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Various miRNAs have been shown to participate in the tumor progression and development of colorectal cancer (CRC). However, the role of miR-3913-5p in CRC are yet to be clearly defined. In the present study, we determine that miR-3913-5p is downregulated in CRC cell lines and CRC tissues. Exogenous miR-3913-5p expression weakens the CRC cells growth, migration and invasion. Mechanistically, miR-3913-5p directly targets the 3'UTR of CREB5. Overexpression of CREB5 reverses the suppression of CRC cells proliferation, migration and invasion induced by miR-3913-5p. Furthermore, ATF2 negatively regulates the transcription of miR-3913-5p by binding to its promoter. CREB5 can cooperate with ATF2. CREB5 is required for ATF2 in regulating miR-3913-5p. Finally, inverse correlations can be found between the expressions of miR-3913-5p and CREB5 or ATF2 in CRC tissues. Thus, a plausible mechanism of ATF2/miR-3913-5p/CREB5 axis regulating CRC progression is elucidated. Our findings suggest that miR-3913-5p functions as a tumor suppressor in CRC. ATF2/miR-3913-5p/CREB5 axis might be a potential therapeutic target against CRC progression. The miRNA miR-3913-5p inhibits colorectal cancer cell proliferation, migration and invasion, in concert with its regulation of and by CREB5 and ATF2. [ABSTRACT FROM AUTHOR]

Previous reports have shown that histone deacetylase inhibitors (HDACi) can alter miRNA expression in a range of cancers. Both the 5p-arm and 3p-arm of mature miRNAs can be expressed from the same precursor and involved in cancer progress. Nevertheless, the detailed mechanism by which vorinostat (SAHA), a HDACi, triggers miR-769-5p/miR-769-3p-mediated suppression of proliferation and induces apoptosis in gastric cancer (GC) cells remains elusive. Here, we showed that the miRNA-seq analysis of GC cells treated with SAHA identified seven differentially expressed miRNAs with both strands of the miRNA duplex. miR-769-5p/miR-769-3p expression was downregulated in GC tissues compared with normal tissues. Functionally, high expression of miR-769-5p/miR-769-3p blocked the malignant abilities of GC cells. Mechanistically, miR-769-5p/miR-769-3p targeted IGF1R and IGF1R overexpression rescued the effects of miR-769-5p/miR-769-3p on GC cells growth and metastasis. Moreover, STAT3 bound to the promoter of miR-769. Furthermore, miR-769-5p/miR-769-3p expression was negatively regulated by the STAT3-IGF1R-HDAC3 complex. Besides, miR-769-5p/miR-769-3p synergized with SAHA to promote GC cells apoptosis. Our studies suggest that miR-769-5p/miR-769-3p acts as a tumor suppressor by the STAT3-IGF1R-HDAC3 complex. Moreover, SAHA triggers miR-769-5p/miR-769-3p-mediated inhibition of proliferation and induces apoptosis in GC cells. [ABSTRACT FROM AUTHOR]

In this article, we have proposed and demonstrated a sensing interrogation scheme of microwave photonic filter (MPF) based on multi‐wavelength fiber laser (MWFL). A Mach‐Zehnder interferometer (FMZI) acts as the wavelength selective component in the laser cavity as well as the sensing element. An erbium doped fiber amplifier (EDFA) and a semiconductor optical amplifier (SOA) are employed as hybrid gain medium to suppress the homogeneous broadening of erbium doped fiber. The MWFL is employed as the optical source to implement the MPF together with a dispersive medium. The free spectrum range of interference pattern of the FMZI changes with the temperature variation, thus changing the central frequency of MPF's passbands. The sensitivities are −12.23 and 6.11 MHz/°C, respectively, when the sensing optical fiber with the length of 2.2 and 1.1 m are used. [ABSTRACT FROM AUTHOR]

