Retrospective Cohort Study Showing Clinical Equivalence of Microendoscopic Laminotomy to Open Fenestration for Patients with Lumbar Spinal Stenosis

Objective Despite the popularity of microendoscopic disectomy, there is currently insufficient studies about microendoscopic laminotomy (MEL) for lumbar spinal stenosis. The purpose of this study was to compare the clinical and radiographic outcomes of MEL and fenestration (laminotomy in open procedure) for lumbar spinal stenosis. Methods This study included 30 patients in the MEL group and 46 patients in the open fenestration group between 2012 and 2016 (follow-up period ≥1 year). The Japanese Orthopedic Association Back Pain Evaluation Questionnaire(JOABPEQ), a visual analog scale(VAS), surgical outcomes, blood test outcomes, and radiographic parameters were studied. Results Mean age was 67 years old in the MEL group and 70 years old in the open fenestration group (p=0.1). There were no significant differences in score change of either domain of JOABPEQ between MEL and fenestration. The 95% confidence intervals of the between-group differences in score change were within clinical important difference (±20 point) in all the domains of JOABPEQ. The MEL group had significantly shorter hospital stays (9 days vs 13 days; p<0.001), smaller increase in C-reactive protein (1.7 mg/dL vs 2.9 mg/dL; p=0.009), and longer operating time (122 min vs 39 min; p<0.001) than the fenestration group. There was no significant difference in hemoglobin level, total protein, albumin, creatine kinase between the groups. The MEL group had one case of dural tear and the fenestration group had two cases(p=1.0). There was no significant differences in complication rate between the groups. There were no significant between-group differences in change of disc height or ROM. Conclusion In the treatment of lumbar spinal stenosis, the clinical effectiveness and safety of MEL was equivalent to that of fenestration, with less invasiveness

Brazilian Propolis Suppresses Angiogenesis by Inducing Apoptosis in Tube-Forming Endothelial Cells through Inactivation of Survival Signal ERK1/2

We recently reported that propolis suppresses tumor-induced angiogenesis through tube formation inhibition and apoptosis induction in endothelial cells. However, molecular mechanisms underlying such angiogenesis suppression by propolis have not been fully elucidated. The aim of this study was to investigate the effects of ethanol extract of Brazilian propolis (EEBP) on two major survival signals, extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt, and to elucidate whether changes in these signals were actually involved in antiangiogenic effects of the propolis. Detection by western blotting revealed that EEBP suppressed phosphorylation of ERK1/2, but not that of Akt. Pharmacological inhibition by U0126 demonstrated that ERK1/2 inactivation alone was enough to inhibit tube formation and induce apoptosis. It was also shown that EEBP and U0126 similarly induced activation of caspase-3 and cleavage of poly ADP-ribose polymerase (PARP) and lamin A/C, all of which are molecular markers of apoptosis. These results indicate that inhibition of survival signal ERK1/2, and subsequent induction of apoptosis, is a critical mechanism of angiogenesis suppression by EEBP

L-PGDS-produced PGD2 in premature, but not in mature, adipocytes increases obesity and insulin resistance

Lipocalin-type prostaglandin (PG) D synthase (L-PGDS) is responsible for the production of PGD2 in adipocytes and is selectively induced by a high-fat diet (HFD) in adipose tissue. In this study, we investigated the effects of HFD on obesity and insulin resistance in two distinct types of adipose-specific L-PGDS gene knockout (KO) mice: fatty acid binding protein 4 (fabp4, aP2)-Cre/L-PGDS flox/flox and adiponectin (AdipoQ)-Cre/L-PGDS flox/flox mice. The L-PGDS gene was deleted in adipocytes in the premature stage of the former strain and after maturation of the latter strain. The L-PGDS expression and PGD2 production levels decreased in white adipose tissue (WAT) under HFD conditions only in the aP2-Cre/L-PGDS flox/flox mice, but were unchanged in the AdipoQ-Cre/L-PGDS flox/flox mice. When fed an HFD, aP2-Cre/L-PGDS flox/flox mice significantly reduced body weight gain, adipocyte size, and serum cholesterol and triglyceride levels. In WAT of the HFD-fed aP2-Cre/L-PGDS flox/flox mice, the expression levels of the adipogenic, lipogenic, and M1 macrophage marker genes were decreased, whereas those of the lipolytic and M2 macrophage marker genes were enhanced or unchanged. Insulin sensitivity was improved in the HFD-fed aP2-Cre/L-PGDS flox/flox mice. These results indicate that PGD2 produced by L-PGDS in premature adipocytes is involved in the regulation of body weight gain and insulin resistance under nutrient-dense conditions

Original Article Brazilian Propolis Suppresses Angiogenesis by Inducing Apoptosis in Tube-Forming Endothelial Cells through Inactivation of Survival Signal ERK1/2

