562 research outputs found
Combined antiproliferative activity of imatinib mesylate (STI-571) with radiation or cisplatin in vitro
Little is known about the interaction of novel anticancer drugs with other treatment modalities. The aim of this study was to examine the effect of combining imatinib mesylate (STI-571) with radiation or cisplatin on the survival of two human solid tumor cell lines β SKNMC cells derived from Ewing sarcoma and breast cancer MCF-7 cells. Methods: Cell proliferation was determined using the sulphorodamine B cytotoxicity assay. Cell cycle analysis was performed with flow cytometry. Apoptosis was determined using a commercial cell death ELISA plus kit. Phosphorylated AKT, which has been suggested to be involved in radiation resistance, was detected by Western blot analysis. Results: Exposure of SKNMC cells to STI-571 resulted in a dose-dependent antiproliferative effect and a decrease in phosphorylated AKT expression. There was no evidence of apoptosis. The combination of STI-571 with radiation or cisplatin had an additive antiproliferative effect in SKNMC cells (60% reduction in cell number). A similar effect was observed in human MCF-7 breast cancer cells. Conclusion: STI-571 improves the outcome of cisplatin or irradiation treatment in vitro. AKT pathway may play a role in the additive effect of STI-571 and irradiation.Π¦Π΅Π»Ρ: ΠΎΡΠ΅Π½ΠΈΡΡ Π°Π½ΡΠΈΠΏΡΠΎΠ»ΠΈΡΠ΅ΡΠ°ΡΠΈΠ²Π½ΡΠΉ ΡΡΡΠ΅ΠΊΡ ΠΈΠΌΠ°ΡΠΈΠ½ΠΈΠ±Π° (STI-571) Π² ΠΊΠΎΠΌΠ±ΠΈΠ½Π°ΡΠΈΠΈ Ρ ΠΎΠ±Π»ΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΠΈΠ»ΠΈ ΡΠΈΡΠΏΠ»Π°ΡΠΈΠ½ΠΎΠΉ ΠΏΠΎ ΠΎΡΠ½ΠΎΡΠ΅Π½ΠΈΡ
ΠΊ Π΄Π²ΡΠΌ ΠΊΠ»Π΅ΡΠΎΡΠ½ΡΠΌ Π»ΠΈΠ½ΠΈΡΠΌ β ΠΊΠ»Π΅ΡΠΊΠ°ΠΌ Π»ΠΈΠ½ΠΈΠΈ SKNMC, ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠΌ ΠΈΠ· ΡΠ°ΡΠΊΠΎΠΌΡ ΠΠ²ΠΈΠ½Π³Π°, ΠΈ ΠΊΠ»Π΅ΡΠΊΠ°ΠΌ ΡΠ°ΠΊΠ° ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ
ΡΠ΅Π»ΠΎΠ²Π΅ΠΊΠ° Π»ΠΈΠ½ΠΈΠΈ MCF-7. ΠΠ΅ΡΠΎΠ΄Ρ: Π΄Π»Ρ ΠΎΡΠ΅Π½ΠΊΠΈ ΠΏΡΠΎΠ»ΠΈΡΠ΅ΡΠ°ΡΠΈΠΈ ΠΊΠ»Π΅ΡΠΎΠΊ ΠΏΡΠΈΠΌΠ΅Π½ΡΠ»ΠΈ ΠΌΠ΅ΡΠΎΠ΄ Π°Π½Π°Π»ΠΈΠ·Π° ΡΠΈΡΠΎΡΠΎΠΊΡΠΈΡΠ½ΠΎΡΡΠΈ Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ
ΡΡΠ»ΡΡΠΎΡΠΎΠ΄Π°ΠΌΠΈΠ½Π° B. ΠΠ»Ρ Π°Π½Π°Π»ΠΈΠ·Π° ΡΠ°ΡΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ ΠΊΠ»Π΅ΡΠΎΠΊ ΠΏΠΎ ΡΠ°Π·Π°ΠΌ ΠΊΠ»Π΅ΡΠΎΡΠ½ΠΎΠ³ΠΎ ΡΠΈΠΊΠ»Π° ΠΏΡΠΈΠΌΠ΅Π½ΡΠ»ΠΈ ΠΌΠ΅ΡΠΎΠ΄ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΠΉ ΡΠΈΡΠΎΠΌΠ΅ΡΡΠΈΠΈ,
