Pancytopenia Due to Possible Drug-Drug Interactions Between Low-Dose Methotrexate and Proton Pump Inhibitors.

Methotrexate (MTX) has been widely used with a wide range of doses in the treatment of certain neoplastic diseases, severe psoriasis, and rheumatoid arthritis. At higher dose, monitoring of serum MTX elimination is performed because delayed elimination can result in serious and potentially life-threatening toxicities. A number of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), salicylates, phenylbutazone, phenytoin, sulfonamides, and some oral antibiotics, are known to interact with MTX therapy through various mechanisms.

Cryptotanshinone ameliorates MPP-induced oxidative stress and apoptosis of SH-SY5Y neuroblastoma cells: the role of STAT3 in Parkinson's disease.

Cryptotanshinone (CTN) has shown its neuroprotective and anti-inflammatory qualities in non-genetic mouse model of Alzheimer's disease. According to bioinformatics analysis, CTN and Signal Transducer and Activator of Transcription 3 (STAT3) may interact to form a drug-target network. This study was conducted to identify the role of CTN-STAT3 interaction in Parkinson's disease (PD).

Effect of Src tyrosine kinase on a rat model of asthma.

Src tyrosine kinase is a protein encoded by the Src gene. The present study aimed to determine the role of Src protein kinase in asthma using small interfering RNA (siRNA) technology. Several Src siRNAs were designed and the most effective siRNA pair was selected.

Plasma mutation abundance affects clinical response to first-line EGFR-TKIs in patients with advanced non-small cell lung cancer.

Background: Activated epidermal growth factor receptor () mutation is the main pathogenic cause of non-small cell lung cancer (NSCLC) in Asia. However, the impact of plasma mutation abundance, especially of the ultra-low abundance of mutation detected by highly sensitive techniques on clinical outcomes of first-line EGFR tyrosine kinase inhibitors (TKIs) for advanced NSCLC patients remains unclear.

Methods: We qualitatively detected baseline status of NSCLC tissues using amplification-refractory mutation system and quantified the plasma abundance of mutations through next-generation sequencing (NGS).

BAP1 promotes viability and migration of ECA109 cells through KLF5/CyclinD1/FGF-BP1.

More than 40 000 patients worldwide die from esophageal cancer annually. The 5-year survival rate of patients is only ~ 15-20%, and thus, there is an ongoing need to improve diagnosis and treatment of esophageal cancer. Breast cancer type 1 susceptibility protein (BRCA1)-associated protein (BAP1) is a marker of poor prognosis in several cancers, including uveal melanoma, renal cell carcinoma, cholangiocarcinoma, non-small cell lung cancer, and colorectal cancer.

Protective effects and mechanisms of Ndfipl on SH-SY5Y cell apoptosis in an in vitro Parkinson's disease model.

The aim of the current study was to examine the protective effects and mechanisms of Ndfipl on neurocytes in an experimental in vitro Parkinson's disease model induced by MPP+. The cell model was developed with dominant negative expression and suppressed expression of Ndfipl by means of transient transfection of Ndfipl-dominant negative and -inhibitory vectors. In total, four different Ndfipl cell models were established.

Effect of HDAC-6 on PD cell induced by lactacystin.

Objective: To explore the effects of histone deacetylase 6(HDAC-6) on the PD cell model induced by proteasome inhibitor lactacystin.

Methods: Human neuroblastoma SK-N-SH cells were cultured. The wild type pcDNA3.

Protein expression levels in the medullary visceral zone of rats with subarachnoid hemorrhage.

We investigated protein expression in the medullary visceral zone (MVZ) of rats with multiple-organ dysfunction syndrome (MODS) caused by subarachnoid hemorrhage (SAH) to discuss the possible regulatory mechanism of the MVZ in the course of SAH-induced MODS. A SAH-induced MODS model was established in rats by injecting arterial blood into the Willis' circle. Protein expression in the MVZ was analyzed by immunohistochemistry assay.

A new method to induce myasthenia gravis models and the protective effect of soluble decay accelerating factors.

It is expensive to induce experimental autoimmune myasthenia gravis (EAMG) by active immunity, and difficult to obtain natural acetylcholine receptor (AChR). We sought a new method of inducing EAMG by immunizing rats with artificially synthesized AChR. The AChR mRNA in TE671 cells was extracted and reverse transcribed.