Social acceptability of psilocybin-assisted therapy for existential distress at the end of life: A population-based survey.

BACKGROUND: Internationally, there is a growing interest in the potential benefits of psilocybin-assisted therapy to treat existential distress at the end of life. However, the social acceptability of this therapy is not yet well known. AIM: This study assesses the social acceptability of the medical use of psilocybin to treat existential distress at the end of life. DESIGN: An online survey was conducted in Canada between November 23 and December 4, 2022. The questionnaire included items pertaining to perceptions, attitudes and concerns towards psilocybin-assisted therapy to treat existential distress at the end of life. PARTICIPANTS: The sample (n = 2800) was stratified by province, age and sex. Participants were adults from four provinces of Canada: Québec, Ontario, Alberta and British Columbia. RESULTS: Overall, 79.3% considered psilocybin-assisted therapy a reasonable medical choice for a patient suffering from existential distress at the end of life, 84.8% agreed that the public health system should cover the costs of the intervention and 63.3% would welcome the legalisation of psilocybin for medical purposes. Previous psilocybin use (p < 0.0001, for all dependent variables), exposure to palliative care (p < 0.05, for all dependent variables) and a progressive political orientation (p < 0.05, for all dependent variables) were associated with more favourable attitudes towards psilocybin-assisted therapy at the end of life. CONCLUSION: The social acceptability of psilocybin-assisted therapy for existential distress at the end of life is rather high in Canada. These findings may contribute to efforts to mobilise resources and improve access to this emerging therapy in palliative and end of life care settings.

Complete mimicry: Rhabdomyosarcoma with FUS::TFCP2 fusion masquerading as carcinoma-diagnostic challenge and report of two cases.

Rhabdomyosarcomas (RMS) are malignant mesenchymal tumors with skeletal muscle differentiation which are classified into alveolar, embryonal, pleomorphic, and spindle cell/sclerosing RMS. Within the spindle cell/sclerosing RMS tumor type there is a recently recognized sub-type categorized as intraosseous spindle cell RMS with TFCP2/NCOA2 gene fusion. This rare tumor is highly aggressive with predominant involvement of the craniofacial and pelvic bones with approximately 30 cases reported to date. Histopathologic features include spindle cell and epithelioid morphology with a characteristic co-expression of epithelial markers, myogenic markers, and ALK1 expression. We report two cases of gnathic spindle cell/sclerosing RMS with FUS::TFCP2 gene fusion that were initially interpreted as carcinomas by referring institutions and later reclassified when encountered in our practice after additional work-up and molecular characterization.

miR-145a-5p/Plexin-A2 promotes the migration of OECs and transplantation of miR-145a-5p engineered OECs enhances the functional recovery in rats with SCI.

BACKGROUND: Olfactory ensheathing cells (OECs) serve as a bridge by migrating at the site of spinal cord injury (SCI) to facilitate the repair of the neural structure and neural function. However, OEC migration at the injury site not only faces the complex and disordered internal environment but also is closely associated with the migration ability of OECs. METHODS: We extracted OECs from the olfactory bulb of SD rats aged <7 days old. We verified the micro ribonucleic acid (miR)-145a-5p expression level in the gene chip after SCI and OEC transplantation using quantitative reverse transcription (qRT)-polymerase chain reaction (PCR). The possible target gene Plexin-A2 of miR-145a-5p was screened using bioinformatics and was verified using dual-luciferase reporter assay, Western blot, and qRT-PCR. The effect of miR-145a-5p/plexin-A2 on OEC migration ability was verified by wound healing assay, Transwell cell migration assay, and immunohistochemistry. Nerve repair was observed at the injured site of the spinal cord after OEC transplantation using tissue immunofluorescence and magnetic resonance imaging, diffusion tensor imaging, and the Basso-Beattie-Bresnahan locomotor rating scale were further used for imaging and functional evaluation. RESULTS: miR-145a-5p expression in the injured spinal cord tissue after SCI considerably decreased, while Plexin-A2 expression significantly increased. OEC transplantation can reverse miR-145a-5p and Plexin-A2 expression after SCI. miR-145a-5p overexpression enhanced the intrinsic migration ability of OECs. As a target gene of miR-145a-5p, Plexin-A2 hinders OEC migration. OEC transplantation overexpressing miR-145a-5p after SCI can increase miR-145a-5p levels in the spinal cord, reduce Plexin-A2 expression in the OECs and the spinal cord tissue, and promote OEC migration and distribution at the injured site. OEC transplantation overexpressing miR-145a-5p can promote the repair of neural morphology and neural function. CONCLUSIONS: Our study demonstrated that miR-145a-5p could promote OEC migration by down-regulating the target gene Plexin-A2, and transplantation of miR-145a-5p engineered OECs was beneficial to enhance neural structural and functional recovery in SCI rats.

