Protocol of a parallel, randomized controlled trial on the effects of a novel personalized nutrition approach by artificial intelligence in real world scenario.

BACKGROUND: Nutrition service needs are huge in China. Previous studies indicated that personalized nutrition (PN) interventions were effective. The aim of the present study is to identify the effectiveness and feasibility of a novel PN approach supported by artificial intelligence (AI). METHODS: This study is a two-arm parallel, randomized, controlled trial in real world scenario. The participants will be enrolled among who consume lunch at a staff canteen. In Phase I, a total of 170 eligible participants will be assigned to either intervention or control group on 1:1 ratio. The intervention group will be instructed to use the smartphone applet to record their lunches and reach the real-time AI-based information of dish nutrition evaluation and PN evaluation after meal consumption for 3 months. The control group will receive no nutrition information but be asked to record their lunches though the applet. Dietary pattern, body weight or blood pressure optimizing is expected after the intervention. In phase II, the applet will be free to all the diners (about 800) at the study canteen for another one year. Who use the applet at least 2 days per week will be regarded as the intervention group while the others will be the control group. Body metabolism normalization is expected after this period. Generalized linear mixed models will be used to identify the dietary, anthropometric and metabolic changes. DISCUSSION: This novel approach will provide real-time AI-based dish nutrition evaluation and PN evaluation after meal consumption in order to assist users with nutrition information to make wise food choice. This study is designed under a real-life scenario which facilitates translating the trial intervention into real-world practice. TRIAL REGISTRATION: This trial has been registered with the Chinese Clinical Trial Registry (ChiCTR2100051771; date registered: 03/10/2021).

Revealing the Enhanced Thermoelectric Properties of Controllably Doped Donor-Acceptor Copolymer: The Impact of Regioregularity.

Albeit considerable attention to the fast-developing organic thermoelectric (OTE) materials due to their flexibility and non-toxic features, it is still challenging to design an OTE polymer with superior thermoelectric properties. In this work, two "isomorphic" donor-acceptor (D-A) conjugated polymers are studied as the semiconductor in OTE devices, revealing for the first time the internal mechanism of regioregularity on thermoelectric performances in D-A type polymers. A higher molecular structure regularity can lead to higher crystalline order and mobility, higher doping efficiency, order of energy state, and thermoelectric (TE) performance. As a result, the regioregular P2F exhibits a maximum power factor (PF) of up to 113.27 µW m-1  K-2 , more than three times that of the regiorandom PRF (35.35 µW m-1  K-2 ). However, the regular backbone also implies lower miscibility with a dopant, negatively affecting TE performance. Therefore, the trade-off between doping efficiency and miscibility plays a vital role in OTE materials, and this work sheds light on the molecular design strategy of OTE polymers with state-of-the-art performances.

Hybrid Photovoltaic/Thermoelectric Systems for Round-the-Clock Energy Harvesting.

Due to their emission-free operation and high efficiency, photovoltaic cells (PVCs) have been one of the candidates for next-generation "green" power generators. However, PVCs require prolonged exposure to sunlight to work, resulting in elevated temperatures and worsened performances. To overcome this shortcoming, photovoltaic-thermal collector (PVT) systems are used to cool down PVCs, leaving the waste heat unrecovered. Fortunately, the development of thermoelectric generators (TEGs) provides a way to directly convert temperature gradients into electricity. The PVC-TEG hybrid system not only solves the problem of overheated solar cells but also improves the overall power output. In this review, we first discuss the basic principle of PVCs and TEGs, as well as the principle and basic configuration of the hybrid system. Then, the optimization of the hybrid system, including internal and external aspects, is elaborated. Furthermore, we compare the economic evaluation and power output of PVC and hybrid systems. Finally, a further outlook on the hybrid system is offered.

A Modified Langmuir Model for Moisture Diffusion in UGFRE of Composite Insulator Considering the Composite Degradation.

