29 research outputs found
Anti-tumor effect of adenovirus-mediated gene transfer of pigment epithelium-derived factor on mouse B16-F10 melanoma
<p>Abstract</p> <p>Background</p> <p>Angiogenesis plays an important role in tumor growth, invasion, and eventually metastasis. Antiangiogenic strategies have been proven to be a promising approach for clinical therapy for a variety of tumors. As a potent inhibitor of tumor angiogenesis, pigment epithelium-derived factor (PEDF) has recently been studied and used as an anticancer agent in several tumor models.</p> <p>Methods</p> <p>A recombined adenovirus carrying PEDF gene (Ad-PEDF) was prepared, and its expression by infected cells and in treated animals was confirmed with Western blotting and ELISA, respectively. Its activity for inhibiting human umbilical vein endothelial cell (HUVEC) proliferation was tested using the MTT assay. C57BL/6 mice bearing B16-F10 melanoma were treated with i.v. administration of 5 Ă— 10<sup>8 </sup>IU/mouse Ad-PEDF, or 5 Ă— 10<sup>8 </sup>IU/mouse Ad-Null, or normal saline (NS), every 3 days for a total of 4 times. Tumor volume and survival time were recorded. TUNEL, CD31 and H&E stainings of tumor tissue were conducted to examine apoptosis, microvessel density and histological morphology changes. Antiangiogenesis was determined by the alginate-encapsulated tumor cell assay.</p> <p>Results</p> <p>The recombinant PEDF adenovirus is able to transfer the PEDF gene to infected cells and successfully produce secretory PEDF protein, which exhibits potent inhibitory effects on HUVEC proliferation. Through inhibiting angiogenesis, reducing MVD and increasing apoptosis, Ad-PEDF treatment reduced tumor volume and prolonged survival times of mouse bearing B16-F10 melanoma.</p> <p>Conclusion</p> <p>Our data indicate that Ad-PEDF may provide an effective approach to inhibit mouse B16-F10 melanoma growth.</p
Recurrence of primary hyperoxaluria: An avoidable catastrophe following kidney transplant
Primary hyperoxaluria is a rare autosomal recessive disease due to
deficiency of an oxalate-metabolizing liver enzyme, which results in
nephrolithiasis and renal failure. Concomitant liver and kidney
transplant is recommended as isolated kidney transplant is inevitably
complicated by recurrence of the disease. We present a 25-year-old man
with end-stage nephrolithiatic renal disease who underwent bilateral
nephrectomy, followed by kidney transplantation. There was progressive
worsening of kidney function two weeks post transplant. Review of
nephrectomy and transplant kidney biopsy showed abundant calcium
oxalate crystals and further workup revealed hyperoxaluria, which was
previously unsuspected. Later he developed fever, breathlessness,
hemiparesis and died 10 weeks after transplant. Autopsy revealed
multi-organ deposits of oxalate crystals as well as widespread
zygomycosis. This case emphasizes the need for careful pre-transplant
evaluation of patients with renal calculus disease in order to exclude
primary hyperoxaluria