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Objective: To investigate the risk factors of postoperative delirium in elderly patients undergoing spine surgery., Methods: The basic case data of 566 patients who underwent spine surgery under general anesthesia from January 2021 to January 2023 were retrospectively analyzed. There were 296 males and 270 females with an average age of (71.58 ± 4.21) years old. There were 195 cases of cervical spine surgery, 26 cases of thoracic spine surgery and 345 cases of lumbar spine surgery.According to the occurrence of postoperative delirium, the patients were divided into postoperative delirium group(41 patients) and non-delirium group (525 patients). Univariate analysis was used to analyze the possible influencing factors such as gender, age, weight, smoking history, drinking history, surgical site, preoperative anxiety, intraoperative hypotension times, blood loss and so on, and binary Logistic regression was used to analyze the univariate factors with P <0.05., Results: A total of 41 patients developed postoperative delirium. Univariate analysis showed that age ( P =0.000), duration of surgery ( P =0.039), preoperative anxiety ( P =0.001), blood loss ( P =0.000), history of opioid use ( P =0.003), history of stroke ( P =0.005), C-reactive protein ( P =0.000), sodium ion( P =0.000) were significantly different between delirium group and non-delirium group. These factors were included in the binary Logistic regression analysis, and the results showed that age [ OR =0.729, 95% CI (0.569, 0.932), P =0.012], opioid use [ OR =21.500, 95% CI (1.334, 346.508), P =0.031], blood loss [ OR =0.932, 95% CI (0.875, 0.993), P =0.029], C-reactive protein [ OR =0.657, 95% CI (0.485, 0.890), P =0.007], preoperative anxiety [ OR =23.143, 95% CI (1.859, 288.090), P =0.015], and sodium [ OR =1.228, 95% CI (1.032, 1.461), P =0.020] were independent risk factors for the development of delirium after spinal surgery in elderly patients., Conclusion: Age, opioid use, blood loss, preoperative anxiety, elevated c-reactive protein, and hyponatremia are independent risk factors for the development of postoperative delirium in elderly patients undergoing spinal surgery.

Objective: To investigate the different impacts on clinical outcomes between regular recall and non-regular recall among incident peritoneal dialysis (PD) patients., Methods: A two-center cohort of 216 new PD patients from 1January 2013, to 31 December 2014, was studied. Informative clinical data were collected from baseline until two years after PD initiation, including demographics, laboratory and PD-related parameters, PD-related peritonitis rates, and frequency of hospitalization. Regular in-person recall (RPR) was defined as having a one-month interval and non-regular in-person recall (NRPR) as an interval ranging from more than one month to less than three months., Results: Percentage of patients with peritonitis was significantly higher among patients in the NRPR group than among those in the RPR group (27.7% vs. 16.5%, p  = .049). PD-related peritonitis rate was higher in the NRPR vs. RPR cohorts (0.16 vs. 0.09 person/year, p  = .019). PD-related hospitalization frequency was also higher in the NRPR cohort (0.8 ± 1.0 vs. 0.5 ± 0.9, p  = .039) over two years. Kt/ V values in the NRPR cohort gradually decreased over two years and were at lower levels than in the RPR cohort., Conclusions: New PD patients with NRPR showed higher rates of PD-related peritonitis and hospitalization frequency than patients with RPR.

Background: It is well known that diabetes mellitus is one of the high-risk factors for periodontitis and also for the failure of implant restorations. Usually, the success of an implant restoration depends on both the good osseointegration and the stable soft tissue interface on the implant neck. A good gingival interface of the implant neck is the barrier that enables implant to resist oral microorganisms and the site of initiation of peri-implantitis. This study sought to investigate the effects of hyperglycemia on the attachment and proliferation of human gingival fibroblasts (HGFs) on pure titanium surfaces., Methods: HGFs were cultured in cell culture mediums with different glucose concentrations (i.e., 5.5, 8. 8, 10, and 15 mmol/L) for 7 d and seeded on pure titanium surfaces. The cells that were seeded on the titanium surfaces had been cultured in cell culture mediums with different glucose concentrations for 3 and 7 d. The attached HGFs on the titanium surfaces were counted for all groups using a blood cell counting plate, and the results were statistically analyzed. The morphologies of the attached HGFs on the titanium surfaces were observed for all the groups using a scanning electronic microscope., Results: As the glucose concentrations increased, the number of attached HGFs on the titanium surfaces decreased. The numbers of attached cells in Groups A and B 7 d after being seeded on the titanium surfaces were more than those 3 d after being seeded (P<0.05). The numbers of attached cells in Groups C and D 3 d after being seeded on the titanium were more than those 7 d after being seeded (P<0.05). The scanning electronic microscope showed that the attached cells in Groups A and B proliferated well, and most cells grew one on top of another. Conversely, the attached cells in Groups C and D proliferated sparsely and the cell morphologies were not good., Conclusions: The attachment and proliferation of HGFs on pure titanium surfaces were inhibited by increases in glucose concentrations, and the inhibition was further enhanced by the passage of time.