Water invasion induced aging and degradation of the unidirectional glass fiber reinforced epoxy resin (UGFRE) rod is inferred as the primary reason for the decay-like fracture of the composite insulator. In this paper, the moisture diffusion processes in the UGFRE from different directions at various test humidities and temperatures are studied. The moisture diffusion of the UGFRE sample obeys the Langmuir diffusion law under the humidity conditions of 53%, 82% and 100% at 40 °C. In deionized water, the moisture diffusion of the UGFRE sample also obeys the Langmuir diffusion law when the invading direction is vertical to the glass fiber. However, when the water invades the UGFRE sample, parallel with the glass fiber, the weight loss caused by composite degradation should not be neglected. A modified Langmuir model, taking Arrhenius Theory and the nonlinear aging characteristic of the composite into consideration, is proposed and can successfully describe the moisture diffusion process. Both the glass fibers and epoxy resin will degrade in the deionized water. The glass fibers show better resistance to degradation than the epoxy resin. The epoxy resin degrades from the glass fiber/epoxy resin interface and become fragments. For composite insulators, the water invasion through the ends should be avoided as far as possible, or the degradation of the UGFRE rod will result in decay-like fracture.

Thermoelectric-Powered Sensors for Internet of Things.

The Internet of Things (IoT) combines various sensors and the internet to form an expanded network, realizing the interconnection between human beings and machines anytime and anywhere. Nevertheless, the problem of energy supply limits the large-scale implementation of the IoT. Fortunately, thermoelectric generators (TEGs), which can directly convert thermal gradients into electricity, have attracted extensive attention in the IoT field due to their unique benefits, such as small sizes, long maintenance cycles, high stability, and no noise. Therefore, it is vital to integrate the significantly advanced research on TEGs into IoT. In this review, we first outline the basic principle of the thermoelectricity effect and summarize the common preparation methods for thermoelectric functional parts in TEGs. Then, we elaborate on the application of TEG-powered sensors in the human body, including wearable and implantable medical electronic devices. This is followed by a discussion on the application of scene sensors for IoTs, for example, building energy management and airliners. Finally, we provide a further outlook on the current challenges and opportunities.

Prognostic Values of Alpha-Fetoprotein and Des-Gamma-Carboxyprothrombin in Hepatocellular Carcinoma in China: An Analysis of 4792 Patients.

BACKGROUND: The importance of alpha-fetoprotein (AFP) and des-gamma-carboxyprothrombin (DCP) in hepatocellular carcinoma (HCC) has been studied extensively in Japan, where hepatitis C virus is the predominant aetiology of HCC. The clinical profiles of HCC regarding the state of AFP and DCP in a hepatitis B virus epidemic area have not been comprehensively investigated, and the value of these tumour markers in evaluating the response to treatment and the detection of recurrence has yet to be determined. PATIENTS AND METHODS: A total of 4792 patients treated in our centre were continuously analysed regarding accessible AFP and DCP data pre- and posttreatment. Baseline characteristics were summarized, and comparisons of progression-free survival (PFS) and overall survival (OS) rates were made independently. The prognostic significance of each factor was tested with the Cox proportional hazards model. Patients who had AFP and DCP data pretreatment, pre- and posttreatment, and those who were continuously monitored more than twice were analysed separately. RESULTS: A total of 2600 patients (53.4%) were positive for AFP and DCP; 362 (7.6%) and 1211 (25.3%) patients were AFP- or DCP-positive, respectively, and 619 patients (12.9%) were negative for both AFP and DCP. Patients in the AFP single-positive or double-negative groups had the best OS (P<0.001). Patients with less than 50% responses in AFP and DCP after treatments suffered from worse prognostic survival (P<0.001). In the multivariate analysis, elevated AFP and DCP were identified as independent prognostic factors of PFS and OS. In addition, different tumour markers were related to different clinical and pathological traits. CONCLUSION: The present study comprehensively explored the clinical value of classical tumour markers for HCC using the "point-to-line" method. Positivity of pretreatment AFP and DCP or less than 50% treatment response rates exhibited more aggressive HCC, resulting in poor PFS and OS in HCC patients.

LINC00958 Promotes The Malignancy Of Nasopharyngeal Carcinoma By Sponging microRNA-625 And Thus Upregulating NUAK1.

