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91.
To determine the cause of a positive direct antiglobulin test (DAT), blood banks routinely perform serologic tests on eluates prepared from DAT-positive red cells. Negative eluates traditionally have been suspected to be associated with drug reactions. This report confirms that the most frequent cause of a positive DAT and a nonreactive eluate is hypergammaglobulinemia. The results of 74 patient samples with positive DATs were analyzed retrospectively. Eluates prepared from the red cells of 54 patients (72.9%) reacted; eluates from 20 patients (27.1%) did not react. This latter group had identical serologic and clinical findings, suggesting that they made up a homogeneous group. In particular, the patients had a positive DAT, a negative indirect antiglobulin test, and a negative eluate; an increased serum concentration of IgG; and no evidence of hemolysis. In a subsequent study, DATs were performed prospectively on red cells from 44 consecutive patients with elevated serum IgG levels. The serum IgG concentration was highest in the three patients whose red cells had a positive DAT. The DAT also became positive in two patients treated with high-dose intravenous gammaglobulin (IV IgG). These studies indicate that a negative eluate from red cells with a positive DAT, a common serologic finding, is often caused by hypergammaglobulinemia. The authors postulate that IgG binds nonspecifically to the red cells because of the hypergammaglobulinemia. 相似文献
92.
A novel homozygous SLC25A1 mutation with impaired mitochondrial complex V: Possible phenotypic expansion
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Idan Cohen Orna Staretz‐Chacham Ohad Wormser Yonatan Perez Ann Saada Rotem Kadir Ohad S. Birk 《American journal of medical genetics. Part A》2018,176(2):330-336
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94.
Birk S Petersen KA Kruuse C Guieu R Jonassen O Eisert W Olesen J 《Cephalalgia : an international journal of headache》2005,25(5):369-377
Adenosine is an endogenous neurotransmitter that is released from the brain during hypoxia and relaxes isolated human cerebral arteries. Many cerebral artery dilators cause migraine attacks. However, the effect of intravenous adenosine on headache and cerebral artery diameter has not previously been investigated in man and reports regarding the effect of intravenous adenosine on cerebral blood flow are conflicting. Twelve healthy participants received adenosine 80, 120 microg kg(-1) min(-1) and placebo intravenously for 20 min, in a double-blind, three-way, crossover, randomized design. Headache was rated on a verbal scale (0-10). Regional cerebral blood flow (rCBF) with 133Xe inhalation and single-photon emission computed tomography (SPECT) and MCA flow velocity (V(MCA)) with transcranial Doppler, were measured in direct sequence. Six participants developed headache during 80 microg kg(-1) min(-1) and six during 120 microg kg(-1) min(-1) compared with none on placebo (P = 0.006). The headache was very mild and predominantly described as a pressing sensation. When correcting data for adenosine-induced hyperventilation, no significant changes in rCBF (P = 0.22) or V(MCA) (P = 0.16) were found between treatments. A significant dilation of the superficial temporal artery (STA) was seen (P < 0.001). These results show that circulating adenosine has no effect on rCBF or V(MCA), while it dilates the STA and causes very mild headache. 相似文献
95.
目的:观察聚乙二醇法在组织工程瓣膜准备中的应用价值,比较聚乙二醇去细胞前后组织工程瓣膜的物理特性。方法:实验于2005-10/2006-03在华中科技大学同济医学院基础医学院生物化学系实验室完成。①实验分组:取猪10只,由于猪主动脉瓣为三叶瓣结构,共取得瓣叶组织30个,麻醉后宰杀取其心脏动脉瓣膜,分为去细胞组和对照组,每组各15个。②实验方法:去细胞组用聚乙二醇和DNase I处理;瓣叶组织放入1kg/L聚乙二醇,室温下浸泡30~45min,振荡器加以振荡;含抗生素磷酸盐缓冲液浸泡24h,反复3次洗脱;以5×104U/L DNase I液浸泡处理1h;对照组仅以含抗生素磷酸盐缓冲液浸泡24h,反复3次洗脱。③实验评估:苏木精-伊红染色、扫描电镜观察去细胞情况,吸光度(A)值,计算去细胞率(%)=(对照组A值-去细胞组A值)/对照组A值×100%。猪去细胞瓣膜条置于力学测试仪测定最大负荷、最大应力、最大应变和弹性模量。结果:纳入猪10只,均进入结果分析。①去细胞组织形态学观察:去细胞组猪瓣膜组织中看不到细胞成分,且细胞外基质结构保存完整,胶原纤维排列整齐,无明显断裂,仍呈波浪状平行排列,结构紧凑,弹性纤维结构清晰,组织无明显水肿。②DNA含量分析:聚乙二醇处理后去细胞百分率为95.32%。③生物力学检测:与对照组比较,去细胞组瓣膜组织最大负荷[(12.586±1.693),(10.242±1.435)N,P>0.05]、最大应力[(2.346±0.342),(1.877±0.572)N/mm,P>0.05]、弹性模量(15.152±1.579,14.549±0.678,P>0.05)、最大应变[(31.685±7.533),(28.118±6.045)mm/N,>0.05]等均无显著差异。P结论:聚乙二醇法去除细胞完全,细胞外基质保存完整,对组织机械性能无明显影响,适于构建组织工程瓣膜。 相似文献
96.
