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After Vogel proposed a dimensionless inflow performance equation, with the rise of the horizontal well production mode, a large number of inflow performance relationship (IPR) equations have emerged. In the productivity analysis of deviated and horizontal wells, the IPR equation proposed by Cheng is mainly used. However, it is still unclear whether these inflow performance models (such as the Cheng, Klins-Majcher, Bendakhlia-Aziz, and Wiggins-Russell-Jennings types) are suitable for productivity evaluations of horizontal and deviated wells in low-permeability reservoirs. In-depth comparisons and analyses have not been carried out, which hinders improvements in the accuracy of the productivity evaluations of horizontal wells in low-permeability reservoirs. In this study, exploratory work was conducted in two areas. First, the linear flow function relationship used in previous studies was improved. Based on the experimental pressure-volume-temperature results, a power exponential flow function model was established according to different intervals greater or less than the bubble point pressure, which was introduced into the subsequent derivation of the inflow performance equation. Second, given the particularity of low-permeability reservoir percolation, considering that the reservoir is a deformation medium, and because of the existence of a threshold pressure gradient in fluid flow, the relationship between permeability and pressure was changed. The starting pressure gradient was introduced into the subsequent establishment of the inflow performance equation. Based on the above two aspects of this work, the dimensionless IPR of single-phase and oil-gas two-phase horizontal wells in a deformed medium reservoir was established by using the equivalent seepage resistance method and complex potential superposition principle. Furthermore, through regression and error analyses of the standard inflow performance data, the correlation coefficients and error distributions of six types of IPR equations applicable to deviated and horizontal wells at different inclination angles were compared. The results show that the IPR equation established in this study features good stability and accuracy and that it can fully reflect the particularity of low-permeability reservoir seepage. It provides the best choice of the IPR between inclined wells and horizontal wells in low-permeability reservoirs. The other types of IPR equations are the Wiggins-Russell-Jennings, Klins-Majcher, Vogel, Fetkovich, Bendakhlia-Aziz, and Harrison equations, listed here in order from good to poor in accuracy.

The hydrogen sulfide (H(2)S)/cystathionine γ-lyase (CSE) signaling pathway is involved in several inflammatory conditions, where tumor necrosis factor-α (TNFα) is one of the inflammatory cytokines activated during sepsis. Therefore, the present study investigated the role of the NF-κB transcription factor binding site in the transcriptional regulation of the CSE gene in 293T cells following treatment with TNFα using luciferase assays, as well as using western blotting and reverse transcription-quantitative PCR to examine the effect of TNFα on CSE expression in HUVECs. After transfected 293T cells were incubated with various concentrations of TNFα for 1, 3, and 6 h, the wild-type promoter of the CSE gene increased significantly at 1 h compared to 0 h. By contrast, after the transfected 293T cells were incubated with various concentrations of TNFα for 1 h, the mutant-type promoter activity of the CSE gene decreased significantly compared to the wild-type. These results revealed that the DNA sequence GGGACATTCC on the CSE gene promoter was directly associated with the transcriptional regulation of the CSE gene in Human cells (293T cells) that's were treated with TNFα. This suggests that TNFα affects CSE gene expression, such that vascular endothelial cells respond to TNFα in the blood by regulating CSE expression. The regulatory mechanisms associated with the effects of TNFα on the transcriptional regulation of the CSE gene in HUVECs and the NF-κB pathway warrant further investigation.

Cystathionine gamma-lyase (CSE) is one of the essential H2S-producing enzymes, and it regulates diverse functions in connection with cardiovascular function. It is crucial how exogenous H2S regulates CSE expression of the vascular endothelial cell during hypoxia. We examined the transcription and expression of CSE in HUVECs regulated by exogenous H2S with 100 μM during hypoxia by Luciferase assay, Western blotting, and quantitative RT-qPCR. Exogenous H2S influenced on the promoter activity of CSE in HUVECs during hypoxia. The effects of 100 μM H2S on CSE mRNA expression in HUVECs is decreased compared with 0 μM H2S. The consequences of 100 μM H2S on the expression level of CSE protein in HUVECs at two h of hypoxia is reduced compared with 0 μM H2S. These findings suggest that vascular endothelial cells can respond to the signals of hypoxia in the blood, and can respond to changes in H2S concentration in the blood, thus affect the blood vessels themselves.

