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Liver-specific protein was isolated from bovine, rabbit, and human liver. A corresponding kidney protein was isolated from rabbit kidney. The liver-specific protein and kidney-specific protein were coupled to activated CH-Sepharose 4B. Affinity chromatography was performed on columns of liver-specific protein and kidney-specific protein CH-Sepharose 4B, with sera containing antimitochondrial antibodies, smooth muscle antibodies, bile canalicular antibodies, reticular tissue antibodies, and antinuclear antibodies. The material eluted from the affinity chromatography columns was studied for immunofluorescence reaction against sections of liver, kidney, and stomach. Reactions were found of the liver-specific protein and kidney-specific protein column eluates against mitochondria, smooth muscle, double-stained bile canaliculi, reticular tissue, and nucleoli. Thus, the antigens belonging to these cell and organ constituents must have been present in the liver-specific protein (and kidney-specific protein) preparations, indicating that liver-specific protein is not a pure liver cell membrane-specific protein.  相似文献   
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We previously demonstrated that the steadiness of shoulder abduction is reduced in patients with subacromial impingement syndrome (SIS), which might be related to shoulder pain associated with the SIS. The aim of the present study was to examine the acute effects of experimental shoulder muscle pain on shoulder motor function in healthy subjects. The fluctuations in exerted force (force steadiness) and electromyographic (EMG) activity from eight shoulder muscles were determined during sub-maximal isometric and dynamic contractions with the shoulder abductors in nine healthy subjects (27.7 ± 4.2 years, mean ± 1 SD) before, during and after experimental pain induction. Experimental pain was induced by bolus injections of 6% hypertonic saline into the supraspinatus muscle. Experimental muscle pain reduced shoulder-abduction force steadiness on average by 21% during isometric contractions (P = 0.012) and tended to do so during concentric contractions (P = 0.083). Middle deltoid, and infraspinatus and lower trapezius muscle activity increased (3–5% EMGmax) during isometric and concentric contractions, respectively (P < 0.05). Thus, experimental shoulder muscle pain reduced the steadiness of isometric shoulder abduction and caused small changes in the abduction activation strategy. The observed effects of experimental pain on shoulder motor function differed from that observed previously in patients with SIS and chronic pain during the same types of contractions. A possible explanation may be that, even though the adopted experimental pain-paradigm may reflect the SIS in terms of the painful structures, it might not reflect the adaptations in the central nervous system seen with chronic pain.  相似文献   
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ABO-incompatibility has been proposed as a cause of neonatal thrombocytopenia. We conducted a study in 1982 of 172 deliveries at Odense University Hospital. We investigated umbilical cord blood in all cases and compared ABO-compatible groups with ABO-incompatible groups. No statistically significant difference in platelet counts or number of thrombo-cytopenic neonates was found. In four detected cases with immune anti-A antibody, no influence on platelet count could be observed, and in the cases with hyperbilirubinaemia during the first 24 h no influence of ABO-incompatibility could be demonstrated either. With the platelet suspension immunofluorescence test, A and B antigens were demonstrated on adult platelets and A antigen on umbilical cord platelets. A slight elevated level of PlIgG was detected on umbilical cord platelets in six samples (3.4%). It seemed that PlIgG correlated with the content of anti-A and anti-B IgG in maternal serum, but did not correlate with a reduction in platelet count, hyperbilirubinaemia or HLA-antibodies. A pathogenetic influence of ABO-incompatibility on umbilical cord platelets could not be detected in this study.  相似文献   
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Background

Data outlining the mortality and the causes of death in patients with type 1 myocardial infarction, type 2 myocardial infarction, and those with myocardial injury are limited.

Methods

During a 1-year period from January 2010 to January 2011, all hospitalized patients who had cardiac troponin I measured on clinical indication were prospectively studied. Patients with at least one cardiac troponin I value >30 ng/L underwent case ascertainment and individual evaluation by an experienced adjudication committee. Patients were classified as having type 1 myocardial infarction, type 2 myocardial infarction, or myocardial injury according to the criteria of the universal definition of myocardial infarction. Follow-up was ensured until December 31, 2014. Data on mortality and causes of death were obtained from the Danish Civil Registration System and the Danish Register of Causes of Death.

Results

Overall, 3762 consecutive patients were followed for a mean of 3.2 years (interquartile range 1.3-3.6 years). All-cause mortality differed significantly among categories: Type 1 myocardial infarction 31.7%, type 2 myocardial infarction 62.2%, myocardial injury 58.7%, and 22.2% in patients with nonelevated troponin values (log-rank test; P < .0001). In patients with type 1 myocardial infarction, 61.3% died from cardiovascular causes, vs 42.6% in patients with type 2 myocardial infarction (P = .015) and 41.2% in those with myocardial injury (P < .0001). The overall mortality and the causes of death did not differ substantially between patients with type 2 myocardial infarction and those with myocardial injury.

Conclusions

Patients with type 2 myocardial infarction and myocardial injury exhibit a significantly higher long-term mortality compared with patients with type 1 myocardial infarction . However, most patients with type 1 myocardial infarction die from cardiovascular causes in contrast to patients with type 2 myocardial infarction and myocardial injury, in whom noncardiovascular causes of death predominate.  相似文献   
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