Body composition in Parkinson's disease: a study with dual-energy X-ray absorptiometry

Some investigators have reported that patients with Parkinson's disease (PD) tend to lose weight, and have a low body mass index. For this reason, it was suggested that PD patients have an increased metabolic rate. Using dual-energy X-ray absorptiometry (DXA) we determined, the body composition in 52 unselected PD patients (28 males, 24 females) and in 80 age and sex-matched healthy controls (40 males, 40 females). The mean+/-SD duration of PD was 5.9+/-4.8 years. PD severity was assesed with the Unified PD Rating Scale (UPDRS) and Hoehn & Yahr staging. PD patients and controls did not differ significantly in height, weight and body mass index. The total fat and percentage of fat were significantly higher (p<0.01) and the lean body mass and water content were lower (p<0.001 for each) in male PD patients when compared with male controls. All these values were similar in female PD patients and female controls. Fat mass, lean body mass and water content did not correlate with the UPDRS scores and Hoehn &Yahr staging, although PD patients with higher UPDRS scores had higher percentage of fat.     

Lipidic profile: evolution,tendency and tracking from infancy to adulthood. PECNA Study

Cardiovascular diseases start during infancy, although the clinical manifestations show themselves during adulthood. Since the year 1987 a (PECNA) study has been underway in Navarra to analyse the epidemiology of the cardiovascular risk factors of the infant-juvenile population. This paper presents the evolution of the lipidic profile from 4 to 23 years of age, the tendency from 1987 to 1993, the evolution of the prevalence of hypercholesterolaemia seric cholesterol >200 mg/dl and the tracking from infancy to adult age. Outstanding amongst the results are the differences between the lipidic profile in both sexes, as well as the observed fall in the average levels of total seric cholesterol and in the prevalence of hypercholesterolaemia. With regard to the tracking, it is concluded that between 50% and 55% of individuals belonging to the extreme quintile of the distribution of the lipidic variables persist at this level six years later.     

Common mutations in the familial Mediterranean fever gene associate with rapid progression to disability in non-Ashkenazi Jewish multiple sclerosis patients

Ancient founder mutations in the Mediterranean fever gene, MEFV, are associated with familial Mediterranean fever, a recessive, episodic, inflammatory disease. Since these mutations are reported to express with above normal levels of acute phase reactants in healthy heterozygotes we postulated that the heterozygous phenotype could aggravate the clinical expression of ongoing autoimmune diseases. This study evaluated progression to disability in relapsing-remitting multiple sclerosis (RR-MS) patients of non-Ashkenazi and Ashkenazi origin carrying an MEFV mutation, particularly the detrimental M694V, using the expanded disability status scale (EDSS). In the non-Ashkenazi patients group (n=48), carriers (n=17) presented with a two-fold higher fraction which reached EDSS=3.0 and 6.0 compared to noncarriers (n=31) despite a comparable mean of MS duration. The median time to reach EDSS=3.0 was 2 years in the carriers vs 10 years in noncarriers (P=0.007); The median time to reach EDSS=6.0 was 6 years vs 23 years, respectively (P=0.003). M694V heterozygous patients reached both EDSS milestones earlier than other patients. Progression to disability was not enhanced in Ashkenazi RR-MS carriers (n=12, noncarriers n=59). In conclusion, non-Asheknazi MS patients carrying one mutated MEFV gene, particularly M694V, expressed rapid progression to disability. The expressed mutation may increase inflammatory damage inflicted by autoimmune responses.     

Functional C8 associated with human platelets

Haemolytic assay for C8 revealed its association in functionally active form with washed human platelets. Platelet-bound C8 haemolytic activity was inhibited by F(ab')2 anti-C8 and was undetectable in the platelet suspension obtained from three C8 deficient patients. Incubation of platelets from C8 deficient individuals in normal plasma did not restore C8 haemolytic activity, indicating that platelets do not absorb C8 from plasma in vitro during platelet preparation. Thrombin, a mediator of the platelet release reaction, did not induce the release of C8 from normal platelets. Conversely, lysis of EAC1-7.9 by platelet bound C8 was not accompanied by release of beta-thromboglobulin or serotonin from the platelets. C8 was detected in a homogenate prepared from platelets as well as in the supernatant collected after high speed centrifugation of the homogenate. The association of C8 with platelets as an individual component rather than as part of the C5b-9 membrane-attack complex was supported by the following evidence: platelet bound C8 eluted from a Sephacryl S-200 column at the same volume as C8 from normal human serum; F(ab')2 anti-C8, but not F(ab')2 anti-C5, inhibited platelet C8 activity; the platelet homogenate, which lysed EAC1-7.9, had no effect on EAC43 which are susceptible to the lytic activity of the C5b-9 complex.     

