FAP Serves as a Prognostic Biomarker in Head and Neck Squamous Cell Carcinoma.

Head and neck squamous cell carcinoma (HNSCC) poses significant challenges with poor survival rates and limited therapeutic strategies. Our study, using The Cancer Genome Atlas (TCGA) data, assesses cancer-associated fibroblast (CAF) gene signatures' clinical relevance. In our analysis across TCGA tumor types, differential gene expression analysis revealed that fibroblast activation protein (FAP) is upregulated in tumor tissues and associated with poorer survival rates in HNSCC. Furthermore, mechanistic studies employing gene-silencing techniques substantiated that FAP knockout led to a significant decrease in cellular proliferation, invasion, and migration in HNSCC cell lines. Through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses, we established that high FAP expression correlates with vital biological processes such as extracellular matrix organization, angiogenesis, and cellular motility. Importantly, FAP was found to regulate these processes by promoting the expression of key proteins involved in epithelial-mesenchymal transition-related pathways. Additionally, our analysis revealed a significant correlation between FAP expression and the expression profiles of immune checkpoint molecules, underscoring its potential role in immune modulation. Collectively, our findings illuminate FAP's pivotal role in HNSCC pathogenesis and its potential as a prognostic biomarker and therapeutic target. This research lays the groundwork for understanding the multifaceted roles and regulatory mechanisms of CAFs in HNSCC, thereby offering valuable perspectives for the development of targeted therapeutic strategies aimed at improving patient outcomes.

Bidirectional associations between periodontitis and inflammatory bowel disease: A systematic review of longitudinal studies with meta-analysis and trial sequential analysis.

The bidirectional associations between periodontitis and inflammatory bowel disease (IBD) with temporal directionality remain inconclusive. This study aims to evaluate the bidirectional associations between periodontitis and IBD through a systematic review and meta-analysis. Five databases (PubMed, Embase, Web of Science, Scopus and Cochrane Library) were systematically searched from inception to 27 February 2024. Two independent reviewers performed a review of the retrieved studies. Longitudinal studies, including cohort and nested case-control studies, were considered eligible for the study design. The pooled risk ratio (RR) and hazard ratio (HR) derived from the meta-analysis were used to assess whether periodontitis (or IBD) was a risk factor for IBD (or periodontitis). Trial sequential analysis (TSA) was performed to evaluate the reliability of the results. Four studies (n = 10 270 912) on the risk of IBD in patients with periodontitis and two (n = 33 420) on the risk of periodontitis in patients with IBD were included. The result suggested that periodontitis did not increase the risk of IBD (pooled RR = 1.04, 95% confidence interval [CI]: 0.99-1.09; p = .164; I-squared statistic [I2] = 27%). For subtypes of IBD, periodontitis was associated with the occurrence of ulcerative colitis (UC) (pooled RR = 1.12, 95% CI: 1.04-1.21; p = .003; I2 = 38%), but not with Crohn's disease (CD) (pooled RR = 0.98, 95% CI: 0.92-1.04; p = .475; I2 = 0%). Specifically, the risk of UC was higher among men (pooled HR = 1.11, 95% CI: 1.01-1.22; p = .025; I2 = 0%) and smokers (pooled HR = 1.23, 95% CI: 1.07-1.42; p = .004; I2 = 0%) with periodontitis than their counterparts without periodontitis. Patients with IBD may have a higher risk of developing periodontitis (pooled HR = 1.37, 95% CI: 1.26-1.49; p < .001; I2 = 18%); however, whether IBD subtypes increased the occurrence of periodontitis remained uncertain. The TSA results confirmed the reliability of the primary findings. Based on limited longitudinal evidence, patients with periodontitis do not exhibit an increased risk of developing IBD overall, but they are at increased risk of UC (not CD). On the contrary, patients with IBD have a higher risk of developing periodontitis over time. More high-quality longitudinal studies are needed to determine the effect of specific subtypes of IBD on periodontitis.

Development and Validation of a Prognostic Nomogram for HR+ HER- Breast Cancer.

