Biomedical subjects

X Chen

Publications and source records attributed to X Chen.

At least 145 records · Page 8Linked to original sources

PubMed2002

Structure of complement receptor (CR) 2 and CR2-C3d complexes.

Using X-ray crystallography, we have determined the structure of the first two short consensus repeats (SCRs) of human complement receptor (CR) 2 in complex with C3d. These studies revealed: (i) a primary site of interaction for C3d within SCR2 of CR2, (ii) a hydrophobic patch holding SCR1 to SCR2 in a rigid V-shape, (iii) a dimer formed by interactions between SCR1 of each molecule, (iv) several non-linear sequences on C3d that interact with CR2 and (v) mutations of C3d amino acids within the co-crystal interface that resulted in decreased binding. In addition, a polymorphism that results in decreased C3d binding and introduces a new glycosylation site predicted to disrupt the dimer interface was found in the New Zealand White autoimmune mouse strain. Although the co-crystal complex results are in agreement with a subset of prior studies, our additional findings, which demonstrate an extended SCR1-SCR2 structure in solution and differences in the kinetics of ligand-receptor interactions with longer forms of CR2, have suggested a more complex receptor-ligand interaction. To characterize this interaction further, several approaches directed at the determination of solution phase interactions as well as the analysis of the three-dimensional structure of CR2 alone and key CR2 mutants will be necessary.

Animals↗

PubMed2002

Obesity, coronary heart disease risk factors and diabetes in Chinese: an approach to the criteria of obesity in the Chinese population.

The aim of this work was to study the relationship between excess body weight and the risks of hypertension and diabetes in the population of northeastern China. Subsections of a cross-sectional survey in Da Qing City were used to assess the relationship of excess weight to risk factors for coronary heart disease (CHD). A 6-year prospective study also assessed the probability of developing Type 2 diabetes. A total of 2856 adults (25-70 years of age) were assessed cross-sectionally and 629 non-diabetic subjects of similar age were followed-up for 6 years. Blood pressure, plasma fasting glucose, triglycerides, high-density lipoporotein (HDL) cholesterol and fibrinogen levels were measured as well as weight, height and waist and hip circumferences. About 45% of adults had a body mass index (BMI) of > or =25.0. Risk factors increased with increasing BMI from a baseline value of 21.0: at a BMI of 23.0-24.9, the risk of hypertension and hypertriglyceridaemia doubled; the risk increased threefold at a BMI of 25.0-26.9. The prevalence of Type 2 diabetes increased progressively in women within the normal BMI range and in men from a BMI of 25.0. Type 2 diabetes was four times as common if the BMI was >27.0. Increasing waist measurements predicted 10-fold increases in hypertension and a three-to-five times increased risk of diabetes. Suitable waist cut-off points were 85cm for men and 80cm for women, with statistical analysis showing waist as the more dominant predictor of risk than age, waist-to-hip ratios or BMIs. Hence, small increases in BMI, and particularly in waist circumference, predict a substantial increase in the risk of diabetes and risk for CHD, especially hypertension, in Chinese adults.

Adult↗

PubMed2002

ADME-AP: a database of ADME associated proteins.

Drug absorption, distribution, metabolism and excretion (ADME) often involve interaction of a drug with specific proteins. Knowledge about these ADME-associated proteins is important in facilitating the study of the molecular mechanism of disposition and individual response as well as therapeutic action of drugs. It is also useful in the development and testing of pharmacokinetics prediction tools. Several databases describing specific classes of ADME-associated proteins have appeared. A new database, ADME-associated proteins (ADME-AP), is introduced to provide comprehensive information about all classes of ADME-associated proteins described in the literature including physiological function of each protein, pharmacokinetic effect, ADME classification, direction and driving force of disposition, location and tissue distribution, substrates, synonyms, gene name and protein availability in other species. Cross-links to other databases are also provided to facilitate the access of information about the sequence, 3D structure, function, polymorphisms, genetic disorders, nomenclature, ligand binding properties and related literatures of each protein. ADME-AP currently contains entries for 321 proteins and 964 substrates.

Databases, Protein↗

PubMed2002

Hyperglycemia induces insulin resistance on angiotensinogen gene expression in diabetic rat kidney proximal tubular cells.

