Quasiparticle-mediated spin Hall effect in a superconductor.

In some materials the competition between superconductivity and magnetism brings about a variety of unique phenomena such as the coexistence of superconductivity and magnetism in heavy-fermion superconductors or spin-triplet supercurrent in ferromagnetic Josephson junctions. Recent observations of spin-charge separation in a lateral spin valve with a superconductor evidence that these remarkable properties are applicable to spintronics, although there are still few works exploring this possibility. Here, we report the experimental observation of the quasiparticle-mediated spin Hall effect in a superconductor, NbN. This compound exhibits the inverse spin Hall (ISH) effect even below the superconducting transition temperature. Surprisingly, the ISH signal increases by more than 2,000 times compared with that in the normal state with a decrease of the injected spin current. The effect disappears when the distance between the voltage probes becomes larger than the charge imbalance length, corroborating that the huge ISH signals measured are mediated by quasiparticles.

Localisation pattern of Foxp3+ regulatory T cells is associated with clinical behaviour in gastric cancer.

It has been reported that the population of regulatory T cells (T regs) is increased in tumour-infiltrating lymphocytes in cancer-bearing hosts. Recently, forkhead/winged helix transcription factor p3, Foxp3, is thought to be the most reliable marker of T regs. In the present study, we investigated the prevalence and localisation pattern of Foxp3+ cells in gastric cancer (n=80) by immunohistochemistry, in relation to the clinical outcome of gastric cancer patients. Immunohistochemical staining was performed with anti-Foxp3 mAb, and Foxp3+ cells were semiquantified. We divided all cases into two groups: Foxp3+ -high (n=40) and Foxp3+ -low (n=40) groups, by the median size of the population of Foxp3+ cells. Furthermore, in terms of the localisation pattern of accumulating Foxp3+ cells in tumours, we classified all cases into three groups: a peri-tumour group (n=30), a diffuse group (n=40), and a follicular group (n=10). As a result, although the populations of Foxp3+ cells in stage IV were significantly larger than those in stage I (P<0.05), there was no significant difference in survival between the patients with high and low population levels of Foxp3+ cells. However, survival in patients with a diffuse pattern of Foxp3+ cells was significantly poorer than in those with a peri-tumoral pattern. In conclusion, the localisation pattern, but not the population size, of Foxp3+ cells was significantly related to patient survival.

Targeting EGFR and HER-2 with cetuximab- and trastuzumab-mediated immunotherapy in oesophageal squamous cell carcinoma.

We previously reported that oesophageal squamous cell carcinoma (SCC) had a relatively high incidence of EGFR and HER-2 overexpression. Thus, anti-HER family targeting may become a promising approach to treat oesophageal SCC. In the present study, we investigated (a) the distribution of EGFR and HER-2 expression in oesophageal SCC (n=66) detected by immunohistochemistry and (b) cetuximab- and/or trastuzumab-mediated biological activity (antiproliferative effect by the MTT assay, apoptosis-inducing activity by the annexin V/propidium iodide assay, and antibody-dependent cellular cytotoxicity (ADCC) by the (51)Cr-release assay) against oesophageal SCC cell lines with various levels of EGFR and HER-2. Twelve of the 66 patients (18%) showed both EGFR- and HER-2 expression. Out of both EGFR- and HER-2-positive cases, nine cases (75%) showed EGFR and HER-2 expression in individually distinct regions. Furthermore, the combination of cetuximab and trastuzumab could induce synergistic antiproliferative effects and additional ADCC activities against not all, but several oesophageal SCC cell lines with EGFR and HER-2 expression. The combination of cetuximab and trastuzumab may be useful in the treatment of oesophageal SCC with EGFR and HER-2 expression.

[A case of primary Sjögren syndrome with repeated purpura].

In Sjögren syndrome, purpura is one of its various well known eruptions. Although this disease state is assumed to be based on hypergammaglobulinemia, the details of its mechanism are unknown. We experienced a case involving a female patient with primary Sjögren syndrome showing repeated purpura on the legs, and examined her blood viscosity and histopathology. This girl developed Sjögren syndrome and was admitted to our hospital at 12-years-old. She underwent steroid treatment because of aggravation of the xerosis state and prominent purpura on the legs. Hypergammaglobulinemia was improved during the course; however, purpura appeared repeatedly. Although her blood viscosity was slightly higher than normal, this had no relation to purpura and serum gamma globulin values. Skin biopsy revealed necrotizing angiitis. These results suggest that the purpura of this case was caused not only by hyperviscosity from the hypergammaglobulinemia but also involvement of vasculitis by the primary disease.

[A patient with recurrent breast cancer whose liver metastasis regressed following combined use of weekly docetaxel and MPA.5'-DFUR].