Safety and Efficacy of Oxaliplatin Pressurized Intraperitoneal Aerosolized Chemotherapy (PIPAC) in Colorectal and Appendiceal Cancer with Peritoneal Metastases: Results of a Multicenter Phase I Trial in the USA.

BACKGROUND: Pressurized intraperitoneal aerosolized chemotherapy (PIPAC) is a laparoscopic locoregional treatment for peritoneal metastases (PM) from colorectal cancer (CRC) or appendiceal cancer (AC) in patients who cannot undergo cytoreductive surgery (CRS). While PIPAC has been studied in Europe and Asia, it has not been investigated in the USA. PATIENTS AND METHODS: We evaluated PIPAC with 90 mg/m2 oxaliplatin alone (cycle 1) and preceded by systemic chemotherapy with fluorouracil (5-FU) and leucovorin (LV) (cycle 2-3) as a multicenter prospective phase I clinical trial (NCT04329494). The primary endpoint was treatment-related adverse events (AEs). Secondary endpoints included survival and laparoscopic, histologic, and radiographic response. RESULTS: 12 patients were included: 8 with CRC and 4 with AC. Median prior chemotherapy cycles was 2 (interquartile range (IQR) 2-3). All patients were refractory to systemic oxaliplatin-based chemotherapy. Median peritoneal carcinomatosis index (PCI) was 28 (IQR 19-32). Six (50%) of twelve patients completed three PIPAC cycles. No surgical complications or dose-limiting toxicities were observed. Two patients developed grade 3 treatment-related toxicities (one abdominal pain and one anemia). Median overall survival (OS) was 12.0 months, and median progression-free survival (PFS) was 2.9 months. OS was correlated with stable disease by Response Evaluation Criteria in Solid Tumors (RECIST) criteria but not with laparoscopic response by PCI or histologic response by peritoneal regression grading system (PRGS). CONCLUSIONS: This phase I trial in the USA demonstrated safety, feasibility, and early efficacy signal of PIPAC with oxaliplatin and chemotherapy in patients with PM from AC or CRC who are refractory to standard lines of systemic chemotherapy.

A microgel of CdSe quantum dots for fluorescent bisphenol A detection.

A fluorescent microgel for BPA detection has been successfully prepared by cross-linking linear poly(styrene-co-glycidyl methacrylate) (poly (STY-co-GMA)) with L-cysteine-capped CdSe quantum dots (Lcys-caped CdSe QDs). The microgel contained specific binding sites created by the covalent grafting of the copolymer onto the QDs via the GMA units, allowing for selective trapping of BPA molecules through π-π and hydrogen bond interactions with phenyl, carboxylic, and amine groups. After binding, electron transfer from the QDs to the analyte quenched the fluorescence at a wavelength of 547 nm when excited at 400 nm. The rational compositional and structural design allows the microgel to accurately detect BPA concentrations over a wide dynamic range of 1.0×10-1 to 1.0×105 µg/L with a low detection limit (7.0×10-2 to 8.0×10-2 µg/L) in deionized, drinking, and tap waters within just 2.0 min. On top of that, the sensitivity for BPA detection was 2.0-4.6 times higher than that of the other 3 structural analogues, even molecular imprinting was not involved. The influence of the STY/GMA compositions in the copolymers and environmental conditions, including pH and ionic strength, on the sensing performance was determined. Moreover, the sensing mechanism and the selectivity with respect to the molecular features were elucidated.

Sleep quality traits correlate with inflammatory markers in the breast tissue of women.

