The market, by type, is sub-segmented into calcium stones, uric acid, struvite kidney stones, and
cystine stones.
Goodyer previously reported data at the WORLDSymposium which showed that ELX-02 decreases the
cystine content in cellular and animal models.
If untreated, elevated
cystine accumulation leads to progressive, irreversible tissue damage and multi-organ failure, including kidney failure, blindness, muscle wasting and premature death.
Although we could not measure his leukocyte
cystine content at that time, direct sequencing of the polymerase chain reaction products was performed.
The enzymatic characterization by API-ZYM test system revealed alkaline-phosphatase, acidic-phosphatase, lipase, valine arylamidase,
cystine arylamidase, naphthol-AS-BI-phosphohydrolase, [beta]-galactosidase, leucine arylamidase, and trypsin as positive enzymes produced by S.
Cystine stones, meanwhile, occur in people with a hereditary disorder that causes the kidneys to excrete an excess of certain amino acids.
CaP, uric acid, or
cystine crystals formed in the renal tubules plug at the terminal collecting ducts.
We found statistically significant correlations between increased resistance to 5-fluorocytosine and higher activity of acid phosphatase; increased resistance to ketoconazole and higher activity of beta-glucuronidase; increased resistance to miconazole and higher activity of beta-glucosidase; increased resistance to itraconazole and higher activity of N-acetyl-beta-D-glucosidase, as well as increased susceptibility to itraconazole and higher enzymatic activity of
cystine arylamidase and naphthyl phosphohydrolase.
Cystinosis is a rare metabolic disease with autosomal recessive inheritance, (1) characterized by the accumulation of
cystine crystals in various tissues including the kidneys, bone marrow, pancreas, thyroid, muscle, brain, and eyes.
After percutaneous nephrolithotomy, stone analysis found a calcium oxalate (CaOX) stone in patient-1 and a
cystine stone in patient-2.
Cystinuria is an autosomal recessive disorder in which the kidney, due to a genetic defect in the
cystine transporter, is unable to reabsorb
cystine in the proximal tubule, resulting in urinary hyperexcretion of amino acids
cystine, ornithine, lysine, and arginine (COLA).
Cystine crystal deposits start in the cornea and lead to increased sensitivity to light (photophobia) and corneal surface deterioration (keratopathy).
Deficiency of CBS results in the accumulation of homocysteine and methionine along with a lack of cysteine and
cystine, the oxidised dimer form.
