Association between glyphosate exposure and cognitive function, depression, and neurological diseases in a representative sample of US adults: NHANES 2013-2014 analysis.

Glyphosate, the most widely used herbicide globally, has been linked to neurological impairments in some occupational studies. However, the potential neurotoxic effects of glyphosate exposure in the general population are still not fully understood. We conducted analyses on existing data collected from 1532 adults of the 2013-2014 National Health and Nutrition Examination Survey (NHANES) to explore the possible relationship between glyphosate exposure and cognitive function, depressive symptoms, disability, and neurological medical conditions. Our results showed a significant negative association between urinary glyphosate levels and the Consortium to Establish a Registry for Alzheimer's Disease Word List Memory Test (CERAD-WLT) trial 3 recall and delayed recall scores in both models, with ß coefficients of -0.288 (S.E. = 0.111, P = 0.021) and -0.426 (S.E. = 0.148, P = 0.011), respectively. Furthermore, the odds ratio did not show a significant increase with the severity of depressive symptoms with a one-unit increase in ln-glyphosate levels. However, the odds ratio for severe depressive symptoms was significantly higher than for no symptoms (odds ratio = 4.148 (95% CI = 1.009-17.133), P = 0.049). Notably, the odds ratio showed a significant increase for individuals with serious hearing difficulty (odds ratio = 1.354 (95% CI = 1.018-1.800), P = 0.039) with a one-unit increase in ln-glyphosate levels, but not for other neurological medical conditions. In conclusion, our findings provide the first evidence that glyphosate exposure may be associated with neurological health outcomes in the US adult population. Additional investigation is necessary to understand the potential mechanisms and clinical significance of these correlations.

Antibody Profiling in COVID-19 Patients with Different Severities by Using Spike Variant Protein Microarrays.

The disease progression of COVID-19 varies from mild to severe, even death. However, the link between COVID-19 severities and humoral immune specificities is not clear. Here, we developed a multiplexed spike variant protein microarray (SVPM) and utilized it for quantifying neutralizing activity, drug screening, and profiling humoral immunity. First, we demonstrated the competition between antispike antibody and ACE2 on SVPM for measuring the neutralizing activity against multiple spike variants. Next, we collected the serums from healthy subjects and COVID-19 patients with different severities and profile the neutralizing activity as well as antibody isotypes. We identified the inhibition of ACE2 binding was stronger against multiple variants in severe compared to mild/moderate or critical patients. Moreover, the serum IgG against nonstructural protein 3 was elevated in severe but not in mild/moderate and critical cases. Finally, we evaluated two ACE2 inhibitors, Ramipril and Perindopril, and found the dose-dependent inhibition of ACE2 binding to all the spike variants except for B.1.617.3. Together, the SVPM and the assay procedures provide a tool for profiling neutralizing antibodies, antibody isotypes, and reagent specificities.

Genetic Loss of Immunoglobulin A Does Not Influence Development of Alcoholic Steatohepatitis in Mice.

BACKGROUND: Chronic alcohol abuse is associated with intestinal dysbiosis and bacterial translocation. Translocated commensal bacteria contribute to alcoholic liver disease. Secretory immunoglobulin A (IgA) in the intestine binds bacteria and prevents bacterial translocation. METHODS: To investigate the functional role of IgA in ethanol (EtOH)-induced liver disease in mice, we subjected wild type (WT) and IgA-deficient littermate mice to Lieber-DeCarli models of chronic EtOH administration and the model of chronic and binge EtOH feeding (the NIAAA model). RESULTS: Chronic EtOH feeding increased systemic levels of IgA, while fecal IgA was reduced in C57BL/6 WT mice. WT and Iga-/- littermate mice showed similar liver injury, steatosis, and inflammation following 4 weeks of EtOH feeding or chronic and binge EtOH feeding. IgA deficiency did not affect intestinal absorption or hepatic metabolism of EtOH. Pretreatment with ampicillin elevated intestinal IgA in WT littermate mice. Despite increased intestinal IgA, WT littermate mice exhibited a similar degree of liver disease compared with Iga-/- mice after 7 weeks of EtOH feeding. Interestingly, bacterial translocation to mesenteric lymph nodes was increased in Iga-/- mice fed an isocaloric diet, but was the same after EtOH feeding relative to WT littermate mice. The absence of intestinal IgA was associated with increased intestinal and plasma IgM in Iga-/- mice after EtOH feeding. CONCLUSIONS: Our findings indicate that absence of IgA does not affect the development of alcoholic liver disease in mice. Loss of intestinal IgA is compensated by increased levels of intestinal IgM, which likely limits bacterial translocation after chronic EtOH administration.