In this paper, a rhodamine derivative was synthesized as a probe for Hg(II) detection. Its spectral response and sensing mechanism towards Hg(II) were discussed carefully. It was found that its absorption and emission were increased by Hg(II), via a direct bonding stoichiometry of 1:1. Its association constant was determined with absorption titration as 2.59 × 105 M−1, which suggested a coordination procedure between Hg(II) and this rhodamine probe. It showed good selectivity towards Hg(II) over competing metal cations, no increased emission or absorption was observed in the presence of interfering metal cations. It was then covalently grafted onto silica (SiO2)-encapsulated upconversion nanoparticles (UCNPs). Upon near-infrared (NIR) excitation (980 nm), RHO accepted energy from these UCNPs through a FRET (fluorescence resonance energy transfer) procedure, quenching their upconversion emission. A sensing response towards Hg(II) was thus constructed. Good linearity and selectivity were still preserved in this composite sample. On the other hand, this work found a different phenomenon from literature cases, which was the emission absence of rhodamine emission in this composite structure. Detailed analysis suggested that rhodamine emission absence was caused by its self-quenching effect.

Hydrogen sulfide (H2S), as an endogenous signaling molecule in mammals, shows a variety of biological effects. Cystathionine gamma-lyase (CSE)/H2S pathway has been implicated in scavenging reactive oxygen species (ROS) in the mammalian cells. Therefore, we first investigated the regulatory effects of exogenously applied hydrogen peroxide (H2O2) on CSE expression in the mammalian cells. African green monkey kidney fibroblastlike cells (COS-7 cells) or human embryonic kidney 293 cells (HEK 293 cells) were transfected with CSE promoter-luciferase reporter constructs and treated with H2O2 of 1, 5, and 10 microM for 0.5 and 1.5 h at 37 degrees C. The transfected cells were assayed for firefly luciferase activities normalized by Renilla luciferase activity. Human lung adenocarcinoma cells (A549 cells) or human liver cancer cells (SMMC-7721 cells) were treated with H2O2 of 1, 5, and 10 microM for 0.5 and 1.5 h at 37 degrees C, and were then harvested and analyzed by Western blotting and quantitative RT-PCR. Our results showed that the treatment of a medium concentration (5 microM) of H2O2 at a longer time (1.5 h) upregulated CSE expression in the mammalian cells at the levels of the promoter, message RNA, and protein. Collectively, exogenously applied H2O2 can not only markedly affect CSE mRNA and protein expression, but also can affect the CSE promoter activity in the mammalian cells. Our observations indicate that that exogenous H2O2 can upregulate the expression of the CSE gene in the mammalian cells, which will provide the possibility of the scavenging effect of the CSE gene indirectly on ROS in the mammalian cells. However, the regulatory mechanism involved in the effects of exogenously applied H2O2 on CSE expression in the mammalian cells need be further studied.

Hydrogen sulfide (H2S), an endogenous signaling molecule in mammalian cells, shows a variety of biological effects. Cystathionine γ-lyase (CSE) is a key enzyme in the trans-sulfuration pathway responsible for the production of endogenous H2S. Whether CSE expression is regulated by hypoxia in mammalian cells remains largely unknown. This study revealed that these regulatory effects changed with time at transcriptional and post-transcriptional levels. Hypoxia regulated CSE expression in mammalian cells in a complex manner; CSE transcription went through a down-regulation and recovery period, while CSE mRNA and protein levels increased during hypoxia. Taken together, the results suggest that CSE can respond to hypoxia through transcriptional and post-transcriptional regulation, and CSE expression can be up-regulated by hypoxia to a certain extent. Therefore, the up-regulation of CSE expression during hypoxia may be useful for increasing the production and concentration of H2S in mammalian cells and indirectly protecting cells from hypoxia.

Cystathionine γ-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using L-cysteine or L-homocysteine as a substrate. The regulatory mechanism of CSE by exogenous H2S remains unknown. The transcription and expression of the CSE gene regulated by exogenous H2S at approximately physiologic concentrations was investigated using luciferase assay, Western blotting, and quantitative RT-PCR. The results revealed that exogenous H2S down-regulates the transcription and expression of CSE in mammalian cells at 10-80 μM. Exogenous H2S at 120 μM increases the transcription and expression of CSE significantly. At a concentration of exogenous H2S over 160 μM, the transcription and expression of CSE are inhibited completely. These findings suggest that CSE expression has not only a feedback to the enzyme itself at lower concentrations of exogenous H2S but also can be up-regulated at higher concentrations, and H2S may become toxic at higher levels.