Sequence variants of human papillomavirus type 16 in clinical samples permit verification and extension of epidemiological studies and construction of a phylogenetic tree.

Genomic variability between different viral isolates provides a powerful epidemiological tool for verifying ultrasensitive diagnostic procedures, understanding infectious pathways in individuals and human populations, and studying viral evolution. The potential of this approach has not yet been exploited for the diagnosis of human papillomaviruses (HPVs) like HPV type 16 (HPV-16), which are involved in genital cancer. Toward this end, we amplified by polymerase chain reaction, cloned, and sequenced a 364-bp noncoding segment of the HPV-16 genome from cell lines, cervical biopsy specimens, and cervical smears. The HPV-16 genomes in the cell lines SiHa and CaSki showed an identical point mutation, and in the SiHa cell line it had an additional 38-bp deletion. Only 4 of 22 cervical lesions biopsied from patients at several hospitals in Singapore contained HPV-16 DNA with the prototype sequence, while the DNAs of the other 18 cervical lesions differed by 1 to 10 mutations. This excludes contaminations with cloned HPV-16 DNA as the source of this DNA. To test whether this diversity was a geographic idiosyncrasy, we analyzed 25 cervical biopsy specimens from Brazil. Eight of these contained the prototype sequence, while 17 were mutated. Altogether, 11 genomic variants were found in the Singaporean samples and 12 genomic variants were found in the Brazilian samples, and only 5 of these occurred identically in both cohorts. All variants could be connected to form a phylogenetic tree, with some branches being specific for each cohort. This suggests that the variants did not originate over a short period in the individual patient but, rather, evolved consecutively while spreading throughout humankind.(ABSTRACT TRUNCATED AT 250 WORDS)     

In vivo leptin expression in cartilage and bone cells of growing rats and adult humans

The present investigation was carried out to analyse, immunohistochemically, in vivo leptin expression in cartilage and bone cells, the latter restricted to the elements of the osteogenic system (stromal cells, osteoblasts, osteocytes, bone lining cells). Observations were performed on the first lumbar vertebra, tibia and femur of four rats and on the humerus, femur and acromion of four patients. Histological sections of paraffin-embedded bone samples were immunostained using antibody to leptin. The results showed that, in growing rat bone, leptin is expressed in chondrocytes and stromal cells, but not in osteoblasts; bone lining cells were not found in the microscopic fields examined. In adult human bone, leptin is expressed in chondrocytes, stromal cells and bone lining cells; osteoblasts were not found in the microscopic fields examined. Osteocytes were found to be leptin positive only occasionally and focally in both rat and human bone. The in vivo findings reported show, for the first time, that leptin appears to be expressed only in the cells of the osteogenic lineage (stromal cells, bone lining cells, osteocytes) that, with respect to osteoblasts, are permanent and inactive, i.e. in those cells that according to our terminology constitute the bone basic cellular system (BBCS). Because the BBCS seems to be primarily involved in sensing and integrating mechanical strains and biochemical factors and then in triggering and driving bone formation and/or bone resorption, it appears that leptin seems to be mainly involved in modulating the initial phases of bone modelling and remodelling processes.     

Immunohistochemical localization of 6-keto-prostaglandin F1 alpha and prostaglandin E2 in the human umbilical cord before and after labor

In this report immunohistochemical localization of 6-keto prostaglandin (PG)F1 alpha (the stable metabolite of prostacyclin (PGI2], PGE2, and its stable metabolite bicyclic PGE2 in umbilical amnion and vasculature is described. Umbilical cords were obtained at cesarean section from women who were not in labor (N = 7) and from women (N = 6) who went through normal labor and delivery at term. Study of both groups of umbilical cords allowed assessment of differential prostanoid metabolite localization pre- and post-labor. Formalin fixed, paraffin-embedded sections were stained by the avidin-biotin peroxidase complex method. PGE2, bicyclic PGE2, and 6-keto-PGF1 alpha localized to the amniotic cells covering the umbilical cord as well as to the endothelium of the umbilical veins in both groups (pre- and post-labor). No immunostaining was identified in the umbilical arteries. These findings suggest that amniotic cells and endothelial cells of the umbilical vein but not arteries are sites of synthesis or storage for the prostanoids 6-keto-PGF1 alpha and PGE2.