Novel self-adaptive boat-shaped complexes with a tetraphosphine ligand.

A series of novel boat-shaped host-guest complexes were designed and synthesized by the combination of a new calixarene fragment-based tetraphosphine ligand L with group 11 metal salts Cu(MeCN)4ClO4 and AgNO3 in a self-assembly process, and by the following anion exchange reactions of complex 1 with sodium p-toluenesulfonate, AcONa, PhCO2Na and sodium 9-anthrylcarboxylate. The host with a novel boat-shaped cavity is capable of self-adaptive encapsulation of various anions of different sizes through M(i)-O coordinations and CHπ interactions between the host and guest anion. The DFT calculations confirmed that the CHπ interaction played a vital role in the self-adaptive phenomenon in complexes 4-6.

Expression and clinical significance of retinoid X receptor α in esophageal carcinoma.

Purpose: Esophageal carcinoma (EC) is one of the most aggressive type cancers and dysregulation of retinoid X receptor α (RXRα) involves various tumors. However, the relationship of RXRα with the clinicopathological factors of EC, particularly prognostic characteristics, remains unclear. This present study was to evaluate the effect of RXRα expression in the development of EC.

Dietary supplementation with docosahexanoic acid (DHA) increases red blood cell membrane flexibility in mice with sickle cell disease.

Humans and mice with sickle cell disease (SCD) have rigid red blood cells (RBCs). Omega-3 fatty acids, such as docosahexanoic acid (DHA), may influence RBC deformability via incorporation into the RBC membrane. In this study, sickle cell (SS) mice were fed natural ingredient rodent diets supplemented with 3% DHA (DHA diet) or a control diet matched in total fat (CTRL diet).

Sickle cell disease increases high mobility group box 1: a novel mechanism of inflammation.

High mobility group box 1 (HMGB1) is a chromatin-binding protein that maintains DNA structure. On cellular activation or injury, HMGB1 is released from activated immune cells or necrotic tissues and acts as a damage-associated molecular pattern to activate Toll-like receptor 4 (TLR4). Little is known concerning HMGB1 release and TLR4 activity and their role in the pathology of inflammation of sickle cell disease (SCD).

Primary small cell carcinoma of the lesser omentum.

Although pulmonary small cell carcinoma (SCC) is seen frequently, SCC that originates from the extrapulmonary organs is extremely rare. We herein report a case of a SCC located in the lesser omentum. A 61-year-old male was admitted to our department due to intermittent epigastralgia for 2 months.

Caveolin-1-dependent apoptosis induced by fibrin degradation products.

In mice lacking the blood coagulation regulator thrombomodulin, fibrinolytic degradation products (FDP) of fibrin induce apoptotic cell death of a specialized cell type in the placenta, polyploid trophoblast giant cells. Here, we document that this bioactivity of FDP is conserved in human FDP, is not limited to trophoblast cells, and is associated with an Aalpha-chain segment of fibrin fragment E (FnE). The majority of proapoptotic activity is arginine-glycine-aspartic acid (RGD)-independent and requires caveolin-1-dependent cellular internalization of FnE.

Vascular dysfunction in a murine model of severe hemolysis.

Spectrin is the backbone of the erythroid cytoskeleton; sph/sph mice have severe hereditary spherocytosis (HS) because of a mutation in the murine erythroid alpha-spectrin gene. sph/sph mice have a high incidence of thrombosis and infarction in multiple tissues, suggesting significant vascular dysfunction. In the current study, we provide evidence for both pulmonary and systemic vascular dysfunction in sph/sph mice.

Fetal gene defects precipitate platelet-mediated pregnancy failure in factor V Leiden mothers.

We describe a mouse model of fetal loss in factor V Leiden (FvL) mothers in which fetal loss is triggered when the maternal prothrombotic state coincides with fetal gene defects that reduce activation of the protein C anticoagulant pathway within the placenta. Fetal loss is caused by disruption of placental morphogenesis at the stage of labyrinth layer formation and occurs in the absence of overt placental thrombosis, infarction, or perfusion defects. Platelet depletion or elimination of protease-activated receptor 4 (Par4) from the mother allows normal placentation and prevents fetal loss.

[Nonalcoholic steatohepatitis: a clinicopathological analysis of liver biopsy in 32 cases].

Objective: To investigate the clinicopathological features of nonalcoholic steatohepatitis (NASH) and elucidate its diagnosis and differential diagnosis.

Methods: Liver biopsy tissues and clinical data of 32 patients with NASH were collected and the clinicopathological findings by HE and Masson staining were evaluated for NASH grading.

Results: Ballooning degeneration of the liver cells and fibrosis around hepatic sinusoid was scarce in mild NASH cases and increased in moderate to severe cases.

[Expression of IGF-I and IGF-IR in bladder cancer].

Background & Objective: Insulin-like growth factors (IGF) is one of polypeptide growth factors that stimulate proliferation, survival, and differentiation in many cell types; their signal pathways implicate development and progression of many kinds of malignant tumor, while less study were undergone on the roles of IGF-I and IGF-IR in bladder cancer genesis. This study was designed to investigate the expression of IGF-I and IGF-IR and proliferation cell nuclear antigen (PCNA) in human normal and carcinomatous bladder cancer, and to explore the mechanism of IGF-I and IGF-IR in cellular proliferation and tumorigenesis of bladder cancer.

Methods: Immunohistochemical methods were adopted to examine expression of IGF-I, IGF-IR, and PCNA in 88 cases with bladder cancer and 12 cases with normal bladder tissues.