BACKGROUND: Several mechanisms have been posited to play a role in the sleep and breast cancer association, including alterations in immune function, but evidence remains inconclusive. A closer look at how sleep quality traits affect the breast microenvironment may provide clues for molecular mechanisms underlying the link between sleep and breast cancer. We examined the association between sleep quality traits (sleep duration, sleep aids, and insomnia) and tissue-based protein levels and gene expression of several inflammatory markers associated with breast cancer. METHODS: Breast tissues (normal n = 165 and adipose n = 74) were surgically obtained from women diagnosed with breast cancer. Protein levels by immunohistochemistry were determined using the quickscore method for 11 inflammatory markers in the normal epithelial breast tissue (interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), cyclooxygenase-2 (COX-2), leptin, serum amyloid A1 (SAA1), lactoferrin, transforming growth factor-beta (TGF-ß), and signal transducer and activator of transcription 3 markers (STAT3). Relative quantification of 4 genes (COX-2, IL-6, TNF-α and LEP) in the adipose breast tissue was carried out using qPCR. Patient characteristics and sleep traits (average sleep duration per night, taking sleeping aids in the past year, and the average number of insomnia episodes per month) were determined by telephone interview. Associations were tested using Spearman's rank correlation (rs) coefficients adjusted (ars) for age at surgery, menopausal status and PCR batch when applicable. Sleep duration categories (<7, 7-9, >9 h) and root- or log-transformed biomarker levels were examined with adjusted linear mixed models. RESULTS: TGF-ß and CRP levels in normal epithelial breast tissue were positively correlated with sleep aids (ars = 0.28, p = 0.013), and insomnia (ars = 0.23, p = 0.044) in postmenopausal women, respectively. IL-6 in the adipose breast tissue was inversely correlated with sleep aids (ars = -0.26, p = 0.029) in all women. None of the sleep traits significantly correlated with inflammatory markers in premenopausal women. Several markers tended to correlate at 0.05 ≥ p ≤ 0.10. Adjusted mean levels of inflammatory markers were significantly different across sleep duration categories (<7, 7-9, >9 h). Higher mean levels of IL-6, CRP, IL-10, and IL-6 and COX-2 expression were noted in the breast tissues of women sleeping < 7, and particularly, >9 h per night (p < 0.05). CONCLUSION: Our findings indicate that sleep duration, sleep aids, and insomnia may differently affect women's breast tissues depending on menopausal status. From a public health perspective, these results warrant further validation in larger studies. Since sleep is a modifiable factor, it may be an interesting approach for breast cancer prevention.

Refractive status, biometric components, and functional outcomes of patients with threshold retinopathy of prematurity: systemic review and a 17-year longitudinal study.

OBJECTIVE: To assess the long-term refractive status, visual outcome, astigmatism, and the change in biometric optic components in older adolescents up to age 17 years with threshold retinopathy of prematurity (ROP) treated with diode laser. METHODS: A retrospective, longitudinal study in which cycloplegic refraction, keratometry, and the biometric measurement of optic components were performed on 28 consecutive preterm eyes with laser-treated threshold ROP at age 17 years. The study results were statistically analysed and compared with age-matched full-term control. RESULTS: All patients with ROP had myopia (average spherical equivalent of - 6.35 D, ranges from - 1.25 to - 12.38 D), and 12 eyes (43%) were highly myopic (spherical equivalent < - 6.0 D). Threshold ROP eyes exhibited a significantly poorer visual acuity (P < 0.001), greater cylinder refractive error (P < 0.001), higher corneal astigmatism (P < 0.001), and flatter horizontal corneal curvature (P = 0.01) compared with age-matched controls. Biometric optic components analysis revealed a significant shallower anterior chamber depth (P < 0.001), thicker lens (P < 0.001), and shorter axial length (P = 0.021) in laser-treated ROP eyes compared with age-matched controls. CONCLUSIONS: In this 17-year longitudinal study, a higher prevalence of myopia and astigmatism was observed in laser-treated threshold ROP eyes compared with age-matched control eyes. Myopia and astigmatism in laser-treated ROP eyes typically progress through adolescence after school age. Therefore, we recommend that preterm patients with laser-treated threshold ROP should attend regular follow-up not only for refractive status but also for structural change of anterior segment until their adolescence.

Lithium alleviated spinal cord injury (SCI)-induced apoptosis and inflammation in rats via BDNF-AS/miR-9-5p axis.

