The inhibition of Beclin1-dependent autophagy sensitizes PTC cells to ABT737-induced death.

ABT737 is used as a specific BCL2 inhibitor, which can treat papillary thyroid carcinoma (PTC). However, the effect of ABT737 on PTC cell apoptosis is limited. Moreover, BCL2 inhibition causes the activation of Beclin1-dependent autophagy. Our study aimed to explore the effects of autophagy and Beclin1 on ABT737 efficacy in PTC. The experimental data showed that ABT737 synchronously enhanced autophagic activity and apoptosis level in PTC cells. ABT737 also promoted the dissociation of BCL2-Beclin1 and BCL2-Bax complexes. Autophagy inhibitors, Bafilomycin A1 and 3-MA, enhanced the inhibitory effect of ABT737 on the survival and function in PTC cells. Consistently, autophagy inhibition with Beclin1 pharmacological inhibitor (spautin-1) also enhanced the efficacy of ABT737. Additionally, ABT737 at low-dose promoted LC3 conversion in PTC cells, and did not affect PTC cell apoptosis and survival. However, The efficacy of low-dose of ABT737 in PTC cell apoptosis and survival was displayed with the addition of Bafilomycin A1, 3-MA or spautin-1. In conclusion, the limited role of ABT737 in PTC cell apoptosis is attributed to its promoting effect on Beclin1-dependent autophagy. Therefore, autophagy inhibition based on Beclin1 downregulation can enhance the sensitivity of PTC cells to ABT737-induced death.

Comprehensive characterization of ERV-K (HML-8) in the chimpanzee genome revealed less genomic activity than humans.

Endogenous retroviruses (ERVs) originate from ancestral germline infections caused by exogenous retroviruses. Throughout evolution, they have become fixed within the genome of the animals into which they were integrated. As ERV elements coevolve with the host, they are normally epigenetically silenced and can become upregulated in a series of physiological and pathological processes. Generally, a detailed ERV profile in the host genome is critical for understanding the evolutionary history and functional performance of the host genome. We previously characterized and cataloged all the ERV-K subtype HML-8 loci in the human genome; however, this has not been done for the chimpanzee, the nearest living relative of humans. In this study, we aimed to catalog and characterize the integration of HML-8 in the chimpanzee genome and compare it with the integration of HML-8 in the human genome. We analyzed the integration of HML-8 and found that HML-8 pervasively invaded the chimpanzee genome. A total of 76 proviral elements were characterized on 23/24 chromosomes, including detailed elements distribution, structure, phylogeny, integration time, and their potential to regulate adjacent genes. The incomplete structure of HML-8 proviral LTRs will undoubtedly affect their activity. Moreover, the results indicated that HML-8 integration occurred before the divergence between humans and chimpanzees. Furthermore, chimpanzees include more HML-8 proviral elements (76 vs. 40) and fewer solo long terminal repeats (LTR) (0 vs. 5) than humans. These results suggested that chimpanzee genome activity is less than the human genome and that humans may have a better ability to shape and screen integrated proviral elements. Our work is informative in both an evolutionary and a functional context for ERVs.

PHACTR1 promotes the mobility of papillary thyroid carcinoma cells by inducing F-actin formation.

Papillary thyroid carcinoma (PTC) limits effective biomarkers for predicting prognosis and targeted therapy. Phosphatase and actin regulator 1 (PHACTR1) is a mobility-promoting molecule due to its regulation on F-actin formation, which is valuable for the investigation of PTC. Our study aimed to investigate the relationship between PHACTR1 and PTC carcinogenesis, especially mobility. Our results displayed that PHACTR1 expression was elevated in metastatic or larger PTC tissues. In addition, PTC cells K1 with more obvious mobility had higher PHACTR1 expression whereas weakly mobile cells TPC-1 was contrary. Moreover, PHACTR1 silencing inhibited the invasion, migration and tumorigenicity of K1 cells, while PHACTR1 overexpression promoted the invasion, migration and tumorigenicity in TPC-1 cells. Furthermore, PHACTR1 overexpression increased the fluorescent intensity of F-actin in TPC-1 cells. Importantly, the enhanced invasion and migration in TPC-1 cells caused by PHACTR1 overexpression were significantly reversed by the disruption of F-actin assembly with swinholide A. In conclusion, PHACTR1 can promote the mobility of PTC cells, which results in the carcinogenesis of PTC. PHACTR1-regulated F-actin formation determines the mobility of PTC cells. Therefore, PHACTR1 can function as a potential biomarker for predicting prognosis and targeting therapy in PTC.