PURPOSE: The aberrant expression of long noncoding RNAs (lncRNAs) indicates progression of various diseases. LINC00958 has been well studied in several types of human cancer; however, the expression profile, functions, and potential mechanism of action of this lncRNA in nasopharyngeal carcinoma (NPC) remain largely unclear and still need to be elucidated. In the present study, we aimed to measure LINC00958 expression in NPC, determine its clinical value, and explore its roles in NPC progression as well as the mechanisms behind these processes. METHODS: The expression profile of LINC00958 in NPC was evaluated by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). A series of functional assays, including the Cell Counting Kit-8 assay, flow cytometry, a Transwell assay, and an in vivo nude mouse model, were utilized to determine the participation of LINC00958 in the malignancy of NPC. RESULTS: LINC00958 was found to be upregulated in NPC tissue specimens and cell lines. The LINC00958 overexpression significantly correlated with tumor size, lymph node status, TNM stage, and worse overall survival among NPC patients. Downregulation of LINC00958 suppressed NPC cell proliferation, migration, and invasion and induced apoptosis in vitro. Additionally, the LINC00958 knockdown impaired tumor growth in vivo. Mechanistically, LINC00958 was found to serve as a molecular sponge of microRNA-625 (miR-625), thereby upregulating NUAK family SNF1-like kinase 1 (NUAK1) in NPC cells. Lastly, rescue experiments validated the involvement of the miR-625-NUAK1 axis in LINC00958-mediated biological functions in NPC. CONCLUSION: Our results demonstrated that LINC00958 works as an oncogene in NPC and plays a key role in the malignant phenotype of NPC cells by sponging miR-625 and increasing NUAK1 expression. The LINC00958-miR-625-NUAK1 pathway might be a target for anticancer therapy in patients with NPC.

NANOG Attenuates Hair Follicle-Derived Mesenchymal Stem Cell Senescence by Upregulating PBX1 and Activating AKT Signaling.

Stem cells derived from elderly donors or harvested by repeated subculture exhibit a marked decrease in proliferative capacity and multipotency, which not only compromises their therapeutic potential but also raises safety concerns for regenerative medicine. NANOG-a well-known core transcription factor-plays an important role in maintaining the self-renewal and pluripotency of stem cells. Unfortunately, the mechanism that NANOG delays mesenchymal stem cell (MSC) senescence is not well-known until now. In our study, we showed that both ectopic NANOG expression and PBX1 overexpression (i) significantly upregulated phosphorylated AKT (p-AKT) and PARP1; (ii) promoted cell proliferation, cell cycle progression, and osteogenesis; (iii) reduced the number of senescence-associated-ß-galactosidase- (SA-ß-gal-) positive cells; and (iv) downregulated the expression of p16, p53, and p21. Western blotting and dual-luciferase activity assays showed that ectopic NANOG expression significantly upregulated PBX1 expression and increased PBX1 promoter activity. In contrast, PBX1 knockdown by RNA interference in hair follicle- (HF-) derived MSCs that were ectopically expressing NANOG resulted in the significant downregulation of p-AKT and the upregulation of p16 and p21. Moreover, blocking AKT with the PI3K/AKT inhibitor LY294002 or knocking down AKT via RNA interference significantly decreased PBX1 expression, while increasing p16 and p21 expression and the number of SA-ß-gal-positive cells. In conclusion, our findings show that NANOG delays HF-MSC senescence by upregulating PBX1 and activating AKT signaling and that a feedback loop likely exists between PBX1 and AKT signaling.

PBX homeobox 1 enhances hair follicle mesenchymal stem cell proliferation and reprogramming through activation of the AKT/glycogen synthase kinase signaling pathway and suppression of apoptosis.