Association between urinary glyphosate levels and serum neurofilament light chain in a representative sample of US adults: NHANES 2013-2014.

BACKGROUND: Glyphosate, the herbicide with the highest global usage, has been found to have links to neurological impairment in some occupational studies. Neurofilament light chain (NfL) is a protein that is released into the bloodstream following neuroaxonal damage and has emerged as a reliable biomarker for various neurological disorders. However, no research has investigated the potential link between glyphosate exposure and neurological damage or serum NfL levels in the general population. OBJECTIVE: The objective of this study was to assess the possible correlation between glyphosate exposure and serum NfL levels in a population that is representative of the United States. METHODS: We analyzed data from 597 adults (aged ≥20 years) from the 2013-2014 National Health and Nutrition Examination Survey (NHANES) to explore the potential correlation between urinary glyphosate levels and serum NfL levels. RESULTS: We found a significant positive association between urinary glyphosate levels and serum NfL levels (ß-coefficient = 0.110; S.E. = 0.040; P = 0.015), indicating that higher levels of glyphosate exposure may be linked to higher levels of neuroaxonal damage. Furthermore, when glyphosate levels were divided into quintiles, we observed a significant trend of increasing mean NfL concentrations with increasing quintiles of glyphosate exposure (P for trend = 0.036). Notably, the association was more pronounced in certain subgroups, including those aged ≥40 years, non-Hispanic whites, and those with a BMI between 25 and 30. IMPACT STATEMENT: This is the first research to suggest an association between glyphosate exposure and biomarkers indicative of neurological damage in general U.S. adults. If the correlation observed is causal, it raises concerns about the potential effects of glyphosate exposure on neurological health among U.S. adults. The study is noteworthy due to its representation of American adults aged 20 and above, as well as the use of reliable and comprehensive data from the NHANES database.

Urinary di-(2-ethylhexyl) phthalate metabolites are independently related to serum neurofilament light chain, a biomarker of neurological diseases, in adults: results from NHANES 2013-2014.

Di (2-ethylhexyl) phthalate (DEHP) is a chemical commonly used in the manufacturing of plastics and can pose human health risks, including endocrine disruption, reproductive toxicity, and potential carcinogenic effects. Children may be particularly vulnerable to the harmful effects of DEHP. Early exposure to DEHP has been linked to potential behavioral and learning problems. However, there are no reports to date on whether DEHP exposure in adulthood has neurotoxic effects. Serum neurofilament light chain (NfL), a protein released into the blood after neuroaxonal damage, has been shown to be a reliable biomarker for many neurological diseases. To date, no study has examined the relationship between DEHP exposure and NfL. For the present study, we selected 619 adults (aged ≥ 20 years) from the 2013-2014 National Health and Nutrition Examination Survey (NHANES) to examine the association between urinary DEHP metabolites and serum NfL. We reported higher urinary levels of ln-mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), ln-mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and ln-mono(2-ethyl-5-carboxypentyl) phthalate (MECPP), and ln-ΣDEHP levels were associated with higher serum levels of ln-NfL (ΣDEHP: ß-coefficient = 0. 075; S.E. = 0.026; P = 0.011). When we divided ΣDEHP into quartiles, mean NfL concentrations increased with quartiles of MEHHP (P for trend = 0.023). The association was more pronounced in males, non-Hispanic white race, higher income, and BMI < 25. In conclusion, higher DEHP exposure was positively associated with higher serum NfL in adults from NHANES 2013-2014. If this finding is causal, it is possible that DEHP exposure in adulthood may also induce neurological damage. Although the causality of this observation and the clinical significance are uncertain, our findings suggest that additional research is needed on DEHP exposure, serum NfL, and neurological disease in adults.