Π°ΠΏΠΎΠΏΡΠΎΠ·Π° β Ρ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ΠΌ ΠΊΠΎΠΌΠΌΠ΅ΡΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π½Π°Π±ΠΎΡΠ° Π΄Π»Ρ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΡ ΠΠ€Π. Π£ΡΠΎΠ²Π΅Π½Ρ ΡΠΎΡΡΠΎΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΠΊΠΈΠ½Π°Π·Ρ ΠΠΠ’,
ΠΏΡΠ΅Π΄ΠΏΠΎΠ»ΠΎΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎ ΡΠ²ΡΠ·Π°Π½Π½ΠΎΠΉ Ρ ΡΠ°Π΄ΠΈΠΎΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΠΎΡΡΡΡ, ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΠ΅ΡΡΠ΅ΡΠ½-Π±Π»ΠΎΡ Π°Π½Π°Π»ΠΈΠ·Π°. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: ΠΈΠ½ΠΊΡΠ±Π°ΡΠΈΡ
ΠΊΠ»Π΅ΡΠΎΠΊ SKNMC STI-571 ΠΏΡΠΈΠ²ΠΎΠ΄ΠΈΠ»Π° ΠΊ Π΄ΠΎΠ·ΠΎΠ·Π°Π²ΠΈΡΠΈΠΌΠΎΠΌΡ Π°Π½ΡΠΈΠΏΡΠΎΠ»ΠΈΡΠ΅ΡΠ°ΡΠΈΠ²Π½ΠΎΠΌΡ ΡΡΡΠ΅ΠΊΡΡ ΠΈ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΡ ΡΠΎΡΡΠΎΡΠΈΠ»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ
AKT, Π½ΠΎ Π½Π΅ Π°ΠΏΠΎΠΏΡΠΎΠ·Ρ ΠΊΠ»Π΅ΡΠΎΠΊ. ΠΠΎΠΌΠ±ΠΈΠ½ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠ΅ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ STI-571 ΠΈ ΠΎΠ±Π»Π΅Π½ΠΈΡ ΠΈΠ»ΠΈ ΡΠΈΡΠΏΠ»Π°ΡΠΈΠ½Ρ ΠΎΠΊΠ°Π·ΡΠ²Π°Π»ΠΎ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ΅
Π°Π½ΡΠΈΠΏΡΠΎΠ»ΠΈΡΠ΅ΡΠ°ΡΠΈΠ²Π½ΠΎΠ΅ Π²ΠΎΠ·Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅ Π½Π° ΠΊΠ»Π΅ΡΠΊΠΈ Π»ΠΈΠ½ΠΈΠΈ SKNMC (60% ΡΠΌΠ΅Π½ΡΡΠ΅Π½ΠΈΡ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π° ΠΊΠ»Π΅ΡΠΎΠΊ). ΠΠ½Π°Π»ΠΎΠ³ΠΈΡΠ½ΡΠ΅ ΡΡΡΠ΅ΠΊΡΡ
ΠΎΡΠΌΠ΅ΡΠ°Π»ΠΈ Π½Π° ΠΊΠ»Π΅ΡΠΊΠ°Ρ
Π»ΠΈΠ½ΠΈΠΈ MCF-7. ΠΡΠ²ΠΎΠ΄Ρ: ΠΎΠ±ΡΠ°Π±ΠΎΡΠΊΠ° ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ STI-571 ΡΡΠΈΠ»ΠΈΠ²Π°Π΅Ρ ΡΡΡΠ΅ΠΊΡ ΠΎΠ±Π»Π΅Π½ΠΈΡ ΠΈ ΡΠΈΡΠΏΠ»Π°ΡΠΈΠ½Ρ
in, ΠΏΡΠΈΡΠ΅ΠΌ ΡΠ°ΠΊΠΎΠ²ΠΎΠΉ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΠΎΠΏΠΎΡΡΠ΅Π΄ΠΎΠ²Π°Π½ ΡΠΈΠ³Π½Π°Π»ΡΠ½ΡΠΌ ΠΊΠ°ΡΠΊΠ°Π΄ΠΎΠΌ AK
The miR-17 similar to 92 cluster collaborates with the Sonic Hedgehog pathway in medulloblastoma
Medulloblastomas (MBs) are the most common brain tumors in children. Some are thought to originate from cerebellar granule neuron progenitors (GNPs) that fail to undergo normal cell cycle exit and differentiation. Because microRNAs regulate numerous aspects of cellular physiology and development, we reasoned that alterations in miRNA expression might contribute to MB. We tested this hypothesis using 2 spontaneous mouse MB models with specific initiating mutations, Ink4c(-/-); Ptch1(+/-) and Ink4c(-/-); p53(-/-). We found that 26 miRNAs showed increased expression and 24 miRNAs showed decreased expression in proliferating mouse GNPs and MBs relative