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1.
Lab Chip ; 20(9): 1621-1627, 2020 05 05.
Artigo em Inglês | MEDLINE | ID: mdl-32334422

RESUMO

Rapid, sensitive and specific detection and reporting of infectious pathogens is important for patient management and epidemic surveillance. We demonstrated a point-of-care system integrated with a smartphone for detecting live virus from nasal swab media, using a panel of equine respiratory infectious diseases as a model system for corresponding human diseases such as COVID-19. Specific nucleic acid sequences of five pathogens were amplified by loop-mediated isothermal amplification on a microfluidic chip and detected at the end of reactions by the smartphone. Pathogen-spiked horse nasal swab samples were correctly diagnosed using our system, with a limit of detection comparable to that of the traditional lab-based test, polymerase chain reaction, with results achieved in ∼30 minutes.


Assuntos
Doenças dos Cavalos/diagnóstico , Dispositivos Lab-On-A-Chip , Técnicas de Diagnóstico Molecular/métodos , Técnicas de Amplificação de Ácido Nucleico/métodos , Transtornos Respiratórios/veterinária , Smartphone , Animais , Betacoronavirus/isolamento & purificação , Técnicas de Laboratório Clínico/métodos , Infecções por Coronavirus/diagnóstico , Herpesvirus Equídeo 1/isolamento & purificação , Herpesvirus Equídeo 4/isolamento & purificação , Doenças dos Cavalos/microbiologia , Doenças dos Cavalos/virologia , Cavalos , Vírus da Influenza A Subtipo H3N8/isolamento & purificação , Aplicativos Móveis , Nariz/microbiologia , Nariz/virologia , Sistemas Automatizados de Assistência Junto ao Leito , Transtornos Respiratórios/diagnóstico , Transtornos Respiratórios/microbiologia , Transtornos Respiratórios/virologia , Streptococcus equi/isolamento & purificação
2.
Artigo em Inglês | MEDLINE | ID: mdl-32296882

RESUMO

PURPOSE: The purpose of this study was to investigate the prognostic value of whole-body metabolic tumor volume (MTV) and other metabolic tumor parameters, obtained from baseline and first restaging 18F-FDG PET/CT scans in melanoma patients treated with immune checkpoint inhibitors (ICIs). METHODS: Eighty-five consecutive melanoma patients (M, 57; F, 28) treated with ICIs who underwent PET/CT scans before and approximately 3 months after the start of immunotherapy were retrospectively enrolled. Metabolic tumor parameters including MTV for all melanoma lesions were measured on each scan. A Cox proportional hazards model was used for univariate and multivariate analyses of metabolic parameters combined with known clinical prognostic factors associated with overall survival (OS). Kaplan-Meier curves for patients dichotomized based on median values of imaging parameters were generated. RESULTS: The median OS time in all patients was 45 months (95% CI 24-45 months). Univariate analysis demonstrated that MTV obtained from first restaging PET/CT scans (MTVpost) was the strongest prognostic factor for OS among PET/CT parameters (P < 0.0001). The median OS in patients with high MTVpost (≥ 23.44) was 16 months (95% CI 12-32 months) as compared with more than 60 months in patients with low MTVpost (< 23.44) (P = 0.0003). A multivariate model including PET/CT parameters and known clinical prognostic factors revealed that MTVpost and the presence of central nervous system lesions were independent prognostic factors for OS (P = 0.0004, 0.0167, respectively). One pseudoprogression case (1.2%) was seen in this population and classified into the high MTVpost group. CONCLUSION: Whole-body metabolic tumor volume from PET scan acquired approximately 3 months following initiation of immunotherapy (MTVpost) is a strong prognostic indicator of OS in melanoma patients. Although the possibility of pseudoprogression must be considered whenever evaluating first restaging PET imaging, it only occurred in 1 patient in our cohort.

