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Cadmium (Cd) is a heavy metal that pollutes the environment and threatens human and animal health via the food chain. The spleen is one of the target organs affected by Cd toxicity. However, the mechanism of Cd toxicity is not fully understood. In this study, 80 chicks were allocated into 4 groups (n = 20) and exposed to different doses of CdCl 2 (0 mg/kg, 35 mg/kg, 70 mg/kg and 140 mg/kg) for 90 d. The pathological changes in the spleen, mitochondrial dynamics-related factors, cytochrome P450 (CYP450) enzyme system contents, activities, transcription levels, nuclear receptors (NRs) response molecule levels, and mitochondrial unfolded protein-related factors were detected. The findings indicate that exposure to Cd significantly leads to spleen injury. In Cd groups, the total contents of CYP450 and cytochrome b5 (Cyt b5) increased, and the activities of the CYP450 enzyme system (APND, ERND, AH, and NCR) changed. The NRs response was induced, and the gene levels of AHR/CAR and corresponding CYP450 isoforms (CYP1B1, CYP1A5, CYP1A1, CYP2C18, CYP2D6 and CYP3A4) were found altered. The study found that Cd exposure altered the mRNA expression levels of mitochondrial dynamics-related factors, such as OPA1, Fis1, MFF, Mfn1, and Mfn2, breaking mitochondrial fusion and cleavage and ultimately leading to mitochondrial dysfunction. Changes were detected in the gene levels of several mitochondrial unfolded protein response (mtUPR)-related factors, namely (SIRT1, PGC-1α, NRF1, TFAM, SOD2, and HtrA2). Cd also altered the gene levels of mitochondrial function-related factors (VDAC1, Cyt-C, COA6, PRDX3, RAF and SIRT3). It is showed that Cd can initiate the NRs response, influence the homeostasis of the CPY450 enzyme system, trigger the mtUPR, impair mitochondrial function, and ultimately lead to Cd toxicity in the spleen of chickens., Competing Interests: DISCLOSURES The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Mycotoxins are ubiquitous natural pollutants that pose a serious threat to public health. Deoxynivalenol (DON) as one of the most prominent mycotoxins has a noticeable adverse effect on intestinal barrier function, which depends on the intestinal barrier integrity. However, the potential mechanisms and effective therapeutic strategies remain unclear. Aryl hydrocarbon receptor (AHR) has been implicated in the modulation of intestinal barrier function and inflammation. The study aims to investigate the unique role of AHR in mediating DON-induced intestinal epithelial barrier function. In the current study, we revealed that DON triggered mitochondrial structural damage and functional impairment, leading to oxidative stress and apoptosis in porcine jejunal epithelial cells (IPEC-J2). DON altered the integrity of IPEC-J2 cells by disrupting the distribution and function of tight junction proteins. Additionally, DON activated TNF-α/NF-κB/MLCK signaling pathway, thereby eliciting inflammatory response. Notably, DON inhibited AHR nuclear translocation and attenuated xenobiotic response element promoter activity and its target genes. However, overexpression of AHR mitigated DON-induced disruption of intestinal epithelial barrier functions by suppressing TNF-α/NF-κB/MLCK pathway in IPEC-J2 cells. Our findings indicate that AHR regulates intestinal epithelial barrier function and therefore is a novel therapeutic molecule for intestinal disorders., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Phthalates (PAEs), especially di (2-ethylhexyl) phthalate (DEHP), are generally considered to have adverse impact on nervous system. The residue of DEHP in the environment has gradually become a widely concerned environmental problem due to its widespread use in plastic items. Lycopene (LYC) as the readily available natural antioxidant is considered to have the potential to alleviate exogenous poisons-induced nerve damage. However, there is currently a lack of strategies to alleviate the neurotoxicity caused by DEHP, and it is also unknown whether LYC can alleviate the neurotoxicity caused by DEHP. The experiment demonstrated that LYC had the potential to mitigate DEHP-induced mitochondrial damage in cerebellum. DEHP induced the disorder of Ca 2+ transport in cerebellum, thereby resulting in the imbalance of protein homeostasis. Such disruption in protein homeostasis further results in the overactivation of mitochondrial unfolded protein response (UPR mt ) and mitochondrial injury. Mechanistically, LYC could alleviate the imbalance of calcium homeostasis and protein homeostasis induced by DEHP via regulating inositol 1, 4, 5-trisphosphate receptor type1 (IP3R1) and sarco/endoplasmic reticulum Ca (2+)-ATPase 2 (SERCA2), further alleviating mitochondrial damage in cerebellum. Subsequently, the present study suggested the mechanism of cerebellar injury induced by DEHP, and provided a novel approach to treating DEHP-induced neurotoxicity., Competing Interests: Declaration of competing interest The authors state that there are no conflicts of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Selenium (Se), a highly beneficial animal feed additive, exhibits remarkable antioxidant and anti-inflammatory properties. Nano‑selenium (Nano-Se) is an advanced formulation of Se featuring a specialized drug delivery vehicle, with good bioavailability, higher efficacy, and lower toxicity compared to the traditional form of Se. With the advancement of industry, cadmium (Cd) contamination occurs in different countries and regions and thereby contaminating different food crops, and the degree of pollution is degree increasing year by year. The present investigation entailed the oral administration of CdCl 2 and/or Nano-Se to male chickens of the Hy-Line Variety White breed, which are one day old, subsequent to a 7-day adaptive feeding period, for a duration of 90 days. The study aimed to elucidate the potential protective impact of Nano-Se on Cd exposure. The study found that Nano-Se demonstrates potential in mitigating the blood-brain barrier (BBB) dysfunction characterized by impairment of adherens junctions (AJS) and tight junctions (TJS) by inhibiting reactive oxygen species (ROS) overproduction. In addition, the data uncovered that Nano-Se demonstrates a proficient ability in alleviating BBB impairment and inflammatory reactions caused by Cd through the modulation of the Wnt7A/β-catenin pathway, highlights its potential to maintain brain homeostasis. Hence, this research anticipates that the utilization of Nano-Se effectively mitigate the detrimental impacts associated with Cd exposure on the BBB., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Porcine Epidemic Diarrhea Virus (PEDV) is a highly contagious virus that causes Porcine Epidemic Diarrhea (PED). This enteric disease results in high mortality rates in piglets, leading to significant financial losses in the pig industry. However, vaccines cannot provide sufficient protection against epidemic strains. Spike (S) protein exposed on the surface of virion mediates PEDV entry into cells. Our findings imply that matrine (MT), a naturally occurring alkaloid, inhibits PEDV infection targeting S protein of virions and biological process of cells. The GLY434 residue in the autodocking site of the S protein and MT conserved based on sequence comparison. This study provides a comprehensive analysis