to mature mouse cerebellum, regardless of genotype. Among the 26 overexpressed miRNAs, 9 were encoded by the miR-17 similar to 92 cluster family, a group of microRNAs implicated as oncogenes in several tumor types. Analysis of human MBs demonstrated that 3 miR-17 similar to 92 cluster miRNAs (miR-92, miR-19a, and miR-20) were also overexpressed in human MBs with a constitutively activated Sonic Hedgehog (SHH) signaling pathway, but not in other forms of the disease. To test whether the miR-17 similar to 92 cluster could promote MB formation, we enforced expression of these miRNAs in GNPs isolated from cerebella of postnatal (P) day P6 Ink4c(-/-); Ptch1(+/-) mice. These, but not similarly engineered cells from Ink4c(-/-); p53(-/-) mice, formed MBs in orthotopic transplants with complete penetrance. Interestingly, orthotopic mouse tumors ectopically expressing miR-17 similar to 92 lost expression of the wild-type Ptch1 allele. Our findings suggest a functional collaboration between the miR-17 similar to 92 cluster and the SHH signaling pathway in the development of MBs in mouse and man
Anisotropic flow at RHIC: How unique is the number-of-constituent-quark scaling?
The transverse momentum dependence of the anisotropic flow for ,
, nucleon, , and is studied for Au+Au collisions at
GeV within two independent string-hadron transport
approaches (RQMD and UrQMD). Although both models reach only 60% of the
absolute magnitude of the measured , they both predict the particle type
dependence of , as observed by the RHIC experiments: exhibits a
hadron-mass hierarchy (HMH) in the low region and a
number-of-constituent-quark (NCQ) dependence in the intermediate region.
The failure of the hadronic models to reproduce the absolute magnitude of the
observed indicates that transport calculations of heavy ion collisions at
RHIC must incorporate interactions among quarks and gluons in the early, hot
and dense phase. The presence of an NCQ scaling in the string-hadron model
results suggests that the particle-type dependencies observed in heavy-ion
collisions at intermediate might be related to the hadronic cross
sections in vacuum rather than to the hadronization process itself.Comment: 10 pages, 5 figures; A new author (H. Petersen) is added; A new
figure (fig.1) on time evolution of elliptic flow and number of collisions is
added; Version accepted for publication in J. Phys.
