Ventricular reservoir migration into the lateral ventricle through the endoscopic tract after unsuccessful third ventriculostomy

We report a case of reservoir migration into the lateral ventricle through an enlarged endoscopic tract. A full-term female infant with a myelomeningocele, which was repaired surgically after birth, came to us with hydrocephalus, and a reservoir was placed after an unsuccessful endoscopic third ventriculostomy. The tract gradually enlarged and the reservoir eventually slipped into the lateral ventricle 16 days after implantation. This complication may be unique to children, in whom the bone is malleable. As endoscopic surgery is being used more often in infants, the risk of this complication may also be increasing with concurrent reservoir implantation. We believe this complication can be avoided with careful attention to several key points during surgery.     

MR imaging findings of spinal posterior column involvement in a case of Miller Fisher syndrome

Summary: The site of lesions causing ataxia in Miller Fisher syndrome (MFS) remains in dispute. A 43-year-old man manifested rapidly progressive left-sided ptosis, bilateral abducens palsy, areflexia, and severe ataxia. Initial MR imaging showed confined lesions of the cauda equina with gadolinium enhancement. A diagnosis of MFS was made, and the patient underwent immunotherapy. His ophthalmoplegia disappeared, but other symptoms remained. Five months after onset, MR imaging disclosed lesions confined to the spinal posterior column, which were considered to result from involvement of posterior nerve roots of the cauda equina and to be responsible for his remaining severe ataxia.     

The point mutation of tyrosine 759 of the IL-6 family cytokine receptor gp130 synergizes with HTLV-1 pX in promoting rheumatoid arthritis-like arthritis

Rheumatoid arthritis (RA) is a polygenic autoimmune disease. The autoimmunity develops from synergistic actions of genetic and environmental factors. We generated a double-mutant mouse by crossing two murine models of RA, a gp130 mutant knock-in mouse (gp130F759/F759) and an HTLV-1 pX transgenic mouse (pX-Tg), in a C57BL/6 background, which is resistant to arthritis. The mice spontaneously developed severe arthritis with a much earlier onset than the gp130F759/F759 mice and with a much higher incidence than did the pX-Tg mice. The symptoms of gp130F759/F759 mice, including lymphoadenopathy, splenomegaly, hyper-gamma-globulinemia, autoantibody production, increases in memory/activated T cells and granulocytes in the peripheral lymphoid organs, and a decrease in the class II MHC(bright) CD11c+ population, were augmented in the double mutants. Marked reductions in incidence, severity and immunological abnormalities were seen in the triple mutant, IL-6-/-/gp130F759/F759/pX-Tg, indicating that the arthritis in the double mutant is IL-6 dependent. gp130F759/F759/pX-Tg is a unique mouse model for RA.     

Role of Dok-1 and Dok-2 in myeloid homeostasis and suppression of leukemia

Dok-1 and Dok-2 are closely related rasGAP-associated docking proteins expressed preferentially in hematopoietic cells. Although they are phosphorylated upon activation of many protein tyrosine kinases (PTKs), including those coupled with cytokine receptors and oncogenic PTKs like Bcr-Abl, their physiological roles are largely unidentified. Here, we generated mice lacking Dok-1 and/or Dok-2, which included the double-deficient mice succumbed to myeloproliferative disease resembling human chronic myelogenous leukemia (CML) and chronic myelomonocytic leukemia. The double-deficient mice displayed medullary and extramedullary hyperplasia of granulocyte/macrophage progenitors with leukemic potential, and their myeloid cells showed hyperproliferation and hypo-apoptosis upon treatment and deprivation of cytokines, respectively. Consistently, the mutant myeloid cells showed enhanced Erk and Akt activation upon cytokine stimulation. Moreover, loss of Dok-1 and/or Dok-2 induced blastic transformation of chronic phase CML-like disease in mice carrying the bcr-abl gene, a cause of CML. These findings demonstrate that Dok-1 and Dok-2 are key negative regulators of cytokine responses and are essential for myeloid homeostasis and suppression of leukemia.     