3.
Cancer Discov ; 8(10): 1227-1236, 2018 10.
Artigo em Inglês | MEDLINE | ID: mdl-30093503

RESUMO

The use of tyrosine kinase inhibitors (TKI) with activity against ALK, ROS1, or TRKA-C can result in significant clinical benefit in patients with diverse tumors harboring ALK, ROS1, or NTRK1-3 rearrangements; however, resistance invariably develops. The emergence of on-target kinase domain mutations represents a major mechanism of acquired resistance. Solvent-front substitutions such as ALKG1202R, ROS1G2032R or ROS1D2033N, TRKAG595R, and TRKCG623R are among the most recalcitrant of these mechanisms. Repotrectinib (TPX-0005) is a rationally designed, low-molecular-weight, macrocyclic TKI that is selective and highly potent against ROS1, TRKA-C, and ALK. Importantly, repotrectinib exhibits activity against a variety of solvent-front substitutions in vitro and in vivo As clinical proof of concept, in an ongoing first-in-human phase I/II trial, repotrectinib achieved confirmed responses in patients with ROS1 or NTRK3 fusion-positive cancers who had relapsed on earlier-generation TKIs due to ROS1 or TRKC solvent-front substitution-mediated resistance.Significance: Repotrectinib (TPX-0005), a next-generation ROS1, pan-TRK, and ALK TKI, overcomes resistance due to acquired solvent-front mutations involving ROS1, NTRK1-3, and ALK Repotrectinib may represent an effective therapeutic option for patients with ROS1-, NTRK1-3-, or ALK-rearranged malignancies who have progressed on earlier-generation TKIs. Cancer Discov; 8(10); 1227-36. ©2018 AACR. This article is highlighted in the In This Issue feature, p. 1195.


Assuntos
Inibidores de Proteínas Quinases/uso terapêutico , Proteínas Tirosina Quinases/antagonistas & inibidores , Proteínas Proto-Oncogênicas/antagonistas & inibidores , Humanos , Mutação , Inibidores de Proteínas Quinases/farmacologia
4.
Exp Neurol ; 275 Pt 3: 436-449, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25450468

RESUMO

Repetitive mild traumatic brain injury (mTBI) is implicated in chronic neurological illness. The development of animal models of repetitive mTBI in mice is essential for exploring mechanisms of these chronic diseases, including genetic vulnerability by using transgenic backgrounds. In this study, the rat model of impact acceleration (IA) was redesigned for the mouse cranium and used in two clinically relevant repetitive mTBI paradigms. We first determined, by using increments of weight dropped from 1m that the 40g weight was most representative of mTBI and was not associated with fractures, brain contusions, anoxic-ischemic injury, mortality, or significant neurological impairments. Quantitative evaluation of traumatic axonal injury (TAI) in the optic nerve/tract, cerebellum and corpus callosum confirmed that weight increase produced a graded injury. We next evaluated two novel repetitive mTBI paradigms (1 time per day or 3 times per day at days 0, 1, 3, and 7) and compared the resulting TAI, neuronal cell death, and neuroinflammation to single hit mTBI at sub-acute (7days) and chronic time points (10weeks) post-injury. Both single and repetitive mTBI caused TAI in the optic nerve/tract, cerebellum, corticospinal tract, lateral lemniscus and corpus callosum. Reactive microglia with phagocytic phenotypes were present at injury sites. Severity of axonal injury corresponded to impact load and frequency in the optic nerve/tract and cerebellum. Both single and repeat injury protocols were associated with retinal ganglion cell loss and optic nerve degeneration; these outcomes correlated with impact load and number/frequency. No phosphorylated tau immunoreactivity was detected in the brains of animals subjected to repetitive mTBI. Our findings establish a new model of repetitive mTBI model featured by TAI in discrete CNS tracts, especially the visual system and cerebellum. Injury in retina and optic nerve provides a sensitive measure of severity of mTBI, thus enabling further studies on mechanisms and experimental therapeutics. Our model can also be useful in exploring mechanisms of chronic neurological disease caused by repetitive mTBI in wild-type and transgenic mice.


