Publication

The Crucial Role of AR-V7 in Enzalutamide-Resistance of Castration-Resistant Prostate Cancer

Prostate cancer (PCa) has the second highest incidence of malignancies occurring in men worldwide. The first-line therapy of PCa is androgen deprivation therapy (ADT). Nonetheless, most patients progress to castration-resistant prostate cancer (CRPC) after being treated by ADT. As a second-generation androgen receptor (AR) antagonist, enzalutamide (ENZ) is the current mainstay of new endocrine therapies for CRPC in clinical use. However, almost all patients develop resistance during AR antagonist therapy due to various mechanisms.

VP.60 Every breath counts! Inspiratory muscle training in children with neuromuscular diseases: a cross-over randomised controlled trial

Progressive respiratory muscle weakness and ineffective cough contributes to morbidity and mortality in children with neuromuscular diseases (NMD). Inspiratory muscle training (IMT) aims to preserve or improve respiratory muscle strength and reduce respiratory morbidity. This study aimed to determine the safety and efficacy of IMT in children with NMD. A randomised cross-over study compared three-month intervention (IMT) with control periods.

FP.29 AAV-CRISPR-Cas13 gene therapy for FSHD: DUX4 gene silencing efficacy and immune responses to Cas13b protein

Facioscapulohumeral muscular dystrophy (FSHD) is among the most prevalent muscular dystrophies, ranging from 1 in 8,333 to 1 in 20,000. Currently no treatment exists that alters the course of FSHD, and therapy development remains an unmet need in the field. Abnormal reactivation of the DUX4 gene in skeletal muscle has emerged as an underlying cause of muscle weakness and wasting in FSHD. We propose that DUX4 silencing is the most direct route to FSHD therapy. Toward this goal, we developed an AAV6-CRISPR-Cas13 strategy to silence DUX4 mRNA.

P.187 SelN expression in activated satellite cells following muscle injury

SELENON-related congenital myopathy is characterized by proximal weakness starting in infancy, early respiratory insufficiency, and early development of severe scoliosis. While changes in the SELENON gene, which encodes the protein SelN, are known to cause this disease the mechanisms through which loss of SelN lead to myopathy are not well understood.

P.188 Early growth and metabolic abnormalities in zebrafish and cellular models of SELENON-related myopathy

SELENON-Related Myopathy (SELENON-RM) is a rare genetic disease caused by recessive mutations of the SELENON gene. It is characterized by the development of rigid spine, axial muscle weakness, and respiratory insufficiency. The most common histopathological feature in SELENON-RM patients is the presence of minicores in skeletal muscle biopsies, which are concentrated areas of mitochondrial depletion within fibers. Natural history data suggest that insulin-resistance as well as altered body mass index (BMI) are correlated with SELENON-RM prognosis.

P.189 Using in situ hybridization to delineate collagen VI genes' expression patterns in skeletal muscles of wild-type and COL6-related dystrophies mice

Collagen VI (COLVI) is a critical myomatrix protein for skeletal muscle health and maintenance. There are 6 COL6 genes (COL6A1-COL6A6). Pathogenic variants in COL6A1, COL6A2, or COL6A3 cause COLVI-related dystrophies (COL6-RDs) with early-onset muscle weakness and loss of ambulation. Identifying novel therapeutic targets is critical for developing COL6-RDs therapies.

P.190 Congenital muscular dystrophy associated to conserved oligomeric Golgi complex subunit 1 homozygous mutation

Congenital disorders of glycosylation (CDG) are a group of clinically and genetically heterogeneous diseases caused by disorders of glycoproteins synthesis. Patients manifest a wide range of symptoms, phenotypes, and severity, usually with neurological compromise. The conserved oligomeric Golgi (COG) complex plays an important role in vesicular tethering in retrograde Golgi transport. Mutation in this complex is considered a multiple-pathway CDG. Only 6 cases of pathogenic variants of COG1 have been reported in the literature.

Independent Skeletal Actions of Pituitary Hormones

Over the past years, pituitary hormones and their receptors have been shown to have non-traditional actions that allow them to bypass the hypothalamus-pituitary-effector glands axis. Bone cells-osteoblasts and osteoclasts-express receptors for growth hormone, follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH), prolactin, oxytocin, and vasopressin.

Distribution of vasopressin 1a and oxytocin receptor protein and mRNA in the basal forebrain and midbrain of the spiny mouse (Acomys cahirinus)

The nonapeptide system modulates numerous social behaviors through oxytocin and vasopressin activation of the oxytocin receptor (OXTR) and vasopressin receptor (AVPR1A) in the brain. OXTRs and AVPR1As are widely distributed throughout the brain and binding densities exhibit substantial variation within and across species. Although OXTR and AVPR1A binding distributions have been mapped for several rodents, this system has yet to be characterized in the spiny mouse (Acomys cahirinus).

Global circRNA expression changes predate clinical and histological improvements of psoriasis patients upon secukinumab treatment

Psoriasis is a common chronic inflammatory skin disease accompanied by heterogenous clinical and histological features, including a characteristic keratinocyte hyperproliferation and dermal immunogenic profile. In addition, psoriasis is associated with widespread transcriptomic alterations including changes in microRNA (miRNA) and circular RNA (circRNA) abundance, which constitute non-coding RNA (ncRNA) classes with specific regulatory capacities in diverse physiological and pathological processes.

Pages

X
Contact Us

Complete one of the three forms below and we will get back to you.

For Quote Requests, please provide more details in the Contact Sales form below

Advanced Cell Diagnostics

Our new headquarters office starting May 2016:

7707 Gateway Blvd.  
Newark, CA 94560
Toll Free: 1 (877) 576-3636
Phone: (510) 576-8800
Fax: (510) 576-8798

 

Bio-Techne

19 Barton Lane  
Abingdon Science Park
Abingdon
OX14 3NB
United Kingdom
Phone 2: +44 1235 529449
Fax: +44 1235 533420

 

Advanced Cell Diagnostics China

20F, Tower 3,
Raffles City Changning Office,
1193 Changning Road, Shanghai 200051

021-52293200
info.cn@bio-techne.com
Web: www.acdbio.com/cn

For general information: Info.ACD@bio-techne.com
For place an order: order.ACD@bio-techne.com
For product support: support.ACD@bio-techne.com
For career opportunities: hr.ACD@bio-techne.com