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1.
BMC Urol ; 24(1): 11, 2024 Jan 06.
Artigo em Inglês | MEDLINE | ID: mdl-38184525

RESUMO

BACKGROUND: The incidence rate of malignant tumors after solid organ transplantation is higher than the normal population. The aim of our study is to identify the risk of renal cell carcinoma (RCC) after liver, kidney, heart and lung transplantation, respectively, and suggest that transplant patients can be screened early for tumors to avoid risk. METHODS: PubMed, Embase and the Cochrane Library from their inception until August 16,2023. Retrospective and cohort studies which focus on the statistical data of standardized incidence ratios (SIRs) of RCC after solid organ transplantation (SOT) more than one year have been included and extracted. The study was registered with PROSPERO, CRD4202022343633. RESULTS: Sixteen original studies have been included for meta-analysis. Liver transplantation could increase the risk of RCC (SIR = 0.73, 95%CI: 0.53 to 0.93) with no heterogeneity(P = 0.594, I2 = 0.0%). And kidney transplantation could increase the risk of RCC(8.54, 6.68 to 10.40; 0.000,90.0%). Besides, heart and lung transplantation also could increase the risk of RCC(SIR = 0.73, 95%CI: 0.53 to 0.93; SIR = 1.61, 95%CI:0.50 to 2.71). Moreover, significance could also be found in most subgroups, especially the European group and retrospective study group. What's more, after removing studies which have a greater impact on the overall outcome in RCC rate after kidney transplantation, heterogeneity did not solve and significant different was also observed in the European group (7.15, 5.49 to 8.81; 0.000, 78.6%). CONCLUSION: Liver, kidney, heart and lung transplantation patients have an increased risk of processing RCC compared to the general population and most subgroups, especially in geographic location of European subgroup, which suggested that patients should be screened frequently after transplantation.


Assuntos
Carcinoma de Células Renais , Neoplasias Renais , Transplante de Rim , Humanos , Carcinoma de Células Renais/epidemiologia , Carcinoma de Células Renais/etiologia , Incidência , Estudos Retrospectivos , Transplante de Rim/efeitos adversos , Neoplasias Renais/epidemiologia , Neoplasias Renais/etiologia
2.
Nanomaterials (Basel) ; 14(2)2024 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-38251115

RESUMO

Super-hydrophilic and oleophobic functional materials can prevent pollution or adsorption by repelling oil, and have good circulation. However, traditional strategies for preparing these functional materials either use expensive fabrication machines or contain possibly toxic organic polymers, which may prohibit the practical application. The research of multifunctional ZnO microstructures or nanoarrays thin films with super-hydrophilic, antifouling, and antibacterial properties has not been reported yet. Moreover, the exploration of underwater oleophobic and self-cleaning antifouling properties in ZnO micro/nanostructures is still in its infancy. Here, we prepared ZnO microstructured films on fluorine-doped tin oxide substrates (F-ZMF) for the development of advanced self-cleaning type super-hydrophilic and oleophobic materials. With the increase of the accelerators, the average size of the F-ZMF microstructures decreased. The F-ZMF shows excellent self-cleaning performance and hydrophilic (water contact angle ≤ 10°) and oleophobic characteristics in the underwater antifouling experiment. Under a dark condition, F-ZMF-4 showed good antibacterial effects against Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) with inhibition rates of 99.1% and 99.9%, respectively. This study broadens the application scope of ZnO-based material and provides a novel prospect for the development of self-cleaning super-hydrophilic and oleophobic materials.

3.
Artigo em Inglês | MEDLINE | ID: mdl-38135863

RESUMO

Certain dietary and physical activity (PA) behaviors may differentially predispose male and female adolescents to obesity and diabetes; however, sex differences in dietary and PA behaviors and in factors that impact these behaviors (e.g., self-efficacy, social support) in this population remain unknown. Using data from a community-based adolescent diabetes prevention intervention conducted in East Harlem in New York City, we examined sex differences in baseline characteristics including clinical measurements, lifestyle behaviors, and behavioral determinants. Among 147 overweight/obese adolescents aged 13-19 years, 61.9% were girls, 69.7% were of Hispanic ethnicity, 24.8% were non-Hispanic Black, and 60.5% were diagnosed with prediabetes. Boys had higher metabolic risk scores than girls (3.8 vs. 3.3, p = 0.002) despite girls reporting more perceived barriers to healthy eating and PA. Boys reported doing more moderate to vigorous PA but also had more sedentary behaviors than girls. Boys reported higher self-efficacy and more peer support for PA. Girls reported more depressive symptoms and were more likely to compare their body images to those in magazines/social media. Overall, among a sample of urban adolescents with high metabolic risk, we found significant sex differences in many dietary and PA behaviors and related factors, which could be used to inform tailored strategies for weight management to reduce cardiometabolic risk among youth from similar high-risk populations.