Genetic Background of Prop1df Mutants Provides Remarkable Protection Against Hypothyroidism-Induced Hearing Impairment
Hypothyroidism is a cause of genetic and environmentally induced deafness. The sensitivity of cochlear development and function to thyroid hormone (TH) mandates understanding TH action in this sensory organ. Prop1df and Pou1f1dw mutant mice carry mutations in different pituitary transcription factors, each resulting in pituitary thyrotropin deficiency. Despite the same lack of detectable serum TH, these mutants have very different hearing abilities: Prop1df mutants are mildly affected, while Pou1f1dw mutants are completely deaf. Genetic studies show that this difference is attributable to the genetic backgrounds. Using embryo transfer, we discovered that factors intrinsic to the fetus are the major contributor to this difference, not maternal effects. We analyzed Prop1df mutants to identify processes in cochlear development that are disrupted in other hypothyroid animal models but protected in Prop1df mutants by the genetic background. The development of outer hair cell (OHC) function is delayed, but Prestin and KCNQ4 immunostaining appear normal in mature Prop1df mutants. The endocochlear potential and KCNJ10 immunostaining in the stria vascularis are indistinguishable from wild type, and no differences in neurofilament or synaptophysin staining are evident in Prop1df mutants. The synaptic vesicle protein otoferlin normally shifts expression from OHC to IHC as temporary afferent fibers beneath the OHC regress postnatally. Prop1df mutants exhibit persistent, abnormal expression of otoferlin in apical OHC, suggesting delayed maturation of synaptic function. Thus, the genetic background of Prop1df mutants is remarkably protective for most functions affected in other hypothyroid mice. The Prop1df mutant is an attractive model for identifying the genes that protect against deafness
Growing pains in children
We review the clinical manifestations of "growing pains", the most common form of episodic childhood musculoskeletal pain. Physicians should be careful to adhere to clear clinical criteria as described in this review before diagnosing a child with growing pain. We expand on current theories on possible causes of growing pains and describe the management of these pains and the generally good outcome in nearly all children
The Reputational Consequences of Failed Replications and Wrongness Admission among Scientists
Scientists are dedicating more attention to replication efforts. While the scientific utility of replications is unquestionable, the impact of failed replication efforts and the discussions surrounding them deserve more attention. Specifically, the debates about failed replications on social media have led to worry, in some scientists, regarding reputation. In order to gain data-informed insights into these issues, we collected data from 281 published scientists. We assessed whether scientists overestimate the negative reputational effects of a failed replication in a scenario-based study. Second, we assessed the reputational consequences of admitting wrongness (versus not) as an original scientist of an effect that has failed to replicate. Our data suggests that scientists overestimate the negative reputational impact of a hypothetical failed replication effort. We also show that admitting wrongness about a non-replicated finding is less harmful to oneβs reputation than not admitting. Finally, we discovered a hint of evidence that feelings about the replication movement can be affected by whether replication efforts are aimed oneβs own work versus the work of another. Given these findings, we then present potential ways forward in these discussions
OP0291β TOFACITINIB FOR THE TREATMENT OF POLYARTICULAR COURSE JUVENILE IDIOPATHIC ARTHRITIS: RESULTS OF A PHASE 3, RANDOMISED, DOUBLE-BLIND, PLACEBO-CONTROLLED WITHDRAWAL STUDY
