Fatty liver-hemorrhagic syndrome observed in commercial layers fed diets containing chelated minerals

This study was originally conducted to determine the effect of various chloride levels and consumption of chelated versus non-chelated minerals on egg production and eggshell breaking strength. However, the focus of this report changed after fatty liver-hemorrhagic syndrome (FLHS) was observed in hens that consumed diets containing chelated minerals. No FLHS was observed in hens that consumed a diet that contained non-chelated minerals. Four hundred thirty-two 35-week-old commercial laying hens were housed in individual cages in groups of nine hens each. The treatments were factorially arranged (3 x 2) such that six experimental diets differing in chloride levels and in source of minerals were fed for six 28-day laying periods. A significantly higher mortality attributed to FLHS was observed in hens that consumed the diets having chelated minerals as compared with hens that consumed the diets with non-chelated minerals. No difference in mortality was observed among the hens fed the various chloride diets.     

The effects of temperature on the interactions between volatile general anaesthetics and a neuronal nicotinic acetylcholine receptor

1. Completely isolated identified neurones from the right parietal ganglion of the pond snail Lymnaea stagnalis were investigated under two-electrode voltage clamp. Neuronal nicotinic acetylcholine receptor (AChR) currents were studied at low acetylcholine concentrations (< or = 200 nM). 2. Inhibition of the ACh-induced currents by three volatile general anaesthetics (halothane, isoflurane and methoxyflurane) and the specific inhibitor (+)-tubocurarine was studied as a function of temperature (over the range 4-25 degrees C). 3. The inhibition by the volatile anaesthetics increased (inhibition constants decreased) with decreasing temperature while the inhibition by (+)-tubocurarine did not change significantly near room temperature, but decreased at lower temperatures. The (+)-tubocurarine inhibition appeared to be competitive in nature and showed no significant voltage-dependence. 4. The van't Hoff plots (logarithms of the dissociation constants against reciprocal absolute temperature) were linear for the anaesthetics, but markedly non-linear for (+)-tubocurarine. From these plots, values for the changes in the standard Gibbs free energy delta G degrees water-->AChR, enthalpy delta H degree water-->AChR, entropy delta S degree water-->AChR and heat capacity delta Cp degree water-->AChR were determined. Tubocurarine was found to bind very much tighter to the receptor than the volatile anaesthetics due, entirely, to a favourable increase in entropy on binding. 5. A comparison between the temperature-dependence of the anaesthetic inhibition of the ACh receptor and that of general anaesthetic potencies in animals indicates that the temperature-dependence of animal potencies might be simply accounted for in terms of changes in anaesthetic/receptor binding.     

Pain perception and cardiovascular responses in men with positive parental history for hypertension

Evidence suggests a reduced pain sensitivity in hypertensive individuals. This study sought to extend this work to normotensive individuals with hypertensive parents. Men with a positive (PH+) or negative (PH-) parental history for hypertension rated their pain every 15 s during a 90-s hand cold pressor test and for 90 s after the cold pressor test. Systolic (SBP) and diastolic (DBP) blood pressures and heart rate were measured throughout. After the cold pressor test, the men recalled their pain using the McGill Pain Questionnaire. PH+ men showed greater SBP and DBP responses to the cold pressor test. Although pain ratings during the cold pressor test did not differ between groups, posttest reported pain receded faster in the PH+ than in the PH- men. The PH+ men also reported less total pain on the McGill. These findings support the hypothesis that risk for hypertension may be associated with attenuated pain responses to nociceptive stimuli.     

Complications resulting from saphenous vein patch graft after carotid endarterectomy

OBJECTIVE: Reducing surgical risks to the minimum in carotid endarterectomy has become crucial, especially with the results of recent clinical trials extending indications to asymptomatic patients. The use of the saphenous vein patch graft (SVPG) has been suggested to reduce early postoperative thrombosis and cerebral infarct as well as late recurrent stenosis. However, the exact risks and complications involved in this technique are not known. METHODS: During a 23-year period (1972-1994), 2888 carotid endarterectomies with SVPG for primary carotid stenosis were performed by the Neurosurgical Cerebrovascular Service at the Mayo Clinic. The data from all patients were retrospectively analyzed, emphasizing postoperative complications related to SVPG. RESULTS: There were five postoperative vein ruptures (0.17%), four cases of aneurysm formation, and three cases of deep infection necessitating surgical intervention. The vein patch ruptured in one male patient and four female patients (mean age, 69 yr). All ruptures occurred within 4 days of the primary operation, including two during the first 24 hours. All patients with rupture underwent emergency surgery and were found to have intact suture lines and tears in the middle of the grafts. Two patients recovered without deficits, one suffered major disability, and the other two died. Aneurysm of the patch developed in two male patients and two female patients (mean age, 71 yr). All of the patients developed painless pulsatile neck masses 1 to 9 years after the initial surgery; two also had recurrent ischemic symptoms. All of the patients with aneurysms underwent surgical correction without consequences. CONCLUSION: Although the benefit of routine use of SVPG in carotid endarterectomy is still the focus of debate, this analysis showed that its use adds a small but definite risk of serious complications related to inherent weakness of the venous tissue. If a surgeon chooses to use a patch graft, our recommendation is for use of a synthetic material rather than vein.     

Acute inferior myocardial infarction complicated by rupture into the coronary sinus: diagnosis by two-dimensional echocardiography

Ventricular rupture is a catastrophic, often fatal complication of myocardial infarction. We present a unique case of left ventricular rupture into the coronary sinus that was diagnosed by two-dimensional Doppler echocardiography in a patient with a recent inferior myocardial infarction. The echocardiographic findings essential to diagnosis were subsequently confirmed at autopsy and are reviewed in detail.     

