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Biomedical subjects

L Chen

Publications and source records attributed to L Chen.

At least 757 records · Page 42Linked to original sources
PubMed1998

Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS): a case report.

Megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS) is a rare congenital disorder characterized by a massively enlarged urinary bladder without mechanical outlet obstruction and microcolon, as well as a hypoperistaltic bowel with normal ganglion cell distribution. We report one such case to discuss the findings of antenatal ultrasound and the radiologic and pathologic features of this condition.

Abnormalities, Multiple↗
PubMed1998

Signaling by HGF and KGF in corneal epithelial cells: Ras/MAP kinase and Jak-STAT pathways.

PURPOSE: To characterize the signaling pathways used by hepatocyte growth factor (HGF) and keratinocyte growth factor (KGF) in human corneal epithelial cells. METHODS: Cultures of SV40 large T antigen-transfected human corneal epithelial cells were treated with recombinant human HGF or KGF at 50 ng/ml to 100 ng/ml for 5 to 30 minutes and harvested for protein isolation. Immunoprecipitation was performed with antisera to signal transducers and activators of transcription 1 (STAT1), STAT3, Janus kinase 1 (Jak1), Shc, Grb2, Sos1, and HGF receptor (met). Immunoprecipitated proteins were analyzed by western blot analysis. Gel retardation experiments were carried out with first-passage human corneal epithelial cells to detect binding of STATs to the high affinity c-sis (platelet-derived growth factor) inducible DNA element (hSIE). Effects of HGF, KGF, and kinase inhibitors on mitogen-activated protein kinase (MAPK) activation were evaluated by western blot analysis and enzymatic assays. RESULTS: In human corneal epithelial cells, the phosphorylation of adapter protein Shc (52- and 66-kDa isoforms) was enhanced by HGF, but not by KGF. Phosphorylated HGF receptor coimmunoprecipitated with Shc, Grb2, and Sos1. Hepatocyte growth factor or KGF rapidly activated MAPK in corneal epithelial cells. The activation of MAPK (p42 and p44) by HGF or KGF was transient and decreased gradually within 1 hour. MAPK kinase 1 (MEK1) inhibitor PD098059 or the protein tyrosine kinase inhibitor genistein blocked MAPK activation. Activation of MAPK induced by HGF was partially inhibited by protein kinase C inhibitor calphostin C. Hepatocyte growth factor and KGF had no effect on the activation of Jak-STAT cascade components that are activated by epidermal growth factor. CONCLUSIONS: Hepatocyte growth factor and KGF activate Ras-MAPK pathways in human corneal epithelial cells. There may be at least two routes used by HGF in transmitting signals from its receptor to the MAPK cascade. One is the receptor-Grb2/Sos complex to the Ras pathway, and the other is through protein kinase C. Hepatocyte growth factor and KGF did not activate the Jak-STAT cascade components STAT1, STAT3, or Jak1 in corneal epithelial cells.

Blotting, Western↗
PubMed1998

Experimental study on the scavenging effects of ginsenosides on oxygen free radicals using model of heterotopic heart transplantation in rats.

Oxygen-derived free radicals play an important role in myocardial injury associated ischemia and reperfusion. To investigate whether ginsenosides, as an additive agent of cardioplegic solution, can decrease toxicity of oxygen free radicals in myocardial injury, a heterotopic heart transplantation model in Wistar rats was employed. St. Thomas II cold cardioplegia containing ginsenosides 80 mg/l was used in the experimental group. St. Thomas II cold cardioplegia alone was used in the control group. After global ischemia for 60 minutes and reperfusion for 30 minutes of a transplanted heart, SOD activity in the myocardium treated with ginsenosides was significantly higher than that in the control group (N=10, p< 0.01), whereas the MDA in the myocardium treated with ginsenosides were markedly lower than that of the control group (p< 0.01). The amounts of oxygen free radicals in the myocardium treated with ginsenosides were significantly lower than that of the control group (p <0.001). This study demonstrates that ginsenosides, as a proper additive agent of cardioplegic solution, can decrease toxicity of oxygen free radicals, suggesting one of the mechanisms for its protective effects against myocardial ischemia and reperfusion injury.

Animals↗
PubMed1998

Association between coronary heart disease and cancers of the breast, prostate, and colon.