Spinal cord injury (SCI) is a major cause of paralysis, disability and even death in severe cases. Lithium has neuroprotective effects on SCI, while the underlying mechanisms remain obscure. In the present study, we established a SCI rat model, which subsequently received lithium treatment. Results displayed that lithium treatment improved the locomotor function recovery and reduced apoptosis by increasing anti-apoptotic molecule expression and decreasing pro-apoptotic factor expression in SCI rats. Furthermore, lithium treatment alleviated the inflammatory response by inactivating the nuclear factor-kappa B (NF-κB) pathway and inhibited the expression of lncRNA brain-derived neurotrophic factor antisense (BDNF-AS) in SCI rats. Subsequent researches indicated that miR-9-5p was targeted and regulated by BDNF-AS. Lithium treatment rescued the upregulation of BDNF-AS expression and downregulation of miR-9-5p expression induced by H2O2 in SH-SY5Y cells. BDNF-AS overexpression or miR-9-5p interference attenuated the anti-apoptotic and anti-inflammatory effects of lithium chloride in SH-SY5Y cells that was damaged by H2O2 induction, revealing that lithium might act through the BDNF-AS/miR-9-5p axis. In vivo studies showed that the injection of BDNF-AS adenovirus vector or miR-9-5p inhibitor reversed the effects of lithium on the histologic morphology of spinal cord, motor function, inflammatory reaction and apoptosis in SCI rats, which was consistent with the results of in vitro studies. In conclusion, our data demonstrated that lithium reduced SCI-induced apoptosis and inflammation in rats via the BDNF-AS/miR-9-5p axis.

A Comparison of Liver-Directed Therapy and Systemic Therapy for the Treatment of Liver Metastases in Patients with Gastrointestinal Neuroendocrine Tumors: Analysis of the California Cancer Registry.

PURPOSE: To compare the outcomes of patients with gastrointestinal neuroendocrine tumor liver metastases treated with liver-directed therapy (LDT) to those treated with systemic therapy (ST) in a statewide cancer database. MATERIALS AND METHODS: A retrospective study was performed of patients with metastatic gastrointestinal tract neuroendocrine tumors treated with either LDT or ST alone between the years 2000-2012 in the California Cancer Registry. Overall survival and disease-specific survival were assessed using multivariable Cox proportional hazards analysis and propensity score matching. RESULTS: A total of 154 patients (ST, n = 87 and LDT, n = 67) were studied. The median overall survival and disease-specific survival for patients that received ST was 29 and 35 months versus 51 and >60 months for patients that received LDT. On multivariate analysis, LDT and the resection of the primary tumor were associated with improved survival (hazard ratio [HR] 0.52, P = .002; HR 0.43, P = .001). Non-white race, Medicaid/uninsured status, and the presence of lung metastases were associated with poor survival (HR 1.76, P = .014; HR 2.29, P = .009; and HR 1.79, P = .031). Propensity score matching demonstrated an improvement in disease-specific survival for LDT compared to ST (HR 0.53, P = .036). The improvement in overall survival on propensity score matching did not achieve statistical significance (HR 0.70, P = .199). CONCLUSIONS: LDT is associated with improved overall and disease-specific survival as compared to ST in patients with gastrointestinal neuroendocrine tumor liver metastases. Further investigation is needed to determine whether combination or sequential treatment can improve outcomes in this population.

Association between the polymorphisms in MMP-2 and MMP-9 with adiposity and mammographic features.

BACKGROUND: Matrix metalloproteinases (MMP)-2 and -9 may play an important role in adipogenesis and carcinogenesis. We investigated whether some polymorphisms located in these genes are associated with body adiposity and mammographic breast density, which are risk factors for breast cancer. METHODS: Our study population included 731 premenopausal women. Multivariate generalized linear models were used to evaluate the association of polymorphisms rs243865 in MMP-2 and rs3918242, rs17576, rs2250889 and rs2274756 in MMP-9 with anthropometric factors that refer to adiposity and mammographic features (percent density, dense area and non-dense area) measured by computer-assisted method. RESULTS: The number of copies of rs243865 T allele in MMP-2 was associated with increased means of anthropometric factors (ptrend < 0.05 for all except waist-to-hip ratio). The same allele of rs243865 was associated with decreased mean percent density (ptrend = 0.036) and increased mean non-dense area (ptrend = 0.031) when adjusted for potential confounders, but these associations were attenuated when further adjusted for adiposity. CONCLUSION: These findings suggest that the relation between rs243865 in MMP-2 and mammographic features could be mediated by adiposity.

