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排序方式: 共有273条查询结果,搜索用时 15 毫秒
1.
Gundula Schaumburg-Lever 《Journal of cutaneous pathology》1995,22(6):483-487
The application of immunostaining techniques to electron microscopy specimens has led to a renewal of interest in electron microscopy in biological research in general, as well as in dermatopathology. Refinements in the preparative procedures have made easier the immunolocalization of antigens both in chemically-fixed and frozen unfixed tissues, embedded in plastic and sectioned. Application of these methods has led to the demonstration of the bullous pemphigoid antigen inside basal keratinocytes. HMB-45 antigen has been found to be present in premelanosomes. Recently, Factor XIIIa has been localized not only in dermal dendrocytes but also in endothelial cells and mast cells. 相似文献
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Claus Neurohr Patrick Huppmann Hanno Leuchte Martin Schwaiblmair Iris Bittmann Gundula Jaeger Rudolf Hatz Lorenz Frey Peter Überfuhr Bruno Reichart Jürgen Behr for the Munich Lung Transplant Group 《American journal of transplantation》2005,5(12):2982-2991
Bronchiolitis obliterans syndrome (BOS) is the limiting factor to long-term survival after lung transplantation. Previous studies suggested respiratory viral tract infections are associated with the development of BOS. To identify the impact of virus detection in bronchoalveolar lavage (BAL) fluid, we analyzed BAL samples from 87 consecutive lung transplant recipients for human herpesvirus (HHV)-6, Epstein-Barr virus, Herpes simplex virus 1/2, Cytomegalovirus, respiratory syncytical virus and adenovirus by PCR. Acute rejection, BOS and death were recorded for a mean follow-up time of 3.27 +/- 0.47 years. Results of PCR analysis and other potential risk factors were entered into a Cox regression analysis of BOS predictors and death. Only acute rejection was a distinct risk factor for BOS of all stages, death and death from BOS. HHV-6 was detected in 20 patients. Univariate and multivariate analysis revealed that HHV-6 was associated with an increased risk to develop BOS > orb = stage 1 and death, separate from the risk attributable to acute rejection. Identification of HHV-6 DNA in BAL fluid is a potential risk factor for BOS. Our results warrant further studies to elucidate a possible causal link between HHV-6 and BOS. 相似文献
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Traditionally, diagnosis and treatment have been seen as two distinct tasks. Consequently, most approaches to computer supported health care focus on one of the two-mostly on diagnosis or rather on the interpretation of measurements which is much better understood and formalised. However, in practice diagnosis and treatment overlap and influence each other in many ways. Combinations range from repeatedly going through the diagnosis-treatment loop over a period of time to permanent monitoring of the patients' health condition as it is done in intensive care units. In this article we describe how to model these combinations using the clinical protocol-representation language ASBRU. It implements treatment steps in a hierarchy of skeletal, time-oriented plans. Diagnosis can either be described in a declarative way in the conditions, under which treatment steps are taken or it can be modelled explicitly as plans of their own right. We demonstrate our approach using examples taken from the American Association of Paediatricians' guideline for the treatment of hyperbilirubinemia in the new-born. 相似文献
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Miksch S Lumsden A Guenther UP Foernzler D Christen-Zäch S Daugherty C Ramesar RK Lebwohl M Hohl D Neldner KH Lindpaintner K Richards RI Struk B 《Human mutation》2005,26(3):235-248
Pseudoxanthoma elasticum (PXE) is a systemic heritable disorder that affects the elastic tissue in the skin, eye, and cardiovascular system. Mutations in the ABCC6 gene cause PXE. We performed a mutation screen in ABCC6 using haplotype analysis in conjunction with direct sequencing to achieve a mutation detection rate of 97%. This screen consisted of 170 PXE chromosomes in 81 families, and detected 59 distinct mutations (32 missense, eight nonsense, and six likely splice-site point mutations; one small insertion; and seven small and five large deletions). Forty-three of these mutations are novel variants, which increases the total number of PXE mutations to 121. While most mutations are rare, three nonsense mutations, a splice donor site mutation, and the large deletion comprising exons 23-29 (c.2996_4208del) were identified as relatively frequent PXE mutations at 26%, 5%, 3.5%, 3%, and 11%, respectively. Chromosomal haplotyping with two proximal and two distal polymorphic markers flanking ABCC6 demonstrated that most chromosomes that carry these relatively frequent PXE mutations have related haplotypes specific for these mutations, which suggests that these chromosomes originate from single founder mutations. The types of mutations found support loss-of-function as the molecular mechanism for the PXE phenotype. In 76 of the 81 families, the affected individuals were either homozygous for the same mutation or compound heterozygous for two mutations. In the remaining five families with one uncovered mutation, affected showed allelic compound heterozygosity for the cosegregating PXE haplotype. This demonstrates pseudo-dominance as the relevant inheritance mechanism, since disease transmission to the next generation always requires one mutant allelic variant from each parent. In contrast to other previous clinical and molecular claims, our results show evidence only for recessive PXE. This has profound consequences for the genetic counseling of families with PXE. 相似文献
6.