Clinical and animal studies have shown that treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II (Ang II) receptor antagonists slows the progression of nephropathy in diabetes, indicating that Ang II plays an important role in its development. We have reported previously that insulin inhibits the stimulatory effect of high glucose levels on angiotensinogen (ANG) gene expression in rat immortalized renal proximal tubular cells (IRPTCs) via the mitogen-activated protein kinase (p44/42 MAPK) signal transduction pathway. We hypothesize that the suppressive action of insulin on ANG gene expression might be attenuated in renal proximal tubular cells (RPTCs) of rats with established diabetes. Two groups of male adult Wistar rats were studied: controls and streptozotocin (STZ)-induced diabetic rats at 2, 4, 8 and 12 weeks post-STZ administration. Kidney proximal tubules were isolated and cultured in either normal glucose (i.e. 5 mM) or high glucose (i.e. 25 mM) medium to determine the inhibitory effect of insulin on ANG gene expression. Immunoreactive rat ANG (IR-rANG) in culture media and cellular ANG mRNA were measured by a specific radioimmunoassay and reverse transcription-polymerase chain reaction assay respectively. Activation of the p44/42 MAPK signal transduction pathway in rat RPTCs was evaluated by p44/42 MAPK phosphorylation employing a PhosphoPlus p44/42 MAPK antibody kit. Insulin (10(-7) M) inhibited the stimulatory effect of high glucose levels on IR-rANG secretion and ANG gene expression and increased p44/42 MAPK phosphorylation in normal rat RPTCs. In contrast, it failed to affect these parameters in diabetic rat RPTCs. In conclusion, our studies demonstrate that hyperglycaemia induces insulin resistance on ANG gene expression in diabetic rat RPTCs by altering the MAPK signal transduction pathway.

Angiotensinogen↗

PubMed2002

Efficient method to generate homologous recombinant baculovirus genomes in E. coli.

Here we describe a convenient method to generate homologous recombinant baculoviral genomes in E. coli. The recombination takes place with the aid of recombination enzymes provided by the phage lambda Red system between a bacmid (a baculoviral genome that can replicate in bacteria) and a linear fragment. Proof of concept was provided when the cathepsin gene (v-cath) of the Helicoverpa armigera single nucleocapsid nucleopolyhedrovirus (HaSNPV) was replaced by the chloramphenicol resistance gene (CmR). First, CmR was inserted between the flanking sequences of the HaS-NPV v-cath. Each of the flanking regions was about 1 kb. The fragment was linearized and electroporated into bacteria containing both the HaSNPV bacmid and the lambda Red system. Recombinant bacmids resistant to chloramphenicol were selected. In comparison to the standard co-transfection/plaque assays, this method significantly reduces the time required to construct baculovirus knockout mutants. It may also be useful in the manipulation of other large viral genomes.

Baculoviridae↗

PubMed2002

The promise and obstacle of p53 as a cancer therapeutic agent.

p53 is a tumor suppressor gene that is mutated in greater than 50% of human cancers. The action of p53 as a tumor suppressor involves inhibition of cell proliferation through cell cycle arrest and/or apoptosis. Loss of p53 function therefore allows the uncontrolled proliferation associated with cancerous cells. While design of most anti-cancer agents has focused on targeting and inactivating cancer promoting targets, such as oncogenes, recent attention has been given to restoring the lost activity of tumor suppressor genes. Because the loss of p53 function is so prevalent in human cancer, this protein is an ideal candidate for such therapy. Several gene therapeutic strategies have been employed in the attempt to restore p53 function to cancerous cells. These approaches include introduction of wild-type p53 into cells with mutant p53; the use of small molecules to stabilize mutant p53 in a wild-type, active conformation; and the introduction of agents to prevent degradation of p53 by proteins that normally target it. In addition, because mutant p53 has oncogenic gain of function activity, several approaches have been investigated to selectively target and kill cells harboring mutant p53. These include the introduction of mutant viruses that cause cell death only in cells with mutant p53 and the introduction of a gene that, in the absence of functional p53, produces a toxic product. Many obstacles remain to optimize these strategies for use in humans, but, despite these, restoration of p53 function is a promising anti-cancer therapeutic approach.

Genes, p53↗

PubMed2002

Isoflavones and bone: animal and human evidence of efficacy.

