Search PubMed⌕ Search

Biomedical subjects

X Chen

Publications and source records attributed to X Chen.

At least 505 records · Page 28Linked to original sources
PubMed2000

Interferon alpha in combination with GM-CSF induces the differentiation of leukaemic antigen-presenting cells that have the capacity to stimulate a specific anti-leukaemic cytotoxic T-cell response from patients with chronic myeloid leukaemia.

Although interferon alpha (IFN-alpha) is able to induce haematological remission in 60-80% of patients with chronic myeloid leukaemia (CML) in early chronic phase, major cytogenetic remissions are only achievable in 30-40%. Recent clinical data suggest that the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) to IFN-alpha therapy can significantly improve the cytogenetic response in some patients, although the mechanism remains unknown. We hypothesized that the combination of GM-CSF and IFN-alpha induces the differentiation of dendritic cells, which subsequently stimulates a specific anti-leukaemic response. Monocytes from CML patients were cultured in GM-CSF and interleukin (IL)-4 (GM/IL-4)or in GM-CSF and IFN-alpha (GM/IFN-alpha). After 7 d, the number of cells exhibiting typical antigen-presenting cell (APC) morphology was equal in both groups, and fluorescence in situ hybridization (FISH) analysis confirmed that the APCs generated with GM/IFN-alpha were of leukaemic origin. Phenotypically, both sets of APCs expressed typical surface markers; however, CD86, CD83, CD11c, HLA-ABC and HLA-DR expression was significantly higher in the GM/IFN-alpha APCs, whereas CD1a expression was significantly lower. In mixed lymphocyte reactions (MLR), GM/IFN-alpha APCs stimulated the proliferation of allogeneic T cells significantly better than GM/IL-4 APCs. However, both groups of APCs stimulated autologous T-cell proliferation equally. Finally, we assessed the ability of GM/IFN-alpha APCs to induce a leukaemia-specific cytotoxic T-cell response. Some samples generated cytotoxic T lymphocytes (CTLs) that specifically lysed bcr-abl-positive target cells. These data show that the combination of GM-CSF and IFN-alpha, when used in vitro, induces the differentiation of malignant APCs with potent T-cell stimulatory capacity. Although there is no in vivo evidence to support these findings, it is possible that, when administered to CML patients, GM-CSF in combination with IFN-alpha results in the generation of highly stimulatory leukaemic APCs.

Antigen-Presenting Cells↗
PubMed2000

Pretreatment with ramiprilat induces cardioprotection against free radical injury in guinea-pig isolated heart: involvement of bradykinin, protein kinase C and prostaglandins.

1. Pretreatment with ramiprilat, an angiotensin-converting enzyme (ACE) inhibitor, induced cardioprotection and its possible mechanism of action was investigated in guinea-pig Langendorff perfused heart. 2. Superoxide anion (*O2-), produced by hypoxanthine and xanthine oxidase, and the 1,1-diphenyl-2-picryl-hydrazyl (DPPH) free radical were used for triggering free radical injury in cardiac tissue. 3. 1,1-Diphenyl-2-picryl-hydrazyl and *O2- significantly reduced left ventricular developed pressure (LVDP), +/-dP/dt(max), heart rate and coronary flow. Left ventricular end-diastolic pressure (LVEDP) was elevated and lactate dehydrogenase (LDH) leakage and the formation of thiobarbituric acid-reactive substances (TBARS) formation were significantly increased. 4. Pretreatment with ramiprilat induced cardioprotection against DPPH and *O2- free radical injury. Cardiac functions (LVDP, LVEDP and +/-dP/dt(max)) were significantly improved. Both LDH and TBARS were reduced. 5. HOE 140 (a selective bradykinin B2 receptor antagonist), calphostin C (a protein kinase C (PKC) inhibitor) and indomethacin (a cyclo-oxygenase inhibitor) all abolished the cardiac protective effect of ramiprilat. However, N(G)-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, had no effect. 6. In conclusion, ramiprilat pretreatment induces cardioprotection against either DPPH or *O2- free radical injury. The protective effect depends on activation of B2 receptors and PKC. Prostaglandin synthesis is also involved.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Factors that affect results of the 13C urea breath test in Japanese patients.