Exposure to phthalate esters from indoor environment

Phthalate esters and phosphate esters in samples of indoor air from 27 houses in the Tokyo Metropolitan area were quantified using gas chromatograph/mass spectrometer and gas chromatograph/flame photometric detector after adsorption on to charcoal and solvent extraction. The median concentrations of diethyl phthalate, dibutyl phthalate (DBP), butylbenzyl phthalate, dicyclohexyl phthalate and diethylhexyl phthalate were 0.10, 0.39, 0.01, 0.07 and 0.11 microg/m(3), respectively. The median concentrations of tributyl phosphate, tris(2-chloroethyl) phosphate, triphenyl phosphate and tris(2-butoxyethyl) phosphate were less than 0.001 microg/m(3). DBP was detected at the highest concentration (6.18 microg/m(3)) in a new residential housing. This research indicated that exposure to phthalate esters through inhalation of air from the indoor environment is as important as dietary intake of phthalate esters, and can contribute to daily intake to a much greater extent than has been assumed hitherto.     

The mechanism of contractile dysfunction in heart failure, focussing on SERCA2a function

Cytosolic Ca(2+) is a key regulator of excitation-contraction coupling in myocardium. Myocardial contractile dysfunction in heart failure is characterized by a decrease in contraction and prolonged relaxation. These alterations are mainly due to changes in 1) intracellular Ca(2+) transients (CaT), 2) Ca(2+) sensitivity of the contractile elements, and/or 3) contractile proteins. It is useful to investigate the relationship between CaT and contraction for understanding of the mechanism of contractile dysfunction in heart failure. There are many reports regarding the alterations in CaT, Ca(2+) sensitivity, and contractile proteins in heart failure. Changes in the activity of the sarcoplasmic Ca(2+) pump protein, SERCA2a, may be involved in the altered contractility in heart failure. We generated cardiac-restricted overexpression of SERCA2a transgenic mice (TG) and non-transgenic littermates (NTG). To investigate the role of SERCA2a activity for ischemic heart, we used acidosis as a model of acute contractile dysfunction. During acidosis and recovery from acidosis, the peaks of CaT and tension in TG were significantly larger than those in NTG. These results suggest that an increase in the activity of SERCA2a could be beneficial to preserve contractility during acidosis and recovery. Thus, a disturbance of the intracellular Ca(2+) homeostasis is one of the key factors for the contractile dysfunction in heart failure.     

Lignan derivatives and a norditerpene from the seeds of Vitex negundo

A new phenyldihydronaphthalene-type lignan, vitedoin A (1), a new phenylnaphthalene-type lignan alkaloid, vitedoamine A (2), and a new trinorlabdane-type diterpene, vitedoin B (3), were isolated from the seeds of Vitex negundo along with five known lignan derivatives (4-8). Their chemical structures were determined mainly on the basis of NMR and MS data. Compounds 1, 2, and 4-7 showed stronger antioxidative activity than alpha-tocopherol using the ferric thiocyanate method. Compounds 1, 2, and 4-7 showed higher radical-scavenging effect on the stable free radical, 1,1-diphenyl-2-picrylhydrazyl, than L-cysteine.     

Comparative efficacy of hormone replacement therapy, etidronate, calcitonin, alfacalcidol, and vitamin K in postmenopausal women with osteoporosis: The Yamaguchi Osteoporosis Prevention Study

