Fabrication of Planar Power Inductor for Embedded Passives in LSI Package for Hundreds Megahertz Switching DC–DC Buck Converter

Recently, research and development of integrated low-voltage dc-dc converter to LSIs has been active. In order to realize such integrated dc power supply, power magnetic devices must be integrated in it. The authors have fabricated planar power inductor embedded in LSI package for hundreds megahertz switching dc-dc buck converter. In this study, two types of planar power inductors have been fabricated: one was spin-sprayed Zn-ferrite thick film magnetic core inductor, and the other was composite magnetic core (Fe-based amorphous/polyimide) inductor. Footprint of the fabricated inductors was 850 x 850 mu m(2), their inductance was about 10 nH, and the quality factor Q was about 20 at 100 MHz. The rating current which depends on the superimposed dc characteristic was at least up to 2 A.ArticleIEEE TRANSACTIONS ON MAGNETICS. 47(10):3204-3207 (2011)journal articl

Fabrication of Planar Power Inductor for Embedded Passives in LSI Package for Hundreds Megahertz Switching DC-DC Buck Converter

Recently, research and development of integrated low-voltage dc-dc converter to LSIs has been active. In order to realize such integrated dc power supply, power magnetic devices must be integrated in it. The authors have fabricated planar power inductor embedded in LSI package for hundreds megahertz switching dc-dc buck converter. In this study, two types of planar power inductors have been fabricated: one was spin-sprayed Zn-ferrite thick film magnetic core inductor, and the other was composite magnetic core (Fe-based amorphous/polyimide) inductor. Footprint of the fabricated inductors was 850 x 850 mu m(2), their inductance was about 10 nH, and the quality factor Q was about 20 at 100 MHz. The rating current which depends on the superimposed dc characteristic was at least up to 2 A.ArticleIEEE TRANSACTIONS ON MAGNETICS. 47(10):3204-3207 (2011)journal articl

Anorexia nervosa-associated pancytopenia mimicking idiopathic aplastic anemia: a case report

Abstract Background Patients with anorexia nervosa (AN) often present with pancytopenia. In most cases described in the literature, AN with pancytopenia demonstrates gelatinous marrow transformation (GMT), which is a typical bone marrow feature of malnutrition. Differentiation of AN-associated pancytopenia from other types of pancytopenia, especially idiopathic aplastic anemia (IAA), has not been studied. We encountered a case of pancytopenia in a patient with AN and relatively poor nutritional status, whose hematological findings mimicked those of IAA, specifically fatty bone marrow and absence of GMT. Case presentation The patient was a 32-year-old woman with poorly controlled AN. At 31 years of age, her body mass index (BMI) had fallen from 17.0 kg/m2 to below 13.8 kg/m2. The patient presented with ongoing fatigue and thus was examined by a hematologist. Hematological findings were consistent with IAA: peripheral blood tests revealed pancytopenia, whereas the bone marrow displayed fatty replacement without GMT. Despite the absence of bone marrow features typically seen in malnutrition, the patient’s hematological abnormalities had manifested after a decrease in body weight. Thus, although the bone marrow findings indicated IAA, we considered that the nutritional etiology of pancytopenia could not be thoroughly ruled out. Using nutritional therapy alone, the hematological abnormalities improved as BMI increased to 16.5 kg/m2. The final diagnosis was pancytopenia secondary to malnutrition because pancytopenia and fatty bone marrow improved after implementation of nutritional therapy alone. Conclusions The present case is the first documented case of AN with pancytopenia for which bone marrow examination confirmed fatty marrow without any evidence of GMT. IAA and pancytopenia secondary to malnutrition can present the same clinical findings. This case is significant because it suggests a need to differentiate between malnutrition and IAA

Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function.

Mobilization of intracellular Ca(2+) stores regulates a multitude of cellular functions, but the role of intracellular Ca(2+) release via the ryanodine receptor (RyR) in the brain remains incompletely understood. We found that nitric oxide (NO) directly activates RyRs, which induce Ca(2+) release from intracellular stores of central neurons, and thereby promote prolonged Ca(2+) signalling in the brain. Reversible S-nitrosylation of type 1 RyR (RyR1) triggers this Ca(2+) release. NO-induced Ca(2+) release (NICR) is evoked by type 1 NO synthase-dependent NO production during neural firing, and is essential for cerebellar synaptic plasticity. NO production has also been implicated in pathological conditions including ischaemic brain injury, and our results suggest that NICR is involved in NO-induced neuronal cell death. These findings suggest that NICR via RyR1 plays a regulatory role in the physiological and pathophysiological functions of the brain

Depletion of R270C Mutant p53 in Osteosarcoma Attenuates Cell Growth but Does Not Prevent Invasion and Metastasis In Vivo

Novel therapeutic targets are needed to better treat osteosarcoma, which is the most common bone malignancy. We previously developed mouse osteosarcoma cells, designated AX (accelerated bone formation) cells from bone marrow stromal cells. AX cells harbor both wild-type and mutant forms of p53 (R270C in the DNA-binding domain, which is equivalent to human R273C). In this study, we showed that mutant p53 did not suppress the transcriptional activation function of wild-type p53 in AX cells. Notably, AXT cells, which are cells derived from tumors originating from AX cells, lost wild-type p53 expression, were devoid of the intact transcription activation function, and were resistant to doxorubicin. ChIP-seq analyses revealed that this mutant form of p53 bound to chromatin in the vicinity of the transcription start sites of various genes but exhibited a different binding profile from wild-type p53. The knockout of mutant p53 in AX and AXT cells by CRISPR–Cas9 attenuated tumor growth but did not affect the invasion of these cells. In addition, depletion of mutant p53 did not prevent metastasis in vivo. Therefore, the therapeutic potency targeting R270C (equivalent to human R273C) mutant p53 is limited in osteosarcoma. However, considering the heterogeneous nature of osteosarcoma, it is important to further evaluate the biological and clinical significance of mutant p53 in various cases