Previous reports of soy extracts and isoflavone-enriched preparations studied in animals and humans have found that these molecules, when given at appropriate doses, have positive effects on the skeleton, including improvements in bone mineral content (BMC) and bone mineral density (BMD). A reduction in fracture risk of human subjects has not yet been shown in a prospective trial. Isoflavones, which exist in significant amounts only in soybeans, exert estrogen-like effects in human bone cells because of their unique organic structures that are similar to that of estradiol. The discovery of the b isoform of the estrogen receptor (ER) suggests that the molecular regulation of bone remodeling by estrogens, or estrogen-like molecules, including isoflavones, is more complex than previously thought. Depending on the type of ER present in a particular tissue, isoflavones may act as weak estrogen agonists or as weak estrogen antagonists. For example, isoflavones act as weak estrogen agonists in osteoblasts, but in reproductive cells, such as in the breast and uterus, they behave as weak estrogen antagonists. Weak agonistic effects of the isoflavones include stimulation of osteoblast proliferation and differentiation and increasing the production of cytokines that may inhibit osteclastic activity. The selective beneficial effects of estrogen-like molecules in bone tissues, compared to the anti-estrogenic effects in cells of reproductive tissues, make isoflavones attractive for the promotion of bone health. Relatively greater values of BMC and BMD of Asian populations with high consumption of soy isoflavones throughout life, compared to those with lower intakes, indirectly support the skeletal benefits of this pattern of intake of these estrogen-like molecules.

Journal Article↗

PubMed2001

Identification of two novel human dynein light chain genes, DNLC2A and DNLC2B, and their expression changes in hepatocellular carcinoma tissues from 68 Chinese patients.

Two full-length cDNAs, DNLC2A and DNLC2B, were cloned and characterized. Their open reading frames respectively encode 96 amino acids which are most closely homologous to roadblock/LC7, one member of an ancient dynein light chain protein family, conserved in nematode, fruit fly, mouse and rat. The DNLC2A was expressed in 12 of 16 human tissues examined, with especially strong expression in heart, liver and brain, whereas there was weak expression in lung, prostate, testis, small intestine and colon. The expression of DNLC2B was generally high compared with that of DNLC2A except in liver. Northern blotting and/or semi-quantitative RT-PCR analysis examined the expression changes of DNLC2A and DNLC2B in 68 hepatocellular carcinoma tissue samples. It was revealed that DNLC2A was up-regulated (45 out of the 68 cases) while DNLC2B was down-regulated (44 out of 68 cases), compared with their adjacent tumor-free liver tissues. Interestingly, among the total 68 liver cancer samples tested, DNLC2A was up-regulated while DNLC2B was down-regulated in 28 cases; DNLC2A was up-regulated while no obvious change was observed for DNLC2B in 10 cases; no obvious change was observed for DNLC2A while DNLC2B was down-regulated in 14 cases. Although the underlying mechanism is not clear to date, the apparent up-regulation of DNLC2A and down-regulation of DNLC2B suggest that these genes might be involved in tumor progression. On the other hand, the different expression changes of the two homologous genes indicate that hepatocellular carcinomas are caused by different pathological mechanisms. In addition, DNLC2A was assigned to human chromosome 20q12-q13.11 near the marker D20S106 by radiation hybrid mapping.

Adult↗

PubMed2001

Expression of vaccinia E3L and K3L genes by a novel recombinant canarypox HIV vaccine vector enhances HIV-1 pseudovirion production and inhibits apoptosis in human cells.

Poxviruses that are attenuated for growth in human cells provide a safe means of HIV antigen expression and are capable of eliciting HIV-specific immune responses, including CD8+ cytotoxic T-lymphocyte (CTL) responses. HIV-1 antigen expression in human cells by attenuated poxvirus vectors may be limited by interferon-mediated host defense mechanisms. To enhance HIV antigen expression in human cells, the vaccinia virus E3L and K3L genes were inserted into a canarypox vector that expresses HIV-1 Gag, Env, and a Nef/Pol polyepitope string. E3L and K3L markedly reduced the activation of the double-stranded RNA-dependent protein kinase, PKR, and led to a significant reduction in apoptosis in HeLa cells. Production and release of HIV-1 antigen in the form of pseudovirions was enhanced in both duration and magnitude by this vector modification. The addition of immunomodulatory genes to attenuated poxviruses represents a novel strategy for enhancing antigen production by live vector HIV vaccine candidates.

