Two-axis control of a singlet-triplet qubit with an integrated micromagnet.

The qubit is the fundamental building block of a quantum computer. We fabricate a qubit in a silicon double-quantum dot with an integrated micromagnet in which the qubit basis states are the singlet state and the spin-zero triplet state of two electrons. Because of the micromagnet, the magnetic field difference ΔB between the two sides of the double dot is large enough to enable the achievement of coherent rotation of the qubit's Bloch vector around two different axes of the Bloch sphere. By measuring the decay of the quantum oscillations, the inhomogeneous spin coherence time T2* is determined. By measuring T2* at many different values of the exchange coupling J and at two different values of ΔB, we provide evidence that the micromagnet does not limit decoherence, with the dominant limits on T2* arising from charge noise and from coupling to nuclear spins.

Characterization of a gate-defined double quantum dot in a Si/SiGe nanomembrane.

We report the fabrication and characterization of a gate-defined double quantum dot formed in a Si/SiGe nanomembrane. In the past, all gate-defined quantum dots in Si/SiGe heterostructures were formed on top of strain-graded virtual substrates. The strain grading process necessarily introduces misfit dislocations into a heterostructure, and these defects introduce lateral strain inhomogeneities, mosaic tilt, and threading dislocations. The use of a SiGe nanomembrane as the virtual substrate enables the strain relaxation to be entirely elastic, eliminating the need for misfit dislocations. However, in this approach the formation of the heterostructure is more complicated, involving two separate epitaxial growth procedures separated by a wet-transfer process that results in a buried non-epitaxial interface 625 nm from the quantum dot. We demonstrate that in spite of this buried interface in close proximity to the device, a double quantum dot can be formed that is controllable enough to enable tuning of the inter-dot tunnel coupling, the identification of spin states, and the measurement of a singlet-to-triplet transition as a function of an applied magnetic field.

Association of Myianoetus muscarum (Acari: Histiostomatidae) With Synthesiomyia nudiseta (Wulp) (Diptera: Muscidae) on Human Remains.

Synthesiomyia nudiseta (Wulp) (Diptera: Muscidae) was identified during the course of three indoor medicolegal forensic entomology investigations in the state of Texas, one in 2011 from Hayes County, TX, and two in 2015 from Harris County, TX. In all cases, mites were found in association with the sample and subsequently identified as Myianoetus muscarum (L., 1758) (Acariformes: Histiostomatidae). This report represents the first records of a mite associated with S. nudiseta in the continental United States. In particular, this association is believed to be of potential future value in forensic investigations, as it lends new insight into the community structure of colonizers on human remains in indoor environments.

A roadmap for bridging basic and applied research in forensic entomology.

The National Research Council issued a report in 2009 that heavily criticized the forensic sciences. The report made several recommendations that if addressed would allow the forensic sciences to develop a stronger scientific foundation. We suggest a roadmap for decomposition ecology and forensic entomology hinging on a framework built on basic research concepts in ecology, evolution, and genetics. Unifying both basic and applied research fields under a common umbrella of terminology and structure would facilitate communication in the field and the production of scientific results. It would also help to identify novel research areas leading to a better understanding of principal underpinnings governing ecosystem structure, function, and evolution while increasing the accuracy of and ability to interpret entomological evidence collected from crime scenes. By following the proposed roadmap, a bridge can be built between basic and applied decomposition ecology research, culminating in science that could withstand the rigors of emerging legal and cultural expectations.

TLR agonists enhance responsiveness of inflammatory innate immune cells in HLA-B*57-positive HIV patients.