Purpose: We aimed to develop a nomogram to predict prognosis of HR+ HER2- breast cancer patients and guide the application of postoperative adjuvant chemotherapy. Methods: We identified 310 eligible HR+ HER- breast cancer patients and randomly divided the database into a training group and a validation group. The endpoint was disease free survival (DFS). Concordance index (C-index), area under the curve (AUC) and calibration curves were used to evaluate predictive accuracy and discriminative ability of the nomogram. We also compared the predictive accuracy and discriminative ability of our nomogram with the eighth AJCC staging system using overall data. Results: According to the training group, platelet-to-lymphocyte ratio (PLR), tumor size, positive lymph nodes and Ki-67 index were used to construct the nomogram of DFS. The C-index of DFS was 0.708 (95% CI: 0.623-0.793) in the training group and 0.67 (95% CI: 0.544-0.796) in the validation group. The calibration curves revealed great consistencies in both groups. Conclusion: We have developed and validated a novel and practical nomogram that can provide individual prediction of DFS for patients with HR+ HER- breast cancer. This nomogram may help clinicians in risk consulting and guiding the application of postoperative adjuvant chemotherapy.

Intramolecular Hydrogen Bonding Rigidifying Flexible Bridge for Solution- and Vacuum-Processed TSCT-TADF Emitters.

To realize strong donor-acceptor face-to-face stacking for efficient through-space charge transfer-type thermally activated delayed fluorescence, a conceptually new design strategy is proposed to couple flexible bridges with adequate rigidity via built-in intramolecular hydrogen bonds (IHBs). The resulting emitter ACE-CN has a planarized benzyl methyl ether bridge self-anchored by the C-H···O IHB and shows a high photoluminescence quantum efficiency of 93%. The solution- and vacuum-processed devices exhibited high external quantum efficiencies of 11.8% and 24.7%, respectively.

Periodontal pathogen Fusobacterium nucleatum infection accelerates hepatic steatosis in high-fat diet-fed ApoE knockout mice by inhibiting Nrf2/Keap1 signaling.

AIMS: This study sought to explore the impact of Fusobacterium nucleatum on hepatic steatosis in apolipoprotein E (ApoE) knockout (KO) mice induced by a high-fat diet (HFD) and elucidate the underlying mechanism. METHODS: ApoE KO mice, on a HFD, received F. nucleatum oral inoculation every other day. After 24 weeks, body weight, liver weight, and liver index were assessed. Serum biochemistry and pro-inflammatory factors in serum and liver were analyzed. The histopathology of right maxilla and live were performed. Oil red O, immunohistochemistry, and immunofluorescence staining for the liver were conducted. Myeloperoxidase (MPO) activity, apoptosis, lipid reactive oxygen species (ROS), ROS, lipid peroxides, and hepatic lipids were also evaluated. Liver inflammation, fibrosis, de novo lipogenesis (DNL)-related molecule, and Nrf2/Keap1-related signaling molecule gene/protein expression were determined by real-time PCR (RT-PCR) and/or Western blot (WB) analysis. RESULTS: HFD-fed ApoE KO mice infected by F. nucleatum demonstrated significant changes, including increased body and liver weight, elevated proinflammatory factors and lipids in serum and liver, as well as neutrophil infiltration, fibrosis, apoptosis, oxidative stress, and lipid peroxidation in the liver. Additionally, F. nucleatum stimulates hepatic lipid accumulation and activates de novo lipogenesis (DNL), while simultaneously suppressing the Nrf2/Keap1 antioxidant pathway. CONCLUSION: In conclusion, our study reveals that oral inoculation of F. nucleatum might promote hepatic steatosis by inhibiting Nrf2/Keap1 pathway.

Photocatalytic regeneration of nicotinamide cofactor biomimetics drives biocatalytic reduction by Old Yellow enzymes.

