Designing laboratory activities is a real challenge for those working in higher education. There is often an acknowledged frustration with the status quo, but a lack of clear guidance on what strategies might be useful in considering a redesign. This article aims to address the question: what considerations should be taken into account when designing a laboratory activity? To address it, we first describe an overarching framework for laboratory learning, describing it as a complex learning environment. The reason for this is that two clear overarching guidelines emerge -the first is that the laboratory curriculum should be structured so that each new challenge for student is adequately supported by their prior learning so that they can draw on their knowledge to address the new learning situation, and the second is that guidelines for the kinds of preparation for laboratory learning emerge. Based on this framework, we advocate four core principles for laboratory learning that should be considered when designing a laboratory activity regarding the overall purpose, the role of preparation, the teaching of technique, and the consideration of affective dimensions of learning. We illustrate this framework in practice with examples from our own practice, with suggestions on using the literature on laboratory education as a source for curriculum reform within an institution.

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Regenerating nonthrombotic and compliant artery, especially in the aging body, remains a major surgical challenge, mainly owing to the inadequate knowledge of the major cell sources contributing to arterial regeneration and insufficient bioactivity of delivered peptides in grafts. Ultrathin nanofibrous sheaths stented with biodegrading elastomer present opening channels and reduced material residue, enabling fast cell recruitment and host remodeling, while incorporating peptides offering developmental cues are challenging. In this study, a recombinant human thymosin β4 dimer (DTβ4) that contains two complete Tβ4 molecules is produced. The adult perivascular adipose is found as the dominant source of vascular progenitors which, when stimulated by the DTβ4‐loaded nanofibrous sheath, enables 100% patency rates, near‐complete structural as well as adequate functional regeneration of artery, and effectively ameliorates aging‐induced defective regeneration. As compared with Tβ4, DTβ4 exhibits durable regenerative activity including recruiting more progenitors for endothelial cells and smooth muscle cells, when incorporated into the ultrathin polycaprolactone sheath. Moreover, the DTβ4‐loaded interface promotes smooth muscle cells differentiation, mainly through promoting M2 macrophage polarization and chemokines. Incorporating artificial DTβ4 into ultrathin sheaths of fast degrading vascular grafts creates an effective interface for sufficient muscular remodeling thus offering a robust tool for vessel replacement.

In bipolar SiC devices, which are promising under ultra-high voltage operation, the carrier lifetime is a highly influential parameter for the device performance. Surface recombination is one of the limiting factors for the carrier lifetime, and quantitative values of the surface recombination velocities are required for the design and development of fabrication processes of the devices. In this study, we observe carrier recombination at various temperatures for the Si- and C-faces of n- and p-type 4H-SiC samples and the a- and m-faces of n-type 4H-SiC samples with a treatment of chemical mechanical polishing or reactive ion etching by using the microwave photoconductivity decay method. From the experimental results, we estimate surface recombination velocities and bulk carrier lifetimes of the samples by using an analytical model. As a result, we found the smallest surface recombination velocity of 150 cm/s for the chemical mechanical polished surface of the Si-face of the n-type samples at room temperature. Surface recombination velocities increased with temperature for the chemical mechanical polished surfaces. The surfaces treated with reactive ion etching showed relatively large surface recombination velocities with weak temperature dependence. Based on these results, we discuss the origins of the recombination centers at surfaces of 4H-SiC.

Liver cancer is a major healthcare problem and one of the leading causes of cancer-associated mortality in the world. To date, chemotherapy remains a common method for treating cancer and cisplatin is one of the most widely used chemotherapeutics. However, owing to drug resistance and side effects, it is imperative to identify a novel approach to improve the anticancer effect of cisplatin. Auxiliary chemotherapy drugs with minor toxicity to normal cells may represent a novel strategy for cancer therapy. Previous studies have indicated that ginkgol C17:1 exhibits anticancer effects in liver cancer cells in vitro and in vivo . The antitumor activity of ginkgol C17:1 has been reported in combination with cisplatin in human liver cancer cells. Owing to the route of systemic administration, liver cancer cells and normal hepatocytes were exposed to chemotherapeutics and auxiliary chemotherapy drugs. However, the effects of ginkgol C17:1 in normal hepatocytes remain unclear. In the present study, the biological effects of ginkgol C17:1 alone and as co-treatment with cisplatin were compared in human hepatoma cells and normal hepatocytes. Consistently, the results confirmed that in human hepatoma HepG2 cells, ginkgol C17:1 or cisplatin alone induced autophagy and apoptosis. The co-treatment increased cisplatin-induced apoptosis and inhibited cisplatin-induced autophagy. In comparison, the treatments in human normal L02 hepatocytes indicated that ginkgol C17:1 alone induced autophagy, whereas cisplatin alone induced apoptosis. The co-treatment inhibited cisplatin-induced apoptosis, but enhanced autophagy in L02 cells. Further investigation revealed that the AMP-activated protein kinase/serine/threonine protein kinase ULK1 and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathways were involved in the underlying regulatory mechanisms. Taken together, the results of the present study provide the first evidence that ginkgol C17:1 protects normal hepatocytes against cisplatin-induced cytotoxicity while potentiating the anticancer effect of cisplatin chemotherapy. The differential effects on normal and cancer cells suggest that ginkgol C17:1 is a promising candidate for auxiliary chemotherapy.