concentrations in the pipette solution. Overall, these results establish the identity of I(AC) K(+) channels, demonstrate the expression of bTREK-1 in a specific endocrine cell, identify potent new TREK-1 antagonists, and assign a pivotal role for these tandem-pore channels in the physiology of cortisol secretion. The activation of I(AC) by ATP indicates that native bTREK-1 channels may function as sensors that couple the metabolic state of the cell to membrane potential, perhaps through an associated ATP-binding protein.

Adenosine Triphosphate↗
PubMed2002

Mitogen-activated protein kinase-activated protein (MAPKAP) kinase 2 deficiency protects brain from ischemic injury in mice.

Mitogen-activated protein (MAP) kinase-activated protein kinase 2 (MK2) is one of several kinases directly regulated by p38 MAP kinase. A role of p38 MAP kinase in ischemic brain injury has been previously suggested by pharmacological means. In the present study, we provide evidence for a role of MK2 in cerebral ischemic injury using MK2-deficient (MK2(-/-)) mice. MK2(-/-) mice subjected to focal ischemia markedly reduced infarct size by 64 and 76% after transient and permanent ischemia, respectively, compared with wild-type mice. Furthermore, MK2(-/-) mice had significant reduction in neurological deficits. Real-time PCR analysis identified a significantly lower expression in interleukin-1beta mRNA (53% reduction) but not in tumor necrosis factor-alpha mRNA in MK2(-/-) mice over wild-type animals after ischemic injury. The significant reduction in interleukin-1beta was also confirmed in MK2(-/-) mice by enzyme-linked immunosorbent assay. The marked neuroprotection from ischemic brain injury in MK2(-/-) mice was not associated with the alteration of hemodynamic or systemic variables, activation of caspase-3, or apoptosis. Our data provide new evidence for the involvement of MAP kinase pathway in focal ischemic brain injury and suggest that this effect might be associated with the expression of interleukin-1beta in the ischemic brain tissue.

Animals↗
PubMed2002

Alpha-2 macroglobulin I1000 V polymorphism in Chinese sporadic Alzheimer's disease and Parkinson's disease.

Several lines of evidence have revealed some overlapping pathologies in Alzheimer's disease (AD) and Parkinson's disease (PD). Although the alpha-2 macroglobulin gene (A2M) might be a risk factor of these two neurodegenerative diseases, conclusions from different studies have remained conflicting. Here we studied the role of A2M I1000 V polymorphism in both AD and PD in a Chinese Han population. We found that the A2M I/V genotype is associated with both AD (odds ratio (OR)=2.55, 95% confidential interval (95% CI): 1.20-5.43, attributable fraction (AF)=13.65%) and PD (OR=3.03, 95% CI: 1.30-7.02, AF=16.51%). After classifying according to the age of onset, this association is only detected in early-onset AD patients (OR=3.96, 95% CI: 1.28-12.26) and late-onset PD patients (OR=2.61, 95% CI: 0.97-7.09). Therefore, we conclude that in our samples, the A2M I/V genotype might be a susceptibility variant, even with minor effect, for both sporadic AD and PD.

Adult↗
PubMed2002

Propofol facilitates the development of long-term depression (LTD) and impairs the maintenance of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats.

Memory is sensitive to the short-acting anesthetic (2,6-diisopropylphenol) propofol, but the underlying mechanism is little known. Here, we have examined the effects of propofol on synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats. We found that low dose of propofol (20 mg/kg, i.p.) did not affect the basal transmission, but enhanced prominently the development of long-term depression (LTD) and impaired the maintenance of long-term potentiation (LTP). The impairment of LTP maintenance and enhancement of LTD development may contribute to propofol-induced deficits in memory following propofol anesthesia.

2-Amino-5-phosphonovalerate↗
PubMed2002

Genetic study of apolipoprotein E gene, alpha-1 antichymotrypsin gene in sporadic Parkinson disease.

Several lines of evidence have suggested some common genetic risk factors for Alzheimer disease (AD) and Parkinson disease (PD) because there are some overlapping pathologies in these two neurodegenerative diseases. In the present study, we investigated the role of Apolipoprotein E gene polymorphism and the signal peptide polymorphism in alpha-1 antichymotrypsin (ACT) gene in idiopathic sporadic PD. The study was performed in a sample consisting of 68 PD cases and 160 healthy subjects in Shanghai China. We found no significant differences of ACT gene polymorphic distribution between PD cases and controls. The ApoE gene epsilon2/epsilon4 genotype was significantly more frequent in PD subjects (chi2 = 7.126, df = 1, P = 0.008) and conferred a 12.70 times susceptibility for PD (OR = 12.62, 95% CI: 1.445-110.17, chi2 = 5.259, P < 0.05, AF = 4.59%). No interaction of ApoE and ACT genes was detected in PD. Therefore, our data suggested that the ApoE epsilon2/epsilon4 genotype might be a susceptibility variant of moderate effect for sporadic idiopathic PD in our samples, whereas the ACT gene signal peptide polymorphism might not.

