THE DYEING PROCESS OF KNITTED FABRICS AT DIFFERENT TEMPERATURES USING ULTRASOUND

The dyeing of knitted fabrics made from 100 % cellulose using on-line procedure vinyl sulfonic reactive dye, with or without ultrasound energy, is carried out in this paper. The impact of temperature has been observed. The dye exhaustion is monitored using the method of absorption spectrophotometry, and the quality control of the coloration is monitored using color measurements. The acting of ultrasound on coloration consistency, as well as on some mechanical characteristics has also been examined. All examples of the ultrasound dyeing process show greater dye exhaustion in comparison to the conventional procedure. In addition, all the samples, which have been dyed with the ultrasound energy at 40°C, are significantly darker and have deeper color in comparison with the referent sample. The temperature has a great influence on kinetic energy of the dye molecules, and therefore on the diffusion processes in the dyeing system. The exhaustion chart indicates that when the temperature is lower the exhaustion degree drops. However, all the samples dyed with the ultrasound energy have bigger exhaustion. Besides that, ultrasound energy contributes to warming up the processing environment, so the additional warm up with the electricity is unnecessary, unlike the conventional way of dyeing. Since the reactive dyes chemically connect themselves with the cellulose substrate and in that way form covalent connection, the dyed fabrics have good washing consistency. Analysis results indicate that the consistencies are identical regardless the applied dyeing procedure. In other words, the dyeing method using the ultrasound energy produces the dyed fabric of the same quality. After analyzing the results of breaking force and elongation at break of knitted fabrics, it is noticeable that there is no degradation of previously mentioned knitted fabrics features (horizontally and vertically) during the ultrasound wave’s activity

DYEING OF KNITTED MICRO-VISCOSE IN THE PRESENCE OF ULTRASOUND WITH DIFFERENT FREQUENCIES

In dyeing process, the object is to transport or diffuse dyes and chemicals into the fibre. Various novel processes, including ultrasound, are being introduced and studied as more environmentally friendly alternatives. Encouraging results have been reported for the use of ultrasound energy in dyeing processes of micro-viscose. The recent studies revealed major ultrasound applications advances: savings of processing time, energy, chemicals, as well as environmental protection. Influence of various ultrasound frequencies (40, 200 and 400 kHz) on dyeing of micro-viscose knitted fabrics, by a reactive dye has been reported in this work. A method of reflection spectrophotometry has been employed to record reemission curves of the colored compounds. A software packet has been employed to calculate CIELab colored coordinates. Then, a comparison has been made with samples colored by conventional procedure according to CIELab76 and CMC (2:1) criteria. The use ultrasound in textile dyeing processing offers many potential advantages. The results prove better dye exhaustion by ultrasound and consequently the better fixing. The exhaustion for the bifunctional dye (containing two vinylsulphone groups) reaches 71.75 % without ultrasound, and 83.69 % with 400 kHz ultrasound. The 40 kHz, 150 W ultrasound causes a cavitation of higher intensity, compared to 200 and 400 kHz ultrasounds. In this particular case, destruction of cavitation bubbles is very intensive. That is why a large amount of cavitation energy is being transformed into a heat, yielding the additional bath heating. The ultrasounds with higher frequencies (200 and 400 kHz) cannot use such a strong power. The applied powering this case reaches 0.6 W. The cavitation bubbles are now smaller the cavitation disintegration is not so strong, and the energy loss is much smaller, i.e. a smaller amount of energy has been transformed into a heat. An ultrasound of an equal power, but of higher frequency contributes to the somewhat higher exhaustion and fixing. The ultrasound dyeing produces much obscured colours, compared the standard. The differences are evident and not negligible. The comparison of the samples treated ultrasound of different frequencies during dyeing revealed the higher coulours intensities with the increase of ultrasound frequencies of the equal power (200 and 400 kHz). However, the increase is not so expressed

The Next-Generation Oral Selective Estrogen Receptor Degrader Camizestrant (AZD9833) Suppresses ER+ Breast Cancer Growth and Overcomes Endocrine and CDK4/6 Inhibitor Resistance