Objective: To investigate the changes of natural killer(NK) cell function, and clarify the effect of granulocytic myeloid derived suppressor cells (G-MDSCs) on NK cell functionality in patients with treatment-naive chronic hepatitis C (CHC) who were cured by direct-acting antiviral agents (DAAs). Methods: Thirteen treatment-naive CHC patients and 13 healthy controls were prospectively included in this study from March 2016 to January 2017. They were divided into case group and control group, respectively. The patients of case group,6 males and 7 females aged 21-65 years old with an average of (37±14),were treated with daclatasvir and asunaprevir combination (DCV/ASV) at the Department of Infectious Diseases, Fifth Medical Center of Chinese PLA General Hospital. While 13 healthy individuals, 6 males and 7 females aged 21-57 (36±11) years old, were enrolled as healthy controls(control group). Flow cytometry was used to determine the immunological characteristics of peripheral blood NK cells subset, and detect the frequencies of gMDSCs in peripheral blood of people in two groups. It was specifically notes that CHC patients of case group would be detected before, during and after treatment. The correlations between gMDSCs and each NK cell subset function were also examined. The impact of gMDSCs on NK cell functionalities and the relevant regulatory mechanisms were explored using co-culture experiments of sorted NK cells and gMDSCs in vitro . Results: Compared with healthy controls, the decreased IFN-γ production[ M ( Q 1, Q 3)] [3.182 (2.757, 4.237) vs 6.675 (4.476, 8.280),1.434 (1.127, 2.434) vs 3.045 (1.680, 4.856), 2.611 (1.749, 3.498) vs 5.160 (4.232, 7.683)] and increased CD107a degranulation [9.314 (7.838, 13.543) vs 3.480 (2.938, 6.824), 2.544 (1.366, 4.768) vs 0.552 (0.408, 1.560), 10.339 (9.145, 12.534) vs 3.488 (3.117, 5.651)] (all P <0.05) were found on NK cell and its subsets. The frequencies of gMDSCs and plasma concentration of arginase-1 in CHC patients was significantly higher than that in healthy controls [7.050 (4.180, 12.538) vs 1.440 (0.444, 2.261), 114.278 (68.492, 163.724) vs 64.753 (50.809, 93.278)](all P <0.05). The production of IFN-γ was increased and the secretion of CD107a was decreased in NK cell and its subsets after DAAs treatment ( P <0.05). The frequencies of gMDSCs and plasma arignase I levels were also decreased in CHC patients treated with DAAs ( P <0.05).The results of the study indicated that the frequencies of G-MDSCs were inversely associated with the levels of IFN-γproduction of NK cells and CD56 dim NK cells in CHC patients ( r =0.668, -0.750, respectively, both P <0.05). In addition, the frequencies of gMDSCs were positively associated with the expression of CD107a in the CD56 bright NK cell subset ( r =0.711, P =0.021). In vitro , the inhibition of gMDSCs on the IFN-γ production of NK cells was demonstrated in the co-culture experiments of sorted NK cells and gMDSCs, and blocking arginase I can significantly increase the ability of NK cells to produce IFN-γ, restore NK cell IFN-γ production. Conclusions: gMDSCs in peripheral blood of CHC patients has been shown to suppress NK cell IFN-γ production in an arginase I-dependent manner. Direct-acting antiviral-mediated clearance of HCV is associated with the normalization of NK cell function and gMDSCs frequency.

Objective: To investigate the effect of serum potassium level and hyperkalemia on the renal function decline in chronic kidney disease (CKD) patients. Methods: The clinical data at baseline and follow-up in stage Ⅲ-Ⅴ CKD patients without dialysis who were followed up for more than one year in Tianjin First Central Hospital from May 2015 to June 2019 and Teikyo University School of Medicine from January 2008 to July 2013 were retrospectively collected. All patients were divided into stable group (337 cases), slow progression group (337 cases) and rapid progression group (338 cases) according to the tertile of estimated glomerular filtration rate (eGFR) slope (the annual average percentage of eGFR decline). Multivariate logistic regression analysis models were used to evaluate the correlations of baseline serum potassium or time-averaged serum potassium level with CKD rapid progression. Results: Three hundred and forty-three cases from Tianjin First Central Hospital and 669 cases from Teikyo University School of Medicine were included in the study, and 635 cases (62.7%) were male. The average age was (61±14) years old and the average eGFR decline slope was 4.0%/year. The levels of baseline serum potassium and time-averaged serum potassium of patients in the slow progression group [(4.47±0.52) and (4.51±0.43) mmo/L] and rapid progression group [(4.62±0.62) and (4.76±0.48) mmo/L] were higher than those in the stable group [(4.37±0.49) and (4.38±0.37) mmo/L] (both P <0.05). Meanwhile, 24.6% (83/338) of the patients in the rapid progression group had hyperkalemia at baseline (serum potassium ≥5.0 mmol/L) and 34.9% (118/338) of the patients had time-averaged serum potassium ≥5.0 mmol/L, which were higher than those in the stable group [10.7% (36/337) and 6.5% (22/337)] (both P <0.001). Multivariate logistic regression analysis showed that compared with the stable group, baseline serum potassium ( OR =1.843, 95% CI : 1.051-3.234) and time-averaged serum potassium ( OR =2.495, 95% CI : 1.040-5.987) were correlated with the rapid progression of CKD. Time-averaged serum potassium ≥5.0 mmol/L was the independent influencing factor for rapid progression of CKD. Conclusions: During the follow-up period, the average level of serum potassium in stage Ⅲ-Ⅴ CKD patients should be controlled under 5.0 mmol/L, which may reduce the risk of rapid decline of renal function.

