Coordinated voltage control for improved power system voltage stability by incorporating the reactive power reserve from wind farms

The absorption and output characteristics of reactive power of the doubly-fed induction generator (DFIG) greatly influence the voltage stability of PCC (Point of Common Coupling) where the wind farms are integrated into the bulk power grid. This study proposes a reactive power compensation strategy for coordinated voltage control (CVC) of PCC with large-scale wind farms to achieve the expected voltage quality of the power grid through a minimum amount of control actions in emergencies. To this end, the mechanism of reactive power and voltage control inside DFIG is first analyzed. Then, the concept of reactive power reserve (RPR) sensitivity concerning control actions is introduced and an index of voltage stability margin is proposed to evaluate and analyze the distance between the current operating point and the voltage collapse point by analyzing the relationship between reactive power reserve and voltage stability margin. In the event of an emergency, critical reactive power reserves are obtained to reduce the dimension and complexity of the control problem. The sensitivity of reactive power reserve and the control are formulated into a convex quadratic programming problem to optimize the control strategies for voltage stability. The proposed technology has been validated on the IEEE 39-bus system

Quantification of dissolved organic carbon (DOC) storage in lakes and reservoirs of mainland China

As a major fraction of carbon in inland waters, dissolved organic carbon (DOC) plays a crucial role in carbon cycling on a global scale. However, the quantity of DOC stored in lakes and reservoirs was not clear to date. In an attempt to examine the factors that determine the DOC storage in lakes and reservoirs across China, we assembled a large database (measured 367 lakes, and meta-analyzed 102 lakes from five limnetic regions; measured 144 reservoirs, and meta-analyzed 272 reservoirs from 31 provincial units) of DOC concentrations and water storages for lakes and reservoirs that are used to determine DOC storage in static inland waters. We found that DOC concentrations in saline waters (Mean/median ± S.D: 50.5/ 30.0 ± 55.97mg/L) are much higher than those in fresh waters (8.1/5.9 ± 6.8 mg/L), while lake DOC concentrations (25.9/11.5 ± 42.04 mg/L) are much higher than those in reservoirs (5.0/3.8 ± 4.5 mg/L). In terms of lake water volume and DOC storage, the Tibet-Qinghai lake region has the largest water volume (552.8 km3), 92% of which is saline waters, thus the largest DOC (13.39 Tg) is stored in these alpine lake region; followed by the Mengxin lake region, having a water volume of 99.4 km3 in which 1.75 Tg DOC was stored. Compared to Mengxin lake region, almost the same amount of water was stored in East China lake region (91.9 km3), however, much less DOC was stored in this region (0.43 Tg) due to the lower DOC concentration (Ave: 3.45 ± 2.68 mg/L). According to our investigation, Yungui and Northeast lake regions had water storages of 32.14 km3 and 19.44 km3 respectively, but relatively less DOC was stored in Yungui (0.13 Tg) than in Northeast lake region (0.19 Tg). Due to low DOC concentration in reservoirs, especially these large reservoirs having lower DOC concentration (V > 1.0 km3: 2.31 ± 1.48 mg/L), only 1.54 Tg was stored in a 485.1 km3 volume of water contained in reservoirs across the entire country

Reversal of bortezomib resistance in myelodysplastic syndrome cells by MAPK inhibitors.

The myelodysplastic syndromes (MDS) comprise a heterogeneous group of malignant neoplasms with distinctive clinicopathological features. Currently, there is no specific approach for the treatment of MDS. Here, we report that bortezomib (BTZ), a proteasome inhibitor that has been used to treat plasma cell myeloma, induced G2/M phase cycle arrest in the MDS cell line SKM-1 through upregulation of Wee1, a negative regulator of G2/M phase transition. Treatment by BTZ led to reduced SKM-1 cell viability as well as increased apoptosis and autophagy. The BTZ-induced cell death was associated with reduced expression of p-ERK. To elucidate the implications of downregulation of p-ERK, we established the BTZ resistant cell line SKM-1R. Our data show that resistance to BTZ-induced apoptosis could be reversed by the MEK inhibitors U0126 or PD98059. Our results suggest that MAPK pathway may play an important role in mediating BTZ resistance

BTZ induces apoptosis.

<p>A. Representative flow cytometry scatter plots showing cells undergoing apoptosis in response to BTZ. B. Bar graph shows percentage of SKM-1 cells undergoing apoptosis in response to 5 and 10 nM BTZ for 24 h. C. Immunoblot analysis of cleaved caspase-3. D. Immumofluorescence staining of cleaved caspase-3. Bar 50 µm. *<i>P</i><0.05.</p

ERK1/2 expression in SKM-1 cells.

<p>Immunoblotting of SKM-1 cells shows that total and p-ERK1/2 are both expressed in untreated SKM-1 cells (control). However, BTZ inhibited the expression of p-ERK1/2 but not total ERK1/2. GAPDH was used as loading control.</p

Cell viability in response to BTZ treatment.

<p>SKM-1 and SKM-1R cells were exposed to 5 nM BTZ for 24 h and the viable cell number was evaluated by MTT assay. The result showed a reduction in cell viability by treating wild type SKM-1 cells with 5 nM BTZ with no notable effect on SKM-1R cells. *<i>P</i><0.05.</p

ERK1/2 expression in BTZ resistant SKM-1R cells.

<p>Immunoblotting of SKM-1R cells shows that both total and phospho-ERK1/2 are upregulated in response to BTZ treatment. Protein expression levels were quantified by ImageJ. Total and phospho-ERK1/2 levels were normalized to GAPDH.</p

BTZ induces autophagy in SKM-1 cells.

<p>SKM-1 cells were treated with 10 nM BTZ for 24 h and immunoblotted for microtubule-associated light chain (LC3-I and LC3-II). GAPDH was used as loading control.</p

Reversal of BTZ resistance by MEK inhibitors in SKM-1R cells.

<p>A. Flow cytometry scatter plots showing Annexin V staining of SKM-1R cells. B. Bar graph shows percentage of SKM-1R cells undergoing apoptosis in response to a 24 h exposure to 5 nM BTZ. Both PD98059 (PD) and U0126 (U0) significantly increased the percentage of cells undergoing apoptosis. *<i>P</i><0.05, ***<i>P</i><0.001.</p

BTZ arrests SKM-1 cells at G2/M phase.

<p>A. SKM-1 cells were treated with vehicle (control) or 10 nM BTZ for 24 h and then stained with PI for FACS analysis. B. The distribution of cells in each cell cycle phase is shown. **<i>P</i><0.01.</p