Assuntos
Aceleração/efeitos adversos , Axônios/patologia , Lesões Encefálicas/patologia , Modelos Animais de Doenças , Degeneração Neural/patologia , Células Ganglionares da Retina/patologia , Animais , Lesões Encefálicas/complicações , Inflamação/etiologia , Inflamação/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Degeneração Neural/etiologia , Nervo Óptico/patologia
5.
Exp Neurol ; 273: 168-76, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26311071

RESUMO

Chronic traumatic encephalopathy (CTE) is associated with repetitive mild traumatic brain injury (mTBI) in the context of contact and collision sports, but not all exposed individuals develop this condition. In addition, experiments in animal models in several laboratories have shown that non-transgenic mice do not develop tauopathy after exposure to repetitive mTBI schedules. It is thus reasonable to assume that genetic factors may play an etiological role in the development of CTE. More than 40 mutations in the tau gene are known to confer proneness to aggregation and are thought to cause neurodegenerative diseases including frontotemporal degeneration (FTD). Transgenic mice harboring these mutations can be used to ask the question whether repetitive mTBI can accelerate onset and course of tauopathy or worsen the outcomes of transgenic disease. In this study, we exposed mice harboring the tau P301S transgene associated with FTD to repetitive mTBI schedules by impact acceleration (IA) that we have previously characterized. We explored the progression of tauopathy in the retina and neocortex based on density of neuronal profiles loaded with tau pS422, a marker of advanced tau hyperphosphorylation. We found that the density of tau pS422 (+) retinal ganglion cells (RGCs) increased twenty fold with one mTBI hit, a little over fifty fold with four mTBI hits and sixty fold with 12 mTBI hits. The severity of mTBI burden (number of hits) was a significant factor in tauopathy outcome. On the other hand, we found no association between repetitive mTBI and density of pS422 (+) neuronal profiles in neocortex, a region that is not featured by significant TAI in our repetitive mTBI model. We observed similar, but less prominent, trends in tauopathy-prone transgenic mice harboring all 6 isoforms of wild-type human tau without mouse tau. Our findings indicate that repetitive mTBI accelerates tauopathy under diverse genetic conditions predisposing to tau aggregation and suggest a vulnerability-stress model in understanding some cases of acquired neurodegenerative disease after repetitive mTBI.


Assuntos
Lesões Encefálicas/complicações , Mutação/genética , Retina/patologia , Tauopatias/patologia , Proteínas tau/genética , Análise de Variância , Animais , Contagem de Células , Córtex Cerebral/patologia , Modelos Animais de Doenças , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Prolina/genética , Tratos Piramidais/patologia , Retina/metabolismo , Células Ganglionares da Retina/patologia , Serina/genética , Tauopatias/complicações , Tauopatias/genética , Vias Visuais/metabolismo , Vias Visuais/patologia , gama-Sinucleína/metabolismo
6.
Proc Natl Acad Sci U S A ; 111(26): 9633-8, 2014 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-24979790

RESUMO

It is generally accepted that healthy cells degrade their own mitochondria. Here, we report that retinal ganglion cell axons of WT mice shed mitochondria at the optic nerve head (ONH), and that these mitochondria are internalized and degraded by adjacent astrocytes. EM demonstrates that mitochondria are shed through formation of large protrusions that originate from otherwise healthy axons. A virally introduced tandem fluorophore protein reporter of acidified mitochondria reveals that acidified axonal mitochondria originating from the retinal ganglion cell are associated with lysosomes within columns of astrocytes in the ONH. According to this reporter, a greater proportion of retinal ganglion cell mitochondria are degraded at the ONH than in the ganglion cell soma. Consistently, analyses of degrading DNA reveal extensive mtDNA degradation within the optic nerve astrocytes, some of which comes from retinal ganglion cell axons. Together, these results demonstrate that surprisingly large proportions of retinal ganglion cell axonal mitochondria are normally degraded by the astrocytes of the ONH. This transcellular degradation of mitochondria, or transmitophagy, likely occurs elsewhere in the CNS, because structurally similar accumulations of degrading mitochondria are also found along neurites in superficial layers of the cerebral cortex. Thus, the general assumption that neurons or other cells necessarily degrade their own mitochondria should be reconsidered.