The Pro-Tumor Biological Function of IL-36α Plays an Important Role in the Tumor Microenvironment of HCC.

Purpose: To investigate the role of IL-36 in the tumorigenesis of hepatocellular carcinoma (HCC). IL-36 composed of a natural antagonist (IL-36Ra) and three agonists (IL-36α, -ß, -γ) that stimulate inflammation by binding to a common receptor consisting of IL-36R and IL-1RAcP. HCC is a common malignancy associated with high morbidity and mortality, often diagnosed at later stages. Although the exact role of IL-36α in HCC remains controversial, it is hypothesized that it may play a significant role in the development and progression of this cancer. Materials and Methods: In the current study, we measured both circulating and intrahepatic levels of IL-36α from HCC patients and healthy controls, using ELISA. The association between IL-36 and the differentiation of HCC was determined. Furthermore, the role IL-36 in both HCC and non-HCC cell lines was evaluated in vitro. Results: Circulating and intra-hepatic IL-36α was inversely correlated with differentiation of HCC, suggesting that IL-36α contribute to protection during the development of HCC. Based on bioinformatics, miR-27b-3p is closely related to downstream IL-36α. Thus, we determined miR-27b-3p expression in HCC tissues, showing upregulated miR-27b-3p was inversely correlated with IL-36α in HCC, perhaps via CXCL1 in HCC cells. It was confirmed that IL-36α inhibited HCC proliferation, viability and migration in vitro, consistent with reduced the expression of cytokines IL-1ß, IL-18, implying that IL-36α inhibited the possible involvement of pyroptosis. Conclusion: Our data suggests that IL-36α may be a potential therapeutic target and a prediction biomarker for the management of HCC.

An Uncommon Cause of Acute Chest Pain.

This case report describes a patient in their 50s with 20 minutes of substernal chest pain radiating to the left shoulder and back, which was accompanied by shortness of breath and sweating.

Irradiance penetration distribution and flashing light frequency simultaneously affected with microalgal cell absorption and CO2 bubble scattering in a raceway pond.

In order to investigate light penetration and flashing light frequency for microalgal cell-CO2 bubble culture system in a raceway pond, user-defined function for CO2 mass transfer and bubble scattering models coupled with discrete ordinates radiation model were adopted to clarify simultaneous effects of microalgal cell absorption and CO2 bubble scattering. Light intensity along the microalgal suspension depth attenuated more rapidly with increased biomass concentration, decreased bubble generation diameter, increased CO2 gas content and incident light intensity. Ratio of light zone decreased from 81.13 % to 20.00 % when biomass concentration increased from 0 to 0.4 g/L because of light absorption and shading effects of microalgae. When bubble generation diameter increased from 0.1 to 1.6 mm, ratio of light zone increased from 37.95 % to 42.64 %, while microalgal flashing light cycle first decreased to a valley of 1.81 s at 0.8 mm and then increased. Local light intensity in the upper layers was more enhanced due to lots of CO2 bubbles gathering and reflecting more light with decreased bubble diameter and increased gas content. Light attenuated more rapidly in microalgal suspension with decreased bubble generation diameter and increased CO2 gas content because of increased bubble diffraction coefficient and contact area. When initial CO2 volume fraction increased from 0.02 to 0.2, flashing light frequency of microalgal cells decreased from 0.55 to 0.29 Hz and light zone time ratio φ decreased from 36.90 % to 18.40 %. At a biomass concentration of 0.1 g/L and a bubble flow rate of 0.1 m/s, the maximum light penetration and microalgal growth rate was achieved when bubble diameter, incident light intensity and gas content were optimally at 0.8 mm, 200 W/m2 and 0.02, respectively. This work provides data support and theoretical guidance for photobioreactor design and optimization of light energy utilization.

TAT-Beclin 1 represses the carcinogenesis of DUSP4-positive PTC by enhancing autophagy.

