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排序方式: 共有792条查询结果,搜索用时 15 毫秒
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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.
相似文献
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Jan M. West Danielle C. Humphris D. George Stephenson 《Journal of muscle research and cell motility》1995,16(3):267-284
Summary Long-(SL>6m) and short-sarcomere (SL<4m) fibres were isolated from the claw muscle of the yabby (Cherax destructor) during limb regeneration and at different stages of the moult cycle. Long-sarcomere fibres were more susceptible to the changes resulting from the moult-induced atrophy compared with the short-sarcomere fibres. Signs of atrophy included fibre erosion, loss of myosin filaments, a reduction in the diameter of myosin filaments and changes associated with the Z line. The intracellular structure of the fibres, however, remained intact in both fibre types. Fibres taken immediately prior to ecdysis could not be fully activated with Ca2+ or Sr2+ without breaking. In contrast fibres taken within 4 h after ecdysis could develop and maintain full force when activated by Ca2+ or Sr2+. The results suggest that loss of myofibrillar proteins via the moult-induced atrophy and/or events associated with fibre elongation may occur in the period just prior to ecdysis and that these changes may be responsible for the fibres inability to function during the premoult stage. Results from this study showed that short-sarcomere fibres add sarcomeres by at least two different mechanisms (1) transverse sarcomere splitting and (2) Z line splitting. Long-sarcomere fibres appear to be elongated by mechanism (s) other than those used by short-sarcomere fibres which possibly involve large electron dense structures which are positioned between the myofibrils and within the A and I bands. Results from the regenerating chelae limb bud showed that sarcomeres form from separate units comprising myosin filaments and actin filaments anchored into Z lines respectively. These sub-sarcomeric units then join together to form sarcomeres. Myofibril formation is aided by electron dense regions which are closely associated with the membrane system. These fibres although short in length and still within the non-functional limb bud could be activated by Ca2+ and Sr2+ suggesting that full fibre function exists before the chelae become functional. Regenerating muscle fibres consisted predominately of fibres with short-sarcomeres. 相似文献
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van Kranen HJ; van Iersel PW; Rijnkels JM; Beems DB; Alink GM; van Kreijl CF 《Carcinogenesis》1998,19(9):1597-1601
The variation in colorectal cancer (CRC) incidence worldwide strongly
suggests a role for dietary influences. Based on epidemiological data,
protective effects of vegetables and fruit intake on CRC are widely
claimed, while other data indicate a possible increased CRC risk from
(higher) dietary fat intake. Therefore, we have investigated single and
interactive effects of dietary fat and a vegetable-fruit mixture (VFM) in
the ApcMin mouse, a mouse model for multiple intestinal neoplasia. In this
study, four different diets (A-D) were compared, which were either low in
fat (20% energy diets A/B) or high in fat (40% energy diets C/D). In
addition, 19.5% (wt/wt) of the carbohydrates in diets B and D were replaced
by a freeze-dried VFM. The diets were balanced so that they only differed
among each other in fat/carbohydrate content and the presence of specific
plant-constituents. Because the initiation of intestinal tumors in ApcMin
mice occurs relatively early in life, exposure to the diets was started in
utero. Without the addition of VFM, mice maintained at a high-fat diet did
not develop significantly higher numbers of small or large intestinal
adenomas than mice maintained at a low-fat diet. VFM added to a low-fat
diet significantly lowered multiplicity of small intestinal polyps (from
16.2 to 10.2/mouse, 15 animals/group), but not of colon tumors in male
ApcMin mice only. Strikingly, addition of VFM to female mice maintained on
a low-fat diet and to both sexes maintained on a high-fat diet
significantly enhanced intestinal polyp multiplicity (from 16.5 to 26.7
polyps/mouse). In conclusion, our results indicate that neither a lower fat
intake nor consumption of VFM included in a high-fat diet decreases the
development of polyps in mice genetically predisposed to intestinal tumor
development.
相似文献
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