4.
JAMA Otolaryngol Head Neck Surg ; 149(12): 1101-1110, 2023 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-37796484

RESUMO

Importance: Cancer survivors are at a higher risk of developing hearing loss (HL) due to older age, chemotherapy, and radiotherapy. However, the prevalence of HL among US cancer survivors remains unknown. Additionally, there is a lack of uniform HL screening guidelines for this enlarging population. Objective: To estimate the prevalence of subjective HL and objective HL by audiometry test among cancer survivors and compare them with the general population as well as to assess the performance of subjective HL questions in detecting true (ie, audiometry-confirmed) HL. Design, Setting, and Participants: In a cross-sectional design, adults between ages 20 and 80 years who had audiometry testing and responded to a hearing questionnaire from the National Health and Nutrition Examination Survey (2011-2012, 2015-2016, and 2017 to March 2020 prepandemic survey cycles) were selected. Data analysis was conducted from August 13, 2022, to July 26, 2023. Main Outcomes and Measures: The weighted prevalence of subjective HL (troublesome hearing and tinnitus) and objective HL (speech-frequency HL and high-frequency HL) by audiometry were calculated. Analyses with χ2 testing and multiadjusted logistic regression models were used to compare HL between cancer survivors and the general population. To evaluate the performance of subjective HL questions as a tool to screen for objective HL by audiometry, areas under the curve were estimated using age- and gender-adjusted logistic regression. Results: Among the total 9337 participants (weighted n = 90 098 441; 51.2% women), 10.3% were cancer survivors. Compared with the general population, cancer survivors had a higher prevalence of troublesome hearing (adjusted odds ratio [AOR], 1.43; 95% CI, 1.11-1.84), tinnitus (AOR, 1.28; 95% CI, 0.94-1.74), speech-frequency HL (AOR, 1.43; 95% CI, 1.11-1.85), and high-frequency HL (AOR, 1.74; 95% CI, 1.29-2.34). When using the subjective HL tool and questioning regarding whether the participants were having troublesome hearing and/or tinnitus in screening for HL, the age- and gender-adjusted area under the curve was 0.88 in detecting speech-frequency HL and 0.90 in detecting high-frequency HL. Conclusion and Relevance: The findings of this study suggest that cancer survivors have a significantly higher prevalence of HL than the general population. Two subjective HL questions could potentially accurately identify those who have true HL and provide a simple and efficient screening tool for health care professionals. Cancer survivors and their families should be educated and encouraged to discuss hearing concerns, and health care professionals should facilitate raising awareness and provide early screening and timely referral when HL is identified.


Assuntos
Sobreviventes de Câncer , Surdez , Neoplasias , Zumbido , Adulto , Humanos , Feminino , Masculino , Zumbido/diagnóstico , Zumbido/epidemiologia , Zumbido/etiologia , Inquéritos Nutricionais , Estudos Transversais , Neoplasias/complicações , Neoplasias/epidemiologia , Perda Auditiva de Alta Frequência , Audiometria de Tons Puros
5.
Phytomedicine ; 121: 155083, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37722244

RESUMO

BACKGROUND: Astrocytes play a vital role in offering functional support for neurons, which are related to the pathogenic mechanism of depression. Ginsenoside Rb1 (GRb1) is demonstrated with antidepressant-like activities. PURPOSE: We aimed to investigate whether GRb1 can inhibit mitophagy-mediated astrocytic pyroptosis to protect neurons in depression. STUDY DESIGN: Model rats were subjected to chronic unpredictable mild stress (CUMS) for determining the in vivo antidepressant activity of GRb1. METHODS: The mitophagy-mediated antipyroptosis role of GRb1 was assessed in lipopolysaccharide (LPS) + ATP-stimulated astrocytes. The mechanism by which GRb1 protects synaptic plasticity was investigated using hippocampal neurons incubated in an astrocyte medium. The rat depressive-like behaviors were determined through sucrose preference, forced swimming, and the open-field tests. Escitalopram was used in the anti-depression control of GRb1. Cyclosporin A (CsA), a mitophagy inhibitor, and interleukin (IL)-1ß were used to reverse the role of GRb1 in mitophagy and pyroptosis, respectively. RESULTS: GRb1 inhibited LPS-induced inflammation and activation in the astrocytes and repressed nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Also, GRb1 repressed LPS + ATP-promoted astrocytic pyroptosis. During GRb1 treatment, the activation of mitophagy with a decrease in ROS was observed in LPS + ATPs-stimulated astrocytes. CsA enhanced GRb1-decreased ROS and promoted astrocytic pyroptosis. The GRb1-treated astrocyte medium suppressed neuron death and increased neuron viability and synaptic density. Escitalopram and GRb1 improved the depressive-like behaviors of the rats. GRb1 activated mitophagy and inhibited astrocytic activation and pyroptosis in rats with depression. It also reduced impairments in synaptic structures and increased synaptic density in depressive-like rats. IL-1ß increased astrocytic pyroptosis and reversed GRb1-enhanced synaptic plasticity in the rats exposed to CUMS. There were no statistical changes in depressive-like behaviors between GRb1 and Escitalopram groups. CONCLUSION: GRb1 modulates mitophagy and the NF-κB pathway to inhibit astrocytic pyroptosis, thereby maintaining neurological homeostasis by repressing inflammation and enhancing synaptic plasticity.


