Developing High-Energy Dissipative Soliton 2 μm Tm3+-Doped Fiber Lasers

In recent years, mid-infrared (mid-IR) lasers have attracted a great interest over the world. During the development of mid-IR laser sources, the 2 μm Tm3+-doped fiber laser (TDFL) has played an important role for its specific emission wavelength between near-IR and mid-IR. Its great potential applications include sensing, medical surgery, ranging, telecommunications, and pump sources for developing 3–5 μm laser systems. Though the continuous-wave (CW) output power of 2 μm TDFLs has been scaled to over 1000 W, high-pulse-energy ultrafast 2 μm TDFLs are still limited by nonlinear optical effects. In traditional soliton mode-locking, the pulse energy has an upper limit defined by the soliton area theorem (or energy quantization principle). For improving the pulse energy of 2 μm fiber lasers, dissipative soliton (DS) mode-locking may be one of the efficient solutions. In this chapter, the current state of the art in high-energy ultrafast DS 2 μm TDFLs developed in our laboratory is reviewed, and the potential and prospect of this theme are analyzed. By introducing a new model, condensed-gain fiber mode-locking, we show that the soliton pulse energy of 2 μm TDFLs can be steadily scaled to over 10 nJ and various soliton dynamics (harmonic mode-locking, soliton molecules, etc.) can be observed. Furthermore, DS mode-locking of TDFLs with one of the two-dimension-like materials (MoS2) is investigated

A semiempirical dynamic model of reversible open circuit voltage drop in a PEM fuel cell

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149313/1/er4127_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149313/2/er4127.pd

Chronic inflammation triggered by the NLRP3 inflammasome in myeloid cells promotes growth plate dysplasia by mesenchymal cells

AbstractSkeletal complications are common features of neonatal-onset multisystem inflammatory disease (NOMID), a disorder caused by NLRP3-activating mutations. NOMID mice in which NLRP3 is activated globally exhibit several characteristics of the human disease, including systemic inflammation and cartilage dysplasia, but the mechanisms of skeletal manifestations remain unknown. In this study, we find that activation of NLRP3 in myeloid cells, but not mesenchymal cells triggers chronic inflammation, which ultimately, causes growth plate and epiphyseal dysplasia in mice. These responses are IL-1 signaling-dependent, but independent of PARP1, which also functions downstream of NLRP3 and regulates skeletal homeostasis. Mechanistically, inflammation causes severe anemia and hypoxia in the bone environment, yet down-regulates the HIF-1α pathway in chondrocytes, thereby promoting the demise of these cells. Thus, activation of NLRP3 in hematopoietic cells initiates IL-1β-driven paracrine cascades, which promote abnormal growth plate development in NOMID mice.</jats:p