勃脉力A注射液对体外循环心脏手术患者肝功能的影响

目的 探讨勃脉力A注射液对体外循环心脏手术患者肝功能的影响.方法 选择术前肝功能正常、无肝炎病史的行体外循环心脏手术患者60名,随机分为勃脉力A组(P组)和林格液组(R组).所有患者均在术前、术后2h、1d、3d、7d分别采肘正中静脉血和挠动脉血:静脉血分离血清后应用自动血生化分析仪检测血清中天冬氨酸转氨酶和丙氨酸氨基转移酶,以了解患者的肝脏功能改变;抽取动脉血查乳酸浓度.术中及术后密切观察患者血压、心率、中心静脉压、尿量等,观察并记录患者拔管及停留ICU时间.结果 与R组相比较,在术后各时间点P组ALT、AST及乳酸浓度均显著降低(P﹤0.05),并且拔除气管导管时间和停留ICU时间均有所缩短.结论 勃脉力A注射液能够显著降低体外循环术中乳酸浓度,并能改善患者肝功能,非常适用于体外循环手术.     

Concordance between Self-Reported and Objective Wakeup Times in Ambulatory Salivary Cortisol Research

Background  

Hypothalamic–pituitary–adrenal (HPA) axis functioning has implications for physical and mental health. One important indicator of HPA axis functioning, the salivary cortisol awakening response (CAR), is sensitive to whether participants provide their samples at the requested times after waking.     

Neonatal lupus is a novel cause of positive newborn screening for X-linked adrenoleukodystrophy

We report three unrelated individuals, each exposed to maternal autoantibodies during gestation and found to have elevated very long-chain fatty acids (VLCFAs) in the newborn period after screening positive by California newborn screening (NBS) for X-linked adrenoleukodystrophy (ALD). Two probands presented with clinical and laboratory features of neonatal lupus erythematosus (NLE); the third had features suggestive of NLE and a known maternal history of Sjogren's syndrome and rheumatoid arthritis. In all three individuals, subsequent biochemical and molecular evaluation for primary and secondary peroxisomal disorders was nondiagnostic with normalization of VLCFAs by 15 months of age. These cases add to the expanding differential diagnosis to consider in newborns who screen positive for ALD via elevated C26:0-lysophosphatidylcholine. Though the pathophysiology of how transplacental maternal anti-Ro antibodies damage fetal tissue is not well-understood, we postulate that the VLCFA elevations reflect a systemic inflammatory response and secondary peroxisomal dysfunction that improves once maternal autoantibodies wane after birth. Additional evaluation of this phenomenon is warranted to better understand the intricate biochemical, clinical, and possible therapeutic overlap between autoimmunity, inflammation, peroxisomal dysfunction, and human disease.     

Assessment of myocardial triglyceride oxidation with PET and 11C-palmitate

Background  The goal of this study was to test whether myocardial triglyceride (TG) turnover including oxidation of TG-derived fatty acids (FA) could be assessed with PET and ¹¹C-palmitate. Methods and Results  A total of 26 dogs were studied fasted (FAST), during Intralipid infusion (IL), during a hyperinsulinemic-euglycemic clamp without (HIEG), or with Intralipid infusion (HIEG + IL). ¹¹C-palmitate was injected, and 45 minutes were allowed for labeling of myocardial TG pool. 3D PET data were then acquired for 60 minutes, with first 15 minutes at baseline followed by 45 minutes during cardiac work stimulated with constant infusion of either phenylephrine (FAST, n = 6; IL, n = 6; HIEG + IL, n = 6) or dobutamine (FAST, n = 4; HIEG, n = 4). Myocardial ¹¹C washout during adrenergic stimulation (AS) was fitted to a mono-exponential function (Km(PET)). To determine the source of this ¹¹C clearance, Km(PET) was compared to direct coronary sinus-arterial measurements of total ¹¹C activity, ¹¹C-palmitate, and ¹¹CO₂. Before AS, PET curves in all groups were flat indicating absence of net clearance of ¹¹C activity from heart. In both FAST groups, AS resulted in negligible net ¹¹C activity and ¹¹CO₂ production higher than net ¹¹C-palmitate uptake. AS with phenylephrine resulted in net myocardial uptake of total ¹¹C activity and ¹¹C-palmitate in IL and HIEG + IL, and ¹¹CO₂ production lower than ¹¹C-palmitate uptake. In contrast, AS with dobutamine in HIEG resulted in net clearance of all ¹¹C metabolites (total ¹¹C activity, ¹¹C-palmitate and ¹¹CO₂) with ¹¹CO₂ contributing 66% to endogenous FA oxidation. The AS resulted in significant Km(PET) in all the groups, except HIEG + IL. However, positive correlation between Km(PET) and ¹¹CO₂ was observed only in HIEG (R ² = 0.83, P = .09). Conclusions  This is the first study to demonstrate that using PET and pre-labeling of intracardiac TG pool with ¹¹C-palmitate, noninvasive assessment of myocardial TG use is feasible under metabolic conditions that favor endogenous TG use such as increased metabolic demand (β-adrenergic stimulation of cardiac work) with limited availability of exogenous substrate (HIEG).     

Time-dependent loss of surface complement regulatory activity during storage of donor blood

The survival of transfused red cells (RBCs) diminishes with time of in vitro storage in blood banks, but the molecular mechanisms underlying the slow but incessant deterioration are incompletely understood. To investigate the possibility that impaired resistance to autologous complement attack could play a role in this phenomenon, packed RBCs stored for variable periods were assayed for decay-accelerating factor (DAF) and CD59, two glycoinositol-phospholipid (GPI)-anchored, membrane- associated complement regulatory proteins that function physiologically to protect blood cells from autologous complement activation on their surfaces. Immunoradiometric and flow cytometric assays employing DAF and CD59 monoclonal antibodies showed that levels of both surface proteins gradually declined over 6 weeks. Digestion analyses with phosphatidylinositol-specific phospholipase C, an enzyme that releases GPI-anchored proteins from cell surfaces, showed that DAF and CD59 molecules with GPI anchors containing unacylated inositol were preferentially lost. These findings suggest: 1) that DAF and CD59 molecules with acylated GPI anchors are more stable in RBC membranes than are molecules with unacylated GPI anchors, and 2) that DAF and CD59 loss may participate with other membrane alterations that occur during in vitro storage in compromising the survival of transfused cells.