In this article, we have proposed and demonstrated a new approach to implementing microwave photonic filter (MPF) with switchable, tunable and reconfigurable passbands based on a multi-wavelength fiber laser (MWFL) cooperating with a fiber Mach–Zehnder interferometer (FMZI). An EDFA and an SOA have been employed as a hybrid gain medium in the laser cavity, to suppress the homogeneous broadening of EDF. By inserting the FMZI in the fiber laser cavity, MWFL with tunable and switchable wavelength spacing has been achieved, which can be used as the multi-wavelength optical source to implement switchable, tunable and reconfigurable MPF together with a dispersive medium. By tuning the length of variable optical delay line (VODL), the wavelength spacing of the MWFL can be changed, and thus the passband's central frequency of the MPF. By adjusting the polarization states, gain of EDFA or SOA of the laser cavity, the shape of the laser output can be adjustable, and as a result, shape-adjustable passbands of the MPF have been realized. By introducing the reflective FMZI structure as the wavelength selective component and carefully adjusting the polarization states, half number of the passband can be suppressed, which means the MPF can be switchable. The proposed MPF exhibits shape-adjustable and switchable passbands and enjoys more flexibility compared to previous methods. [ABSTRACT FROM AUTHOR]

• MFC signals with four switchable frequencies have been generated, which can be switched by simply rotating the PC. • By cascading a dual-loop structure, MFC signals with supermode noise suppression can be obtained. • By applying the longer length of the PMFs, the higher switchable central frequency of the MFC can be achieved. In this paper, we propose and experimentally demonstrate a flexibly frequency switchable active mode-locking optoelectronic oscillator (FSAML-OEO) in which a multi-passband microwave photonic filter (MPF) with two polarization-maintaining fibers (PMF) based Solc-Sagnac interferometer is used. Microwave frequency combs (MFCs) signals with four switchable central frequencies of 217 MHz, 453 MHz, 662 MHz and 1101 MHz are generated by controlling the polarization state of the Sagnac interferometer via rotating the polarization controller (PC). By cascading a dual-loop structure, MFCs signals with adjustable comb spacing of 1 MHz, 3 MHz, and 5 MHz are obtained with fundamental and harmonic FSAML-OEO, in which the supermode noise suppression ratios of the dominate modes and the super-modes are measured to be about 30 dB. [ABSTRACT FROM AUTHOR]

• A dual channel photonic crystal fiber is proposed for dual-parameter sensing. • The gold is coated on the outer surface of the sensor to measure the salinity. • The polydimethylsiloxane is coated on the half-side of the surface of the sensor. • The temperature sensitivity is −4.937 nm/°C in the sensing range from 25 °C to 50 °C. • The salinity sensitivity is 0.307 nm/‰ in the sensing range from 0‰ to 100‰. A novel half-side PDMS-coated photonic crystal fiber (PCF) sensor based on surface plasmon resonance (SPR) is proposed for simultaneous detection of seawater salinity and temperature. The plasmonic material gold is coated on the outer surface of the PCF to measure the seawater salinity by exciting SPR effect. Moreover, the polydimethylsiloxane (PDMS) layer is coated on the upper half-side of the surface of the sensor as an independent temperature sensing channel. The properties of modes coupling between surface plasmon polaritons (SPPs) mode and four different core modes are investigated. Meanwhile, the influence of various geometrical parameters on the sensing characteristics are theoretically simulated by using finite element method (FEM). The numerical results show that the salinity sensitivity of the designed sensor can reach 0.307 nm/‰ with a resolution of 0.3257‰. Additionally, the temperature sensitivity of −4.937 nm/°C with the resolution of 0.0203 °C in the sensing range from 25 °C to 50 °C has been obtained. The proposed sensor, possessing advantages such as ease of fabrication, excellent sensing performance and low cost, not only realizes the simultaneous measurement of two parameters, but also has potential in the field of seawater monitoring. [ABSTRACT FROM AUTHOR]

Background: The transcription factor HOXD9 is one of the members of the HOX family, which plays an important role in neoplastic processes. However, the role of HOXD9 in the growth and metastasis of gastric cancer (GC) remains to be elucidated. Methods: In vitro functional role of HOXD9 and RURY3 in GC cells was determined using the TMA-based immunohistochemistry, western blot, EdU incorporation, gelatin zymography, luciferase, chromatin Immunoprecipitation (ChIP) and cell invasion assays. In vivo tumor growth and metastasis were conducted in nude mice. Results: HOXD9 is overexpressed in GC cells and tissues. The high expression of HOXD9 was correlated with poor survival in GC patients. Functionally, HOXD9 expression significantly promoted the proliferation, invasion and migration of GC cells. Mechanically, HOXD9 directly associated with the RUFY3 promoter to increase the transcriptional activity of RUFY3. Inhibition of RUFY3 attenuated the proliferation, migration and invasiveness of HOXD9-overexpressing GC cells in vitro and in vivo. Moreover, both HOXD9 and RUFY3 were highly expressed in cancer cells but not in normal gastric tissues, with their expressions being positively correlated. Conclusions: The evidence presented here suggests that the HOXD9-RUFY3 axis promotes the development and progression of human GC. [ABSTRACT FROM AUTHOR]