Assuntos
Axônios/fisiologia , Mitofagia/fisiologia , Disco Óptico/citologia , Células Ganglionares da Retina/fisiologia , Animais , Astrócitos/metabolismo , Tomografia com Microscopia Eletrônica , Exocitose/fisiologia , Imageamento Tridimensional , Imuno-Histoquímica , Hibridização in Situ Fluorescente , Marcação In Situ das Extremidades Cortadas , Proteínas Luminescentes , Lisossomos/metabolismo , Camundongos , Fagocitose/fisiologia , Células Ganglionares da Retina/citologia
7.
Proc Natl Acad Sci U S A ; 110(10): 4045-50, 2013 Mar 05.
Artigo em Inglês | MEDLINE | ID: mdl-23431148

RESUMO

Glaucoma, a major cause of blindness worldwide, is a neurodegenerative optic neuropathy in which vision loss is caused by loss of retinal ganglion cells (RGCs). To better define the pathways mediating RGC death and identify targets for the development of neuroprotective drugs, we developed a high-throughput RNA interference screen with primary RGCs and used it to screen the full mouse kinome. The screen identified dual leucine zipper kinase (DLK) as a key neuroprotective target in RGCs. In cultured RGCs, DLK signaling is both necessary and sufficient for cell death. DLK undergoes robust posttranscriptional up-regulation in response to axonal injury in vitro and in vivo. Using a conditional knockout approach, we confirmed that DLK is required for RGC JNK activation and cell death in a rodent model of optic neuropathy. In addition, tozasertib, a small molecule protein kinase inhibitor with activity against DLK, protects RGCs from cell death in rodent glaucoma and traumatic optic neuropathy models. Together, our results establish a previously undescribed drug/drug target combination in glaucoma, identify an early marker of RGC injury, and provide a starting point for the development of more specific neuroprotective DLK inhibitors for the treatment of glaucoma, nonglaucomatous forms of optic neuropathy, and perhaps other CNS neurodegenerations.


Assuntos
MAP Quinase Quinase Quinases/genética , MAP Quinase Quinase Quinases/fisiologia , Células Ganglionares da Retina/enzimologia , Células Ganglionares da Retina/patologia , Animais , Morte Celular/genética , Morte Celular/fisiologia , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/genética , Sobrevivência Celular/fisiologia , Células Cultivadas , Modelos Animais de Doenças , Regulação para Baixo , Glaucoma/tratamento farmacológico , Glaucoma/etiologia , Humanos , MAP Quinase Quinase Quinases/antagonistas & inibidores , Masculino , Camundongos , Doenças do Nervo Óptico/etiologia , Doenças do Nervo Óptico/patologia , Traumatismos do Nervo Óptico/tratamento farmacológico , Traumatismos do Nervo Óptico/enzimologia , Traumatismos do Nervo Óptico/patologia , Piperazinas/farmacologia , Inibidores de Proteínas Quinases/farmacologia , Interferência de RNA , Ratos , Ratos Wistar , Células Ganglionares da Retina/efeitos dos fármacos , Transdução de Sinais , Regulação para Cima
8.
Proc Natl Acad Sci U S A ; 108(3): 1176-81, 2011 Jan 18.
Artigo em Inglês | MEDLINE | ID: mdl-21199938

