Approximation of a melting plateau of large area HTFP cells used for spectral irradiance realization.

This paper adopted an approximation of a melting plateau to solve the problem that temperature data cannot be monitored continuously when measuring the spectral irradiance of a large area tungsten carbide-carbon high-temperature fixed-point blackbody at each measured wavelength. Tests with fully measured curves showed that the method has a rather small deviation from the measured data of 0.017 K maximum, which corresponds to the spectral irradiance deviation of 0.005% at 500 nm. The maximum relative deviation between the Akima fitting method and the measured temperature in terms of spectral irradiance was 0.002%, which was better than -0.067% of a single temperature of 3020.11 K method and 0.026% of a linear interpolation method.

A method for spectral irradiance measurement based on a large area WC-C fixed point blackbody.

We have proposed a novel method for the spectral irradiance measurement of the standard lamp. The measurement has been realized by using national primary scale based on a large area WC-C fixed point blackbody for the first time. The wavelength range is from 450 nm to 1000 nm. The spectral irradiance of the standard lamp has been measured based on the traditional variable temperature blackbody and large area WC-C fixed point blackbody. The results of the two methods agree within the uncertainties. Compared with the traditional measurement method, the fixed point method can reduce the major component of the spectral irradiance measurement uncertainty related to the temperature measurement.

A method for optimizing the reference temperature in the effective emissivity calculation of nonisothermal blackbody cavities.

For a nonisothermal blackbody cavity, different reference temperatures have influence on the calculation of effective emissivity. Previous studies proposed a weighted average method which can be indicated by a priori to calculate the reference temperature. However, these studies did not mention how to define the weight function but used some arbitrary temperature or the temperature of a fixed position like the central bottom of the cavity as the reference temperature. In this study, a quantitative analysis and calculation method, which is implemented in the Monte Carlo method based optical simulation software Tracepro, is proposed to define the weight coefficients and optimize the reference temperature. To do so, in the Tracepro software, a surface source is placed in front of the cavity opening and emits radiation to the blackbody cavity. The radiation from this surface source can be absorbed or reflected many times in the cavity, and finally the incident radiation distribution in the cavity can be obtained. According to the principle of light path reversibility, the normalized incident radiation can be considered as the contribution of its position to the effective emissivity. In the experiment, the actual temperatures of two different-shaped blackbody cavities are measured with the non-contact method in 873 K temperature. By dividing the inner surface of each blackbody cavity into several regions based on the positions of the actually measured temperature points, the incident radiation from the surface source to each segmented region is calculated and normalized to the total incident radiation across all regions as its weight coefficient; the reference temperature is the sum of the weighted temperature (by multiplying each weight coefficient with its measured temperature) in each region. Different from previous studies, this study optimizes the reference temperature by considering the contribution of the whole cavity to the effective emissivity, which should be more consistent with the actual situation. Moreover, the influences of different shapes of the blackbody cavities, different radiation characteristics of the inner surface materials and different viewing conditions of the effective emissivity on the reference temperature are discussed and compared. The results suggest that the optimization of reference temperature has close link with above factors and thus should be calculated individually.

Spectral irradiance primary scale realization and characterization of deuterium lamps from 200 to 400 nm.

To meet the increasing metrology demand of spectral irradiance in the short UV spectral range, a new spectral irradiance scale from 200 to 400 nm was realized at National Institute of Metrology (NIM) based on a high-temperature blackbody BB3500M, and a group of stable deuterium lamps are used as the transfer standards. Accurate real-time temperature of a blackbody is derived to reduce the temperature drift during the measurement period. A combination of an absolute and relative measurement system is designed to reduce repeatability uncertainty, and a selective optical filter method is used to remove fluorescence with a peak at 330 nm. A seven-point bandwidth novel correction method based on differential quadrature formula is put forward to correct the bandwidth error of the monochromator. The expanded uncertainties of the new spectral irradiance scale are 5.3% at 200 nm, 1.8% at 250 nm, 1.9% at 330 nm, and 3.6% at 400 nm, respectively. In the overlap wavelength from 250 to 400 nm, the average deviation between two types transfer standards, deuterium lamps and tungsten halogen lamps, is verified to be 0.39%, which are consistent with the associated measurement uncertainties.

Case of systemic sclerosis overlapping with psoriasis.

Coexistence of the skin manifestations of systemic sclerosis and psoriasis is rare. The link between systemic sclerosis and psoriasis has been poorly investigated. We report a case of a 70-year-old woman, who was diagnosed with diffuse cutaneous systemic sclerosis and psoriasis vulgaris and was treated with oral azathioprine (50 mg/d) and prednisolone (10 mg/d), topical corticosteroids, and calcipotriols. The erythema and plaques almost disappeared after 1 week, and the symptoms of discoloration in cold, regurgitation, and dysphagia abated after 3 months.