Background: In the post-pandemic era, a wide range of COVID-19 sequelae is of growing health concern. However, the risks of digestive diseases in long COVID have not been comprehensively understood. To investigate the long-term risk of digestive diseases among COVID patients. Methods: In this large-scale retrospective cohort study with up to 2.6 years follow-up (median follow-up: 0.7 years), the COVID-19 group (n = 112,311), the contemporary comparison group (n = 359,671) and the historical comparison group (n = 370,979) predated the COVID-19 outbreak were built using UK Biobank database. Each digestive outcome was defined as the diagnosis 30 days or more after the onset of COVID-19 infection or the index date. Hazard ratios (HRs) and corresponding 95% confidence intervals (CI) were computed utilizing the Cox regression models after inverse probability weighting. Results: Compared with the contemporary comparison group, patients with previous COVID-19 infection had higher risks of digestive diseases, including gastrointestinal (GI) dysfunction (HR 1.38 (95% CI 1.26 to 1.51)); peptic ulcer disease (HR 1.23 (1.00 to 1.52)); gastroesophageal reflux disease (GERD) (HR 1.41 (1.30 to 1.53)); gallbladder disease (HR 1.21 (1.06 to 1.38)); severe liver disease (HR 1.35 (1.03 to 1.76)); non-alcoholic liver disease (HR 1.27 (1.09 to 1.47)); and pancreatic disease (HR 1.36 (1.11 to 1.66)). The risks of GERD were increased stepwise with the severity of the acute phase of COVID-19 infection. Even after 1-year follow-up, GERD (HR 1.64 (1.30 to 2.07)) and GI dysfunction (HR 1.35 (1.04 to 1.75)) continued to pose risks to COVID-19 patients. Compared to those with one SARS-CoV-2 infection, reinfected patients were at a higher risk of pancreatic diseases (HR 2.57 (1.23 to 5.38)). The results were consistent when the historical cohort was used as the comparison group. Conclusions: Our study provides insights into the association between COVID-19 and the long-term risk of digestive system disorders. COVID-19 patients are at a higher risk of developing digestive diseases. The risks exhibited a stepwise escalation with the severity of COVID-19, were noted in cases of reinfection, and persisted even after 1-year follow-up. This highlights the need to understand the varying risks of digestive outcomes in COVID-19 patients over time, particularly those who experienced reinfection, and develop appropriate follow-up strategies. [ABSTRACT FROM AUTHOR]

Previous studies have shown an association between coiled-coil domain-containing (CCDC) genes and different cancers. Our previous studies revealed that CCDC43 is highly expressed in colorectal cancer, but the expression and molecular mechanisms of CCDC43 in gastric cancer (GC) are yet to be determined. Here, we show that CCDC43 is overexpressed in gastric tissues. CCDC43 expression is closely related to tumor differentiation, lymph-node-metastasis, and prognosis of gastric cancer. Overexpression of CCDC43 promotes the proliferation, invasion, and metastasis of GC cells. CCDC43 may upregulate and stabilize ADRM1, resulting in the construction of the ubiquitin-mediated proteasome. In contrast, inhibition of ADRM1 could reverse the function of CCDC43 in GC both in vitro and in vivo. Our data demonstrate that transcription factor YY1 directly binds to CCDC43 and ADRM1 gene promoters, leading to over-expression of CCDC43 and ADRM1. Furthermore, in vitro experiments demonstrate that knock down of CCDC43 or ADRM1 attenuates the YY1-mediated malignant phenotypes. Finally, the association among YY1, CCDC43 and ADRM1 is validated in clinical samples. Our findings suggest that the CCDC43-ADRM1 axis regulated by YY1, promotes proliferation and metastasis of GC, and the axis may be a potential therapeutic target for GC. [ABSTRACT FROM AUTHOR]