BACKGROUND: DUSP4 is a pro-tumorigenic molecule of papillary thyroid carcinoma (PTC). DUSP4 also exists as an autophagic regulator. Moreover, DUSP4, as a negative regulator of MAPK, can prevent Beclin 1 from participating in autophagic response. This study aimed to explore whether TAT-Beclin 1, a recombinant protein of Beclin 1, could inhibit the tumorigenesis of DUSP4-positive PTC by regulating autophagy. METHODS: First, we divided PTC tissues into three groups according to DUSP4 expression levels by immunohistochemical analyses, and evaluated the relationship between autophagic molecules (Beclin 1 and LC3II) and DUSP4 using Western blotting assays. After overexpression of DUSP4 by lentiviral transduction, the in vitro and in vivo roles of TAT-Beclin 1 on DUSP4-overexpressed PTC cells were assessed (including autophagic activity, cell survival and function, and tumor growth). The roles of TAT-Beclin 1 in the survival of DUSP4-silenced PTC cells were also evaluated. RESULTS: Our results showed that the expression levels of autophagic proteins decreased with the increase of DUSP4 expression in PTC tissues. In PTC cells, DUSP4 overexpression-inhibited autophagic activity (including Beclin 1 expression, LC3 conversion rate and LC3-puncta formation) and -promoted cell proliferation and migration were reversed by TAT-Beclin 1 administration. In vivo assays also showed that DUSP4-overexpressed PTC cells had stronger tumorigenic ability and weaker autophagic activity, which was blocked by TAT-Beclin 1 administration. CONCLUSION: TAT-Beclin 1, as an autophagic promoter, could repress the carcinogenesis of DUSP4-positive PTC, which implies that the use of TAT-Beclin 1 for the PTC patients' treatment might be determined according to the DUSP4 level in their tumors.

Using Iron Tailings for Phosphate Removal in Cemented Phosphogypsum (PG) Backfill.

Compared with the post-treatment of pollutants, such as the removal of phosphate from wastewater, it is more important to develop effective emission control strategies to reduce phosphate pollution. Phosphogypsum (PG) is a typical solid waste byproduct of phosphate production and contains high amounts of residual phosphate. In order to control the phosphate emissions during the recycling of PG aggregates for cemented backfill, another solid waste product­iron tailings (ITs)­was added during the preparation of backfill slurry. The results showed that the ITs effectively accelerated the phosphate removal in cemented PG backfill, enabling the quick reduction in the phosphate concentration to the discharge standard (<0.5 mg/L) within 15 min. This means that the emissions of phosphate to bleeding water were effectively controlled. The adsorption experiment showed that phosphate was adsorbed by the ITs, and the adsorption data fitted well with the Langmuir adsorption model (R2 = 0.98) and pseudo-second-order kinetic model (R2 = 0.99), indicating that the phosphate adsorption of ITs was a monolayer chemical adsorption. Furthermore, an unconfined compressive strength (UCS) test was performed on the backfill with the addition of ITs. Compared to the control group (without ITs), the UCS of backfill with 20% ITs increased from 1.08 MPa to 1.33 MPa, indicating that the addition of solid waste could be beneficial to the strength development of the backfill by mitigating the interference of phosphate with the hydration process. The backfill cured for 28 d was selected for the toxic leaching test, and the phosphate concentration in the leachates was always below 0.02 mg/L, indicating that ITs can effectively immobilize phosphate in backfill for a long time.

[Research Progress of Pharmacological Therapy and Nutritional Support for Cachexia 
in Lung Cancer Patients].

Cachexia is a common complication in patients with lung cancer. It aggravates the toxic and side effects of chemotherapy, hinders the treatment plan, weakens the responsiveness of chemotherapy, reduces the quality of life, increases complications and mortality, and seriously endangers the physical and mental health of patients with lung cancer. The causes and pathogenesis of tumor cachexia are extremely complex, which makes its treatment difficult and complex. Controlling cachexia in lung cancer patients requires many means such as anti-tumor therapy, inhibition of inflammatory response, nutritional support, physical exercise, and relief of symptoms to exert the synergistic effect of multimodal therapy against multiple mechanisms of tumor cachexia. To date, there has been a consensus within the discipline that no single therapy can control the development of cachexia. Some therapies have made some progress, but they need to be implemented in combination with multimodal therapy after fully assessing the individual characteristics of lung cancer patients. This article reviews the application of drug therapy and nutritional support in lung cancer patients, and looks forward to the research direction of cachexia control in lung cancer patients.
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MiR-379-5p inhibits the proliferation, migration, and invasion of breast cancer by targeting KIF4A.