Adult↗
PubMed2002

c-Raf/MEK/ERK pathway controls protein kinase C-mediated p70S6K activation in adult cardiac muscle cells.

p70S6 kinase (S6K1) plays a pivotal role in hypertrophic cardiac growth via ribosomal biogenesis. In pressure-overloaded myocardium, we show S6K1 activation accompanied by activation of protein kinase C (PKC), c-Raf, and mitogen-activated protein kinases (MAPKs). To explore the importance of the c-Raf/MAPK kinase (MEK)/MAPK pathway, we stimulated adult feline cardiomyocytes with 12-O-tetradecanoylphorbol-13-acetate (TPA), insulin, or forskolin to activate PKC, phosphatidylinositol-3-OH kinase, or protein kinase A (PKA), respectively. These treatments resulted in S6K1 activation with Thr-389 phosphorylation as well as mammalian target of rapamycin (mTOR) and S6 protein phosphorylation. Thr-421/Ser-424 phosphorylation of S6K1 was observed predominantly in TPA-treated cells. Dominant negative c-Raf expression or a MEK1/2 inhibitor (U0126) treatment showed a profound blocking effect only on the TPA-stimulated phosphorylation of S6K1 and mTOR. Whereas p38 MAPK inhibitors exhibited only partial effect, MAPK-phosphatase-3 expression significantly blocked the TPA-stimulated S6K1 and mTOR phosphorylation. Inhibition of mTOR with rapamycin blocked the Thr-389 but not the Thr-421/Ser-424 phosphorylation of S6K1. Therefore, during PKC activation, the c-Raf/MEK/extracellular signal-regulated kinase-1/2 (ERK1/2) pathway mediates both the Thr-421/Ser-424 and the Thr-389 phosphorylation in an mTOR-independent and -dependent manner, respectively. Together, our in vivo and in vitro studies indicate that the PKC/c-Raf/MEK/ERK pathway plays a major role in the S6K1 activation in hypertrophic cardiac growth.

Adenoviridae↗
PubMed2002

A programmable fragmentation analysis of proteins by in-source decay in MALDI-TOF mass spectrometry.

Here we describe an algorithm for identifying peptides/ proteins of known sequence and unknown peptides from partial spectra generated by an in-source decay (ISD) technique coupled with matrix-assisted laser desorption/ ionization time-of-flight mass spectrometry. The identification of protein fragments is processed with a software program called CMATCH, which generates candidate subsequences for both known peptides/proteins and unknown peptides for the major product ions in the spectral range m/z 400-5000 and then matches these to known protein sequences contained in a reference database for the known peptides/proteins. CMATCH, which is compiled for MSDOS or WINDOWS95/NT, has two main advantages: first, the candidate subsequences are generated automatically without the need for supplementary information concerning the distribution of either N-terminal or C-terminal ions in the spectra for both known peptides/proteins and unknown peptides; second, the highest coordinated homologous sequences are picked up automatically from the reference database as the best matches with known peptides/proteins. Examples from the ISD spectra of several test proteins demonstrate the efficacy of this protein identification software.

Algorithms↗
PubMed2002

Cardiac-specific expression and hypertrophic upregulation of the feline Na(+)-Ca(2+) exchanger gene H1-promoter in a transgenic mouse model.

The NCX1 gene contains three promoters (H1, K1, and Br1), and as a result of alternative promoter usage and alternative splicing, there are multiple tissue-specific variants of the Na(+)-Ca(2+) exchanger. We have proposed that for NCX1, the H1 promoter regulates expression in the heart, the K1 promoter regulates expression in the kidney, and the Br1 promoter regulates expression in the brain as well as low-level ubiquitous expression. Here, using a transgenic mouse model, we test the role of the DNA region including -1831 to 67 bp of intron 1, encompassing exon H1 of the feline NCX1 gene (NCX1H1). The NCX1H1 promoter was sufficient for driving the normal spatiotemporal pattern of NCX1 expression in cardiac development. The luciferase reporter gene was expressed in a heart-restricted pattern both in early embryos (embryonic days 8 to 14) and in later embryos (after embryonic day 14), when NCX1 is also expressed in other tissues. In the adult, no luciferase activity was detected in the kidney, liver, spleen, uterus, or skeletal muscle; minimal activity was detected in the brain; and very high levels of luciferase expression were detected in the heart. Transverse aortic constriction-operated mice showed significantly increased left ventricular mass after 7 days. In addition, there was a 2-fold upregulation of NCX1H1 promoter activity in the left ventricle in animals after 7 days of pressure overload compared with both control and sham-operated animals. This work demonstrates that the NCX1H1 promoter directs cardiac-specific expression of the exchanger in both the embryo and adult and is also sufficient for the upregulation of NCX1 in response to pressure overload.

Animals↗
PubMed2002

Relationship between glucocorticoid-induced osteoporosis and vitamin D receptor genotypes.

By means of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay, the association between vitamin D receptor (VDR) genotypes and bone mineral density (BMD) in the patients receiving long-term glucocorticoid therapy was studied. The clinical data and blood of 71 patients with rheumatosis who received long-term glucocorticoid therapy were collected. BMD was measured by dual-energy X-ray absorptimometry. VDR gene fragment (about 185 bp) was amplified by PCR from the extracted genomic DNA, then digested with restriction endonuclease Bsm I. The genotypes were evaluated based on the fragment length following endonuclease digestion and the association between genotypes and BMD or Z-score values was analyzed. Among the 71 cases, the detected genotypes were Bb and bb with the distribution frequency being 11.3% and 88.7% respectively. The distribution frequency of the alleles was in agreement with the Hardy-Weinberg equilibrium. There was no significant difference between the two genotypes in age, gender, body mass index (BMI), disease duration, disease types, time of glucocorticoid administration and cumulative dosage (P > 0.05). Osteoporosis rate of the patients with Bb or bb genotype was 37.5% and 33.3% respectively, with the difference being not significant (chi 2 = 0.05, P = 0.8). The BMD and Z-score values at lumbar spine and femur in two genotypes were not similar, but the difference had no significant (P > 0.05). The distribution frequency of bb type of VDR genotypes in Han populations of China was more prevalent, followed by Bb and bb types in turn. In the patients receiving long-term glucocorticoid therapy, there was no significant difference in BMD between Bb and bb genotypes. The data suggest that the VDR genotypes may not be means of identifying patients at greater risk of glucocorticoid-induced osteoporosis, which await to be further confirmed by a large sample size.

Adolescent↗