BACKGROUND: The 13C urea breath test (UBT) is considered to be the most accurate way of diagnosing Helicobacter pylori infection. Our objective was to investigate the accuracy of the UBT in Japanese patients and the association of UBT values with histological findings. MATERIALS AND METHODS: A total of 169 consecutive patients were studied by endoscopy with histology, by serology with IgG antibody and test serum pepsinogen (PG), and by UBT. The association between UBT values and histological findings and the PG I / II ratio were analyzed in H. pylori-positive patients. RESULTS: Of 169 Japanese patients, 135 were H. pylori-positive on both histology and serology analysis, 27 were H. pylori-negative on both histology and serology analysis, and 7 patients showed differing results. Using a cutoff value of 2.5 per thousand, test sensitivity was 100%, while specificity was 96%. Among the 135 H. pylori-positive patients, a significant relation was observed between UBT value and H. pylori colonization density of the corpus and antrum, neutrophil activity of the antrum, atrophy, and intestinal metaplasia of the corpus in the H. pylori-positive patients. Also, UBT values correlated with the PG I /II ratio. In multivariate analysis, the PG I /II ratio was the most important factor related to UBT values (odds ration [OR], 4. 99; 95% confidence interval, 1.60-15.55). CONCLUSIONS: The UBT is an accurate method for detecting H. pylori infection in the Japanese population, which shows a high prevalence of atrophic gastritis. Values are affected by H. pylori infection and by the severity of atrophic gastritis.

Adolescent↗
PubMed2000

The familial mediterranean fever protein interacts and colocalizes with a putative Golgi transporter.

The biological function of pyrin, the protein mutated in Familial Mediterranean Fever (FMF), has not been elucidated. Based on sequence homology, a transcription factor activity was proposed for this neutrophil-specific protein. In a yeast two-hybrid assay, neither transcription activation activity nor any self interaction was detected for pyrin. Screening of an expression cDNA library of peripheral blood leukocytes using as bait the carboxyl portion of pyrin (amino acids 557-781), which contains most of the FMF mutations, led to the identification of P/M-IP1 (pyrin/marenostrin interacting protein 1). A splice variant of P/M-IP1, GTC-90, had previously been described as a component of the 13S hetero-oligomeric protein complex that stimulates in vitro Golgi transport. We have now shown that P/M-IP1 colocalizes with pyrin in the perinuclear cytoplasm of Cos-7 cells and that the interaction between these two proteins is impaired by FMF causing mutations in pyrin. These data suggest that, at some stage of its functional pathway, pyrin resides in the cytoplasm and might be involved in, or impacted by, cellular protein sorting by the Golgi apparatus. The data also imply that P/M-IP1 may be involved in the abnormal inflammatory response that occurs in patients with FMF.

Adaptor Proteins, Vesicular Transport↗
PubMed2000

Protein gamma-radiolysis in frozen solutions is a macromolecular surface phenomenon: fragmentation of lysozyme, citrate synthase and alpha-lactalbumin in native or denatured states.

PURPOSE: To test whether radiolysis-induced fragmentation in frozen aqueous protein solution is dependent on solvent access to the surface of the protein or to the molecular mass of the polypeptide chain. MATERIALS AND METHODS: 60Co gamma-irradiation of three proteins at -78 degrees C: lysozyme, citrate synthase and alpha-lactalbumin in their native state, with or without bound substrate, or denatured (random coil in urea/acid-denatured state). RESULTS: By SDS-polyacrylamide gel electrophoresis/analysis of the protein-fragmentation process, it was found that for a given protein D37 values (dose to decrease the measured amount of protein, with an unaltered polypeptidic chain, to 37% of the initial amount) varied according to the state of the protein. D37 for denatured proteins was always much smaller than for native states, indicating a greater susceptibility to fragmentation. In urea, contrary to the native state, no well-defined fragments were observed. Radiolysis decay constants (K= 1/D37) increased with solvent-accessible surface area of these proteins estimated from their radii of gyration in the various states. This is shown also in previous data on native or SDS-denatured proteins. Denatured proteins which have a large surface area exposed to the solvent compared with native ones are more fragmented at equal doses. CONCLUSIONS: It is concluded that D37 is directly related to the exposed surface area and not to the molecular mass of the polypeptide chain.

Animals↗
PubMed2000

Predicting the standard enthalpy (deltaH0f) and entropy (S0) of alkanes by artificial neural networks.

