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71.
72.
A novel dynamic matrix detachment model reveals a shift from apoptosis to necrosis in melanoma cells
Tzukert K Gorodestky R Avrahami I Krasny L Shimony N Elkin G Nettelbeck DM Haviv YS 《Cancer letters》2008,272(2):345-354
Anchorage-independence is a hallmark of invasive cancer. The setback of the classical poly-HEMA static matrix detachment (SMD) anoikis model is the absence of dynamic fluid circulation, resulting in cell aggregates. We addressed this problem by developing a novel 3D cell culture dynamic matrix detachment (DMD) model with a turbulent-free laminar flow, yielding a very low shear stress. In this study, we focused on melanoma cells where apoptosis was evaluated both via annexin V flow cytometry and caspase cleavage. The DMD model was superior to SMD in the induction of melanoma cell death and in revealing a shift from apoptosis to necrotic cell death, as evident by failure to activate caspase 9 and a decrease in annexin V stain. Combination of DMD with cisplatin could further accentuate necrotic cell death in cisplatin-resistant melanoma cells. Thus, the DMD model may be a useful matrix deprivation model to identify necrotic vs. apoptotic cell death pathways. 相似文献
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74.
Victor V. Lonasescu Charles C. Searby Rebecca Ionasescu Shivanand Patil 《American journal of medical genetics. Part A》1989,33(1):113-116
A recombinant DNA study for deletion evaluation was performed in a 4 generation family with Duchenne muscular dystrophy (DMD) in twins. The patients were 6 years old, had a history of progressive difficulty in walking since age 4, and showed weak gluteals, iliopsoas, latissimus dorsi, rhomboids, lower trapezius, sternocleidomastoids, pseudohypertrophic calves, and tight heelcords. Both patients had high serum creatine kinase of 19,000 and 11,000 IU, respectively, and the muscle biopsy of the left vastus lateralis showed dystrophic alterations. Both twins had the same red cell types for ABO, Rh, CDE, MNSs, Kelly, Lewis, Duffy, and Kidd. HLA typing also detected the same antigens in both twins: A2, B44, DR4, and DR5. Cytogenetic studies were consistent with 46, XY male individuals with normal banding pattern. By cDNA probes the entire DMD gene was surveyed for missing or abnormal-sized restriction fragments. Both twin boys showed absence of 8.5, 8.0, 4.6, 4.2, and 3.1 kb fragments on Hind III blots and absence of 13.5, 3.7, 2.9, and 1.4 kb fragments on Bgl II blots both hybridized with cDNA l-2a corresponding to most 5′ region of the DMD gene. The mother and other relatives of the patient did not show deletion. These findings strongly suggest that the deletion in the DMD monozygotic twins represents a new mutation. 相似文献
75.
先将样品乙酰化以消除主药之间的干扰,再用单纯形最优化法选择实验条件,不经分离提取,直接测定双嘧啶和复方新诺明片中TMP、SD、SMZ的含量。TMP回收率分别是99.68±0.17%,100.0±0.03%。双嘧啶片中SD和复方新诺明片中SMZ的回收率各为:99.97±0.10%,100.0±0.04%。 相似文献
76.
Ruth Shomrat Nava Driks Cyril Legum Yosef Shiloh 《American journal of medical genetics. Part A》1992,42(3):281-287
Duchenne muscular dystrophy (DMD) results from mutations in the X-linked gene coding for the muscular protein dystrophin. The isolation of genomic and cDNA probes for this gene has greatly facilitated the detection of DMD carriers, which previously relied mainly on measurements of serum creatine kinase (CK), and has enabled prenatal diagnosis of this disease. However, the relatively large size of the gene and the high frequency of recombination and mutation events within the dystrophin locus continue to pose difficulties in the genetic counselling and prenatal diagnosis of DMD, and render the conclusions of molecular analysis less clear cut. This communication presents examples of two such difficulties: the distinction between sporadic and inherited cases in families with a single patient and normal CK levels in all females, and the distinction between mutant and normal dystrophin alleles in families in which the patients have died. The combined use of genomic and cDNA probes allows one to make these distinctions. An additional complicating factor, gonadal mosaicism, is demonstrated. 相似文献
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78.