Metabolic disease, including diabetes mellitus, hypertension, dyslipidemia, obesity, and hyperuricemia, is a common complication after liver transplantation and a risk factor for cardiovascular disease and death. The development of metabolic disease is closely related to the side effects of immunosuppressants. Therefore, optimization of the immunosuppressive regimen is very important for the prevention and treatment of metabolic disease. The Chinese Society of Organ Transplantation has developed an expert consensus on the management of metabolic diseases in Chinese liver transplant recipients based on recent studies. Emphasis is placed on the risk factors of metabolic diseases, the effect of immunosuppressants on metabolic disease, and the prevention and treatment of metabolic diseases., Competing Interests: Conflict-of-interest statement: All the authors have no conflict of interest related to the manuscript., (©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.)

Background: The clinical course of Viridans streptococci (VS) peritonitis in patients undergoing peritoneal dialysis (PD) is rarely reported. This study examined the association of clinical factors with VS peritonitis., Methods: We retrospectively reviewed clinical data from patients with VS peritonitis from March 1990 to February 2016 in a PD center in Taiwan and evaluated clinical profiles and treatment outcomes., Results: A total of 109 episodes of VS peritonitis in 71 patients identified. Among these patients, 57 had mono-VS peritonitis and 14 had concurrent polymicrobial infections. The median time interval from PD initiation to the first VS peritonitis episode was 18 months (range, 0.6-144 months). Among clinical outcomes, most VS peritonitis episodes were completely cured regardless of a history of peritonitis. All episodes with catheter removal occurred in those without a history of recent antibiotic use., Conclusion: VS peritonitis in patients undergoing PD typically has favorable treatment outcomes. Antibiotic therapy should be started promptly.

Uric acid (UA) remains a risk factor for the progression of chronic kidney disease (CKD). Most observational studies showed a slight elevation in the serum UA level and this independently predicts the incidence and development of CKD. The recent meta-analysis, however, did not reach the conclusion that urate-lowering therapy with allopurinol retards the progression of CKD. The target level of serum UA if treated is another issue of debate. Our recent analysis by propensity score analysis has shown that the serum UA should be targeted below 6.0 mg/dL to inhibit the progression towards end-stage renal disease. Underlying mechanisms whereby an increase in serum UA induces kidney injury have been elucidated in animal models. Hyperuricemic models can lead to systemic hypertension, arteriolosclerosis including afferent arteriolopathy as well as albuminuria probably due to the activation of oxidative stress. Discoveries of urate transporters have elucidated the novel mechanism of UA transport in the kidney and intestine. The intestinal ABCG2 may play a compensatory role in light of decreased renal clearance of UA in CKD model rats, the trigger of which is not a uremic toxin but serum UA itself. Insulin directly upregulates URAT1 and downregulates ABCG2 in the kidney tubules, suggesting a possible link between UA and metabolic syndrome. This review summarizes the recent knowledge on the causal effect of serum UA on the kidney injury., (© 2018 S. Karger AG, Basel.)