Coronary heart disease (CHD) and cancers of the breast, prostate, and colon are more common in industrialized countries than in the developing world, and to some degree, these conditions appear to share risk factors. To investigate whether there is an association between these cancers and a prior history of CHD, a hospital-based case-control study was conducted at Columbia-Presbyterian Medical Center in New York. The study was based on 252 breast cancer cases, 256 colorectal cancer cases, and 322 benign surgical controls, all of whom underwent biopsy or surgery between January 1989 and December 1992, and on 319 prostate cancer cases and 189 benign prostatic hypertrophy controls diagnosed between January 1984 and December 1986 (prior to widespread use of prostate-specific antigen screening). Medical records were reviewed on each, focusing on the preoperative anesthesia and surgical clearances. No association was found between a history of CHD and breast or colorectal cancer, but an elevated risk was found for prostate cancer (odds ratio, 2.00; 95% confidence interval, 1.18-3.39), using unconditional logistic regression with adjustment for appropriate confounders. No association was found between cigarette smoking and any of the three cancers. Aspirin use was protective for colorectal cancer (odds ratio, 0.35; 95% confidence interval, 0.17-0.73) but had no association with breast or prostate cancer. The study suggests that individuals with CHD are at elevated risk for prostate cancer but not breast or colorectal cancer. Etiological risk factors associated with CHD should be investigated with regard to prostate cancer. Patients with CHD may represent a high-risk group for prostate cancer and potential future targets for prostate cancer screening interventions.

Aged↗
PubMed1998

The effect of location of transcutaneous electrical nerve stimulation on postoperative opioid analgesic requirement: acupoint versus nonacupoint stimulation.

UNLABELLED: Transcutaneous electrical nerve stimulation (TENS) has been used as a complementary (supplemental) therapy to opioid analgesics for pain relief after surgery. Simultaneous stimulation at a classical Chinese acupoint site and periincisional dermatomes significantly decreases the postoperative analgesic requirement. This sham-controlled study was designed to assess the relative effectiveness of acupoint versus nonacupoint stimulation on the postoperative hydromorphone (HM) requirement, the incidence of opioid-related side effects, and the overall recovery profile. One hundred women undergoing total abdominal hysterectomy or myomectomy procedures with a standardized general anesthesia were randomly assigned to one of four postoperative analgesic treatment regimens (n = 25 each): Group I = sham-TENS (no electrical current) at the Zusanli (ST36) acupoints, Group II = nonacupoint-TENS at the shoulders, Group III = dermatomal-TENS at the level of the surgical incision, and Group IV = acupoint-TENS at the Zusanli acupoints. The frequency of TENS was set in the standard dense-and-disperse mode of 2/100 Hz. The intensity of stimulation was set at 0 mA for patients in Group I and at 9-12 mA for patients in Groups II, III, and IV. A patient-controlled analgesia (PCA) device programmed to deliver bolus doses of HM 0.2-0.4 mg IV on demand with a minimal lockout interval of 10 min was used to quantify the postoperative opioid analgesic requirement. Standard 100-mm visual analog scales were used to assess pain, as well as sedation, fatigue, and nausea, at specific intervals after surgery. The numbers of PCA demands and delivered bolus doses, requirements for supplemental medication, and any opioid-related side effects were recorded. In the first 24 h postoperatively, the opioid requirements in Groups III and IV were decreased by 37% and 39%, respectively, compared with the control (sham) group and 35% and 38%, respectively, compared with Group II. The duration of PCA usage and the incidences of nausea and dizziness were also significantly decreased in Groups III and IV compared with Groups I and II. We conclude that periincisional dermatomal and Zusanli acupoint stimulation were equally effective in decreasing the postoperative opioid analgesic requirement and in reducing opioid-related side effects. Both of these positions were more effective than the nonacupoint (shoulder) location. IMPLICATIONS: The location of the stimulating electrodes seems to be an important determinant of the efficacy of transcutaneous electrical nerve stimulation in decreasing the need for opioid analgesics in the postoperative period. This study demonstrates that transcutaneous electrical nerve stimulation applied at the dermatomal level of the skin incision is as effective as Zusanli acupoint stimulation, and both were more effective than stimulation at a nonacupoint (shoulder) location.

Acupuncture Points↗
PubMed1998

Bone morphogenic proteins 2 and 4 and their receptors in the adult human cornea.

