Screening for depression and anxiety in lung cancer patients: A real-world study using GAD-7 and HADS.

BACKGROUND: The psychological well-being of lung cancer patients is critical in-patient care but frequently overlooked. METHODS: This study, employing a cross-sectional, questionnaire-based design, aimed to elucidate the prevalence of depressive and anxiety symptoms among lung cancer patients and identify associated risk factors. Participants' demographic, medical history, disease stage, and pathology were systematically collected. Psychological assessment was conducted using the general anxiety disorder-7 (GAD-7), patient health questionnaire-9 (PHQ-9), and hospital anxiety and depression scale (HADS). Statistical analyses were performed using SPSS software (version 25.0). RESULTS: Out of 294 distributed questionnaires, 247 lung cancer patients were included in the final analysis, with an average completion time of 9.08 min. Notably, 32.4% exhibited depressive symptoms, while 30% displayed signs of anxiety. A significant correlation was found between both depressive and anxiety symptoms and a history of tobacco and alcohol consumption. Specifically, increased nicotine dependence and greater cumulative tobacco use were linked to higher rates of depressive symptoms, whereas cumulative alcohol consumption was associated with increased risks of anxiety symptoms. CONCLUSION: The study affirms the feasibility of GAD-7, PHQ-9, and HADS as screening tools for depressive and anxiety symptoms in lung cancer patients. It further highlights tobacco and alcohol consumption as significant risk factors for poor psychological health in this population.

Inhibition of testosterone synthesis induced by oral TiO2 NPs is associated with ROS-MAPK(ERK1/2)-StAR signaling pathway in SD rat.

Titanium dioxide nanoparticles (TiO2 NPs) have been widely used in food, medical, and other fields; their reproductive toxicity has been reported in numerous studies. However, the relevant toxicity mechanism still requires further exploration. In this paper, the effect of oral exposure to 500 mg/kg TiO2 NPs (anatase and rutile) in adult male SD rats was studied over 3 and 7 days. Results showed that the total sperm count and testosterone level of 7 days of exposure in serum decreased in the experimental group. Testicular tissue lesions, such as disappearance of Leydig cells, disorder of arrangement of spermatogenic cells in the lumen of convoluted seminiferous tubules, and disorder of arrangement of germ cells, were observed. Meanwhile, the expression of steroidogenic acute regulatory (StAR; the key factors of testosterone synthesis), MAPK (ERK1/2), and phosphorylated ERK1/2 in testes of SD rats after exposure to TiO2 NPs for 7 days decreased, while the malondialdehyde content increased and superoxide dismutase activity decreased in serum. The present study showed that TiO2 NPs could cause reproductive toxicity. Notably, anatase is more toxic than rutile. In addition, exposure to 500 mg/kg TiO2 NPs for 7 days inhibited testosterone synthesis in male rat, which may be related to the reactive oxygen species (ROS)-MAPK (ERK1/2)-StAR signal pathway. Warning that the use of TiO2 NPs should be regulated.

Toxic effects of TiO2 NPs in the blood-milk barrier of the maternal dams and growth of offspring.

Titanium dioxide nanoparticles (TiO2 NPs) are amongst the most frequently used nanomaterial in everyday consumer products, and their widespread applications have raised concerns of the consequent deleterious effects on human health, particularly to vulnerable populations, such as lactating females remains elusive. Therefore, this study was initiated to investigate the detrimental effects and toxic mechanisms induced by TiO2 NPs in maternal dams and offspring during the lactation period. Dams were randomly divided into three groups. The water (Control; Group I) and TiO2 NPs (100 mg/kg; Group II) were orally administered from postnatal day 1-20, respectively. The results indicated that TiO2 NPs could cause toxicity in the dams, such as pathological damages to mammary gland tissues. The excessive accumulation of TiO2 NPs could induce oxidative stress in the mammary gland, leading to the dysfunctional blood-milk barrier; besides, TiO2 NPs could also be transferred to offspring via breastfeeding, causing abnormal development of infant. We further accessed the possible underlying molecular mechanism; for this, we orally administered TiO2 NPs with vitamin E (100 mg/kg; Group III). The results revealed that toxicity induced by TiO2 NPs was rescued. Collectively, this study presented the deleterious pathological effects of oral exposure to TiO2 NPs in the mammary gland tissues and blood-milk barrier via the production of reactive oxygen species (ROS) in dams and developmental concerns in offspring. However, the administration of VE could mitigate the toxic effects induced by the TiO2 NPs.