Objective To investigate the association between the polymorphism of C-689T in the peroxisome proliferator-activated receptor-γ2 (PPARγ2) promoter and coronary heart disease (CHD). Methods This case-controlled study was conducted in nondiabetic Chinese Han people, which enrolled 455 patients with CHD (cases) and 693 subjects without CHD (controls). Data of clinical indexes were collected, including height, body weight, waist circumstance, systolic blood pressure (SBP), diastolic blood pressure (DBP), smoking, drinking, physical activity, as well as body mass index (BMI). Fasting blood glucose (FBG), plasma total cholesterol (TC) and triglyceride (TG) levels were measured. Polymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) was used to determine the PPARγ2 promoter C-689→T substitution. The genotype distribution of PPARγ2 promoter C-689T, allelic frequency, clinical indexes, and laboratorial measurements were compared between the two groups. The effect of genotype on the risk of CHD was assessed using univariate and multivariate regression model. Results The genotype frequencies of CC, CT and TT in PPARγ2 promoter C-689T were 89.7%, 9.9% and 0.4% in the case group, and 93.1%, 6.6% and 0.3% in the control group, respectively (CC vs. CT+TT, χ 2 = 6.243, P=0.041). Carriers of -689T allele (n=95) had significantly higher TC level than non-carriers (n=1053) (5.12±1.26 vs. 4.76±1.22 mmol/L, P=0.001). Male carriers of -689T allele (n=51) were significantly higher in waist circumference, body weight, TC and TG than male non-carriers (n=656) (all P<0.05). In subjects whose BMI was over 25 kg/m 2 , carriers of -689T allele (n=82) had significantly higher levels of waist circumference, BMI, SBP and TC than non-carriers (n=231) (all p<0.05). The -689T allele was an independent risk factor for CHD (OR=1.668, 95%CI: 1.031-2.705, P=0.037) after adjusting for age, gender, waist circumference, body weight, BMI, smoking, physical activities, SBP, DBP, FBG, TC and TG level. Conclusion These data support the hypothesis that the -689T allele is associated with an increased risk of CHD, in Chinese Han people and correlates significantly with the profiles of CHD-related risk factors.

Aldosterone plays an important role in regulating Na-Cl reabsorption and blood pressure. Epithelial Na + channel, Na + -Cl - cotransporter, and Cl - /HCO 3 - exchanger pendrin are the major mediators of Na-Cl transport in the aldosterone-sensitive distal nephron. Existing evidence also suggests that plasma K + concentration affects renal Na-Cl handling. In this study, we posited that hypokalemia modulates the effects of aldosterone on pendrin in hyperaldosteronism. Chronic aldosterone infusion in mice increased pendrin levels at the plasma membrane, and correcting hypokalemia in this model almost completely blocked pendrin upregulation. However, hypokalemia induced by a low-K + diet resulted in pendrin downregulation along with reduced plasma aldosterone levels, indicating that both hypokalemia and aldosterone excess are necessary for pendrin induction. In contrast, decreased plasma K + levels were sufficient to increase Na + -Cl - cotransporter levels. We found that phosphorylation of mineralocorticoid receptor that prevents aldosterone binding in intercalated cells was suppressed by hypokalemia, which resulted in enhanced pendrin response to aldosterone, explaining the coordinated action of aldosterone and hypokalemia in pendrin regulation. Finally, to address the physiological significance of our observations, we administered aldosterone to mice lacking pendrin. Notably, plasma K + levels were significantly lower in pendrin knockout mice (2.7±0.1 mmol/L) than in wild-type mice (3.0±0.1 mmol/L) after aldosterone infusion, demonstrating that pendrin alleviates hypokalemia in a state of aldosterone excess. These data indicate that the decreased plasma K + levels promote pendrin induction by aldosterone, which, in concert with Na + -Cl - cotransporter, counteracts the progression of hypokalemia but promotes hypertension in primary aldosterone excess., (© 2017 American Heart Association, Inc.)

Uric acid (UA) remains a possible risk factor of chronic kidney disease (CKD) but its potential role should be elucidated given a fact that multidisciplinary treatments assure a sole strategy to inhibit the progression to end-stage renal disease (ESRD). In clinical setting, most observational studies showed that elevation of serum uric acid (SUA) independently predicts the incidence and the development of CKD. The meta-analysis showed that SUA-lowering therapy with allopurinol may retard the progression of CKD but did not reach conclusive results due to small-sized studies. Larger scale, randomized placebo-controlled trials to assess SUA-lowering therapy are needed. Our recent analysis by propensity score methods has shown that the threshold of SUA should be less than 6.5 mg/dL to abrogate ESRD. In animal models an increase in SUA by the administration of oxonic acid, uricase inhibitor, or nephrectomy can induce glomerular hypertension, arteriolosclerosis including afferent arteriolopathy and tubulointerstitial fibrosis. The ever-growing discoveries of urate transporters prompt us to learn UA metabolism in the kidney and intestine. One example is that the intestinal ABCG2 may play a compensatory role at face of decreased renal clearance of UA in nephrectomized rats, the trigger of which is not a uremic toxin but SUA itself. This review will summarize the recent knowledge on the relationship between SUA and the kidney and try to draw a conclusion when and how to treat asymptomatic hyperuricemia accompanied by CKD. Finally we will address a future perspective on UA study including a Mendelian randomization approach.