RESUMO

Optic nerve head (ONH) astrocytes have been proposed to play both protective and deleterious roles in glaucoma. We now show that, within the postlaminar ONH myelination transition zone (MTZ), there are astrocytes that normally express Mac-2 (also known as Lgals3 or galectin-3), a gene typically expressed only in phagocytic cells. Surprisingly, even in healthy mice, MTZ and other ONH astrocytes constitutive internalize large axonal evulsions that contain whole organelles. In mouse glaucoma models, MTZ astrocytes further up-regulate Mac-2 expression. During glaucomatous degeneration, there are dystrophic processes in the retina and optic nerve, including the MTZ, which contain protease resistant γ-synuclein. The increased Mac-2 expression by MTZ astrocytes during glaucoma likely depends on this γ-synuclein, as mice lacking γ-synuclein fail to up-regulate Mac-2 at the MTZ after elevation of intraocular pressure. These results suggest the possibility that a newly discovered normal degradative pathway for axons might contribute to glaucomatous neurodegeneration.


Assuntos
Astrócitos/metabolismo , Galectina 3/metabolismo , Glaucoma/fisiopatologia , Fibras Nervosas Mielinizadas/metabolismo , Nervo Óptico/metabolismo , Fagocitose/fisiologia , gama-Sinucleína/metabolismo , Animais , Astrócitos/fisiologia , Astrócitos/ultraestrutura , Axônios/metabolismo , Axônios/patologia , Glaucoma/metabolismo , Imuno-Histoquímica , Hibridização In Situ , Camundongos , Microscopia Eletrônica de Varredura
10.
J Biol Chem ; 286(5): 3579-86, 2011 Feb 04.
Artigo em Inglês | MEDLINE | ID: mdl-21115494

RESUMO

Sororin is a positive regulator of sister chromatid cohesion that interacts with the cohesin complex. Sororin is required for the increased stability of the cohesin complex on chromatin following DNA replication and sister chromatid cohesion during G(2). The mechanism by which sororin ensures cohesion is currently unknown. Because the primary sequence of sororin does not contain any previously characterized structural or functional motifs, we have undertaken a structure-function analysis of the sororin protein. Using a series of mutant derivatives of sororin, we show that the ability of sororin to bind to chromatin is separable from both its role in sister chromatid cohesion and its interaction with the cohesin complex. We also show that derivatives of sororin with deletions or mutations in the conserved C terminus fail to rescue the loss-of-cohesion phenotype caused by sororin RNAi and that these mutations also abrogate the association of sororin with the cohesin complex. Our data suggest that the interaction of the highly conserved motif at the C terminus of sororin with the cohesin complex is critical to its ability to mediate sister chromatid cohesion.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/fisiologia , Proteínas de Ciclo Celular/metabolismo , Proteínas de Ciclo Celular/fisiologia , Cromátides/metabolismo , Proteínas Cromossômicas não Histona/metabolismo , Sequência Conservada/fisiologia , Proteínas Adaptadoras de Transdução de Sinal/genética , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Motivos de Aminoácidos/fisiologia , Animais , Proteínas de Ciclo Celular/genética , Sequência Conservada/genética , Células HeLa , Humanos , Mutação , Ligação Proteica
11.
Nat Cell Biol ; 12(11): 1094-100, 2010 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-20972425

RESUMO

S-nitrosylation of proteins by nitric oxide is a major mode of signalling in cells. S-nitrosylation can mediate the regulation of a range of proteins, including prominent nuclear proteins, such as HDAC2 (ref. 2) and PARP1 (ref. 3). The high reactivity of the nitric oxide group with protein thiols, but the selective nature of nitrosylation within the cell, implies the existence of targeting mechanisms. Specificity of nitric oxide signalling is often achieved by the binding of nitric oxide synthase (NOS) to target proteins, either directly or through scaffolding proteins such as PSD-95 (ref. 5) and CAPON. As the three principal isoforms of NOS--neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS)--are primarily non-nuclear, the mechanisms by which nuclear proteins are selectively nitrosylated have been elusive. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is physiologically nitrosylated at its Cys 150 residue. Nitrosylated GAPDH (SNO-GAPDH) binds to Siah1, which possesses a nuclear localization signal, and is transported to the nucleus. Here, we show that SNO-GAPDH physiologically transnitrosylates nuclear proteins, including the deacetylating enzyme sirtuin-1 (SIRT1), histone deacetylase-2 (HDAC2) and DNA-activated protein kinase (DNA-PK). Our findings reveal a novel mechanism for targeted nitrosylation of nuclear proteins and suggest that protein-protein transfer of nitric oxide groups may be a general mechanism in cellular signal transduction.