Urine Di-(2-ethylhexyl) Phthalate Metabolites Are Independently Related to Body Fluid Status in Adults: Results from a U.S. Nationally Representative Survey.

PURPOSE: Di-(2-ethylhexyl) phthalate (DEHP) has been utilized in many daily products for decades. Previous studies have reported that DEHP exposure could induce renin-angiotensin-aldosterone system activation and increase epithelial sodium channel (ENaC) activity, which contributes to extracellular fluid (ECF) volume expansion. However, there is also no previous study to evaluate the association between DEHP exposure and body fluid status. METHODS: We selected 1678 subjects (aged ≥18 years) from a National Health and Nutrition Examination Survey (NHANES) in 2003-2004 to determine the relationship between urine DEHP metabolites and body composition (body measures, bioelectrical impedance analysis (BIA)). RESULTS: After weighing the sampling strategy in multiple linear regression analysis, we report that higher levels of DEHP metabolites are correlated with increases in body measures (body weight, body mass index (BMI), waist circumference), BIA parameters (estimated fat mass, percent body fat, ECF, and ECF/intracellular fluid (ICF) ratio) in multiple linear regression analysis. The relationship between DEHP metabolites and the ECF/ICF ratio was more evident in subjects of younger age (20-39 years old), women, non-Hispanic white ethnicity, and subjects who were not active smokers. CONCLUSION: In addition to being positively correlated with body measures and body fat, we found that urine DEHP metabolites were positively correlated with ECF and the ECF/ICF ratio in the US general adult population. The finding implies that DEHP exposures might increase ECF volume and the ECF/ICF ratio, which may have adverse health outcomes on the cardiovascular system. Further research is needed to clarify the causal relationship.

Saccharomyces Boulardii Ameliorates Non-alcoholic Steatohepatitis in Mice Induced by a Methionine-Choline-Deficient Diet Through Gut-Liver Axis.

Non-alcoholic steatohepatitis (NASH) is affecting people worldwide. Changes in the intestinal microbiome are crucial to NASH. A previous study showed that eradicating intestinal fungi ameliorates NASH; however, the role of intestinal fungi in the development of NASH remains unclear. Saccharomyces boulardii (SB), a dietary supplement yeast, has been reported to restore the integrity of the intestine. Here, we tested the effect of SB in the treatment of NASH. For this study, we fed eight-week-old C57/BL6 male mice either a methionine-choline deficient (MCD) diet or a normal chow diet (NCD) for eight weeks. Half of the MCD diet-fed mice were gavaged with SB (5 mg/day) once daily. The remainder of the NCD-fed mice were gavaged with normal saline as a control. The MCD diet-fed mice on SB supplement showed better liver function, less hepatic steatosis, and decreased inflammation. Both hepatic inflammatory gene expression and fibrogenic gene expression were suppressed in mice with SB gavage. Intestinal damage caused by the MCD diet was tampered with, intestine inflammation decreased, and gut permeability improved in mice that had been given the SB supplement. Deep sequencing of the fecal microbiome showed a potentially increased beneficial gut microbiota and increased microbiota diversity in the SB-supplemented mice. The SB supplement maintains gut integrity, increases microbial diversity, and increases the number of potentially beneficial gut microbiota. Thus, the SB supplement attenuates gut leakage and exerts a protective effect against NASH. Our results provide new insight into the prevention of NASH.

Selenium status is independently related to bone mineral density, FRAX score, and bone fracture history: NHANES, 2013 to 2014.

