Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The continuous shortage of human donor organs for transplantation has led to new interest in the application of pig organs. However, reports of pig endogenous retroviruses (PERV), which are able to infect human cells in vitro, have raised concerns about the transmission of PERV to the recipients or even to other community members. In this study, PK15 and human 7721 cell lines were implanted into each flank of nude mice and tumors appeared several weeks postimplantation. PERV infection was detected by PCR, using cytochrome oxidase B sequences as the specific marker for pig DNA. The results showed that PERV gag sequence were positive in mice livers, kidneys, hearts, and lungs, but no cytochrome oxidase B sequences detected, which indicates the absence of pig-mouse microchimerism. The results also showed that PERV did not infect human 7721 tumors in mice. This study confirmed the presence of PERV transmission from pig-to-mouse tissue and strengthened the concern of the risk of transmitting PERV through pig cells xenotransplantation.
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PMID:Porcine endogenus retrovirus transmission from pig cell line to mouse tissues but not human cells in nude mice. 1580 87

Mitochondrial disorders comprise a heterogenous group. A neonate who presented with episodes of severe truncal hypertonia and apnea progressed to a hypokinetic rigid syndrome characterized by hypokinesia, tremulousness, profound head lag, absent suck and gag reflexes, brisk deep tendon reflexes, ankle and jaw clonus, and evidence of autonomic dysfunction. Analysis of cerebrospinal fluid neurotransmitters from age 7 weeks demonstrated low levels of amine metabolites (homovanillic acid and 5-hydroxyindoleacetic acid), tetrahydrobiopterin, and pyridoxal phosphate. Mitochondrial DNA quantitative studies on muscle homogenate demonstrated a mitochondrial DNA depletion disorder. Respiratory chain enzymology demonstrated decreased complex IV activity. Screening for mitochondrial DNA rearrangement disorders and sequencing relevant mitochondrial genes produced negative results. No clinical or biochemical response to treatment with pyridoxal phosphate, tetrahydrobiopterin, or l-dopa occurred. The clinical course was progressive, and the patient died at age 19 months. Mitochondrial disorders causing secondary neurotransmitter diseases are usually severe, but are rarely reported. This diagnosis should be considered in neonates or infants who present with hypertonia, hypokinesia rigidity, and progressive neurodegeneration.
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PMID:"Stiff neonate" with mitochondrial DNA depletion and secondary neurotransmitter defects. 2211 5