Apoptosis↗

PubMed2001

Ratiometric pulsed alkylation/mass spectrometry of the cysteine pairs in individual zinc fingers of MRE-binding transcription factor-1 (MTF-1) as a probe of zinc chelate stability.

Metal-response element (MRE)-binding transcription factor-1 (MTF-1) is a zinc-regulated transcriptional activator of metallothionein (MT) genes in mammalian cells. The MRE-binding domain of MTF-1 (MTF-zf) has six canonical Cys(2)-His(2) zinc finger domains that are distinguished on the basis of their apparent affinities for zinc and their specific roles in MRE-binding. In this paper, pulsed alkylation of the zinc-liganding cysteine thiolate pairs with the sulfhydryl-specific alkylating reagent d(5)-N-ethylmaleimide (d(5)-NEM) is used as a residue-specific probe of the relative stabilities of the individual zinc finger coordination complexes in Zn(6) MTF-zf. A chase with excess H(5)-N-ethylmaleimide (H(5)-NEM) to fully derivatize MTF-zf concomitant with complete proteolysis, followed by MALDI-TOF mass spectrometry allows quantitation of the mole fraction of d(5),d(5)-, d(5),H(5)-, and H(5),H(5)-NEM derivatized peptides corresponding to each individual zinc finger domain as a function of d(5)-NEM pulse time. This experiment establishes the hierarchy of cysteine thiolate reactivity in MTF-zf as F5 > F6 >> F1 > F2 approximately F3 approximately F4. The apparent second-order rate of reaction of F1 thiolates is comparable to that determined for the DNA binding domain of Sp1, Zn(3) Sp1-zf, under identical solution conditions. The reactivities of all Cys residues in MTF-zf are significantly reduced when bound to an MREd-containing oligonucleotide. An identical experiment carried out with Zn(5) MTF-zf26, an MTF-zf domain lacking the N-terminal F1 zinc finger, reveals that MTF-zf26 binds to the MREd very weakly, and is characterized by strongly increased reactivity of nonadjacent F4 thiolates. These findings are discussed in the context of existing models for metalloregulation by MTF-1.

Alkylation↗

PubMed2001

Local delivery of mithramycin restores vascular reactivity and inhibits neointimal formation in injured arteries and vascular grafts.

Arterial restenosis is responsible for the high failure rates of vascular reconstruction procedures. Local sustained drug delivery has shown promise in the prevention of restenosis. The drug release rate from mithramycin-loaded EVA matrices (0.1%) was evaluated, and their antirestenotic effect was studied in the rat carotid model and rabbit model of vascular grafts. The modulation of c-myc expression by mithramycin treatment was examined by immunohistochemistry in the rat carotid model. The proliferative response of injured rat arteries was studied by bromdeoxyuridine (BrdU) immunostaining. The impact of mithramycin treatment on vasomotor responses of the venous segments grafted into arterial circulation was studied ex vivo using vasoreactive compounds. Mithramycin was released exponentially from EVA matrices in PBS. Matrices co-formulated with PEG-4600 revealed enhanced release kinetics. The perivascular implantation of drug-loaded EVA-PEG matrices led to 50% reduction of neointimal formation, and reduced the c-myc expression and BrdU labeling in comparison to control implants. Decreased sensitivity of mithramycin-treated grafts to serotonin-induced vasoconstriction was observed. Local perivascular mithramycin treatment limits the functional alteration caused by the grafting of venous segments in high-pressure arterial environment, and potently inhibits stenosis secondary to grafting and angioplasty injury. The antirestenotic effect is associated with reduced c-myc expression and with subsequent decrease in SMC proliferation.

Animals↗

PubMed2001

Impact of the media and the internet on oncology: survey of cancer patients and oncologists in Canada.

