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C Caruso G Di Lorenzo M A Modica G Candore M R Portelli G Crescimanno A Ingrassia G B Sangiorgi A Salerno 《Mechanisms of ageing and development》1991,59(1-2):27-35
The evidence from several studies indicates that as individuals age, they may display immune dysfunctions, mostly T cell dysfunctions. Recently, a soluble form of the receptor for interleukin-2 (IL-2) (sIL-2R) has been demonstrated in human sera and in vitro stimulated culture supernatants from human T lymphocytes. In the present paper, we report in vitro sIL-2R production from peripheral blood mononuclear cells in elderly subjects. The results show that no difference exists for unstimulated cultures, whereas after mitogen stimulation the elderly subjects showed the lowest values compared with young ones. These findings suggest that sIL-2R may provide a new tool for the study of T lymphocyte dysfunctions in old age. 相似文献
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Polycystic kidney disease is an autosomal dominant disease that may be associated with cystic disease of the liver. In women, the cysts may develop early and be more troublesome than in men. Cystadenocarcinoma of the pancreas is uncommon, comprising 1% of primary pancreatic malignancies. This case report is the first to describe a familial association between polycystic kidney disease and cystadenocarcinoma of the pancreas and liver in the English medical literature. A patient with autosomal dominant polycystic kidney disease (ADPKD) and multiple hepatic cysts developed cystadenocarcinoma of the pancreas with multiple malignant liver cysts. The patient's mother, sister, and niece had ADPKD, and the patient's sister also died of pancreatic cystadenocarcinoma. We believe that the development of these two disease entities in which the primary pathology is cyst formation has a genetic association. (Gastroenterology 1997 Jun;112(6):2104-7) 相似文献
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In this review we describe the developmental mechanisms involved in the making of a limb, by focusing on the nature and types of interactions of the molecules that play a part in the regulation of limb patterning and characterizing clinical conditions that are known to result from the abnormal function of these molecules. The latter subject is divided into sections dealing with syndromal and nonsyndromal deficiencies, polydactylies, and brachydactylies. Conditions caused by mutations in homeobox genes and fibroblast growth factors and their receptor genes are listed separately. Since the process of limb development has been conserved for more than 300 millions years, with all the necessary adaptive modifications occurring throughout evolution, we also take into consideration the evolutionary aspects of limb development in terms of genetic repertoire, molecular pathways, and morphogenetic events. 相似文献
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Annika?E?StenbergEmail author Lisskulla?Sylvén Carl?GM?Magnusson Malou?Hultcrantz 《Journal of negative results in biomedicine》2004,3(1):6
Disturbances in the immune system has been described in Turner syndrome, with an association to low levels of IgG and IgM
and decreased levels of T- and B-lymphocytes. Also different autoimmune diseases have been connected to Turner syndrome (45,
X), thyroiditis being the most common. 相似文献
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A point mutation in the 5' splice site of the dystrophin gene first intron responsible for X-linked dilated cardiomyopathy 总被引:3,自引:4,他引:3
Milasin J; Muntoni F; Severini GM; Bartoloni L; Vatta M; Krajinovic M; Mateddu A; Angelini C; Camerini F; Falaschi A; Mestroni L; Giacca M 《Human molecular genetics》1996,5(1):73-79
X-linked dilated cardiomyopathy (XLDC) is a familial heart disease
presenting in young males as a rapidly progressive congestive heart
failure, without clinical signs of skeletal myopathy. This condition has
recently been linked to the dystrophin gene in some families and deletions
encompassing the genomic region coding for the first muscle exon have been
detected. In order to identify the defect responsible for this disease at
the molecular level and to understand the reasons for the selective heart
involvement, a family with a severe form of XLDC was studied. In the
affected members, no deletions of the dystrophin gene were observed.
Analysis of the muscle promoter, first exon and intron regions revealed the
presence of a single point mutation at the first exon-intron boundary,
inactivating the universally conserved 5' splice site consensus sequence of
the first intron. This mutation introduced a new restriction site for MseI,
which cosegregates with the disease in the analyzed family. Expression of
the major dystrophin mRNA isoforms (from the muscle-, brain- and Purkinje
cell-promoters) was completely abolished in the myocardium, while the
brain- and Purkinje cell- (but not the muscle-) isoforms were detectable in
the skeletal muscle. Immunocytochemical studies with anti- dystrophin
antibodies showed that the protein was reduced in quantity but normally
distributed in the skeletal muscle, while it was undetectable in the
cardiac muscle. These findings indicate that expression of the muscle
dystrophin isoform is critical for myocardial function and suggest that
selective heart involvement in dystrophin- linked dilated cardiomyopathy is
related to the absence, in the heart, of a compensatory expression of
dystrophin from alternative promoters.
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