Selenium is an essential trace mineral element for humans. Although previous in vitro and animal studies have reported the vital role of selenium in bone, the results of the relationship between the selenium status and bone health were inconsistent in epidemiological studies. The risk of selenium deficiency is negligible for U.S. general population, however, the relationship between selenium status and bone health has never been surveyed in a nationally representative sample. In this study, we analyzed the data of 2983 adults (aged ≥40 years) in the National Health and Nutrition Examination Survey (NHANES) 2013-2014 to investigate the association among three markers of the selenium status (measured from whole blood, serum, and dietary intake), total spine and femur bone mineral density (BMD), and FRAX scores, and history of bone fractures. We found a one-unit increase in the ln-whole-blood selenium level was correlated with an increase in the total femur BMD of 0.064 g/cm2 (S.E. = 0.025; P = 0.022) in all participants and 0.086 g/cm2 (S.E. = 0.031; P = 0.013) in menopausal women. Additionally, a one-unit increase in the ln-selenium intake amount was associated with an increase in the total femur BMD of 0.014 g/cm2 (S.E. = 0.007; P = 0.043) in all participants. We also found that the dietary and whole-blood selenium statuses were negatively associated with the FRAX score, while levels of all the three selenium biomarkers were negatively associated with a history of bone fractures. In conclusion, increased selenium status is correlated with an increased total femur BMD, decreased FRAX scores, and a reduced incidence of previous bone fractures in the U.S. representative survey of adults. Further study is warranted to clarify the causal inference.

Zinc status is independently related to the bone mineral density, fracture risk assessment tool result, and bone fracture history: Results from a U.S. nationally representative survey.

PURPOSE: Previous reports have identified the important role of zinc in bone health. Although the risk of zinc deficiency is still a concern in the U.S., there has never been an in-depth study of the association between zinc status and bone health in a sample representing the country. METHODS: We included 2,895 subjects (aged ≥ 40 years) from National Health and Nutrition Examination Survey (NHANES) 2013-2014 to explore the relationship among three biomarkers of zinc (serum, food, and total intake), the bone mineral density (BMD) of the total spine and femur, the FRAX® scores, and the previous history of bone fractures. RESULTS: We showed a one-unit increase in the ln-serum zinc level was associated with an increase in the total spine BMD (ß = 0.068; S.E. = 0.028; P = 0.030) and total femur BMD (ß = 0.061; S.E. = 0.017; P = 0.003), while a one-unit increase in the ln-food zinc intake amount was correlated with an increase in the total femur BMD in the participants (ß = 0.023; S.E. = 0.009; P = 0.021). The ln-total zinc intake amount was correlated with an increase in the total femur BMD in women (ß = 0.016; S.E. = 0.007; P = 0.041). We also found food zinc intake was negatively correlated with the FRAX® score, while increased levels of all three zinc biomarkers were associated with a decreased incidence of previous bone fractures. CONCLUSIONS: In this representative survey of American adults above 40 years old, higher zinc status was associated with higher total spine and femoral BMD, lower FRAX® scores, and lower incidence of previous fractures. If this finding is causal, increased zinc intake remains an important issue for Americans.

PRKCSH genetic mutation was not found in Taiwanese patients with polycystic liver disease.

Polycystic liver disease (PCLD) without polycystic kidney is infrequent in clinical setting. Family clustering is found in patients with PCLD, and it is inherited in an autosomal dominant fashion. Through positional cloning in North America and Europe (mostly in Dutch and Finnish descents), mutations in PRKCSH gene on chromosome 19 were found to be responsible for the disease. We investigated the prevalence of liver cysts and PCLD in Taiwan and investigated whether the PRKCSH mutations exist in Taiwanese. The prevalence of liver cysts is only 0.17% in people under 30 years old and increased gradually to 14.29% in people between 55 and 60 years old and 14.19% in people over 65 years old. PCLD was not found in people under 40 years old. The prevalence is 0.15% between 40 and 45 years old, and increased to 1.37% between 55 and 60 years old, 1.21% between 60 and 65 years old, and 0.99% over 65 years old. There is only one polymorphism (deletion of one GAG repeat in exon 11) found, and the genotype and allele frequency were the same in Taiwanese patients and controls. No mutation, even polymorphism reported in the literature, was found in the 20 cases of PCLD. Our results suggest that PRKCSH gene is not a major genetic cause of PCLD and there may be at least another locus responsible for the disease in Taiwan.