HLA-B*57 affects the course of HIV infection. Under antiretroviral therapy, its effects cannot be explained by outstandingly efficient T cell responses alone but may also involve cells of innate immunity. Studying in vitro stimulation with Pam3CSK4, E. coli LPS-B5 and CpG-ODN-2216, we observed greater induction of IL-6/IL-1beta double-positive CD14+CD16++ monocytes as well as IFN-gamma-positive cytotoxic CD56highCD16neg NK cells in HLA-B*57- versus HLA-B*44-positive HIV patients, while TNF-alpha induction remained unchanged. Differences were not seen in the other monocyte and NK cell subsets or in HLA-matched healthy controls. Our findings show that, in virally suppressed HIV infection, HLA-B*57 is associated with enhanced responsiveness of inflammatory innate immune cells to TLR ligands, possibly contributing to increased vulnerability in sepsis. KEY MESSAGES: • HLA-B*57 is a host factor affecting clinical outcomes of HIV infection. • HLA-B*57 modifies inflammatory subsets of NK cells and monocytes in HIV infection. • In HLA-B*57-positive HIV patients TLR agonists induce enhanced IL-6/IL-1beta in monocytes. • NK cells from HLA-B*57 HIV patients release more IFN-gamma upon TLR costimulation. • HLA-B*57 is linked to enhanced inflammatory responsiveness to TLR ligands.

Routine use of bilateral skeletonized internal thoracic artery grafting: long-term results.

BACKGROUND: Skeletonized harvesting of the internal thoracic artery (ITA) decreases the severity of sternal devascularization, thus reducing the risk of postoperative sternal complications in patients undergoing bilateral ITA grafting. METHODS AND RESULTS: Between 1996 and 2001, 1515 consecutive patients underwent skeletonized bilateral ITA grafting. Of the 1179 male and 336 female patients, 641 (42.3%) were >70 years of age, and 519 (34.2%) had diabetes mellitus. Operative mortality was 2.8%. Early postoperative morbidity included sternal infection (1.6%), cerebrovascular accident (3%), and perioperative myocardial infarction (1%). Multiple regression analysis showed chronic obstructive pulmonary disease (odds ratio, 11.3; 95% confidence interval [CI], 4.45 to 28.55), repeat operation (odds ratio, 12.7; 95% CI, 3.25 to 49.56), and diabetes mellitus (non-insulin dependent: odds ratio, 4.64; 95% CI, 1.85 to 11.59; insulin dependent: odds ratio, 6.9; 95% CI, 1.35 to 35.27) to be associated with increased risk of sternal infection. Follow-up (between 5 and 12 years) revealed 305 late deaths. Kaplan-Meier 10-year survival rates for patients <65, 65 to 74, and >75 years of age were 87%, 75%, and 52%, respectively. Cox regression analysis revealed increased overall mortality (early and late) in patients with peripheral vascular disease (hazard ratio [HR], 1.8; 95% CI, 1.39 to 2.33), patients >75 years of age (HR, 7.23; 95% CI, 4.16 to 12.55), those undergoing repeat operations (HR, 2.22; 95% CI, 1.27 to 3.89), patients with preoperative congestive heart failure (HR, 1.64; 95% CI, 1.29 to 3.75), and those with chronic renal failure (HR, 1.52; 95% CI, 1.11 to 2.01). Operations performed without cardiopulmonary bypass were associated with better postoperative survival (HR, 0.66; 95% CI, 0.49 to 0.87). CONCLUSIONS: Bilateral ITA grafting is associated with low morbidity and good long-term results. Use of skeletonized bilateral ITA is appropriate for the elderly and most patients with diabetes; however, it is not recommended for repeat operations or for patients with chronic obstructive pulmonary disease.

Mutation of unique region of Bruton's tyrosine kinase in immunodeficient XID mice.

The cytoplasmic tyrosine kinase, Bruton's tyrosine kinase (Btk, formerly bpk or atk), is crucial for B cell development. Loss of kinase activity results in the human immunodeficiency, X-linked agammaglobulinemia, characterized by a failure to produce B cells. In the murine X-linked immunodeficiency (XID), B cells are present but respond abnormally to activating signals. The Btk gene, btk, was mapped to the xid region of the mouse X chromosome by interspecific backcross analysis. A single conserved residue within the amino terminal unique region of Btk was mutated in XID mice. This change in xid probably interferes with normal B cell signaling mediated by Btk protein interactions.

