Domestic activities after myocardial infarction. Their impact is underestimated.

BACKGROUND: Although aptitude for resumption of work is usually evaluated after myocardial infarction, the return home often entails significant daily obligations whose cardiovascular implications are poorly described and may well be underestimated. AIM: The aim of this study was to evaluate the consequences of domestic activities on blood pressure and heart rate in patients with recent myocardial infarction DESIGN: This was an observational study. SETTING: Inpatients, at the end of a three week period of cardiovascular rehabilitation. POPULATION: Patients with recent myocardial infarction. METHODS: We studied patients who had benefited from a three-week period of cardiovascular rehabilitation after a myocardial infarction, all treated with beta-blockers. At the end of the rehabilitation period, patients were submitted to a standardized exercise test with measurement of V.O2. They also carried out, on a separate day, four standardized domestic tasks in a random order along with an automated measurement of blood pressure and heart rate. RESULTS: We included 16 men and 11 women, aged 35 to 74 years. Vacuum cleaning led to a much greater increase in the product of heart rate and systolic blood pressure (DP) than did window cleaning, bathroom cleaning or ironing. It also led to an increase in heart rate to 70-90% of maximum heart rate during the exercise test and 47-65% of the maximal DP on the exercise test. Although the women were more accustomed to these tasks than the men, they did not appear to benefit from any training effect. The average level of DP observed in some patients during domestic tasks was comparable to that of a maximum exercise test indicating that they were not adequately prepared for a return to household activities. CONCLUSION: Domestic tasks should not be underestimated as they can lead to a significant increase in DP. They tend not to be taken into account in the rehabilitation of patients after a myocardial infarction. CLINICAL REHABILITATION IMPACT: The traditional methods of rehabilitation are not well adapted for resumption of domestic life, especially for women who are most involved in these activities. We recommend an individual approach involving performance of real life tasks taking account of the personality of the patients, their lifestyle and home environment.

Src-family kinases play an essential role in differentiation signaling downstream of macrophage colony-stimulating factor receptors mediating persistent phosphorylation of phospholipase C-gamma2 and MAP kinases ERK1 and ERK2.

Macrophage colony-stimulating factor (M-CSF) has been found to be involved in multiple developmental processes, especially production of cells belonging to the mononuclear phagocyte system. The decision of myeloid progenitor cells to commit to differentiation depends on activation levels of the mitogen-activated protein kinases (MAPK), ERK1 and ERK2. Using the murine myeloid progenitor cell line FD-Fms, we show here that persistent activity of Src-family kinases (SFK) is necessary for FD-Fms cell differentiation to macrophages in response to M-CSF. Chemical inhibition of SFK blocked FD-Fms cell differentiation while it caused strong inhibition of the late phosphorylation of phospholipase C (PLC)-gamma2 and MAPK. The PLC inhibitor U73122, previously shown to block M-CSF-induced differentiation, strongly decreased long-term MAPK phosphorylation. Interestingly, inhibiting SFK with SU6656 or the MAPK kinases MEK with U0126 significantly impaired development of mononuclear phagocytes in cultures of mouse bone marrow cells stimulated with M-CSF. Collectively, results support a model in which SFK are required for sustained PLC activity and MAPK activation above threshold required for commitment of myeloid progenitors to macrophage differentiation.

PtdIns(3)P regulates the neutrophil oxidase complex by binding to the PX domain of p40(phox).

The production of reactive oxygen species (ROS) by neutrophils has a vital role in defence against a range of infectious agents, and is driven by the assembly of a multi-protein complex containing a minimal core of five proteins: the two membrane-bound subunits of cytochrome b(558) (gp91(phox) and p22(phox)) and three soluble factors (GTP-Rac, p47(phox) and p67(phox) (refs 1, 2). This minimal complex can reconstitute ROS formation in vitro in the presence of non-physiological amphiphiles such as SDS. p40(phox) has subsequently been discovered as a binding partner for p67(phox) (ref. 3), but its role in ROS formation is unclear. Phosphoinositide-3-OH kinases (PI(3)Ks) have been implicated in the intracellular signalling pathways coordinating ROS formation but through an unknown mechanism. We show that the addition of p40(phox) to the minimal core complex allows a lipid product of PI(3)Ks, phosphatidylinositol 3-phosphate (PtdIns(3)P), to stimulate specifically the formation of ROS. This effect was mediated by binding of PtdIns(3)P to the PX domain of p40(phox). These results offer new insights into the roles for PI(3)Ks and p40(phox) in ROS formation and define a cellular ligand for the orphan PX domain.

