En Bloc removal of soft tumors within the brain parenchyma using spoon retractors: traction-dissection method. Technical note

BACKGROUND: En bloc removal of soft tumors within the brain parenchyma has rarely been performed. We describe a safe technique for en bloc removal of the tumors using a spoon retractor, which enables retraction while holding the soft mass upward. METHODS: Dissection of a tumor mass is performed under traction of the surrounding brain tissue by retracting the mass using a spoon retractor. A dissection plane is first established in a relatively safe area, not opposite the critical area, after a corticotomy. The dissection plane is then extended toward the critical side. After circumferential dissection of the tumor mass, the dissection is continued spirally into deeper regions by retracting and holding the mass upward using a spoon retractor. In this way, the tumor is removed en bloc. CONCLUSIONS: The traction-dissection method using spoon retractors is useful in performing en bloc removal of soft tumors within the brain parenchyma less invasively and provides an appropriate operating field even at depth, reducing intraoperative bleeding, and in vascular rich tumors, possibly preventing tumor seeding in cases of malignant tumors.     

Anesthetic management for clipping a giant basilar artery aneurysm with moderate hypothermia,extracorporeal circulation assistance,and propofol infusion

A 65-year-old female patient underwent surgery to clip a giant basilar artery aneurysm with closed-chest extracorporeal circulation using femorofemoral bypass. Moderate hypothermia (27 degrees C-30 degrees C), retention of spontaneous circulation, and propofol infusion (3-5 mg. kg(-1). h(-1)) were used under general anesthesia. Blood outflow via femoral vein was sufficient to maintain cardiopulmonary bypass and to induce hypothermia. Hemodynamics were controlled with dopamine and noradrenaline. In this case, extracorporeal circulation under moderate hypothermia was used to assist rather than substitute for spontaneous circulation, and spontaneous circulation was maintained at all times. We think that this method had advantages over deep hypothermic circulatory arrest with regard to intraoperative risks and postoperative complications.     

Potentiation of proopiomelanocortin gene expression in cultured pituitary cells by benzodiazepines

BACKGROUND: Benzodiazepines are frequently used not only as a part of general anesthesia but also for the purpose of sedation during regional anesthesia. Effects of these drugs on the hypothalamic-pituitary-adrenal axis activity have been studied, but are still controversial. It is not known whether benzodiazepines affect expression of proopiomelanocortin, precursor protein of adrenocorticotropic hormone and related peptides. METHODS: AtT20PL cell line, a clone of AtT20/D16v mouse corticotroph tumor cells stably transfected with approximately 0.7 kilobases (kb) of the rat proopiomelanocortin 5' promoter-luciferase fusion gene, was used. In the presence or absence of diazepam or midazolam, cells were stimulated by corticotropin-releasing hormone (CRH) or forskolin. Proopiomelanocortin gene expression was estimated by measurement of luciferase activity. Furthermore, to study the mechanism of benzodiazepine effects, cyclic adenosine 3',5'-monophosphate (cyclic AMP) efflux was measured by enzyme immunoassay. RESULTS: Diazepam and midazolam dose-dependently increased the proopiomelanocortin gene expression induced by CRH or forskolin. The potentiating effect was not affected by benzodiazepine receptor antagonists flumazenil and PK11195, but was abolished by a cyclic AMP-dependent protein kinase inhibitor H89. Cyclic AMP efflux induced by CRH or forskolin was also enhanced by diazepam and midazolam. In the presence of isobutylmethylxanthine, a nonspecific phosphodiesterase inhibitor, potentiation of proopiomelanocortin gene expression and enhancement of cyclic AMP efflux by benzodiazepines were not observed. CONCLUSIONS: Benzodiazepines potentiate the effect of CRH or forskolin on proopiomelanocortin gene expression. The potentiating effect is not mediated by the benzodiazepine receptors, but its mechanism probably involves inhibition of phosphodiesterase.     

