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Biomedical subjects

A Limaye

Publications and source records attributed to A Limaye.

6 recordsLinked to original sources
PubMed2004

Investigation of microstructural features in regenerating bone using micro computed tomography.

We illustrate some of the uses of micro-computed tomography (micro-CT) to study tissue-engineered bone using a micro-CT facility for imaging and visualizing biomaterials in three dimensions (3-D). The micro-CT is capable of acquiring 3D X-ray CT images made up of 2000(3) voxels on specimens up to 5 cm in extent with resolutions down to 2 microm. This allows the 3-D structure of tissue-engineered materials to be imaged across orders of magnitude in resolution. This capability is used to examine an explanted, tissue-engineered bone material based on a polycaprolactone scaffold and autologous bone marrow cells. Imaging of the tissue-engineered bone at a scale of 1 cm and resolutions of 10 microm allows one to visualize the complex ingrowth of bone into the polymer scaffold. From a theoretical viewpoint the voxel data may also be used to calculate expected mechanical properties of the tissue-engineered implant. These observations illustrate the benefits of tomography over traditional techniques for the characterization of bone morphology and interconnectivity. As the method is nondestructive it can perform a complimentary role to current histomorphometric techniques.

Animals↗
PubMed2001

Adeno-associated viral vector-mediated gene transfer results in long-term enzymatic and functional correction in multiple organs of Fabry mice.

Fabry disease is a lysosomal storage disorder caused by a deficiency of the lysosomal enzyme alpha-galactosidase A (alpha-gal A). This enzyme deficiency leads to impaired catabolism of alpha-galactosyl-terminal lipids such as globotriaosylceramide (Gb3). Patients develop painful neuropathy and vascular occlusions that progressively lead to cardiovascular, cerebrovascular, and renal dysfunction and early death. Although enzyme replacement therapy and bone marrow transplantation have shown promise in the murine analog of Fabry disease, gene therapy holds a strong potential for treating this disease in humans. Delivery of the normal alpha-gal A gene (cDNA) into a depot organ such as liver may be sufficient to elicit corrective circulating levels of the deficient enzyme. To investigate this possibility, a recombinant adeno-associated viral vector encoding human alpha-gal A (rAAV-AGA) was constructed and injected into the hepatic portal vein of Fabry mice. Two weeks postinjection, alpha-gal A activity in the livers of rAAV-AGA-injected Fabry mice was 20-35% of that of the normal mice. The transduced animals continued to show higher alpha-gal A levels in liver and other tissues compared with the untouched Fabry controls as long as 6 months after treatment. In parallel to the elevated enzyme levels, we see significant reductions in Gb3 levels to near normal at 2 and 5 weeks posttreatment. The lower Gb3 levels continued in liver, spleen, and heart, up to 25 weeks with no significant immune response to the virus or alpha-gal A. Also, no signs of liver toxicity occurred after the rAAV-AGA administration. These findings suggest that an AAV-mediated gene transfer may be useful for the treatment of Fabry disease and possibly other metabolic disorders.

Animals↗
PubMed1987

Propylthiouracil-induced fatal hepatic necrosis.

We present a fatal case of acute submassive hepatic necrosis occurring in a 42-yr-old black woman treated for hyperthyroidism with propylthiouracil for 1 yr. Alcohol and drug abuse were ruled out and all serological tests for hepatitis A and B, cytomegalovirus, and Epstein-Barr virus infection were negative. At autopsy the liver was shrunken and presented a yellow granular appearance. Microscopy disclosed submassive necrosis with bile stasis and severe chronic inflammation, as well as mild bile duct proliferation. Although non-A, non-B hepatitis cannot be ruled out (there was no transfusion of blood or its products), this is considered to be the third fatal case and ninth instance of propylthiouracil-induced hepatic necrosis.

Adult↗