Assuntos
Astrócitos , NF-kappa B , Ratos , Animais , Astrócitos/metabolismo , NF-kappa B/metabolismo , Piroptose , Escitalopram , Lipopolissacarídeos , Mitofagia , Espécies Reativas de Oxigênio/metabolismo , Antidepressivos/uso terapêutico , Neurônios/metabolismo , Hipocampo/metabolismo , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Trifosfato de Adenosina/metabolismo , Depressão/tratamento farmacológico , Depressão/metabolismo
6.
Tob Prev Cessat ; 9: 18, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37274934

RESUMO

INTRODUCTION: Hospital staff discussing smoking with children and their families can impact tobacco control, which is crucial in reducing the harmful effects of tobacco smoke exposure. Our study aims to assess staff comfort level in discussing smoking with patients or their families, and coworkers, after the implementation of a hospital-wide tobacco control policy. METHODS: This cross-sectional study included 2340 staff members who completed an anonymous online survey in a large urban children's hospital in 2019. The main outcomes of interest were the comfort level in discussing smoking with patients or their families, and co-workers. We used multivariable logistic regression to identify whether the comfort level varied by sex, age, job type, and smoking status. RESULTS: Most of the respondents (83.8%) were female, 41.2% were aged 18-35 years, 57.6% worked as clinical staff, and 15.5% were ever smokers. Compared to males, females were less likely to feel very comfortable in asking patients or their families about their smoking tobacco (adjusted odds ratio, AOR=0.72; 95% CI: 0.56-0.92) or talking to co-workers about the health risks associated with their smoking (AOR=0.71; 95% CI: 0.54-0.93). Staff who were non-smokers were less likely to feel very comfortable in talking to co-workers about the health risks associated with their smoking (AOR=0.60; 95% CI: 0.45-0.78). The odds of feeling very comfortable in discussing smoking were consistently lower among those aged 18-35 years than their older counterparts. Clinical staff were more likely than non-clinical staff to feel very comfortable in discussing with patients and their parents about smoking, but there was no difference when talking to co-workers. CONCLUSIONS: We found differences in staff comfort level in discussing smoking with patients or their families, and coworkers, by sex, age, job type, and smoking status. These results can guide training and identify potential barriers and improve tailored tobacco control training programs and policies for hospital staff.

7.
Bioorg Med Chem Lett ; 91: 129370, 2023 07 15.
Artigo em Inglês | MEDLINE | ID: mdl-37301522

RESUMO

Plinabulin is a promising microtubule destabilizing agent in phase 3 clinical stage for treating non-small cell lung cancer. However, the high toxicity and the poor water solubility of plinabulin limited its use and more plinabulin derivatives need to be explored. Here, two series of 29 plinabulin derivatives were designed, synthesized and evaluated for their anti-tumor effect against three types of cancer cell lines. Most of derivatives exerted obvious inhibition to the proliferation of the cell lines tested. Among them, compound 11c exerted stronger efficiency than plinabulin, and the reason might be the additional hydrogen bond between the nitrogen atom of the indole ring in compound 11c and Gln134 of ß-tubulin. Immunofluorescence assay showed that compound 11c at 10 nM significantly disrupted tubulin structure. Compound 11c also significantly induced G2/M cell cycle arrest and apoptosis in dose dependent manner. These results suggest that compound 11c might be a potential candidate for cancer treatment as antimicrotubule agent.


Assuntos
Antineoplásicos , Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Humanos , Tubulina (Proteína)/metabolismo , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Moduladores de Tubulina/química , Neoplasias Pulmonares/tratamento farmacológico , Antineoplásicos/química , Proliferação de Células , Ensaios de Seleção de Medicamentos Antitumorais , Linhagem Celular Tumoral , Relação Estrutura-Atividade , Apoptose
8.
J Neuroinflammation ; 20(1): 31, 2023 Feb 10.
Artigo em Inglês | MEDLINE | ID: mdl-36765376