Assuntos
Proteína Quinase Ativada por DNA/metabolismo , Gliceraldeído-3-Fosfato Desidrogenases/metabolismo , Histona Desacetilase 2/metabolismo , Proteínas Nucleares/metabolismo , Sirtuína 1/metabolismo , Células Cultivadas , Humanos , Óxido Nítrico/metabolismo , Doadores de Óxido Nítrico/farmacologia , Transdução de Sinais , Sirtuína 1/antagonistas & inibidores
12.
Pediatr Nurs ; 36(3): 138-45, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20687305

RESUMO

In this randomized, controlled multi-site study, the pacifier-activated-lullaby system (PAL) was used with 68 premature infants. Dependent variables were (a) total number of days prior to nipple feeding, (b) days of nipple feeding, (c) discharge weight, and (d) overall weight gain. Independent variables included contingent music reinforcement for non-nutritive sucking for PAL intervention at 32 vs. 34 vs. 36 weeks adjusted gestational age (AGA), with each age group subdivided into three trial conditions: control consisting of no PAL used vs. one 15-minute PAL trial vs. three 15-minute PAL trials. At 34 weeks, PAL trials significantly shortened gavage feeding length, and three trials were significantly better than one trial. At 32 weeks, PAL trials lengthened gavage feeding. Female infants learned to nipple feed significantly faster than male infants. It was noted that PAL babies went home sooner after beginning to nipple feed, a trend that was not statistically significant.


Assuntos
Recém-Nascido Prematuro , Musicoterapia/métodos , Enfermagem Neonatal/métodos , Chupetas , Reforço Psicológico , Comportamento de Sucção , Análise de Variância , Pesquisa em Enfermagem Clínica , Nutrição Enteral/métodos , Nutrição Enteral/enfermagem , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Recém-Nascido Prematuro/fisiologia , Recém-Nascido Prematuro/psicologia , Terapia Intensiva Neonatal/métodos , Tempo de Internação/estatística & dados numéricos , Masculino , Encaminhamento e Consulta , Caracteres Sexuais , Comportamento de Sucção/fisiologia , Ganho de Peso
13.
Optom Vis Sci ; 87(9): E705-9, 2010 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-20601911

RESUMO

PURPOSE: Full-thickness macular holes affect 0.3% of the population, worldwide. This condition has a predilection for females in their sixth to seventh decade. Patients can present with severe impairment of their central vision or can be relatively asymptomatic. We believe that an optic disc hemangioblastoma adhered to the vitreous, causing an anterior displacement of the hyaloid membrane that resulted in a form of vitreomacular traction that pulled the macular hole nasally, toward the optic nerve. CASE REPORT: A 66-year-old white male presented to our clinic with decreased vision. He had a previously stable, longstanding optic disc hemangioblastoma. On presentation, an early developing full-thickness macular hole was noted. The outcome was a full-thickness macular hole that was disproportionately more detached on the nasal side of the macula. Treatment regimen included repeated intravitreal off-label injections with bevacizumab, followed by external beam radiation therapy, ultimately followed by surgery. CONCLUSIONS: Treatment in this case was especially complicated because of the presence of the macular hole in addition to the hemangioblastoma. The plan was to decrease vascular activity of the hemangioblastoma before proceeding with macular hole repair. First, off-label bevacizumab injections were administered, followed by external beam radiation therapy, and finally combined surgery. Surgery was successful, and to date, the macula is flat and intact.