Survival of HIV/HCV co-infected patients before introduction of HCV direct acting antivirals (DAA).

HIV/HCV infection is supposed to substantially reduce survival as compared to HIV mono-infection. Here, we compared longtime-survival and causes of death in a cohort of HIV- and HIV/HCV-co-infected patients on combined antiretroviral therapy (cART), before introduction of HCV direct acting antivirals (DAA). 322 Caucasian patients with HIV (n = 176) and HIV/HCV-infection (n = 146) were enrolled into this study. All patients were recruited between 2003 and 2004 and followed until 01.01.2014. We compared overall survival between the two groups by the Kaplan-Meyer method and identified independent factors associated with long-time survival by conditional Cox regression analysis. In total 46 (14.3%) patients died during the observation period (HIV infection: n = 23 (13.1%), HIV/HCV infection: n = 23 (15.8%) but overall-survival did not differ significantly between HIV/HCV-infected and HIV mono-infected patients (p = 0.619). Survival was substantially better in patients with complete suppression of HIV replication below the level of detection than in those with residual viremia (p = 0.001). Age (p = 0.008), γ-glutamyltranspeptidase (p < 0.0001) and bilirubin (p = 0.008) were significant predictors of survival irrespective from HCV co-infection. Complete repression of HIV replication on cART is the key factor determining survival both in HIV- and HIV/HCV-co-infected patients, while HCV co-infection and therapy without DAAs seem to affect survival to a lesser extent. Thus, patients with HIV/HCV co-infection require particularly intensive cART.

Kir, a novel Ras-family G-protein, induces invasive pseudohyphal growth in Saccharomyces cerevisiae.

Kir belongs to a novel class of Ras-family G-proteins which includes Gem and Rad. These proteins are unique among Ras super-family G-proteins since their expression is under transcriptional regulation in mammalian cells. To gain insight into the function of Kir, we took advantage of the well-defined signal transduction pathways of yeast. When kir is expressed in Saccharomyces cerevisiae, the transformants form pseudohyphae and exhibit invasive properties characteristics of yeast cells undergoing a developmental transition induced by nitrogen starvation. Analysis of pseudohyphal signaling pathway mutants suggests that the Kir-induced pseudohyphae formation requires a MAP kinase cascade involving ste20, ste11, ste7 but not ste5 gene products. Furthermore, our results are consistent with the idea that Kir functions upstream of the STE20 kinase which plays a critical role in two distinct MAP kinase cascades.

Tumor necrosis factor-alpha is released from the isolated heart undergoing ischemia and reperfusion.

OBJECTIVES: The purpose of this study was to examine whether tumor necrosis factor-alpha (TNF-alpha) is released directly from the ischemic myocardium undergoing reperfusion. BACKGROUND: Tumor necrosis factor-alpha is a protein hormone produced by systemic leukocytes (primarily by activated macrophages). It has been implicated as a systemic mediator in the development of septic shock and other pathologic conditions. Serum TNF-alpha has also been detected in a variety of cardiac disease states and after myocardial ischemia-reperfusion injury. METHODS: Nine isolated rat hearts undergoing 30 min of perfusion, followed by warm cardioplegic arrest, 1 h of global ischemia and 30 min of reperfusion, were investigated using the modified Langendorff model. RESULTS: Significant amounts of TNF-alpha (752 +/- 212 pmol/ml) were detected in the effluent during the first minute of reperfusion. Tumor necrosis factor-alpha levels correlated with postischemic deterioration in peak systolic pressures (r = 0.7882, p = 0.012), dP/dt max (r = 0.6795, p = 0.044), time-pressure integral (r = 0.7661, p = 0.0016) and postischemic creatine kinase levels (r = 0.8367, p = 0.005). The deterioration in coronary flow, however, was inversely correlated with TNF-alpha levels (r = -0.7581, p = 0.018). CONCLUSIONS: To our knowledge, this study is the first to suggest that the isolated rat myocardium synthesizes and releases TNF-alpha in response to ischemia and reperfusion, which directly correlates with the postischemic deterioration in myocardial mechanical performance and the amount of cellular necrosis.