of viral attachment, entry, and virucidal effects to investigate how that MT inhibits virus replication. MT inhibits PEDV attachment and entry by targeting S protein. MT was added to cells before, during, or after infection, it exhibits anti-PEDV activities and viricidal effects. Network pharmacology focuses on addressing causal mechanisms rather than just treating symptoms. We identified the key genes and screened the cell apoptosis involved in the inhibition of MT on PEDV infection in network pharmacology. MT significantly promotes cell apoptosis in PEDV-infected cells to inhibit PEDV infection by activating the MAPK signaling pathway. Collectively, we provide the biological foundations for the development of single components of traditional Chinese medicine to inhibit PEDV infection and spread., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Atrazine (ATR) is widely used worldwide as a commercial herbicide, Diaminochlorotriazine (DACT) is the main metabolite of ATR in the organism. Both of them disrupt the production of steroids and induce abnormal reproductive development. The granulosa cells (GCs) are important for growth and reproduction of animals. However, the toxicity of ATR on the GCs of birds is not well clarified. To evaluate the effect of the environmental pollutant ATR on bird GCs. The quail GCs were allotted into 7 groups, C (The medium of M199), A20 (20 µM ATR), A100 (100 µM ATR), A250 (250 µM ATR), D20 (20 µM DACT), D100 (100 µM DACT) and D200 (200 µM DACT). The results demonstrated that ATR reduced the viability of GCs, disrupted mitochondrial structure (including mitochondrial cristae fragmentation and the mitochondrial morphology disappearance) and decreased mitochondrial membrane potential. Meanwhile, ATR interfered with the expression of key factors in the steroid synthesis pathway, inducing the secretion of the sex hormones E 2 and P in GCs. which in turn induced apoptosis. Furthermore, the Nrf2/ARE pathway as a potential target to ameliorate ATR-induced endocrine disruption in GCs for proper reproductive functions. Our research provides a new perspective for understanding the effects of ATR on reproductive functions in birds., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Cadmium (Cd) is a well-known testis toxicant. The blood-testis barrier (BTB) is a crucial component of the testis. Cd can disrupt the integrity of the BTB and reproductive function. However, the mechanism of Cd-induced disruption of BTB and testicular damage has not been fully elucidated. Here, our study investigates the effects of Cd on BTB integrity and testicular dysfunction. 80 (aged 1 day) Hy-Line white variety chickens were randomly designed into 4 groups and treated for 90 days, as follows: control group (essential diet), 35 Cd, 70 Cd and 140 Cd groups (35, 70 and 140 mg/kg Cd). The results found that Cd exposure diminished volume of the testes and induced histopathological lesions in the testes. Exposure to Cd induced an inflammatory response, disrupted the structure and function of the FAK/occludin/ZO-1 protein complex and disrupted the tight junction and adherens junction in the BTB. In addition, Cd exposure reduced the expression of steroid-related proteins and inhibited testosterone synthesis. Taken together, these data elucidate that Cd disrupts the integrity of the BTB and further inhibits spermatogenesis by dissociating the FAK/occludin/ZO-1 complex, which provides a basis for further investigation into the mechanisms of Cd-induced impairment of male reproductive function and pharmacological protection., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Transport stress (TS) not only weakens poultry performance but also affects animal welfare. Additionally, TS can evoke cardiac damage by triggering sterile inflammation in chicks, but the underlying mechanism is not fully understood. Here, we aimed to elucidate how TS induces sterile inflammation and heart injury and to clarify the antagonism effect of astragalus polysaccharides (APS). We randomly divided 60 chicks (one-day-old female) into 5 groups (n = 12): Control_0h (Con_0h) group (chicks were slaughtered at initiation), Control group (stress-free control), TS group (simulated TS exposure for 8 h), TS plus water (TS+W) group, and TS plus APS (TS+APS) group. Before simulation transport, the chicks of TS+W and TS+APS groups were, respectively, dietary with 100 μL of water or APS (250 μg/mL). H&E staining was employed for cardiac histopathological observation. ELISA assay was used to measure oxidative stress marker levels (GSH, GPX, GST, and MDA). A commercial kit was used to isolate the mitochondrial portion, and qRT-PCR was employed to measure the mitochondrial DNA (mtDNA) levels. Furthermore, we evaluated the activity of mtDNA-mediated NF-κB, NLRP3 inflammasome, and cGAS-STING inflammatory pathways and the expression of downstream inflammatory factors by Western Blotting or qRT-PCR. Our findings revealed that APS notably relieved TS-induced myocardial histopathological lesions and infiltrations. Likewise, the decrease in proinflammatory factors (TNF-α, IL-1β, and IL-6) and IFN-β by APS further supported this result. Meanwhile, TS caused severe oxidative stress in the chick heart, as evidenced by decreased antioxidant enzymes and increased MDA. Importantly, APS prevented mtDNA stress and leakage by reducing oxidative stress. Interestingly, TS-induced mtDNA leakage caused a series of inflammation events via mtDNA-PRRs pathways, including TLR21-NF-κB, NLRP3 inflammasome, and cGAS-STING signaling. Encouragingly, all these adverse changes related to inflammation events induced by mtDNA-PRRs activation were all relieved by APS treatment. In summary, our findings provide the first evidence that inhibition of mtDNA-PRRs pathway-mediated sterile inflammation by APS could protect against TS-induced cardiac damage in chicks., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Atrazine (ATZ) is the most prevalent herbicide that has been widely used in agriculture to control broadleaf weeds and improve crop yield and quality. The heavy use of ATZ has caused serious environmental pollution and toxicity to human health. Lycopene (LYC), is a carotenoid that exhibits numerous health benefits, such as prevention of cardiovascular diseases and nephropathy. However, it remains unclear that whether ATZ causes cardiorenal injury or even cardiorenal syndrome (CRS) and the beneficial role of LYC on it. To test this hypothesis, mice were treated with LYC and/or ATZ for 21 days by oral gavage. This study demonstrated that ATZ exposure caused cardiorenal morphological alterations, and several inflammatory cell infiltrations mediated by activating NF-κB signaling pathways. Interestingly, dysregulation of MAPK signaling pathways and MAPK phosphorylation caused by ATZ have been implicated in cardiorenal diseases. ATZ exposure up-regulated cardiac and renal injury associated biomarkers levels that suggested the occurrence of CRS. However, these all changes were reverted, and the phenomenon of CAR was disappeared by LYC co-treatment. Based on our findings, we postulated a novel mechanism to elucidate pesticide-induced CRS and indicated that LYC can be a preventive and therapeutic agent for treating CRS by targeting MAPK/NF-κB signaling pathways., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2024. Published by Elsevier B.V.)