Uridine diphosphate glucuronosyl transferase 1A1 promoter polymorphism is associated with choledocholithiasis in Taiwanese patients.

BACKGROUND AND AIMS: The gene product of the uridine diphosphate glucuronosyl transferase 1A1 (UGT1A1) is crucial to bilirubin metabolism. Mutations in this gene subsequently result in disease presented with unconjugated hyperbilirubinemia. A previous study showed that a TA-repeat polymorphism in the promoter region of this gene might play a role in the metabolism of bilirubin. Whether this polymorphism might predispose choledocholithiasis is unclear. METHODS: We recruited 32 patients who were diagnosed with pigment choledocholithiasis (common bile duct stones) by endoscopic retrograde cholangiopancreatography (ERCP) morphology and 107 population controls. The TA-repeat in the UGT1A1 promoter was genotyped. RESULTS: We found that among the 32 patients, 15 (46.9%) were wild type (A[TA](6)TAA homozygous); 15 (46.9%) were a heterozygous variation (A[TA[(6)TAA/A[TA](7)TAA) and 2 (6.2%) were a homozygous variation (A[TA](7)TAA). Among the controls, 81 (75.7%) were wild type, 23 (21.5%) were a heterozygous variation and 3 (2.8%) were a homozygous variation. The genotype distribution was significantly different between patients and controls. CONCLUSIONS: The results suggest that the UGT1A1 promoter TA-repeat polymorphism is associated with choledocholithiasis in Taiwanese patients.

[Effect of Free Nitrous Acid on the Activity of Nitrifying Bacteria in Different Sludge Concentrations Under Anoxic Conditions].

This study investigated the inhibitory effect of free nitrous acid (FNA) on the activity of ammonia oxidizing bacteria (AOB) and nitrite oxidizing bacteria (NOB) under anoxic conditions with different mixed liquid suspended solids (MLSS). Sequencing batch reactors were used to study the changes in the activity of AOB and NOB in nitrifying activated sludge based on four different MLSS (8398, 11254, 15998, and 19637 mg·L-1), after treatment, under anoxic conditions with FNA (at an initial concentration of 1.3 mg·L-1) for 48 h. The results showed that the pH increased by approximately 0.9, but the concentration of NO2--N did not decrease significantly. With over-aeration, the concentration of NH4+-N gradually degraded to 0 mg·L-1, and the removal rate of NH4+-N gradually increased to a maximum of 4.4-6.8 mg·(L·h)-1 which time used was shorter with the increase of the inhibition MLSS. The nitrite accumulation rate was more than 92% when the sludge concentration was 8398, 11254, 15998, and 19637 mg·L-1 and with over-aeration for 0-396 h, 0-396 h, 0-372 h, and 0-168 h, respectively. When aerated for 468 h, 468 h, 444 h, and 264 h, the NO2--N concentration and NAR decreased to 0, and NO3--N concentrations increased to their highest with the values of 42.6, 49.9, 42.9, and 47.9 mg·L-1 respectively.

Intestinal fungi contribute to development of alcoholic liver disease.

Chronic liver disease with cirrhosis is the 12th leading cause of death in the United States, and alcoholic liver disease accounts for approximately half of all cirrhosis deaths. Chronic alcohol consumption is associated with intestinal bacterial dysbiosis, yet we understand little about the contribution of intestinal fungi, or mycobiota, to alcoholic liver disease. Here we have demonstrated that chronic alcohol administration increases mycobiota populations and translocation of fungal ß-glucan into systemic circulation in mice. Treating mice with antifungal agents reduced intestinal fungal overgrowth, decreased ß-glucan translocation, and ameliorated ethanol-induced liver disease. Using bone marrow chimeric mice, we found that ß-glucan induces liver inflammation via the C-type lectin-like receptor CLEC7A on Kupffer cells and possibly other bone marrow-derived cells. Subsequent increases in IL-1ß expression and secretion contributed to hepatocyte damage and promoted development of ethanol-induced liver disease. We observed that alcohol-dependent patients displayed reduced intestinal fungal diversity and Candida overgrowth. Compared with healthy individuals and patients with non-alcohol-related cirrhosis, alcoholic cirrhosis patients had increased systemic exposure and immune response to mycobiota. Moreover, the levels of extraintestinal exposure and immune response correlated with mortality. Thus, chronic alcohol consumption is associated with an altered mycobiota and translocation of fungal products. Manipulating the intestinal mycobiome might be an effective strategy for attenuating alcohol-related liver disease.

