Amoxicillin is an antibiotic which belongs to the group of penicillins. It is approved in Taiwan for treating bacterial infections caused by Streptococcus sp. and Photobacterium sp. in anguilliformes, perciformes and salmoniformes. The pharmacokinetics of amoxicillin were determined in pompano following oral administration of a single dose of 40 mg/kg. Residue studies were performed to determine residues in liver and kidney tissues of healthy fish after oral gavage of amoxicillin at a daily dose of 40 mg/kg for five consecutive days. Amoxicillin residues were analyzed by HPLC using Hypersil-100 C18 column (150 mm × 4.6 mm i.d.) and mobile phase consists of 10 mM K 2 HPO 4 (pH 8.5) with acetonitrile (80:20, v/v), at a flow rate of 1 mL/min. The effluent was monitored using a fluorescence detector set as 358 and 440 nm as excitation and emission wavelengths. Following a single oral dose, amoxicillin residues in 0.5 h post-dosing pompano were at a maximum of 6.17 μg/g in liver and 4.27 μg/g in kidney; the concentration of amoxicillin in liver and kidney declined with half-lives of 18.3 and 12.0 h. Amoxicillin residues in pompano liver and kidney tissues were proved to be under the MRL, 0.5 ug/g (liver and kidney) after a withdrawal period of five days.
Introduction: Reducing mean population sodium intake by ~1200 mg is projected to reduce thousands of deaths from heart disease and stroke and save billions of health care dollars annually. Twenty-four hour urine collection is recommended for assessing changes in mean population sodium intake, but can be difficult to implement. Predicting 24-hour urine sodium excretion using spot urines is not recommended due to diurnal variations in excretion. Further, sodium excretion patterns differ between black and white persons. We assessed the validity of previously published prediction equations for 24-hour sodium excretion in black and other young adults by timing of spot urine collection. Design: Of 481 adult volunteers aged 18-39 years (50% Blacks) asked to participate in a 2011 study in the Metropolitan DC area, 407 collected each urine void in a separate container for 24 hours. Four timed voids from the 24-h urine collection were selected (morning, afternoon, evening, and overnight) to use with previously published predictive equations. Predictive equations were based on one of two approaches; 1) an indirect approach using spot urine sodium-to-creatinine concentrations and predicted 24-hour creatinine excretion ( Tanaka, Kawasaki, Mage ), and 2) a direct approach using spot urine sodium, potassium, and creatinine concentrations, and age, and body mass index with separate equations by sex ( Brown ). We assessed mean differences between predicted and measured 24-hour sodium excretion (bias) and individual differences across levels of sodium excretion using Bland-Altman plots. Results: Among participants, mean measured 24-hour sodium excretion was ~3300 mg (SD ~1400 mg). Of the equations evaluated, mean bias in predicted 24-hour sodium excretion was least from Brown equations when using morning (-165 mg, 95% confidence interval [CI], -295, -36 mg), afternoon (-90 mg, 95% CI, -208, 28 mg) or evening ( -120 mg, 95% CI -230, -11 mg) spot urines. When using overnight spot urines, mean bias from Brown equations was greatest and statistically significant (-247 mg, 95% CI, -348, -151 mg). When using overnight spot urines, mean bias from Tanaka (-23 mg) or Mage (-145 mg) equations was not significant, however, when stratified by sex, mean biases were significant and in opposite directions. Among Blacks, mean biases from Brown were not significant (-167 to 122 mg) except using overnight specimens among Black females (-267 mg, 95% CI, -525, -47 mg). Across equations and time periods, Bland-Altman plots indicated significant bias at the individual level. Conclusions: Of the evaluated equations, predicted 24-hour urine sodium excretion using the Brown equations with morning, afternoon, or evening specimens may provide the least biased estimates of group mean sodium intake among young US adults. None of the equations adequately predicted individual 24-hour sodium excretion measured on the same day.
Abstract Mutations in the septin (SEPT) family lead to male infertility. Septin 14 (SEPT14) is abundantly expressed in the testis, and its expression is significantly reduced in individuals with teratozoospermia, suggesting that SEPT14 may play a role in spermatogenesis. Here, we demonstrated that Sept14 is expressed mainly at the acroplaxome, manchette, neck, and annulus during spermiogenesis. To study the role of SEPT14 in sperm morphogenesis and function, the Sept14 knockout ( Sept14 −/− ) mice were generated. The Sept14 −/− male mice were subfertile and presented phenotypes such as irregular acrosomes, DNA damage, disorganized mitochondria, and displaced annuli. These abnormalities contributed to reduced sperm motility and impaired capacitation. Mechanistically, in the sperm head, SEPT14 interacted and colocalized with microtubules and actin during the manchette formation at the sperm metamorphosis phase. In the annulus, SEPT14 interacted with SEPT9, SEPT7, and SEPT2 to form the septin filaments to maintain the localization of the annulus. The GTP‐binding domain (GBD) of SEPT14 interacted with the GBD of SEPT2, whereas the C‐terminus of SEPT14 interacted with the GBD of SEPT7. Thus, our study reveals a role of SEPT14 in mediating sperm morphogenesis.