The green tea polyphenol epigallocatechin-3-gallate attenuates age-associated muscle loss via regulation of miR-486-5p and myostatin.

(-)-Epigallocatechin-3-gallate (EGCG), the most abundant catechin component in green tea, has been reported to attenuate age-associated insulin resistance, lipogenesis and loss of muscle mass through restoring Akt activity in skeletal muscle in our previous and present studies. Accumulated data has suggested that polyphenols regulate signaling pathways involved in aging process such as inflammation and oxidative stress via modulation of miRNA expression. Here we found that miRNA-486-5p was significantly decreased in both aged senescence accelerated mouse-prone 8 (SAMP8) mice and late passage C2C12 cells. Thus, we further investigated the regulatory effect of EGCG on miRNA-486-5p expression in age-regulated muscle loss. SAMP8 mice were fed with chow diet containing without or with 0.32% EGCG from aged 32 weeks for 8 weeks. Early passage (<12 passages) and late passage (>30 passages) of C2C12 cells were treated without or with EGCG at concentrations of 50 µM for 24h. Our data showed that EGCG supplementation increased miRNA-486-5p expression in both aged SAMP8 mice and late passage C2C12 cells. EGCG stimulated AKT phosphorylation and inhibited FoxO1a-mediated MuRF1 and Atrogin-1 transcription via up-regulating the expression of miR-486 in skeletal muscle of 40-wk-old SAMP8 mice as well as late passage C2C12 cells. In addition, myostatin expression was increased in late passage C2C12 cells and anti-myostatin treatment upregulated the expression of miR-486-5p. Our results identify a unique mechanism of a dietary constituent of green tea and suggest that use of EGCG or compounds derived from it attenuates age-associated muscle loss via myostatin/miRNAs/ubiquitin-proteasome signaling.

Lymphovascular Invasion Predicts Lymph Node Involvement in Small Pancreatic Neuroendocrine Tumors.

INTRODUCTION: Pancreatic neuroendocrine tumors (p-NETS) are increasing in incidence, and prognostic factors continue to evolve. The benefit of lymphadenectomy for p-NETS ≤2 cm remains unclear. We sought to determine the significance of lymphovascular invasion (LVI) for small p-NETS. METHODS: The National Cancer Database was queried for patients with p-NETS ≤2 cm and with ≥1 evaluated lymph node (LN), years 2004-2015. Demographic, clinical, and treatment characteristics were analyzed. Multivariate logistic regression was performed to identify predictors of LN positivity. RESULTS: Among 2,499 patients identified, tumor location was delineated as the head (26%), body (18%), tail (38%), or unspecified (18%); 74% were well-differentiated versus 10% moderate, 2% poor, and 14% unknown. LVI occurred in 11%. A median of 9 LNs were evaluated; overall positivity was 18%. Mean survival was significantly longer in node-negative patients (115 vs. 95 months, log-rank p < 0.0001). LVI was the strongest predictor of node involvement (OR 10.4, p < 0.0001) when controlling for tumor size, grade, and location. Subset analysis of patients with known LVI status, grade, location, and mitoses found that LVI was more likely in the setting of moderate-to-high tumor grade, 1-2 cm size, pancreatic head location, and high mitotic rate. Among patients with ≥2 of these 4 factors, 25% were node-positive. CONCLUSIONS: Presence of LVI was the strongest predictor of node positivity. LVI on endoscopic biopsy should prompt resection and regional LN dissection to fully stage patients with small p-NETS. Patients with other high-risk factors should also be considered for resection and regional lymphadenectomy.

Dysregulations of mitochondrial quality control and autophagic flux at an early age lead to progression of sarcopenia in SAMP8 mice.

