RESUMO
Fully integrated monolithic, multi-channel InP-based coherent receiver PICs and transceiver modules with extended C-band tunability are described. These PICs operate at 33 and 44 Gbaud per channel under dual polarization (DP) 16-QAM modulation. Fourteen-channel monolithic InP receiver PICs show integration and data rate scaling capability to operate at 44 Gbaud under DP 16-QAM modulation for combined 4.9 Tb/s total capacity. Six channel simultaneous operation of a commercial transceiver module at 33 Gbaud is demonstrated for a variety of modulation formats including DP 16-QAM for >1.2Tbit/s aggregate data capacity.
RESUMO
In this work, a 10-wavelength, polarization-multiplexed, monolithically integrated InP coherent QPSK transmitter PIC is demonstrated to operate at 112 Gb/sec per wavelength and total chip superchannel bandwidth of 1.12 Tb/s. This demonstration suggests that increasing data capacity to multi-Tb/s per chip is possible and likely in the future.
RESUMO
OBJECTIVES: Relationship between diabetes and periodontal disease is well established. It has been shown that advanced glycation end-products (AGEs) might exert noxious effects on gingival tissues through its receptor. Evidence for the role of receptors of AGE (RAGE) in periodontal disease was verified in a murine model for diabetes. However, the presence of RAGE in human gingival tissues has not been demonstrated previously. In this study we demonstrate the presence of RAGE in human periodontium in patients with chronic periodontitis with and without type 2 diabetes. MATERIAL AND METHODS: Gingival biopsies from eight patients with both type 2 diabetes and chronic periodontitis and 14 healthy control subjects with chronic periodontitis were immunohistochemically stained for RAGE. Five samples from the study groups and four controls were subjected to reverse transcriptase coupled to polymerase chain reaction (RT-PCR) for quantitative determination of mRNA for RAGE. RESULTS: On immunohistochemistry, positive staining for RAGE was seen in the endothelium and the basal and spinous layer of the inflamed gingival epithelium in both type 2 diabetes and non-diabetes tissue with no statistically significant difference between both groups. RT-PCR, however, showed a 50% increase in mRNA for RAGE in the gingiva of diabetic patients when compared with controls (p<0.05). CONCLUSIONS: Although there was no change in the staining intensity for RAGE between both groups, the increase in the mRNA for RAGE in the type 2 diabetes gingival epithelium may indicate a possible involvement of this receptor in the periodontal destruction in type 2 diabetes.