We presented a distance-based detection method for visual quantification of mercury ions on a microfluidic paper-based analytical device (μPAD). Dithizone in NaOH solution was used as chromogenic reagent and deposited onto paper channel delimited by hydrophobic wax barrier. Reactions happened between mercury ions and dithizone to form an insoluble colored complex, producing colored precipitate on the paper channel. The length of colored precipitate could be readily measured using the printed ruler along each device. The length of precipitate increase linearly with the mercury concentrations, mercury in sample solution could be quantified by measuring the length of the colored precipitate. Being free of any electronic instruments, this method has the advantages of portability, ease of use, low cost and disposability. This presented method was used to detect mercury ions in a synthetic sample, demonstrating its potential in on-site and real time analysis.

Hydrogen sulfide (H2S) is regarded as the third endogenous gaseous signaling molecule. Cystathioine γ-lyase (CSE), one of the three enzymes in the transsulfuration pathway, is responsible for the production of endogenous H2S. The H2S/CSE signaling pathway is involved in the inflamma - tion induced by lipopolysaccharides (LPS). Therefore, in this study, we investigated the effects of the binding site (on the CSE promoter) for the transcription factor, nuclear factor (NF)-κB, on the transcriptional regulation of the CSE gene in mammalian cells treated with LPS. For this purpose, HEK-293 and COS-7 cells were transfected with 5 µg pGL4.12-KM1478 or 5 µg pGL4.12-KM1478m (mutant) together with the pRL-CMV control vector (0.032 µg for the HEK-293 cells, 0.0032 µg for the COS-7 cells). Subsequently, the cells were treated with LPS for 6 h. The expression of CSE was measured by RT-qPCR. cDNA pooled from J774.1A and RAW264.7 cells treated with LPS for 6 h was used to estimate the quantity of the transcripts. Our results revealed that LPS markedly increased the mRNA and protein expression levels of the CSE gene in the J774.1A and RAW264.7 cells following treatment with LPS for 6 h. In addition, we found that the GGGACATTCC DNA sequence on the promoter of the CSE gene was closely associated with the transcriptional regulation of the CSE gene in the HEK-293 and COS-7 cells treated with LPS. Taken together, our data suggest that the NF-κB binding site on CSE promoter is critical for LPS-induced CSE expression in mammalian cells.

Cystathionine gamma-lyase (CSE) is the predominant enzyme responsible for the production of endogenous hydrogen sulfide (H2S) in cardiovascular system, and hypoxia is one of the pathogenetic conditions frequently encountered by the cardiovascular system. We would like to answer the question whether hypoxia affects CSE expression on levels of promoter, message RNA and protein. In the present study, we studied the effect of hypoxia on CSE expression in the mammalian cells during hypoxia. Our results showed that hypoxia regulated CSE expression in the mammalian cells in a complex manner, and CSE transcription went through a repression and recovery period while total mRNA and protein levels increased during hypoxia. Based on the above analysis, we proposed a hypothesis about the mechanism of CSE protection on the myocardial cells. This hypothesis explained the mechanism as follows. Under the hypoxic condition which induced some cardiomyocyte apoptosis, the peroxisomes of cardiomyocyte released hydrogen peroxide (H2O2) out into the vascular endothelial cells of small arteries in the heart. The proper concentration of H2O2 promoted the recovery increase of CSE expression in the vascular endothelial cells via the nuclear factor kappa-B signal pathway. The up-regulation of CSE expression in the vascular endothelial cells produced more hydrogen sulfide H2S, which accelerated vascular smooth muscular cells (SMCs) vasodilation. Therefore, the improvement of blood circulation increased the quantity of oxygen supply to the heart, decreased the infarct size, and attenuated cardiomyocyte apoptosis. Taken together, we believe that the CSE gene in the mammalian cells is a prominent protective component in response to hypoxia through transcriptional and post transcriptional mRNA regulation. Meanwhile, we speculate that the up-regulation of CSE expression provides one of the effective protections on the mammalian cells under hypoxic conditions.