Di(2-ethylhexyl) phthalate (DEHP) is a synthetic chemical applied as a plasticizer. As an environmental toxicant, DEHP poses a serious health threat. Many studies have revealed that DEHP can cause lead to various degrees of damage to the kidney. However, the evidence of DEHP-induced renal ferroptosis has not been reported. The purpose of this work was to probe the specific role of lipophagy in DEHP-induced renal injury and to investigate the relationship between lipophagy and ferroptosis. Quail were treated with DEHP (250 mg/kg BW/day, 500 mg/kg BW/day and 750 mg/kg BW/day) for 45 days. Microstructural and ultrastructural observations showed that DEHP caused damage to glomerular and tubular cells, and autophagy with multilayer structures were observed, suggesting that DEHP can induce lipophagy. The results indicated that the iron homeostasis was abnormal and the lipid peroxidation was increased. SLC7A11 and SLC3A2 were down-regulated. PTGS2, ACSL4 and LPCAT3 were elevated. In conclusion, DEHP could induce lipid peroxidation, lead to ferroptosis, and damage renal cells. Therefore, the relationship between lipophagy and ferroptosis was elucidated, which provided a new basis for intervention and prevention of DEHP increased diseases., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The global prevalence of Neurological disorders has increased alarmingly in response to environmental and lifestyle changes. Atrazine (ATZ) is a difficult to degrade soil and water pollutant with well-known neurotoxicity. Melatonin (MT), an antioxidant with chemoprotective properties, has a potential therapeutic effect on cerebellar damage caused by ATZ exposure. The aim of this study was to explore the effects and underlying mechanisms of MT on the cerebellar inflammatory response and pyroptosis induced by ATZ exposure. In this study, C57BL/6J mice were treated with ATZ (170 mg/kg BW/day) and MT (5 mg/kg BW/day) for 28 days. Our results revealed that MT alleviated the histopathological changes, ultrastructural damage, oxidative stress and decrease of mitochondrial membrane potential (ΔΨm) in the cerebellum induced by ATZ exposure. ATZ exposure damaged the mitochondria leading to release of mitochondrial DNA (mtDNA) to the cytoplasm, MT activated the cyclic GMP-AMP synthetase interferon gene stimulator (cGAS-STING) axis to alleviate inflammation and pyroptosis caused by ATZ exposure. In general, our study provided new evidence that the cGAS-STING-NLRP3 axis plays an important role in the treatment of ATZ-induced cerebellar injury by MT., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)

The granulosa cells (GCs) of birds are essential for the reproduction and maintenance of populations in nature. Atrazine (ATR) is a potent endocrine disruptor that can interfere with reproductive function in females and Diaminochlorotriazine (DACT) is the primary metabolite of ATR in the organism. Melatonin (MT) is an endogenous hormone with antioxidant properties that plays a crucial role in development of animal germ cells. However, how ATR causes mitochondrial dysfunction, abnormal secretion of steroid hormones, and whether MT prevents ATR-induced female reproductive toxicity remains unclear. Thus, the purpose of this study is to investigate the protective effect of MT against ATR-induced female reproduction. In the present study, the GCs of quail were divided into 6 groups, as follows: C (Serum-free medium), MT (10 µM MT), A250 (250 µM ATR), MA250 (10 µM MT+250 µM ATR), D200 (200 µM DACT) and MD200 (10 µM MT+200 µM DACT), and were cultured for 24 h. The results revealed that ATR prevented GCs proliferation and decreased cell differentiation. ATR caused oxidative damage and mitochondrial dysfunction, leading to disruption of steroid synthesis, which posed a severe risk to GC's function. However, MT supplements reversed these changes. Mechanistically, our study exhibited that the ROS/SIRT1/STAR axis as a target for MT to ameliorate ATR-induced mitochondrial dysfunction and steroid disorders in GCs, which provides new insights into the role of MT in ATR-induced reproductive capacity and species conservation in birds., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Due to the wide use of atrazine (ATR), the concern has increased regarding the negative impact of ATR on reproduction. Nevertheless, the reproductive effects caused by different exposure concentrations and the severity of toxic damage are poorly understood. In organisms, ATR is metabolized and degraded through phase II enzyme systems, and changes in cytochrome P450 (CYP) enzymes may have a regulatory role in the harm of ATR. However, less information is available on the induction of CYPs by ATR in avian organisms, and even less on its effects on the testis. Birds are exposed to ATR mainly through food residues and contaminated water, the purpose of this study was to examine reproductive toxicity by different exposure concentrations and elaborate metabolic disorders caused by ATR in European quail (Coturnix coturnix). In this study, the quail were given ATR at 50 mg/kg, 250 mg/kg and 500 mg/kg by oral gavage for 45 days, and the testicular weight coefficients, histopathology and ultrastructure of testes, primary biochemical functions, sex steroid hormones, critical protein levels in the testosterone synthesis pathway, the expression of genes involved CYPs, gonad axis and nuclear receptors expression were investigated. Altogether, testicular coefficient decreased significantly in the high-dose group (1.22%) compared with the control group (3.03%) after 45 days of ATR exposure, and ATR is a potent CYP disruptor that acts through the NXRs and steroid receptor subfamily (APND, CAR, ERND and ERα) without a dose-dependent manner. Notably, ATR interfered with the homeostasis of hormones by triggering the expression of hormones on the gonad axis (LH and E 2 ). These results suggest that exposure to ATR can cause testicular toxicity involving accommodative disorder of phase II enzyme and testosterone synthesis in European quail., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Cadmium (Cd) is widespread globally in the environment as a toxic metal. Although it is well known to induce hepatotoxicity in the cells, defense mechanisms against the detrimental effects of Cd are still unknown. We examined the role of autophagy (a cellular defense mechanism) on Cd-induced cytotoxicity in bird hepatocytes. Primary chicken hepatocytes were cultured with different concentrations (0, 1, 2.5, 5, and 10 μM) of cadmium chloride (CdCl 2 ) for 