目的 分析散发型DMD/BMD家系中患者的致病突变,为部分家系的胎儿进行产前基因诊断,明确该类家庭中女性成员是否致病突变携带者,分析该类家系新发突变的比例.方法 共收集30个散发DMD/BMD家系,应用传统mPCR方法 分析DMD基因缺失热区中的18个外显子;应用MLPA方法,对家系中的30例患者及23个家系中的28位女性成员,进行DMD基因全部79个外显子的定量分析,并为其中19个家系进行20例产前诊断.结果 mPCR检测到19例缺失突变;MLPA检测到21例缺失突变和3例重复突变,并明确缺失突变范围.在检测到突变的家系中,10例母亲为缺失突变携带者,2例为重复突变携带者,9例母亲不是携带者,新发突变比例为37.5%.7例患者的姐妹中5例为携带者(3例缺失,2例莺复),2例不是携带者.经产前诊断,12例男性胎儿中5例为患者,8例女性胎儿中2例为携带者.结论 MLPA方法 可全面检测DMD基因缺失及重复突变、明确女性携带者,为产前诊断提供准确信息. 相似文献
79.
Letizia Brogi Maria Marchese Alessandro Cellerino Rosario Licitra Valentina Naef Serena Mero Carlo Bibbiani Baldassare Fronte 《Nutrients》2021,13(5)
Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular childhood disorder that causes progressive muscle weakness and degeneration. A lack of dystrophin in DMD leads to inflammatory response, autophagic dysregulation, and oxidative stress in skeletal muscle fibers that play a key role in the progression of the pathology. β-glucans can modulate immune function by modifying the phagocytic activity of immunocompetent cells, notably macrophages. Mitochondrial function is also involved in an important mechanism of the innate and adaptive immune responses, owing to high need for energy of immune cells. In the present study, the effects of 1,3-1,6 β-glucans on five-day-old non-dystrophic and dystrophic (sapje) zebrafish larvae were investigated. The effects of the sonication of β-glucans and the dechorionation of embryos were also evaluated. The results showed that the incidence of dystrophic phenotypes was reduced when dystrophic embryos were exposed to 2 and 4 mg L−1 of 1,3-1,6 β-glucans. Moreover, when the dystrophic larvae underwent 8 mg L−1 treatment, an improvement of the locomotor performances and mitochondrial respiration were observed. In conclusion, the observed results demonstrated that 1,3-1,6 β-glucans improve locomotor performances and mitochondrial function in dystrophic zebrafish. Therefore, for ameliorating their life quality, 1,3-1,6 β-glucans look like a promising diet supplement for DMD patients, even though further investigations are required. 相似文献
80.
Aravindhan Veerapandiyan MD Kathryn R. Wagner MD PhD Susan Apkon MD Craig M. McDonald MD Katherine D. Mathews MD Julie A. Parsons MD Brenda L. Wong MD Katy Eichinger PT PhD Perry B. Shieh MD PhD Russell J. Butterfield MD PhD Vamshi K. Rao MD Edward C. Smith MD Crystal M. Proud MD Anne M. Connolly MD Emma Ciafaloni MD 《Muscle & nerve》2020,62(1):41-45
The coronavirus disease 2019 (COVID-19) pandemic has resulted in the reorganization of health-care settings affecting clinical care delivery to patients with Duchenne and Becker muscular dystrophy (DBMD) as well as other inherited muscular dystrophies. The magnitude of the impact of this public health emergency on the care of patients with DBMD is unclear as they are suspected of having an increased risk for severe manifestations of COVID-19. In this article, the authors discuss their consensus recommendations pertaining to care of these patients during the pandemic. We address issues surrounding corticosteroid and exon-skipping treatments, cardiac medications, hydroxychloroquine use, emergency/respiratory care, rehabilitation management, and the conduct of clinical trials. We highlight the importance of collaborative treatment decisions between the patient, family, and health-care provider, considering any geographic or institution-specific policies and precautions for COVID-19. We advocate for continuing multidisciplinary care for these patients using telehealth. 相似文献