Effects of QDs exposure on the reproductive and embryonic developmental toxicity in mice at various pregnancy stages.

Quantum dots (QDs) have recently attracted considerable attention in the biomedical fields because of their unique and excellent optical properties. However, information on their health effects, particularly in the reproductive system, is limited. The present study focuses on the effects of intravenous injection of CdSe/ZnS QDs on the reproductive system and embryo development at various stages of pregnancy in mice. The CdSe/ZnS QDs intravenously injected in mice during pregnancy accumulated in the maternal liver, uterus and placenta. This accumulation affected the growth and development of the embryo during the early and middle stages of pregnancy. Moreover, genotoxicity to the placenta after exposure to CdSe/ZnS QDs was demonstrated by the increased expression levels of genes related to oxidative stress and apoptosis and the reduced expression levels of genes related to the nutrient and waste transportation. Alterations in the gene expression levels have hindered the transport of metabolites across the placenta, which in turn affected the ability of the fetus to obtain nutrients.

Protective effect of the NAC and Sal on zinc oxide nanoparticles-induced reproductive and development toxicity in pregnant mice.

The growing use of zinc oxide nanoparticles (ZnO NPs) in various applications has raised many concerns about the potential risks to human health. In this research, the protective effects of cellular oxidative stress inhibitor N-Acetyl-cysteine (NAC) and endoplasmic reticulum (ER) stress inhibitor Salubrinal (Sal) on reproductive toxicity induced by ZnO NPs were investigated. The results showed that application of these two kinds of cell stress inhibitors after oral ingestion of ZnO NPs could prevent the weight loss of pregnant mice; reduce zinc content in the uterus, placenta and fetus; reduce abnormal development of the offspring; and decrease fetal abortion. Furthermore, RT-qPCR, Western blot and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta. Sal decreased the expression of ATF4, JNK and Caspase-12, and increased the expression of eNOS and IGF-1caused by the oral ingestion of ZnO NPs. These results indicated that treatment with NAC and Sal after oral exposure could reduce reproductive and development toxicity caused by ZnO NPs which induced reproductive and development toxicity that was probably caused by the activation of oxide stress and ER stress.

Oral exposure of titanium oxide nanoparticles induce ileum physical barrier dysfunction via Th1/Th2 imbalance.

In this work, we aimed to evaluate the adverse effects and the mechanism of intestinal barrier caused by titanium dioxide nanoparticles (TiO2 NPs). Here, the effects of two different dosages (300 and 1200 mg/kg) of TiO2 NPs on female mice (n = 5) were investigated. After 28-day oral exposure, the results of Ti content were significantly increased in the ileum in comparison with the control. The histopathological structure index of the ileum was significantly changed after TiO2 NPs exposure; villi height and crypt depth were decreased and increased, respectively. Meanwhile, TiO2 NPs treatment also significantly altered the transcription levels of genes. First, the GATA-3 and STAT-4 were upregulation and downregulation, respectively. Second, gene expressions of the Zonula Occludens-1, claudin (CLDN)-12, occludin, and myosin light chain kinase were significantly upregulated, while the CLDN-3 was decreased. Finally, the caspase-3, caspase-9, and caspase-12 were upregulated. The results of TUNEL staining indicated apoptosis in the ileum. In general, TiO2 NPs treatment significantly changed the intestine physical barrier in a dose-dependent manner. The toxicity of TiO2 NPs could be through the imbalance in the Th1/Th2.

Nano Zinc Oxide Induced Fetal Mice Growth Restriction, Based on Oxide Stress and Endoplasmic Reticulum Stress.