Interaction between paracrine tumor necrosis factor-alpha and paracrine angiotensin II during myocardial ischemia.

OBJECTIVES: The purpose of this study was to explore interactions between paracrine angiotensin II (Ang-II) and tumor necrosis factor-alpha (TNF-alpha) during myocardial ischemia. BACKGROUND: Ischemic myocardium releases significant amounts of TNF-alpha. This paracrine release correlated with postischemic myocardial injury. Other studies showed myocardial protection obtained by the use of angiotensin-converting enzyme inhibitors (i.e., captopril) and the Ang-II type 1 receptor antagonist losartan after ischemia. The possibility that these agents decrease TNF-alpha synthesis has not yet been investigated. METHODS: Using the modified Langendorff model, isolated rat hearts underwent either 90 min of nonischemic perfusion (control group) or 1 h of global cardioplegic ischemia. In both groups, either captopril (360 micromol/liter) or losartan (182.2 micromol/liter) was added before ischemia. The hearts were assayed for messenger ribonucleic acid (mRNA) expression and effluent TNF-alpha levels. In addition, cardiac myocytes were incubated in cell culture with Ang-II. RESULTS: After ischemia, TNF-alpha mRNA expression intensified from 0.63 +/- 0.06 (control group) to 0.92 +/- 0.12 (p < 0.03), and effluent TNF-alpha levels were 711 +/- 154 pg/ml. The TNF-alpha mRNA expression declined to 0.46 +/- 0.07 (p < 0.01) and 0.65 +/- 0.08 (p < 0.02) in captopril- and losartan-treated hearts, respectively. Effluent TNF-alpha was below detectable levels. Concentrations of TNF-alpha in supernatants of incubated cardiac myocytes treated with 10 and 50 nmol/liter of Ang-II were 206.0 +/- 47.0 pg/ml and 810 +/- 130 pg/ml, respectively (p < 0.004). When pretreated with 700 micromol/liter of losartan, TNF-alpha was below detectable levels. CONCLUSIONS: This study presents an original explanation for previously reported myocardial protection after ischemia, obtained by the use of captopril and losartan. These drugs reduce TNF-alpha synthesis, providing strong evidence of active interactions between paracrine TNF-alpha and Ang-II in the evolution of the ischemic cascade.

Anti-tumor necrosis factor-alpha improves myocardial recovery after ischemia and reperfusion.

OBJECTIVES: This study sought to assess the importance of locally released or paracrine myocardial tumor necrosis factor-alpha (TNF-alpha) in the evolution of postischemic myocardial dysfunction and to use immunohistochemical studies to localize TNF-alpha within the myocardium. BACKGROUND: TNF-alpha is implicated as a systemic mediator in the development of myocardial ischemia-reperfusion injury by promoting leukocyte myocardial infiltration, and it has been shown to originate from noncardiac peripheral mononuclear cells. We have recently documented in a blood-free environment the release of TNF-alpha from the ischemic-reperfused myocardium. METHODS: Isolated rat hearts undergoing 1 h of global cardioplegia-induced ischemia and 30 min of reperfusion were investigated with use of the modified Langendorff model. Hearts were randomly divided into three subgroups: group A, control group; and groups B and C, isolated hearts receiving cardioplegic solution containing monoclonal hamster antimurine TNF-alpha antibodies (group B) or hamster IgG (group C). RESULTS: Significant amounts of TNF-alpha were detected in group A and group C effluent on 1 min of reperfusion (752 +/- 212 and 958 +/- 409 pmol/ml, respectively). However, in group B, TNF-alpha was below detectable levels. In this group, postischemic left ventricular peak systolic pressures, first derivative of the rise in left ventricular pressure (dP/dtmax), pressure-time integral, coronary flow and O2 consumption improved (analysis of variance [ANOVA] p < 0.0001 for all variables) compared with values in groups A and C; creatine kinase levels decreased (p < 0.005); and myocardial structure was preserved. Immunohistochemical staining localized TNF-alpha to cardiac myocytes and to endothelial cells. CONCLUSIONS: Anti-TNF-alpha neutralizes local TNF-alpha release from cardiac myocytes after ischemia and improves myocardial recovery during reperfusion, indicating that postischemic paracrine TNF-alpha release plays an active role in myocardial dysfunction.