12 h. We assessed the effects of CdCl 2 on the cell viability, antioxidant status, reactive oxygen species (ROS) generation, autophagy response and endoplasmic reticulum (ER) stress. Further, it is also evaluated that insight into underling molecular mechanisms involved in the study. In this study, CdCl 2 -induce hepatotoxicity was caused by drastically increased ROS generation as well as a reduction level of antioxidant enzymes. It was also demonstrated that marked activation of ER stress markers (GRP78, IRE1, PERK, ATF4, ATF6 and XBP-1 s) was observed. Simultaneously, increased activation of autophagy in low-dose CdCl 2 (1 μM) exposed group was observed, but high-dose CdCl 2 (10 μM) inhibited autophagy and significantly promoted apoptosis, as indicated by the expression of the autophagy related genes for P62, Beclin-1, ATG3, ATG5, ATG9, and the detection of autophagic vacuoles. Pretreatment with autophagy agonist Rapamycin (RAP) has successfully reduced ROS production, attenuated ER stress and enhanced hepatocytes viability, while the autophagy inhibitor 3-Methyladenine (3-MA) had the opposite effect. Hence, these findings stipulate that Cd could inhibit viability of hepatocytes in a dose-dependent manner. Autophagy relieves hepatotoxicity of Cd via reducing ROS generation and regulating ER stress. We identified autophagy as a novel protective mechanism involved in Cd-mediated chicken hepatotoxicity., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Inc.)

Di-(2-ethylhexyl) phthalate (DEHP) is an environmental toxicant that is widely used in the whole world as a plasticizer that can enhance plastic properties. A number of reserarches have demonstrated that DEHP could cause varying degrees of damage to the normal function of nerve. The research aimed to investigate the mechanism of DEHP-induced cerebellar toxicity. In present study, we set DEHP-caused cerebellar injury models of quail and implied that DEHP induced cerebellar dysplasia by abnormity of Purkinje cell and reduction of cerebellar granule cell. Furthermore, the mitochondrial damage was confirmed by the swelling, cristae reduction, membrane rupture of mitochondria or even the occurrence of autophagic vacuole. To clarified DEHP-induced mitochondrial damage in cerebellum, we examined the relevant genes of mitochondrial biogenesis, mitochondrial dynamics, oxidative damage, the pathways related to Nrf2 and PINK1/Parkin in cerebellum. Based on data, it appeared that DEHP treatment had a damaging effect on the cerebellum and led to mitophagy as well as oxidative stress. In conclusion, the research indicated that DEHP-actuated mitochondrial injury has a directly relationship with mitophagy. DEHP-actuated reduced mitochondrial biogenesis and dysregulation of mitochondrial dynamics. The increase of oxidative stress damaged mitochondria, and the redundant ROS in damaged mitochondria that gave rise to cerebellar harm., Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Stress or stress-induced intestinal disturbances, especially diarrhea, are the main triggers for inflammatory bowel disease and irritable bowel syndrome. Diarrhea and intestinal inflammatory disease afflict patients around the world, and it has become a huge burden on the global health care system. Drinking sodium metasilicate-based alkaline mineral water (SM-based AMW) exerts a potential therapeutic effect in gastrointestinal disorders, including gut inflammation, and diarrhea, but the supportive evidence on animal studies and mechanism involved remain unreported. The maternally separated (MS) piglet (Newly weaned piglet) is an excellent model to investigate the treatment of diarrhea in infant. This study aims to determine whether drinking SM-based AMW confers diarrhea resistance in maternally separated (MS) piglets under weaning stress and what the underlying mechanisms are involved. 240 newly weaned piglets were randomly divided into the Control group and the sodium metasilicate pentahydrate (SMP) group. A decreased diarrhea incidence was observed in SMP treatment piglets. The intestine injury and activated stress hormones (COR and ACTH) induced by weaning was alleviated by SM-based AMW. This may be related to the improvement of intestinal microflora structure and function by SMP, especially the increase of s_copri abundance. Meanwhile, SMP maintained the integrity of the duodenal mucus barrier in MS piglets. Importantly, by targeting NF-κB inhibition via the microbiota-gut interaction, SM-based AMW alleviated intestinal inflammation, maintained fluid homeostasis by modulating aquaporins and fluid transporter expression, and enhanced barrier integrity by suppressing MLCK/p-MLC signaling. Therefore, drinking metasilicate-based alkaline mineral water confers diarrhea resistance in MS piglets via the microbiota-gut interaction., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Declaration of Competing Interest There is no conflict of interest to declare., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Male infertility is an attracting growing concern owing to decline in sperm quality of men worldwide. Phthalates, in particular to di (2-ethylhexyl) phthalate (DEHP) or its main metabolite mono-2-ethylhexyl phthalate (MEHP), affect male reproductive development and function, which mainly accounts for reduction in male fertility. Lycopene (LYC) is a natural antioxidant agent that has been recognized as a possible therapeutic option for treating male infertility. Testosterone (T)/androgen receptor (AR) signaling pathway is involved in maintaining spermatogenesis and male fertility. How DEHP causes spermatogenesis disturbance and whether LYC could prevent DEHP-induced male reproductive toxicity have remained unclear. Using in vivo and vitro approaches, we demonstrated that DEHP caused T biosynthesis reduction in Leydig cell and secretory function disorder in Sertoli cell, and thereby resulted in spermatogenic impairment. Results also showed that MEHP caused mitochondrial damage and oxidative damage, which imposes a serious threat to the progress of spermatogenesis. However, LYC supplement reversed these changes. Mechanistically, DEHP contributed to male infertility via perturbing T/AR signaling pathway during spermatogenesis. Overall, our study reveals critical role for T/AR signal transduction in male fertility and provides promising insights into the protective role of LYC in phthalate-induced male reproductive disorders., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Transport stress (TS) not only affects animal welfare but