ZnO NPs have been assessed to show adverse effects on reproductive organs, but the molecular mechanisms of reproductive toxicity have not been sufficiently studied. In this research, the dosage effects from the oral exposure of ZnO NPs (30 nm) to pregnant mice in gestation day 10.5 to 17.5 was analyzed. Pregnant mice exposed to ZnO NPs induced dam injury, mice fetal growth restriction, and the fetus number decreased. The pathological evaluation showed that ZnO NPs exposure caused placental spongiotrophoblast area decease and structural damage. The RT-qPCR and immunocytochemistry data indicated that ZnO NPs could induce placenta oxide stress, endoplasmic reticulum stress responses, apoptosis, and altered placental function. These findings indicated that ZnO NPs could induce dam injury and fetal growth restriction. Reproductive toxicity of ZnO NPs may be due to placental injury and function alteration caused by apoptosis, oxide stress, and endoplasmic reticulum stress after ZnO NPs exposure.

ZnO Nanoparticles Induced Male Reproductive Toxicity Based on the Effects on the Endoplasmic Reticulum Stress Signaling Pathway.

PURPOSE: The aim of this study was to evaluate the adverse effects of ZnO NPs on male reproductive system and explore the possible mechanism. METHODS: In this study, the effect of oral administration of 50, 150 and 450 mg/kg zinc oxide nanoparticles (ZnO NPs) in adult male mice was studied over a 14-day period. RESULTS: The results showed that the number of sperms in the epididymis and the concentration of testosterone in serum were decreased with an increased dose of ZnO NPs. Testicular histopathological lesions like detachment, atrophy and vacuolization of germ cells were observed. The results showed that increased dosage of ZnO NPs correspondingly up-regulated the IRE1α, XBP1s, BIP, and CHOP (P<0.05) which are genes related to ER stress. These observations indicated that ZnO NPs had adverse effects on the male reproductive system in a dose-dependent manner possibly through ER stress. The expression of caspase-3 was significantly increased in all the treated groups (P<0.001), which reflected the possible activation of apoptosis. Additionally, there was significant down-regulation of the gene StAR (P<0.05), a key player in testosterone synthesis. When an ER-stress inhibitor salubrinal was administered to the 450 mg/kg ZnO NPs treatment group, the damages to the seminiferous tube and vacuolization of Sertoli and Leydig cells were not observed. Furthermore, the testosterone levels in the serum were similar to the control group after the subsequent salubrinal treatment. CONCLUSION: It may be inferred that the ZnO NP's reproductive toxicity in male mice occurred via apoptosis and ER-stress signaling pathway.

[Progress in rolling circle amplification in biological detection].

Rolling circle amplification is a rapid, sensitive and isothermal single-stranded DNA amplification technique that can be used with staining or probes to amplify the detection signal. This technology has been widely used in biological detection and other aspects. The present paper introduces how to design rolling circle amplification, summarize its application in the detection of pathogens, nucleic acid tumor markers, proteins, biological small biomolecules, and viruses in recent years and prospects for future development.

CdSe/ZnS Quantum Dots Impaired the First Two Generations of Placenta Growth in an Animal Model, Based on the Shh Signaling Pathway.

The toxicity, especially the transgenerational toxicity of quantum dots (QDs) in vivo, is still scarcely understood in spite of great promising applications of QDs in biomedicine. In this study, the maternal status, pregnancy outcome, and fetus development of parental generation (P0) to offspring in three generations (F3) were investigated after Kunming mice perinatal (GD 13-PND 5) exposure to Cd containing QDs (CdSe/ZnS QDs) and CdCl2. The results show CdSe/ZnS QDs induced placenta injuries in P0 and diminished placenta diameters in F1 and F2. Bodyweight growth decreased in the CdSe/ZnS QDs treatment group in the F1 and F2 generation. Additionally, CdSe/ZnS QDs significantly altered the expression of key genes in the Shh signal pathway. Overall, this study exhibited that the CdSe/ZnS QDs exposure during perinatal period impaired placenta growth in the first two generations, but not on the third generation. The toxicological actions of the CdSe/ZnS QDs might be through the effects on the Shh signal pathway.

Transbronchoscopic patient biopsy-derived xenografts as a preclinical model to explore chemorefractory-associated pathways and biomarkers for small-cell lung cancer.

