Identification of Single Nucleotide Polymorphism Markers in the Laccase Gene of Shiitake Mushrooms (Lentinula edodes)

We identified single nucleotide polymorphism (SNP) markers in the laccase gene to establish a line-diagnostic system for shiitake mushrooms. A total of 89 fungal isolates representing four lines, including Korean registered, Korean wild type, Chinese, and Japanese lines, were analyzed. The results suggest that SNP markers in the laccase gene can be useful for line typing in shiitake mushrooms

Decreased expression of CCL17 in the disrupted nasal polyp epithelium and its regulation by IL-4 and IL-5.

BACKGROUND:In airway epithelium, thymus and activation-regulated chemokine (CCL17) and macrophage-derived chemokine (CCL22) are induced by defective epithelial barriers such as E-cadherin and attract the effector cells of Th2 immunity. However, the association between the epithelial barrier and CCL17 expression has not been studied in chronic rhinosinusitis with nasal polyp (CRSwNP). Thus, we aimed to evaluate the expression of CCL17 and its regulation by Th cytokines in nasal polyp (NP) epithelial cells. METHODS:The expression and distribution of CCL17, CCL22, E-cadherin and/or epidermal growth factor receptor (EGFR) were measured using real-time PCR, western blot, and immunohistochemistry and compared between normal ethmoid sinus epithelium and NP epithelium. In addition, the expression level of CCL17 was determined in cultured epithelial cells treated with IL-4, IL-5, IL-13, TNF-α, and IFN-γ. RESULTS:The expression of CCL17 was decreased in the NP epithelium compared to the epithelium of normal ethmoid sinus, whereas the expression of CCL22 was not decreased. E-cadherin was differentially distributed between the epithelium of normal ethmoid sinus and NP epithelium. EGFR was also decreased in NPs. Interestingly, the stimulation of cultured epithelial cells with Th2 cytokines, IL-4 and IL-5, resulted in an upregulation of CCL17 expression only in NP epithelial cells whereas the expression of CCL17 was increased in both normal epithelial cells and NP epithelial cells by Th1 cytokines. CONCLUSION:Our results suggest that the decreased expression of CCL17 in defective NP epithelium may be closely connected to NP pathogenesis and can be differentially regulated by cytokines in the NP epithelium of patients with CRSwNP

PDZ Domain-containing 1 (PDZK1) Protein Regulates Phospholipase C-beta 3 (PLC-beta 3)-specific Activation of Somatostatin by Forming a Ternary Complex with PLC-beta 3 and Somatostatin Receptors

Phospholipase C-beta(PLC-beta) is a key molecule in G protein-coupled receptor (GPCR)-mediated signaling. Many studies have shown that the four PLC-beta subtypes have different physiological functions despite their similar structures. Because the PLC-beta subtypes possess different PDZ-binding motifs, they have the potential to interact with different PDZ proteins. In this study, we identified PDZ domain-containing 1 (PDZK1) as a PDZ protein that specifically interacts with PLC-beta 3. To elucidate the functional roles of PDZK1, we next screened for potential interacting proteins of PDZK1 and identified the somatostatin receptors (SSTRs) as another protein that interacts with PDZK1. Through these interactions, PDZK1 assembles as a ternary complex with PLC-beta 3 and SSTRs. Interestingly, the expression of PDZK1 and PLC-beta 3, but not PLC-beta 1, markedly potentiated SST-induced PLC activation. However, disruption of the ternary complex inhibited SST-induced PLC activation, which suggests that PDZK1-mediated complex formation is required for the specific activation of PLC-beta 3 by SST. Consistent with this observation, the knockdown of PDZK1 or PLC-beta 3, but not that of PLC-beta 1, significantly inhibited SST-induced intracellular Ca2+ mobilization, which further attenuated subsequent ERK1/2 phosphorylation. Taken together, our results strongly suggest that the formation of a complex between SSTRs, PDZK1, and PLC-beta 3 is essential for the specific activation of PLC-beta 3 and the subsequent physiologic responses by SST.close4