also eventually leads to higher morbidity and mortality. Moreover, TS could induce heart injury in animals, but the possible mechanism has yet to be fully explored. Astragalus polysaccharide (APS) is a main active component of Radix Astragali, which has an extensive anti-stress effect. However, the effect of APS on TS-induced heart injury has not yet been elucidated. In this study, a chick model of simulated TS was used. 240 newly hatched chicks were arranged into 4 groups: Control (Con), Transport group (T), Transport + water group (TW), and Transport + APS group (TA). Before transport, the chicks of the TW and TA groups were treated with deionized water and APS (0.25 mg/mL, 100 µL) by oral drops respectively. The histopathological analysis of myocardial tissue was assessed by hematoxylin and eosin staining. qRT-PCR and Western Blotting assays were employed to measure the expression of genes and proteins. Semiquantitative PCR was performed for the X box-binding protein-1 (XBP-1) mRNA splicing assay. The results indicated that APS significantly reduced TS-induced myocardial histopathological changes. Meanwhile, TS induced endoplasmic reticulum stress (ERS), evidenced by an activation of the unfolded protein response (UPR) signaling pathway and up-regulation of ERS-markers (P < 0.05). Moreover, TS markedly triggered autophagy induction by activating AMP-activated protein kinase (AMPK), reflected by augmented LC3-II/LC3-I, AMPK phosphorylation and autophagy-related genes (ATGs) expression (P < 0.05). Importantly, our study manifested that treatment of APS could reduce TS-induced ERS and AMPK-activated autophagy, accordingly alleviating heart injury of transported chicks. In summary, these findings indicate that TS induces heart injury in chicks via an ERS-UPR-autophagy-dependent pathway, and APS as an effective therapeutic method to alleviate it., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Cadmium (Cd) is a widely used heavy metal which is reported to exert extensive harm to the environment and human health. Owing to Cd being an element it is continuously enriched in the environment. The mechanism of splenic toxicity by Cd, however, is not yet clear. In order to explore the toxic mechanism of Cd exposure to the spleen, we added 0, 35, 70 and 140 mg/kg of Cd to the diet of chicken and fed them this diet for 90 days. Analysis of histopathological sections showed that Cd exposure damaged the spleen structure, the spleen red pulp, the white pulp boundary disappeared and the number of lymphocytes decreased significantly, suggesting that Cd exposure leads to organ injury to the spleen. Particularly, Cd-induced anoikis - a special form of programmed cell death caused by the loss of contact between cells and extracellular matrix and other cells - is associated with integrin-related cell detachment and activation of apoptotic signaling pathways. Moreover, Cd exposure leads to an increase in free radicals content and affects the activity of antioxidant enzymes resulting in oxidative stress. Simultaneously, Cd activated the body's antioxidant defense system mediated by the Nuclear factor related factor 2 (Nrf2) signaling pathway. Based on our results Cd-induced splenic lymphocytes anoikis is not mitigated by Nrf2-mediated antioxidative defense response., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Di-(2-ethylhexyl) phthalate (DEHP), an extensively used plasticizer, can cause environmental pollution and organ injury. Lycopene (LYC) is a natural carotene that has the potential to prevent chronic diseases. To reveal the effect of DEHP and/or LYC on the kidney, male mice were treated with LYC (5 mg/kg) and/or DEHP (500 mg/kg or 1000 mg/kg) by gavage for 28 days. The study indicated that DEHP caused glomerular atrophy, tubular expansion, disappearance of the mitochondrial membrane, and cristae rupture. DEHP exposure can increase the expression of aquaporin (AQP) subunits and the activity of Ca 2+ -Mg 2+ -ATPase and decrease the activity of Na + -K + -ATPase, which results in ion disorder. However, LYC can relieve kidney injury by regulating the activity of ATPase, the expression of ATPase subunits, and AQP subunit expression. The results indicated that AQP was a target for LYC in antagonizing the disturbance of DEHP-induced renal damage., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Cadmium (Cd) has been confirmed as an environmental contaminant, which potential threats health impacts to humans and animals. Selenium (Se) as a beneficial element that alleviates the negative effects of Cd toxicity. Se mainly exists in two forms in food nutrients including organic Se usually as (Se-enriched yeast (SeY)) and inorganic Se (sodium selenite (SSe)). Nanoparticle of Se (Nano-Se), a new form Se, which is synthesized by the bioreduction of Se species, which attracted significant attention recently. However, compared the superiority alleviation effects of Nano-Se, SeY or SSe on Cd-induced toxicity and related mechanisms are still poorly understood. The purpose of this study was to compare the superiority antagonism effects of Nano-Se, SeY and SSe on Cd-induced inflammation response via NF-kB/IκB pathway in the heart. The present study demonstrated that exposed to Cd obviously increased the accumulation of Cd, disruption of ion homeostasis and depressed the ratios of K + /Na + and Mg 2+ /Ca 2+ via ion chromatography mass spectrometry (ICP-MS) detecting the heart specimens. In the results of histological and ultrastructure observation, typical inflammatory infiltrate characteristics and mitochondria and nuclear structure alterations in the hearts of Cd group were confirmed. Cd treatment enhanced the inducible nitric oxide synthase (iNOS) activities and NOS isoforms expression via NF-kB/IκB pathway to promote inflammation response. However, the combined treatment of Cd-exposed animals with Nano-Se was more effective than SeY and SSe in reversing Cd-induced histopathological changes and iNOS activities increased, reducing Cd accumulation and antagonizing Cd-triggered inflammation response via NF-kB/IκB pathway in chicken hearts. Overall, Se applications, especially Nano-Se, can be most efficiently used for relieving cardiotoxicity by exposed to Cd compared to other Se compound., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Cadmium (Cd) is a ubiquitous environmental pollutant, which mainly input to the aquatic environment through discharge of industrial and agricultural waste, can be a threat to human and animal health. Selenium (Se) possesses a beneficial