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Biomedical subjects

J Coll

Publications and source records attributed to J Coll.

At least 91 records · Page 5Linked to original sources
PubMed1990

[The waiting times in a health center].

Variables of geographical and functional accessibility were evaluated with a questionnaire in 322 users of a health center with spontaneous demand of medical care. A remarkable finding was that, while the time from the patient's home to the health center was 9.3 minutes, the mean waiting time in the clinic was over two hours (121 min). Surprisingly, only 30.2% of the surveyed population considered this waiting time as "long or very long". By contrast, when they were asked about what would be their optimal waiting time the mean response was 35.5 min. The factors possibly involved in those long waiting times and their relation with the user's satisfaction are evaluated. It becomes obvious that a widespread "time-oriented" appointment system should be implemented.

Age Factors↗
PubMed1989

Septic shock and bacteremia associated with laparoscopic guided liver biopsy, report on two cases.

Two cases of infectious complications after liver biopsy are reported. Klebsiella pneumoniae and beta-hemolytic Streptococcus were cultured. In both cases the biopsy was obtained under laparoscopic control. A 28-year-old woman with liver cirrhosis died 24 hours after liver biopsy as a result of septic shock and disseminated intravascular coagulation. A 67-year-old man with hepatic fibrosis suffered from transient bacteremia and recovered uneventfully after antibiotic therapy. In these patients, there was evidence to implicate pre-existing cholangitis as factor predisposing to postbiopsy bacteremia.

Adult↗
PubMed1989

Exocrine pancreatic function in Sjögren's syndrome.

Pancreatic function testing was carried out in 19 patients with Sjögren's syndrome (SS) (nine primary type, ten secondary) by the N-benzoyl-tyrosil-p-aminobenzoic acid (PABA) test, serum immunoreactive trypsin (IRT) levels, and stool fat measurements to evaluate the incidence and type of exocrine pancreatic alterations in this disease. Exocrine pancreatic impairment was found to be present in 63% of the patients. Three types of secretory patterns were observed: (1) normal PABA test results and normal IRT levels (37% [7/19] of the patients); (2) normal PABA test results and elevated IRT levels (42% [8/19]; and (3) low PABA test results and elevated IRT levels (21% [4/19]), including two patients with steatorrhea. Functional pancreatic impairment tended to be more severe in patients with longer disease duration and it was related to the degree of alteration of salivary flow but not to labial salivary gland histologic changes or the type of SS. Inasmuch as hypertrypsinemia was the common marker of pancreatic dysfunction in all patients, we suggest a periodic measurement of serum IRT levels in the follow-up of patients with SS to detect early stages of pancreatic involvement.

4-Aminobenzoic Acid↗
PubMed1988

Replacement of lys 622 in the ATP binding domain of P100gag-mil abolishes the in vitro autophosphorylation of the protein and the biological properties of the v-mil oncogene of MH2 virus.

Lysine 622 in the ATP-binding domain of P100gag-mil, the translation product of the v-mil oncogene of MH2, has been replaced with methionine using oligonucleotide site-directed mutagenesis. This substitution results in the inactivation of the serine/threonine-specific autophosphorylation of P100gag-mil in vitro, indicating that this activity is an intrinsic property of the viral protein. This substitution also suppresses two of the biological properties of MH2 which have previously been shown to be dependant upon the expression of v-mil, namely, the production of chicken myelomonocytic growth factor (cMGF) by v-myc-transformed chicken macrophages and the sustained proliferation of chicken neuroretina cells. These data strongly suggest that the biological properties of v-mil are mediated by the phosphorylation at serine/threonine residues of key cellular substrates. In contrast to the in vitro situation, both the mutant and wild-type proteins appear to be phosphorylated at the same sites and to the same extent in either transformed fibroblasts or macrophages. This, together with the fact that the sites phosphorylated in vivo and in vitro are essentially different indicate that most of the phosphate associated with P100gag-mil in transformed cells does not result from an obligate autophosphorylation event but from the phosphorylation by as yet uncharacterized cellular kinase(s).

Adenosine Triphosphate↗
PubMed1988

[Cell proliferation and cooperation of v-mil and v-myc oncogenes].

Retroviruses which possess the property to recombine with genetic material from the cell, have cloned and activated some oncogenes and hence are a privileged source for the study of these genes. Cellular oncogene activation can occur following two non mutually exclusive ways: (i) by over-expression of their products; (ii) by modifications of their products through mutations. Retroviruses can combine these two ways of activation leading to the over-expression of a modified product. In this paper, we present results obtained in the study of MH2, a retrovirus containing two oncogenes. We have shown that the two oncogenes of MH2 (v-mil and v-myc) cooperate in vitro to transform neuroretina cells from chicken embryos. These cells which normally do not grow in a defined medium, are induced to proliferate and become transformed upon infection by MH2. Our data enabled us to show that in MH2 v-mil was responsible for the induction of proliferation and v-myc for the transformation of the proliferating cells. Using in vitro constructs we located two regions in the protein encoded by v-mil which are important for its mitogenic property. We have also cloned the cellular counterpart of v-mil and the study of its biological activity on neuroretina cells enabled us to propose a mechanism of activation of the cellular gene by truncation of its 5' part.

Animals↗
PubMed1988

Mapping by in vitro constructs of the P100gag-mil region, accounting for induction of chicken neuroretina cell proliferation.

The v-mil oncogene of the avian retrovirus MH2 is expressed as a fusion protein with viral gag determinants in infected cells. This P100gag-mil protein accounts for the proliferation of chicken embryo neuroretina cells (CNR) induced by MH2 in vitro. We constructed a series of mutants by in-frame deletions in different parts of the gag and mil domains and tested their ability to induce CNR growth. We show that gag sequences, as well as 200-base-pair 5' mil sequences, were not required to induce such a proliferation. However, gag sequences seem to contribute to a full proliferation of growing CNR. In contrast, deletions in the kinase domain abolish this induction. In particular, by deleting only 9 nucleotides localized around the unique SphI site of v-mil, we produced a totally inactive mutant (BalSp). This mutant directs the synthesis of a v-mil protein lacking the dipeptide Tyr-Leu, which is conserved in almost all the members of the large protein kinase family, and a histidine residue highly conserved in Ser-Thr protein kinase members.

Animals↗
PubMed1988

Alternative splicing of RNAs transcribed from the chicken c-mil gene.

Two distinct c-mil-related cDNA clones have been isolated from a chicken embryo cDNA library. Results presented here show that the single chicken c-mil gene is coding for two c-mil mRNA species, different by at least 60 base pairs and generated by an alternative splicing mechanism. These mRNA molecules can be translated into two distinct proteins of 73 and 71 kilodaltons.

Amino Acid Sequence↗
PubMed1988

Chronic intestinal pseudoobstruction and ophthalmoplegia in a patient with mitochondrial myopathy.

A 38 year old woman having chronic intestinal pseudoobstruction associated with mitochondrial myopathy is reported. The clinical and radiographic features suggested the diagnosis of chronic intestinal pseudoobstruction. Muscular atrophy and ophthalmoplegia led to muscle biopsy, which disclosed accumulation of normal and abnormal mitochondria ('ragged red fibres'), characteristic of mitochondrial myopathy.

Adult↗