The relationship between serum alkaline phosphatase (ALP) concentrations and mortality in peritoneal dialysis (PD) patients is rarely reported. We enrolled 667 PD patients in one PD centre in Taiwan to retrospectively examine the association between three ALP concentrations (baseline, time-averaged, time-dependent) and mortality over a 5-year period (2011-2015). Baseline data collection included demographics, clinical, and laboratory parameters. Multivariable-adjusted Cox models were used to analyse the association. Four ALP quartiles were defined at the baseline: ≤62, 63-82, 83-118, and ≥119 U/L. Of 667 patients, 65 patients died, of which 8 patients died due to cardiovascular disease. Females were predominant in the higher ALP quartiles, and 24-h urine volume was significantly proportionately decreased in the higher ALP quartiles. ALP quartiles expressed by the three models were not associated with all-cause or cardiovascular mortalities after adjusting for demographics, liver function, bone metabolism, mortality, hemoglobin, and 24-h urine volume. In conclusion, ALP concentrations were not associated with death risk in PD patients over the 5-year period.

Background/aims: Higher level of serum uric acid (SUA) predicts early entry to dialysis in chronic kidney disease (CKD) patients. However, a short-term effect of SUA remains to be elucidated using a novel surrogate endpoint., Methods: Japanese CKD stage 3 to 4 patients were retrospectively examined (n= 701). The follow-up level of SUA was estimated as time-averaged uric acid (TA-UA). A propensity score for 6.0, 6.5 or 7.0 mg/dL of TA-UA was respectively calculated using baseline 23 covariates. The time-to-event analysis was performed for 30% decline in estimated GFR over 2 years., Results: Incidence rates over 2 years were 90 of 440 in men and 36 of 261 in women (p = 0.03). Despite the negative result of baseline SUA, stratified Cox regression on the quintiles of the estimated propensity score showed that higher TA-UA of the three thresholds were all significant (crude HR 2.10 to 2.44) even after adjusting for the confounders. Kaplan-Meier analysis after propensity score matching likewise showed worse survival in the patients with the higher TA-UA (HR 3.11 to 4.26)., Conclusion: Higher SUA increases likelihood of reaching a surrogate endpoint over 2 years. Early intervention for SUA less than 6.0 mg/dL is recommended for slowing CKD progression., (© 2017 The Author(s). Published by S. Karger AG, Basel.)

Background: Although hyperphosphatemia is deemed a risk factor of the progression of chronic kidney disease (CKD), it remains unclear whether the normal range of serum phosphorus likewise deteriorates CKD. A propensity score analysis was applied to examine the causal effect of the normal range of serum phosphorus on the incidence of end-stage renal disease (ESRD)., Methods: A retrospective CKD cohort of 803 participants in a single institution was analyzed. Propensity score was estimated using 22 baseline covariates by multivariate binary logistic regression for the different thresholds of time-averaged phosphorus (TA-P) in the normal range of serum phosphorus incremented by 0.1 mg/dL from 3.3 to 4.5 mg/dL., Results: The incidence rate of ESRD was 33.9 per 1,000 person-years over median follow-up of 4.3 years. Total patients showed the mean baseline phosphorus of 3.37 mg/dL and were divided to quartile. The higher quartile was associated with the parameters consistent with the advancement of CKD. A stratified Cox regression showed the highest hazard ratio (HR) at TA-P 3.4 mg/dL (HR 17.60, 95% CI 3.92-78.98) adjusted for baseline covariates such as sex, age, diabetic nephropathy, estimated GFR, serum albumin, Na-Cl, phosphorus, LDL-C and proteinuria. Adjusted HRs remained high up to TA-P 4.2 mg/dL (HR 2.22, 95% CI 1.33-3.71). After propensity score matching conducted at the thresholds of TA-P 3.4, 3.6, 3.8 and 4.0 mg/dL, the higher levels of TA-P showed the higher HRs by Kaplan-Meier analysis (p < 0.05 by stratified log-rank test). The numbers needed to treat were calculated as 3.9 to 5.3 over 5 years., Conclusions: The propensity score analysis shows that even the normal range of serum phosphorus clearly accelerates CKD progression to ESRD. Our results encourage clinicians to target serum phosphorus to inhibit CKD progression in the manner of 'the lower the better.'

Background: Targeting the modifiable risk factors may help halt the progression of CKD, thus risk factor analysis is better performed using the parameters in the follow-up. This study aimed to examine the time-dependent risk factors for CKD progression using time-averaged values and to investigate the characteristics of rapid progression group., Methods: This is a retrospective cohort study enrolling 770 patients of CKD stage 3-4. Time-dependent parameters were calculated as time-averaged values by a trapezoidal rule. % decline of estimated GFR (eGFR) per year from entry was divided to three groups: <10% (stable), 10-25% (moderate progression), and ≥25% (rapid progression). Multivariate regression analyses were employed for the baseline and the time-averaged datasets., Results: eGFR decline was 2.83 ± 4.04 mL/min/1.73 m(2)/year (8.8 ± 12.9 %) in male and 1.66 ± 3.23 mL/min/1.73 m(2)/year (5.4 ± 11.0%) in female (p < 0.001). % decline of eGFR was associated with male, proteinuria, phosphorus, and systolic blood pressure as risk factors and with age, albumin, and hemoglobin as protective factors using either dataset. Baseline eGFR and diabetic nephropathy appeared in the baseline dataset, while uric acid appeared in the time-averaged dataset. The rapid progression group was associated with proteinuria, phosphorus, albumin, and hemoglobin in the follow-up., Conclusion: These results suggest that time-averaged values provide insightful clinical guide in targeting the risk factors. Rapid decline of eGFR is strongly associated with hyperphosphatemia, proteinuria, and anemia indicating that these risk factors should be intervened in the follow-up of CKD.