PURPOSE: To assess the comparative effectiveness of several medications on bone mineral density, biochemical bone markers, and the incidence of vertebral fractures in postmenopausal women with osteoporosis. METHODS: A total of 396 postmenopausal women, aged 50 to 75 years, were allocated randomly to six equal-sized groups: hormone replacement therapy, etidronate, eel calcitonin, alfacalcidol, vitamin K (menatetrenone), or control (no treatment). Thoracic and lumbar spine radiographs, bone mineral density at the distal radius, and markers of bone turnover were assessed at baseline and every 3 months during the 2-year study. RESULTS: Compared with baseline, the 2-year mean changes in bone mineral density were 2.0% for hormone replacement therapy, -0.5% for etidronate, 1.6% for calcitonin, -3.6% for alfacalcidol, -1.9% for vitamin K, and -3.3% for control. Seventeen (26%) of the 66 control patients developed new vertebral fractures. Compared with controls, the relative risks of vertebral fracture were 0.35 (95% confidence interval [CI]: 0.14 to 0.83) for hormone replacement therapy, 0.40 (95% CI: 0.17 to 0.92) for etidronate, 0.41 (95% CI: 0.17 to 0.93) for calcitonin, 0.56 (95% CI: 0.26 to 1.12) for alfacalcidol, and 0.44 (95% CI: 0.20 to 0.99) for vitamin K. CONCLUSION: We observed significant reductions in the incidence of vertebral fractures with hormone replacement therapy, etidronate, and calcitonin, and significant improvements in bone mineral density with hormone replacement therapy and calcitonin.     

Therapeutic orthosis and electrical stimulation for upper extremity hemiplegia after stroke: a review of effectiveness based on evidence

Upper extremity hemiplegia after stroke is common and disabling. Apart from conventional physical and occupational therapy, a number of additional approaches that use devices such as orthoses, prostheses, electrical stimulation, and robots have been introduced. The purpose of this review was to assess the clinical efficacy of such devices used for the affected upper extremities of acute, subacute, and chronic stroke patients. Assessments of their effectiveness and recommendations were based on the weight of published scientific evidence. The amount of evidence with respect to hand splints and shoulder slings is limited. Further study with a well-designed randomized controlled trial (RCT) is required to investigate accurately their short- and long-term efficacy. A number of studies suggested that the use of electrical stimulation for reducing shoulder subluxation or improving the function of wrist and finger extensors is effective during or shortly after the daily treatment period. The robotic approach to hemiplegic upper extremities appears to be a novel therapeutic strategy that may help improve hand and arm function. However, the longer term effectiveness after discontinuation as well as the motor recovery mechanism of electrical stimulation or robotic devices remains unclear. More research is needed to determine the evidence-based effectiveness of electrical stimulation or other devices for stroke survivors.     

Image of a line is not shrunk but neglected. Absence of crossover in unilateral spatial neglect

Patients with left unilateral spatial neglect following right hemisphere lesions usually err rightward when bisecting a horizontal line. For very short lines (e.g. 25 mm), however, leftward errors or seemingly 'right' neglect is often observed. To explain this paradox of crossover in the direction of errors, rather complicated models have been introduced as to the distribution of attention. Neglect may be hypothesized to occur in representational process of a line or estimation of the midpoint on the formed image, or both. We devised a line image task using a computer display with a touch panel and approached the representational image of a line to be bisected. Three patients with typical left neglect were presented with a line and forced to see its whole extent with cueing to the left endpoint. After disappearance of the line, they pointed to the right endpoint, the left endpoint, or the subjective midpoint according to their representational image. The line image between the reproduced right and left endpoints was appropriately formed for the 200 mm lines. However, the images for the shorter 25 and 100 mm lines were longer than the physical lengths with overextension to the left side. These results proved the context effect that short lines may be perceived longer when they are presented in combination with longer lines. One of our patients had an extensive lesion that involved the frontal, temporal, and parietal lobes, and the other two had a lesion restricted to the posterior right hemisphere. The image for a fully perceived line may be represented far enough into left space even when left neglect occurs after a lesion that involves the right parietal lobe. The patients with neglect placed the subjective midpoint rightward from the centre of the stimulus line for the 100 and 200 mm lines and leftward for the 25 mm lines. This crossover of bisection errors disappeared when the displacement of the subjective midpoint was measured from the centre of the representational line image. Left neglect may occur consistently in estimation of the subjective midpoint on the representational image, which may be explained by a simple rightward bias of attentional distribution.