Based on the Seebeck effect, the CMOS compatible micromachined thermopile is widely used in infrared detection for its advantages of low-cost, high batch yield, broad spectral response and insensitivity to ambient temperature. We present two integrated thermopile IR detectors on stacked dielectric layers realized by a standard P-well CMOS technology, followed by one CMOS compatible maskless XeF2 isotropic dry-etching step. Characterizations of CMOS devices, before and after XeF2 etching, respectively, were performed to investigate the effects of XeF2 etching on the CMOS devices. With a 2.5 µm thick stacked silicon oxide–nitride–oxide layer as an absorber, the rectangular thermopile detector and the circular thermopile detector provided responsivity of 14.14 and 10.26 V W−1, specific detectivity of 4.15 × 107 and 4.54 × 107 cm Hz1/2 W−1, and time constant of 23.7 and 14.6 ms, respectively. Compared with the rectangular thermopile detector, the circular thermopile detector is mechanically more stable, because its circular structure design eases the internal stress problem in the CMOS layers. After XeF2 etching, the maximum changes of threshold voltage, maximum transconductance and switching threshold voltage were 0.97%, 1.25% and 0.08%, respectively. Experimental results show that the effects of XeF2 etching on the CMOS devices are insignificant, and XeF2 etching is suitable for post-CMOS micromachining.

Quinolone(s) (QNs) is widely used in infection therapy due to its good antimicrobial characteristics. However, QNs-induced arthropathy of immature animals has led to restrictions on the therapeutic use of these antimicrobial agents. The exact mechanism(s) of QNs-induced chondrotoxicity remain unknown. In the present study, we investigated the possible mechanism of ofloxacin (one typical QNs)-induced injuries of chondrocytes. Juvenile rabbit joint chondrocytes cultured in alginate microspheres were incubated with ofloxacin at concentrations of 0, 2, 5, 10, 20, and 40 g/ml for up to 96 h. Concentration of 10 g/ml ofloxacin induced apoptosis of chondrocyte with visible apoptotic signs, including degradation of poly(ADP-ribose) polymerase, caspase-3 activation, and DNA ladder formation. Furthermore, extracellular signal-regulated kinase 1/2 (phospho-ERK1/2) and growth factor receptor-bound protein 2 (Grb2) were significantly reduced, and similar changes were also observed in the ␤ 1 -integrin receptor as assessed by immunoblotting. However, the mRNA level of ␤ 1 -integrin obtained from reverse transcription-polymerase chain reaction remained unchanged. Results of ␤ 1 -integrin immunoprecipitation have also shown that ␤ 1 -integrin did not interact with activated intracellular signaling proteins. In addition, ofloxacin did not induce apoptosis and decrease ␤ 1 -integrin expression in chondrocytes supplemented with Mg 2ϩ , and the ofloxacin-induced apoptosis was caspase-8-dependent, inhibition of which did not affect the expression mode of phospho-ERK1/2 and ␤ 1 -integrin. Our results demonstrate that ofloxacin affects ␤ 1 -integrin receptor functions and the ERK mitogen-activated protein kinase signaling pathway, causing caspase-8-dependent apoptosis after exposure of 48 h.

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