Background. This study evaluated the association between achieving target chronic kidney disease-mineral and bone disorder (CKD-MBD) marker levels and mortality in Taiwanese hemodialysis (HD) patients. Target levels were based on the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. Methods. We performed a retrospective medical record review of 1126 HD patients between 2009 and 2013. A logistic regression model was used to evaluate the relationship between achieving target marker levels and the risk for all-cause and cardiovascular (CV) mortality. Reference target ranges were 7.9 ≤ calcium (Ca) ≤ 9.9 mg/dL, 2.4 ≤ phosphate (P) ≤ 4.7 mg/dL, and 144 ≤ intact parathyroid hormone (iPTH) ≤ 648 pg/mL. Results. Achievement of target P levels was associated with a lower risk for all-cause mortality compared to achievement of either target Ca or iPTH levels. Achieving target P + iPTH levels (OR 1.32) was associated with a lower odds ratio for all-cause mortality compared to achieving target Ca + P (OR 1.66) and Ca + iPTH (OR 1.43) levels. Similar trends were observed for CV mortality risk. Conclusions. The present study demonstrated that achieving serum P levels within the KDIGO target range is the most important factor for lowering mortality in HD patients., Competing Interests: The authors declare that there is no conflict of interests regarding the publication of this paper.

Background/aims: Abnormal potassium profiles are common in peritoneal dialysis (PD) patients. We studied the factors associated with serum potassium profiles in incident PD patients., Methods: Patients were enrolled from two hospital-facilitated PD centers from May 2013 to May 2016 and January 2009 to December 2015. A total of 319 incident PD patients were examined for factors associated with serum potassium profile. Average serum potassium levels were obtained for analysis during the first 3 months after PD initiation. Clinically factors and parameters associated with PD were assessed by logistic regression., Results: There were 168 men and 151 women (mean age, 50.8 years). Blood urea nitrogen (BUN), creatinine (Cr), and intact parathyroid hormone levels were significantly increased in patients in the higher serum potassium group. There were no significant risk factors for hypokalemia, including sex, age, diabetes, blood examination parameters, medication use, or PD-related parameters by multivariate logistic regression analysis. BUN (adjusted odds ratio [OR] 1.02, 95% CI 1.01-1.03, p = 0.001) and Cr (adjusted OR 1.08, 95% CI 1.01-1.16, p = 0.029) levels were significant risk factors for hyperkalemia by multivariate logistic regression analysis., Conclusion: Hyperkalemia and blood BUN and Cr levels were significantly associated in incident PD patients., (© 2016 The Author(s) Published by S. Karger AG, Basel.)

Background: The role of uric acid (UA) in the progression of chronic kidney disease (CKD) remains controversial due to the unavoidable cause and result relationship. This study was aimed to clarify the independent impact of UA on the subsequent risk of end-stage renal disease (ESRD) by a propensity score analysis., Methods: A retrospective CKD cohort was used (n = 803). Baseline 23 covariates were subjected to a multivariate binary logistic regression with the targeted time-averaged UA of 6.0, 6.5 or 7.0 mg/dL. The participants trimmed 2.5 percentile from the extreme ends of the cohort underwent propensity score analyses consisting of matching, stratification on quintile and covariate adjustment. Covariate balances after 1:1 matching without replacement were tested for by paired analysis and standardized differences. A stratified Cox regression and a Cox regression adjusted for logit of propensity scores were examined., Results: After propensity score matching, the higher UA showed elevated hazard ratios (HRs) by Kaplan-Meier analysis (≥ 6.0 mg/dL, HR 4.53, 95%CI 1.79-11.43; ≥ 6.5 mg/dL, HR 3.39, 95%CI 1.55-7.42; ≥ 7.0 mg/dL, HR 2.19, 95%CI 1.28-3.75). The number needed to treat was 8 to 9 over 5 years. A stratified Cox regression likewise showed significant crude HRs (≥ 6.0 mg/dL, HR 3.63, 95%CI 1.25-10.58; ≥ 6.5 mg/dL, HR 3.46, 95%CI 1.56-7.68; ≥ 7.0 mg/dL, HR 2.05, 95%CI 1.21-3.48). Adjusted HR lost its significance at 6.0 mg/dL. The adjustment for the logit of the propensity scores showed the similar results but with worse model fittings than the stratification method. Upon further adjustment for other covariates the significance was attained at 6.5 mg/dL., Conclusions: Three different methods of the propensity score analysis showed consistent results that the higher UA accelerates the progression to the subsequent ESRD. A stratified Cox regression outperforms other methods in generalizability and adjusting for residual bias. Serum UA should be targeted less than 6.5 mg/dL.