PURPOSE: To examine the expression of transforming growth factor family members bone morphogenic proteins 2 and 4 (BMP2, BMP4), their receptor mRNAs, and BMP2 and BMP4 proteins in the cells of the human cornea. The effects of BMP2 and BMP4 on corneal fibroblast proliferation and apoptosis were also examined. METHODS: Reverse transcription-polymerase chain reaction, immunoprecipitation, and western blot analysis were used to examine mRNA and protein expression in cultured human corneal cells. Immunocytochemistry was applied to examine protein localization in fresh frozen human cornea cells. Stimulation and inhibition of nuclear factor-kappaB (NF-kappaB) activation was evaluated by gel shift assay. Apoptosis was examined using trypan blue exclusion, laddering of DNA, CPP32 assay, and transmission electron microscopy. Proliferation was monitored by counting cells. RESULTS: BMP2 and BMP4 mRNAs and proteins were expressed in cultured human corneal epithelial cells, keratocytes, and corneal endothelial cells. BMP2 and BMP4 were detected in each major corneal cell type in fresh frozen human cornea. BMP receptor IA, IB, and II mRNAs were also detected in cultured human corneal epithelial cells, keratocytes, and endothelial cells. BMP2 and BMP4 stimulated activation of NF-kappaB. Actinomycin D and SN50 peptide, but not SN50M control peptide, inhibited NF-kappaB activation in response to BMP2 or BMP4. BMP2 and BMP4 stimulated apoptosis of corneal fibroblast cells when NF-kappaB activation was inhibited with the nonselective inhibitor actinomycin D or selective inhibitor SN50. The nonsteroidal anti-inflammatory agents ketorolac tromethamine and diclofenac sodium augmented the effect of BMP2 on corneal fibroblast apoptosis. BMP2 and BMP4 both stimulated proliferation of corneal fibroblast cells in the absence of inhibitors of NF-kappaB activation. CONCLUSIONS: BMP2, BMP4, and their receptors are expressed in the cells of the adult human cornea. The functions regulated by these cytokines may include keratocyte proliferation and apoptosis.

Adult↗
PubMed1997

Nitroglycerin enhances the ability of dobutamine stress echocardiography to detect hibernating myocardium.

BACKGROUND: A biphasic response of wall thickening with initial improvement and subsequent deterioration during dobutamine stress echocardiography (DSE) has been increasingly used for detection of hibernating myocardium. However, the improvement of wall thickening at low-dose DSE may be limited in hibernating myocardium by severe hypoperfusion. Nitroglycerin (NTG) improves myocardial perfusion, reduces oxygen demand, and may enhance low-dose dobutamine to improve wall thickening. METHODS AND RESULTS: A pig model of myocardial hibernation of 24 hours to 7 days was created through severe left anterior descending coronary artery stenosis with coronary flow reductions of approximately 40%, producing severe regional left ventricular dysfunction but no infarction in seven pigs. Myocardial infarction was produced in five pigs with occlusion of the artery. DSE was performed with incremental doses with and without an NTG infusion of 50 to 100 microg/min. In the hibernating group, NTG alone improved wall thickening in the hibernating region modestly from 11.4+/-7.2% at baseline to 19.1+/-7.0%. The improvement was associated with increased regional coronary flow from 0.46+/-0.12 to 0.55+/-0.13 mL x beat(-1) x 100 g myocardium(-1) (P<.05). There was an additive effect of NTG to low-dose (2.5 to 5 microg x kg(-1) x min(-1)) dobutamine on wall thickening in the hibernating region. The improvement of wall thickening of hibernating myocardium with NTG and dobutamine, from 23.7+/-11.1% to 31.1+/-8.9% (P<.001), was associated with an increase in regional coronary flow (P<.01). NTG did not prevent high doses of dobutamine from inducing deterioration of wall thickening in hibernating myocardium. In the infarcted group, no improvement in wall thickening was observed in infarcted regions during NTG infusion, dobutamine infusion, or the combination. CONCLUSIONS: NTG enhances the improvement of wall thickening at low-dose dobutamine and does not prevent high-dose dobutamine from inducing ischemia in hibernating myocardium. Thus, NTG augments the biphasic response of wall thickening and improves the accuracy of DSE for detecting viable myocardium.

Animals↗
PubMed1997

Molecular cloning and analysis of novel cDNAs specifically expressed in adult mouse testes.