Cox-Maze III procedure with valvular surgery in an autopneumonectomized patient

<p>Abstract</p> <p>Destructive pulmonary inflammation can leave patients with only a single functional lung, resulting in anatomical and physiological changes that may interfere with subsequent cardiac surgeries. Such patients are vulnerable to perioperative cardiopulmonary complications. Herein, we report the first case, to our knowledge, of an autopneumonectomized patient who successfully underwent a modified Cox-Maze III procedure combined with valvular repairs. The three major findings in this case can be summarized as follows: (1) a median sternotomy with peripheral cannulations, such as femoral cannulations, can provide an optimal exposure and prevent the obstruction of vision that may occur as a result of multiple cannulations through a median sternotomy; (2) a modified septal incision combined with biatrial incisions facilitate adequate exposure of the mitral valve; and (3) the aggressive use of intraoperative ultrafiltration may be helpful for the perioperative managements as decreasing pulmonary water contents, thereby avoiding the pulmonary edema associated with secretion of inflammatory cytokines during a cardiopulmonary bypass. We also provide several suggestions for achieving similar satisfactory surgical outcomes in patients with a comparable condition.</p

Immunoblotting analysis of E-cadherin, CCL17, and EGFR in epithelial cells from normal ethmoid and nasal polyp cells.

<p>Representative immunoblot images (A) and graphical and statistical analysis of relative CCL17 expression (B), relative mature E-cadherin expression (C), the ratio of cleaved E-cadherin to mature E-cadherin (D), and relative EGFR expression (E). * <i>p</i><0.05.</p

Patients characteristics.

<p>Patients characteristics.</p

Analysis of CCL17 expression in epithelial cells treated with DECMA or cytokines.

<p>Epithelial cells from the normal ethmoid were incubated with DECMA, anti-E-cadherin antibody, and the cell extract was analysed by immunoblotting with anti-E-cadherin and anti-CCL17 antibody. Representative immunoblot images (A) and graphical and statistical analysis of relative CCL17 expression (B). Epithelial cells from the normal ethmoid (C) and nasal polyp (D) were treated with Th1 cytokines TNF-α and IFN-γ or Th2 cytokines IL-4, IL-5 and IL-13 as indicated. The expression of IL-4 and IL-5 in nasal polyp epithelial cells was significantly greater than that of normal ethmoid epithelial cells. * <i>p</i><0.05.</p

A Randomized, Multicenter, Phase II Study of Cetuximab With Docetaxel and Cisplatin as Induction Chemotherapy in Unresectable, Locally Advanced Head and Neck Cancer

Background. We investigated the efficacy of cetuximab when added to induction chemotherapy followed by concurrent chemoradiotherapy (CCRT) in patients with locally advanced head and neck squamous cell carcinoma. Methods. Patients were randomized to receive three cycles of docetaxel and cisplatin (TP regimen) with or without cetuximab (TP plus cetuximab [CTP] vs. TP) as induction chemotherapy. Patients in the CTP arm received CCRT with cetuximab and cisplatin, whereas patients in the TP arm received cisplatin alone. The primary endpoint was the objective response rate (ORR) after induction chemotherapy. Results. Overall, 92 patients were enrolled. The ORRs for induction chemotherapy in the CTP and TP arms were not different (81% vs. 82%). Adding cetuximab lowered the completion rate of induction chemotherapy and CCRT and resulted in more frequent dose reductions of the induction chemotherapy, although this did not reach statistical significance. In the CTP and TP arms, respectively, the 3-year progression-free survival (PFS) rates were 70% and 56%(p=.359), and the overall survival (OS) rates were 88% and 74% (p =.313). When limited to patients who completed induction chemotherapy, 3-year PFS rates of 78% and 59% (p =.085) and OS rates of 94% and 73% (p =.045) were observed in the CTP and TP arms, respectively. Conclusion. Adding cetuximab to sequential treatment did not increase the treatment efficacy and resulted in greater toxicity. In the intent-to-treat population, neither PFS nor OS was improved by the addition of cetuximab to sequential treatment; however, a suggestion of improved survival outcomes was observed in patients completing cetuximab-containing induction chemotherapy.