RESUMO

OBJECTIVE: Patients with hypertension have a risk of depression. Morinda officinalis oligosaccharides (MOOs) have anti-depressant properties. In this study, we aimed to determine whether MOOs can improve the symptoms of depression in individuals with hypertension. METHODS: Dahl salt-sensitive rats fed with a high-salt diet were stimulated by chronic unpredictable mild stress to mimic hypertension with depression. Primary astrocytes and neurons were isolated from these rats. Astrocytes underwent LPS stimulation to simulate the inflammatory astrocytes during depression. MOOs were administrated at 0.1 mg/g/day in vivo and 1.25, 2.5, and 5 mg/mL in vitro. Mitophagy was inhibited using 5 mM 3-methyladenine (3-MA). Astrocyte-mediated neurotoxicity was detected by co-culturing astrocytes and neurons. RESULTS: MOOs decreased systolic pressure, diastolic pressure, and mean arterial pressure, thereby improving depression-like behavior, including behavioral despair, lack of enthusiasm, and loss of pleasure during hypertension with depression. Furthermore, MOOs inhibited inflammation, astrocytic dysfunction, and mitochondrial damage in the brain. Then, MOOs promoted autophagosome and lysosome enriched in mitochondria in LPS-stimulated astrocytes. MOOs suppressed mitochondrial damage and the release of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1ß in astrocytes undergoing LPS stimulation. Importantly, MOOs rescued the impaired neurons co-cultured with astrocytes. The effects of MOOs on LPS-stimulated astrocytes were reversed by 3-MA. Finally, MOOs upregulated LPS-downregulated Mfn2 expression in astrocytes. Mfn2 inhibition partly reversed the effects of MOOs on hypertension with depression. Intriguingly, Mfn2 suppression activated PI3K/Akt/mTOR pathway during MOOs treatment. CONCLUSIONS: Astrocytes develop neuroinflammation in response to mitochondrial damage during hypertension with depression. MOOs upregulated Mfn2 expression to activate the PI3K/Akt/mTOR pathway-mediated mitophagy, thereby removing impaired mitochondria in astrocytes. HIGHLIGHTS: 1. MOOs have anti-hypertensive and anti-depressive properties. 2. MOOs inhibit inflammation and injury in astrocytes during hypertension with depression. 3. MOOs induce mitophagy activation in inflammatory astrocytes with mitochondrial damage. 4. MOOs upregulate Mfn2 expression in astrocytes. 5. Mfn2 activates mitophagy to resist mitochondrial damage in astrocytes.


Assuntos
Hipertensão , Morinda , Ratos , Animais , Mitofagia , Depressão/tratamento farmacológico , Depressão/etiologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Lipopolissacarídeos/farmacologia , Fosfatidilinositol 3-Quinases/metabolismo , Ratos Endogâmicos Dahl , Inflamação/metabolismo , Interleucina-6/metabolismo , Hipertensão/metabolismo , Serina-Treonina Quinases TOR/metabolismo , Oligossacarídeos/metabolismo , Oligossacarídeos/farmacologia , Astrócitos/metabolismo
9.
Molecules ; 28(2)2023 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-36677726

RESUMO

Cyanidin-3-O-glucoside (C3G), an active ingredient in anthocyanins, mainly exists in dark cereals. C3G was investigated for its effect on human gastric cancer (GC) cells, together with its molecular mechanism. The CCK-8 assay results showed that C3G had significant antiproliferative effects on GC cells, but it had little effect on normal cells. Western blot and flow cytometry results showed that C3G regulated the reduction of mitochondrial membrane potential and arrested the cell cycle in the G2/M phase through the AKT signaling pathway, causing the cells to undergo apoptosis. Additionally, in MKN-45 cells, C3G markedly raised intracellular reactive oxygen species (ROS) levels. The wound healing assay and Transwell assay results showed that MKN-45 cell migration was significantly inhibited. Western blot results showed that the expression of E-cadherin protein was upregulated and the expressions of ß-catenin, N-cadherin, and Vimentin were downregulated. Additionally, following N-acetylcysteine treatment, the expression levels of these proteins were reduced. In conclusion, C3G caused MKN-45 cells to undergo apoptosis; arrested the cell cycle in the G2/M phase; hindered cell migration; and activated the MAPK, STAT3, and NF-κB signaling pathways, by inducing an increase in ROS levels. Thus, C3G may be a promising new medication for the treatment of GC.


Assuntos
Antocianinas , Neoplasias Gástricas , Humanos , Antocianinas/farmacologia , Antocianinas/uso terapêutico , Espécies Reativas de Oxigênio/metabolismo , Neoplasias Gástricas/tratamento farmacológico , Glucosídeos/farmacologia , Glucosídeos/uso terapêutico , Transdução de Sinais , Apoptose
10.
CNS Neurosci Ther ; 29(2): 669-681, 2023 02.
Artigo em Inglês | MEDLINE | ID: mdl-36550591

RESUMO

OBJECTIVE: This investigation aims to determine the antidepressant role of Xingpijieyu formula (XPJYF) mediated via gut microbiota (GM)-brain axis. METHODS: We collected fecal microbiota from patients with depressive disorder (DD) and cultured microbiota in vitro. Some of microbiota were transplanted into germ-free rats with the intragastric administration of XPJYF grain at the dose of 1.533 g/kg/day. The behaviors were studied by forced swimming test, open field test, sucrose preference test, and body weight. Products of hypothalamus-pituitary-adrenocortical (HPA) axis, neurotransmitter, and serum cytokines were investigated by enzyme linked immunosorbent assay. Glial fibrillary acidic protein (GFAP), a biomarker of astrocyte, was quantified using immunofluorescence. Microbiota culturing in vitro after XPJYF treatment was analyze by 16 s RNA sequencing technology. We used lipopolysaccharide (LPS) to mimic activated rat primary astrocyte in vitro. Brain-derived neurotrophic factor (BDNF), cytokines, and oxidative stress factors were determined by western blotting, and glycometabolism in astrocyte was investigated by 2-deoxy-D-glucose (2-DG) uptake, adenosine triphosphate (ATP), and glucose-1-phosphate (G1P) kits. RESULTS: Microbiota composition during 8 mg/ml of XPJYF (H12-8) for 12 h showed the more consistency. Lactococcus is enriched in DD-derived microbiota composition, and Biffdobacterium and Lactobacillus in H12-8 group. GLUCOSE1PMETAB-PWY and PWY-7328 of which biofunctions were dominantly encoded by Biffdobacterium were the top two of altered pathways. XPJYF improved behaviors and repressed astrocyte activation in depression rats. XPJYF elevated 2-DG uptake, ATP, glucose-1-phosphate, and brain-derived neurotrophic factor (BDNF), and inhibited cytokines and oxidative stress in LPS-induced astrocyte. CONCLUSION: XPJYF treatment targets inflammation, activation, and glycometabolim in astrocyte via gut microbiota modulation, thereby improve animal behaviors, HPA axis dysfunction, and neurotransmitter synthesis in depression rats.


