The usefulness of the urine protein:creatine ratio
(UPCR) in management of molecular targeted therapy has not been studied,
although urine protein dipstick testing (uPr) is widely used. The authors
investigated the usefulness of UPCR as compared to uPr in patients undergoing
molecular targeted therapy for advanced renal cell carcinoma (RCC). They found that
uPr-based grade tends to be higher than UPCR-based grade, which may lead to
overestimate of proteinuria and unnecessary interruption of treatment. UPCR may
be a better tool for evaluation of proteinuria in RCC patients receiving molecular
targeted therapy.
Introduction: The present study was
designed to explore the impacts of sinomenine on cell proliferation and
invasion ability of RB cells and the related mechanism. WERI-RB-1 and Y79 cells
were cultured and treated by different concentration of sinomenine. The authors
found that sinomenine was able to decrease the proliferation and promote the
apoptosis of RB cells in a dose-dependent manner; and also significantly
suppressed the migration as well as invasion ability of WERI-RB-1 and Y79 cells
in vitro via regulating the PI3K/AKT signaling pathway, suggesting that
sinomenine has the potential to become an alternative medication for the
treatment of RB.
The
rapid degradation in kidney function caused by contrast media usually is
temporary, but it can result in chronic kidney disease or even end-stage renal
disease. Contrast-induced nephropathy (CIN) is a common clinical problem for
which there is no effective medical treatment. The aim of this study was to
examine the protective effects of agmatine, which is a polyamine found in mammals,
in a rat and a rabbit model of CIN. The results indicate that agmatine prevents
the development of CIN-induced renal insufficiency in rabbits, and the effect
is accompanied by activation of nitric oxide synthase and subsequent increase
of blood flow.
Elaidic
acid (EA) is the most abundant food-derived trans-fatty
acid (TFA), whose intake is associated with neurodegenerative diseases (NDs)
including Alzheimer’s disease. Hirata et
al. provide evidence implicating a novel microglial apoptosis signaling
pathway in TFA-related NDs. In microglial cell lines such as MG6 and BV2,
extracellular ATP, a damage-associated molecular pattern (DAMP) leaked from
injured cells, triggered reactive oxygen species (ROS)-dependent activation of
the apoptosis signal-regulating kinase 1 (ASK1)-p38 MAP kinase pathway, and ultimately
apoptosis. EA strongly enhanced activation of the microglial apoptosis pathway,
which may account for the underlying pathological mechanisms of TFA-related NDs
that are closely associated with neuronal cell death and inflammation.
Cinacalcet
is a calcimimetic that permits impaired endothelial functions to be recovered
via inhibiting parathyroid hormone (PTH) production in SHPT patients receiving
hemodialysis. However, the underlying mechanism for its action remains unknown.
The article by Imafuku et al. reported cinacalcet improves the redox status of
human serum albumin (HSA) by inhibiting PTH production and partially by its
radical scavenging action and increaed the anti-oxidant defense system in the
blood circulation of SHPT patients. Such an anti-oxidative action of cinacalcet
may, in part, explain the reduced risk for cardiovascular and all-cause
mortality during cinacalcet treatment.