The senescence-accelerated mouse (SAM) prone 8 (SAMP8) has been demonstrated for muscular aging research including sarcopenia, but its underlying mechanisms remain scarce. Physiological indices and histology of skeletal muscle were analyzed in SAMP8 mice at different ages. SAMP8 mice exhibited typical features of sarcopenia at 40 weeks of age and were more time-efficient than that at 88 weeks of age in bothSAM resistant 1 (SAMR1) and C57BL/6 mice. Increase in FoxO3a-mediated transcription of Atrogin-1 and MuRF1 and decrease in phosphorylated mTOR/P70s6k were observed at week 40 in SAMP8 mice. High oxidative stress was observed from week 24 and persisted to week 40 in SAMP8 mice evidenced by overexpression of protein carbonyl groups and reduced activities of CAT, SOD, and GPx. Downregulation of genes involved in mitochondrial biogenesis (PGC-1α, Nrf-1, Tfam, Ndufs8, and Cox5b) and in mitochondrial dynamics fission (Mfn2 and Opa1) from week 24 indicated dysregulation of mitochondrial quality control in SAMP8 mice. Impaired autophagic flux was observed in SAMP8 mice evidenced by elevated Atg13 and LC3-II accompanied with the accumulation of P62 and LAMP1. Increases in inflammatory factors (IL-6 and MCP-1), adipokines (leptin and resistin), and myostatin in serum at week 32 and decline in Pax7+ satellite cell resided next to muscle fibers at week 24 implied that muscle microenvironment contributed to the progression of sarcopenia in SAMP8 mice. Our data suggest that early alterations of mitochondrial quality control and autophagic flux worsen muscle microenvironment prior to the onset of sarcopenia.

A Pathology Review of the Lower Gastrointestinal Tract in Relation to Ulcerative Colitis in Rats and Cynomolgus Macaques Treated With Ammonium Perfluorooctanoate.

Among many short-term, subchronic, and chronic toxicology studies with ammonium perfluorooctanoate (PFOA), the gastrointestinal tract has not been identified as a target organ for PFOA-related toxicity in laboratory animals where the corresponding serum PFOA concentrations typically approach several orders of magnitude higher than the general human population. These lack of gastrointestinal tract-related findings were in direct contrast to an epidemiological observation where a positive trend was observed for ulcerative colitis, an idiopathic chronic inflammatory condition of the gut, in a Mid-Ohio River community whose drinking water contained higher levels of PFOA. This study was conducted to perform a histological reevaluation of large intestine sections in laboratory animals from 2 long-term toxicological studies: one was with Sprague Dawley rats that received ammonium PFOA in their diet for 2 years and the other one was with cynomolgus macaques that received daily capsules of ammonium PFOA for 6 months. In both studies, there was a lack of histological evidence of treatment-related inflammatory lesions that was suggestive of the occurrence of ulcerative colitis in these laboratory animals even under the most rigorous treatment schedules. These findings do not offer support for the biological plausibility of the epidemiological associations reported.

EGR1 interacts with DNMT3L to inhibit the transcription of miR-195 and plays an anti-apoptotic role in the development of gastric cancer.

EGR1 regulates the expression of its downstream target genes and may exert different biological effects in different tumours. We found that the expression of EGR1 was increased in gastric cancer (GC), and silencing the expression of EGR1 promoted the apoptosis of GC cells. Moreover, overexpression of EGR1 repressed the apoptosis of GC cells. Bioinformatics analysis showed that EGR1 had binding sites at the upstream promoter region of miR-195; ChIP assays were applied to determine EGR1 occupancy of the miR-195 promoter. The RT-PCR results showed that EGR1 suppressed the expression of miR-195. The mechanism by which EGR1 acts as a transcriptional repressor is still unclear. Bioinformatics analysis showed that EGR1 may interact with DNMT3L. We confirmed that EGR1 and DNMT3L formed a complex, and EGR1 was an important player in the transcriptional control of miR-195. Overexpression of miR-195 inhibited proliferation and promoted apoptosis in GC cells. We found a well-matched miR-195 binding site at the AKT3 3'-UTR. Double luciferase reporter assays showed that AKT3 was a target of miR-195, and silencing AKT3 repressed cell proliferation and promoted apoptosis. Our results indicated EGR1 may interact with DNMT3L to inhibit the miR-195-AKT3 axis and regulate the GC cell apoptosis.

Mechanism of Photocatalytic CO2 Reduction by Bismuth-Based Perovskite Nanocrystals at the Gas-Solid Interface.