role in protecting animals and ameliorating the toxic effects of Cd. However, the comparative antagonistic effects of different Se sources such as inorganic, organic Se and nano-form Se on Cd toxicity are still under-investigated. Hence, the purpose of this study was to evaluate the comparative of Se sources antagonism on Cd-induced nephrotoxicity via oxidative stress and selenoproteome transcription. In the present study, Cd-diet disturbed in the system balance of 5 trace elements (Zinc (Zn), copper (Cu), Iron (Fe), Se, Cd) and impaired renal function. Se sources, including nano- Se (NS), Se- yeast (SY), sodium selenite (SS) and mixed selenium (MS) significantly recovered the balance of 4 trace elements (Zn, Cu, Cd, Se) and renal impaired indexes (blood urea nitrogen (BUN) and creatinine (CREA)). Histological appearance of Cd-treated kidney indicated renal tubular epithelial vacuoles, particle degeneration and enlarged capsular space. Ultrastructure observation results illustrated that Cd-induced mitochondrial cristae reduction, membrane disappearance, and nuclear deformation. Treatment with Se sources, NS appeared a better impact on improving kidney tissues against the pathological alterations resulting from Cd administration. Meanwhile, NS reflected a significant impact on relieving Cd-induced kidney oxidative damage, and significantly restored the antioxidant defense system of the body. Our findings also showed NS ameliorated the Cd-induced downtrends expression of selenoproteome and selenoprotein synthesis related transcription factors. Overall, NS was the most effective Se source in avoiding of Cd cumulative toxicity, improving antioxidant capacity and regulating of selenoproteome transcriptome and selenoprotein synthesis related transcription factors expression, which contributes to ameliorate Cd-induced nephrotoxicity in chickens. These results demonstrated diet supplement with NS may prove to be an effective approach for alleviating Cd toxicity and minimizing Cd -induced health risk., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

An increasing number of epidemiologic studies show that women have a special exposure profile to phthalates, and the exposures have attracted attention regarding their potential health hazards. Here, we developed a model for studying the ovarian action of di-(2-ethylhexyl) phthalate (DEHP) and its major metabolite monoethylhexyl phthalate (MEHP). In vivo, treatment with DEHP (250, 500, and 1000 mg kg^-1) induced decreased thickness of ovarian granulosa cell layer and mitochondrial damage in quail, caused oxidative stress, interfered with the transcription of hypothalamic-pituitary-ovarian axis (HPOA) steroid hormone-related factors (increased transcription of StAR, 3β-HSD, P450scc, and LH and decreased transcription of 17β-HSD, P450arom, FSH, and ERβ), and blocked the secretion of steroid hormones (decreased FSH, E 2 , and T levels and increased LH, P, and PRL levels). In vitro, granulosa cells were cultured with MEHP (50, 100, and 200 μM), activator of PPARγ (rosiglitazone, 50 μM), or antagonist of PPARγ (GW9662, 10 μM) for 24 h and gene and protein expression were analyzed by real time RT-PCR and western blot. Rosiglitazone, like MEHP, significantly decreased mRNA and protein levels of P450arom. Antagonist GW9662 partially blocked the suppression of P450arom by MEHP, suggesting that MEHP acts through PPARγ, but not exclusively. Our model shows that MEHP acts on granulosa cells in quail by stimulating PPARs, which leads to decreased gene and protein expression of P450arom. Therefore, the environmental endocrine disruptor DEHP and its major metabolite MEHP act through a receptor-mediated signaling pathway to inhibit the production of estradiol, interfere with the modulation of HPOA, suppress the synthesis of sex hormones, and cause sex hormone secretion disorders, resulting in severe toxicity in the female reproductive system. A framework for an adverse outcome pathway of DEHP/MEHP-induced ovarian toxicity was constructed, which can facilitate an improved understanding of the mechanism of female reproductive toxicity., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

A series of benzothiazole-based compounds were synthesized and characterized. Among them, probe Z showed significant dual-functional performance which was capable of sensing pH change and Cu 2+ . Probe Z displayed fluorescent turn-on under alkaline conditions due to deprotonation of the hydroxyl group along with the obviously color change from colorless to mint green. Interestingly, it further achieved in ratiometric detection of Cu 2+ through absorbance or fluorescence signals in strong alkaline condition. The limit of detection was calculated correspondingly as 0.37 μM and 1.35 μM, respectively. Especially, the combination of the XNOR and INHIBIT logic gates could be used to confirm that one medium was in neutrality or alkalinity condition. Moreover, Z was successfully used in real water samples and test paper for fast identification of Cu 2+ , respectively., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Cadmium (Cd) is a widespread environmental pollutant that accumulates in living systems and represents a significant global health hazard. Cd poses a toxicity threat to both human and animal health, including that of birds. Further knowledge of Cd toxicology pathways will allow for a better understanding of Cd-induced nephrotoxicity. To evaluate Cd-induced nephrotoxicity through potential oxidative damage, male chickens were treated with 0 mg/kg, 35 mg/kg or 70 mg/kg CdCl 2 in diet for 90 days. Markedly, histopathology indicated renal tubular epithelial cell swelling, renal function CREA content abnormalities, biochemical and morphologic indices indicative of Cd-induced kidney injury. Cd toxicity induced the up-regulation of Nrf2 and downstream target genes that relieve oxidative stress. Meanwhile, Cd disrupted the homeostasis of trace elements and promoted oxidative damage. Cd interfered with mitochondrial unfolded protein response (UPR mt )-related factors (SIRT1, SIRT3, PGC-1α, TFAM, Nrf1, and HTRA2) and disrupted the homeostasis of mitochondrial dynamics (OPA1, MFN1, MFN2, Fis1 and MFF), thereby exacerbating mitochondrial structural damage and mitochondrial dysfunction. In conclusion, our study demonstrated that the nephrotoxicity of Cd exposure results in oxidative stress and mitochondrial dysfunction by activating the Nrf2 signaling pathway and inhibiting UPR mt in the kidneys., (Copyright © 2019 Elsevier B.V. All rights reserved.)