Clinical analysis of multiple primary malignancies in the digestive system: a hospital-based study.

AIM: To analyze the characteristics of multiple primary malignancies (MPMs) of digestive system; including incidence, types of tumor combinations, time intervals between development of multiple tumors, clinical course, and prognostic factors affecting survival and mortality. METHODS: Data from a total of 129 patients treated from January 1991 to December 2000 for pathologically proved MPMs, including at least one originating from the digestive system, were reviewed retrospectively. RESULTS: Among 129 patients, 120 (93.02%) had two primary cancers and 9 (6.98%) had three primary cancers. The major sites of MPMs of the digestive system were large intestine, stomach, and liver. Associated non-digestive cancers included 40 cases of gynecological cancers, of which 31 were carcinoma of cervix and 10 cases of genitourinary cancers, of which 5 were bladder cancers. Other cancers originated from the lung, breast, nasopharynx, larynx, thyroid, brain, muscle, and skin. Reproductive tract cancers, especially cervical, ovarian, bladder, and prostate cancers were the most commonly associated non-GI cancers, followed by cancer of the lung and breasts. Forty-three cases were synchronous, while the rest (86 cases) were metachronous cancers. Staging of MPMs and treatment regimes correlated with the prognosis between survival and non-survival groups. CONCLUSION: As advances in cancer therapy bring about a progressively larger percentage of long-term survivors, the proportion of patients with subsequent primary lesions will increase. Early diagnosis of these lesions, based on an awareness of the possibility of second and third cancers, and multidisciplinary treatment strategies will substantially increase the survival of these patients.

Methods to determine intestinal permeability and bacterial translocation during liver disease.

Liver disease is often times associated with increased intestinal permeability. A disruption of the gut barrier allows microbial products and viable bacteria to translocate from the intestinal lumen to extraintestinal organs. The majority of the venous blood from the intestinal tract is drained into the portal circulation, which is part of the dual hepatic blood supply. The liver is therefore the first organ in the body to encounter not only absorbed nutrients, but also gut-derived bacteria and pathogen associated molecular patterns (PAMPs). Chronic exposure to increased levels of PAMPs has been linked to disease progression during early stages and to infectious complications during late stages of liver disease (cirrhosis). It is therefore important to assess and monitor gut barrier dysfunction during hepatic disease. We review methods to assess intestinal barrier disruption and discuss advantages and disadvantages. We will in particular focus on methods that we have used to measure increased intestinal permeability and bacterial translocation in experimental liver disease models.

Interleukin 10 promoter haplotype is associated with alcoholic liver cirrhosis in Taiwanese patients.