Estrogen receptor; Breast cancer; Endocrine inhibitorReceptor d'estrògens; Càncer de mama; Inhibidor endocríReceptores de estrógenos; Cáncer de mama; Inhibidor endocrinoOral selective estrogen receptor degraders (SERD) could become the backbone of endocrine therapy (ET) for estrogen receptor–positive (ER+) breast cancer, as they achieve greater inhibition of ER-driven cancers than current ETs and overcome key resistance mechanisms. In this study, we evaluated the preclinical pharmacology and efficacy of the next-generation oral SERD camizestrant (AZD9833) and assessed ER–co-targeting strategies by combining camizestrant with CDK4/6 inhibitors (CDK4/6i) and PI3K/AKT/mTOR-targeted therapy in models of progression on CDK4/6i and/or ET. Camizestrant demonstrated robust and selective ER degradation, modulated ER-regulated gene expression, and induced complete ER antagonism and significant antiproliferation activity in ESR1 wild-type (ESR1wt) and mutant (ESR1m) breast cancer cell lines and patient-derived xenograft (PDX) models. Camizestrant also delivered strong antitumor activity in fulvestrant-resistant ESR1wt and ESR1m PDX models. Evaluation of camizestrant in combination with CDK4/6i (palbociclib or abemaciclib) in CDK4/6-naive and -resistant models, as well as in combination with PI3Kαi (alpelisib), mTORi (everolimus), or AKTi (capivasertib), indicated that camizestrant was active with CDK4/6i or PI3K/AKT/mTORi and that antitumor activity was further increased by the triple combination. The response was observed independently of PI3K pathway mutation status. Overall, camizestrant shows strong and broad antitumor activity in ER+ breast cancer as a monotherapy and when combined with CDK4/6i and PI3K/AKT/mTORi. Significance: Camizestrant, a next-generation oral SERD, shows promise in preclinical models of ER+ breast cancer alone and in combination with CDK4/6 and PI3K/AKT/mTOR inhibitors to address endocrine resistance, a current barrier to treatment

Risk factors associated with poor clinical outcome in pyogenic spinal infections : 5-years’ intensive care experience

Introduction: Management of pyogenic spinal infections (PSI) after the development of neurological deficit has not been specifically addressed in the literature. We aimed to describe real-life clinical outcomes of PSI in patients admitted to an intensive care unit with neurological deficit and identify factors associated with good prognosis. Methodology: Consecutive patients admitted to ICU with a possible diagnosis of spinal infection over five years’ period were included. Descriptive statistics were performed to examine the demographics and clinical parameters. Results: The majority (71%) of patients were male. The mean age was 57.4 years (27-79), and 71% were > 50 years old. At least one underlying risk factor was identified in 68% of the patients; the most common comorbidity was diabetes mellitus (DM). All patients have presented with fever accompanied by a neurological deficit (86%) and back pain (79%). A complete recovery was achieved in 25% of patients. However, the majority of patients had adverse outcomes with 21.4% mortality, and 43% remaining neurological sequelae. Increased age with a cut-off of 65 years and pre-existing DM were identified as being associated with poor outcome. Conclusion: Mortality among patients admitted to ICU with PSI was significantly higher than reported in the literature. The residual neurological deficit was common, one-third of patients had remaining neurological sequelae, and only one-fourth had complete recovery. Increased age and background DM were the most important determinants of poor clinical outcome. The impact of DM appears to be much more important than currently recognised in this population.Publisher PDFPeer reviewe

Tumour stroma-derived lipocalin-2 promotes breast cancer metastasis

Tumour cell-secreted factors skew infiltrating immune cells towards a tumour-supporting phenotype, expressing pro-tumourigenic mediators. However, the influence of lipocalin-2 (Lcn2) on the metastatic cascade in the tumour micro-environment is still not clearly defined. Here, we explored the role of stroma-derived, especially macrophage-released, Lcn2 in breast cancer progression. Knockdown studies and neutralizing antibody approaches showed that Lcn2 contributes to the early events of metastasis in vitro. The release of Lcn2 from macrophages induced an epithelial–mesenchymal transition programme in MCF-7 breast cancer cells and enhanced local migration as well as invasion into the extracellular matrix, using a three-dimensioanl (3D) spheroid model. Moreover, a global Lcn2 deficiency attenuated breast cancer metastasis in both the MMTV–PyMT breast cancer model and a xenograft model inoculating MCF-7 cells pretreated with supernatants from wild-type and Lcn2-knockdown macrophages. To dissect the role of stroma-derived Lcn2, we employed an orthotopic mammary tumour mouse model. Implantation of wild-type PyMT tumour cells into Lcn2-deficient mice left primary mammary tumour formation unaltered, but specifically reduced tumour cell dissemination into the lung. We conclude that stroma-secreted Lcn2 promotes metastasis in vitro and in vivo, thereby contributing to tumour progression. Our study highlights the tumourigenic potential of stroma-released Lcn2 and suggests Lcn2 as a putative therapeutic target