A key approach in developing green chemistry involves converting solar energy into chemical energy of biomolecules through photocatalysis. Photocatalysis can facilitate the regeneration of nicotinamide cofactors during redox processes. Nicotinamide cofactor biomimetics (NCBs) are economical substitutes for natural cofactors. Here, photocatalytic regeneration of NADH and reduced NCBs (NCBsred) using graphitic carbon nitride (g-C3N4) was developed. The process involves g-C3N4 as the photocatalyst, Cp*Rh(bpy)H2O2+ as the electron mediator, and Triethanolamine as the electron donor, facilitating the reduction of NAD+ and various oxidative NCBs (NCBsox) under light irradiation. Notably, the highest reduction yield of 48.32 % was achieved with BANA+, outperforming the natural cofactor NAD+. Electrochemical analysis reveals that the reduction efficiency and capacity of cofactors relies on their redox potentials. Additionally, a coupled photo-enzymatic catalysis system was explored for the reduction of 4-Ketoisophorone by Old Yellow Enzyme XenA. Among all the NCBsox and NAD+, the highest conversion ratio of over 99 % was obtained with BANA+. After recycled for 8 times, g-C3N4 maintained over 93.6 % catalytic efficiency. The photocatalytic cofactor regeneration showcases its outstanding performance with NAD+ as well as NCBsox. This work significantly advances the development of photocatalytic cofactor regeneration for artificial cofactors and its potential application.

Prognostic value and immunological role of MMRN1: a rising star in cancer.

BACKGROUND: Multimerin 1 (MMRN1) is a factor V binding protein, which can support platelet adhesion and thrombus formation. In recent years, the role of MMRN1 in cancer has begun to attract attention. But systematic studies in this area are lacking. Therefore, we used bioinformatics methods to analyze MMRN1 in tumors to reveal the possible role of MMRN1. METHODS: Using the Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) database, we obtained relevant data for analyzing MMRN1. Using Gene Expression Profiling Interactive Analysis (GEPIA), Human Protein Atlas (HPA), TCGA, GeneMANIA, and cBioPortal, we explored the potential role of MMRN1 in different types of tumors. Tumor Immune System Interactions and Drug Bank (TISIDB) and Sangerbox were used to analyze the correlation between MMRN1 and tumor immunity. Gene set cancer analysis (GSCA) and UALCAN were used to analyze the methylation of MMRN1. GSCA was also used to analyze the drug sensitivity of MMRN1. RESULTS: MMRN1 is down-regulated in most cancer types and is closely related to the prognosis of cancer patients. Interestingly, in most tumors, MMRN1 is positively correlated with immune -related genes. In addition, we observed different levels of methylation and mutations in different types of tumors. Drug sensitivity analysis found that MMRN1 was negatively correlated with several drugs, including GW-2580 and TL-1-85, suggesting that it can be used to develop potential anticancer therapies. CONCLUSION: Our analysis demonstrated a significant relationship between MMRN1 and prognosis, tumor immunity, and drug sensitivity of several tumors. As a rising star in cancer, it needs further research.

Hepatoid Adenocarcinoma of the Esophagus with Thyroid Metastasis: A Case Report.

Rare hepatoid adenocarcinomas are highly heterogeneous. In this case, hepatoid adenocarcinoma occurred in both the esophagus and thyroid, and the combination of chemotherapy and immunotherapy may be a promising therapeutic tool for rare tumors. Laryngoscope, 2024.

Epidermolysis Bullosa: Two rare case reports of COL7A1 and EBS-GEN SEV KRT14 variants with review of literature.

EPIDERMOLYSIS: Bullosa is a rare hereditary skin condition that causes blisters. Genes encoding structural proteins at or near the dermal-epidermal junction are mutated recessively or dominantly, and this is the primary cause of EB. Herein, two Chinese boys were diagnosed with the condition, each with a different variant in a gene that serves as a reference for EB genetic counseling. Skincare significantly impacted their prognosis and quality of life. CASE PRESENTATION: Two Chinese boys, with phenotypically normal parents, have been diagnosed with distinct blister symptoms, one with Dominant Dystrophic Epidermolysis Bullosa and the other with a severe form of Epidermolysis Bullosa Simplex. The first patient had a G-to-A variant in the COL7A1 allele, at nucleotide position 6163 which was named "G2055A". The proband is heterozygous for Dystrophic Epidermolysis Bullosa due to a COL7A1 allele with a glycine substitution at the triple helix domain. A similar variant has been discovered in his mother, indicating its potential transmission to future generations. Another patient had severe Epidermolysis Bullosa Simplex with a rare c.377T > A  variant resulting in substitution of amino acid p.Leu126Arg (NM_000526.5 (c.377T > G, p.Leu126Arg) in the Keratin 14 gene. In prior literature, Keratin 14 has been associated with an excellent prognosis. However, our patient with this infrequent variant tragically died from sepsis at 21 days old. There has been a reported occurrence of the variant only once. CONCLUSION: Our study reveals that Epidermolysis Bullosa patients with COL7A1 c.6163G > A and KRT14 c.377T>A variants have different clinical presentations, with dominant forms of Dystrophic EB having milder phenotypes than recessive ones. Thus, the better prognosis in the c.6163G > A patient. Furthermore, c.377T>A patient was more prone to infection than the patient with c.6163G>A gene variant. Genetic testing is crucial for identifying the specific variant responsible and improving treatment options.

