Increasing evidence shows that the heterogeneity of individual cells within a genetically identical population can be critical to their peculiar function and fate. Conventional cell based assays mainly analysis the average responses from a population cells, while the difference within individual cells may often be masked. The cell size, RNA transcripts and protein expression level are quite different within individual cells and these variations are key point to answer the problems in cancer, neurobiology, stem cell biology, immunology and developmental biology. To better understand the cell-to-cell variations, the single cell analysis can provide much more detailed information which may be helpful for therapeutic decisions in an increasingly personalized medicine. In this review, we will focus on the recent development in single cell analysis, including methods used in single cell isolation, analysis and some application examples. The review provides the historical background to single cell analysis, discusses limitations, and current and future possibilities in this exciting field of research.

Depression and anxiety disorders are the two most prevalent psychiatric diseases that affect hundreds of millions of individuals worldwide. Understanding the etiology and related mechanisms is of great importance and might yield new therapeutic strategies to treat these diseases effectively. During the past decades, a growing number of studies have pointed out the importance of the stress-induced inflammatory response in the amygdala, a kernel region for processing emotional stimuli, as a potentially critical contributor to the pathophysiology of depression and anxiety disorders. In this review, we first summarized the recent progress from both animal and human studies toward understanding the causal link between stress-induced inflammation and depression and anxiety disorders, with particular emphasis on findings showing the effect of inflammation on the functional changes in neurons in the amygdala, at levels ranging from molecular signaling, cellular function, synaptic plasticity, and the neural circuit to behavior, as well as their contributions to the pathology of inflammation-related depression and anxiety disorders. Finally, we concluded by discussing some of the difficulties surrounding the current research and propose some issues worth future study in this field.

Glioblastoma multiforme is the most common and aggressive form of primary malignant brain tumor. Previous evidence demonstrates that β‑adrenergic receptors (β‑ARs) are closely associated with the occurrence and development of brain tumors. However, the functional role of β‑ARs in human glioblastoma and the underlying mechanisms are not fully understood. In the present study, by using the MTT assay, western blotting, and the reverse transcription polymerase chain reaction, it was revealed that isoproterenol (ISO), an agonist of β‑ARs, promoted the proliferation of U251 cells but not U87‑MG cells, and that this effect was blocked by the β‑ARs antagonist propranolol. It was also demonstrated that ISO transiently induced extracellular signal‑related kinase 1/2 (ERK1/2) phosphorylation, and that blocking the mitogen-activated protein kinase pathway by U0126 inhibited ERK1/2 phosphorylation and suppressed U251 cell proliferation. In addition, β‑ARs activation increased the expression of matrix metalloproteinase (MMP) family members MMP‑2 and MMP‑9 mRNA through ERK1/2 activation. In conclusion, these data suggest that β‑ARs induce ERK1/2 phosphorylation, which may in turn increase MMPs expression to promote U251 cell proliferation. These results provide additional insight into the specific roles of β‑ARs in glioblastoma.