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J C Bigot

Publications and source records attributed to J C Bigot.

7 recordsLinked to original sources
PubMed2002

[Epidemiologic study of urinary calculi in Western France].

OBJECTIVES: An epidemiologic study of urinary calculi (N = 1843) was conducted in Western France: distribution according to the main chemical compounds, age and sex. Comparison with the results of a study with national recruitment (N = 10,617) and a study with regional recruitment (N = 1774). METHOD: The study involved 1843 stones characterized beforehand by morphological analysis associated with infra-red spectrophotometry (FTIR). If analysis of the composition of the stones was carried out on the totality of calculi, studies related to age and sex included only 1583 cases. Comparison of percentages was made using chi 2 test. RESULTS: The composition in main compounds of calculi was comparable with the results of other studies; minor significant compounds presented great differences, raising the problem of interpretation of the infra-red spectra of the latter. Hence, our work was directed towards the analysis of the major compounds and we showed, like most authors, that monohydrate calcium oxalate is predominant in male (46%) as well as in females (37%). Calculi average sex-ratio was 2.19 but dehydrated calcium oxalate sex-ratio was 4.42, suggesting that this compound is found mainly in men. Conversely, for the majority of phosphate stones, the sex-ratio was lower or equal to one, indicating that they predominate in women. Infectious calculi (particularly struvite calculi) appeared slightly more frequent in our population than in other studies, whereas the number of uric acid calculi was lower. This, however, remains to be confirmed. CONCLUSION: The population studied was not significantly different from the national population regarding lithiasis, except perhaps for uric acid and struvite calculi, despite specific regional differences in diet and the role of nutritional factors in lithogenesis.

Adolescent↗
PubMed1993

[Results of dietary evaluation during calcium oxalate and calcium phosphate lithiasis].

In order to better understand the role of diet in etiology of urolithiasis, 84 oxalo-phospho-calcic-lithiasic patients (52 men, 32 women) have been studied by a nutritional week-interview and by urinary and blood testing. Diet data were compared to an ideal standard. Total caloric intake was 2428 +/- 651 calories/d; this intake is high in 7% women and 40% men. 79% out of patients are fat. Protidic intake is 87 +/- 21 g/d higher than 1 g/kg/d in 84.5% of patients. Lipids are high in 38.9 +/- 7%, glucid are low in 45.3 +/- 7%. Calcium intake is 934 +/- 406 mg/d, sodium intake is 12.9 + 3 g/d. Water intake is 2305 +/- 759 ml/d. Different groups of patients are studied: a) 21 patients with mean age of 43 +/- 12 years have recurrent lithiasis (R). This group is compared to 48 patients with 37 +/- 44 years who have a single lithiasis. Half of (R) patients have hypercalciuria, hyperphosphaturia and hyperoxaluria. Diet study is no different between these two groups. b) Other groups are studied: 21 have hyperophosphaturia (HPU) without hypophosphoremia and they have hypercalciuria, hyperuraturia and high urinary urea; diet shows higher glucicid and potassium intake than group with normal phosphaturia; 23 have hypercalciuria (HCU) and high uraturia and phosphaturia: diet study shows no difference with a group with normal calciuria. 21 have hyperoxaluria (HOU): diet study of a normal oxaluric group shows higher lipid intake, lower glucidic and calcium intake; 22 have hyperuraturia (HAU) and higher urinary urea, sodium and potassium than normouraturia group: in this group potassium intake is higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Changes in striatal and cortical amino acid and ammonia levels of rat brain after one hyperbaric oxygen-induced seizure.

Changes in amino acids (AA) and ammonia were investigated in the cerebral cortex and striatum of rats after the following conditions: 1) one hyperbaric oxygen (HBO)-induced seizure (6 ATA O2); 2) exposure to 6 ATA air; and 3) exposure to atmospheric pressure (no seizures in both latter groups). Exposure to 6 ATA air produced no change with respect to atmospheric pressure. After HBO seizure, AA levels (except for gamma-amino butyric acid, GABA, and glutamine), with respect to 6 ATA air levels, were altered in the striatum with a concomitant rise in ammonia (+70%) at variance with the cortex. These changes could be explained by increased oxidative deamination in the striatum. Decrease in taurine content (-66%) in the striatum, where HBO lipoperoxidation exists, suggests an alteration of glial function leading to blockade of uptake and loss of released products in interstitial fluid. This pattern of change recalls the one seen in ischemic conditions, but cannot be confirmed in the absence of measurements of extracellular amino acid levels under HBO conditions. The maintenance in the level of GABA would favor its role in controlling seizure. In the cortex, only a few AA levels decreased, along with a nonsignificant trend for ammonia to increase. The remaining abnormalities in the striatum, after the first HBO seizure, may explain the already known repetition of seizures in continuously exposed animals and are consistent with previous data on the important role of the striatum.

Amino Acids↗
PubMed1990

Ammonia and monoamine concentrations in two brain areas in rats after one hyperoxic seizure.

Monoamines (catecholamines, serotonin, and metabolites) and ammonia were studied within two areas of the rat brain--the frontal cortex (FC) and the striatum (SA)--after exposure to hyperbaric oxygen (HBO) at 6 ATA up to the first seizure. An increase of norepinephrine (NE), dopamine (DA), and metabolites (HVA, DOPAC) measured by the HPLC/EC method were found in SA with a parallel increase of ammonia at variance with the FC where no monoamine changes, but a slight increase of ammonia, were found. Blood ammonia did not change with HBO. So, 20 min after one HBO seizure, there are regional differences in the brain, which are consistent with the previous findings of an SA start of electrocortical abnormalities at the onset of a seizure. Elevated DA, and possibly NE, levels may contribute to the accumulation of ammonia in the brain. During prolonged HBO exposure, this rise of ammonia could be one of the mechanisms involved in the relapse of seizures. It might also be implicated in initiation of the first seizure. By their situations and contents, SA glial cells could play an important role in brain HBO susceptibility.

Ammonia↗
PubMed1985

[Alcoholic epilepsy. Decrease of tryptophan levels in the blood and cerebrospinal fluid].

The initial, functional stage of alcoholic epilepsy has been attributed to disturbances in neuromediators, including serotonin. Tryptophan, a precursor of serotonin, was assayed in 10 alcoholic patients with epilepsy and in a group of subjects with normal tryptophan metabolism and undisrupted blood-brain barrier. Tryptophan levels were measured in the cerebrospinal fluid and free and total tryptophan levels in plasma, using an automatized continuous flow method. Compared with controls, the alcoholic patients showed a highly significant decrease of all tryptophan fractions.

Adult↗