Structure-Guided Evolution of Cyclohexanone Monooxygenase Toward Bulky Omeprazole Sulfide: Substrate Migration and Stereoselectivity Inversion.

Structure-guided engineering of a CHMO from Amycolatopsis methanolica (AmCHMO) was performed for asymmetric sulfoxidation activity and stereoselectivity toward omeprazole sulfide. Initially, combinatorial active-site saturation test (CASTing) and iteratively saturation mutagenesis (ISM) were performed on 5 residues at the "bottleneck" of substrate tunnel, and MT3 was successfully obtained with a specific activity of 46.19 U/g and R-stereoselectivity of 99 % toward OPS. Then, 4 key mutations affecting the stereoselectivity were identified through multiple rounds of ISM on residues at the substrate binding pocket region, resulting MT8 with an inversed stereoselectivity from 99 % (R) to 97 % (S). MT8 has a greatly compromised specific activity of 0.08 U/g. By introducing additional beneficial mutations, MT11 was constructed with significantly increased specific activity of 2.29 U/g and stereoselectivity of 97 % (S). Enlarged substrate tunnel is critical to the expanded substrate spectrum of AmCHMO, while reshaping of substrate binding pocket is important for stereoselective inversion. Based on MD simulation, pre-reaction states of MT3-OPSproR, MT8-OPSproS, and MT11-OPSproS were calculated to be 45.56 %, 17.94 %, and 28.65 % respectively, which further confirm the experimental data on activity and stereoselectivity. Our results pave the way for engineering distinct activity and stereoselectivity of BVMOs toward bulky prazole thioethers.

Cellular senescence gene TACC3 associated with colorectal cancer risk via genetic and DNA methylated alteration.

Cell senescence genes play a vital role in the pathogenesis of colorectal cancer, a process that may involve the triggering of genetic variations and reversible phenotypes caused by epigenetic modifications. However, the specific regulatory mechanisms remain unclear. Using CellAge and The Cancer Genome Atlas databases and in-house RNA-seq data, DNA methylation-modified cellular senescence genes (DMCSGs) were validated by Support Vector Machine and correlation analyses. In 1150 cases and 1342 controls, we identified colorectal cancer risk variants in DMCSGs. The regulatory effects of gene, variant, and DNA methylation were explored through dual-luciferase and 5-azacytidine treatment experiments, complemented by multiple database analyses. Biological functions of key gene were evaluated via cell proliferation assays, SA-ß-gal staining, senescence marker detection, and immune infiltration analyses. The genetic variant rs4558926 in the downstream of TACC3 was significantly associated with colorectal cancer risk (OR = 1.35, P = 3.22 × 10-4). TACC3 mRNA expression increased due to rs4558926 C > G and decreased DNA methylation levels. The CpG sites in the TACC3 promoter region were regulated by rs4558926. TACC3 knockdown decreased proliferation and senescence in colorectal cancer cells. In addition, subjects with high-TACC3 expression presented an immunosuppressive microenvironment. These findings provide insights into the involvement of genetic variants of cellular senescence genes in the development and progression of colorectal cancer.

Long non-coding RNA ACTA2-AS1 suppresses metastasis of papillary thyroid cancer via regulation of miR-4428/KLF9 axis.

