Oscillating thromboemboli within the extracranial internal carotid artery demonstrated by ultrasonography in patients with acute cardioembolic stroke

BACKGROUND: Gunshot wounds to the kidney have been managed traditionally by surgical exploration. Concerns over increased nephrectomy rates and unnecessary explorations have placed this method under scrutiny. Selective renal exploration based on solid clinical and radiographic criteria may be a safer alternative and deserves evaluation. METHODS: The medical records of 52 consecutive patients with renal gunshot wounds, who were managed between September 1994 and August 1995 by a protocol of selective exploration, were reviewed. Renal injuries were explored only if they involved the hilum or were accompanied by signs of continued bleeding. Main outcome measures were the numbers of kidneys lost, as well as the morbidity and mortality related to the management of the renal injury. RESULTS: Three patients died from associated injuries shortly after admission. Fifteen patients suffered complications but only two had complications directly associated with the renal injury. Thirty-two patients underwent renal exploration and 17 of them required nephrectomy for major renovascular or parenchymal trauma (grade IV and V). Renal exploration was successfully avoided in the remaining 20 patients. No kidneys were lost unnecessarily as a result of this policy. CONCLUSION: Mandatory exploration of all gunshot wounds to the kidney is not necessary. Injuries that produce stable peripheral haematomas do not require exploration.     

In vitro parathyroid hormone release in patients with secondary hyperparathyroidism

BACKGROUND: The purpose of this study was to determine the precise endocrine characteristics of parathyroid function in secondary hyperparathyroidism (sHPT). METHODS: We examined the effects of extracellular ionized calcium (Ca2+) varying from 0.5 to 2.0 mM on parathyroid hormone (PTH) release in parathyroid cell suspensions using a mid-regional PTH assay. Cells were obtained from 26 patients with sHPT who were divided into two groups according to the type of hyperplasia they exhibited, either nodular (n = 16) or diffuse (n = 10). For comparison, we also analyzed data from nine patients with primary hyperparathyroidism (pHPT; adenomas). RESULTS: Significant in vitro suppression of PTH release by Ca2+ was observed in the majority of subjects, regardless of the histologic abnormality. The pHPT group exhibited no significant relationship between clinical and in vitro data. In contrast, in the sHPT group (taken as a whole), suppression of PTH release by Ca2+ exhibited a plateau at a total serum calcium concentration of 2.5 mmol/L, and a parathyroid gland weight of 2 g. CONCLUSIONS: These findings suggest that there is a curvilinear relationship in sHPT, but not pHPT, between the in vitro calcium sensitivity of parathyroid cells and total serum calcium, as well as gland weight. The in vitro calcium sensitivity in sHPT remains constant when the total serum calcium concentration exceeds 2.5 mmol/L, or when the gland weight exceeds 2 g.     

Portal-hepatic venous shunt through a portal aneurysm complicated by hepatic encephalopathy and pulmonary hypertension

We report a rare case of portal-hepatic venous shunt through an enormous portal aneurysm complicated by pulmonary hypertension. A 66-year-old woman was admitted to our hospital for hepatic encephalopathy. Chest roentgenography revealed pulmonary hypertension. Computed tomography and ultrasound examination demonstrated a shunt between the portal and hepatic veins through an enormous portal aneurysm. The diagnoses of portal-hepatic venous shunt and pulmonary hypertension were confirmed by hepatic venous catheterization and cardiac catheterization. Pulmonary hypertension might result from the effects of vasoconstrictive agents, which should be metabolized by the liver in normal subjects, passing through the intrahepatic shunt into the lung.     

Continuous reactor system of monosized colloidal particles

A reactor system, which continuously hydrolysed the metal alkoxide in an alcohol solution, was designed using an electromagnetic stirrer and an ageing tube. Several monosized colloidal particles were produced by this reactor system, which had high reproducibility and reliability for long-term production. The relation between powder characteristics and experimental parameters such as reagent concentration, mixing rate, ageing time, temperature, was investigated. These parameters had an effect on the particle size, size distribution, morphology and state of agglomeration. It is possible to control the particle size to between 0.1 and 1.0 μm by varying the experimental conditions. A narrower size distribution of powders was obtained by using an electromagnetic stirrer with greater flow rate. Physical and chemical properties of monosized colloidal particles obtained by this reactor were comparable to those of monosized colloidal particles obtained by the batch process.     