Assuntos
Transtorno Depressivo , Microbioma Gastrointestinal , Ratos , Animais , Depressão/tratamento farmacológico , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Sistema Hipotálamo-Hipofisário/metabolismo , Lipopolissacarídeos , Sistema Hipófise-Suprarrenal/metabolismo , Citocinas/metabolismo , Transtorno Depressivo/tratamento farmacológico , Estresse Psicológico/metabolismo
11.
Pharmaceuticals (Basel) ; 15(12)2022 Dec 12.
Artigo em Inglês | MEDLINE | ID: mdl-36558992

RESUMO

Isoorientin (ISO) is a flavonoid compound containing a luteolin structure, which can induce autophagy in some tumor cells. This study investigated the impact of ISO in gastric cancer AGS cells, and performed an experimental analysis on the main signaling pathways and transduction pathways it regulates. CCK-8 assay results showed that ISO reduced the survival rate of gastric cancer AGS cells, but the toxicity to normal cells was minimal. Hoechst 33342/PI double staining assay results showed that ISO induced apoptosis in gastric cancer AGS cells. Further analysis by flow cytometry and Western blot showed that ISO induced apoptosis via a mitochondria-dependent pathway. In addition, the level of reactive oxygen species (ROS) in gastric cancer AGS cells also increased with the extension of the ISO treatment time. However, cell apoptosis was inhibited by preconditioning cells with N-acetylcysteine (NAC). Moreover, ISO arrested the cell cycle at the G2/M phase by increasing intracellular ROS levels. Cell migration assay results showed that ISO inhibited cell migration by inhibiting the expression of p-AKT, p-GSK-3ß, and ß-catenin and was also related to the accumulation of ROS. These results suggest that ISO-induced cell apoptosis by ROS-mediated MAPK/STAT3/NF-κB signaling pathways inhibited cell migration by regulating the AKT/GSK-3ß/ß-catenin signaling pathway in gastric cancer AGS cells.

12.
J Cancer Surviv ; 2022 Oct 12.
Artigo em Inglês | MEDLINE | ID: mdl-36222970

RESUMO

PURPOSE: As the life expectancy of cancer survivors continues to improve, cancer survivors start or resume their life roles as caregivers themselves. We aim to assess the associations between caregiving, cancer diagnosis, and self-reported well-being. METHODS: Data were obtained from the Behavioral Risk Factor Surveillance System (BRFSS) 2016, 2018, and 2020. Outcomes included self-reported general health, physical health, mental health, depression, physical inactivity, and poor sleep. Weighted multivariable logistic regression models were used to calculate self-reported well-being's adjusted odds ratio (aOR). RESULTS: Comparable to the proportion of caregivers in the general population, approximately 1 out of 5 cancer survivors were caregivers to others. Individuals with dual roles were significantly more likely to report poor general health (aOR = 2.45; 95%CI: 1.46-4.11), physical health (aOR = 2.17; 95%CI: 1.32-3.56), mental health (aOR = 2.47; 95%CI: 1.31-4.64), depression (aOR = 1.64; 95%CI: 1.15-2.41), physical inactivity (aOR = 1.56; 95%CI: 1.05-2.31), and poor sleep (aOR = 1.48; 95%CI: 1.00-2.19) than the general population. Differential impacts of an additional cancer diagnosis on the well-being of caregivers were observed by sex, race, and time since cancer diagnosis. CONCLUSIONS: Nearly four million cancer survivors in the USA are concomitant caregivers. Individuals with dual roles reported diminished well-being across a variety of measures than caregivers only. IMPLICATIONS FOR CANCER SURVIVORS: Significant unmet health and psychosocial needs exist among individuals with dual roles. Our findings urge for increased awareness of this additional role/responsibility in cancer survivors and provide direct evidence for healthcare providers and policymakers to develop substantial support from the structural level.

