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Biomedical subjects

L Capron

Publications and source records attributed to L Capron.

At least 19 recordsLinked to original sources
PubMed2005

[Workshop to teach elderly patients how to get up from the ground: pilot prospective assessment in a hospital department of internal medicine].

BACKGROUND: Falls occur frequently among the elderly and often lead to hospitalization. Even if uninjured, some of them cannot get up again, and prolonged time on the floor and failed efforts to get up can cause complications. Training methods and exercises for getting up from the floor exist but have not been evaluated. METHODS: We set up a training course to teach elderly patients to get up from the ground and assessed it over the short term by a prospective observational study of 29 patients over 3 months. Each week, a group training session took place, followed 2-9 days later by an individual assessment conducted according to a written protocol. RESULTS: Of the 29 patients (16% of those older than 65 years admitted to our internal medicine department during this period) who received the training, 24 (80%) underwent the subsequent evaluation. Training was effective: before training, only 2 of 29 assessable patients were able to get up on their own, while at the reassessment, 11 of 24 succeeded (p=0.003). Significant improvement was observed for the first two-and most difficult-steps of the maneuver: rolling over from a supine to a prone position (p=0.003), and then moving up into a quadrupedal position (getting up onto all four limbs) (p=0.006). The only variable that appeared to predict a poor result was a Mini Mental Status (MMS) score lower than 26/30. CONCLUSION: Teaching elderly patients how to get up from the floor can be accomplished in an inpatient internal medicine department and appears to be effective in the short term. Although further studies involving more patients followed for a longer period are required to confirm and assess the actual benefits, this training is safe and can be recommended.

Accidental Falls↗
PubMed2003

What's in a risk factor? "He who strikes the ball".

A major aim of epidemiology is to explore the prognosis and aetiology of diseases, in order to improve treatment and prevention. To avoid misleading interpretations of observed associations between a modifier and the occurrence of a disease, the all-purpose idiom "risk factor" should be replaced by 3 locutions with narrower meanings: a risk marker is a modifier which is associated (correlated) with disease prevalence (case-control studies) or incidence (cohort studies); a risk marker truly becomes a risk factor if its experimental correction (intervention studies) does improve the disease incidence or prognosis; a risk factor is promoted to the rank of cause if it is proved to be necessary (sine qua non) for the occurrence of the disease. A more rigorous vocabulary avoids premature claims for unsubstantiated treatments or preventions, and helps defining sound priorities in aetiological research.

Adult↗
PubMed2001

Transient down-regulation of L-type Ca(2+) channel and dystrophin expression after balloon injury in rat aortic cells.

OBJECTIVE: Migration and proliferation of arterial smooth muscle cells are critical responses during restenosis after balloon angioplasty. We investigated the changes in the expression of Ca(2+) channels and dystrophin, two determinants of contraction, after balloon injury of rat aortas. METHODS: Proliferation and migration of aortic myocytes were triggered in vivo by the passage of an inflated balloon catheter in the aortas of 12-week-old male Wistar rats. We used the whole-cell patch clamp technique to investigate Ba(2+) currents (I(Ba)) through Ca(2+) channels in single cells freshly isolated from media and neointima at various times after injury (days 2, 7, 15, 30 and 45). RESULTS: No T-type Ca(2+) channel current was recorded in any cell at any time. In contrast, a dihydropyridine (DHP)-sensitive L-type I(Ba)was recorded consistently in the media of intact aorta. After aortic injury, I(Ba) decreased dramatically (at days 2 and 7) but recovered over time to reach normal amplitude on days 30 and 45. In the neointima, I(Ba) was absent on day 15 but also increased gradually over time as observed at days 30 and 45. The use of a specific antibody directed against the L-type Ca(2+) channel alpha(1C) subunit showed, both by immunostaining and by Western blotting, no expression of the Ca(2+) channel protein on day 15. Parallel immunodetection of dystrophin showed that this marker of the contractile phenotype of SMCs was also not detectable at this stage in neointimal cells. Both proteins were re-expressed at days 45 and 63. Balloon injury induces a transient down-regulation of I(Ba) in arterial cells. CONCLUSIONS: Cell dedifferentiation and proliferation in vivo abolish the expression of L-type Ca(2+) channels and dystrophin in neointimal cells. These changes may be critical in the regulation of Ca(2+) homeostasis and, thereby, contraction of the arterial SMCs during restenosis following angioplasty.