Dissection of signaling pathways and cloning of new signal transducers in tyrosine kinase-induced pathways by genetic selection.

We used genetic strategies which have been proven valuable to decipher signaling pathways in comparatively simple organisms such as Drosophila and Caenorhabditis elegans, to dissect signaling network activated by tyrosine kinases in mammals. The strategy was developed further towards a generally applicable expression cloning system to identify signal transducers in tyrosine kinase pathways. This system is based on the ability of downstream acting genes to rescue the transformation phenotype of partial loss-of-function mutants of BCR-ABL which still retain tyrosine kinase activity. Using this strategy we have previously shown that overexpression of c-Myc and Cyclin D1 can rescue a signaling defective SH2 mutant of BCR-ABL for transformation. In an unbiased approach to identify new compensating genes, a cDNA library was introduced by retroviral infection into fibroblasts which express the BCR-ABL SH2 mutant. CDNA clones, capable of rescuing the SH2 mutant for transformation should result in colony formation in soft agar. A PCR approach was used to recover these compensating genes from the genomic DNA of the transformed fibroblasts. Sequencing analysis of the initial cDNAs identified three known genes, the adapter molecule Shc, the kinases SPRK and p38 MAPK. These genes have been found to interact functionally with BCR-ABL for fibroblast and hematopoietic cell transformation. Currently, we are constructing and screening new libraries to identify novel genes which complement the BCR-ABL SH2 mutant. Our results demonstrate that this cloning approach is an effective means of identifying and characterizing signaling molecules that function in specific signaling pathways. This in turn may identify specific targets for mechanism-based therapeutic intervention to block altered signaling.

High-dose MTX/5-FU and adriamycin for gastric cancer.

In a phase II trial we tried to evaluate the efficacy of a sequential combination of high-dose methotrexate (MTX) and 5-fluorouracil (5-FU) combined with Adriamycin (ADM). In a pilot study we had found high-dose MTX effective as a single agent in gastric cancer. MTX and 5-FU were combined sequentially because Cadman et al had shown synergism for this combination. The therapy protocol consisted of high-dose MTX, 1.5 g/m2 of body surface, and high-dose 5-FU, 1.5 g/m2. MTX was administered 1 hr prior to 5-FU. Both drugs were given as a bolus. Twenty-four hours after MTX administration, citrovorum factor rescue was started, 15 mg/m2, q.6h. X 12, orally. Forty-eight hours after MTX administration, serum concentration of the drug was measured by high performance liquid chromatography (HPLC). Fourteen days after MTX was given, ADM, 30 mg/m2, was injected as a bolus. This protocol was repeated every 28 days. Patients eligible for this treatment should have a creatinine clearance of greater than 60 ml/min. The study included 30 patients with metastasizing gastric cancer and performance status between 40% and 70%. The response rate was 63% (19 of 30 patients). Two of 30 patients had complete remissions, which are still maintained. The median survival for responders is not yet evaluable: 68% are living after 17+ mo. The median survival for nonresponders was only 5 mo. The difference in survival curves is significant at a level of p less than 0.05. Cytostatic treatment was well tolerated. Fifty percent of the patients could be treated on an outpatient basis. Total alopecia was observed in only 10% of the patients. Severe leukopenia, thrombocytopenia, and kidney disorders were not observed.

Side effects of ofloxacin in clinical trials and in postmarketing surveillance.