13.
Appl Microbiol Biotechnol ; 106(19-20): 6625-6640, 2022 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-36097174

RESUMO

Biogenic volatile organic compounds hold remarkable potential for controlling fungal decay in agro- and food products. Recently, we reported that linalool, the major volatile component of the Zanthoxylum schinifolium pericarp, showed great potential as a biofumigant to control Aspergillus flavus growth in postharvest grains. In this study, the inhibitory effects of linalool on A. flavus growth in stored grains and its underlying mechanism were investigated through transcriptomic and biochemical analyses. Linalool vapor at 800 µL/L can effectively prevent A. flavus growth in 22% moisture wheat grains. Linalool at 2 µL/mL completely inhibited the germination of A. flavus spores, and 10 µL/mL caused spore death. Scanning electron microscopy revealed that linalool treatment caused wrinkling and spore breakage. Transcriptomics showed that 3806 genes were significantly differentially expressed in A. flavus spores exposed to 2 µL/mL linalool, predominantly showing enrichment regarding the ribosome, DNA replication, glutathione metabolism, peroxisome, and MAPK signaling pathways. Flow cytometry showed that linalool treatment caused hyperpolarization of mitochondrial membrane potential. 4,6-Diamidino-2-phenylindole staining indicated that linalool caused DNA fragmentation in A. flavus spores, and monodansylcadaverine staining confirmed that linalool induced autophagy in A. flavus spores. We thus propose that linalool can damage the plasma membrane, cause mitochondrial dysfunction and DNA damage, and induce autophagy in A. flavus spores. These findings considerably improve our understanding of the mechanisms underlying the inhibitory effects of linalool on A. flavus, which is crucial regarding the development of applications to prevent postharvest grain spoilage due to A. flavus infestations. KEY POINTS: • The inhibitory potency of linalool on A. flavus spore germination was determined. • Transcriptomic analyses were performed to identify differentially expressed genes of A. flavus exposed to linalool. • A functional mechanism underlying the inhibitory effects of linalool on A. flavus spore germination is proposed.


Assuntos
Aspergillus flavus , Compostos Orgânicos Voláteis , Monoterpenos Acíclicos , Antifúngicos/farmacologia , Glutationa/metabolismo , Esporos Fúngicos , Compostos Orgânicos Voláteis/metabolismo
14.
Drug Dev Res ; 83(7): 1683-1696, 2022 11.
Artigo em Inglês | MEDLINE | ID: mdl-36048972

RESUMO

Peimine (PM), a natural product extracted from Fritillaria, has anti-inflammatory, drug resistance reversal, and other pharmacological effects. The purpose of this study was to investigate the antitumor effects and the molecular mechanisms of PM using gastric cancer MKN-45 cells. Cell counting kit-8 assays were used to evaluate the viability of gastric cancer cells after treatment with PM. The results showed that PM significantly reduced the activity of gastric cancer cells, and the effect was most obvious in MKN-45 cells. Annexin V-FITC/propidium iodide staining and flow cytometry were used to assess apoptosis of MKN-45 cells after PM treatment. Our results showed that PM-induced apoptosis of MKN-45 cells. Flow cytometry was also used to determine the mitochondrial membrane potential and reactive oxygen species (ROS) levels, and to assess PM-induced cell-cycle arrest. Additionally, Western blot was used to analyze the expression of signaling pathway proteins and the relationship between apoptosis and ROS accumulation. Our findings showed that PM destroyed the mitochondria by diminishing the mitochondrial membrane potential. In addition, PM regulated the mitogen-activated protein kinase (MAPK), signal transducer and activator of transcription 3, and nuclear factor kappa-B signaling pathways by promoting the accumulation of ROS in MKN-45 cells. PM also caused cell-cycle arrest in the G2/M phase by increasing ROS accumulation. Furthermore, PM inhibited cell migration by regulating the Wnt/ß-catenin pathway. In conclusion, PM plays an anticancer role through endogenous apoptosis pathways and by inhibiting cell migration, and it has the potential to be a useful treatment for gastric cancers.


Assuntos
Fator de Transcrição STAT3 , Neoplasias Gástricas , Humanos , Espécies Reativas de Oxigênio/metabolismo , Fator de Transcrição STAT3/metabolismo , NF-kappa B/metabolismo , Neoplasias Gástricas/metabolismo , Via de Sinalização Wnt , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Proteínas Quinases Ativadas por Mitógeno/farmacologia , Linhagem Celular Tumoral , Apoptose
15.
Rural Remote Health ; 22(3): 7339, 2022 09.
Artigo em Inglês | MEDLINE | ID: mdl-36088935