Musholt TJ Musholt PB Petrich T Oetting G Knapp WH Klempnauer J 《World journal of surgery》2000,24(11):1409-1417
Hereditable predisposition to papillary thyroid carcinoma (PTC) and multinodular goiter (MNG) without evidence of an association
with other malignancies as a distinct entity was recognized only recently. A meta-review of the literature on familial PTC
(FPTC) was undertaken, and characteristics of families with frequent occurrence of PTC or MNG (or both) were summarized. A
database on thyroid cancer patients maintained in our institution was searched for potential FPTC families. Clinical examinations
were performed in 6 of 12 Hannover kindreds identified, and blood samples of all family members were collected for genetic
analyses. Clinical presentations and histopathologic features of the FPTC cases were compiled. Based on the FPTC meta-review
and own experience, predictive criteria to identify families at risk were developed: Exclusion criteria were previous radiation
exposure and coincidence with neoplasia syndromes. Primary criteria for susceptibility to FPTC are (1) PTC in two or more
first-degree relatives and (2) MNG in at least three first- or second-degree relatives of a PTC patient. Secondary criteria
are diagnosis in a patient younger than 33 years, multifocal or bilateral PTC, organ-exceeding tumor growth (T4), metastasis
(N1, M1), and familial accumulation of adolescent-onset thyroid disease. A hereditary predisposition to PTC is considered
if both primary criteria or one primary criterion plus three secondary criteria are present. Family history-taking is recommended
for all PTC patients to identify FPTC kindreds at risk. Blood relatives of FPTC index patients who harbor MNG should undergo
thorough and regular clinical screening. Suspicious lesions should prompt early surgical intervention. 相似文献
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Catharina Busch Georg Girke Benjamin Kohl Christiane Stoll Marion Lemke Senat Krasnici Wolfgang Ertel Sandeep Silawal Thilo John Gundula Schulze-Tanzil 《Molecular immunology》2013,53(4):363-373
Interplay between complement factors, regulatory proteins, anaphylatoxins and cytokines could be involved in tendon healing and scar formation. The expression and regulation of complement factors by cytokines or anaphylatoxins are completely unclear in tendon.Hence, the gene expression of the anaphylatoxin receptors C3aR, C5aR and cytoprotective complement regulatory proteins (CRPs) was analysed in human tendon, cultured primary tenocytes and to directly compare the general expression level, additionally in human leukocytes. Time-dependent regulation of complement by cytokines and the anaphylatoxin C3a was assessed in cultured tenocytes.Gene expression of the anaphylatoxin receptors C3aR, C5aR and the CRPs CD46, CD55 and CD59 was detected in tendon, cultured tenocytes and leukocytes, whereas CD35 could only be found in tendon and leukocytes. Compared with cultured tenocytes, complement expression was higher in tendon and compared with leukocytes C3aR, C5aR, CD35 and CD55, but not CD46 and CD59 gene expression levels were lower in tendon. C3aR mRNA was up-regulated by both TNFα and C3a in cultured tenocytes in a time-dependent manner whereby C5aR gene expression was only induced by C3a. IL-6 or C3a impaired the CRP gene expression. C3a stimulation lead to an up-regulation of TNFα and IL-1β mRNA in tenocytes. Degenerated tendons revealed an increased C5aR and a reduced CD55 expression.The expression profile of the investigated complement components in tendon and cultured tenocytes clearly differed from that of leukocytes. Tenocytes respond to the complement split fragment C3a with CRP suppression and enhanced pro-inflammatory cytokine gene expression suggesting their sensitivity to complement activation. 相似文献
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