Assuntos
Neoplasias dos Nervos Cranianos/complicações , Hemangioblastoma/complicações , Doenças do Nervo Óptico/complicações , Perfurações Retinianas/etiologia , Idoso , Inibidores da Angiogênese/administração & dosagem , Anticorpos Monoclonais/administração & dosagem , Anticorpos Monoclonais Humanizados , Bevacizumab , Braquiterapia , Neoplasias dos Nervos Cranianos/terapia , Hemangioblastoma/terapia , Humanos , Injeções Intraoculares , Terapia a Laser , Masculino , Doenças do Nervo Óptico/terapia , Radioterapia Adjuvante , Perfurações Retinianas/terapia , Corpo Vítreo
14.
Indian J Radiol Imaging ; 19(4): 266-77, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-19881101

RESUMO

In the USA, the use of the American College of Radiology Breast Imaging-Reporting and Data System (ACR BI-RADS) has served not only as a quality assurance tool and guide to standardizing breast imaging reports but has also improved communication between referring physicians, researchers, and patients. In fact, in the USA, the Mammography Quality Standards Act of 1997 requires that all mammograms be assigned a BI-RADS category based on the finding of most concern. In this manuscript, we aim to review the recommendations provided in the 4 th edition of the ACR BI-RADS for mammography, USG, and MRI. We also review the major controversies surrounding the use of ACR BI-RADS .

15.
J Music Ther ; 45(3): 349-59, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18959455

RESUMO

The physiological and psychological stress that brain tumor patients undergo during the entire surgical experience can considerably affect several aspects of their hospitalization. The purpose of this study was to examine the effects of live music therapy on quality of life indicators, amount of medications administered and length of stay for persons receiving elective surgical procedures of the brain. Subjects (N = 27) were patients admitted for some type of surgical procedure of the brain. Subjects were randomly assigned to either the control group receiving no music intervention (n = 13) or the experimental group receiving pre and postoperative live music therapy sessions (n = 14). Anxiety, mood, pain, perception of hospitalization or procedure, relaxation, and stress were measured using a self-report Visual Analog Scale (VAS) for each of the variables. The documented administration of postoperative pain medications; the frequency, dosage, type, and how it was given was also compared between groups. Experimental subjects live and interactive music therapy sessions, including a pre-operative session and continuing with daily sessions until the patient was discharged home. Control subjects received routine hospital care without any music therapy intervention. Differences in experimental pretest and posttest scores were analyzed using a Wilcoxon Matched-Pairs Signed-Rank test. Results indicated statistically significant differences for 4 of the 6 quality of life measures: anxiety (p = .03), perception of hospitalization (p = .03), relaxation (p = .001), and stress (p = .001). No statistically significant differences were found for mood (p > .05) or pain (p > .05) levels. Administration amounts of nausea and pain medications were compared with a Two-Way ANOVA with One Repeated Measure resulting in no significant differences between groups and medications, F(1, 51) = 0.03; p > .05. Results indicate no significant differences between groups for length of stay (t = .97, df = 25, p > .05). This research study indicates that live music therapy using patient-preferred music can be beneficial in improving quality of life indicators such as anxiety, perception of the hospitalization or procedure, relaxation, and stress in patients undergoing surgical procedures of the brain.


Assuntos
Neoplasias Encefálicas/psicologia , Procedimentos Cirúrgicos Eletivos/psicologia , Musicoterapia/métodos , Satisfação Pessoal , Qualidade de Vida , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Análise de Variância , Ansiedade/prevenção & controle , Neoplasias Encefálicas/cirurgia , Criança , Feminino , Humanos , Tempo de Internação , Masculino , Pessoa de Meia-Idade , Dor/prevenção & controle , Medição da Dor/métodos , Resultado do Tratamento
16.
J Mol Cell Cardiol ; 36(4): 597-601, 2004 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15081319