We recently reported that propolis suppresses tumor-induced angiogenesis through tube formation inhibition and apoptosis induction in endothelial cells. However, molecular mechanisms underlying such angiogenesis suppression by propolis have not been fully elucidated. The aim of this study was to investigate the effects of ethanol extract of Brazilian propolis (EEBP) on two major survival signals, extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt, and to elucidate whether changes in these signals were actually involved in antiangiogenic effects of the propolis. Detection by western blotting revealed that EEBP suppressed phosphorylation of ERK1/2, but not that of Akt. Pharmacological inhibition by U0126 demonstrated that ERK1/2 inactivation alone was enough to inhibit tube formation and induce apoptosis. It was also shown that EEBP and U0126 similarly induced activation of caspase-3 and cleavage of poly ADP-ribose polymerase (PARP) and lamin A/C, all of which are molecular markers of apoptosis. These results indicate that inhibition of survival signal ERK1/2, and subsequent induction of apoptosis, is a critical mechanism of angiogenesis suppression by EEBP

Combined immunohistochemistry of β-catenin, cytokeratin 7, and cytokeratin 20 is useful in discriminating primary lung adenocarcinomas from metastatic colorectal cancer

BACKGROUND: It is important to discriminate between primary and secondary lung cancer. However, often, the discriminating diagnosis of primary lung acinar adenocarcinoma and lung metastasis of colorectal cancer based on morphological and pathological findings is difficult. The purpose of this study was to evaluate the clinical usefulness of immunohistochemistry of β-catenin, cytokeratin (CK) 7, and CK20 for the discriminating diagnosis of lung cancer. METHODS: We performed immunohistochemistry of β-catenin, CK7, and CK20 in 19 lung metastasis of colorectal cancer samples, 10 corresponding primary colorectal cancer samples and 11 primary lung acinar adenocarcinoma samples and compared the levels of accuracy of the discriminating diagnosis by using antibodies against these antigens. RESULTS: Positive staining of β-catenin was observed in all the lung metastasis of colorectal cancer samples as well as in the primary colorectal cancer samples but in none of the primary lung acinar adenocarcinoma samples. Positive staining of CK7 was observed in 90.9% of the primary lung acinar adenocarcinoma samples and in 5.3% of the lung metastasis of colorectal cancer samples, but in none of the primary colorectal cancer samples. Positive staining of CK20 was observed in all the primary colorectal cancer samples and in 84.2% of the lung metastasis of colorectal cancer samples, but in none of the primary lung acinar adenocarcinoma samples. CONCLUSION: Combined immunohistochemistry of β-catenin, CK7, and CK20 is useful for making a discriminating diagnosis between lung metastasis of colorectal cancer and primary lung acinar adenocarcinoma. This method will enable accurate diagnosis of a lung tumor and will be useful for selecting appropriate therapeutic strategies, including chemotherapeutic agents and operation methods

radioprotective effect of zinc yeast is p53 dependent to human lymphoblastoid cells

It was shown that the administration of zinc-containing yeast (zinc-yeast) to the abdominal cavity significantly increased the survival of mice irradiated with 7.5 Gy X-rays (LD50/30 assay result). In order to elucidate the molecular mechanism of this radio-protection effect, we examined TK6 (p53 wild type) and WTK1 (p53 mutant) lymphoblast cell lines exposed to 0.1mg/ml zinc-yeast. In TK6 cells, the cell growth was impaired after administration of zinc-yeast and the cells seem to accumulate at S/G2 phase in the cell cycle. On the other hand, in WTK1 cells, no effect on cell growth was observed. Furthermore, we measured the occurrence of apoptosis in X-irradiated cells (10 Gy) treated with zinc-yeast post-irradiation. In TK6 cells, a significant reduction in apoptosis was observed with the combined treatment, while there was no clear difference observed in WTK1 cells under the same treatment. These data indicate that the radio-protective effect induced by zinc-yeast might be affected by the p53 status of irradiated cells.13th International Congress of Radiation Researc

Radioprotective effect of zinc yeast is p53 dependent to human lymphoblastoid cells

It was shown that the administration of zinc-containing yeast (zinc-yeast) to the abdominal cavity significantly increased the survival of mice irradiated with 7.5 Gy X-rays (LD50/30 assay result). In order to elucidate the molecular mechanism of this radio-protection effect, we examined TK6 (p53 wild type) and WTK1 (p53 mutant) lymphoblast cell lines exposed to 0.1mg/ml zinc-yeast. In TK6 cells, the cell growth was impaired after administration of zinc-yeast and the cells seem to accumulate at S/G2 phase in the cell cycle. On the other hand, in WTK1 cells, no effect on cell growth was observed. Furthermore, we measured the occurrence of apoptosis in X-irradiated cells (10 Gy) treated with zinc-yeast post-irradiation. In TK6 cells, a significant reduction in apoptosis was observed with the combined treatment, while there was no clear difference observed in WTK1 cells under the same treatment. These data indicate that the radio-protective effect induced by zinc-yeast might be affected by the p53 status of irradiated cells.13th International Congress of Radiation Researc