Golden Retriever Handbook

Golden Retriever Guide

Do you want to know everything that there is to know about America's favorite breed of dogs? All that you have to do is read this ebook guide, written by true lovers of Goldens and experts in their behavior. Have you ever wondered why your Golden does the things that it does or if you are giving him or her the proper type of love? You can make sure you know what you need to know with this complete guide to Golden retrievers! You will learn how to select a puppy if you're getting one for the first time, how to prepare your home for your golden puppy, and how to train your adorable new dog. You will also learn the foods that your dog needs to stay healthy and happy for years to come! You will also learn grooming tips, and how to play with your dog!

Golden Retriever Guide Summary


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Contents: Ebook
Author: Marco Santini
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This is one of the best e-books I have read on this field. The writing style was simple and engaging. Content included was worth reading spending my precious time.

As a whole, this book contains everything you need to know about this subject. I would recommend it as a guide for beginners as well as experts and everyone in between.

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Intracavitary Injection

During the postnatal period, the abilities of intraperitoneal or intrapleural administration of different vectors to transduce the diaphragm have also been evaluated. Howell et al. (1997) reported that after intraperitoneal injection of plasmid DNA containing a LacZ transgene together with lipofectin in Golden Retriever Muscular Dystrophy (GRMD) dog pups, positive staining could be found in the diaphragm, intercostal and abdominal muscles, albeit at extremely low levels. Huard et al (1995) performed intraperitoneal injection of first-generation adenoviral vectors in 2-day old rats, and showed significant transgene expression after 5 days in the diaphragm. In this study, a substantial adenovirus level in the blood was also demonstrated in the first few hours after intraperitoneal injection of the vector, raising a question as to whether transduction of the diaphragm may have been mediated through the systemic circulation. In adult mice, Mah et al (2004) compared the efficiencies of...

Summary and Future Direction

In summary, AAV-mediated gene therapy for muscular dystrophies on small animal models by systemic therapeutic gene delivery has been very successful. It can fundamentally restore the defective gene leading to functional recovery of the disease phenotype. In this chapter, we described how gene therapy was applied to multiple forms of muscular dystrophies, particularly, DMD, congenital muscular dystrophy, as well as limb-girdle muscular dystrophy. These studies, along with the work of many other groups, have laid a solid foundation for the development of gene therapy regime for muscular dystrophy patients. In recent years, tremendous efforts have been made to translate the encouraging results from small animal models to large animal models, and eventually to muscular dystrophy patients. One of the examples is the translation from mdx mice to the golden retriever muscular dystrophy (GRMD) dogs and to DMD patients. A number of new challenges absent in the mouse studies are met in the...

Cells Possibly Involved In Muscle Regeneration

Isolating mesoangioblast-like cells also from post-natal mouse, dog and human tissues. When injected into the blood circulation, mesoangioblasts accumulate in the first capillary filter they encounter and are able to migrate outside the vessel, but only in the presence of inflammation, as in the case of dystrophic muscle. We thus reasoned that if these cells were injected into an artery, they would accumulate into the capillary filter and from there into the interstitial tissue of downstream muscles. Indeed, intra-arterial delivery of wild type mesoangioblasts in the a-sarcoglycan KO mouse, a model for limb girdle muscular dystrophy, corrects morphologically and functionally the dystrophic phenotype of all the muscles downstream of the injected vessel Furthermore, mesoangioblasts isolated from a-sarcoglycan null mice and transduced with a lentiviral vector expressing a-sarcoglycan, reconstituted skeletal muscle similarly to wild type cells (Sampaolesi et al., 2003). These data...

Muscular Dystrophy Human Disease and Animal Models

Most of the gene therapy trials for genetic diseases are aimed at sustained expression of therapeutic genes by introducing the vector in the target tissue with minimal or no tissue damage. Activation of T cells is dependent on the danger or inflammatory signal. Thus, the context of antigen presentation for the treatment of DMD has a significant role in T cell activation, since the health status of target tissue, the nature of the vector, and tissue injury associated with the vector delivery all impose additional risks of unwanted T cell activation. Early studies on the prevalence of the expression of MHC class I in skeletal muscle of DMD revealed a remarkable variation. More recently, muscle biopsies of humans with muscular dystrophy or idiopathic inflammatory myopathies revealed upregulation of MHC class I in the sarcolemma in 11 and > 60 of patients, respectively (van der Pas et al. 2004). Interestingly, prolonged immunosuppression was associated with significant reduction in MHC...

The Therapeutic Threshold for Duchenne Cardiomyopathy Gene Therapy

Massons Trichrome Dmd

Fig. 9.3 Animal models for Duchenne dilated cardiomyopathy. (a) Representative photomicrographs of cardiac Masson trichrome staining from 21-m-old BL10 and mdx mice. Fibrotic tissue is in blue color. (b) Representative pressure-volume loops from 21-m-old BL10 and mdx mice. Vertical arrow, end-diastolic volume Horizontal arrow, maximal pressure Double arrow, stroke volume. (c) Representative necropsy photomicrographs of sex matched 2-year-old dog hearts. Left panel, normal golden retriever dog heart Right panel, golden retriever muscular dystrophy (GRMD) dog heart. Bracket, ventricular free wall thickness Asterisk, ventricular free wall trabe-culation Arrow, sporadic calcification seen only in the GRMD heart. (Panels a and b were previously published in Bostick et al. 2008b)

Canine Model for Duchenne Cardiomyopathy

Dystrophin-deficient dogs are exceedingly valuable to DMD gene therapy studies. The dog has a body size closer to that of humans. Additionally, dystrophin-deficient dogs faithfully recapitulate the clinical course of the human disease (reviewed in (Shelton and Engvall 2005 Wieczorek et al. 2006)). The most well studied dog model is the Golden Retriever Muscular Dystrophy (GRMD) model (Cooper et al. 1988 Kornegay et al. 1988). Similar to human patients, GRMD dogs develop severe cardiomyopathy (Chetboul et al. 2004a, b Moise et al. 1991 Valentine et al. 1989 Yugeta et al. 2006). On necropsy, the ventricular chamber of GRMD dogs is clearly enlarged compared to that of the age and sex-matched normal golden retriever dogs (Fig. 9.3c). Also evident in the heart of affected dogs are thin ventricular walls, prominent trabeculations, fibrosis and sporadic calcification (Fig. 9.3c). There is no doubt that dystrophin-deficient dogs will be extremely valuable to define the parameters for Duchenne...


Canine DMD has been diagnosed much more commonly than feline DMD, probably due to the severity of the disease in this species. Among the breeds in which DMD has been described are the Golden Retriever (Sharp et al. 1992), German Short-haired Pointer (Schatzberg et al. 1999), Rottweiler (Winand and Cooper 1994), Labrador Retriever (Bergman et al. 2002), Welsh Corgi (Woods et al. 1998), West Highland White (Smith, unpublished), English Springer Spaniel (Smith unpublished), Australian Labradoodle (Smith unpublished), Old English Sheepdog (Wieczorek et al. 2006) Grand Basset Griffon Vendeen (Klarenbeek et al. 2007) and Japanese Spitz (Jones et al. 2004). The Golden Retriever was the first Golden retriever dog model of DMD identified and the first in which the mutation was determined. The mutation in this breed was found to be a point mutation in the splice acceptor site of intron 6 (Sharp et al. 1992). This results in exon 7 being spliced out of the mRNA, causing a frame-shift and...