Understanding measurement error in sodium and potassium intake is essential for assessing population intake and studying associations with health outcomes.The aim of this study was to compare sodium and potassium intake derived from 24-h dietary recall (24HDR) with intake derived from 24-h urinary excretion (24HUE).Data were analyzed from 776 nonpregnant, noninstitutionalized US adults aged 20-69 y who completed 1-to-2 24HUE and 24HDR measures in the 2014 NHANES. A total of 1190 urine specimens and 1414 dietary recalls were analyzed. Mean bias was estimated as mean of the differences between individual mean 24HDR and 24HUE measurements. Correlations and attenuation factors were estimated using the Kipnis joint-mixed effects model accounting for within-person day-to-day variability in sodium excretion. The attenuation factor reflects the degree to which true associations between long-term intake (estimated using 24HUEs) and a hypothetical health outcome would be approximated using a single 24HDR: values near 1 indicate close approximation and near 0 indicate bias toward null. Estimates are reported for sodium, potassium, and the sodium: potassium (Na/K) ratio. Model parameters can be used to estimate correlations/attenuation factors when multiple 24HDRs are available.Overall, mean bias for sodium was -452 mg (95% CI: -646, -259), for potassium -315 mg (CI: -450, -179), and for the Na/K ratio -0.04 (CI: -0.15, 0.07, NS). Using 1 24HDR, the attenuation factor for sodium was 0.16 (CI: 0.09, 0.21), for potassium 0.25 (CI:0.16, 0.36), and for the Na/K ratio 0.20 (CI: 0.10, 0.25). The correlation for sodium was 0.27 (CI: 0.16, 0.37), for potassium 0.35 (CI: 0.26, 0.55), and for the Na/K ratio 0.27 (CI: 0.13, 0.32).Compared with 24HUE, using 24HDR underestimates mean sodium and potassium intake but is unbiased for the Na/K ratio. Additionally, using 24HDR as a measure of exposure in observational studies attenuates the true associations of sodium and potassium intake with health outcomes.
Abstract Oxygen is essentially required by most eukaryotic organisms as a scavenger to remove harmful electron and hydrogen ions or as a critical substrate to ensure the proper execution of enzymatic reactions. All nucleated cells can sense oxygen concentration and respond to reduced oxygen availability (hypoxia). When oxygen delivery is disrupted or reduced, the organisms will develop numerous adaptive mechanisms to facilitate cells survived in the hypoxic condition. Normally, such hypoxic response will cease when oxygen level is restored. However, the situation becomes complicated if hypoxic stress persists (chronic hypoxia) or cyclic normoxia-hypoxia phenomenon occurs (intermittent hypoxia). A series of chain reaction-like gene expression cascade, termed hypoxia-mediated gene regulatory network, will be initiated under such prolonged or intermittent hypoxic conditions and subsequently leads to alteration of cellular function and/or behaviors. As a result, irreversible processes occur that may cause physiological disorder or even pathological consequences. A growing body of evidence implicates that hypoxia plays critical roles in the pathogenesis of major causes of mortality including cancer, myocardial ischemia, metabolic diseases, and chronic heart and kidney diseases, and in reproductive diseases such as preeclampsia and endometriosis. This review article will summarize current understandings regarding the molecular mechanism of hypoxia in these common and important diseases.
Preeclampsia is a severe gestational hypertensive disorder that occurs after 20 weeks' of gestation. It involves several maternal systems, such as cardiovascular, renal, coagulatory systems, and poses a major threat to the maternal and fetal health. Recent clinical evidence showed that aspirin is an effective preventative treatment for reducing the incidence of premature preeclampsia among high-risk pregnant women, however, the mechanism of drug action is not clear. miR-200 family has been shown to be associated with preeclampsia and upregulated in the plasma and placenta of preeclamptic patients. Here we revealed that miR-200 family inhibited trophoblast invasion and epithelial-mesenchymal transition (EMT) process by stimulating epithelial marker expression (E-cadherin and ZO-1) and repressing mesenchymal marker expression (ZEB1 and TGFβ1). Similarly, EMT markers in the placenta of preeclamptic patients showed higher E-cadherin and lower ZEB1 and TGF-β1 protein expression. Moreover, aspirin was shown to suppress miR-200 family and these miR-200 family-mediated cell functions, including cell invasion and EMT changes, were completely reversed. In conclusion, this study demonstrates the effect of miR-200 family on trophoblast invasion and EMT. For the first time, aspirin was shown to fully reverse miR-200-mediated trophoblast biology and act through the network signaling of TGF-β1/ZEB1/miR-200. These results provide a plausible mechanism explaining aspirin's effect on preeclampsia prevention and a therapeutic target for disease intervention.
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