tick borne encephalitis in serbia a case series

Introduction: In the Europe, the number of tick-borne encephalitis (TBE) has been increased in the last decade, and the number of endemic areas has been also increased and is still growing. In the present case series, we present clinical and socio-epidemiological data of patients with TBE hospitalized in the period of TBE virus epidemic in Serbia. Methodology: A case series was conducted in Serbia in 2017. Patients with confirmed TBE were included in the study. Biochemical and serological analysis of blood and CSF, as well as radiological imaging (CT and MRI) were done. Results: In total, 10 patients with TBE were included in the study. M:F ratio was 1.5:1, while average age was 45.1 years. Half of the patients had severe clinical picture. Endocranial CT scan and MRI did not reveal any abnormality, except in the patient with the most severe CNS infection (meningoencephalomyelitis). Mean value of sedimentation and CRP was slightly elevated (29.6 mm/1hours and 20.1 mg/L, respectively) in 80% of the patients, although elevation was almost negligible. The average number of leucocytes in the cerebrospinal fluid (CSF) was 171×106/L, the mean value of the CSF protein was 1.1g/L. There were no fatal outcomes. Conclusion: Since other CNS infections have similar clinical picture and CSF finding as TBE, serological analysis for TBE should be included in routine diagnostic practice

RARRES3 suppresses breast cancer lung metastasis by regulating adhesion and differentiation

In estrogen receptor-negative breast cancer patients, metastatic relapse usually occurs in the lung and is responsible for the fatal outcome of the disease. Thus, a better understanding of the biology of metastasis is needed. In particular, biomarkers to identify patients that are at risk of lung metastasis could open the avenue for new therapeutic opportunities. Here we characterize the biological activity of RARRES3, a new metastasis suppressor gene whose reduced expression in the primary breast tumors identifies a subgroup of patients more likely to develop lung metastasis. We show that RARRES3 downregulation engages metastasis-initiating capabilities by facilitating adhesion of the tumor cells to the lung parenchyma. In addition, impaired tumor cell differentiation due to the loss of RARRES3 phospholipase A1/A2 activity also contributes to lung metastasis. Our results establish RARRES3 downregulation as a potential biomarker to identify patients at high risk of lung metastasis who might benefit from a differentiation treatment in the adjuvant programme.We would like to thank the Functional Genomics, Microscopy, and Cytometry core facilities of IRB Barcelona, and the UB. We thank C. Caelles for the 3AOX-luc construct. We thank Angel Nebreda for his scientific suggestions. EJA is supported by "La Caixa" PhD fellowship programme, and JU is a Juan de la Cierva Researcher (MICINN). JM is a Howard Hughes investigator. The work of A. C. and S.F-R is supported by the Ramon y Cajal award to AC (Spanish Ministry of Education) and the ERC (336343). JM was supported by HHMI. RRG and XS are ICREA Research Professors (Institucio Catalana de Recerca i Estudis Avancats). Support and structural funds were provided by the Associacion Espanola Contra el Cancer (AECC), Fundacion BBVA, Generalitat de Catalunya (2009 SGR 1429), and Spanish Ministerio de Ciencia e Innovacion (MICINN) (SAF2010-21171) to RRG

Stratification and therapeutic potential of PML in metastatic breast cancer.

Patient stratification has been instrumental for the success of targeted therapies in breast cancer. However, the molecular basis of metastatic breast cancer and its therapeutic vulnerabilities remain poorly understood. Here we show that PML is a novel target in aggressive breast cancer. The acquisition of aggressiveness and metastatic features in breast tumours is accompanied by the elevated PML expression and enhanced sensitivity to its inhibition. Interestingly, we find that STAT3 is responsible, at least in part, for the transcriptional upregulation of PML in breast cancer. Moreover, PML targeting hampers breast cancer initiation and metastatic seeding. Mechanistically, this biological activity relies on the regulation of the stem cell gene SOX9 through interaction of PML with its promoter region. Altogether, we identify a novel pathway sustaining breast cancer aggressiveness that can be therapeutically exploited in combination with PML-based stratification.The work of A.C. is supported by the Ramón y Cajal award, the Basque Department of Industry, Tourism and Trade (Etortek), Health (2012111086) and Education (PI2012-03), Marie Curie (277043), Movember Foundation (GAP1), ISCIII (PI10/01484, PI13/00031), FERO (VIII Fellowship) and ERC (336343). N.M.-M. and P.A. are supported by the Spanish Association Against Cancer (AECC), AECC JP Vizcaya and Guipuzcoa, respectively. J.U. and F.S. are Juan de la Cierva Researchers (MINECO). L.A., A.A.-A. and L.V.-J. are supported by the Basque Government of education. M.L.-M.C. acknowledges SAF2014-54658-R and Asociación Española contra el Cancer. R.B. acknowledges Spanish MINECO (BFU2014-52282-P, Consolider BFU2014-57703-REDC), the Departments of Education and Industry of the Basque Government (PI2012/42) and the Bizkaia County. M.S., V.S. and J.B. acknowledge Banco Bilbao Vizcaya Argentaria (BBVA) Foundation (Tumour Biomarker Research Program). M.S. and J.B. are supported by NIH grant P30 CA008748. M.dM.V. is supported by the Institute of Health Carlos III (PI11/02251, PI14/01328) and Basque Government, Health Department (2014111145). A.M. is supported by ISCIII (CP10/00539, PI13/02277) and Marie Curie CIG 2012/712404. V.S. is supported by the SCIII (PI13/01714, CP14/00228), the FERO Foundation and the Catalan Agency AGAUR (2014 SGR 1331). R.R.G. research support is provided by the Spanish Ministry of Science and Innovation grant SAF2013-46196, BBVA Foundation, the Generalitat de Catalunya (2014 SGR 535), Institució Catalana de Recerca i Estudis Avançats, the Spanish Ministerio de Economia y Competitividad (MINECO) and FEDER funds (SAF2013-46196).This is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/10.1038/ncomms1259

