John L Mcanally

US Patent:

20100251768, Oct 7, 2010

Filed:

Apr 6, 2009

Appl. No.:

12/418734

Inventors:

John R. McAnally - Grand Prairie TX, US

International Classification:

A44C 5/00
A44C 5/02
A44C 25/00

US Classification:

63 3, 63 38

Abstract:

A bracelet comprising interconnected blocks for use in the Pro-Life movement for reminding people of the reproductive process associated with the human fetuses, each block containing an individualized prayer on the reverse side. The bracelet portrays continual development from the fertilization stage and through the last month of birth. The present invention is a Pro-life religious bracelet designed for use by the Pro-life movement to help people understand the various stages of conception and perhaps dissuade individuals from performing abortions.

US Patent:

20160058889, Mar 3, 2016

Filed:

Aug 11, 2015

Appl. No.:

14/823563

Inventors:

- Austin TX, US
Chengzu LONG - Dallas TX, US
John R. MCANALLY - Dallas TX, US
John M. SHELTON - Dallas TX, US

International Classification:

A61K 48/00
C12N 15/113
A61K 38/46

Abstract:

Duchenne muscular dystrophy (DMD) is an inherited X-linked disease caused by mutations in the gene encoding dystrophin, a protein required for muscle fiber integrity. The disclosure reports CRISPR/Cas9-mediated gene editing (Myo-editing) is effective at correcting the dystrophin gene mutation in the mdx mice, a model for DMD. Further, the disclosure reports optimization of germline editing of mdx mice by engineering the permanent skipping of mutant exon (exon 23) and extending exon skipping to also correct the disease by post-natal delivery of adeno-associate virus (AAV). AAV-mediated Myo-editing can efficiently rescue the reading frame of dystrophin in mdx mice in vivo. The disclosure reports means of Myo-editing-mediated exon skipping has been successfully advanced from somatic tissues in mice to human DMD patients-derived iPSCs (induced pluripotent stem cells). Custom Myo-editing was performed on iPSCs from patients with differing mutations and successfully restored dystrophin protein expression for all mutations in iPSCs-derived cardiomyocytes.