BACKGROUND: Metastasis is the primary cause of recurrence and death in patients with papillary thyroid carcinoma (PTC). LncRNA ACTA2-AS1, a long non-coding RNA, acts as a tumor suppressor in multiple types of human malignancies, while the role of ACTA2-AS1 in PTC metastasis remains unclear. METHODS: The ACTA2-AS1 expression in PTC tissues was analyzed. The sponged roles of ACTA2-AS1 via miR-4428/KLF9 axis were identified using starBase tool. The function of ACTA2-AS1 in PTC was performed with in vitro and in vivo experiments. The correlation between DNA methylation and mRNA expressions of these gene in the TCGA dataset was explored. RESULTS: ACTA2-AS1 expression was downregulated in PTC tissues without metastasis and further decreased in PTC tissues with lymph node metastasis compared with that in normal tissues. Functionally, the overexpression of ACTA2-AS1 inhibited the growth, proliferation, and invasion of PTC cells, whereas its depletion exerted opposite effect. In vivo, ACTA2-AS1 expression inhibited PTC metastasis. Furthermore, ACTA2-AS1 acted as a competing endogenous RNA for miR-4428, thereby positively regulating the expression of miR-4428 target gene, KLF9. Finally, miR-4428 overexpression enhanced invasive potential of PTC cells and significantly weakened the effects of ACTA2-AS1 on promotion and inhibition of KLF9 expression as well as invasive ability of PTC cells, respectively. In the TCGA dataset, the methylation level of ACTA2-AS1 was significantly correlated with its mRNA expression (r = 0.21, p = 2.1 × e-6). CONCLUSIONS: Our findings demonstrate that ACTA2-AS1 functions as a tumor suppressor in PTC progression at least partly by regulating the miR-4428-dependent expression of KLF9.

A comparative study of two aldehyde dehydrogenases from Sphingobium sp.: the substrate spectrum and catalytic mechanism.

Biocatalytic oxidation is one of the most important and indispensable organic reactions for the development of green and sustainable biomanufacturing processes. NAD(P)+-dependent aldehyde dehydrogenase (ALDH) catalyzes the oxidation of aldehydes to carboxylic acids. Here, two ALDHs, SpALDH1 and SpALDH2, were identified from Sphingobium sp. SYK-6. They belong to different ALDH families and share only 32.30% amino acid identity. Interestingly, SpALDH1 and SpALDH2 exhibit significantly different enzymatic properties and substrate profiles. SpALDH2 has better thermostability than SpALDH1. SpALDH1 is a metalloenzyme and is activated by potassium ions, while SpALDH2 is not metallic-dependent. Compared with SpALDH1, SpALDH2 has a relatively broad substrate spectrum toward aromatic aldehydes. Based on homology modeling and molecular docking analysis, mechanisms underlying the substrate specificity of ALDHs were elucidated. For both ALDHs, hydrophobicity of substrate binding pockets is important for the catalytic properties, especially substrate specificity. Notably, optimization of the flexible loop 444-457 reforms a hydrogen bond between pyridine substrates and SpALDH1, contributing to the high catalytic activity. Finally, a coupling reaction catalyzed by ALDHs and NOX was constructed for efficient production of aromatic carboxylic acids.

Genetic variants in hypoxia-inducible factor pathway are associated with colorectal cancer risk and immune infiltration.

Hypoxia-inducible factor (HIF) pathway genes influence tumorigenesis and immune status. However, the associations between genetic variants in hypoxia-related genes and colorectal cancer risk and the immune status of hypoxia-associated genes in colorectal cancer have not been systematically characterized. The associations between genetic variants and colorectal cancer risk were evaluated in Chinese, Japanese and European populations using logistic regression analysis. The relationships between target genes and tumour immune infiltration were predicted by Tumour Immune Estimation Resource (TIMER). We found that rs34533650 in EPAS1 was associated with colorectal cancer risk (OR = 1.43, 95% CI = 1.20-1.70, P(FDR) = 8.35 × 10-4 ), and this finding was validated in two independent populations (Japanese: OR = 1.07, 95% CI = 1.01-1.15, p = 3.38 × 10-2 ; European: OR = 1.11, 95% CI = 1.03-1.19, p = 6.04 × 10-3 ). EPAS1-associated genes were enriched in immune-related pathways. In addition, we found that EPAS1 copy number variation (CNV) was associated with the degree of infiltration of immune cells and observed correlations between EPAS1 expression and immune cell infiltration levels in colorectal cancer. These results highlight that genetic variants of hypoxia-related genes play roles in colorectal cancer risk and provide new insight that EPAS1 might be a promising predictor of colorectal cancer susceptibility and immune status.

A structural color hydrogel for diagnosis of halitosis and screening of periodontitis.