In an effort to examine the molecular basis of spermatogenesis, we isolated two types of novel cDNA clones specifically expressed in mouse testes. Type A cDNA (2,071 nucleotides) is predicted to encode 347 amino acid residues, whereas type B cDNA (1,536 nucleotides) has a deletion of 535 bp from nucleotides 1,206 to 1,740 of type A cDNA, probably due to alternative splicing. This deletion causes a frame shift of the putative open reading frame at the C-terminal portion of type A cDNA to encode 366 amino acid residues. Northern blot analysis using adult ICR organs demonstrated that both types of mRNAs were specifically expressed in testis, although type B mRNA was more abundant than type A mRNA. RT-PCR analysis revealed that these two mRNAs were also expressed in immature testes at 1, 5, 11, 16 and 24 days after birth. In situ hybridization analysis of adult ICR testes demonstrated that these two mRNAs were expressed in spermatogonia, Sertoli cells and Leydig cells. In the W/ WV mouse testis which lacks c-kit activity and spermatogonia, but contains Sertoli and Leydig cells, both mRNAs were found to be expressed in the latter two types of cells. We therefore termed these novel clones tsec-1, testis-specifically expressed cDNAs-1. The protein products of tsec-1 may play an important role in mammalian spermatogenesis.

Amino Acid Sequence↗
PubMed1997

Potentiation of cytochrome P450/cyclophosphamide-based cancer gene therapy by coexpression of the P450 reductase gene.

Intratumoral expression of cytochrome P450 2B1 sensitizes tumor cells to the cytotoxic action of the alkylating agent prodrug cyclophosphamide (CPA) and provides a novel strategy for cancer gene therapy that may enhance the selectivity and the effectiveness of this class of antitumor drugs [L. Chen and D. J. Waxman, Cancer Res., 55: 581-589, 1995]. P450-catalyzed drug metabolism is obligatorily dependent on electron input from the flavoenzyme NADPH-P450 reductase (RED), which is widely expressed in many cell types, including tumor cells. Here, we investigate the potential utility of combining RED gene transfer with CPA-based P450 gene therapy. Rat 9L gliosarcoma cells stably expressing either basal or elevated (up to 10-fold increase) levels of RED, in the presence or absence of P450 2B1, were selected and characterized. RED overexpression substantially increased the sensitivity of these cells to CPA, but only when combined with P450 2B1 expression. An enhanced cytotoxic response was also obtained when recombinant adenovirus encoding P450 2B1 was used to deliver the P450 gene to RED-overexpressing tumor cells. CPA cytotoxicity was substantially decreased by the RED inhibitor diphenyleneiodonium chloride or by the P450 inhibitor metyrapone, providing evidence of its dependence on the catalytic contributions of both protein components of the P450 metabolic pathway. Conditioned media from P450 2B1-expressing and RED-overexpressing tumor cells treated with CPA exhibited increased formation of the primary 4-hydroxy metabolite and greater cell contact-independent bystander cytotoxic potential compared to tumor cells containing P450 2B1 and basal levels of RED. Evaluation of the impact of P450/RED combination gene therapy using a s.c. solid tumor model/tumor excision assay revealed a dramatic 50-100-fold increase in tumor cell kill in vivo over that provided by liver drug activation alone. These findings establish the importance of endogenous RED levels as a determinant of the sensitivity of tumor cells to CPA/P450 gene therapy and demonstrate the striking therapeutic effectiveness of an anticancer prodrug activation strategy based on the combination of a cytochrome P450 gene with the gene encoding RED.

Adenoviridae↗
PubMed1997

Redundant expression but selective utilization of nuclear factor of activated T cells family members.

Nuclear factor of activated T cells (NF-AT) complexes regulate the induction of many early T cell activation molecules. Four related proteins can function as the cytoplasmic subunit of NF-AT, and their overlapping expression patterns and the mild phenotype of the NF-ATp null mice suggest that they may be functionally redundant. We characterized the distribution and activation of cytoplasmic NF-AT proteins in mature lymphocytes and found that NF-ATc, NF-ATp, and NF-AT4/x/c3 are co-expressed and co-regulated in mature T and B cells. Each protein forms independent DNA binding complexes, and at physiologic concentrations, NF-ATc and NF-ATp complexes out-compete NF-AT4/x/c3 for occupancy of NF-AT sites from the IL-2, IL-3/granulocyte-macrophage CSF, IL-4, and CD40 ligand genes. This predicts heavily redundant immune regulatory functions of NF-ATp and NF-ATc, but distinct activities for NF-AT4/x/c3. Additionally, Ab interaction with NF-ATp induces high affinity NF-kappaB site interaction, suggesting that nuclear partners may dramatically vary the specificity of the NF-AT family.

