Medical students expressed an early interest in academic medicine but lacked clarity about the career path. Black and Hispanic students' perceptions of having greater difficulty succeeding in academia may be an obstacle to engaging them in the prospective pool of academicians. Strategic and dedicated institutional resources are needed to encourage racial and ethnic minority medical students to explore careers in academic medicine.

Mesenchymal stem cells (MSCs) are a group of multipotent cells with key properties of multi-lineage differentiation, expressing a set of relatively specific surface markers and unique immunomodulatory functions. IDO1, a catabolic enzyme of tryptophan, represents a critical molecule mediating immunomodulatory functions of MSCs. However, the signaling pathways involved in regulating these key properties still remain elusive. To investigate the involvement of Notch signaling as well as other potential signaling pathway(s) in regulating these critical properties of MSCs, we treated human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) with γ-secreatase inhibitor I (GSI-I), which inhibits both Notch signaling and ubiquitin-proteasome activities. It was shown that the GSI-I treatment resulted in apoptosis, reduced expression of surface markers CD73, CD90 and CD105, reduced osteogenic differentiation, and reduction of the hUC-MSCs-mediated suppression of Th1 lymphocyte proliferation and the IFN-γ-induced IDO1 expression. Through distinguishing the effects of GSI-I between Notch inhibition and proteasome inhibition, it was further observed that, whereas both Notch inhibition and proteasome inhibition were attributable to the reduced CD105 expression and osteogenic differentiation, but not to the induced apoptosis. However, Notch inhibition, but not proteasome inhibition, only contributed to the significant effect of GSI-I on Th1 proliferation probably through reducing IDO1 promoter activity. In conclusion, the Notch signaling may represent a very important cell signaling capable of regulating multiple critical properties, especially the immunomodulatory functions of MSCs.

Animal embryonic stem cells (ESCs) provide powerful tool for studies of early embryonic development, gene targeting, cloning, and regenerative medicine. However, the majority of attempts to establish ESC lines from large animals, especially ungulate mammals have failed. Recently, another type of pluripotent stem cells, known as induced pluripotent stem cells (iPSCs), have been successfully generated from mouse, human, monkey, rat and pig. In this study we show sheep fibroblasts can be reprogrammed to pluripotency by defined factors using a drug-inducible system. Sheep iPSCs derived in this fashion have a normal karyotype, exhibit morphological features similar to those of human ESCs and express AP, Oct4, Sox2, Nanog and the cell surface marker SSEA-4. Pluripotency of these cells was further confirmed by embryoid body (EB) and teratoma formation assays which generated derivatives of all three germ layers. Our results also show that the substitution of knockout serum replacement (KSR) with fetal bovine serum in culture improves the reprogramming efficiency of sheep iPSCs. Generation of sheep iPSCs places sheep on the front lines of large animal preclinical trials and experiments involving modification of animal genomes.

Background information. STAT3 (signal transducer and activator of transcription 3) is an important transcription factor involved in many biological events, including apoptosis, tumorigenesis, angiogenesis and epithelial-tomesenchymal transition. However, no direct evidence for a role of STAT3 in 3T3-L1 adipocyte differentiation has been reported.Results. In the present study, we found that rapid activation of STAT3, lasting for more than 48 h, was elicited upon induction of adipogenesis. Both the STAT3-selective inhibitor stattic and the JAK2 (Janus kinase 2)/STAT3-selective inhibitors AG490 and Gö6976 inhibited STAT3 activation, leading to the suppression of adipocyte differentiation. Adipocyte differentiation was also suppressed by STAT3 siRNA (small interfering RNA) or dominant-negative STAT3. Interestingly, the PPARγ (peroxisome-proliferator-activated receptor γ) agonist TAZ (troglitazone) abolished the STAT3-inhibitor-and RNAi (RNA interference)-mediated suppression of adipogenesis. However, TAZ treatment had no effect on the stattic-and AG490-mediated down-regulation of STAT3 activation, suggesting that STAT3 regulates adipocyte differentiation through signalling that occurs upstream of PPARγ.Conclusion. These data indicate that STAT3 functions as a critical factor for adipogenesis via a mechanism involving the PPARγ activation pathway.

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II (6) in 62% yield, which provides an alternate method for the preparation of 6. Treatment of 3 with 2 equiv of indene(C 9 H 8 ) produced the ytterbium(III) complex (η 5 -C 9 H 7 ) 2 Yb III N(SiMe 3 ) 2 (7). Treatment of 3 with 1 equiv of 1,2-bis(indenyl)ethane also produced the ytterbium(III) complex meso-[ethylenebis(η 5 -indenyl)ytterbium III bis(trimethylsily)amide ((EBI)Yb III N(SiMe 3 ) 2 ) (8). All the compounds were fully characterized by spectroscopic methods and elemental analyses. Complexes 3, 4, 5, 6, and 8 were additionally characterized by a single-crystal X-ray diffraction study. The formation pathway for the ytterbium(II) complexes is proposed. The study showed that ytterbuim(II) complexes 4, 5, and 6 can function as single-component MMA polymerization catalysts with good activity.

Metastable h-MoO 3 hexagonal prisms have been fabricated through a simple green ultrasonic-assisted chemical route. After calcination at 440 C for 2 h, the thermodynamically stable a-MoO 3 nanoplate-based rods have been achieved through a process of in situ phase transformation. The as-synthesised products have been characterised by powder X-ray diffraction, field emission scanning electron microscopy, Fourier transform infrared spectrum, UVÀvis diffuse reflection spectroscopy and photoluminescence spectroscopy. The phase transformation from metastable h-MoO 3 to stable a-MoO 3 is observed at 419 C according to the differential scanning calorimetry results. The possible growth mechanism of MoO 3 crystals has been proposed based on the experimental results. The prepared two kinds of MoO 3 samples both display higher photocatalytic performance for degrading rhodamine B compared to that of commercial MoO 3 . In the present system, a-MoO 3 nanoplate-based rods exhibit slightly higher degradation activity than h-MoO 3 hexagonal prisms, which is possibly due to its smaller band gap energy, smaller scale of nanoplate, better adsorption capacity and lower recombination of photogenerated electrons and holes.

4 H 8 ) 2 Eu (4), via tandem silylamine elimination/homolysis of the Eu-N bond reactions. The formation pathway for complex 3 was proposed. All the compounds were fully characterized by spectroscopic methods and elemental analyses, and the structures of complexes 3 and 4 were additionally determined by single-crystal X-ray diffraction analyses. It was found that complexes 3 and 4 can function as single-component MMA polymerization initiators, which represent the first examples of europium(II) complexes as single-component MMA polymerization catalysts. The solvents and temperature effects' on the activities of the catalysts were also discussed.