Data derived from clinical trials of ofloxacin in 15,962 patients show that the incidence rate of adverse drug events was 4.27 per 100 patients. Symptoms were generally mild and related to the gastrointestinal tract, nervous system or hypersensitivity reactions in rank order. On the other hand, spontaneous reports obtained during postmarketing surveillance involving 1.5 million patients showed that the most frequent adverse drug events were related to the nervous system; next in order of frequency were hypersensitivity reactions and gastrointestinal symptoms. A comparison of the data obtained from clinical trials and postmarketing surveillance revealed no change in the favourable overall benefit:risk ratio of ofloxacin. Possible reasons for the different patterns of adverse drug events are discussed.

A monoclonal antibody to the galactan from Helix pomatia snails recognizes beta-(1,6)-linked D-galactose residues.

Using the hybridoma technique, a series of four monoclonal antibodies to the galactan isolated from albumin glands of wine yard snails (Helix pomatia) could be generated. Characterization of the binding properties of one of these antibodies revealed a specificity for beta-(1,6)-glycosidically linked D-galactose residues. This could be demonstrated by reaction of the antibody with beta-(1,6)-D-galactans and by the D-galactose-inhibitable binding to group B streptococci of type II, which possess beta-(1,6)-linked D-galactose as immuno-determinant group.

Coronary artery bypass without cardiopulmonary bypass: analysis of short-term and mid-term outcome in 220 patients.

Two hundred twenty patients, preferentially those with high-risk conditions, underwent coronary artery bypass grafting without cardiopulmonary bypass. Early unfavorable outcome events included operative mortality (7 patients, 3.2%), nonfatal perioperative myocardial infarction (6 patients, 2.7%), cerebrovascular accident (1 patient, 0.4%), and sternal infection (3 patients, 1.4%). There were two deaths (13%) among 15 patients with calcified aorta and four (12%) in 33 patients who underwent emergency operation. Multivariate analysis revealed these two risk factors to be the only predictors of early mortality (odds ratios, 8.0 and 9.8, respectively). Preoperative risk factors such as left ventricular dysfunction (ejection fraction < or = 35%) (40 patients, 18%), congestive heart failure (46 patients, 21%), acute myocardial infarction (59 patients, 27%), cardiogenic shock (7 patients, 3%), age 70 years or older (59 patients, 27%), renal failure (19 patients, 9%), and cerebrovascular accident and carotid disease (11 patients, 5%) were not found to be major predictors of early mortality or unfavorable outcome. During 12 months of follow-up (range 1 to 21 months), there were four cardiac and three noncardiac deaths (1-year actuarial survival 93%) and 17 cases (7.7%) of early return of angina. Calcified aorta, nonuse of the internal mammary artery, reoperation, and diabetes mellitus were independent predictors of unfavorable events. We conclude that coronary artery bypass grafting without cardiopulmonary bypass can be done with relatively low operative mortality, although there seems to be an increased risk for early return of angina. This procedure should therefore be considered for patients with appropriate coronary anatomy, in whom cardiopulmonary bypass poses a high risk. This procedure is still hazardous with calcified aorta or emergency operation.

Prevention of supraventricular tachyarrhythmia with low-dose propranolol after coronary bypass.

Eighty-five patients receiving long-term propranolol therapy were randomized after aorta-coronary bypass grafting either to receive minidose propranolol (Group I) or to serve as controls (Group II). They were compared with 18 patients (Group III) who did not receive beta blocking agents prior to operation but were given propranolol postoperatively. Poor-risk patients (those having left ventricular aneurysms, low ejection fraction, or congestive heart failure) as well as patients who required catecholamines postoperatively were included in the study. All three groups were comparable with respect to all risk factors. Propranolol (5 to 10 mg/6 hr) was started through a nasogastric tube 6 hours after operation and continued orally in all patients in Groups I and III. Supraventricular tachyarrhythmia appeared in two of 37 patients in Group I (5%), 19 of 48 patients in Group II (40%), and five of 18 patients in Group III (27%). The incidence of supraventricular tachyarrhythmia was significantly lower in Group I than in Groups II and III (p less than 0.001, Group I versus Group II; p less than 0.01, Group I versus Group III). In conclusion, low-dose propranolol is very effective in preventing supraventricular tachyarrhythmia following aorta-coronary bypass in patients receiving beta blockers preoperatively. The increased tendency for postoperative supraventricular tachyarrhythmia to develop in these patients is attributed to hypersensitivity to adrenergic stimulation after propranolol withdrawal. The tachyarrhythmia can be prevented by early reinstitution of propranolol in low doses after the operation.