Animals↗
PubMed1997

Proteolytic cleavage of the mdm2 oncoprotein during apoptosis.

The mdm2 oncogene encodes a 90-kDa protein that can bind to the p53 tumor suppressor protein and negatively regulate its functions in transcription, cell cycle arrest, and apoptosis. The mdm2 gene is frequently amplified in human sarcomas, which may be responsible for the malignant transformations. We present evidence that the mdm2 oncoprotein is cleaved by an interleukin 1beta-converting enzyme-like protease (caspase) during p53-mediated apoptosis. The protease that cleaves mdm2 has a specificity similar to that of CPP32 (caspase-3), and recombinant caspase-3 is able to cleave mdm2 in vitro. The protease cleavage site has been mapped to between residue 361 and 362 of human mdm2. The proteolytic cleavage removes the COOH-terminal RING finger domain of mdm2, resulting in the loss of RNA binding activity. The p53 binding and inhibition functions of mdm2 are not affected by the cleavage. The cleavage site sequence of mdm2 is evolutionarily conserved, suggesting that regulation by caspase cleavage during apoptosis is an important feature of mdm2.

Amidohydrolases↗
PubMed1997

Gut epithelial cells as targets for gene therapy of hemophilia.

Gut epithelium is an attractive target for gene therapy of hemophilia due to the large number of rapidly dividing cells that should be readily accessible to a wide range of vectors by a noninvasive route of administration. We have performed in vitro tests to determine the suitability of gut epithelial cells for gene transfer, protein synthesis, and secretion of coagulation factors VIII and IX. The results with retroviral vectors indicate that transduced epithelial cells from human, rat, or porcine small or large intestine can synthesize significant amounts of factor VIII or factor IX and that two-thirds or more of the recombinant protein is secreted in a basolateral direction (i.e., away from the lumen and toward underlying capillaries and lymphatics). Furthermore, we have demonstrated that intestinal epithelial cells are susceptible to efficient gene transfer by lipofection and adenovirus vectors. In the case of factor IX, we have produced a high-titer adenovirus vector capable of transducing gut epithelial cells resulting in synthesis of factor IX. The results of our in vitro studies indicate that gene transfer targeting gut epithelium as a new approach to hemophilia gene therapy is rational and merits in vivo studies in hemophilia animal models.

Adenoviridae↗
PubMed1997

Transcriptional regulation of N-acetylglucosaminyltransferase V by the src oncogene.

Transformation of baby hamster kidney fibroblasts by the Rous sarcoma virus causes a significant increase in the GlcNAcbeta(1, 6)Man-branched oligosaccharides by elevating the activity and mRNA transcript levels encoding N-acetylglucosaminyltransferase V (GlcNAc-T V). Elevated activity and mRNA levels could be inhibited by blocking cell proliferation with herbimycin A, demonstrating that Src kinase activity can regulate GlcNAc-T V expression. 5' RACE analysis was used to identify a 3-kilobase 5'-untranslated region from GlcNAc-T V mRNA and locate a transcriptional start site in a 25-kilobase pair GlcNAc-T V human genomic clone. A 6-kilobase pair fragment of the 5' region of the gene contained AP-1 and PEA3/Ets binding elements and, when co-transfected with a src expression plasmid into HepG2 cells, conferred src-stimulated transcriptional enhancement upon a luciferase reporter gene. This stimulation by src could be antagonized by co-transfection with a dominant-negative mutant of the Raf kinase, suggesting the involvement of Ets transcription factors in the regulation of GlcNAc-T V gene expression. The src-responsive element was localized by 5' deletion analysis to a 250-base pair region containing two overlapping Ets sites. src stimulation of transcription from this region was inhibited by co-transfection with a dominant-negative mutant of Ets-2, demonstrating that the effects of the src kinase on GlcNAc-T V expression are dependent on Ets.

Animals↗
PubMed1997

Both overlapping and distinct signaling pathways for somatostatin receptor subtypes SSTR1 and SSTR2 in pituitary cells.

