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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.

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.

In this paper, a sparse reconstruction based approach to estimate Stokes parameters and 2-D DOAs of polarized sources is proposed in case of unknown number of sources. An L-shaped coprime array composed of dipole-dipole pairs, where a dipole in the dipole-dipole pair is placed on x-axis and the other is placed on z-axis, is used to reduce the mutual coupling across two dipoles in the dipole-dipole pair. In order to estimate the elevation of polarized sources, an orthogonal matching pursuit algorithm with the identification of the sources' number (OMP-isn) is proposed. In our proposed approach, the quasi deterministic maximum likelihood (qDML) test step is added in each iteration of algorithm. In addition, a refining grid step is also added in each iteration to reduce the estimation error incurred by the grid mismatch. The OMP algorithm and sparse iterative covariance-based estimation (SPICE) method are employed to estimate the azimuth of polarized sources. In order to pari the azimuth with the elevation, a pair-matching method is proposed based on the l 2 -norm and l 1 -norm ( l 2 / l 1 ) minimization. Based on the pairing azimuth and elevation, Stokes parameters of polarized sources are estimated by using Least Squares (LS) or Total Least Squares (TLS). The stochastic CRB is derived for the 2-D DOAs and Stokes parameters of polarized sources. Simulations are used to verify the performance of the proposed approach.

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, χ2= 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

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.

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.

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.

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

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.

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.

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.

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.

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.’

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.

In this paper, a new “particle-velocity-field and spatial smoothing” (PVFSS) algorithm is proposed for direction-finding of coherent signals, using the cylindrical vector-hydrophones array in the underwater acoustic medium. In contrast to the customary “spatial smoothing” technique, it provides a smaller reduction in the overall array’s spatial aperture. While in contrast to the “particle-velocity-field smoothing” technique, it may increase the number of decorrelate-able coherent signals. Moreover, an ESPRIT-based, closed-form direction-finding algorithm is proposed and a method of removing cyclic ambiguity is provided. Finally, the theoretical performance of the proposed algorithm is analyzed. Simulation results are shown to verify the efficacy of the proposed algorithm.

A new 'particle-velocity-field smoothing' (PVFS) algorithm is proposed to decorrelate up to three coherent sources for azimuth-elevation direction-finding using vector-hydrophones in the underwater acoustic medium. The coherency among the incident sources would reduce the data correlation matrix's rank to below the number of incident sources, but this proposed algorithm restores the rank by summing the individual particle-velocity-field component's data correlation matrices. This scheme uses identically oriented underwater-acoustic vector-hydrophones, its locations may be arbitrary. Each underwater-acoustic vector-hydrophone consists of two or three collocated but orthogonally oriented velocity-hydrophones, and a pressure-hydrophone. In contrast to the customary 'spatial smoothing' technique, this proposed PVFS algorithm does not reduce the array's spatial aperture and does not require any 'virtual array interpolation' even for an irregularly shaped array grid. Monte Carlo simulations verify this proposed scheme's efficacy.

A new vector field smoothing algorithm for direction-of-arrival (DOA) estimation of multiple coherent, underwater acoustic signals is proposed based on the array with vector hydrophones, which is located at or near a reflecting boundary. The performance of the proposed algorithm is examined in two practical applications: hull-mounted and seabed array. The advantage of the vector field smoothing scheme is no reduction in the overall array's spatial aperture.

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.

The problem of estimating direction of arrivals (DOA) and Doppler frequency for many sources is considered in the presence of general array errors (such as amplitude and phase error of sensors, setting position error of sensors). Adopting direct array manifold in a uniform circular array (UCA), the estimation of Doppler frequency can be obtained by DOA matrix. Based on analyzing the statistic characters of general array errors, the estimation of DOA can be obtained by Weight Total Least Squares. Numerical results illustrate that the estimator is robust to general array errors and show the capabilities of the estimator.

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.

Motivated by the benefits of array signal processing in quaternion domain, we investigate the problem of adaptive beamforming based on complex quaternion processes in this paper. First, a complex quaternion least-mean squares (CQLMS) algorithm is proposed and its performance is analyzed. The CQLMS algorithm is suitable for adaptive beamforming of vector-sensor array. The weight vector update of CQLMS algorithm is derived based on the complex gradient, leading to lower computational complexity. Because the complex quaternion can exhibit the orthogonal structure of an electromagnetic vector-sensor in a natural way, a complex quaternion model in time domain is provided for a 3-component vector-sensor array. And the normalized adaptive beamformer using CQLMS is presented. Finally, simulation results are given to validate the performance of the proposed adaptive beamformer.

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 quaternionsemiwidelylinear (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.

In the paper, the problem of MVDR beam former based on hyper complex processes is investigated in a scenarios where there exist one signal and one interference that are uncorrelated. First, a quaternion model of linear array with two-components EM vector-sensors is presented. Based on the quaternion model, a quaternion MVDR (QMVDR) beam former is derived. The quaternion-valued output $y(n)$ of the QMVDR consists of two complex components $y_1(n)$ and $y_2(n)$. In $y_2(n)$, there exist only the interference and noise components, but no desired signal. The desired signal is included in $y_1(n)$ and it is corrupted by the interference and noise. To extract the desired signal, we can employ $y_2(n)$ to cancel partly the interference component in $y_1(n)$. Thus, an interference and noise cancellation (INC) algorithm of QMVDR is proposed. The INC algorithm of QMVDR beam former is similar to the generalized side lobe canceller. Simulation results show that the proposed algorithm can achieve a much better performance in terms of output SINR than existing ones.

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).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.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, P0.01),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,P0.01). 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,P0.05), 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, P0.05). 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, P0.05). 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%.The expression of I Kappa B-alpha mRNA level can be a useful guide for determining the prognosis of patients with MODS.

In presence of general array error in a uniform circular arrays (UCAs), estimation of azimuth and elevation for a source is proposed. Based on array manifold in UCAs, the spatial frequency that is related to DOA is gained and theoretical expression for its asymptotic variance and the Cramer-Rao bound (CRB) of estimation is derived. The ambiguous problem is analyzed. The azimuth and elevation of source are estimated by weighted total least squares. The results of simulation show that the performance of the estimation is close to the CRB.

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 stratifi ed 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 signifi cant 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 specifi city 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.