This perspective gives an overview of recent developments in surface-enhanced Raman scattering (SERS) for biosensing. We focus this review on SERS papers published in the last 10 years and to specific applications of detecting biological analytes. Both intrinsic and extrinsic SERS biosensing schemes have been employed to detect and identify small molecules, nucleic acids, lipids, peptides, and proteins, as well as for in vivo and cellular sensing. Current SERS substrate technologies along with a series of advancements in surface chemistry, sample preparation, intrinsic/extrinsic signal transduction schemes, and tip-enhanced Raman spectroscopy are discussed. The progress covered herein shows great promise for widespread adoption of SERS biosensing.

To this day, glioblastoma (GBM) remains an incurable brain tumor. Previous research has shown that metformin, an oral anti-diabetic drug, may decrease GBM cell proliferation and migration especially in brain tumor initiating cells (BTICs). As transforming growth factor β 2 (TGF-β2) has been reported to promote high-grade glioma and is inhibited by metformin in other tumors, we explored whether metformin directly interferes with TGF-β2-signaling. Functional investigation of proliferation and migration of primary BTICs after treatment with metformin+/-TGF-β2 revealed that metformin doses as low as 0.01 mM metformin thrice a day were able to inhibit proliferation of susceptible cell lines, whereas migration was impacted only at higher doses. Known cellular mechanisms of metformin, such as increased lactate secretion, reduced oxygen consumption and activated AMPK-signaling, could be confirmed. However, TGF-β2 and metformin did not act as functional antagonists, but both rather inhibited proliferation and/or migration, if significant effects were present. We did not observe a relevant influence of metformin on TGF-β2 mRNA expression (qRT-PCR), TGF-β2 protein expression (ELISA) or SMAD-signaling (Western blot). Therefore, it seems that metformin does not exert its inhibitory effects on GBM BTIC proliferation and migration by altering TGF-β2-signaling. Nonetheless, as low doses of metformin are able to reduce proliferation of certain GBM cells, further exploration of predictors of BTICs' susceptibility to metformin appears justified.

Unraveling the highly interconnected nature of complex biological systems is fundamental to a wide range of modern research questions. At the heart of any coordinated biological network is cell-cell communication, and researching the means by which different cell types communicate is an essential prerequisite to fully understanding many aspects of biology. One major mechanism of cell signaling is the regulated release of chemical messengers from preformed vesicles in the cytoplasm. The process of transporting these vesicles to the exterior of the cell and the subsequent release of vesicular contents via membrane fusion is known as exocytosis. In recent decades, carbon-fiber microelectrodes have become increasingly useful for the measurement and study of exocytosis in a variety of biological contexts. This article details the critical background concepts of carbon-fiber microelectrode amperometry (CFMA) and carbon-fiber microelectrode fast scan cyclic voltammetry (FSCV) and reviews a variety of applications for monitoring exocytosis from single in vitro cells. Although the authors recognize the importance of several other complimentary methods including various electron microscopy and patch-clamp techniques, the scope of this article will focus only on CFMA and FSCV and their contributions to the field of single cell exocytosis measurements.

The Mpv17 mouse strain is a recessive transgenic mouse mutant that develops glomerulosclerosis and nephrotic syndrome at a young age. The phenotype results from a loss of function of a gene coding for a hydrophobic peroxisomal protein of 176 amino acids of 20 kDa following its destruction by retroviral integration. To investigate a potential effect of the missing Mpv17 function on the inner ear light and electron microscopic investigations were performed on the inner ears of Mpv17 mice and controls. These revealed degeneration of the stria vascularis and spiral ligament, loss of cochlear neurons and degeneration of the organ of Corti. The alterations observed here were similar to those described for Alport's syndrome, an inherited disorder characterized by progressive nephritis and neurosensory deafness. These findings indicate that although the molecular cause is different, the Mpv17 mouse model may share pathological mechanisms involved in patients with Alport's syndrome. At present the Mpv17 mouse appears to be a suitable animal model for this disease and may help to further elucidate the relationship between the kidney and the inner ear.