A simple naphthalene derivative, 6-hydroxy-2-naphthohydrazide (NAH), was designed and synthesized through two facile steps reactions with the 6-hydroxy-2-naphthoic acid (NCA) as the starting material. In neat H 2 O (10% 0.01 M HEPES buffer, v/v, pH = 7.4), probe NAH showed a highly selective and sensitive response towards Fe 3+ via perceptible color change and displayed "turn-on" dual-emission fluorescence response for Cu 2+ . The binding stoichiometry ratio of NAH/Cu 2+ and NAH/Fe 3+ were all confirmed as 1:1 by the method of fluorescence job's plot and UV-Vis job's plot, respectively. Probe NAH can be used over a wide pH range for the determination of Fe 3+ (2.0-10.0) and Cu 2+ (6.0-10.0) without interference from other co-existing metal ions. A possible detection mechanism was the hydrolysis of NAH upon the addition of Fe 3+ or Cu 2+ , thereby leading to the formation of 6-hydroxy-naphthalene-2-carboxylic acid (NCA) which was further confirmed by the various spectroscopic techniques including FT-IR, 1 H NMR titration and HRMS. Moreover, NAH was successfully applied to the detection of Cu 2+ and Fe 3+ in tap water, ultrapure water and BSA., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Among ubiquitously found environmental contaminants in the ecosystem, di(2-ethylhexyl) phthalate (DEHP) is an important environmental contaminant used as plasticizer in medical and consumer goods. The bioaccumulation and environmental persistence of DEHP cause serious global health effects in wildlife animals and human, especially hepatotoxicity. Herein, to explore the mechanisms of DEHP induced hepatotoxicity, quail were exposed with 0, 250, 500 and 1000 mg/kg BW/day DEHP by gavage administration daily for 45 days. Notably, the adipose tissue degeneration was observed in the liver of DEHP-exposed quail under the histopathological analysis. DEHP exposure increased the peroxidation product (MDA), GSH and GST, but decreased antioxidant function (T-AOC, SOD and GPX). DEHP induced the oxidative stress and pulsed on NRF2 signal pathway through activating downstream genes. Furthermore, DEHP induced mitochondrial ultrastructural abnormalities and mitochondrial dysfunctions. Mitochondrial unfolded protein response (mtUPR) was activated to relieve mitochondrial dysfunctions and mitigated oxidative stress. These findings showed that mitochondrial functions and redox homeostasis were affected by DEHP and resulted in irreversible hepatic injury. In Conclusion, this study suggested that DEHP-induced hepatotoxicity in quail was associated with activating the NRF2 mediated antioxidant defense and mtUPR. These results provided new evidence on molecular mechanism of DEHP induced hepatotoxicity., (Copyright © 2018 Elsevier B.V. All rights reserved.)

A new naphthalene-quinoline based chemosensor L was prepared and structurally characterized. L exhibited excellent selectivity and sensitivity to Al 3+ through distinct fluorescence enhancement (335-fold) and ratiometric detection in DMF/H 2 O (v/v, 1/9) based on the combined mechanisms of ESIPT and CHEF. The recognizing behavior of L toward Al 3+ had been investigated in detail through Job's Plot, FT-IR, HNMR, and HRMS analysis. The limit of detection (LOD) for Al 3+ was as low as and 3.67 × 10 -8  M. L was successfully applied in real sample detection and construction of molecular logic gate. Moreover, L was verified to be of low cytotoxicity and good imaging characteristics for the detection of Al 3+ in cells HSC., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The bioaccumulation and environmental persistence of atrazine (ATZ) poses a severe hazard to animal ecosystem. Quail has strong sensitivity to environmental pollutant, thus it is one of the most important ecological pollution indicator. However, true proof for the effects of ATZ exposure on the liver of quails is lacking. To evaluate the liver injury and the role of Nrf2-mediated defense responses during ATZ exposure, male quails were treated with ATZ (0, 50, 250 and 500mg/kg) by oral gavage for 45 days. Histopathological and ultrastructural changes, oxidative stress indices, apoptosis-related factors and Nrf2 pathway were detected. ATZ caused irreparable mitochondrial damage and destroyed morphophysiological integrity of the quail liver. Lower level ATZ (<250mg/kg) activated Nrf2 signaling pathway to protect liver against oxidative stress and apoptosis via enhancing antioxidative activity. Higher level ATZ (>500mg/kg) induced oxidative stress and apoptosis through decrease of non-enzymatic antioxidant, antioxidant enzymes and anti-apoptosis factors and increase of apoptosis factors expressions. Taken together, our results suggested that ATZ-induced hepatotoxicity in quails was associated with blocking Nrf2-mediated defense response., (Copyright © 2016 Elsevier Inc. All rights reserved.)