Alcoholic liver cirrhosis is a severe form of alcohol-related liver damage. More than 95% of heavy drinkers develop a fatty liver, but only 35% of them develop cirrhosis. We postulate that genetic factors may play a role in this difference. Genetic polymorphisms of the cytokine genes may influence Kupffer cells cytokine genes expression. In this study, we evaluated the promoter polymorphisms of interleukin (IL) 1ß, IL 6, IL 10, and tumor necrosis factor alpha (TNFα) and aimed to clarify the association between the polymorphisms and the disease. Forty alcoholic patients with liver cirrhosis and 64 healthy volunteers were included in our investigation. Genotyping on IL 1ß -511 T>C, IL 6 -572 G>C, IL 10 -819 C>T, IL 10 -1082 G>A, and TNFα -308 G>A was done. Another 36 patients with recurrent alcoholic pancreatitis were included as an additional control group. Genotyping on IL 10 -819 C>T and IL 10 -1082 G>A was done. The polymorphisms on IL 1 and IL 6 showed no significant association. The p value for TNFα -308 G>A was 0.028 in comparison with healthy volunteers. Although the p value was less than 0.05, it did not reach significance after Bonferroni correction. The p values for IL 10 -819 C>T and IL 10 -1082 G>A were respectively 0.031 and 0.026 in healthy volunteers and 0.028 and 0.023 in the alcoholic pancreatitis group. The results also did not reach significance after Bonferroni correction. Among the participants with the GCC haplotype, healthy volunteers had p = 0.027 (p < 0.05) and an odds ratio (OR) of 0.124 [confidence interval (95%) CI, 0.015-0.997], whereas the alcoholic pancreatitis group had p = 0.023 (p < 0.05) and an OR of 0.106 (95% CI, 0.012-0.912). The odds ratio of people having one ATA haplotype was 6.233 (95% CI, 0.739-52.547) in healthy volunteers and 6.588 (95% CI, 0.727-59.679) in the alcoholic pancreatitis group; the corresponding rate was 10.521 (95% CI, 1.252-88.440) and 12.833 (95% CI 1.408-117.008) for people with two ATA haplotypes. The p values in these groups were 0.031 (p < 0.05) and 0.028 (p < 0.05), respectively. The presence of a GCC haplotype could have protective effect against alcoholic liver disease, whereas the presence of an ATA haplotype could predispose carriers to the disease. The IL 10 promoter haplotype is associated with alcoholic liver cirrhosis in Taiwanese patients.

[Optimization of a modified UCT step feed process treating municipal wastewater].

A pilot-scale modified UCT step feed process was proposed to treat the municipal wastewater with lower COD/N in a large-scale wastewater treatment plant. Effects of influent distribution ratios and nutrients ratios (COD/N, COD/P and TN/P) on nutrients removal capabilities were importantly investigated. The removal mechanisms of organics and nutrients and sludge characteristics were ultimately discussed. According to the continuous experiments, the stable and high process performance was obtained. The average COD removal efficiencies and effluent concentration of (83.8 +/- 3.86)% and (43.7 +/- 8.35) mg/L were achieved in the influent COD loading of 0.79-0.93 kg/(m3 x d). The COD removal in anaerobic and anoxic zones accounted for 60.2% - 76.2%. With the influent distribution ratio of 40%: 30%: 30%, as much as 88.2% of TN removal efficiency was observed. It should be considered the removal of 32.8% through simultaneous nitrification and denitrification process. The average effluent NH(4+)-N and TN were (0.21 +/- 0.20) mg/L and (7.90 +/- 1.27) mg/L, respectively. It was extremely important that as much as 32.6% - 39.5% of the denitrifying phosphorus accumulation organisms contributed to the high phosphorus removal efficiency of 97.2%. A linear positive relationship was observed between nitrogen removal efficiency and COD/N in the range of 4.64 and 7.41 (R2 = 0.96). Phosphorus removal efficiency was found to be a function of the influent COD/P and TN/P, varying from 35.0 to 92.5 and from 6.24 to 12.5, respectively (R2 = 0.87 and R2 = 0.89). In addition, the great sludge settleability was obtained with the mean SVI of (82.6 +/- 4.99) mL/g.

[Research on the organic biodegradability of secondary effluent treated by ozonation].

The secondary effluent of three WWTPs was treated by ozonation to investigate organic biodegradability enhancement. The bulk experimental method was used. Ozone adding dosage was controlled to be 2, 4, 6, 8, 10 mg/L by adjusting the adding time. Results showed, UV254 and SUVA(UV254/DOC)decreased with the increasing of the ozone dosage. When ozone adding dosage was 6 mg/L, UV254 and SUVA decreased about 54.4% and 56.6% respectively; while BOD5/COD, BDOC and BDOC/DOC were improved above 30%, 360% and 360% respectively. It could be concluded that suitable ozonation could improve the biodegradation of the organic substances in the secondary effluent. The organic substance was analyzed by the excitation-emission matrix (EEM) to investigate the variation regularity of organic matter changes of the ozoned and non-ozoned secondary effluent. The main organic substances of the secondary effluent in the plant were aromatic protein like substances and humic substances, ozone could significantly remove these types of organic substance.