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Biomedical subjects

J Pie

Publications and source records attributed to J Pie.

7 recordsLinked to original sources
PubMed2003

Preperitoneal repair for recurrent inguinal hernia: laparoscopic and open approach.

BACKGROUND: The aim of this study was to investigate the outcome of preperitoneal repair using laparoscopic (TEP) and open (OPM) approach in recurrent inguinal hernia. METHODS: We performed a prospective controlled nonrandomized clinical study in 188 patients with 207 recurrent inguinal hernias over a period of 5 years. TEP repair was employed for 86 repairs, and OPM was used in 121 procedures. The main outcome measurements were: recurrence rate, operating time, hospital stay, and postoperative complications. RESULTS: There were three recurrences (1.7%). Two in the OPM group (1.8%) and one (1.3%) in the TEP group [ P=NS (not significant)]. The TEP procedure was faster than OPM for unilateral repair (40.8 vs 46.3 min) (P<0.001). Postoperative complications were more frequent in the OPM group (23.9%) than the TEP group (13.9%) ( P=NS). Hospital stay was significantly shorter in the TEP group (1.2 vs 3.9 days) (P<0.001). CONCLUSIONS: Preperitoneal approach (open or laparoscopic) seems to be a good option in recurrent inguinal hernia when these procedures are done by experienced surgeons.

Adult↗
PubMed2003

Molecular basis of 3-hydroxy-3-methylglutaric aciduria.

3-Hydroxy-3-methylglutaric aciduria is a human autosomal recessive metabolic disorder that usually appears within the first year of life. The causes of this aciduria are lethal mutations in the gene encoding for 3-hydroxy-3-methylglutaryl coenzyme A lyase (HL). HL is a mitochondrial matrix enzyme that catalyzes the last step of ketogenesis and leucine catabolism. This gene has been mapped to chromosome 1 at locus 1pter-p33 and its genomic organisation comprises 9 exons whose sizes vary between 64-678 bp. The human cDNA sequence was reported in 1993 with the first genetic study of two Acadian-French Canadian siblings. To date, 24 mutations in 36 patients have been described; most of them are single-base substitutions causing amino acid replacements and a variety of splicing defects. In the population studied two mutations appear predominant: g.122GA (8 patients and 15 alleles) frequent in Saudi Arabia, and g.109GT (6 patients and 12 alleles), prevalent in Spain. At least seven mutations are clustered in the second half of exon 2 affecting aminoacids E37, R41 and D42 and conforming a possible hot spot. The genotype-phenotype correlation is difficult to establish since the probands received different treatments, and the onset of an acute episode frequently depends on external factors such as fasting or acute illness.

Alternative Splicing↗
PubMed2001

Apoptosis of PC12 cells by 4-hydroxy-2-nonenal is mediated through selective activation of the c-Jun N-terminal protein kinase pathway.

Cytotoxic lipid peroxides such as 4-hydroxy-2-nonenal (HNE) are produced when cells are exposed to toxic chemicals. However, the mechanism by which HNE induces cell death has been poorly understood. In this study, we investigated the molecular mechanism of HNE-induced apoptosis in PC12 cells by measuring the activities of the mitogen-activated protein (MAP) kinases involved in early signal transduction pathways. Within 15-30 min after HNE treatment, c-Jun N-terminal protein kinase (JNK) was maximally activated, before returning to control level after 1 h post-treatment. In contrast, activities of extracellular signal regulated kinase (ERK) and p38 MAP kinase remained unchanged from their basal levels. SEK1, an upstream kinase of JNK, was also activated (phosphorylated) within 5 min after HNE treatment and remained activated for up to 60 min. Marked activation of the JNK pathway through SEK1 was demonstrated by the transient transfection of cDNA for wild type SEK1 and JNK into COS-7 cells. Furthermore, significant reductions in JNK activation and HNE-induced cell death were observed when the dominant negative mutant of SEK1 was co-transfected with JNK. Pretreatment of PC12 cells with a survival promoting agent, 8-(4-chlorophenylthio)-cAMP, prevented both the HNE-induced JNK activation and apoptosis. Nonaldehyde, a nontoxic aldehyde, caused neither apoptosis nor JNK activation. Pretreatment of PC12 cells with SB203580, a specific inhibitor of p38 MAP kinase, had no effect on HNE-induced apoptosis. All these data suggest that the HNE-mediated apoptosis of PC12 cells is likely to be mediated through the selective activation of the SEK1-JNK pathway without activation of ERK or p38 MAP kinase.

Aldehydes↗
PubMed1998

Oxidative toxicity in models of neurodegeneration: responses to melatonin.

In this brief review the antioxidative actions of melatonin are summarized and they are discussed relative to several models of oxidative neurotoxicity. Melatonin is a ubiquitously acting antioxidant. It has been shown to scavenge the hydroxyl radical, peroxyl radical, singlet oxygen and the peroxynitrite anion; secondarily, it also scavenges the superoxide anion radical. In addition, melatonin reportedly stimulates a number of antioxidative enzymes including glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase. On the other hand, melatonin inhibits the pro-oxidative enzyme nitric oxide synthase. Besides these actions which help to resist oxidative damage, melatonin prevents membrane rigidity, reduces polymorphonuclear cell infiltration into damaged tissue, limits the adhesion of leucocytes to endothelial cells, thereby increasing blood flow and reducing edema. Some or all of these actions may have been operative in the experimental models of oxidative neurotoxicity that were improved by melatonin treatment. In brief, melatonin has been found to protect the CNS from beta-amyloid toxicity, experimental models of Parkinsonism, excitotoxicity, nitric oxide toxicity, aminolevulinic acid, lipopolysaccharide, hyperbaric hyperoxia, L-cysteine, cyanide and ischemia/reperfusion injury.

Journal Article↗
PubMed1987

Thyroxine in unextracted urine.

The aim of this work was to estimate the daily urinary excretion of free and conjugated thyroxine using a direct radioimmunoassay and enzyme hydrolysis. The renal clearance of free T4 was also determined. The mean urinary values of free and total T4 (mean +/- 1 SD) in 112 euthyroid controls were 1353 +/- 496 and 1855 +/- 651 pmol/24 h, respectively. Urinary excretion of free hormone in 13 hyperthyroid patients was 5552 +/- 4320 pmol/24 h and total T4 was 8122 +/- 7219 pmol/24 h. Urinary free T4 excretion was 223 +/- 223 pmol/24 h in hypothyroid patients and total T4 was 542 +/- 490 pmol/24 h. These results indicate that daily urinary T4 excretion is a good indicator of thyroid function. The mean renal clearance of free T4 was 52 +/- 19 ml/min (mean +/- 1 SD) in euthyroid patients, 53.7 +/- 12.3 ml/min in hyperthyroid patients, and 67.6 +/- 13.1 ml/min in hypothyroid patients. We estimated the endogenous creatinine renal clearance as a control of the renal filtration rate. The data suggest that there is T4 filtration of unbound T4 and partial tubular reabsorption. Further experimental studies will be necessary to clarify the renal handling of thyroxine as well as the fate of reabsorbed T4.

Adult↗