Imaginary part of the refractive index of sulfates and nitrates in the 0.7-2.6-microm spectral region.

We have carried out the transmission spectroscopy and obtained the imaginary part of the refractive index k of sulfate and nitrate aqueous solutions in the spectral range between 0.7 and 2.6 microm for several concentrations at temperatures of T = 24 degrees C and T = -24 degrees C. A linear interpolation with volume fraction is found to reproduce the measured k spectra of the ammonium solutions.

Evaluation of the automated fluorescent analysis of the H-ras minisatellite after optimized PCR amplification in comparison with a standardized Southern blot technique.

Determination of allele sizes? loss of heterozygosity or genetic instability at minisatellite VNTR loci, are routinely performed by the conventional Southern technique. We have investigated the potential use of automated DNA sequencer for the analysis of the H-ras minisatellite. We report the modifications of amplification parameters and electrophoresis conditions on the sequencer. Seventy-one colorectal carcinomas and the corresponding normal tissues were amplified with fluorescent-labeled primers, analyzed on sequencer, and concurrently controlled by Southern blotting. The results on sequencer showed that a Hydrolink matrix used in non-denaturing conditions and a specific analysis software facilitate a more accurate fragment size calculation.

Refractive index of ice in the 1.4-7.8-µm spectral range.

New accurate values of the imaginary part of the refractive index k of polycrystalline ice at T = -22 °C are reported. The k spectrum in the 1.43-2.89-µm region was found to be in excellent agreement with the most recent study, and the data in the 3.35-7.81-µm range eliminate the large existing uncertainty in the 3.5-4.3-µm region.

Analyses of linkage to 17q11-q23 in 3 French hereditary nonpolyposis colon-cancer families.

Hereditary non-polyposis colorectal cancer (HNPCC) is an autosomal dominant disease, accounting for approximately 6% of colorectal cancers. We performed linkage analyses with the aim of proving or excluding the existence of a susceptibility locus on 17q. Three HNPCC families (102 collected members, 25 colorectal cancers, 9 other cancers and 6 colorectal adenomas) were studied with 7 polymorphic DNA markers Mfd15, THRA 1, D17S800, D17S855, Mfd 188, 42D6, 46E6 localized in the 17q11-q23 region. After in vitro enzymatic amplification, the different alleles were separated by classic vertical poly-acrylamide gel electrophoresis or analyzed with the automatic sequencing machine 373A (Applied Biosystems). Results showed that none of the 7 studied markers of the chromosome 17q were linked to the HNPCC disease.

Linkage analyses of 3 French families to Loci on chromosome-2p and chromosome-3p predisposing to hereditary nonpolyposis colon-cancer.

Hereditary, non-polyposis colon cancer (HNPCC) is caused by mutations in different loci. One gene causing HNPCC was mapped to chromosome 2p and recently a tight linkage between a polymorphic marker on the chromosome 3p and the disease locus has been demonstrated and these families also manifest signs of a general DNA replicator disorder. We report detailed genetic studies of three French HNPCC families with D2S123 and D3S1029. In one of the families (F 230), the segregation pattern for markers on chromosomes 2 and 3 suggests absence of linkage. The two other families are not informative enough to conclude on linkage status with chromosomes 2 and 3. If confirmed, this result would mean that the inherited colon cancer in this family is linked to another HNPCC gene. Implication for genetic counselling is discussed. Even with cloned genes, linkage analysis with flanking microsatellite markers for informative families may help to avoid tedious work of seeking point mutations in HNPCC genes.

Hereditary colorectal-cancer (review).

Knowledge of the genetics of colon cancer has already started to have an impact on prevention, early detection and control strategies for large bowel malignancy. This report reviews the genetics of colorectal cancer, both the epidemiological and molecular aspects. It includes a description of the syndromes of inherited colorectal cancer and a discussion of recent molecular genetic work about tumor suppressor genes.