Oral pathogens can produce volatile sulfur compounds (VSCs), which is the main reason for halitosis and indicates the risk of periodontitis. High-sensitivity detection of exhaled VSCs is urgently desired for promoting the point-of-care testing (POCT) of halitosis and screening of periodontitis. However, current detection methods often require bulky and costly instruments, as well as professional training, making them impractical for widespread detection. Here, a structural color hydrogel for naked-eye detection of exhaled VSCs is presented. VSCs can reduce disulfide bonds within the network, leading to expansion of the hydrogel and thus change of the structural color. A linear detection range of 0-1 ppm with a detection limit of 61 ppb can be achieved, covering the typical VSC concentration in the breath of patients with periodontitis. Furthermore, visual and in situ monitoring of Porphyromonas gingivalis responsible for periodontitis can be realized. By integrating the hydrogels into a sensor array, the oral health conditions of patients with halitosis can be evaluated and distinguished, offering risk assessment of periodontitis. Combined with a smartphone capable of color analysis, POCT of VSCs can be achieved, providing an approach for the monitoring of halitosis and screening of periodontitis.

Copper homeostasis and cuproptosis in mitochondria.

Mitochondria serve as sites for energy production and are essential for regulating various forms of cell death induced by metal metabolism, targeted anticancer drugs, radiotherapy and immunotherapy. Cuproptosis is an autonomous form of cell death that depends on copper (Cu) and mitochondrial metabolism. Although the recent discovery of cuproptosis highlights the significance of Cu and mitochondria, there is still a lack of biological evidence and experimental verification for the underlying mechanism. We provide an overview of how Cu and cuproptosis affect mitochondrial morphology and function. Through comparison with ferroptosis, similarities and differences in mitochondrial metabolism between cuproptosis and ferroptosis have been identified. These findings provide implications for further exploration of cuproptotic mechanisms. Furthermore, we explore the correlation between cuproptosis and immunotherapy or radiosensitivity. Ultimately, we emphasize the therapeutic potential of targeting cuproptosis as a novel approach for disease treatment.

Characterizing distinct profiles of immune and inflammatory response with age to Omicron infection.

Background: Understanding inflammatory and immune responses to Omicron infection based on age is crucial when addressing this global health threat. However, the lacking of comprehensive elucidation hinders the development of distinct treatments tailored to different age populations. Methods: 1299 cases of Omicron infection in Shanghai were enrolled between April 10, 2022 and June 3, 2022, dividing into three groups by ages: Adult group (18-59 years), Old group (60-79 years), and Elder group (≥ 80 years). Laboratory data including inflammatory cytokines, cellular, and humoral immunity were collected and analyzed. Results: The mean age of Adult, Old, and Elder groups were 44.14, 69.98, and 89.35 years, respectively, with 40.9% being men. The Elder group patients exhibited higher white blood cell (WBC) counts and elevated levels of inflammatory cytokines, but their lymphocyte counts were relatively lower. In comparison to the Old group patients, the Elder group patients demonstrated significantly lower CD3+ T-cell counts, CD3+ T-cell proportion, CD4+ T-cell counts, CD8+ T-cell counts, and CD19+ B-cell counts, while the NK-cell counts were higher. Omicron negative patients displayed a higher proportion of CD19+ B-cells and higher levels of Complement-3 and IL-17 compared to the positive patients in the Old group. Omicron negative patients had lower WBC counts, CD3+CD8+ T-cells proportion, and the levels of serum amyloid A and IgA in the Elder group, but the CD4+/CD8+ ratio was higher. Conclusions: Our study identified the distinct profiles of inflammatory and immune responses to Omicron infection varying with age and highlighted the diverse correlations between the levels of various biomarkers and Omicron infected/convalescent patients.

A closed loop case study of decentralized food waste management: System performance and life cycle carbon emission assessment.