PURPOSE: To evaluate the use of the news media and the Internet as sources of medical information by patients and oncologists in Canada and to investigate the impact on patients' treatment decisions and the patient-doctor relationship. PATIENTS AND METHODS: During a 2-week period, 191 ambulatory patients participated in the survey. Questionnaires were also mailed to Canadian oncologists: 410 of 686 questionnaires were returned (response rate = 60%). RESULTS: Of the 191 patients, 86% wanted as much information as possible about their illness, 54% reported receiving insufficient information, 83% cited physicians as their primary information source, and 7% cited the Internet. Seventy-one percent of patients actively searched for information, and 50% used the Internet. Patients' opinions about the balance, accuracy, and relevance of news media reports were evenly split. English as the first language, access to the Internet, and use of alternative treatments predicted a higher rate of information seeking. Most oncologists routinely pay some attention to medical news and believe that it is difficult for patients to interpret medical information in the media and on the Internet accurately. Both patients and oncologists agree that information seeking does not affect the patient-physician relationship. CONCLUSION: Information searching is common among cancer patients in Canada. It does not affect the patient-doctor relationship. The media and the Internet are powerful means of medical information dissemination. Strategic efforts are needed to improve the quality of medical news reporting by the media, and to provide guidance for patients to understand their disease and interpret such information better.

Adolescent↗

PubMed2001

Opioid receptor modulation of a metabolically sensitive ion channel in rat amygdala neurons.

We have used single-channel patch-clamp recordings to study opiate receptor effects on freshly dissociated neurons from the rat amygdalohippocampal area (also called the posterior nucleus of the amygdala), an output nucleus of the amygdala implicated in appetitive behaviors. Dissociated cells included a distinct subpopulation that was 30-40 micrometer in diameter, multipolar or pyramidal in shape, and immunoreactive for neuron-specific enolase, mu opioid receptors, and galanin. In whole-cell perforated-patch recordings, these cells responded to low concentrations of mu opioid agonists with a hyperpolarization. In cell-attached single channel recordings, these cells expressed a large variety of K(+)-permeable ion channels, including 20-100 pS inward rectifiers and 150-200 pS apparent Ca(2+)-activated K(+) channels, none of which appeared sensitive to the presence of opioid drugs. In contrast, a 130 pS inwardly rectifying channel was selectively activated by mu opioid receptors in this same subpopulation of cells and was active only in the presence of opioid agonists, and inhibited in the presence of antagonists. Channels identical to the 130 pS channel in conductance and voltage sensitivity were activated in the absence of opioids, when the cells were treated with glucose-free medium or with the metabolic inhibitor rotenone. The sulfonylurea drug tolbutamide inhibited 130 pS channel openings elicited by opioids. Thus, a subpopulation of amygdala projection neurons expresses a metabolically sensitive ion channel that is selectively modulated by opiate receptors. This mechanism may allow opioid neurotransmitters to regulate ingestive behaviors, and thus, opiate drugs to influence reward pathways.

Amygdala↗

PubMed2001

Variable deletion and duplication at recombination junction ends: implication for staggered double-strand cleavage in class-switch recombination.

Immunoglobulin class-switch recombination (CSR) gives rise to looped-out circular DNA of a cleaved S segment, which is lost eventually after cell divisions. To understand the molecular mechanism of S region cleavage during CSR, we constructed artificial CSR substrates in which inversion-type CSR takes place to retain the cleaved S segment. Sequencing analyses of recombinant clones of these substrates revealed that varying degrees of deletions and duplications exist at CSR breakpoints, suggesting the involvement of staggered cleavage of the S region in CSR. In addition, mutations frequently found near junctions showed a similar profile of base replacement to Ig somatic hypermutation. These findings suggest that single-strand tails of staggered cleavage may be repaired by error-prone DNA synthesis.

Animals↗

PubMed2001

Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients.

Proximal spinal muscular atrophy (SMA) is a common motor neuron disorder caused by mutation of the telomeric survival of motor neuron gene SMN1. The centromeric survival of motor neuron SMN2 gene is retained in all SMA patients but does not produce sufficient SMN protein to prevent the development of clinical symptoms. The SMN1 and SMN2 genes differ functionally by a single nucleotide change. This change affects the efficiency with which exon 7 is incorporated into the mRNA transcript. Thus, SMN2 produces less full-length mRNA and protein than SMN1. We have screened a library of compounds in order to identify ones that can alter the splicing pattern of the SMN2 gene. Here, we report that the compound aclarubicin increases the retention of exon 7 into the SMN2 transcript. We show that aclarubicin effectively induces incorporation of exon 7 into SMN2 transcripts from the endogenous gene in type I SMA fibroblasts as well as into transcripts from a SMN2 minigene in the motor neuron cell line NSC34. In type I fibroblasts, treatment resulted in an increase in SMN protein and gems to normal levels. Our results suggest that alteration of splicing pattern represents a new approach to modification of gene expression in disease treatment and demonstrate the feasibility of high throughput screens to detect compounds that affect the splicing pattern of a gene.

