Arteriovenous Fistula Flow Dysfunction Surveillance: Early Detection Using Pulse Radar Sensor and Machine Learning Classification.

Vascular Access (VA) is often referred to as the "Achilles heel" for a Hemodialysis (HD)-dependent patient. Both the patent and sufficient VA provide adequacy for performing dialysis and reducing dialysis-related complications, while on the contrary, insufficient VA is the main reason for recurrent hospitalizations, high morbidity, and high mortality in HD patients. A non-invasive Vascular Wall Motion (VWM) monitoring system, made up of a pulse radar sensor and Support Vector Machine (SVM) classification algorithm, has been developed to detect access flow dysfunction in Arteriovenous Fistula (AVF). The harmonic ratios derived from the Fast Fourier Transform (FFT) spectrum-based signal processing technique were employed as the input features for the SVM classifier. The result of a pilot clinical trial showed that a more accurate prediction of AVF flow dysfunction could be achieved by the VWM monitor as compared with the Ultrasound Dilution (UD) flow monitor. Receiver Operating Characteristic (ROC) curve analysis showed that the SVM classification algorithm achieved a detection specificity of 100% at detection thresholds in the range from 500 to 750 mL/min and a maximum sensitivity of 95.2% at a detection threshold of 750 mL/min.

Site-specific N-glycosylation regulates the GPS auto-proteolysis of CD97.

Auto-proteolysis at the G protein-coupled receptor (GPCR) proteolytic site (GPS) is a hallmark of adhesion-GPCRs. Although defects in GPS auto-proteolysis have been linked to genetic disorders, information on its regulation remains elusive. Here, we investigated the GPS proteolysis of CD97, a human leukocyte-restricted and tumor-associated adhesion-GPCR. We found that CD97 is incompletely processed, unlike its close homolog, epidermal growth factor-like module-containing mucin-like hormone receptor 2. A unique pattern of N-glycosylation within the GPS motif of related adhesion-GPCRs was identified. The use of N-glycosylation inhibitors and mutants confirm site-specific N-glycosylation is an important determinant of GPS proteolysis in CD97. Our results suggest that N-glycosylation may regulate the processing of adhesion-GPCRs leading to the production of either cleaved or uncleaved molecules.

Exploring the effects of C-reactive protein (CRP) and interleukin-1 beta single nucleotide polymorphisms on CRP concentration in patients with established coronary artery disease. Classification tree approach.

PURPOSE: This study was designed to illustrate the effects of C-reactive protein (CRP) and interleukin polymorphisms on serum CRP levels. METHODS: A total of 390 patients with coronary heart disease (CHD) were recruited and high-sensitivity CRP levels were measured. Six polymorphic alleles on the genes of CRP, IL-1, and the IL-1 receptor antagonist were identified. A classification tree was applied to determine their effects and interactions on serum CRP levels. RESULTS: In the hypertensive CHD patients, the presence of CRP + 1059 GC heterozygotes was associated with a lower risk for elevated CRP levels (OR = 0.318, P = 0.001). The coexistence of CRP + 1059 GC and IL-1beta-511 (CT or TT) might result in reduction in the CRP levels compared to IL-1beta-511 CC (OR = 0.222, P = 0.088 and OR = 0.148, P = 0.060, respectively). CONCLUSION: The results demonstrated the distribution of CRP-related polymorphisms and the interactions in Taiwanese patients with CHD.

The effects of metabolic syndrome versus infectious burden on inflammation, severity of coronary atherosclerosis, and major adverse cardiovascular events.

BACKGROUND: The clinical predictors of inflammation in atherosclerosis remain controversial. The objective of this study was to compare the associations of metabolic factors vs. infectious burden (IB) with inflammation, the severity of coronary atherosclerosis, and major adverse cardiovascular events (MACEs). DESIGN, SETTING, AND PATIENTS: Coronary angiography with Gensini score was applied to assess the severity of coronary atherosclerosis in 568 patients with coronary artery disease. Metabolic syndrome (MS) score (0-5) was defined according to the modified criteria of National Cholesterol Education Program Adult Treatment Panel III. IB score (0-7) was defined as the number of seropositivities to several agents. RESULTS: IB score was not associated with plasma C-reactive protein (CRP) concentration, Gensini score, or the risk of MACE. In contrast, MS score significantly correlated with both plasma CRP concentration and Gensini score (P < 0.001 for both). MS score and plasma CRP concentration were also significantly associated with the risk of MACE (hazard ratios 1.51, P < 0.001; and 1.90, P = 0.002, respectively). CONCLUSION: Compared with IB, metabolic abnormalities have a more prominent association with the degree of inflammation, the severity of coronary atherosclerosis, and the risk of MACE in patients with coronary artery disease.

mbgA-dependent lactose utilization by Bacillus megaterium.

The beta-galactosidase-encoding mbgA gene has recently been cloned from Bacillus megaterium. We now report that disruption of the chromosomal mbgA rendered B. megaterium unable to utilize lactose as a sole carbon source. Complementation of the mbgA mutant with a multicopy plasmid carrying intact mbga restored the ability to utilize lactose for cell growth. Crude extracts from the wild-type B. megaterium cells grown in the presence of lactose exhibited a significant level of lactose-hydrolyzing activity, whereas no activity was observed in crude extracts of the mbgA mutant grown under the same condition. The mbgA gene could also confer the ability of lactose utilization on a lacZ deletion mutant of Escherichia coli. Lactose-hydrolyzing activity was also observed in crude extracts of the lacZ deletion mutant carrying mbgA on a multicopy plasmid. In addition, inactivation of the chromosomal mbgA did not affect lactose induction of expression of the mbgA promoter-xylE transcriptional fusion. Taken together, these results suggest that mbgA is essential for lactose utilization by B. megaterium, but is not involved in generation of the intracellular inducer for lactose induction of mbgA expression.