Near-Ideal Copper Oxide Heterostructure Design for Photoelectrochemical Water Splitting.

In recent years, photoelectrochemical (PEC) hydrogen generation through water splitting has gained significant attention as a carbon-free solar-to-energy conversion strategy. Among various materials, copper oxides, specifically cupric oxide (CuO) and cuprous oxide (CuO), have been extensively investigated for their suitable band positions and prominent performance, particularly in heterostructures. However, previously reported heterostructures, such as CuO layers on CuO, are not ideal configurations in terms of photoelectrical properties.

Phase II study of ifosfamide, etoposide, and oxaliplatin (IFETOx) chemotherapy for relapsed or refractory non-Hodgkin's lymphoma.

As part of an effort to develop a more effective and safe treatment for relapsed or refractory non-Hodgkin's lymphoma (NHL), we conducted a phase II study of the oxaliplatin, etoposide, and ifosfamide (IFETOx) regimen. Patients with relapsed or refractory NHL and a performance status of 0-2 were eligible. The IFETOx consisted of etoposide at 100 mg/m(2) on days 1-3, oxaliplatin at 130 mg/m(2) on day 2, and ifosfamide 5,000 mg/m(2) on day 2, every 21 days.

Addition of rituximab to reduced-dose CHOP chemotherapy is feasible for elderly patients with diffuse large B-cell lymphoma.

Purpose: The aim of this study was to evaluate the efficacy and toxicity of reduced-dose (RD) RCHOP (rituximab combined with cyclophosphamide, doxorubicin, vincristine, and prednisolone) chemotherapy for elderly patients with diffuse large B-cell lymphoma (DLBCL).

Methods: This study comprised 85 patients, aged ≥ 60 years, who were diagnosed with DLBCL; patients were enrolled at a single center between June 2004 and December 2009. Patients received either 6 or 8 cycles of RD-RCHOP, spaced 3 weeks apart, at the physician's discretion.

The Toxoplasma gondii dense granule protein GRA7 is phosphorylated upon invasion and forms an unexpected association with the rhoptry proteins ROP2 and ROP4.

The obligate intracellular parasite Toxoplasma gondii infects warm-blooded animals throughout the world and is an opportunistic pathogen of humans. As it invades a host cell, Toxoplasma forms a novel organelle, the parasitophorous vacuole, in which it resides during its intracellular development. The parasite modifies the parasitophorous vacuole and its host cell with numerous proteins delivered from rhoptries and dense granules, which are secretory organelles unique to the phylum Apicomplexa.

Toxoplasma gondii dysregulates IFN-gamma-inducible gene expression in human fibroblasts: insights from a genome-wide transcriptional profiling.

Toxoplasma gondii is an obligate intracellular parasite that persists for the life of a mammalian host. The parasite's ability to block the potent IFN-gamma response may be one of the key mechanisms that allow Toxoplasma to persist. Using a genome-wide microarray analysis, we show here a complete dysregulation of IFN-gamma-inducible gene expression in human fibroblasts infected with Toxoplasma.

Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors.

The protozoan parasite Toxoplasma gondii blocks the innate aversion of rats for cat urine, instead producing an attraction to the pheromone; this may increase the likelihood of a cat predating a rat. This is thought to reflect adaptive, behavioral manipulation by Toxoplasma in that the parasite, although capable of infecting rats, reproduces sexually only in the gut of the cat. The "behavioral manipulation" hypothesis postulates that a parasite will specifically manipulate host behaviors essential for enhancing its own transmission.

The BSR4 protein is up-regulated in Toxoplasma gondii bradyzoites, however the dominant surface antigen recognised by the P36 monoclonal antibody is SRS9.

The protozoan parasite, Toxoplasma gondii, interconverts between fast-growing tachyzoites and slow-growing bradyzoites within intermediate hosts. The surface of T. gondii is covered by the SAG1-related sequence (SRS) superfamily of glycosyl phosphatidyl inositol-anchored proteins, many of which are stage-specific.

Bradyzoite-specific surface antigen SRS9 plays a role in maintaining Toxoplasma gondii persistence in the brain and in host control of parasite replication in the intestine.

Toxoplasma gondii is a ubiquitous parasite that persists for the life of a healthy mammalian host. A latent, chronic infection can reactivate upon immunosuppression and cause life-threatening diseases, such as encephalitis. A key to the pathogenesis is the parasite's interconversion between the tachyzoite (in acute infection) and bradyzoite (in chronic infection) stages.

Stage-specific expression of surface antigens by Toxoplasma gondii as a mechanism to facilitate parasite persistence.

Toxoplasma persists in the face of a functional immune system. This success critically depends on the ability of parasites to activate a strong adaptive immune response during acute infection with tachyzoites that eliminates most of the parasites and to undergo stage conversion to bradyzoites that encyst and persist predominantly in the brain. A dramatic change in antigenic composition occurs during stage conversion, such that tachyzoites and bradyzoites express closely related but antigenically distinct sets of surface Ags belonging to the surface Ag 1 (SAG1)-related sequence (SRS) family.

Prevention of type I diabetes transfer by glutamic acid decarboxylase 65 peptide 206-220-specific T cells.

Glutamic acid decarboxylase (GAD) 65 is one of the major pancreatic antigens targeted by self-reactive T cells in type I diabetes mellitus. T cells specific for GAD65 are among the first to enter inflamed islets and may be important for the initiation of autoimmune diabetes. However, we previously reported that nonobese diabetic (NOD) mice transgenic for a T cell antigen receptor (TCR) specific for one of the immunodominant epitopes of GAD65, peptide 286-300 (G286), are protected from insulitis and diabetes.

CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer.

Glutamic acid decarboxylase (GAD)65 is an early and important antigen in both human diabetes mellitus and the nonobese diabetic (NOD) mouse. However, the exact role of GAD65-specific T cells in diabetes pathogenesis is unclear. T cell responses to GAD65 occur early in diabetes pathogenesis, yet only one GAD65-specific T cell clone of many identified can transfer diabetes.