RESUMO

Although extracellular matrix-degrading enzymes matrix metalloproteinases (MMPs) are activated within minutes after myocardial infarction (MI), the time course of early MI-induced type I cardiac collagen degradation has not been assessed, nor has the ability of MMP inhibitor compounds, such as doxycycline (DOX), to limit these events. The objective of this study was to assess serum biomarker evidence of myocardial type I collagen degradation early (<48 h) after coronary occlusion (CO) and determine the capacity of DOX to ameliorate its release. CO studies were performed in untreated and DOX pre-treated pigs. Treated animals received DOX at 30 mg/kg/d. Radioimmunoassays were performed for serum levels of C-terminal telopeptide of collagen type I (ICTP) fragments. ICTP groups peaked by 6 h after MI. However, in DOX-treated animals, ICTP values returned to normal by 8 h. Average serum concentrations for ICTP values from 0 to 48 h post-MI were significantly inhibited by DOX treatment. In conclusion, serum biomarker results indicate that type I collagen degradation occurs within minutes after MI and that DOX likely reduces its degradation.


Assuntos
Colágeno Tipo I/química , Infarto do Miocárdio/sangue , Animais , Monóxido de Carbono/química , Colágeno/química , Colágeno/metabolismo , Doxiciclina/farmacologia , Imuno-Histoquímica , Masculino , Miocárdio/patologia , Peptídeos/química , Radioimunoensaio , Suínos , Fatores de Tempo , Remodelação Ventricular
17.
Circulation ; 108(12): 1487-92, 2003 Sep 23.
Artigo em Inglês | MEDLINE | ID: mdl-12952845

RESUMO

BACKGROUND: Myocardial infarction (MI) is associated with early metalloproteinase (MMP) activation and extracellular matrix (ECM) degradation. We hypothesized that preserving the original ECM of the infarcted left ventricle (LV) by use of early short-term doxycycline (DOX) treatment preserves cardiac structure and function. METHODS AND RESULTS: LV morphometry and function were measured in 3 groups of rats (sham, MI, and MI+DOX). DOX (30 mg/kg per day) was given orally 48 hours before and 48 hours after MI. Rats were examined at 2 and 4 weeks after MI. By 4 weeks, DOX significantly decreased (P<0.05 versus MI) the heart weight to body weight ratio, myocyte cross-sectional area, and internal LV diameter, whereas it preserved anterior wall thickness within the infarct. Collagen/muscle area fraction did not change in the region of the infarct/scar. Parallel left shifts (versus MI) were observed in pressure-volume relationships of DOX MI rats at all pressures. DOX treatment also shifted passive epicardial strains within the scar area toward normal values. No differences were observed in LV end-diastolic or peak systolic pressures, peak positive or negative LV dP/dt, or isovolumic relaxation rates. Assessment of LV global MMP and MMP-2/9 activities 1 hour after MI using fluorescent probes yielded significant differences with DOX. CONCLUSIONS: Brief, early MMP inhibition after MI yields preservation of LV structure and global as well as scar area passive function, supporting the concept that preserving the original ECM early after coronary occlusion lessens ventricular remodeling.


Assuntos
Doxiciclina/farmacologia , Infarto do Miocárdio/tratamento farmacológico , Remodelação Ventricular/efeitos dos fármacos , Animais , Peso Corporal/efeitos dos fármacos , Modelos Animais de Doenças , Progressão da Doença , Esquema de Medicação , Ativação Enzimática/efeitos dos fármacos , Matriz Extracelular/efeitos dos fármacos , Matriz Extracelular/metabolismo , Coração/efeitos dos fármacos , Coração/fisiopatologia , Hemodinâmica/efeitos dos fármacos , Masculino , Inibidores de Metaloproteinases de Matriz , Metaloproteinases da Matriz/metabolismo , Infarto do Miocárdio/fisiopatologia , Tamanho do Órgão/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Fatores de Tempo , Função Ventricular Esquerda/efeitos dos fármacos
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