To gain insights into nutrient biomarkers and setting of dietary nutrient requirements, selenium biomarker levels and requirements in response to multiple graded levels of dietary selenium were compared between day-old turkeys and chickens versus weanling rats and mice and 2-d-old lambs supplemented with sodium selenite. In rodents, there was no significant effect of dietary selenium on growth, indicating that the minimum selenium requirement was <0.007 μg Se/g diet. In contrast, there was a significant effect in turkeys, chicks, and lambs, which showed selenium requirements for growth of 0.05, 0.025, and 0.05 μg Se/g diet, respectively. Liver glutathione peroxidase (GPX) 1 activity fell in all species to <4% of selenium-adequate levels, plasma GPX3 activity fell to <3% in all species except for mice, and liver GPX4 activity fell to <10% in avians but only to ∼50% of selenium-adequate levels in rodents. Selenium-response curves for these biomarkers reached well-defined plateaus with increasing selenium supplementation in all species, collectively indicating minimum selenium requirements of 0.06-0.10 μg Se/g for rats, mice, and lambs but 0.10-0.13 μg Se/g for chicks and 0.23-0.33 μg Se/g for turkeys. In contrast, increasing dietary selenium did not result in well-defined plateaus for erythrocyte GPX1 activity and liver selenium in most species. Selenium-response curves for GPX1 mRNA for rodents and avians had well-defined plateaus and similar breakpoints. GPX4 mRNA was not significantly regulated by dietary selenium in rodents, but GPX4 mRNA in avians decreased in selenium deficiency to ∼35% of selenium-adequate plateau levels. Notably, no selenoprotein activities or mRNA were effective biomarkers for supernutritional selenium status. Robust biomarkers, such as liver GPX1 and plasma GPX3 activity for selenium, should be specific for the nutrient, fall dramatically in deficiency, and reach well-defined plateaus. Differences in biomarker-response curves may help researchers better understand nutrient metabolism and targeting of tissues in deficiency, thus to better characterize requirements., Competing Interests: 2 Author disclosures: RA Sunde, J-L Li, and RM Taylor, no conflicts of interest., (© 2016 American Society for Nutrition.)

Cadmium (Cd), a potent hepatotoxin, has been reported to induce endoplasmic reticulum (ER) stress in various cell types. However, whether such effect exists in bird is still unclear. To delineate the effects of Cd exposure on ER stress response, we examined the expression of 78-kDa glucose-regulated protein (GRP78) and alteration in calcium homeostasis in primary chicken hepatocytes treated with 2-22 µM Cd for 24 h. A significant decrease of cell viability was observed in chicken hepatocytes following Cd administration. In cells treated with Cd, GRP78 protein levels increased in a dose-dependent manner. In addition, GRP78 and GRP94mRNA levels were elevated in response to Cd exposure. The increase of the intracellular Ca(2+) concentration in chicken hepatocytes was found during Cd exposure. Cd significantly decreased the CaM mRNA levels in hepatocytes. These results show that Cd regulates the expression of GRP78 and calcium homeostasis in chicken hepatocytes, suggesting that ER stress induced by Cd plays an important role in the mechanisms of Cd cytotoxicity to the bird hepatocytes., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Cadmium (Cd) is one of the most toxic metal compounds released into the environment. It was well known that Cd induced hepatotoxicity in animal models. However, little is known about the negative effects of Cd toxicity in the liver of birds. To investigate the Cd hepatotoxicity in birds and the protective effects of selenium (Se) against subchronic exposure to dietary Cd, 100-day-old cocks received either Se (as 10mg Na2SeO3 per kg of diet), Cd (as 150mg CdCl2 per kg of diet) or Cd+Se in their diets for 60 days. Histological and ultrastructural changes in the liver, the concentrations of Cd and Se, the lipid peroxidation (LPO) and nitric oxide (NO) production, the activities of the antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GPx), nitric oxide synthase (NOS) activities and apoptosis were determined. Exposure to Cd significantly reduced SOD and GPx activity, Se content in the liver tissue. It increased the LPO and NO production, the numbers of apoptotic cells and Cd concentration and caused obvious histopathological changes in the liver. Concurrent treatment with Se reduced the Cd-induced liver histopathological changes, oxidative stress, overexpression of NO and apoptosis, suggesting that the toxic effects of Cd on the liver is partly ameliorated by inorganic Se. Se supplementation also modified the distribution of Cd in the liver., (Copyright © 2013 Elsevier Inc. All rights reserved.)

This study examined the concentrations of carbon monoxide, carbon dioxide, TVOC, TSP, PM(10), PM(2.5), PM(1), benzene, toluene and xylene in passenger cars of the Beijing Ground Railway Transit System (Line No. 13). This system connects the northern suburb and downtown, and is equipped with air-conditioned passenger cars. In-train air quality monitoring was performed in both summer (July and August) and winter (December). To obtain representative data, the sampling design considered both rush and regular hours, urban and suburban areas, as well as the number of passengers. Meanwhile, questionnaires were distributed to the passengers. The monitoring results indicated that, overall, the air quality in the passenger cars was acceptable with a few exceptions, which is consistent with the passengers' perception. Concentrations of some air pollutants showed significant seasonal variations and had the significant difference between rush hour and regular hour. Furthermore, the in-train air quality was greatly influenced by the number of passengers. This paper describes the experimental design, and presents the preliminary results.

Objective: To estimate the operative mortality in patients with malignant obstructive jaundice., Methods: Twelve risk factors were analyzed using multivariate discriminant analysis in 90 patients who had been operated on., Results: Operative mortality was significantly related to the following factors: age, duration of jaundice, packed RBC volume, white blood cell count and concentration of blood urine nitrogen; it was not significantly related to diseases and types of operation. The following formula was obtained: packed RBC volume x 0.09954-age x 0.04018- blood urine nitrogen x 0.23693-duration of jaundice x 2.07388-WBC count x 0.21118+ 5.26593. With this formula, an operative mortality of 77.8% was predicted., Conclusion: With a positive value from the formula, the patient should be operated on; otherwise non-operative treatment is advocated.