BACKGROUND: Many studies have shown that microRNAs (miRNAs) play an essential role in gene regulation and tumor development. This study aimed to explore the expression of miR-379-5p and its mechanisms of affecting proliferation, migration, and invasion in breast cancer (BC). METHODS: MiRNAs and mRNAs expression data of BC and normal breast tissue samples were downloaded from the TCGA and GEO databases. qRT-PCR was used to detect the expression of miR-379-5p in human normal breast epithelial cell lines and human BC cell lines. The proliferation ability of transfected cells was detected by colony formation and EdU assays. The mobility and invasion ability of transfected cells was measured by wound healing and transwell assays. The relative protein expression of transfected cells was detected by western blot. Dual luciferase reporter assay was performed to identify the targeted binding of miR-379-5p and KIF4A. RESULTS: MiR-379-5p was lowly expressed in BC tissue samples and BC cell lines. The target genes of miR-379-5p were involved in many cancer-related signaling pathways. PPI analysis and the cytoHubba algorithm of Cytoscape identified 10 genes as the hub genes. Survival analysis showed that only KIF4A expression in 10 hub genes was significantly associated with the prognosis of BC patients and was significantly upregulated in BC. Overexpression of miR-379-5p inhibited proliferation, migration, and invasion in the BC cell line MDA-MB-231, which could be reversed by KIF4A. CONCLUSIONS: MiR-379-5p inhibits proliferation, migration, and invasion of BC by targeting KIF4A.

miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis.

BACKGROUND: The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of aerobic glycolysis. miR-183-5p, an oncogenic miRNA, is highly expressed in HCC, but the regulatory mechanism of miR-183-5p in migration, invasion and aerobic glycolysis in HCC remains unclear. PURPOSE: To elucidate whether miR-183-5p affects aerobic glycolysis to regulate the migration and invasion of HCC, and to explore its regulatory mechanism. METHODS: We attempted to observe the effects of miR-183-5p on the migration and invasion of HepG2 cells by a wound-healing assay and Transwell assays. The effect of miR-183-5p on glycolysis was determined by glucose uptake and lactate generation. Western blot and qPCR were used to detect the relevant proteins and miRNA expression. RESULTS: Our results show that miR-183-5p promoted migration and invasion, enhanced glycolysis via increasing glucose uptake and lactate generation, and up-regulated glycolysis-related gene (PKM2, HK2, LDHA, GLUT1) expression in HepG2 cells. Further experiments indicated that miR-183-5p could decrease PTEN expression, but increased Akt, p-Akt and mTOR expression in HepG2 cells. CONCLUSION: These findings suggest that miR-183-5p may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/mTOR signaling.

miR­122­5p suppresses the oncogenesis of PTC by inhibiting DUSP4 expression.

MicroRNAs (miRNAs or miRs) play an important role in regulating the occurrence and development of papillary thyroid carcinoma (PTC). miR­122­5p is widely considered a tumour inhibitor, which has not been fully explored in PTC. Bioinformatics analysis identified dual specificity phosphatase 4 (DUSP4), a tumour promoter gene for PTC, as a downstream target of miR­122­5p. The aim of the present study was to investigate the role and molecular mechanism of miR­122­5p in PTC oncogenesis. In this study, the expression pattern of miR­122­5p in PTC cancer tissues and PTC cell lines was investigated via reverse transcription­quantitative PCR. Furthermore, the roles of miR­122­5p in PTC were explored using gain­of­function and loss­of­function assays. The results revealed that the expression of miR­122­5p was significantly lower in PTC cancer tissues, especially in cancer tissues with significant invasion or metastasis. Overexpression of miR­122­5p caused by miR­122­5p mimics inhibited the proliferation, invasion, and migration of the PTC cell line K1, while knockdown of miR­122­5p by miR­122­5p inhibitors exhibited the opposite effect. Furthermore, in vivo assays revealed that miR­122­5p overexpression inhibited tumour growth. In addition, miR­122­5p was negatively correlated with DUSP4 expression in PTC cancer tissues. miR­122­5p overexpression inhibited DUSP4 expression in K1 cells, while miR­122­5p downregulation produced the inverse effect. Specifically, a luciferase reporter assay confirmed the binding sites of miR­122­5p on the 3'­UTR of DUSP4, demonstrating the targeting effect of miR­122­5p on DUSP4. miR­122­5p inhibited the oncogenesis of PTC by targeting DUSP4, revealing the potential application value of miR­122­5p in the diagnosis and treatment of PTC.

Orange light spectra filtered through transparent colored polyvinyl chloride sheet enhanced pigment content and growth of Arthrospira cells.