The metabolic co-regulator PGC1α suppresses prostate cancer metastasis

Cellular transformation and cancer progression is accompanied by changes in the metabolic landscape. Master co-regulators of metabolism orchestrate the modulation of multiple metabolic pathways through transcriptional programs, and hence constitute a probabilistically parsimonious mechanism for general metabolic rewiring. Here we show that the transcriptional co-activator peroxisome proliferator-activated receptor gamma co-activator 1α (PGC1α) suppresses prostate cancer progression and metastasis. A metabolic co-regulator data mining analysis unveiled that PGC1α is downregulated in prostate cancer and associated with disease progression. Using genetically engineered mouse models and xenografts, we demonstrated that PGC1α opposes prostate cancer progression and metastasis. Mechanistically, the use of integrative metabolomics and transcriptomics revealed that PGC1α activates an oestrogen-related receptor alpha (ERRα)-dependent transcriptional program to elicit a catabolic state and metastasis suppression. Importantly, a signature based on the PGC1α–ERRα pathway exhibited prognostic potential in prostate cancer, thus uncovering the relevance of monitoring and manipulating this pathway for prostate cancer stratification and treatment

Constitutive activation of B-Raf in the mouse germ line provides a model for human cardio-facio-cutaneous syndrome

RASopathies are a class of developmental syndromes that result from congenital mutations in key elements of the RAS/RAF/MEK signaling pathway. A well-recognized RASopathy is the cardio-facio-cutaneous (CFC) syndrome characterized by a distinctive facial appearance, heart defects, and mental retardation. Clinically diagnosed CFC patients carry germ-line mutations in four different genes, B-RAF, MEK1, MEK2, and K-RAS. B-RAF is by far the most commonly mutated locus, displaying mutations that most often result in constitutive activation of the B-RAF kinase. Here, we describe a mouse model for CFC generated by germ-line expression of a B-RafLSLV600E allele. This targeted allele allows low levels of expression of B-RafV600E, a constitutively active B-Raf kinase first identified in human melanoma. B-Raf+/LSLV600E mice are viable and display several of the characteristic features observed in CFC patients, including reduced life span, small size, facial dysmorphism, cardiomegaly, and epileptic seizures. These mice also show up-regulation of specific catecholamines and cataracts, two features detected in a low percentage of CFC patients. In addition, B-Raf +/LSLV600E mice develop neuroendocrine tumors, a pathology not observed in CFC patients. These mice may provide a means of better understanding the pathophysiology of at least some of the clinical features present in CFC patients. Moreover, they may serve as a tool to evaluate the potential therapeutic efficacy of B-RAF inhibitors and establish the precise window at which they could be effective against this congenital syndrome.Work in the laboratory of M.D. was funded by Consorcios Estratégicos Nacionales en Investigación Técnica Program (CDTEAM) Grant TEC2008-06715-C02-01, Centro de Investigación Biomédica en Red Program Grants CB06/01/0079 and PNSD 2007-2010, Fondo de Investigación Sanitaria (FIS) Grant CP08/00017, and Fundación de la Mutua Madrileña del Automovil (FMMA). E.M.B.W. was the holder of a United Kingdom National Institute for Health Research Academic Clinical Fellowship and was supported by the Manchester Biomedical Research Centre. Work in the laboratory of X.R.B. was funded by National Institutes of Health Grant R01CA073735, Spanish Ministry of Science and Innovation (MICINN) Grants SAF2009-07172 and RD06/0020/0001, Autonomous Government of Castilla y León (GR97), and Asociación Española contra el Cáncer. Work in the laboratory of M.B. was supported by European Union- Framework Programme Grants LSHG-CT-2006-037188 and LSHG-CT-2007-037665 (to M.B.), European Research Council Grant ERC-AG/250297-RAS AHEAD (to M.B.), MICINN Grants SAF2006-11773 and CSD2007-00017 (to M.B.), FMMA (to M.B.), FIS Grant PI042124, and Autonomous Community of Madrid Grant GR/SAL/0349/2004.Peer Reviewe