Aclarubicin↗

PubMed2001

Nitrogen deposition and leaching from two forested catchments in Southwest China--preliminary data and research needs.

Increased nitrogen deposition has resulted in increased nitrogen pools and nitrogen leaching in European and North American forest soils. The development in Asia in general, and China in particular, suggests increased deposition of reduced nitrogen from changes in agricultural practices and of oxidized nitrogen from rapid growth of the transportation sector. Decreased nitrogen retention in forested areas in the future may cause increased NO3- leaching and, thus, acidification and eutrophication in surface waters. The differences in climate, ecosystems, land use, and deposition history make direct application of knowledge from studies in Europe and North America difficult. In Southwest China the potential for nitrogen mobilization from forest soils may be high because of the warm and humid climate, resulting in high decomposition rates of soil organic matter. However, there are very few data available for quantifying the suspected potential for increased nitrogen leaching in forest ecosystems. Here we present data from two forested catchments, dominated by Masson pine (Pinus massoniana), near Guiyang and Chongqing, respectively, in Southwest China. The present nitrogen deposition is moderate, estimated in the range from 10 to 40 kg N ha(-1) year(-1). The C/N ratios of the soils are generally below 15. Nitrate concentrations in soil water are rather variable in space, with highest values of several hundred microequivalents per liter. The turnover rate of nitrogen in the forest ecosystem is quite high compared to the atmospheric deposition rate. At present, nitrate runoff from the catchments is low and intermediate in Guiyang and Chongqing, respectively. More research is needed to improve our ability to predict future nitrogen leaching from subtropical Asian coniferous forests.

Carbon↗

PubMed2001

Inhibition of pancreatic protein secretion by ghrelin in the rat.

1. The role of ghrelin in the regulation of pancreatic protein secretion was investigated in vivo using anaesthetized rats with pancreatic ductal cannulas, and in isolated pancreatic acinar cells and pancreatic lobules in vitro. 2. In vivo, pancreatic protein output stimulated by CCK-8 (400 pmol kg(-1) h(-1)) was dose-dependently inhibited by continuous ghrelin infusion (1.2 and 12 nmol kg(-1) h(-1)) by 45 +/- 8 and 84 +/- 7 %, respectively. 3. In rats with acute subdiaphragmatic vagotomy, ghrelin (12 nmol kg(-1) h(-1)) significantly inhibited CCK-stimulated pancreatic protein secretion by 75 +/- 18 %. 4. Infusion of ghrelin (12 nmol kg(-1) h(-1)) abolished pancreatic protein secretion caused by the central vagal stimulant 2-deoxy-D-glucose (75 mg kg(-1)), whereas bethanechol-stimulated pancreatic protein output was inhibited by only 59 +/- 7 %. 5. In vitro, ghrelin (10(-11)-10(-7) M) produced no change in basal amylase release from dispersed, purified acinar cells. Co-incubation of ghrelin (10(-11)-10(-7) M) with CCK-8 (10(-10) M) demonstrated no inhibition of CCK-stimulated amylase release from dispersed acini. In contrast, ghrelin (10(-9)-10(-7) M) dose-dependently inhibited amylase release from pancreatic lobules exposed to 75 mM potassium. 6. Our results show that (1) ghrelin is a potent inhibitor of pancreatic exocrine secretion in anaesthetized rats in vivo and in pancreatic lobules in vitro; and (2) the actions of ghrelin are indirect and may be exerted at the level of intrapancreatic neurons.

Animals↗

PubMed2001

Crystallization and preliminary X-ray analysis of a Trx domain of human thioredoxin-like protein.

The Trx domain of human thioredoxin-like protein has been purified and crystallized using ammonium sulfate as precipitant. The crystal belongs to space group C2, with unit-cell parameters a = 87.5, b = 48.5, c = 29.8 A, beta = 99.59 degrees. It has one molecule per asymmetric unit and diffracts beyond 2.2 A under cryoconditions (100 K) using an in-house Cu rotating-anode X-ray generator.

Crystallization↗