Paraquat (PQ) is a highly toxic herbicide which is able to induce pulmonary fibrosis in humans and animals. The epithelial‑to‑mesenchymal transition (EMT) was demonstrated to be an important factor in pulmonary fibrosis. However, it has remained elusive whether PQ induces pulmonary fibrosis via EMT, which was therefore investigated in the present study. In addition, the underlying mechanisms of PQ‑induced EMT were examined in vitro. Hematoxylin and eosin staining of rat lung tissues demonstrated that PQ induced pulmonary fibrosis in vivo. Western blot analysis then revealed that the expression of epithelial cell marker E‑cadherin was significantly decreased, while the expression of mesenchymal markers α‑smooth‑muscle actin and vimentin was significantly increased in rat lung tissues and A549 cells following PQ treatment. Transforming growth factor (TGF)‑β/Smad signaling was also induced by PQ as evidenced by increased expression of TGF‑β1 and Smad2. However, PQ‑induced EMT in A549 cells was abolished by transfection with TGF‑β1‑specific small hairpin RNA. In conclusion, the present study demonstrated that PQ induced EMT in vivo and in vitro, which may be an important process in the development of PQ‑induced pulmonary fibrosis. In addition, TGF-β/Smad signaling was involved in PQ-induced EMT.

Background: A goal of searching risk factors for chronic kidney disease (CKD) is to halt progressing to end-stage renal disease (ESRD) by potential intervention. To predict the future ESRD, 30% decline in estimated GFR over 2 years was examined in comparison with other time-dependent predictors., Methods: CKD patients who had measurement of serum creatinine at baseline and 2 years were enrolled (n = 701) and followed up to 6 years. Time-dependent parameters were calculated as time-averaged values over 2 years by a trapezoidal rule. Risk factors affecting the incidence of ESRD were investigated by the extended Cox proportional hazard model with baseline dataset and 2-year time-averaged dataset. Predictive significance of 30% decline in estimated GFR over 2 years for ESRD was analyzed., Results: For predicting ESRD, baseline estimated GFR and proteinuria were the most influential risk factors either with the baseline dataset or the 2-year time-averaged dataset. Using the 2-year time-averaged dataset, 30% decline in estimated GFR over 2 years by itself showed the highest HR of 31.6 for ESRD whereas addition of baseline estimated GFR, proteinuria, serum albumin and hemoglobin yielded a better model by a multivariate Cox regression model. This novel surrogate was mostly associated with time-averaged proteinuria over 2 years with the cut-off of ~1 g/g creatinine., Conclusion: These results suggest that decline in estimated GFR and proteinuria are the risk factors while serum albumin and hemoglobin are the protective factors by the time-to-event analysis. Future incidence of ESRD is best predicted by 30% decline in eGFR over 2 years that can be modified by intervention to proteinuria, hemoglobin, uric acid, phosphorus, blood pressure and use of renin-angiotensin system inhibitors in the follow-up of 2 years.

We investigate the problem of quaternion beamforming based on widely linear processing. First, a quaternion model of linear symmetric array with two-component electromagnetic (EM) vector sensors is presented. Based on array's quaternion model, we propose the general expression of a quaternion semiwidely linear (QSWL) beamformer. Unlike the complex widely linear beamformer, the QSWL beamformer is based on the simultaneous operation on the quaternion vector, which is composed of two jointly proper complex vectors, and its involution counterpart. Second, we propose a useful implementation of QSWL beamformer, that is, QSWL generalized sidelobe canceller (GSC), and derive the simple expressions of the weight vectors. The QSWL GSC consists of two-stage beamformers. By designing the weight vectors of two-stage beamformers, the interference is completely canceled in the output of QSWL GSC and the desired signal is not distorted. We derive the array's gain expression and analyze the performance of the QSWL GSC in the presence of one type of interference. The advantage of QSWL GSC is that the main beam can always point to the desired signal's direction and the robustness to DOA mismatch is improved. Finally, simulations are used to verify the performance of the proposed QSWL GSC.

Background: The bispectral (BIS) index is a processed electroencephalogram (EEG) parameter with extensive validation and demonstrated clinical utility. The study aimed to investigate the correlation between the BIS index and the prognosis of patients with coma in the ICU., Methods: A total of 208 patients with coma in the ICU were enrolled in this study. According to the BIS value, the patients were divided into four groups: group I, BIS value 0 to 20; group II, BIS value 21 to 40; group III, BIS value 41 to 60; and group IV, BIS value greater than 60. The difference in BIS values with the differences in prognosis of patients with coma was compared between the four groups, and the prognosis of patients with coma was stratified into consciousness, coma, vegetative state, and brain death. Subsequently, the best cut-off score of BIS values calculated for determining the correlation between BIS value and mental state was proposed., Results: There are no significant differences in the age and APACHE II scores between the four groups (P>0.05). An inverse correlation was observed between BIS value and mental state (r= -0.749, P=0.00). According to the ROC curve, as BIS value was greater than 42.5, there were higher sensitivity and specificity in conscious-coma patients., Conclusion: BIS value is correlated with the prognosis of patients with coma in ICU, and BIS value can be a useful marker for estimating the prognosis of comatose patients.