Background:Tofacitinib is an oral JAK inhibitor that is being investigated for JIA.Objectives:To assess tofacitinib efficacy and safety in JIA patients (pts).Methods:This was a Phase 3, randomised, double-blind (DB), placebo (PBO)-controlled withdrawal study in pts aged 2β<18 years with polyarticular course JIA (pcJIA), PsA or ERA (NCT02592434). In the 18-week open-label Part 1, pts received weight-based tofacitinib doses (5βmg BID or lower). Pts with β₯JIA ACR30 response at Week (W)18 were randomised 1:1 in the DB Part 2 (W18β44) to continue tofacitinib or switch to PBO. Primary endpoint: disease flare rate by W44. Key secondary endpoints: JIA ACR50/30/70 response rates; change from Part 2 baseline (Ξ) in CHAQ-DI at W44. Other efficacy endpoints: time to disease flare in Part 2; JADAS27-CRP in Parts 1 and 2. PsA/ERA pts were excluded from these efficacy analyses. Safety was evaluated in all pts up to W44.Results:225 enrolled pts with pcJIA (n=184), PsA (n=20) or ERA (n=21) received tofacitinib in Part 1. At W18, 173/225 (76.9%) pts entered Part 2 (pcJIA n=142, PsA n=15, ERA n=16). In pcJIA pts, disease flare rate in Part 2 was significantly lower with tofacitinib vs PBO by W44 (p=0.0031; Fig 1a). JIA ACR50/30/70 response rates (Fig 1b) and ΞCHAQ-DI (Fig 1c) at W44, and time to disease flare in Part 2 (Fig 2a), were improved with tofacitinib vs PBO. Tofacitinib reduced JADAS27-CRP in Part 1; this effect was sustained in Part 2 (Fig 2b). Overall, safety was similar with tofacitinib or PBO (Table): 77.3% and 74.1% had adverse events (AEs); 1.1% and 2.4% had serious AEs. In Part 1, 2 pts had herpes zoster (non-serious) and 3 pts had serious infections (SIs). In Part 2, SIs occurred in 1 tofacitinib pt and 1 PBO pt. No pts died.Conclusion:In pcJIA pts, tofacitinib vs PBO resulted in significantly fewer disease flares, and improved time to flare, disease activity and physical functioning. Tofacitinib safety was consistent with that in RA pts.Table.Safety in all ptsPart 1Part 2TofacitinibaN=225TofacitinibaN=88PBO N=85Pts with events, n (%)AEs153 (68.0)68 (77.3)63 (74.1)SAEs7 (3.1)1 (1.1)2 (2.4)Permanent discontinuations due to AEs26 (11.6)16 (18.2)29 (34.1)AEs of special interestβDeath000βGastrointestinal perforationb000βHepatic eventb3 (1.3)00βHerpes zoster (non-serious and serious)2 (0.9)c00βInterstitial lung diseaseb000βMajor adverse cardiovascular eventsb000βMalignancy (including non-melanoma skin cancer)b000βMacrophage activation syndromeb000βOpportunistic infectionb000βSI3 (1.3)1 (1.1)d1 (1.2)βThrombotic event (deep vein thrombosis, pulmonary embolismbor arterial thromboembolism)000βTuberculosisb000a5βmg BID or equivalent weight-based lower dose in pts <40 kgbAdjudicated eventscBoth non-seriousdOne SAE of pilonidal cyst repair was coded to surgical procedures instead of infections, and was inadvertently not identified as an SI. Following adjudication, the SAE did not meet opportunistic infection criteria; it is also included in the table as an SIAE, adverse event; BID, twice daily; PBO, placebo; pts, patients; SAE, serious AE; SI, serious infectionAcknowledgments:Study sponsored by Pfizer Inc. Medical writing support was provided by Sarah Piggott of CMC Connect and funded by Pfizer Inc.Disclosure of Interests:Nicolino Ruperto Grant/research support from: Bristol-Myers Squibb, Eli Lily, F Hoffmann-La Roche, GlaxoSmithKline, Janssen, Novartis, Pfizer, Sobi (paid to institution), Consultant of: Ablynx, AbbVie, AstraZeneca-Medimmune, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lily, EMD Serono, GlaxoSmithKline, Hoffmann-La Roche, Janssen, Merck, Novartis, Pfizer, R-Pharma, Sanofi, Servier, Sinergie, Sobi, Takeda, Speakers bureau: Ablynx, AbbVie, AstraZeneca-Medimmune, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lily, EMD Serono, GlaxoSmithKline, Hoffmann-La Roche, Janssen, Merck, Novartis, Pfizer, R-Pharma, Sanofi, Servier, Sinergie, Sobi, Takeda, Olga Synoverska Speakers bureau: Sanofi, Tracy Ting: None declared, Carlos Abud-Mendoza Speakers bureau: Eli Lilly, Pfizer Inc, Alberto Spindler Speakers bureau: Eli Lilly, Yulia Vyzhga Grant/research support from: Pfizer Inc, Katherine Marzan Grant/research support from: Novartis, Vladimir Keltsev: None declared, Irit Tirosh: None declared, Lisa Imundo: None declared, Rita Jerath: None declared, Daniel Kingsbury: None declared, BetΓΌl SΓΆzeri: None declared, Sheetal Vora: None declared, Sampath Prahalad Grant/research support from: Novartis, Elena Zholobova Grant/research support from: Novartis and Pfizer Inc, Speakers bureau: AbbVie, Novartis, Pfizer Inc and Roche, Yonatan Butbul Aviel: None declared, Vyacheslav Chasnyk: None declared, Melissa Lerman Grant/research support from: Amgen, Kabita Nanda Grant/research support from: Abbott, AbbVie, Amgen and Roche, Heinrike Schmeling Grant/research support from: Janssen, Pfizer Inc, Roche and USB Bioscience, Heather Tory: None declared, Yosef Uziel Speakers bureau: Pfizer Inc, Diego O Viola Grant/research support from: Bristol-Myers Squibb, GSK, Janssen and Pfizer Inc, Speakers bureau: AbbVie and Bristol-Myers Squibb, Holly Posner Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Keith Kanik Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Ann Wouters Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Cheng Chang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Richard Zhang Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Irina Lazariciu Consultant of: Pfizer Inc, Employee of: IQVIA, Ming-Ann Hsu Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Ricardo Suehiro Shareholder of: Pfizer Inc, Employee of: Pfizer Inc, Alberto Martini Consultant of: AbbVie, Eli Lily, EMD Serono, Janssen, Novartis, Pfizer, UCB, Daniel J Lovell Consultant of: Abbott (consulting and PI), AbbVie (PI), Amgen (consultant and DSMC Chairperson), AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb (PI), Celgene, Forest Research (DSMB Chairman), GlaxoSmithKline, Hoffman-La Roche, Janssen (co-PI), Novartis (consultant and PI), Pfizer (consultant and PI), Roche (PI), Takeda, UBC (consultant and PI), Wyeth, Employee of: Cincinnati Children's Hospital Medical Center, Speakers bureau: Wyeth, Hermine Brunner Consultant of: Hoffman-La Roche, Novartis, Pfizer, Sanofi Aventis, Merck Serono, AbbVie, Amgen, Alter, AstraZeneca, Baxalta Biosimilars, Biogen Idec, Boehringer, Bristol-Myers Squibb, Celgene, EMD Serono, Janssen, MedImmune, Novartis, Pfizer, and UCB Biosciences, Speakers bureau: GSK, Roche, and Novarti
Differences sustained between diffuse and limited forms of juvenile systemic sclerosis in expanded international cohort. www.juvenile-scleroderma.com
OBJECTIVES: To evaluate the baseline clinical characteristics of juvenile systemic sclerosis (jSSc) patients in the international Juvenile SSc Inception Cohort (jSScC), compare these characteristics between the classically defined diffuse (dcjSSc) and limited cutaneous (lcjSSc) subtypes, and among those with overlap features. METHODS: A cross-sectional study was performed using baseline visit data. Demographic, organ system evaluation, treatment, and patient and physician reported outcomes were extracted and summary statistics applied. Comparisons between dcjSSc and lcSSc subtypes and patients with and without overlap features were performed using Chi-square and Mann Whitney U-tests. RESULTS: At data extraction 150 jSSc patients were enrolled across 42 centers, 83% were Caucasian, 80% female, dcjSSc predominated (72%), and 17% of the cohort had overlap features. Significant differences were found between dcjSSc and lcjSSc regarding the modified Rodnan Skin Score, presence of Gottron's papules, digital tip ulceration, 6 Minute walk test, composite pulmonary and cardiac involvement. All more frequent in dcSSc except for cardiac involvement. DcjSSc patients had significantly worse scores for physician rated disease activity and damage. A significantly higher occurrence of Gottron's papules, musculoskeletal involvement and composite pulmonary involvement, and significantly lower frequency of Raynaud's phenomenon, were seen in those with overlap features. CONCLUSION: Results from a large international jSSc cohort demonstrate significant differences between dcjSSc and lcjSSc patients including more globally severe disease and increased frequency of ILD in dcjSSc patients, while those with lcSSc have more frequent cardiac involvement. Those with overlap features had an unexpected higher frequency of interstitial lung disease
Passage of charmed particles through the mixed phase in high-energy heavy-ion collisions
We employ a modified cascade hydrodynamics code to simulate the phase
transition of an expanding quark-gluon plasma and the passage of a charmed
particle through it. When inside the plasma droplets, the charmed quark
experiences drag and diffusion forces. When outside the plasma, the quark
travels as a meson and experiences collisions with pions. Additional energy
transfer takes place when the quark enters or leaves a droplet. We find that
the transverse momentum of mesons provides a rough thermometer of the phase
transition.Comment: 20 pages, 9 Postscript figures included with epsfig.st
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