BACKGROUND: PBX homeobox 1 (PBX1) is involved in the maintenance of the pluripotency of human embryonic and hematopoietic stem cells; however, the effects of PBX1 in the self-renewal and reprogramming of hair follicle mesenchymal stem cells (HF-MSCs) are unclear. The AKT/glycogen synthase kinase (GSK) 3ß pathway regulates cell metabolism, proliferation, apoptosis, and reprogramming, and p16 and p21, which act downstream of this pathway, regulate cell proliferation, cell cycle, and apoptosis induced by reprogramming. Here, we aimed to elucidate the roles of PBX1 in regulating the proliferation and reprogramming of HF-MSCs. METHODS: A lentiviral vector designed to carry the PBX1 sequence or PBX1 short hairpin RNA sequence was used to overexpress or knock down PBX1. The roles of PBX1 in proliferation and apoptosis were investigated by flow cytometry. Real-time polymerase chain reaction was performed to evaluate pluripotent gene expression. Dual-luciferase reporter assays were performed to examine the transcriptional activity of the NANOG promoter. Western blotting was performed to identify the molecules downstream of PBX1 involved in proliferation and reprogramming. Caspase3 activity was detected to assess HF-MSC reprogramming. The phosphatidylinositol 3-kinase/AKT inhibitor LY294002 was used to inhibit the phosphorylation and activity of AKT. RESULTS: Overexpression of PBX1 in HF-MSCs increased the phosphorylation of AKT and nuclear translocation of ß-catenin, resulting in the progression of the cell cycle from G0/G1 to S phase. Moreover, transfection with a combination of five transcription factors (SOMKP) in HF-MSCs enhanced the formation of alkaline phosphatase-stained colonies compared with that in HF-MSCs transfected with a combination of four transcription factors (SOMK). PBX1 upregulated Nanog transcription by activating the promoter and promoted the expression of endogenous SOX2 and OCT4. Furthermore, PBX1 expression activated the AKT/glycogen synthase kinase (GSK) 3ß pathway and reduced apoptosis during the early stages of reprogramming. Inhibition of phospho-AKT or knockdown of PBX1 promoted mitochondrion-mediated apoptosis and reduced reprogramming efficiency. CONCLUSIONS: PBX1 enhanced HF-MSC proliferation, and HF-MSCs induced pluripotent stem cells (iPSC) generation by activating the AKT/GSK3ß signaling pathway. During the reprogramming of HF-MSCs into HF-iPSCs, PBX1 activated the NANOG promoter, upregulated NANOG, and inhibited mitochondrion-mediated apoptosis via the AKT/GSK3ß pathway during the early stages of reprogramming.

miR-93 enhances cell proliferation by directly targeting CDKN1A in nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy of the head and neck with the highest incidence rate in southern China. The aim of the present study was to understand the molecular mechanisms that underlie the progression of NPC. The relative expression of miR-93 and CDKN1A was detected by the reverse-transcription quantitative PCR. Western blot analysis was applied to detect the protein levels of genes. Luciferase activity report was applied to verify the target of miRNA. Cell growth was assayed by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. miR-93 was upregulated in NPC tissues and cell lines compared with normal samples. Re-expression of miR-93 promoted cell growth in vitro as determined by the MTT assay. CDKN1A was identified by luciferase reporter as a direct target of miR-93. Its expression was downregulated by miR-93. Furthermore, the results showed that the expression of miR-93 was inversely correlated with the expression of CDKN1A protein. miR-93 enhanced cell proliferation in NPC by directly targeting CDKN1A. It is suggested that miR-93/CDKN1A axis may present a new target for the treatment of NPC.

Epidermal Growth Factor Induces Proliferation of Hair Follicle-Derived Mesenchymal Stem Cells Through Epidermal Growth Factor Receptor-Mediated Activation of ERK and AKT Signaling Pathways Associated with Upregulation of Cyclin D1 and Downregulation of p16.