To elucidate the signaling events mediated by specific somatostatin receptor (SSTR) subtypes, we expressed SSTR1 and SSTR2 individually in rat pituitary GH12C1 and F4C1 cells, which lack endogenous somatostatin receptors. In transfected GH12C1 cells, both SSTR1 and SSTR2 coupled to inhibition of Ca2+ influx and hyperpolarization of membrane potential via a pertussis toxin (PTx)-sensitive mechanism. These effects reflected modulation of ion channel activities which are important for regulation of hormone secretion. Somatostatin analogs MK678 and CH275 acted as subtype selective agonists as expected. In transfected F4C1 cells, both SSTR1 and SSTR2 mediated somatostatin-induced inhibition of adenylyl cyclase via a PTx-sensitive pathway. In addition, activation of SSTR2 in F4C1 cells, but not SSTR1, stimulated phospholipase C (PLC) activity and an increase in [Ca2+]i due to release of Ca2+ from intracellular stores. Unlike adenylyl cyclase inhibition, the PLC-mediated response was only partially sensitive to PTx. To determine the structural determinants in SSTR2 necessary for activation of PLC, we constructed chimeric receptors in which domains of SSTR2 were introduced into SSTR1. Chimeric receptors containing only the third intracellular loop, or all three intracellular loops from SSTR2, mediated inhibition of adenylyl cyclase, but failed to stimulate PLC activity as did wild-type SSTR2. Furthermore, the C-terminal tail of SSTR2 was not required for coupling to PLC. Thus, by expressing individual somatostatin receptor subtypes in pituitary cells, we have identified both overlapping and distinct signaling pathways for SSTR1 and SSTR2, and have shown that sequences other than simply the intracellular domains are required for SSTR2 to couple to the PLC signaling pathway.

Adenylate Cyclase Toxin↗
PubMed1997

Antigenic cancer cells grow progressively in immune hosts without evidence for T cell exhaustion or systemic anergy.

One enigma in tumor immunology is why animals bearing malignant grafts can reject normal grafts that express the same nonself-antigen. An explanation for this phenomenon could be that different T cell clones react to the normal graft and the malignant cells, respectively, and only the tumor-reactive clonotypes may be affected by the growing tumor. To test this hypothesis, we used a T cell receptor transgenic mouse in which essentially all CD8(+) T cells are specific for a closely related set of self-peptides presented on the MHC class I molecule Ld. We find that the tumor expressed Ld in the T cell receptor transgenic mice but grew, while the Ld-positive skin was rejected. Thus, despite an abundance of antigen-specific T cells, the malignant tissue grew while normal tissue expressing the same epitopes was rejected. Therefore, systemic T cell exhaustion or anergy was not responsible for the growth of the antigenic cancer cells. Expression of costimulatory molecules on the tumor cells after transfection and preimmunization by full-thickness skin grafts was required for rejection of a subsequent tumor challenge, but there was no detectable effect of active immunization once the tumor was established. Thus, the failure of established tumors to attract and activate tumor-specific T cells at the tumor site may be a major obstacle for preventive or therapeutic vaccination against antigenic cancer.

Animals↗
PubMed1997

Crystallographic study of yeast copper amine oxidase.

The copper-containing amine oxidase from the yeast Hansenula polymorpha (YAO) has been crystallized and partially solved by molecular replacement. It catalyzes the oxidative deamination of primary amines by molecular oxygen to the corresponding aldehydes, ammonia and hydrogen peroxide. It contains a covalently bound redox cofactor, topa quinone, generated by post-translational modification of a single tyrosine side chain. The crystals of YAO are orthorhombic, with space-group symmetry P2(1)2(1)2(1) and unit-cell dimensions a = 138.8, b = 148.2, c = 234.0 A and diffract X-rays beyond 2.0 A resolution. Solution by molecular replacement using the E. coli amine oxidase structure [Parsons, Convery, Wilmot, Yadav, Blakeley, Corner, Philips, McPherson & Knowles (1995). Structure, 3, 1171-1184] as a search model reveals that there are three dimers in the asymmetric unit in a trigonal arrangement having 32 point-group symmetry. The solution agrees well with the self-rotation function of YAO. The non-crystallographic threefold axis lies parallel to a crystallographic twofold screw axis and each dimer has twofold symmetry. Phases from the refined model based on the molecular-replacement solution were used to solve one heavy-atom derivative. Model building from the unbiased isomorphous replacement phases is in progress.

Journal Article↗