Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:6.3.5.5 (
CPS
)
1,262
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Twelve patients with peripheral arterial occlusive disease were evaluated prospectively in an effort to further investigate the etiology of pedal and lower leg edema that occurs following revascularization (e.g., aorto-iliac or femoropopliteal bypass). Serum total protein, albumin, blood urea nitrogen, and
creatinine
levels were measured (in addition to peripheral venous pressure), and lymphoscintigraphy of the lower leg was performed. These parameters were assessed just prior to surgery, four weeks postoperatively, and again at follow-up. The serum levels obtained four weeks after surgery and on subsequent follow-ups were significantly higher than the preoperative values. Preoperative peripheral venous pressure was not significantly different from that obtained after surgery. There was no correlation between these pressure measurements and the degree of edema (Grades I to IV correspond to increasing degrees of severity). For both the supine and upright positions, lymphoscintigraphic counts in the inguinal region were significantly higher after surgery. However, the relative increase was dependent upon the severity of edema. The postoperative lymphoscintigraphic count in the upright position was 77 +/- 33
CPS
in patients with Grades I and II edema (n = 6) and 20.6 +/- 16.2
CPS
in patients with Grades III and IV edema (n = 10) (p less than 0.01). Thus, a lesser degree of postoperative pedal and lower leg edema was associated with higher lymphoscintigraphic counts. We conclude that major contributors to the development of lower extremity edema following arterial reconstruction are failed capillary hydrostatic pressure and interrupted lymphatic drainage.
...
PMID:99mTc-HSA lymphoscintigraphy and leg edema following arterial reconstruction. 175 91
Benzoylcarnitine was identified in the urine of a patient with a
carbamoyl-phosphate synthase
I deficiency for whom sodium benzoate and L-carnitine had been used to treat hyperammonemia. This is a newly identified metabolite of benzoate. Its excretion in the urine was increased day by day at the administration of both sodium benzoate and L-carnitine from 0.10 to 2.25 mmol/g
creatinine
. Since there is the possibility of a secondary carnitine deficiency and an increase of benzoyl toxicity after long-term therapy with benzoate supplementation and protein restriction, it is important to monitor the urinary excretion of benzoylcarnitine.
...
PMID:Identification of benzoylcarnitine in the urine of a patient of hyperammonemia. 260 32
A water-soluble polysaccharide (
CPS
-2), isolated from the cultured Cordyceps sinensis, was obtained by hot-water extraction, anion-exchange and gel permeation chromatography. Its structural characteristics were investigated by PMP pre-column derivation, periodate oxidation, methylation analysis, FTIR and NMR spectroscopy.
CPS
-2 was found to be mostly of alpha-(1-->4)-D-glucose and alpha-(1-->3)-D-mannose, branched with alpha-(1-->4,6)-D-glucose every twelve residues on average.
CPS
-2 had a molecular weight of 4.39x10(4) Da. The protective effect of
CPS
-2 on the model of chronic renal failure was established by fulgerizing kidney. The changes in blood urea nitrogen and serum
creatinine
revealed that
CPS
-2 could significantly relieve renal failure caused by fulgerizing kidney.
...
PMID:Protection of chronic renal failure by a polysaccharide from Cordyceps sinensis. 1996 45
Hyperlipidic diets limit glucose oxidation and favor amino acid preservation, hampering the elimination of excess dietary nitrogen and the catabolic utilization of amino acids. We analyzed whether reduced urea excretion was a consequence of higher NO x ; (nitrite, nitrate, and other derivatives) availability caused by increased nitric oxide production in metabolic syndrome. Rats fed a cafeteria diet for 30 days had a higher intake and accumulation of amino acid nitrogen and lower urea excretion. There were no differences in plasma nitrate or nitrite. NO(x) and
creatinine
excretion accounted for only a small part of total nitrogen excretion. Rats fed a cafeteria diet had higher plasma levels of glutamine, serine, threonine, glycine, and ornithine when compared with controls, whereas arginine was lower. Liver
carbamoyl-phosphate synthetase
I activity was higher in cafeteria diet-fed rats, but arginase I was lower. The high
carbamoyl-phosphate synthetase
activity and ornithine levels suggest activation of the urea cycle in cafeteria diet-fed rats, but low arginine levels point to a block in the urea cycle between ornithine and arginine, thereby preventing the elimination of excess nitrogen as urea. The ultimate consequence of this paradoxical block in the urea cycle seems to be the limitation of arginine production and/or availability.
...
PMID:Altered nitrogen balance and decreased urea excretion in male rats fed cafeteria diet are related to arginine availability. 2470 2