Reconstructions of phase contrast,phased array multicoil data

We present a reconstruction method for phased array multicoil data that is compatible with phase contrast MR angiography. The proposed algorithm can produce either complex difference or phase difference angiograms. Directional flow and quantitative information are preserved with the phase difference reconstruction. The proposed method is computationally efficient and avoids intercoil cancellation errors near the velocity aliasing boundary. Feasibility of the method is demonstrated on human scans.     

Monte Carlo simulation of spontaneous miniature excitatory postsynaptic currents in rat hippocampal synapse in the presence and absence of desensitization

 Using the Monte Carlo method, spontaneous fast excitatory postsynaptic currents (mEPSCs) at a hippocampal synapse were simulated by releasing 150–20,000 glutamate molecules from a point source centred 15 nm above a rectangular grid of 14 × 14 α-amino-3-hydroxy-methyl-isoxazole (AMPA) receptors and assuming the channel kinetics to be as reported by Jonas et al. [J Physiol (Lond) 472:615; 1993]. The relationship between the amplitudes of mEPSCs and their time constants of decay is positive, but not pronounced in physiological conditions (except when the number of molecules released is very high). It increases as desensitization is reduced and becomes highly pronounced when it is eliminated. mEPSCs are prolonged with repeated opening of AMPA channels due to enhancement of two concentration-dependent processes: (1) binding of glutamate molecules by AMPA receptors, and (2) occupancy of both activatable bound states. In contrast, the time constant of decay of the patch currents evoked by a short glutamate pulse is independent of glutamate concentration and current amplitude in control conditions, and only moderately concentration dependent in the absence of desensitization. The fast application protocol thus fails to reproduce synaptic currents reliably when there is repeated binding of glutamate molecules to AMPA receptors. During an mEPSC, the occupancy of desensitized states increases rapidly and it strongly depends on the number of glutamate molecules released. Desensitization reaches its maximum after an mEPSC decays to very low levels, and recovers very slowly (from tens to hundreds of milliseconds), and in a concentration-dependent manner. In conclusion, under physiological conditions the desensitization of AMPA receptors plays a major role in shaping the time course of mEPSCs by minimizing the repeated opening of AMPA channels. Received: 17 April 1997 / Received: after revision: 11 August 1997 / Accepted: 1 September 1997     

Insulin resistance and decreased insulin response to glucose in lean type 2 diabetics

In an attempt to determine the mechanism of decreased glucose tolerance in lean type 2 diabetics, glucose turnover in such subjects and controls was studied under basal conditions and during hyperglycemia induced by intravenous administration of glucose. The diabetics had decreased intravenous glucose tolerance and a fasting plasma glucose of 6-8 mM (108-144 mg/dl). Glucose was infused for 2 hr at 2 mg/kg per min in the controls (n = 16) and diabetics (n = 9). Furthermore, 11 healthy subjects were infused also with glucose at 4 mg/kg per min to match the glycemia of the diabetics. Glucose production, utilization, and metabolic clearance were assessed by the primed constant tracer infusion technique. In the basal state, diabetics showed normal plasma insulin, C peptide, and glucagon concentrations. Their increased basal plasma glucose levels were associated with normal rates of glucose production and utilization, but the metabolic glucose clearance was 21% lower than in the controls (P < 0.001), indicating decreased sensitivity to insulin. During infusion of glucose at 2 mg/kg per min, the hyperglycemia attained in the diabetics (170 mg/dl) was higher than that in controls (115 mg/dl) but comparable to that of the controls exposed to the higher glucose load. With the lower glucose load, metabolic clearance rate decreased more markedly in diabetics, again suggesting insulin resistance. This was further substantiated by the fact that, at the same insulin levels, glucose utilization did not increase more in the diabetics than in the controls, although the glycemia reached was considerably higher in the diabetics. With the lower glucose load, glucose production was suppressed to the same degree in the controls and diabetics, although the attained glycemia was much more marked in the latter. Because both insulin and hyperglycemia can suppress glucose production, some defect in the regulation of glucose production of the diabetics is also indicated. The insulin and C peptide levels were much higher in the controls than in the diabetics at the same levels of glycemia, demonstrating the inadequacy of insulin response to glycemia of the diabetics. Glucagon concentration was equally suppressed in all groups. In conclusion, impaired glucose tolerance of mild type 2 diabetics resulted both from inadequate insulin response and from decreased sensitivity to insulin. The insulin resistance could mainly be ascribed to inadequate glucose uptake, but a defect in glucose-induced suppression of glucose production may also have contributed.     