Artificial Neural Networks (ANNs) with Extended Delta-Bar-Delta (EDBD) back propagation learning algorithm have been developed to predict the standard enthalpy and entropy of 87 acyclic alkanes. Molecular weight, boiling point and density of the compounds were used as input parameters. The network's architecture and parameters were optimized to give maximum performances. The best network was a 3-6-2 ANN, and the optimum learning epoch was about 1320. The results show that the maximum relative errors of enthalpy and entropy are less than 3%. They reveal that the performances of ANNs for predicting the enthalpy and entropy of alkanes are satisfying.

Algorithms↗
PubMed2000

Mechanism of antihypertensive effect of dietary potassium in experimental volume expanded hypertension in rats.

Dietary potassium supplementation lowers blood pressure (BP) and attenuates complications in hypertensive subjects, particularly those with the low renin volume expanded (LRVE) variety. We and others have shown that the plasma level of a digitalis like substance (DLS) is elevated in this type of hypertension. We therefore, examined the effect of increases in dietary potassium on the plasma level of endogenous DLS, myocardial and renal Na+, K+-ATPase (NKA) activities, BP, and renal excretory function in reduced renal mass (RRM)-salt hypertension in the rat, a classical model of LRVE hypertension. 70% RRM rats were divided in 4 groups, namely those consuming: 1) a sodium free and normal potassium (1.3% as KCl) diet (RRM-0 Na), 2) a normal sodium and normal potassium diet (RRM-NaK), 3) a normal sodium and high potassium (2 X normal) diet (RRM-Na2K), and 4) a normal sodium and 4 times normal potassium diet (RRM-Na4K). At the end of 4 weeks of dietary treatment, direct BP was recorded, plasma level of DLS determined by bioassay and with a radioimmunoassay for digoxin (DIF) and myocardial and renal NKA activities were measured. As expected, compared to RRM-0Na rats, RRM-NaK rats developed hypertension. BP increased significantly less in RRM-Na2K, whereas BP did not increase in RRM-Na4K rats. Hypertension in RRM-NaK rats was associated with an increase in plasma DLS and DIF and decrease in renal and myocardial NKA activities. DLS was increased (DIF was not changed) and myocardial NKA also decreased in rats consuming double potassium. However, quadrupling potassium in the diet (RRM-Na4K) normalized DLS and DIF and increased myocardial and renal NKA activities, compared to RRM-0Na rats. Also compared to RRM-0Na, water consumption, urinary volume excretion, sodium, and potassium increased in the other 3 groups, more so in RRM-Na4K rats. These data show that quadrupling the potassium in the diet prevents the BP increase in RRM rats and this is associated with diuresis/natriuresis and normalization of DLS, perhaps because the diuresis/natriuresis normalizes blood volume.

Animals↗
PubMed2000

Cytotoxic activity of 2',2'-difluorodeoxycytidine (gemcitabine) in poorly differentiated thyroid carcinoma cells.

Poorly differentiated and anaplastic thyroid cancers are aggressive and usually fatal neoplasms, despite aggressive treatment. We performed an in vitro study to assess the activity of gemcitabine (2',2' difluorodeoxycytidine), a new fluorinated nucleoside analogue, against three poorly differentiated human thyroid carcinoma cell lines (ARO, WRO, and NPA). Each cell line was exposed to increasing concentrations of gemcitabine (0.0003 to 3000 mumol/L) for 24, 48, and 72 hours. Maximal reduction in cell viability was seen after 72 hours of gemcitabine for all three cell lines as measured by 3-(4,5-dimethyl thiazolyl-2)-2,5-diphenyl tetrazolium bromide (MTT) assay. NPA cells were more sensitive than the other two lines after 24 and 48 hours of exposure, but all cell lines were similarly sensitive at 72 hours. A cytotoxic effect was confirmed by DNA assay of adherent cells. IC50 concentrations for reduction in cell viability ranged from 0.731 and 0.986 mumol/L for each cell line after 72 hours of exposure. These concentrations are lower than serum levels in phase 1 clinical trials of gemcitabine for other malignancies. In summary, gemcitabine has activity against poorly differentiated thyroid cancer cell lines in vitro. In vivo studies using xenograft models are warranted to confirm these promising observations.