The maintenance of highly proliferative capacity and full differentiation potential is a necessary step in the initiation of stem cell-based regenerative medicine. Our recent study showed that epidermal growth factor (EGF) significantly enhanced hair follicle-derived mesenchymal stem cell (HF-MSC) proliferation while maintaining the multilineage differentiation potentials. However, the underlying mechanism remains unclear. Herein, we investigated the role of EGF in HF-MSC proliferation. HF-MSCs were isolated and cultured with or without EGF. Immunofluorescence staining, flow cytometry, cytochemistry, and western blotting were used to assess proliferation, cell signaling pathways related to the EGF receptor (EGFR), and cell cycle progression. HF-MSCs exhibited surface markers of mesenchymal stem cells and displayed trilineage differentiation potentials toward adipocytes, chondrocytes, and osteoblasts. EGF significantly increased HF-MSC proliferation as well as EGFR, ERK1/2, and AKT phosphorylation (p-EGFR, p-ERK1/2, and p-AKT) in a time- and dose-dependent manner, but not STAT3 phosphorylation. EGFR inhibitor (AG1478), PI3K-AKT inhibitor (LY294002), ERK inhibitor (U0126), and STAT3 inhibitor (STA-21) significantly blocked EGF-induced HF-MSC proliferation. Moreover, AG1478, LY294002, and U0126 significantly decreased p-EGFR, p-AKT, and p-ERK1/2 expression. EGF shifted HF-MSCs at the G1 phase to the S and G2 phase. Concomitantly, cyclinD1, phosphorylated Rb, and E2F1expression increased, while that of p16 decreased. In conclusion, EGF induces HF-MSC proliferation through the EGFR/ERK and AKT pathways, but not through STAT-3. The G1/S transition was stimulated by upregulation of cyclinD1 and inhibition of p16 expression.

G1/S-specific cyclin-D1 might be a prognostic biomarker for patients with laryngeal squamous cell carcinoma.

OBJECTIVE: To investigate the prognostic role of antigen KI-67 (Ki-67) and G1/S-specific cyclin-D1 (cyclin-D1) in patients with laryngeal squamous cell carcinoma (LSCC). METHODS: Immunohistochemical staining (IHS) was used to determine the protein expression of Ki-67 and cyclin-D1 in LSCC tissues. Kaplan-Meier survival curves was calculated with reference to Ki-67 and cyclin-D1 levels. RESULTS: Cyclin-D1 and Ki67 were expressed in the nuclei of cancer cells. Among the total of 92 cancer tissues examined by immunohistochemistry, 60 (65.22%) had cyclin-D1 overexpression and 56 (60.87%) had Ki67 overexpression. Cyclin-D1 overexpression is associated with the advanced stage of the cancer (P=0.029), but not with gender, age, stage of cancer, histological differentiation, anatomical site, smoking history and alcohol consumption history. Ki67 overexpression is not associated with the advanced stage, gender, age, histological differentiation, anatomical site, smoking history and alcohol consumption history. A statistically significant correlation was found between lymph node status and the expression of Ki67 (p=0.025). Overexpression of cyclin-D1 was correlated to shorter relapse-free survival period (P<0.001). CONCLUSIONS: Overexpression of cyclin-D1 can be used as a marker to predict relapse in patients with LSCC after primary curative resection.

Role of centromere protein H and Ki67 in relapse-free survival of patients after primary surgery for hypopharyngeal cancer.

PURPOSE: Centromere protein H (CENP-H) and Ki67 are overexpressed in some malignancies, but whether they are predictors of survival after primary resection for hypopharyngeal squamous cell carcinoma (HSCC) remains unknown. METHODS: We assessed immunohistochemical expression of CENP-H and Ki67 in 112 HSCC specimens collected between March 2003 and March 2005 for analysis by clinical characteristics. The Kaplan-Meier method was used to analyze relapse-free survival and logistic multivariate regression to determine risk factors of relapse-free survival. Cholecystokinin octapeptide assays and flow cytometry were used to examine cell proliferation and apoptosis after siRNA inhibition of CENP-H in HSCC cells. RESULTS: Overall, 50 (44.6%) HSCC specimens showed upregulated CENP-H expression and 69 (61.6%) upregulated Ki67. An increased CENP-H protein level was associated with advanced cancer stage and alcohol history (P=0.012 and P=0.048, respectively) but an increased Ki67 protein level only with advanced cancer stage (P=0.021). Increased CENP-H or Ki67 were associated with short relapse-free survival (P<0.001 or P=0.009, respectively) and were independent predictors of relapse-free survival (P=0.001 and P=0.018, respectively). siRNA knockdown of CENP-H mRNA inhibited cell proliferation and promoted cancer cell apoptosis in vitro. CONCLUSIONS: Upregulated CENP-H and Ki67 levels are significantly associated with short relapse-free survival in HSCC. These factors may be predictors of a relapsing phenotype in HSSC cases.