In this paper, a structured light vision measurement method using a scanning laser line and a positioning laser line is proposed. The novel method enables the scanning laser plane to slide along a slide rail while maintaining intersection with the positioning laser plane, eliminating the need to determine the scanning direction and moving step. During the measurement process, the laser plane equations need to be recalibrated for each new position, so a real-time calibration method is given. Initially, the geometric barycenter method is employed to detect the subpixel coordinates of the light stripe intersection point. Subsequently, these coordinates are projected into the camera coordinate system using the initial equations of the positioning laser plane. Finally, leveraging the normal information of the initial equation of the scanning laser plane and the three-dimensional coordinates of the light stripe intersection point, the real-time calibration of the scanning laser plane equations can be accomplished. The proposed method enables the three-dimensional reconstruction of objects, and its accuracy is verified through measurements on gauge blocks. Experimental results demonstrate that this method achieves precise and stable three-dimensional reconstruction of object surface shape. [ABSTRACT FROM AUTHOR]

A multi-line structured light measurement method that combines a single-line and a three-line laser, in which precision sliding rails and displacement measurement equipment are not required, is proposed in this paper. During the measurement, the single-line structured light projects onto the surface of an object and the three-line structured light remains fixed. The single-line laser is moved and intersects with the three-line laser to form three intersection points. The single-line light plane can be solved using the camera coordinates of three intersection points, thus completing the real-time calibration of the scanned light plane. The single-line laser can be scanned at any angle to determine the overall complete three-dimensional (3D) shape of the object during the process. Experimental results show that this method overcomes the difficulty of obtaining information about certain angles and locations and can effectively recover the 3D shape of the object. The measurement system's repetition error is under 0.16 mm, which is sufficient to measure the 3D shapes of complicated workpieces. [ABSTRACT FROM AUTHOR]

• A dual-parameter sensor based on four-core fiber (FCF) with a hybrid sensing mechanism is proposed. • The surface of FCF is covered with gold film to excite the SPR and MZI for measuring refractive index (RI) and temperature. • The proposed sensor exhibits a high RI sensitivity of 2091 nm/RIU and a temperature sensitivity of 0.0398 nm/°C. A dual-parameter sensor based on a hybrid sensing mechanism of surface plasmon resonance (SPR) and Mach–Zehnder interference (MZI) using a four-core fiber (FCF), is proposed and implemented. The designed sensor is fabricated by cascading a sandwich structure of the FCF, multimode fiber and lead-in/out single-mode fiber. The gold-coated FCF as the critical component, enabling the excitation of the SPR and MZI for measuring refractive index (RI) and temperature. The proposed sensor exhibits a high RI sensitivity of 2091 nm/RIU and a temperature sensitivity of 0.0398 nm/°C. The proposed dual-parameter sensor based on FCF provides a new insight for the design of fiber SPR sensor, which can be used to measure multiple physical parameters in various fields such as biochemistry, gene diagnosis, environmental monitoring, and so on. [ABSTRACT FROM AUTHOR]

• Balloon-like and waist-enlarged structures are proposed for RI and temperature measurement. • The sensor is constructed using single-mode optical fiber, which is simple and inexpensive. • The RI and temperature sensitivity of the proposed sensor can be up to 340.9 nm/RIU and −0.162 nm/°C, respectively. A balloon-like composite optical fiber interferometer, integrated with a waist-enlarged structure, is presented for measuring refractive index (RI) and temperature. The waist-enlarged fusion tapers (WEFTs) are spliced to the single-mode fiber (SMF) to form a Mach-Zehnder interferometer (MZI). Meanwhile, the WEFTs structure is curved into a balloon-like structure. When the two structures are integrated, a larger evanescent field is formed, which can interact with the external environment better. The experiment results indicate that the best sensitivity of RI and temperature can achieve 340.9 nm/RIU and −0.162 nm/℃, respectively. In addition, the interferometer is small, easy to manufacture, and can be widely applied in various measurement applications. [ABSTRACT FROM AUTHOR]

