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101.
Myocardial micronecrosis produced by microsphere embolization. Role of an alpha-adrenergic tonic influence on the coronary microcirculation 总被引:2,自引:0,他引:2
Microspheres approximately 25 or 50 micrometers in diameter were systemically embolized from the left ventricular cavity. The number of microspheres given was empirically chosen to minimize the possibility of more than one microsphere lodging in an arteriole (3 mg/kg), yet was sufficient to allow for adequate histological assessment. The dogs were sacrificed after 24 hours, and focal areas of myocytolytic necrosis were noted in the myocardium. Groups of dogs were given pretreatment with drugs 10 minutes before embolization. Dogs pretreated with phentolamine (n = 8) and prazosin (n = 2) did not reveal any areas of myocardial necrosis after embolization with 25-micrometers microspheres. Cardiac lesions were also prevented in four of five dogs pretreated with verapamil. In contrast, cardiac lesions were not prevented by pretreatment with yohimbine (n = 2), dipyridamole (n = 3), propranolol (n = 2), or atropine (n = 2). Drug pretreatment with phentolamine or verapamil was not able to prevent cardiac lesions after embolization with 50-micrometers microspheres. Furthermore, despite a greater number of microspheres physically present in the subendocardial layer, the necrotic lesions were more frequent in the mid-wall and epicardial layers. Lesions produced by 25- or 50-micrometers emboli were also significantly smaller in the endocardium. Systemic embolization with microspheres excluding the coronary circulation did not produce cardiac lesions. We conclude that mechanical interruption of the coronary circulation with a 25-micrometers microsphere may be a necessary but not sufficient condition to produce cardiac necrosis. An alpha 1-adrenergic mechanism is also involved in the production of these lesions.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
102.
Reappearance of HBsAg with compartmentalized different HBV strains in allograft versus PBMC of the recipient 总被引:1,自引:0,他引:1
A woman who was positive for anti-hepatitis B surface antigen (anti-HBs) and anti-hepatitis B core antigen (anti-HBc) received
an orthotopic liver transplantation from an anti-HBc-seropositive donor in November 1985. Reappearance of hepatitis B surface
antigen (HBsAg) was noted 5 months after the transplantation, but it was not associated with significant liver inflammation.
Ten years after the transplantation, results of serum hepatitis B virus (HBV) DNA study, by nested polymerase chain reaction,
were negative. However, HBV DNA was detected in the transplanted liver tissues and peripheral blood mononuclear cells. Different
strains were identified in these two organs. An adw strain was found in the transplanted liver, whereas an adr strain with
long segment deletions in the core gene was found in the peripheral blood mononuclear cells. Covalently closed circular HBV
DNA was not detected in any of the tissues examined. Occult HBV infection in the donor as well as the recipient is common
in HBV endemic areas. The recipient in this case had reappearance of hepatitis B surface antigen (HBsAg) in the serum after
transplantation. Nevertheless, 10 years later, two different strains of HBV were identified in different organs, without cross
infection. The present case demonstrates that HBsAg reappearance was not associated with reactivation of the virus and liver
inflammation. This type of HBsAg reappearance did not appear to produce a significant hazard to the transplanted liver.
Received: December 16, 1999 / Accepted: May 26, 2000 相似文献
103.
Hanzhang Xu Deidre Anne De Silva Fung Peng Woon Marcus Eng Hock Ong David B. Matchar Janet Prvu Bettger Daniel T. Laskowitz Ying Xian 《Journal of stroke and cerebrovascular diseases》2021,30(3):105551
ObjectivesThe efficacy of thrombolytic therapy with tissue plasminogen activator (tPA) is highly time dependent. Although clinical guidelines do not recommend written informed consent as it may cause treatment delays, local policy can supersede and require it. From 2014 to 2017, three out of five public hospitals in Singapore changed from written to verbal consent at different time points. We aimed to examine the association of hospital policy changes regarding informed consent on door-to-needle (DTN) times.Materials and MethodsUsing data from the Singapore Stroke Registry and surveys of local practice, we analyzed data of 915 acute ischemic stroke patients treated with tPA within 3 hours in all public hospitals between July 2014 to Dec 2017. Patient-level DTN times before and after policy changes were examined while adjusting for clinical characteristics, within-hospital clustering, and trends over time.ResultsPatient characteristics and stroke severity were similar before and after the policy changes. Overall, the median DTN times decreased from 68 to 53 minutes after the policy changes. After risk adjustment, changing from written to verbal informed consent was associated with a 5.6 minutes reduction (95% CI 1.1-10.0) in DTN times. After the policy changed, the percentage of patients with DTN ≤60 minutes and ≤45 minutes increased from 35.6% to 66.1% (adjusted OR 1.75; 95% CI 1.12-2.74) and 9.3% to 36.0% (adjusted OR 2.42; 95% CI 1.37-4.25), respectively.ConclusionChanging from written to verbal consent is associated with significant improvement in the timeliness of tPA administration in acute ischemic stroke. 相似文献
104.