97.
Pharmacokinetics of total and unbound ertapenem in healthy elderly subjects 总被引:2,自引:0,他引:2
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Musson DG Majumdar A Holland S Birk K Xi L Mistry G Sciberras D Muckow J Deutsch P Rogers JD 《Antimicrobial agents and chemotherapy》2004,48(2):521-524
Ertapenem is a new once-a-day parenteral carbapenem antimicrobial agent. The pharmacokinetics of unbound and total concentrations of ertapenem in plasma were investigated in elderly subjects and compared with historical data from young adults. In a single- and multiple-dose study, healthy elderly males and females (n = 14) 65 years old or older were given a 1-g intravenous (i.v.) dose once daily for 7 days. Plasma and urine samples collected for 24 h on days 1 and 7 following administration of the 1-g doses were analyzed by reversed-phase high-performance liquid chromatography. Areas under the concentration-time curve from 0 h to infinity (AUC(0- infinity )) for elderly females and males were similar following administration of 1-g single i.v. doses, and thus, the genders were pooled in subsequent analyses. Concentrations in plasma and the half-life of ertapenem were generally higher and longer, respectively, in elderly subjects than in young adults. The mean AUC(0- infinity ) of total ertapenem in the elderly was 39% higher than that in young subjects following administration of a 1-g dose. The differences were slightly greater for the mean AUC(0- infinity ) of unbound ertapenem (71%). The unbound fraction of ertapenem in elderly subjects ( approximately 5 to 11%) was generally greater than that in young adults ( approximately 5 to 8%). As in young adults, ertapenem did not accumulate upon multiple dosing in the elderly. The pharmacokinetics of ertapenem in elderly subjects, while slightly different from those in young adults, do not require a dosage adjustment for elderly patients. 相似文献
98.
Galron D Birk OS Kazanovitz A Moses SW Hershkovitz E 《Journal of inherited metabolic disease》2004,27(2):267-273
Carnitine-acylcarnitine translocase CACT deficiency is a very rare autosomal recessive disease. The neonatal phenotype of CACT deficiency is characterized by hypoketotic hypoglycaemia, hyperammonaemia, cardiomyopathy and skeletal muscle weakness culminating in early death. The disease is caused by mutations in the CACT gene, which encodes a protein transporting long-chain fatty acid carnitine esters into the mitochondrial matrix. In this report, we describe the first case of CACT deficiency in the Bedouin population in Israel. The patient, the first son of consanguineous parents, was born at term after uneventful delivery. During the second day of life, he developed clinical signs of an acute metabolic crisis with severe hypoglycaemia and hyperammonaemia. Biochemical investigation suggested the diagnosis of CACT deficiency. Genetic molecular analysis confirmed this diagnosis by demonstrating that the affected child was homozygous for a novel missense mutation 793A>G, substituting glutamine by arginine (Q238R) in exon 7 of the CACT gene. Despite medical treatment and adequate nutrition, the patient died at 6 months of age. 相似文献
99.
Chen S Sun M Meng X Iozzo RV Kao WW Birk DE 《The American journal of pathology》2011,179(5):2409-2419
Autosomal-dominant congenital stromal corneal dystrophy (CSCD) is a human genetic disease characterized by corneal opacities beginning shortly after birth. It is linked to a frameshift mutation in decorin, resulting in a C-terminal truncation lacking 33 amino acids that includes the "ear" repeat, a feature specific for small leucine-rich proteoglycans. Our goals are to elucidate the roles of the mutant decorin in CSCD pathophysiology and to decipher the mechanism whereby mutant decorin affects matrix assembly. A novel animal model that recapitulates human CSCD was generated. This transgenic mouse model targets expression of truncated decorin to keratocytes, thereby mimicking the human frameshift mutation. Mutant mice expressed both wild-type and mutant decorin. Corneal opacities were found throughout, with increased severity toward the posterior stroma. The architecture of the lamellae was disrupted with relatively normal lamellae separated by regions of abnormal fibril organization. Within abnormal zones, the interfibrillar spacing and the fibril diameters were increased. Truncated decorin negatively affected the expression of endogenous decorin, biglycan, lumican, and keratocan and positively affected fibromodulin. Our results provide a mechanistic explanation for the generation of corneal opacities in CSCD. Thus, truncated decorin acts in a dominant-negative manner to interfere dually with matrix assembly and binding to receptor tyrosine kinases, thereby causing abnormal expression of endogenous small leucine-rich proteoglycans leading to structural abnormalities within the cornea and vision loss. 相似文献