Purpose: Growing evidence indicates that aberrant expression of microRNAs contributes to tumor development. However, the biological role of microRNA-4490 (miR-4490) in gastric cancer (GC) remains to be clarified. Methods: To explore the function of miR-4490 in GC, we performed colony formation, EdU incorporation, qRT-PCR, Western blotting, in situ hybridization (ISH), immunohistochemistry (IHC), flow cytometry, ChIP and dual-luciferase reporter assays. In addition, the growth, migration and invasion capacities of GC cells were evaluated. Results: We found that miR-4490 was significantly downregulated in primary GC samples and in GC-derived cell lines compared with normal controls, and that this expression level was negatively correlated with GC malignancy. Exogenous miR-4490 expression not only reduced cell cycle progression and proliferation, but also significantly inhibited GC cell migration, invasion and epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, we found that miR-4490 directly targets USP22, which mediates inhibition of GC cell proliferation and EMT-induced metastasis in vitro and in vivo. Moreover, we found through luciferase and ChIP assays that transcription factor POU2F1 can directly bind to POU2F1 binding sites within the miR-4490 and USP22 promoters and, by doing so, modulate their transcription. Spearman's correlation analysis revealed a positive correlation between USP22 and POU2F1 expression and negative correlations between miR-4490 and USP22 as well as miR-4490 and POU2F1 expression in primary GC tissues. Conclusion: Based on our results we conclude that miR-4490 acts as a tumor suppressor, and that the POU2F1/miR-4490/USP22 axis plays an important role in the regulation of growth, invasion and EMT of GC cells. [ABSTRACT FROM AUTHOR]

Background: HOXD9, a Hox family member, is involved in cancer growth and metastasis. But, its regulation mechanism at the molecular level particularly in colorectal cancer (CRC), is mostly unknown. Methods: The HOXD9 protein expression levels were analyzed using immunofluorescence, immunohistochemistry (IHC) assays, and western blot. The in vivo and in vitro roles of HOXD9 in CRC were determined using colony formation and EdU incorporation, CCK‐8, wound scratch and transwell invasion assay, and animal models. Results: Expression of HOXD9 was higher in CRC than in matched healthy tissues. High expression of HOXD9 has significantly associated with the American Joint Committee on Cancer (AJCC) stages, tumor differentiation, lymph node metastasis, and other serious invasions, and it had a poor prognosis. In vitro, HOXD9 encouraged proliferation, movement and EMT processes in cells of CRC. Also, TGF‐β1 promoted the expression of HOXD9 and this effect was dependent on the dose and downregulation of HOXD9 repressed TGF‐β1 ‐induced EMT. In vivo, HOXD9 promoted the invasive and metastasis of CRC cells via orthotopic implantation. Conclusions: The ectopic expression of HOXD9 promoted the invasion metastasis in cells of the colorectal tumor by induction of EMT in vitro and vivo. [ABSTRACT FROM AUTHOR]

• A highly sensitive surface plasmon resonance (SPR) sensor based on seven-core photonic crystal fiber (SCPCF) is proposed. • The surface of SCPCF is covered with gold film as the sensing region for refractive index (RI) and temperature measurement. • Gold film covers SCPCF surface for RI sensing, with polydimethylsiloxane (PDMS) coating for temperature sensing on one part of the gold film. • The experiment results show that the RI sensitivity and temperature sensitivity of the proposed sensor reach 1644 nm/RIU and −2.59 nm/°C, respectively. A highly sensitive surface plasmon resonance (SPR) sensor based on seven-core photonic crystal fiber (SCPCF) is proposed and experimentally demonstrated for refractive index (RI) and temperature measurement. The dual-parameter sensor is fabricated by inserting an SCPCF between two multimode fibers (MMFs). The surface of SCPCF is covered with gold film as the sensing region. One part of the gold film is additionally coated with polydimethylsiloxane (PDMS) to enable temperature sensing, while the rest is used for RI sensing. The experiment results show that the RI sensitivity and temperature sensitivity of the proposed sensor reach 1644 nm/RIU and −2.59 nm/°C, respectively. Additionally, the SPR dual-parameter sensor based on SCPCF has good stability and repeatability, which has great application potential in the field of environmental monitoring, disease diagnosis, and biochemical sensing. [ABSTRACT FROM AUTHOR]