Glibenclamide-sensitive mechanism is involved in helodermin-produced vasodilatation in rat mesenteric artery

Helodermin-caused vascular relaxation was simultaneously measured with intracellular Ca2+ concentration ([Ca2+]i) in rat mesenteric artery. Helodermin caused concentration-dependent relaxation in the mesenteric artery preconstricted with norepinephrine (NE). Helodermin-caused relaxation was accompanied by decrease in [Ca2+]i, D-cis-Diltiazem, a Ca2+ channel blocker, also lowered the [Ca2+]i and tension increased by NE. However, helodermin relaxed the artery more efficiently than D-cis-diltiazem, suggesting that the peptide decreased myofilament Ca2+ sensitivity. The vascular relaxation and the corresponding decrease in [Ca2+]i induced by helodermin were partly, but significantly attenuated by glibenclamide. Helodermin-induced vascular responses were mimicked by vasoactive intestinal polypeptide (VIP) or forskolin. Furthermore, helodermin increased cAMP contents in the mesenteric artery. These findings show that vasodilatation induced by helodermin is attributable to lowered [Ca2+]i of arterial smooth muscle partly through the activation of glibenclamide-sensitive K+ channels, and to decrease in the myofilament Ca2+ sensitivity. The increase in the cellular cAMP content probably plays a key role in the peptide-induced vasorelaxation.     

In situ measurement of lithium mass transfer during charging and discharging of a Ni–Sn alloy electrode

The charging (lithiation) and discharging (delithiation) of a Ni–Sn alloy electrode was examined by means of holographic interferometry and laser scanning confocal microscopy (LSCM). The developing concentration profile of Li⁺ ion during discharging (delithiation) of the Ni–Sn alloy electrode agreed reasonably well with the prediction based on transient diffusion theory, indicating that the cell configuration successfully suppressed natural convection due to the electrochemical reaction. The morphological variation of Ni–Sn alloy electrode during charge/discharge cycle could be observed very clearly by in situ LSCM. It was found that the contraction of active material during the discharge (delithiation) initiates cracks in the Ni–Sn alloy electrode.     

First-principles study of structure,vacancy formation,and strength of bcc Fe/V<Subscript>4</Subscript>C<Subscript>3</Subscript> interface

Voids are representative of the damage process in both creep and ductile fractures. Although the matrix/precipitate interface has been considered the preferential nucleation site for voids, the relationship between the atomic structure of this interface and the nucleation mechanism of a void has never been sufficiently investigated. In this study, the bcc Fe/V₄C₃ interface is selected as a model interface between a matrix and precipitate. The vacancy formation energy and intrinsic mechanical strength at this interface are investigated using a first-principles calculation because they should be related with the nucleation of creep and ductile voids, respectively. Within the considered interface, the Fe vacancy is found to be dominant. When the Baker–Nutting orientation relationship is satisfied at the interface, the calculated intrinsic mechanical strength of the interface is 23.8 GPa. However, when the geometric coherence at the interface is low as compared to that of the Baker–Nutting orientation relationship, it is found that the interfacial mechanical strength is significantly weakened. At each interface, it is found that the back-bond of the interface determined the interfacial strength because of the strongly bonded Fe–C on the interface. The nucleation mechanism of a void at the matrix/precipitate interface is discussed based on the present findings. It is suggested that local decohesion at the matrix/precipitate interface should be the origin of the nucleation of a ductile void.     

An intrinsic guanine nucleotide exchange inhibitor in Gi2 alpha. Significance of G-protein self-suppression which antagonizes receptor signal

The alpha subunit of Gi2 (Gi2 alpha) is a member of the heterotrimeric G protein family, which transduces receptor signals as a proto-oncogene product. We have found a novel self-suppressive region in Gi2 alpha near its C terminus. A polypeptide consisting of residues 338-352 of Gi2 alpha (Gi2 alpha-339-352) antagonizes receptor- and receptor peptide-stimulated Gi2 alpha activation, without affecting basal activity. Antagonism by Gi2 alpha-338-352 is attributable to an interaction with activated Gi2 alpha, which is not competitive with receptor polypeptides. Combined with the reports suggesting the presence of self-suppressive domains in a juxta-C-terminal portion of Gi2 alpha and G(o) alpha, this study supports the hypothesis that Gi2 alpha-338-352 constitutes an intrinsic guanine nucleotide exchange inhibitor, which in turn antagonizes receptor stimulation, suggesting that G proteins are activated by receptors through relaxation of a self-suppressive conformation.