Microalgae are significantly affected by the spectra composition with various wavelengths. The development of light harvesting pigments can be controlled with specific wavelength of filtered light received by microalgae. Coverage of open raceway pond using transparent colored polyvinyl chloride sheets (PVCS) to filter light spectra, was assessed for the capacity to enhance biomass growth rate. Results showed that orange PVCS filtered light spectra at wavelengths from 480 to 665 nm, increased biomass dry weight (3.3 g/L) by 61% compared with control condition (white PVCS = 350-750 nm). Light spectra filtered through orange PVCS were more easily absorbed by the light harvesting pigment protein complex (phycobilisome) of Arthrospira platensis cells and subsequently transferred to intracellular photosynthesis reaction centers. Therefore, A. platensis cells cultivated with light spectra filtered through orange PVCS contained 62.7 mg/L chlorophyll-a and 23.5 mg/L carotenoid, which were 40% and 29% higher than control condition (with white PVCS).

Developing staggered woven mesh aerator with three variable-micropore layers in recycling water pipeline to enhance CO2 conversion for improving Arthrospira growth.

A staggered woven mesh (SWM) aerator equipped with three variable-micropore layers was developed to enhance the CO2 conversion into HCO3- in a recycling water pipeline for promoting CO2 utilization efficiency and Arthrospira growth in large-scale raceway ponds. The input CO2 gas was broken into smaller bubbles (0.78- 2.43 mm) through the first-stage shear with axial rectangles, second-stage shear with radial rectangles (equivalent pore diameter = 150 µm), and third-stage shear with uniform micropores. A high-speed camera (MotionXtra HG-100K CMOS) and an Image J image processing software were employed to capture the bubble pictures. Compared to the traditional steel pipe (TSP) aerator, the bubble generation diameter and time in the SWM aerator reduced by 72.3% and 48.6%, respectively. The optimized structure (ε = 14, pore = 23 µm) of the SWM aerator promoted the carbonization efficiency and HCO3- conversion efficiency into biomass by 78.6% and 64.6% than the TSP aerator. Further, the chlorophyll fluorescence and biomass measurements showed an increase in the actual photochemical efficiency (analyzed by Hansatech FMS1 chlorophyll fluorescence instrument) and biomass yield by 1.8 times and 80.1%.

SQR mediates therapeutic effects of H2S by targeting mitochondrial electron transport to induce mitochondrial uncoupling.

Hydrogen sulfide (H2S) is a gasotransmitter and a potential therapeutic agent. However, molecular targets relevant to its therapeutic actions remain enigmatic. Sulfide-quinone oxidoreductase (SQR) irreversibly oxidizes H2S. Therefore, SQR is assumed to inhibit H2S signaling. We now report that SQR-mediated oxidation of H2S drives reverse electron transport (RET) at mitochondrial complex I, which, in turn, repurposes mitochondrial function to superoxide production. Unexpectedly, complex I RET, a process dependent on high mitochondrial membrane potential, induces superoxide-dependent mitochondrial uncoupling and downstream activation of adenosine monophosphate-activated protein kinase (AMPK). SQR-induced mitochondrial uncoupling is separated from the inhibition of mitochondrial complex IV by H2S. Moreover, deletion of SQR, complex I, or AMPK abolishes therapeutic effects of H2S following intracerebral hemorrhage. To conclude, SQR mediates H2S signaling and therapeutic effects by targeting mitochondrial electron transport to induce mitochondrial uncoupling. Moreover, SQR is a previously unrecognized target for developing non-protonophore uncouplers with broad clinical implications.

Mitochondrial Uncouplers Confer Protection by Activating AMP-Activated Protein Kinase to Inhibit Neuroinflammation Following Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is a disease with high disability and mortality rates. Currently, the efficacy of therapies available for ICH is limited. Microglia-mediated neuroinflammation substantially exacerbates brain damage following ICH. Here, we investigated whether mitochondrial uncouplers conferred protection by suppressing neuroinflammation following ICH. To mimic ICH-induced neuroinflammation in vitro, we treated microglia with red blood cell (RBC) lysate. RBC lysate enhanced the expression of pro-inflammatory cytokines in microglia. A clinically used uncoupler, niclosamide (Nic), reduced the RBC lysate-induced expression of pro-inflammatory cytokines in microglia. Moreover, Nic ameliorated brain edema, decreased neuroinflammation, and improved neurological deficits in a well-established mouse model of ICH. Like niclosamide, the structurally unrelated uncoupler carbonyl cyanide p-triflouromethoxyphenylhydrazone (FCCP) reduced brain edema, decreased neuroinflammation, and improved neurological deficits following ICH. It has been reported that mitochondrial uncouplers activate AMP-activated protein kinase (AMPK). Mechanistically, Nic enhanced AMPK activation following ICH, and AMPK knockdown abolished the beneficial effects of Nic following ICH. In conclusion, mitochondrial uncouplers conferred protection by activating AMPK to inhibit microglial neuroinflammation following ICH.