Angioplasty, Balloon↗
PubMed1999

[Etiology of atherosclerosis].

The object of aetiology is to unveil causes, conditions that are necessary (although not sufficient) for the occurrence of a disease. No authentic cause of atherosclerosis has been identified yet. So far, aetiologic research has only established risk factors, modifiable conditions that are neither necessary nor sufficient, which provide efficient but incomplete means for prevention. Other aetiologic tracks must be explored, where the levers for truly mastering atherosclerosis are to be found. Infection is but one example which is presently the object of keen interest, but remains quite far from definitive proof.

Arteriosclerosis↗
PubMed1998

Galectin-3 gene (LGALS3) expression in experimental atherosclerosis and cultured smooth muscle cells.

The galectin-3 gene (LGALS3) encodes a beta-galactose binding lectin. LGALS3 expression is associated with neoplastic transformation and with differentiation of monocytes to macrophages. Factors involved in migration, proliferation, adhesion and differentiation of vascular smooth muscle cells (SMC) play a major role during atherosclerosis development. Expression of the galectin-3 gene was not detected in quiescent SMC but was activated in aortas of hypercholesterolemic rabbits, in aortas of rats after balloon injury and in cultured SMC. These results suggest that galectin-3 production is involved in the developmental process of atherogenesis.

Animals↗
PubMed1998

Insulin-like growth factor-1 stimulates vascular smooth muscle cell proliferation in rat aorta in vivo.

IGF-I is a mitogen for vascular smooth muscle cells (SMC) in vitro and enhances SMC proliferation in vivo in diabetic rats. In this study, we examined the effect of IGF-I on SMC proliferation in vivo in normal rats. Recombinant human IGF-I (0.87 and 3.1 mg/kg/day), was infused via osmotic minipumps in normal rats starting 3 days before they were subjected to aortic injury with a balloon catheter. IGF-I at an infusion rate of 3.1 mg/kg/day caused a significant increase in 3H-thymidine incorporation into DNA (+53%, P < 0.01) in the rat aortic intima-media 2 days after injury and DNA content (+13%, P < 0.05) after 11 days. The elastin and collagen contents were not changed by IGF-I infusion after 11 days. Body weight increased slightly while blood glucose was not affected. At an infusion rate of 0.87 mg/kg/day, IGF-I had no significant effects. These results suggest that circulating levels of IGF-I can stimulate SMC proliferation in vivo in normal rats but only at high concentrations.

Animals↗
PubMed1998

[The infection theory in atherosclerosis].

Atherosclerosis displays all the features of a chronic inflammatory process. Aggressions that ignite and fuel atherosclerotic inflammation warrant keen attention. Infection is a potential clue, implying microbes with certain discrete characteristics: a wide epidemiologic distribution, a tropism for the arterial wall, and an aptitude for persistence, latency and recurrence. The infectious theory has built up from the pioneering observations of Fabricant et al. (1978) on the arterial lesions provoked by Marek's disease herpesvirus in chicken. So far one virus (cytomegalovirus) and two bacteria (Chlamydia pneumoniae and Helicobacter pylori) have been implicated in human atherosclerosis, based upon experimental, sero-epidemiologic, or pathologic evidence. None of these potential contributions has yet been established beyond reasonable doubt. However, grounded on the suspicion about C. pneumoniae, provocative therapeutic evidence has added recently: according to two pilot studies, treatment with macrolide antibiotics appear to improve the prognosis of coronary artery disease in both its chronic and acute forms. If ongoing larger-scale studies confirm these preliminary results, a novel era will open in our capacity for explaining, treating and preventing atherosclerosis. An infectious aetiology of atherosclerosis is now to be considered earnestly, and is already being submitted to more intensive clinical and experimental investigation.

Arteriosclerosis↗
PubMed1997

[Severe hemorrhagic complications during treatment with low molecular weight heparin. Apropos of 2 cases].

Two cases of fatal bleeding in patients treated with low molecular weight heparin for deep vein thrombosis are reported. Risk factors for bleeding were: severe underlying disease (cancer in one case, morbid obesity and cardiac failure in the other), age over 80 years and worsening of renal insufficiency in both cases, recent surgical procedure in one case. Anti-Xa activity was beyond the therapeutic range at the time of bleeding in both cases. The usefulness of biologically monitoring the treatment of deep vein thrombosis with low molecular weight heparin is discussed.

Aged↗