Ji-Hyun Park Yoshihiko Nakamura Wenlu Li Gen Hamanaka Ken Arai Eng H Lo Kazuhide Hayakawa 《Journal of cerebral blood flow and metabolism》2021,41(7):1523
Mitochondria may be transferred from cell to cell in the central nervous system and this process may help defend neurons against injury and disease. But how mitochondria maintain their functionality during the process of release into extracellular space remains unknown. Here, we report that mitochondrial protein O-GlcNAcylation is a critical process to support extracellular mitochondrial functionality. Activation of CD38-cADPR signaling in astrocytes robustly induced protein O-GlcNAcylation in mitochondria, while oxygen-glucose deprivation and reoxygenation showed transient and mild protein modification. Blocking the endoplasmic reticulum – Golgi trafficking with Brefeldin A or slc35B4 siRNA reduced O-GlcNAcylation, and resulted in the secretion of mitochondria with decreased membrane potential and mtDNA. Finally, loss-of-function studies verified that O-GlcNAc-modified mitochondria demonstrated higher levels of neuroprotection after astrocyte-to-neuron mitochondrial transfer. Collectively, these findings suggest that post-translational modification by O-GlcNAc may be required for supporting the functionality and neuroprotective properties of mitochondria released from astrocytes. 相似文献
105.
Noor H. A. Suaini Evelyn Xiu-Ling Loo Rachel L. Peters Gaik Chin Yap Katrina J. Allen Hugo Van Bever David J. Martino Anne Eng Neo Goh Shyamali C. Dharmage Marjorelee T. Colega Mary Foong Fong Chong Anne-Louise Ponsonby Kok Hian Tan Mimi L. K. Tang Keith M. Godfrey Bee Wah Lee Lynette Pei-Chi Shek Jennifer J. Koplin Elizabeth Huiwen Tham 《Allergy》2021,76(10):3171-3182
106.
Lauren Desrosiers Sarah Scollon Rebecca Littlejohn Kimberly Nugent Rebecca Althaus Jessica Corredor Emily Berenson Rachel Wyatt Timothy Griffin Kelly Vallance Jonathan Gill Gail Tomlinson Juan Carlos Bernini Angshumoy Roy George Miles Jacquelyn Reuther Shashikant Kulkarni Christine Eng Sharon Plon 《Molecular genetics and metabolism》2021
107.
Martin H. Berryer Fadi F. Hamdan Laura L. Klitten Rikke S. Møller Lionel Carmant Jeremy Schwartzentruber Lysanne Patry Sylvia Dobrzeniecka Daniel Rochefort Mathilde Neugnot‐Cerioli Jean‐Claude Lacaille Zhiyv Niu Christine M. Eng Yaping Yang Sylvain Palardy Céline Belhumeur Guy A. Rouleau Niels Tommerup LaDonna Immken Miriam H. Beauchamp Gayle Simpson Patel Jacek Majewski Mark A. Tarnopolsky Klaus Scheffzek Helle Hjalgrim Jacques L. Michaud Graziella Di Cristo 《Human mutation》2013,34(2):385-394
De novo mutations in SYNGAP1, which codes for a RAS/RAP GTP‐activating protein, cause nonsyndromic intellectual disability (NSID). All disease‐causing point mutations identified until now in SYNGAP1 are truncating, raising the possibility of an association between this type of mutations and NSID. Here, we report the identification of the first pathogenic missense mutations (c.1084T>C [p.W362R], c.1685C>T [p.P562L]) and three novel truncating mutations (c.283dupC [p.H95PfsX5], c.2212_2213del [p.S738X], and (c.2184del [p.N729TfsX31]) in SYNGAP1 in patients with NSID. A subset of these patients also showed ataxia, autism, and a specific form of generalized epilepsy that can be refractory to treatment. All of these mutations occurred de novo, except c.283dupC, which was inherited from a father who is a mosaic. Biolistic transfection of wild‐type SYNGAP1 in pyramidal cells from cortical organotypic cultures significantly reduced activity‐dependent phosphorylated extracellular signal‐regulated kinase (pERK) levels. In contrast, constructs expressing p.W362R, p.P562L, or the previously described p.R579X had no significant effect on pERK levels. These experiments suggest that the de novo missense mutations, p.R579X, and possibly all the other truncating mutations in SYNGAP1 result in a loss of its function. Moreover, our study confirms the involvement of SYNGAP1 in autism while providing novel insight into the epileptic manifestations associated with its disruption. 相似文献
108.