We report here a series of nontoxic and stable bismuth-based perovskite nanocrystals (PeNCs) with applications for photocatalytic reduction of carbon dioxide to methane and carbon monoxide. Three bismuth-based PeNCs of general chemical formulas A3Bi2I9, in which cation A+ = Rb+ or Cs+ or CH3NH3+ (MA+), were synthesized with a novel ultrasonication top-down method. PeNC of Cs3Bi2I9 had the best photocatalytic activity for the reduction of CO2 at the gas-solid interface with formation yields 14.9 µmol g-1 of methane and 77.6 µmol g-1 of CO, representing a much more effective catalyst than TiO2 (P25) under the same experimental conditions. The products of the photocatalytic reactions were analyzed using a gas chromatograph coupled with a mass spectrometer. According to electron paramagnetic resonance and diffuse-reflectance infrared spectra, we propose a reaction mechanism for photoreduction of CO2 via Bi-based PeNC photocatalysts to form CO, CH4, and other possible side products.

miR-99b-3p is induced by vitamin D3 and contributes to its antiproliferative effects in gastric cancer cells by targeting HoxD3.

Vitamin D3 is known to have anticancer actions by affecting tumorigenesis including the cell cycle and cell apoptosis in gastric cancer (GC) cells; the genes including microRNAs (miRNAs) regulated by vitamin D3 signaling remain discovered. miR-99b-3p, the tumor suppressor gene, is not only decreased in GC tissues, but is also induced by vitamin D3 through the vitamin D receptor (VDR) binding on the promoter domain of miR-99b. Further study indicates that miR-99b-3p inhibits cell viability and induces cell arrest in the S-phase in GC cells, the direct target gene of miR-99b-3p is verified to be HoxD3, which is also overexpressed in GC cell lines. Overall, our results show that miR-99b-3p mediates the antiproliferative of vitamin D3 in GC cells and might hold promise for prognosis and therapeutic strategies for GC treatment.

MicroRNA-1297 inhibits proliferation and promotes apoptosis in gastric cancer cells by downregulating CDC6 expression.

Gastric cancer (GC), one of the most common malignant tumors and the second most common leading cause of cancer-related death worldwide, is a biologically heterogeneous disease accompanied by various genetic and epigenetic alterations. However, the molecular mechanisms underlying this disease are complex and not completely understood. Increasing studies have shown that aberrant microRNA (miRNA) expression is associated with GC tumorigenesis and growth. MiR-1297 has been confirmed to be a cancer suppressor in diverse tumors in humans. However, to date, the function and mechanism of miR-1297 in GC have not been determined. Here, we found that the expression of miR-1297 was significantly reduced in GC tissues or GC cell lines compared with paracarcinoma normal tissue or normal cell lines. Exogenic overexpression of miR-1297 in GC cell lines can inhibit cell proliferation and colony formation and induce apoptosis, and inhibition of miR-1297 in GC cell lines can promote cell proliferation and colony formation, and reduce apoptosis in vitro. We further confirmed that miR-1297 acted as a tumor suppressor through targeting cell division control protein 6 (CDC6) in GC. Moreover, the inverse relationship between miR-1297 and CDC6 was verified in GC cell lines. Our results indicated that miR-1297 is a potent tumor suppressor in GC, and its antiproliferative and gene-regulatory effects are, in part, mediated through its downstream target gene, CDC6. These findings implied that miR-1297 might be used as a novel therapeutic target of GC.

Physicochemical characteristics of microbial content in a modified anaerobic inclining-baffled reactor (MAI-BR) treating recycled paper mill effluent (RPME).

Microbial content formed in bioreactors plays a significant role in the anaerobic process. Therefore, the physicochemical characteristics of microbial content in a modified anaerobic inclining-baffled reactor (MAI-BR) treating recycled paper mill effluent (RPME) were investigated using Fourier transform infrared (FTIR), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), thermogravimetric (TG), and derivative thermogravimetric (DTG) analyses, scanning electron microscopy-energy dispersive X-ray spectroscopy (SEM-EDS), Brunauer-Emmett-Teller (BET), and surface area analyzer. FTIR spectra revealed that the microbial content had stronger characteristic peaks corresponding to alcohols, water, lipids carbohydrates, proteins, and mineral compounds. Calcite, muscovite, and lepidolite were the prevalent mineral phases found by XRD analysis. The elemental of these minerals like C, Ca, N, O, and Si was confirmed by XPS results. The microbial content samples from each compartment showed similar thermal behavior. SEM images showed that straight rod-shaped and Methanosaeta-like microorganisms were predominant, whereas C, O, and Ca were noticed by EDS on the surface of granules. The BET surface areas and pores of granules are found to decline throughout the reactor's compartment, where Compartment 1 had the largest values. Thus, the findings of this study establish further understanding of the physicochemical properties of microbial content formed in MAI-BR during the RPME treatment.