Insufficient tumor tissue is a major barrier for cancer biology research in small-cell lung cancer (SCLC) and has driven the development of patient-derived xenografts (PDXs) from biopsy tumor tissues. Here, we utilized transbronchoscopic biopsy specimens from SCLC tumors to establish PDXs and evaluated the genomic profile using next-generation sequencing and an RNA sequencing platform. The PDX establishment rate was 54.1% (40/74). PDXs largely recapitulated the major characteristics of their corresponding primary tumors, such as histopathology, genetic profile, and chemo-responsiveness. Compared with chemosensitive (chemo-S) PDXs, chemorefractory (chemo-R) PDXs demonstrated significant gene aberrances in the mitogen-activated protein kinase (MAPK) pathway and a higher frequency of receptor tyrosine kinase (RTK)-related genes. Phosphorylated ERK (pERK) was associated with chemo-R status. Patients with positive pERK expression demonstrated significantly inferior progression-free survival after first-line chemotherapy compared with that of patients who were negative for pERK (p < 0.001). Collectively, transbronchoscopic biopsy SCLC PDXs can serve as a model for genomic profiling and identifying biomarkers predictive of chemo-R status. Using PDXs, RTK-related gene aberrances and pERK expression were found to be associated with chemo-R SCLC.

Nano and bulk ZnO trigger diverse Zn-transport-related gene transcription in distinct regions of the small intestine in mice after oral exposure.

The oral ingestion of ZnO nanoparticles (NPs) has attracted considerable attention because of the wide usage in food packaging and additives. The small intestine is the major absorption site for ZnO NPs. Unfortunately, studies on the absorption of ZnO NPs in the GIT were still scarce. This study evaluated the absorption characteristics of ZnO NPs (30 nm) and bulk ZnO (rod morphology with a mean size of 139-846 nm). Results showed that ZnO NPs and bulk ZnO were absorbed and redistributed in various organs of mice at 4 h after exposure. Significantly higher levels of MT1 were observed in the duodenums of bulk ZnO and ZnO NPs groups than those of the control (9.8 and 5660.11 fold increases, respectively). The MT4 levels in the bulk ZnO and ZnO NPs groups also showed 4.07 and 43.21fold increases, respectively. In addition, the transcript levels of ZIPs, ZnTs, and MTs in the jejunum of bulk ZnO group were higher than those of ZnO NPs group. And the transcript levels of ZIPs, ZnTs, and MTs were all lower in the ileum than in the jejunum. The results suggested that ZnO NPs were mainly absorbed in the duodenum in the form of particles and can be absorbed as Zn2+ in the jejunum and secondly in the ileum. By contrast, bulk ZnO was more easily absorbed as Zn2+ in the jejunum and secondly in the ileum.

A new application of a sodium deoxycholate-propidium monoazide-quantitative PCR assay for rapid and sensitive detection of viable Cronobacter sakazakii in powdered infant formula.

A rapid, reliable, and sensitive method for the detection of Cronobacter sakazakii, a common foodborne pathogen that may cause serious neonatal disease, has been developed. In this study, a rapid real-time quantitative PCR (qPCR) assay combined with sodium deoxycholate (SD) and propidium monoazide (PMA) was developed to detect C. sakazakii contamination in powdered infant formula (PIF). This method could eliminate the interference from dead or injured bacteria. Optimization studies indicated that SD and PMA at 0.08% (wt/vol) and 5µg/mL, respectively, were the most appropriate. In addition, qPCR, PMA-qPCR, SD-PMA-qPCR, and plate count assays were used to account for the number of viable bacteria in cell suspensions that were exposed to a 55°C water bath at different length of time. As a result, the viable number by PMA-qPCR showed significantly higher than of the number from SD-PMA-qPCR or plate counts. The number of viable bacteria was consistent between SD-PMA-qPCR and traditional plate counts, which indicated that SD treatment could eliminate the interference from dead or injured cells. Using the optimized parameters, the limit of detection with the SD-PMA-qPCR assay was 3.3×102 cfu/mL and 4.4×102 cfu/g in pure culture and in spiked PIF, respectively. A similar detection limit of 5.6×102 cfu/g was obtained in the presence of the Staphylococcus aureus (107 cfu/mL). The combined SD-PMA-qPCR assay holds promise for the rapid detection of viable C. sakazakii in PIF.