Variation in phosphoric acid concentration and treatment time and HEMA diffusion through dentin

IGF-1 and its receptors have been identified in many tissues including the central nervous system (CNS). We have previously demonstrated that injection of insulin directly into the cerebral ventricles (ICV) is followed by a drop in mean arterial pressure (MAP) associated with an increase in skeletal muscle blood flow. Given the similarities between the IGF-1 and insulin molecules and their respective receptors, we have investigated the effect of ICV administration of IGF-1 on systemic blood pressure and blood flow in selected vascular beds. ICV cannulas were implanted into normal rats and the animals were allowed to recover for 3 to 4 days. The femoral artery and vein were cannulated for blood pressure monitoring and blood sampling and blood flow probes placed around the iliac, the renal and the superior mesenteric artery were used to assess regional blood flow. ICV injection of IGF-1 resulted in a significant decrease in MAP with a nadir at 15 minutes and a gradual return to baseline by 60 minutes; heart rate increased 40 minutes after the injection. IGF-1 significantly enhanced vascular flow and conductance in the iliac, but not in the renal and superior mesenteric arteries. The effects of IGF-1 were much smaller than those observed previously with equimolar amounts of insulin. We conclude that IGF-1 can decrease MAP by selectively increasing blood flow to skeletal muscle through a direct action on the central nervous system.     

Disulfide bond structure determination and biochemical analysis of glycoprotein C from herpes simplex virus

A biochemical analysis of glycoprotein C (gC of herpes simplex virus was undertaken to further characterize the structure of the glycoprotein and to determine its disulfide bond arrangement. We used three recombinant forms of gC, gC1(457t), gC1(delta33-123t), and gC2(426t), each truncated prior to the transmembrane region. The proteins were expressed and secreted by using a baculovirus expression system and have been shown to bind to monoclonal antibodies which recognize discontinuous epitopes and to complement component C3b in a dose-dependent manner. We confirmed the N-terminal residues of each mature protein by Edman degradation and confirmed the internal deletion in gC1(delta33-123t). The molecular weight and extent of glycosylation of gC1 (457t), gC1(delta33-123t), and gC2(426t) were determined by treating each protein with endoglycosidases and then subjecting it to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and mass spectrometric analysis. The data indicate that eight to nine of the predicted N-linked oligosaccharide sites on gC1(457t) are occupied by glycans of approximately 1,000 Da. In addition, O-linked oligosaccharides are present on gC1(457t), primarily localized to the N-terminal region (amino acids [aa] 33 to 123) of the protein. gC2(426t) contains N-linked oligosaccharides, but no O-linked oligosaccharides were detected. To determine the disulfide bond arrangement of the eight cysteines of gC1(457t),the protein was cleaved with cyanogen bromide. SDS-PAGE analysis followed by Edman degradation identified three cysteine-containing fragments which are not connected by disulfide linkages. Chemical modification of cysteines combined with matrix-assisted laser desorption ionization mass spectrometry identified disulfide bonds between cysteine 1 (aa 127) and cysteine 2 (aa 144) and between cysteine 3 (aa 286) and cysteine 4 (aa 347). Further proteolysis of the cyanogen bromide-generated fragment containing cysteine 5 through cysteine 8, combined with mass spectrometry and Edman degradation, showed that disulfide bonds link cysteine 5 (aa 386) to cysteine 8 (aa 442) and cysteine 6 (aa 390) to cysteine 7 (aa 419). A similar disulfide bond arrangement is postulated to exist in gC homologs from other herpesviruses.     

Myocardial acoustics in pediatric allograft rejection

BACKGROUND: Ultrasonographic tissue characterization is the assessment of physical properties of biologic tissue on the basis of quantitative analysis of its acoustic characteristics. Abnormalities in microscopic structure that occur with cardiac allograft rejection may result in characteristic alterations in myocardial acoustics. Ultrasonographic tissue characterization may allow noninvasive detection of rejection. METHODS: Findings in 22 pediatric heart transplant patients undergoing routine surveillance for rejection by endomyocardial biopsy were prospectively evaluated. Off-line ultrasonographic tissue characterization analysis was done on transthoracic echocardiograms obtained at each biopsy. Within patients, tissue characterization texture measures derived from the ultrasonographic image data were compared with histologic findings. Univariate multiple regression analysis was used to identify texture measures associated with acute allograft rejection in a subgroup (n = 8) with at least one biopsy-proven episode of moderate rejection. RESULTS: Measures of homogeneity (co-occurrence matrix correlation and heterogeneity (run-length nonuniformity) decreased with moderate rejection (p < 0.03). Homogeneity measures decreased if the patient had a previous episode of rejection. Several measures of heterogeneity (gray level difference and run-length statistics) were affected by the presence of edema. Run-length nonuniformity was the only measure that differentiated moderate rejection from edema. Discriminant analysis on all 22 patients correctly identified 96% of first rejection episodes (sensitivity 80%, specificity 64%), 93% of moderate and severe rejection episodes (sensitivity 71%; specificity 62%), and 69% of all rejection episodes (sensitivity 51%, specificity 91%). CONCLUSIONS: Histologic changes associated with moderate and severe pediatric allograft rejection as reflected by characteristic alterations in myocardial acoustics can be assessed with ultrasonographic tissue characterization. Histologic changes associated with transplantation itself (resolution of rejection and edema) also affect myocardial acoustics and must be taken into account in rejection surveillance.