The triquetrum-hamate joint: an anatomic and in vivo three-dimensional kinematic study

PURPOSE: To obtain anatomic and kinematic information regarding the relative motion of the triquetrum-hamate (TqH) joint. METHODS: In this anatomic study the contact surface constraints of the TqH joint that affect TqH motion were investigated by passively simulating TqH motion according to the kinematic data. Two fresh and 28 embalmed cadaver wrists were dissected. In the kinematic study we studied the in vivo 3-dimensional (3D) kinematics of the TqH joint during radioulnar deviation (RUD) and wrist flexion and extension motion (FEM) in 5 healthy wrists using a magnetic resonance image (MRI)-based markerless bone registration algorithm. Animations of the relative motion of the TqH joint were created and accurate estimates of the relative positions and orientations of the bones and axes of rotation of TqH motion during RUD and FEM were obtained. RESULTS: The anatomic study revealed that the contact surface constraints of the TqH joint include primarily the oval convex surface of the hamate. In the kinematic study TqH motion was likely to be not helicoidal but rotational around an oval convex surface of the hamate. In RUD the triquetral movement was rotation in an ulnoflexion-radial extension plane of the wrist. In FEM it was rotation in an almost flexion-extension plane of the wrist. The axes of rotation of the TqH joint in all wrist motions always ran distal to the TqH joint. CONCLUSIONS: Typical motion of the TqH joint in functional range of motion is not a helicoidal motion on the saddle, but rather a rotational motion on an oval, whose axes of rotation are located on the distal side of the joint.     

NPHS2 mutations in sporadic steroid-resistant nephrotic syndrome in Japanese children

Podocin is an integral membrane protein encoded by NPHS2, which is mapped to 1q25-31 and is exclusively expressed in glomerular podocytes. NPHS2 mutations are responsible for autosomal recessive familial steroid-resistant nephrotic syndrome (SRNS) with minor glomerular abnormalities or focal segmental glomerulosclerosis (FSGS), which is characterized by early childhood onset (age less than 6 years) and rapid progression to chronic renal insufficiency. This gene mutation is also responsible for an adolescent/adult onset form of autosomal recessive familial FSGS with heavy proteinuria. It has been demonstrated that sporadic SRNS and heavy proteinuria are also due to NPHS2 gene mutations. We isolated genomic DNA from 36 Japanese children with chronic renal insufficiency caused by SRNS or heavy proteinuria, and analyzed all eight exons and exon-intron boundaries of NPHS2 using the polymerase chain reaction and direct sequencing. The age at onset of disease was 3.9+/-0.5 years. There were 29 patients with SRNS and 7 with heavy proteinuria without nephrotic syndrome at the onset, but all patients developed chronic renal insufficiency 4.6+/-0.8 years after the onset. A new homozygous missense variant of NPHS2, G34E (G101A) in exon 1, was detected in 1 of 36 patients. However, this homozygous variant was also found in 1 of 44 normal controls, suggesting that the mutation is a polymorphism. Two silent variants (T954C and A1038G) in exon 8 of this gene were also identified in some of the patients and normal controls, indicating that the silent variants are also polymorphisms. There was no significant difference in the genotypic and allelic frequencies of T954C and A1038G polymorphisms between the patients and normal controls. In conclusion, NPHS2 gene mutations are not a major cause of chronic renal insufficiency caused by sporadic SRNS or heavy proteinuria in Japanese children.     

Renal involvement in children with influenza A virus infection

Renal involvement in influenza A virus infection has been rarely reported. To define the clinical characteristics and the factors contributing to the development of renal involvement in influenza A virus infection, we reviewed the clinical characteristics, laboratory data, pediatric risk of mortality (PRISM) score, and the number of systemic inflammatory response syndrome (SIRS) criteria and dysfunctional organs in 45 hospitalized children with influenza A virus infection. Eleven (24.4%) patients had renal involvement. All patients with renal involvement suffered from sepsis and multiple organ dysfunction syndrome (MODS) and 5 developed acute renal failure (ARF). The incidences of dehydration, hypotension, disseminated intravascular coagulation (DIC), and rhabdomyolysis were significantly higher in patients with renal involvement. PRISM scores, the numbers of SIRS criteria and dysfunctional organs, and mortality rate were also higher in patients with renal involvement. Influenza A RNA was absent in the renal tissues of 3 patients with ARF. These results suggested that renal involvement in influenza A virus infection occurred in patients with sepsis and MODS; dehydration, hypotension, DIC, and rhabdomyolysis were factors contributing to its development; direct viral injury to the kidney did not seem to occur in influenza A virus infection.