Food waste (FW) has become a worldwide issue, while anaerobic digestion (AD) has appeared as a widely adopted technology to recover energy and resources from FW. Compared to many existing case studies of centralized AD system, the comprehensive study of decentralized micro-AD system from both system energy efficiency and carbon emission perspective is still scanty, particularly system operated under ambient temperature conditions. In this study, an actual decentralized micro-AD system with treating capacity of 300 kg FW/d for a local hawker center in Singapore was reported and evaluated. The results showed that 1894.5 kg of FW was treated and 173 m3 biogas with methane content of 53 % was produced during the experimental period of 75 days. The methane yield results showed a high FW degradation efficiency (87.87 %). However, net energy consumption and net carbon emission were observed during the experimental period. Nevertheless, energy self-efficiency and carbon neutrality, even net energy output and carbon reduction, can be achieved by increasing daily FW loading and biogas engine efficiency. Specifically, the FW loading for system energy self-efficiency was identified as 159 kg/d for engine efficiency of 35 % at a high kitchen waste/table waste ratio (63 %/37 %, with covid-19 dine-in restrictions); while they were 112 and 58 kg/d for engine efficiency of 25 % and 35 %, respective, at a low kitchen waste/table waste ratio (31 %/69 %, without covid-19 dine-in restrictions). The carbon emission ranged from 156.08 kg CO2-eq/t FW to -77.35 kg CO2-eq/t FW depending on the FW loading quantity and engine efficiency. Moreover, the sensitivity analysis also showed that the used electricity source for substitution influenced the carbon emission performance significantly. The obtained results imply that the decentralized micro-AD system could be a feasible FW management solution for energy generation and carbon reduction when the FW loading and engine electrical efficiency are carefully addressed.

Periodontal health status in cirrhotic patients: a systematic review and meta-analysis.

OBJECTIVES: Liver cirrhosis is a disease with widespread prevalence and high mortality. Oral manifestations, particularly periodontal-related manifestations such as bleeding gums, red and swollen gums, are common in cirrhotic patients but may often be overshadowed by other systemic complications, making them easy to ignore. So this article conducts a systematic review and meta-analysis of periodontal health status in patients with cirrhosis. MATERIAL AND METHODS: We performed electronic searches on the following databases: PubMed, EMBASE, Scopus, Web of Science, and Cochrane Library. Risk of bias evaluation was carried out according to the Fowkes and Fulton guidelines. Meta-analyses were performed with tests for sensitivity and statistical heterogeneity. RESULTS: Of the 368 potentially eligible articles, 12 studies were included for qualitative analysis, and 9 contributed to the meta-analysis. In terms of periodontal-related parameters, cirrhotic patients presented a greater mean of clinical attachment loss (CAL) (weighted mean differences [WMD] = 1.078, 95% confidence interval [95% CI]: 0.546-1.609, p < 0.001), probing depth (PD) (WMD = 0.796, 95% CI: 0.158 to 1.434, p = 0.015) and alveolar bone loss (ABL) (WMD = 3.465, 95% CI: 2.946-3.984, p < 0.001) than those without, while no statistical difference was found in the papillary bleeding index (PBI) (WMD = 0.166, 95% CI: -0546 to 0.878, p = 0.647) and bleeding on probing (BOP) (WMD = 4.913, 95% CI: -3.099 to 12.926, p = 0.229). The prevalence of periodontitis was higher in cirrhotic patients than in the control group (odds ratio [OR] = 2.630, 95% CI: 1.531-4.520, p < 0.001). CONCLUSIONS: The results indicate that cirrhotic patients have poor periodontal conditions and a higher prevalence of periodontitis. We advocate that they should receive regular oral hygiene and basic periodontal treatment.

Engineering Glucose Dehydrogenase to Favor Totally Synthetic Biomimetic Cofactors Containing Carboxyl Group.

The utilization of unnatural nicotinamide cofactors for reactions catalyzed by oxidoreductases has gained increasing interest. Totally synthetic nicotinamide cofactor biomimetics (NCBs) are cost-effective and convenient to synthesize. Thus, it has become increasingly important to develop enzymes that accept NCBs. Here, we have engineered SsGDH to favor a newly synthesized unnatural cofactor 3-carbamoyl-1-(4-carboxybenzyl) pyridin-1-ium (BANA+ ). Using in situ ligand minimization tool, sites 44 and 114 were identified as hotspots for mutagenesis. All the double mutants demonstrated 2.7-7.7-fold improvements in catalytic activity, and the best double mutant E44D/E114 L exhibited 10.6-fold increased catalytic efficiency toward BANA+ . These results provide valuable information for the rational engineering of oxidoreductases with versatile NCBs-dependency, as well as the design of novel biomimetic cofactors.