Antimetabolites, Antineoplastic↗
PubMed2000

Oxidative damage in an esophageal adenocarcinoma model with rats.

Oxidative damage has long been related to carcinogenesis in human cancers and animal cancer models. Recently a rat esophageal adenocarcinoma (EAC) model was established in our laboratory by using esophagoduodenal anastomosis (EDA) plus iron supplementation. Our previous study suggested that iron supplementation enhanced inflammation and the production of reactive nitrogen species in the esophageal epithelium, which could contribute to esophageal adenocarcinogenesis. Here we further characterized oxidative damage in this model. We were particularly interested in how excess iron was deposited in the esophagus, and which cells were targeted by oxidative damage. Male Sprague-Dawley rats received iron supplementation (50 mg Fe/kg/month, i.p.) starting 4 weeks after EDA. The animals were killed at 11, 30 or 35 weeks after surgery. EAC appeared as early as week 11 after surgery, and increased over time, up to 60% at 35 weeks after surgery. All EACs were well-differentiated mucinous adenocarcinoma at the squamocolumnar junction. Iron deposition was found at the squamocolumnar junction and in the area with esophagitis. Esophageal iron overload could result from transient increase of blood iron after i.p. injection, and the overexpression of transferrin receptor in the premalignant columnar-lined esophagus (CLE) cells. Oxidative damage to DNA (8-hydroxy-2'-deoxyguanosine), protein (carbonyl content) and lipid (thiobarbituric acid reactive substance) in the esophagus was significantly higher than that of the non-operated control. CLE cells were believed to be the target cells of oxidative damage because they overexpressed heme oxygenase 1 and metallothionein, both known to be responsive to oxidative damage. We propose that oxidative damage plays an important role in the formation of EAC in the EDA model, and a similar situation may occur in humans with gastroesophageal reflux and iron over-nutrition.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2000

Genetic analysis of the Drosophila DNAprim gene. The function of the 60-kd primase subunit of DNA polymerase opposes the fat facets signaling pathway in the developing eye.

The Drosophila DNAprim gene encodes the large subunit (60 kD) of DNA primase, the part of DNA polymerase alpha that synthesizes RNA primers during DNA replication. The precise function of the 60-kD subunit is unknown. In a mutagenesis screen for suppressors of the fat facets (faf) mutant eye phenotype, we identified mutations in DNAprim. The faf gene encodes a deubiquitinating enzyme required specifically for patterning the compound eye. The DNA sequences of four DNAprim alleles were determined and these define essential protein domains. We show that while flies lacking DNAprim activity are lethal, flies with reduced DNAprim activity display morphological defects in their eyes, and unlike faf mutants, cell cycle abnormalities in larval eye discs. Mechanisms by which DNA primase levels might influence the faf-dependent cell communication pathway are discussed.

Alleles↗
PubMed2000

In vivo Structure/Function analysis of the Drosophila fat facets deubiquitinating enzyme gene.

The Drosophila Fat facets protein is a deubiquitinating enzyme required for patterning the developing compound eye. Ubiquitin, a 76-amino-acid polypeptide, serves as a tag to direct proteins to the proteasome, a protein degradation complex. Deubiquitinating enzymes are a large group of proteins that cleave ubiquitin-protein bonds. Fat facets belongs to a class of deubiquitinating enzymes called Ubps that share a conserved catalytic domain. Fat facets is unique among them in its large size and also because Fat facets is thought to deubiquitinate a specific substrate thereby preventing its proteolysis. Here we asked which portions of the Fat facets protein are essential for its function. P-element constructs that express partial Fat facets proteins were tested for function. In addition, the DNA sequences of 12 mutant fat facets alleles were determined. Finally, regions of amino acid sequence similarity in 18 Drosophila Ubps revealed by the Genome Project were identified. The results indicate functions for specific conserved amino acids in the catalytic region of Fat facets and also indicate that regions of the protein both N- and C-terminal to the catalytic region are required for Fat facets function.

Alleles↗
PubMed2000

Carbon dioxide absorbents containing potassium hydroxide produce much larger concentrations of compound A from sevoflurane in clinical practice.