Klapholz M Thomas I Eng C Iteld BJ Ponce GA Niederman AL Bilsker M Heywood JT Synhorst D 《The American journal of cardiology》2001,88(6):657-661
Omapatrilat, a novel vasopeptidase inhibitor, is a highly potent and selective inhibitor of neutral endopeptidase and angiotensin-converting enzyme; its therapeutic potential is being investigated for treatment of hypertension and heart failure. In the present study, the safety, tolerability, and hemodynamic effects of single oral doses of omapatrilat (1 to 50 mg) are compared with placebo in patients with heart failure. Patients with heart failure (New York Heart Association functional class II to IV) and a resting left ventricular ejection fraction < or = 40% were enrolled in a double-blind, placebo-controlled, sequential-panel study of single doses of omapatrilat of 1, 2.5, 5, 10, 25, or 50 mg, followed by hemodynamic assessment for 24 hours. At 4 to 6 hours after dosing, the 25- and 50-mg doses of omapatrilat, compared with placebo, reduced mean pulmonary capillary wedge pressure by approximately 6 mm Hg from 20 and 23 mm Hg at baseline to 14 and 16 mm Hg. The 50-mg omapatrilat dose maintained this effect compared with placebo with an approximately 2.5-mm Hg reduction in mean pulmonary capillary wedge pressure at 24 hours. Omapatrilat improved additional hemodynamic parameters, including cardiac index, systemic vascular resistance, stroke volume index, and mean arterial pressure. Additionally, by 2 hours after dosing with omapatrilat 25 and 50 mg, a trend in peak increases from baseline in plasma atrial natriuretic peptide (twofold) and cyclic guanosine monophosphate (nearly twofold) was observed. Moreover, omapatrilat was well tolerated. Thus, omapatrilat administered orally to patients with heart failure was safe and well tolerated and resulted in improved hemodynamic performance. 相似文献
109.
Plasma radioiron kinetics in man: explanation for the effect of plasma iron concentration.
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K Skarberg M Eng H Huebers G Marsaglia C Finch 《Proceedings of the National Academy of Sciences of the United States of America》1978,75(3):1559-1561
The plasma iron turnover was measured in 19 normal subjects. A correlation was found between plasma iron concentration and plasma iron turnover. In addition to the turnover of 55Fe at normal plasma iron concentration (predominantly monoferric transferrin), a second turnover in which the labeled plasma was saturated with iron (to produce predominantly diferric transferrin) was studied with 50Fe. It was demonstrated that diferric transferrin had a greater rate of iron turnover but that the distribution between erythroid and non-erythroid tissues was unchanged. It was concluded that plasma iron turnover is dependent on the monoferric/diferric transferrin ratio in the plasma but that the internal distribution of iron is unaffected. 相似文献
110.
ANEES THAJUDEEN M.D. WARREN M. JACKMAN M.D. BRIAN STEWART M.S. IVAN COKIC M.D. HIROSHI NAKAGAWA M.D. Ph.D. MICHAEL SHEHATA M.D. ALLEN M. AMORN M.D. AVINASH KALI M.S. EZH LIU M.D. DORON HARLEV M.Sc. NATHAN BENNETT M.Eng. ROHAN DHARMAKUMAR Ph.D. SUMEET S. CHUGH M.D. XUNZHANG WANG M.D. 《Pacing and clinical electrophysiology : PACE》2015,38(6):663-674