Involvement of intracellular free Ca(2+ )in enhanced release of herpes simplex virus by hydrogen peroxide

BACKGROUND: It was reported that elevation of the intracellular concentration of free Ca(2+ )([Ca(2+)]i) by a calcium ionophore increased the release of herpes simplex virus type 1 (HSV-1). Freely diffusible hydrogen peroxide (H(2)O(2)) is implied to alter Ca(2+ )homeostasis, which further enhances abnormal cellular activity, causing changes in signal transduction, and cellular dysfunction. Whether H(2)O(2 )could affect [Ca(2+)]i in HSV-1-infected cells had not been investigated. RESULTS: H(2)O(2 )treatment increased the amount of cell-free virus and decreased the proportion of viable cells. After the treatment, an elevation in [Ca(2+)]i was observed and the increase in [Ca(2+)]i was suppressed when intracellular and cytosolic Ca(2+ )were buffered by Ca(2+ )chelators. In the presence of Ca(2+ )chelators, H(2)O(2)-mediated increases of cell-free virus and cell death were also diminished. Electron microscopic analysis revealed enlarged cell junctions and a focal disintegration of the plasma membrane in H(2)O(2)-treated cells. CONCLUSION: These results indicate that H(2)O(2 )can elevate [Ca(2+)]i and induces non-apoptotic cell death with membrane lesions, which is responsible for the increased release of HSV-1 from epithelial cells

2008 Inter-laboratory Comparison Study of a Reference Material for Nutrients in Seawater

Autoclaved natural seawater collected in the North Pacific Ocean was used as a reference material for nutrients in seawater (RMNS) during an inter-laboratory comparison (I/C) study conducted in 2008. This study was a follow-up to previous studies conducted in 2003 and 2006. A set of six samples was distributed to each of 58 laboratories in 15 countries around the globe, and results were returned by 54 of those laboratories (15 countries). The homogeneities of samples used in the 2008 I/C study, based on analyses for three determinants, were improved compared to those of samples used in the 2003 and 2006 I/C studies. Results of these I/C studies indicate that most of the participating laboratories have an analytical technique for nutrients that is sufficient to provide data of high comparability. The differences between reported concentrations from the same laboratories in the 2006 and 2008 I/C studies for the same batch of RMNS indicate that most of the laboratories have been maintaining internal comparability for two years. Thus, with the current high level of performance in the participating laboratories, the use of a common reference material and the adaptation of an internationally accepted nutrient scale system would increase comparability among laboratories worldwide, and the use of a certified reference material would establish traceability. In the 2008 I/C study we observed a problem of non-linearity of the instruments of the participating laboratories similar to that observed among the laboratories in the 2006 I/C study. This problem of non-linearity should be investigated and discussed to improve comparability for the full range of nutrient concentrations. For silicate comparability in particular, we see relatively larger consensus standard deviations than those for nitrate and phosphate

腎摘除術後の対側腎の代償性肥大と腎機能の変移

腎摘除術後の対側腎の体積と腎機能の変移を検討した.対象は腎細胞癌で腎摘除術を受け, 対側腎に明らかな異常がなく, 当院で少なくとも2年以上経過観察している25例であった.25例中12例で毎年CT検査を受けていた.腎の体積は造影CT上の腎の3方向の径を測定し楕円体体積の公式に当てはめて求めた。対側腎の体積は術後3年目まで増加し, 術前体積(100%)に比べて2～7年後の平均最終体積は120%であった.対側腎の腎摘前の体積と術後の最終体積の間に有意な相関はなかったが, 術前に小さい腎は腎摘後の最終体積比率が大きい傾向にあった.血清クレアチニン値は術後1年目に有意に増加したが, 1年目の値に比べてその後数年の経過で有意に低下した.つまり, 代償性腎肥大と腎機能の改善は術後数年以内に完成されるものの, 腎肥大に比べて血清クレアチニン値の改善は遅れた.この理由として, 術後早期の腎血漿流量の増加に伴って代償性腎肥大は起こるが, 糸球体濾過率の上昇は2-一一3年遅れるため, 上昇していた血清クレアチニン値の低下も遅れたことが考えられた.We studied the changes in the serum creatinine level and the volume of the remaining kidney following nephrectomy using contrast-enhanced compounded tomogram (CT) scans. Twenty-five patients undergoing nephrectomy for renal cell carcinoma without obvious disease in the remaining kidney were carefully followed for a period of at least two years at our hospital. Twelve patients received follow-up CT scans each year after nephrectomy. The ellipsoid volume of the kidney was calculated by measuring the 3-dimensional size on CT scans. The mean relative volume (%) of the remaining kidney increased up to year 3 postoperatively, and the final mean relative volume at varying periods from years 2 to 7 was 120%. Kidneys that were smaller prior to nephrectomy showed a tendency to have a larger final relative volume after nephrectomy, although there was no significant correlation between the kidney volume prior to nephrectomy and at final measurement. The mean serum creatinine level was significantly increased at one year after nephrectomy, but it decreased significantly over time. Therefore, both compensatory renal hypertrophy and improved renal function seemed to be established within several years after nephrectomy. However, the improvement of serum creatinine was delayed compared with the increase of kidney volume. That is, renal plasma flow might be increased early by compensatory renal hypertrophy, followed within a few years by an increase in glomerular filtration and a decrease of serum creatinine

Non-functioning pancreatic neuroendocrine tumor accompanied with multiple liver metastases: remorseful case and literature review.

Context Pancreatic neuroendocrine tumor (P-NET) is a rare and slow-growing tumor. Unfortunately, there is no clear consensus on the role and timing of surgery for primary tumor and liver metastases, although current reports refer to liver surgery including LT for unresectable liver metastases. Case report A thirty-nine-year-old man was diagnosed with nonfunctioning pancreatic neuroendocrine tumor (P-NET) in the pancreatic head, with multiple liver metastases. The tumor was 2.5 cm in diameter and he was asymptomatic. Small but multiple metastases were detected in the liver, and no extrahepatic metastases were observed. We initially intended to control the liver metastases before resection of the primary tumor. To begin with, transarterial chemoembolization (TACE) and transcatheter arterial infusion (TAI) were repeated. Thereafter, systemic chemotherapy and biotherapy were introduced according to follow-up assessments. Unfortunately, imaging assessment at about 10 months later revealed that liver metastases were partially enlarged, although some were successfully treated. Therefore, these therapies were switched to other regimens, and TACE/TAI, systemic chemotherapies and biotherapies were repeated. Although liver metastases seemed to be stable for a while, the primary tumor was enlarged even after therapy. At 3.5 years after initial diagnosis, the primary tumor became symptomatic (pain and jaundice). Liver metastases enlarged and massive swelling of the para-aortic lymph nodes was observed. Thereafter, palliative therapy was the main course of action. He died at 4.3 years after initial diagnosis. Conclusion Our young patient could have been a candidate for initial surgery for primary tumor and might have had a chance of subsequent liver transplantation for unresectable metastases. Surgeons still face questions in deciding the best surgical scenario in patients with P-NET with liver metastases