Enhanced production of volatile fatty acids by adding a kind of sulfate reducing bacteria under alkaline pH.

Anaerobic digestion could make sludge stable and harmless, and the volatile fatty acids (VFAs) produced from it. The objective of this study was to reduced sludge production and realize the resource utilization of VFAs through enhance anaerobic sludge fermentation by adding sulfate reducing bacteria (SRB) under alkaline pH. Under the neutral and alkaline pH, SRB was added into the sludge fermentation liquid with sole stock solution and sterilization treatment respectively, while the liquid without any additives was used as control. The results indicated that obvious increase of the production of VFAs was observed after adding SRB under alkaline pH. And, more protein and polysaccharide were obtained which were the main substrates for the production of VFAs. The concentration of ammonia nitrogen (NH4+-N) and phosphate (PO43--P) were also increased with the addition of SRB. So, a high yield production of VFAs could be achieved through the addition of SRB + alkaline pH.

Development of a single helical baffle to increase CO2 gas and microalgal solution mixing and Chlorella PY-ZU1 biomass yield.

A single helical baffle (SHB), consisting of twisted turns, was developed to convert straight flow into spiral flow in a Chlorella PY-ZU1 open raceway pond (ORWP) bubbled with 15% CO2. Microalgal solution flowing through the SHB alternative helical interspaces generated whirling flow both vertically and horizontally, which decreased mixing and increased mass transfer rates. The optimized SHB had a pitch length to total SHB length ratio of 0.13 and SHB diameter to ORWP single channel width ratio of 0.30, which decreased mixing times and increased mass transfer coefficients by 41.1% and 38.4% respectively. SHB moved Chlorella PY-ZU1 from the ORWP bottom to the top, increasing light exposure for photosynthesis. Cellular electron transfer rates and photochemical efficiency (φPSII) increased by 18%, chlorophyll a content increased by 16% and variable to maximum fluorescence ratio increased by 13%. The microalgal biomass of SHB ORWP was 23% higher than that of conventional ORWP.

Three-dimensional numerical simulation of light penetration in an optimized flow field composed of microalgae cells, carbon dioxide bubbles and culture medium.

In order to evaluate light penetration and its influence on microalgae growth in a raceway pond with alternatively permutated conic baffles (RWP-APCB), 3D numerical simulation of light penetration was performed using computational fluid dynamics in an optimized flow field composed of microalgae cells, CO2 bubbles and culture medium. Results showed that light intensity in the culture medium attenuated faster in accordance with solution depth, with increased microalgae cell concentration, increased bubble volume fraction and decreased CO2 bubble diameter. Light zone fraction (i.e. ratio of light zone length to solution depth) increased with promoted incident irradiation. It was found that around 75% of microalgae cells were distributed in light zone and non-photochemical quenching coefficient of microalgae decreased by 32% in RWP-APCB. This resulted in a 16% increase of the Chlorella pyrenoidosa biomass growth rate, to 0.36 g/L/d.

Self-rotary propellers with clockwise/counterclockwise blades create spiral flow fields to improve mass transfer and promote microalgae growth.

In this work, self-rotary propellers (SRPs) with clockwise/counterclockwise blades were investigated to create spiral flow fields without external power to strengthen gas-liquid mixing and promote microalgal growth in an open raceway pond. The rotational flow around the propellers and spiral flow between the propellers generated extensive wall shear stress in three dimensions. Four-clockwise blades on the propellers exerted better mixing than three-counterclockwise blades. The bubble generation diameter was reduced by 69% and the mass transfer coefficient increased by 49% when the propeller diameter was increased from 32 to 60 mm. The photochemical efficiency (φPSII) of Arthrospira platensis cells was enhanced by 25%, while the helix pitch and trichome lengths were enlarged by 7-16%. Self-rotary propellers (60 mm diameter) with four-clockwise blades enhanced the growth rate of A. platensis biomass by 35% compared to that in an unmodified raceway pond without propellers.