In human gastric cancer (GC), the upregulation of FOXK1 and vimentin is frequently observed in cancer cells and correlates with increased malignancy. We report that FOXK1 synergizes with vimentin to promote GC invasion and metastasis via the induction of epithelial-mesenchymal transition (EMT). We showed that higher expression levels of FOXK1 were significantly associated with GC development. FOXK1 can physically interact with and stabilize vimentin. Moreover, a positive correlation between the expression of FOXK1 and vimentin was found in GC cells. Higher expression levels of these two proteins were significantly associated with differentiation, lymph node metastasis, AJCC stage, and poorer prognosis. Furthermore, the coexpression of FOXK1 and vimentin enhances cell metastasis through the induction of EMT in GC cells. However, the siRNA-mediated repression of vimentin in FOXK1-overexpressing cells reversed the EMT-like phenotype and reduced GC cell migration and invasion in vitro and in vivo. Altogether, our findings suggest that the vimentin-FOXK1 axis provides new insights into the molecular mechanisms underlying EMT regulation during GC progression and metastasis. [ABSTRACT FROM AUTHOR]

The Editors-in-Chief therefore consider the data reported in this the article to be unreliable. Figure 4f: the AGS and BGC-823 panels for miR-4490/USP22 appear to partially overlap. [Extracted from the article]

The coiled-coil domain-containing protein 43 (CCDC43) is essential to promote gastric cancer (GC) proliferation and invasion, while four and a half LIM domains 1 (FHL1) involves GC cells apoptosis. We attempted to address inter-relationship between CCDC43 and FHL1 in modulating GC cells growth and apoptosis. Levels of protein expression were assessed by western blot, immunofluorescence. Using EdU, plate colony formation, Matrigel invasion and animal models, we evaluated the function in vitro and in vivo. Apoptosis was evaluated by flow cytometry and Hoechst 33258 staining. Reciprocal co-immunoprecipitation (co-IP) analyses indicated that CCDC43 physically interacted with FHL1. The expression of CCDC43 was negatively correlated with FHL1. Moreover, up-regulation of CCDC43 resulted in FHL1 level decline, and the reverse is also true. CCDC43 expressed jointly with FHL1 group significantly decreases the ability of the growth, metastasis and invasion of GC cells compared with that of the CCDC43 group. Furthermore, siRNA-mediated repression of CCDC43 results in dissociation from FHL1 and causes suppression of GC cell proliferation and metastasis. CCDC43 repression mediates the stability of FHL1 protein. In addition, CCDC43 interacts with FHL1. Knockdown of CCDC43 plus FHL1 overexpression inhibits proliferation and migration and induces apoptosis of GC cells in vitro and vivo. • CCDC43 interacts and colocates with FHL1 in GC. • The decrease of FHL1 by CCDC43 promotes the growth and migration of GC cells. • CCDC43 inhibits the stability of FHL1 protein and promotes apoptosis in GC cells. [ABSTRACT FROM AUTHOR]

Background: The deubiquitinating enzyme ubiquitin-specific protease 3 (USP3) plays a crucial role in numerous biological processes. The aberrant expression of USP3 may have an important role in tumor development. However, the mechanism by which USP3 promotes gastric cancer (GC) metastasis remains largely unknown. Methods: Effects of USP3 on the progression of GC in vivo and in vitro and the potential underlying mechanisms have been investigated utilizing proteomics, RT-PCR, western blotting, immunohistochemistry, immunofluorescence, cell invasion and migration assays and xenograft tumor models. Results: USP3 expression was upregulated in GC compared with matched normal tissues and was predictive of poor survival. USP3 also promoted migration and epithelial-to-mesenchymal transition (EMT) in GC cells. Moreover, TGF-β1 induced USP3 expression, and USP3 knockdown inhibited TGF-β1-induced EMT. Furthermore, we utilized Isobaric Tag for Relative and Absolute Quantitation (iTRAQ) to identify differentially expressed proteins in USP3-overexpressing cells compared with control cells. Importantly, we found that SUZ12 is indispensable for USP3-mediated oncogenic activity in GC. We observed that USP3 interacted with and stabilized SUZ12 via deubiquitination. SUZ12 knockdown inhibited USP3-induced migration and invasion, as well as EMT in GC cells. Examination of clinical samples confirmed that USP3 expression was positively correlated with SUZ12 protein expression and that the levels of USP3 or SUZ12 protein were negatively correlated with the levels of E-cadherin protein. Conclusions: These findings identify USP3 as a critical regulator. The USP3-SUZ12 axis might promote tumor progression and could be a potential therapeutic candidate for human GC. [ABSTRACT FROM AUTHOR]