A 28-year-old woman who was 10 months pregnant was diagnosed with left breast cancer. She received preoperative chemotherapy and underwent mastectomy after parturition. Endocrine therapy and adjuvant CMF and CAF was administered, but a bone metastasis appeared 2 years later and a liver metastasis 3 years later. Weekly docetaxel and MPA plus 5'-DFUR combination therapy were successively and simultaneously administered. The liver tumor regressed, and the survival time was prolonged by 1 year and 6 months. This case suggests that the combined use of both therapies was safe for the patient in serious bad condition and had a strong antitumor effect.

Antisense oligonucleotide complementary to the BamHI-H gene family of Marek's disease virus induced growth arrest of MDCC-MSB1 cells in the S-phase.

DNA synthesis was effectively inhibited by antisense oligonucleotide A1 complementary to the BamHI-H gene family in Marek's disease virus (MDV)-derived lymphoblastoid MDCC-MSB1 cells. When a cell cycle distribution of a total cell population was analyzed by flow cytometry, the proportion of S-phase cells increased in the cell populations by treatment with oligonucleotide A1. Approximately 60-70% of the cells appeared in the S phase for 24 and 36 hr of incubation in the presence of oligonucleotide A1 (20-30% in the untreated control cells). The inhibition of cell cycle progression by treatment with oligonucleotide A1 was reversible. When the cells were treated with 5 microM aphidicolin for 12 hr, a similar pattern of cell cycle distribution was observed to that obtained after treatment with oligonucleotide A1. Aphidicolin is an inhibitor of cellular DNA polymerase alpha, and it halts progression of the cell cycle at the G1/S border or early S phase. When the cells were treated with aphidicolin for 12 hr and subsequently incubated with oligonucleotide A1, no significant difference was observed in the cycle phase distribution of cells in the presence and absence of oligonucleotide A1. In contrast, when the cells were treated with oligonucleotide A1 for 12 hr and subsequently incubated with aphidicolin, the cell cycle did not progress from the G1/S border or early S phase to the next phase.

Successful interstitial treatment for bilateral tongue cancer.

We report three cases of bilateral tongue cancer who received interstitial brachytherapy successively for each tumour. Tumour control following treatment are as good as that for unilateral tongue cancer and there have been no severe complications in, or around, the tumour area after using a mandibular protective spacer and dose reduction for the second treatment.

Increased serum levels of vascular endothelial growth factor in Kawasaki disease.

Vascular endothelial growth factor (VEGF) is an angiogenic mitogen that specifically targets vascular endothelial cells. The objective of this study was to evaluate the role of VEGF in Kawasaki disease (KD), the most common cause of systemic vasculitis in childhood. Serum VEGF levels were measured by ELISA in 22 patients with KD, 22 febrile children with infection, and 19 healthy children. Samples from KD patients were divided into three groups: acute stage (n = 20), subacute stage (n = 13), and convalescent stage (n = 15). The results showed that KD patients in the acute and subacute stages had significantly higher levels of VEGF than did patients with infectious diseases and the healthy control subjects. When compared with the VEGF levels of patients with and without coronary artery lesions (CAL), significantly higher levels of VEGF were observed in the subacute stage in patients with CAL and in patients without CAL in the acute stage. Serial examination revealed that the serum VEGF levels in KD patients with CAL increased from a relatively low level in the acute stage to an extremely high level in the subacute stage. In contrast, patients without CAL were found to have extremely high levels of VEGF only in the acute stage of KD. In KD patients, the serum VEGF levels did not correlate with the inflammatory markers and clinical symptoms. Our results raise the possibility that VEGF is involved in the pathogenesis of KD, especially in the development of CAL. Further study is needed to clarify the biologic effect of VEGF on coronary arteries in KD.

[Data analysis by statistical models].

The basic idea for the realization of effective statistical data analysis is illustrated with an example. The use of statistical models is explained and the feasibility of objective comparison of the models by an information criterion AIC is demonstrated. Further, the possibility of practical use of Bayesian models for complex data analysis is explained. Finally, the necessity of cooperation between the experts of respective fields and statisticians for further development of statistical data analysis is mentioned.

Inhibitory factor of actomyosin ATPase in the cardiac conduction system.

ATPase activation and superprecipitation of natural actomyosin in the cardiac conduction system (specialized myocardium) and ventricle were compared. The ATPase activity and superprecipitation of natural actomyosin from the specialized myocardium were much lower than those from the ventricle. The sensitivity of natural actomyosin ATPase to calcium was higher in the specialized myocardium than in the ventricle, whereas the maximum activity of the specialized myocardium was lower than that of the ventricle. The Ca2+-desensitized actomyosin of the specialized myocardium presented scarcely any superprecipitation. Addition of the 0-40% ammonium sulfate fraction (mainly containing myosin and actin) of natural actomyosin from the specialized myocardium to ventricular natural actomyosin inhibited superprecipitation of the latter. On the other hand, addition of the 40-60% ammonium sulfate fraction (mainly containing troponins and tropomyosin) of natural actomyosin from the specialized myocardium enhanced superprecipitation of ventricular natural actomyosin. These results suggested that the specialized myocardium contains some factor(s) that inhibits actin-myosin interaction.