Objective: To probe into the effect of electroacupuncture (EA) at Shuigou (GV 26) on mild and moderate shock., Methods: With 3-center randomized control study method, 276 cases were assigned to an EA plus medicine group and a medication group, 138 cases in each group. They were treated respectively with western medicine plus EA at Shuigou (GV 26), and simple western medicine. Their curative effects were observed after treatment for 6 hours., Results: The blood pressure was immediately increased in the EA plus medicine group and the increase of blood pressure was earlier than that in the medication group (P<0.001). The markedly effective rate of 52.9% in the EA plus medicine group was significantly higher than 18.1% in the medication group (P<0.001)., Conclusion: The therapeutic effect of EA at Shuigou (GV 26) plus western medicine on mild and moderate shock is better than that of simple western medicine.

Objective: To observe the value of nuclear factor-KappaB(NF-KappaB) and I Kappa B mRNA expression estimation on determining the prognosis of patients with multiple organ dysfunction syndrome (MODS)., Methods: Forty-three MODS patients were divided into two groups based on their prognosis: the survivor group (n =28) and the non-survivor group (n=15). Another group of 10 healthy persons served as normal control group. The expression of NF-Kappa B and I Kappa B-alpha mRNA levels in monocytes/neutrophils of patients and controls were detected by reverse transcription-polymerase reaction (RT-PCR), and the results were compared among groups., Results: The expression of NF-KappaB mRNA levels of MODS patients was higher than that of normal control group(1. 35+/-0.53 vs. 0.74+/-0.25, P<0.01),and the expression of I Kappa B-alpha mRNA levels were lower than those of the control group (1. 24+/-0.60 vs. 1. 97+/-0.71,P<0.01). There was no significant difference in NF-KappaB mRNA levels between the survivor group and the non-survivor group (1. 27+/-0.37 vs. 1.39+/-0.60,P>0.05), but the expression of I Kappa B-alpha mRNA levels in the non-survivor group was significantly lower than that of survivors(0.94+/-0.46 vs. 1. 40+/-0.61, P<0.05). The results suggested that there was a negative correlation between the expression of I Kappa B-alpha mRNA level and acute physiology and chronic health evaluation II (APACHE II)(r=-0.340, P<0.05). Moreover, when the cutoff value of the expression of I Kappa B-alpha mRNA level was 1. 34, the Youden index was 0.51, and it was the highest in all the cutoff values, and the specificity was 90.72%,the sensitivity was 60.75%., Conclusion: The expression of I Kappa B-alpha mRNA level can be a useful guide for determining the prognosis of patients with MODS.

Objective: To observe the therapeutic effect of Shennong No. 33 (SN33) in treating multiple organ dysfunction syndrome (MODS) by APACHE II and APACHE II scoring., Methods: One hundred and twenty-nine patients of MODS were randomly divided into the treated group (n = 72) and the control group (n = 57), they were treated with comprehensive therapy and to the treated group, SN33 was given additionally. The changes of APACHE II and APACHE III scores and blood endotoxin level were observed at the time points of within 24 hrs after hospitalization, and the 3rd, 5th and 7th day., Results: In the treated group, 50 patients survived and 22 died, while in the control group, 25 survived and 32 died. The APACHE II and APACHE III scores of the survivors were higher than those of the decedent (P<0.05), which in the treated group was lower than those in the control group (P<0.05). The blood level of endotoxin in the treated group was also lower than that in the control group (P<0.05)., Conclusion: SN33 in treating MODS could improve patients' condition, lead to the lowering of APACHE scores. APACHE scoring system could be applied as the criteria for evaluating the condition and prognosis of critical patients, and the APACHE III scoring is more accurate.

We screened a midgut cDNA library from diamondback moth, Plutella xylostella, with a probe generated using sequence information from an aminopeptidase N gene from Manduca sexta (MsAPN-1). The sequence recovered (PxAPN-A) encodes a protein of 988 resides with a 60% sequence identity to MsAPN-1. The two proteins share a signal peptide which directs processing by the endoplasmic reticulum, a C-terminal hydrophobic region satisfying the criterion for a GPI anchor and cleavage, and the possibility of an O-glycosylated rigid stalk attached to the GPI anchor. PxAPN-A is more closely related to MsAPN-1 than it is to another aminopeptidase recently reported from P. xylostella. Sequence comparisons with other species suggests that at least one aminopeptidase gene duplication occurred in an ancestral lepidopteran.