Spinal cord stimulation (SCS) has been reported to be effective for complex regional pain syndrome (CRPS). This is a case report of a patient with CRPS who was successfully treated with a combination of temporary SCS lead placement and physical therapy. A 19-year-old man presented with severe pain for a few months since receiving plaster cast fixation as treatment for an ankle sprain injury at the previous hospital. At his first visit to our pain center, he could not walk without crutches because of severe pain accompanied by symptoms such as allodynia, decreased skin temperature, redness, edema, muscle weakness, and changes in the appearance of the affected area. The symptoms met the diagnostic criteria for CRPS. Temporary SCS lead placement was performed to alleviate the pain and peripheral circulatory disorder, along with physiotherapy to improve the flexibility and restore the normal appearance of the affected limb. The interdisciplinary treatment effectively improved our patient's leg edema and walking ability, which consequently led to pain relief.

Spinal cord stimulation (SCS) has been reported to be effective for complex regional pain syndrome (CRPS). This is a case report of a patient with CRPS who was successfully treated with a combination of temporary SCS lead placement and physical therapy. A 19-year-old man presented with severe pain for a few months since receiving plaster cast fixation as treatment for an ankle sprain injury at the previous hospital. At his first visit to our pain center, he could not walk without crutches because of severe pain accompanied by symptoms such as allodynia, decreased skin temperature, redness, edema, muscle weakness, and changes in the appearance of the affected area. The symptoms met the diagnostic criteria for CRPS. Temporary SCS lead placement was performed to alleviate the pain and peripheral circulatory disorder, along with physiotherapy to improve the flexibility and restore the normal appearance of the affected limb. The interdisciplinary treatment effectively improved our patient's leg edema and walking ability, which consequently led to pain relief.

New drug discovery is under growing pressure to satisfy the demand from a wide range of domains, especially from the pharmaceutical industry and healthcare services. Assessment of drug efficacy and safety prior to human clinical trials is a crucial part of drug development, which deserves greater emphasis to reduce the cost and time in drug discovery. Recent advances in microfabrication and tissue engineering have given rise to organ-on-a-chip, an in vitro model capable of recapitulating human organ functions in vivo and providing insight into disease pathophysiology, which offers a potential alternative to animal models for more efficient pre-clinical screening of drug candidates. In this review, we first give a snapshot of general considerations for organ-on-a-chip device design. Then, we comprehensively review the recent advances in organ-on-a-chip for drug screening. Finally, we summarize some key challenges of the progress in this field and discuss future prospects of organ-on-a-chip development. Overall, this review highlights the new avenue that organ-on-a-chip opens for drug development, therapeutic innovation, and precision medicine.

Identification of the precise molecular pathways involved in oncogene-induced transformation may help us gain a better understanding of tumor initiation and promotion. Here, we demonstrate that SOX2 foregut epithelial cells are prone to oncogenic transformation upon mutagenic insults, such as Kras and p53 deletion. GFP-based lineage-tracing experiments indicate that SOX2 cells are the cells-of-origin of esophagus and stomach hyperplasia. Our observations indicate distinct roles for oncogenic KRAS mutation and P53 deletion. p53 homozygous deletion is required for the acquisition of an invasive potential, and Kras expression, but not p53 deletion, suffices for tumor formation. Global gene expression analysis reveals secreting factors upregulated in the hyperplasia induced by oncogenic KRAS and highlights a crucial role for the CXCR2 pathway in driving hyperplasia. Collectively, the array of genetic models presented here demonstrate that stratified epithelial cells are susceptible to oncogenic insults, which may lead to a better understanding of tumor initiation and aid in the design of new cancer therapeutics.