Enhanced protection of myocardial function by systemic deep hypothermia during cardioplegic arrest in multiple coronary bypass grafting.

The effectiveness of deep systemic hypothermia (20 degrees C) in myocardial protection during aortic cross-clamping was elevated. Seventy-one consecutive patients undergoing coronary artery bypass grafting were divided into two groups. In group A (32 patients) systemic temperature was reduced to an average of 26.8 degrees C (range 24 degrees to 28 degrees C) and the amount of cardioplegic solution infused totalled 1,000 to 1,200 cc. In Group B (39 patients) systemic temperature was reduced to an average of 20.8 degrees C (17 degrees to 23 degrees C) and the total amount of cardioplegic solution infused was 100 to 300 cc. The mean number of coronary (distal) anastomoses per patient was 4.46 in Group A and 4.51 in Group B. There were no surgical deaths, perioperative infarcts, or neurologic damage in either group. Postoperative catecholamine dependence was used as an indicator for inadequate myocardial protection. Catecholamine support was required by 18 patients (56.25%) in Group A and two patients (5.13%) in Group B (p less than 0.0001). Patients of both groups who received five or six coronary anastomoses, whose aortic cross-clamp time was 60 minutes or more, and whose preoperative left ventricular ejection fractions were above 50% were compared: Ten of the 11 (91%) in Group A required catecholamine support as opposed to none of the 12 in Group B (p less than 0.0001). No significant difference in the incidence of catecholamine requirement was found between patients of both groups whose aortic cross-clamp time was less than 60 minutes (2/13 patients in Group A and 2/21 patients in Group B), regardless of their preoperative left ventricular ejection fraction. We conclude that when aortic cross-clamp time exceeds 60 minutes, that is, when multiple distal anastomoses are performed, deep systemic hypothermia is a simple and effective method for myocardial preservation.

Inaccuracy of radial artery pressure measurement after cardiac operations.

The phenomenon of a pressure gradient between central and radial arteries was evaluated in 48 patients immediately after coronary artery bypass operations. All were in stable hemodynamic condition, none receiving catecholamine support. In eight patients (Group A) mean femoral pressure was significantly higher than mean radial pressure (range 10 to 30 mm Hg). In the remaining 40 (Group B) radial and femoral pressures were equal. Mean cardiac index (thermodilution) was 3.3 +/- 0.68 versus 2.1 +/- 0.4 L/min/m2, systemic vascular resistance 1,181 +/- 218.4 versus 2,049 +/- 501 dynes/sec/cm-5, toe temperature 23.8 degrees +/- 1.2 degrees C versus 24.02 degrees +/- 0.9 degrees C, core temperature 33.9 degrees +/- 0.5 degrees C versus 34.1 degrees +/- 0.6 degrees C, mixed venous oxygen saturation 78% +/- 3% versus 62% +/- 5%, and peak radial dP/dt 1,485 +/- 366 versus 2,028 +/- 392 in Groups A and B, respectively. These data indicate, first, that the low radial pressures measured in Group A patients did not represent the true central aortic pressures; that is, they were false. Second, these low pressures had nothing to do with compromised cardiac function; rather, they were due to peripheral constriction and volume factors and also probably to proximal shunting. It is therefore recommended that while the chest is still open, if a discrepancy exists between a low radial artery pressure, a high palpable aortic pressure, and a satisfactory cardiac contraction, a femoral cannula for pressure measurement should be inserted. Treatment is by blood infusion until the femoral-radial gradient has been abolished.