RESUMO

INTRODUCTION: Prior research has revealed rural populations have lower rates of breast and colorectal cancer screening compared to their urban counterparts in the USA. An increasing number of rural hospitals have closed, with rural residents reporting skipping diagnosing imaging and preventative care due to a lack of access. Considering increasing rural hospital closures, this study investigated disparities in breast and colorectal cancer screening between urban and rural women in the USA. METHODS: This cross-sectional study analyzed the Behavioral Risk Factor Surveillance System (BRFSS) data 2014-2019. Focusing on women aged 50-74 years, this study evaluated the prevalence of breast cancer and colorectal cancer (CRC) screening overall and by urban-rural location using multivariable logistic regressions. RESULTS: During the study period, the adjusted prevalences of breast cancer screening were 80.0% and 77.1% (p<0.001) in urban and rural settings, respectively. The adjusted CRC screening prevalences were 72.8% and 68.4% (p<0.001) in urban and rural settings, respectively. By year, this study found that by 2019 there was no significant difference between urban and rural screening: 80.8% versus 79.6% in breast cancer and 78.9% versus 76.6% in CRC screening in urban and rural groups, respectively. Screening disparities existed between different racial groups. CONCLUSION: Breast cancer and CRC screening disparities between urban and rural women have narrowed; however, they continue to exist within these groups. The implementation of screening initiatives targeting underscreened rural regions and racial groups continues to be necessary.


Assuntos
Neoplasias da Mama , Neoplasias Colorretais , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/epidemiologia , Neoplasias Colorretais/diagnóstico , Neoplasias Colorretais/epidemiologia , Neoplasias Colorretais/prevenção & controle , Estudos Transversais , Detecção Precoce de Câncer/métodos , Feminino , Humanos , População Rural
16.
Int J Cancer ; 151(8): 1291-1303, 2022 10 15.
Artigo em Inglês | MEDLINE | ID: mdl-35666524

RESUMO

Despite the overall decreasing incidence, nasopharyngeal cancer (NPC) continues to cause a significant health burden among Asian Americans (AAs), who are a fast-growing but understudied heterogeneous racial group in the United States. We aimed to examine the racial/ethnic disparities in NPC incidence, treatment, and mortality with a specific focus on AA subgroups. NPC patients aged ≥15 years were obtained from the Surveillance, Epidemiology, and End Results (SEER) 18 (1975-2018). AAs were divided into Chinese, Filipino, Vietnamese, Hawaiian, Japanese, Laotian, Korean, Cambodian, Indian/Pakistani and other Asian/Pacific Islanders (APIs). Age-adjusted incidence was calculated using the SEER*Stat software. Cox proportional and Fine-Gray subdistribution hazard models were used to calculate overall and cause-specific mortalities after adjusting for confounders. Among the total 11 964 NPC cases, 18.4% were Chinese, 7.7% Filipino, 5.0% Vietnamese, 1.2% Hawaiian, 1.0% Japanese, 0.8% Laotian, 0.8% Korean, 0.6% Cambodian, 0.5% Indian/Pakistani and 4.4% other APIs. Laotians had the highest age-adjusted NPC incidence (9.21 per 100 000), which was 18.04 times higher than it in non-Hispanic Whites (NHWs). Chinese and Filipinos observed lower overall mortalities, however, Chinese saw increased NPC-specific mortality than NHWs. Disparities in mortality were also found across different histology subtypes. This is the first and largest study examining the NPC incidence and outcomes in AA subgroups. The significant disparities of NPC within AAs underline the importance of adequate AA-subgroup sample size in future studies to understand the prognostic role of ethnicity in NPC and advocate more ethnically and culturally tailored cancer prevention and care delivery.


Assuntos
Asiático , Neoplasias Nasofaríngeas , Etnicidade , Humanos , Carcinoma Nasofaríngeo , Grupos Raciais , Estados Unidos/epidemiologia , População Branca
17.
CNS Neurosci Ther ; 28(9): 1409-1424, 2022 09.
Artigo em Inglês | MEDLINE | ID: mdl-35713215

RESUMO

AIM: The investigation aims to evaluate the potential effect of Shugan Granule (SGKL) on the gut, brain, and behaviors in rats exposed to chronic restraint stress (CRS). METHODS: The fecal microbiota and metabolite changes were studied in rats exposed to CRS and treated with SGKL (0.1 mg/kg/day). Depressive behaviors of these rats were determined through an open-field experiment, forced swimming test, sucrose preference, and weighing. Moreover, LPS-stimulated microglia and CRS-stimulated rats were treated with SGKL to investigate the regulation between SGKL and the PI3K/Akt/pathway, which is inhibited by LY294002, a PI3K inhibitor. RESULTS: (i) SGKL improved the altered behaviors in CRS-stimulated rats; (ii) SGKL ameliorated the CRS-induced neuronal degeneration and tangled nerve fiber and also contributed to the recovery of intestinal barrier injury in these rats; (iii) SGKL inhibited the hippocampus elevations of TNF-α, IL-1ß, and IL-6 in response to CRS modeling; (iv) based on the principal coordinates analysis (PCoA), SGKL altered α-diversity indices and shifted ß-diversity in CRS-stimulated rats; (v) at the genus level, SGKL decreased the CRS-enhanced abundance of Bacteroides; (vi) Butyricimonas and Candidatus Arthromitus were enriched in SGKL-treated rats; (vii) altered gut microbiota and metabolites were correlated with behaviors, inflammation, and PI3K/Akt/mTOR pathway; (viii) SGKL increased the LPS-decreased phosphorylation of the PI3K/Akt/mTOR pathway in microglia and inhibited the LPS-induced microglial activation; (ix) PI3K/Akt/mTOR pathway inactivation reversed the SGKL effects in CRS rats. CONCLUSION: SGKL targets the PI3K/Akt/mTOR pathway by altering gut microbiota and metabolites, which ameliorates altered behavior and inflammation in the hippocampus.