Predictors and Outcomes of Staged Versus One-Time Multivessel Revascularization in Multivessel Coronary Artery Disease: Insights From the VA CART Program

Objectives

The aim of this study was to determine predictors and outcomes associated with staged percutaneous coronary intervention (PCI) versus one-time multivessel revascularization (OTMVR) in patients with multivessel coronary artery disease.

The increase in human plasma antioxidant capacity after red wine consumption is due to both plasma urate and wine polyphenols

By using red wine, dealcoholized red wine, polyphenols-stripped red wine, ethanol-water solution and water, the role of wine polyphenols and induction of plasma urate elevation on plasma antioxidant capacity was examined in humans (n=9 per beverage). Healthy males randomly consumed each beverage in a cross-over design. Plasma antioxidant capacity (measured by ferric reducing antioxidant power, FRAP), ethanol, catechin and urate concentrations were determined before and 30, 60, 90, 120 and 180 min after beverage intake. Dealcoholized red wine and polyphenols-stripped red wine induced similar increase in FRAP values which represented nearly half the effect of the original red wine. This indicates that consumption of red wine involves two separate mechanisms in elevation of plasma FRAP values and both wine phenols and plasma urate contribute to that effect.     

Quantitative measurement of islet glucagon response to hypoglycemia by confocal fluorescence imaging in diabetic rats

We have shown that the glucagon irresponsiveness to hypoglycemia in diabetic rats is markedly improved by correction of hyperglycemia independent of insulin. In contrast, normalization of glycemia by insulin did not improve this response. To find out whether these glucagon responses reflect changes in islet glucagon, we directly quantified glucagon area and content in each pancreatic islet by using fluorescent immunostaining and computerized image analysis with confocal laser scanning microscopy (CLSM). The pancreases were analyzed in four groups of rats.

How to Use the Left Internal Thoracic Artery Which Has Been Damaged During Harvesting?

The established superiority of the internal thoracic artery as a coronary arterial conduit has led to its mandatory use in coronary artery bypass grafting surgery. Therefore, the damage of the internal thoracic artery during harvesting is an abysmal complication, after which the conduit is usually discarded. An alternative approach is presented here, which has allowed us to use the distal two thirds of the proximally damaged left internal thoracic artery as an in situ (with retrograde blood supply from superior epigastric and musculophrenic arteries), reversed arterial conduit to revascularize the left anterior descending coronary artery.     

Systolic ventricular filling.

The evidence of the ventricular myocardial band (VMB) has revealed unavoidable coherence and mutual coupling of form and function in the ventricular myocardium, making it possible to understand the principles governing electrical, mechanical and energetical events within the human heart. From the earliest Erasistratus' observations, principal mechanisms responsible for the ventricular filling have still remained obscured. Contemporary experimental and clinical investigations unequivocally support the attitude that only powerful suction force, developed by the normal ventricles, would be able to produce an efficient filling of the ventricular cavities. The true origin and the precise time frame for generating such force are still controversial. Elastic recoil and muscular contraction were the most commonly mentioned, but yet, still not clearly explained mechanisms involved in the ventricular suction. Classical concepts about timing of successive mechanical events during the cardiac cycle, also do not offer understandable insight into the mechanism of the ventricular filling. The net result is the current state of insufficient knowledge of systolic and particularly diastolic function of normal and diseased heart. Here we summarize experimental evidence and theoretical backgrounds, which could be useful in understanding the phenomenon of the ventricular filling. Anatomy of the VMB, and recent proofs for its segmental electrical and mechanical activation, undoubtedly indicates that ventricular filling is the consequence of an active muscular contraction. Contraction of the ascendent segment of the VMB, with simultaneous shortening and rectifying of its fibers, produces the paradoxical increase of the ventricular volume and lengthening of its long axis. Specific spatial arrangement of the ascendent segment fibers, their interaction with adjacent descendent segment fibers, elastic elements and intra-cavitary blood volume (hemoskeleton), explain the physical principles involved in this action. This contraction occurs during the last part of classical systole and the first part of diastole. Therefore, the most important part of ventricular diastole (i.e. the rapid filling phase), in which it receives >70% of the stroke volume, belongs to the active muscular contraction of the ascendent segment. We hope that these facts will give rise to new understanding of the principal mechanisms involved in normal and abnormal diastolic heart function.