UNLABELLED: We investigated the concentrations of degraded sevoflurane Compound A during low-flow anesthesia with four carbon dioxide (CO(2)) absorbents. The concentrations of Compound A, obtained from the inspiratory limb of the circle system, were measured by using a gas chromatograph. In the groups administered 2 L/min fresh gas flow with 1% sevoflurane, when the conventional CO(2) absorbents, Wakolime(TM) (Wako, Tokyo, Japan) and Drägersorb(TM) (Dräger, Lübeck, Germany), were used, the concentrations of Compound A increased steadily from a baseline to 14.3 ppm (mean) and 13.2 ppm, respectively, at 2 h after exposure to sevoflurane. In contrast, when the other novel types of absorbents containing decreased or no potassium hydroxide/sodium hydroxide, Medisorb(TM) (Datex-Ohmeda, Louisville, CO) and Amsorb(TM) (Armstrong, Coleraine, Northern Ireland), were used, Compound A remained at baseline (<2 ppm) throughout the study. In the groups administered 1 L/min fresh gas flow with 2% sevoflurane, Wakolime(TM) and Drägersorb(TM) produced much larger concentrations of Compound A (35.4 ppm and 34.2 ppm, respectively) at 2 h after exposure to sevoflurane. Medisorb(TM) showed measurable concentrations of Compound A (8.6 ppm at 2 h), but they were significantly smaller than those produced by the two conventional absorbents. In contrast, when Amsorb(TM) was used, Compound A concentrations remained at baseline throughout the study period. IMPLICATIONS: Carbon dioxide absorbents containing potassium hydroxide/sodium hydroxide produce much larger concentrations of Compound A from sevoflurane in clinical practice. An absorbent containing neither potassium hydroxide nor sodium hydroxide produces the smallest concentrations of Compound A.

Absorption↗
PubMed2000

Interaction between volatile anesthetics and hypoxia in porcine tracheal smooth muscle.

UNLABELLED: We investigated the direct interaction between the volatile anesthetics, isoflurane and sevoflurane, and hypoxia in porcine tracheal smooth muscle in vitro by simultaneously measuring muscle tension and intracellular concentration of free Ca(2+) ([Ca2+]i). Muscle tension was measured by using an isometric transducer, and [Ca2+]i was measured by using fura-2, an indicator of Ca2+. Under the condition of bubbling with 95% O2/5% CO2, [Ca2+]i was increased by 1 microM carbachol with a concomitant contraction. Volatile anesthetics significantly inhibited both carbachol-induced muscle contraction and increase in [Ca2+]i. Hypoxia bubbled with 95% N(2)/5% CO2 inhibited the muscle contraction by 30% with an increase in [Ca2+]i by 20%. Exposure to hypoxia substantially enhanced the inhibitory effects of these anesthetics on carbachol-induced muscle contraction, whereas the decreases in [Ca2+]i were significantly prevented by hypoxia. Under Ca2+-free conditions, hypoxia significantly decreased the muscle contraction by 20%; however, it still increased [Ca2+]i by 15%. Exposure to the anesthetics significantly enhanced the inhibitory effect of hypoxia on the muscle contraction; however, it appeared to have little effect on [Ca2+]i. Hypoxia inhibits airway smooth muscle contraction independently of intracellular Ca2+, and it substantially potentiates the inhibitory effects of volatile anesthetics on airway smooth muscle contraction. IMPLICATIONS: Hypoxia inhibits agonist-induced tracheal smooth muscle contraction with an increase in free Ca2+ [Ca2+]i, which comes from intracellular Ca2+ stores. Hypoxia also potentiates the inhibitory effect of volatile anesthetics on airway smooth muscle contraction. Conversely, there is a possibility that the treatment of asthmatic patients with oxygen partially attenuates the inhibitory effect of volatile anesthetics on airway smooth muscle contractility.

Analysis of Variance↗
PubMed2000

Estrogen modulates a large conductance chloride channel in cultured porcine aortic endothelial cells.