Assuntos
Depressão , Medicamentos de Ervas Chinesas , Microbioma Gastrointestinal , Estresse Psicológico , Animais , Doença Crônica , Depressão/tratamento farmacológico , Depressão/etiologia , Depressão/metabolismo , Medicamentos de Ervas Chinesas/farmacologia , Microbioma Gastrointestinal/efeitos dos fármacos , Inflamação/tratamento farmacológico , Lipopolissacarídeos/toxicidade , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos , Restrição Física/efeitos adversos , Estresse Psicológico/tratamento farmacológico , Estresse Psicológico/etiologia , Estresse Psicológico/metabolismo , Serina-Treonina Quinases TOR/metabolismo
19.
Molecules ; 27(9)2022 May 05.
Artigo em Inglês | MEDLINE | ID: mdl-35566297

RESUMO

Atractylodin (ATR) has anticancer effects on some tumor cells by inducing apoptosis, but its mechanism in lung cancer remains unclear. This study investigates the inhibitory effect of ATR on A549 lung cancer cells. Cell viability was detected by the Cell Counting Kit-8 assay, and results showed that ATR could significantly inhibit the proliferation of A549 cells. Apoptosis was detected by Annexin V-FITC/PI staining, and apoptosis rate and mitochondrial membrane potential were detected by flow cytometry. Results showed that the effect of ATR on the apoptosis of A549 cells was negatively correlated with the change in mitochondrial membrane potential. Western blot analysis showed that ATR regulated apoptosis induced by mitogen-activated protein kinase, signal transducer and activator of transcription 3, and nuclear factor kappa B signaling pathways. Analyses of reactive oxygen species (ROS), cell cycle, and cell migration showed that ATR induced intracellular ROS accumulation as an initiation signal to induce cell cycle arrest regulated by the AKT signaling pathway and cell migration inhibition regulated by the Wnt signaling pathway. Results showed that ATR can inhibit cell proliferation, induce cell apoptosis, induce cell cycle arrest, and inhibit the migration of A549 cells (p < 0.05 was considered statistically significant, * p < 0.05, ** p < 0.01 and *** p < 0.001).


Assuntos
Neoplasias Pulmonares , Células A549 , Apoptose , Pontos de Checagem do Ciclo Celular , Linhagem Celular Tumoral , Proliferação de Células , Furanos , Humanos , Neoplasias Pulmonares/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais
20.
Mol Neurobiol ; 59(5): 2855-2873, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-35230663

RESUMO

Ginsenoside Rg1 is the principal active ingredient in ginseng. The antidepressant effects of Rg1 have been validated; however, the specific underlying mechanism of this effect needs further research. Rats were subjected to the chronic restraint stress (CRS) depression model. Rg1, or a positive control drug, was administered to the rats. Depression-like behaviours were evaluated through behavioural experiments. Cytokine, mRNA, protein, ATP, and mitochondria DNA levels were detected using the indicated methods. Lentivirus-packaged plasmids were injected into the rat brain for GAS5 overexpression or knockdown. In vitro mitochondrial dysfunction was evaluated by detecting mitochondrial reactive oxygen species and mitochondrial membrane potential. Direct interaction between GAS5 and EZH2 was validated by RNA immunoprecipitation and RNA pull-down assay. The enrichment of EZH2 and H3K27me3 was evaluated through chromatin immunoprecipitation quantitative real-time PCR. Rg1 treatment alleviated depression-like behaviours, microglial activation, and mitochondrial dysfunction in CRS rats. Similarly, GAS5 knockdown revealed a similar protective effect of Rg1 treatment. GAS5 overexpression in the rat brain compromised the protective effect of Rg1 treatment. Moreover, Rg1 treatment or GAS5 knockdown attenuated microglial activation and mitochondrial dysfunction in vitro. Mechanically, GAS5 was suppressed SOCS3 and NRF2 expression by facilitating EZH2-mediated transcriptional repression. Rg1 attenuated microglial activation and improved mitochondrial dysfunction in depression by downregulating GAS5 expression. Mechanically, GAS5 might regulate microglial activation and mitochondrial dysfunction via the epigenetic suppression of NRF2 and SOCS3.


Assuntos
Ginsenosídeos , Fator 2 Relacionado a NF-E2 , Animais , Depressão/tratamento farmacológico , Proteína Potenciadora do Homólogo 2 de Zeste/metabolismo , Ginsenosídeos/farmacologia , Ginsenosídeos/uso terapêutico , Microglia/metabolismo , Mitocôndrias/metabolismo , Fator 2 Relacionado a NF-E2/metabolismo , RNA/metabolismo , Ratos , Proteína 3 Supressora da Sinalização de Citocinas/metabolismo , Proteínas Supressoras da Sinalização de Citocina/metabolismo
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