Gut microbiota mediated inflammation, neuroendocrine and neurotrophic functions involved in the antidepressant-like effects of diosgenin in chronic restraint stress.

BACKGROUND: Diosgenin is a well-known steroid saponin possessing neuroprotective activities. However, it is unknown whether diosgenin could alleviate depression-like symptoms. METHODS: The antidepressant-like effect of diosgenin was investigated in mice induced by chronic restraint stress. The effects of diosgenin on behaviors, inflammation, neuroendocrine, neurotrophic function, and gut microbiota were evaluated. RESULTS: The results showed that diosgenin alleviated the depressive-like behaviors in mice. In addition, diosgenin was found to reduce serum concentrations of proinflammatory cytokines and the activity of the hypothalamic-pituitary-adrenal (HPA) axis. Besides, diosgenin could activate hippocampal brain-derived neurotrophic factor (BDNF)/TrkB/ERK/CREB signaling pathway and improve the expression of postsynaptic protein PSD95. Meanwhile, the neurogenesis which was inhibited by chronic restraint stress, was totally reversed by diosgenin. Moreover, diosgenin increased the abundance of phylum Firmicutes and the genus Lactobacillus in stressed mice. The results further showed that diosgenin caused a strong correlation between gut microbiota composition and inflammation, the HPA axis activity, or hippocampus neurotrophic function. LIMITATIONS: Only male mice were used for evaluation in the present study, which limits the understanding of effects of diosgenin on the both sexes. In addition, the results only indicate microbiota at the phylum or genus mediate the regulation of neuroinflammation, neuroendocrine, and neurotrophic function, but does not elucidate how microbiota modulate the systems via their primary or secondary metabolites. CONCLUSIONS: The present study shows that diosgenin exerts the antidepressant activity, which is associated with the enhancement of neurotrophic function and the inhibition of inflammatory and neuroendocrine activities via the regulation of gut microbiota.

The degradation of Rap1GAP via E6AP-mediated ubiquitin-proteasome pathway is associated with HPV16/18-infection in cervical cancer cells.

BACKGROUND: Cervical cancers are closely associated with persistent high-risk human papillomaviruses (HR HPV) infection. The main mechanism involves the targeting of tumor suppressors, such as p53 and pRB, for degradation by HR HPV-encoded oncoproteins, thereby leading to tumorigenesis. Rap1GAP, a tumor suppressor gene, is down-regulated in many cancers. Previous studies have revealed that down-regulation of Rap1GAP is correlated with HPV16/18 infection in cervical cancer. However, the molecular mechanism remains unclear. In this study, we aimed to address the degradation pathway of Rap1GAP in HPV-positive cervical cancer cells. METHODS: HPV-positive (HeLa and SiHa) and negative (C33A) cervical cancer cells were used to analyze the pathways of Rap1GAP degradation. MG132 (carbobenzoxy-leucyl-leucyl-leucine) was used to inhibit protein degradation by proteasome. Co-immunoprecipitation (co-IP) was used to detect the interaction between Rap1GAP and E6AP. siRNA for E6AP was used to silence the expression of E6AP. Rapamycin was used to induce cell autophagy. Western blotting was used to check the levels of proteins. RESULTS: Following treatment with MG132, the levels of Rap1GAP were increased in the HR HPV-positive HeLa and SiHa cells, but not in the HPV-negative C33A cells. Co-immunoprecipitation assay revealed ubiquitinated Rap1GAP protein in HeLa and SiHa cells, but not in C33A cells. E6-associated protein (E6AP) mediated the ubiquitination of Rap1GAP by binding to it in HeLa and SiHa cells, but not in C33A cells. However, the levels of Rap1GAP were decreased in HeLa and SiHa cells after knocking down E6AP by siRNA. Silencing of E6AP did not affect the levels of Rap1GAP in C33A cells. Autophagy marker p62 was decreased and LC3 II/LC3 I was increased after knocking down E6AP in HeLa cells, but not in C33A cells. The levels of Rap1GAP were decreased after treating the cells with rapamycin to induce cell autophagy in HeLa and C33A cells. CONCLUSION: Rap1GAP may be degraded by autophagy in cervical cancer cells, but HPV infection can switch the degradation pathway from autophagy to E6AP-mediated ubiquitin-proteasome degradation. E6AP may be a key component of the switch.