Estrogen is known to exert a protective effect on cardiovascular disease, but the mechanism for this effect is unclear. It has, however, been reported that estrogen and antiestrogen modify ionic currents and membrane potential in various cells. The aim of this study was to clarify whether the chloride channel of aortic endothelial cells was, in fact, modified by estrogen and antiestrogen with inside-out patch and cell-attached patch recording methods. Tamoxifen activated a large-conductance (368 +/- 23 pS, n = 6, in symmetric 150 mM Cl- solution) chloride channel of endothelial cells grown in the presence of 1 microg/ml colchicine. The channels were activated mainly between +/-40 mV, but were inactivated at more extreme potentials. The open probability of channels in cell-attached patches increased from <0.01 to 0.37 +/- 0.08 (n = 8) when cells were treated with 15 microM tamoxifen. This effect can be blocked by 17beta-estradiol, but not by progesterone. The results showed that tamoxifen increased chloride channel activity in the presence of colchicine in cultured endothelial cells, and this action was suppressed by 17beta-estradiol but not by progesterone. This rapid effect by estrogens suggests that these hormones exert nongenomic, short-term activity and do not appear to affect the nuclear estrogen receptor. With these effects, estrogen and antiestrogen bind to the endothelial cells plasma membrane site and subsequently may activate an intracellular second messenger pathway.

Animals↗
PubMed2000

Parallel genotyping of human SNPs using generic high-density oligonucleotide tag arrays.

Large scale human genetic studies require technologies for generating millions of genotypes with relative ease but also at a reasonable cost and with high accuracy. We describe a highly parallel method for genotyping single nucleotide polymorphisms (SNPs), using generic high-density oligonucleotide arrays that contain thousands of preselected 20-mer oligonucleotide tags. First, marker-specific primers are used in PCR amplifications of genomic regions containing SNPs. Second, the amplification products are used as templates in single base extension (SBE) reactions using chimeric primers with 3' complementarity to the specific SNP loci and 5' complementarity to specific probes, or tags, synthesized on the array. The SBE primers, terminating one base before the polymorphic site, are extended in the presence of labeled dideoxy NTPs, using a different label for each of the two SNP alleles, and hybridized to the tag array. Third, genotypes are deduced from the fluorescence intensity ratio of the two colors. This approach takes advantage of multiplexed sample preparation, hybridization, and analysis at each stage. We illustrate and test this method by genotyping 44 individuals for 142 human SNPs identified previously in 62 candidate hypertension genes. Because the hybridization results are quantitative, this method can also be used for allele-frequency estimation in pooled DNA samples.

Blood Pressure↗
PubMed2000

Initial binding of preproteins involving the Toc159 receptor can be bypassed during protein import into chloroplasts.

Two integral outer envelope GTPases, Toc34 and Toc86, are proposed to regulate the recognition and translocation of nuclear-encoded preproteins during the early stages of protein import into chloroplasts. Defining the precise roles of Toc86 and Toc34 has been complicated by the inability to distinguish their GTPase activities. Furthermore, the assignment of Toc86 function is rendered equivocal by recent reports suggesting that the standard protocol for the isolation of chloroplasts results in significant proteolysis of Toc86 (B. Bolter, T. May, J. Soll [1998] FEBS Lett 441: 59-62; G. Schatz [1998] Nature 395: 439-440). We demonstrate that Toc86 corresponds to a native protein of 159 kD in pea (Pisum sativum), designated Toc159. We take advantage of the proteolytic sensitivity of Toc159 to selectively remove its 100-kD cytoplasmic GTPase domain and thereby distinguish its activities from other import components. Proteolysis eliminates detectable binding of preproteins at the chloroplast surface, which is consistent with the proposed role of Toc159 as a receptor component. Remarkably, preprotein translocation across the outer membrane can occur in the absence of the Toc159 cytoplasmic domain, suggesting that binding can be bypassed. Translocation remains sensitive to GTP analogs in the absence of the Toc159 GTP-binding domain, providing evidence that Toc34 plays a key role in the regulation of translocation by GTP.

Amino Acid Sequence↗
PubMed2000

Potassium sodium tin selenide, K3NaSn3Se8

The title compound, tripotassium sodium tritin octaselenide, K(3)NaSn(3)Se(8), has a molecular (zero-dimensional) structure containing trimeric [Sn(3)Se(8)](4-) units which consist of three edge-sharing SnSe(4) tetrahedra. The [Sn(3)Se(8)](4-) anions and the tetrahedrally coordinated Na(+) cations are arranged in an alternating fashion along the c axis to form SiS(2)-like chains, which are then separated by eight-coordinate K(+) cations. The Sn-Se bond distances are normal, being in the range 2.477 (1)-2.612 (1) A.

Journal Article↗