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Diastolic mitral regurgitation is a type of functional mitral regurgitation that develops via a reversal of the left atrioventricular pressure gradient during diastole. This study aimed to explore the mechanism underlying early diastolic mitral regurgitation (EDMR) in patients with left ventricular (LV) aneurysms after anterior myocardial infarction (AMI) by assessing the intraventricular pressure difference using vector flow mapping. We enrolled 23 consecutive patients with LV aneurysms (with and without EDMR) and 15 healthy men as controls. In the control group, LV suction began from the apex during early diastole. In contrast, the blood that pooled in the apical aneurysm during systole generated a relatively higher pressure at the apex than at the basal LV during early diastole; consequently, the pressure reversal phenomenon occurred in the LV. Compared to the EDMR– group, the EDMR + group (n = 7) exhibited a significantly higher diastolic time ratio ([time from the second heart sound to the pressure inversion point]/[total diastolic time]) (P

Given an undirected graph G with n vertices, the independent feedback vertex set problem is to find a vertex subset F of G with the minimum number of vertices such that F is both an independent set and a feedback vertex set of G, if it exists. This problem is known to be NP-hard for bipartite planar graphs of maximum degree four. In this paper, we study the approximability of the problem. We first show that, for any fixed e > 0 , unless P = NP , there exists no polynomial-time n 1 − e -approximation algorithm even for bipartite planar graphs. We then give an α ( Δ − 1 ) / 2 -approximation algorithm for bipartite graphs G of maximum degree Δ, which runs in t ( α , G ) + O ( Δ n ) time, under the assumption that there is an α-approximation algorithm for the original feedback vertex set problem on bipartite graphs which runs in t ( α , G ) time. This algorithmic result also yields a polynomial-time (exact) algorithm for the independent feedback vertex set problem on bipartite graphs of maximum degree three.

Background Sedentary behavior may be an independent risk factor for cardiovascular events. This study aimed to clarify the effects of extended sedentary time in patients with diabetic kidney disease (DKD) on the risk of all-cause death and new events.Methods and Results:A prospective cohort study was performed over 39 months. The study included 173 patients with DKD who completed the International Physical Activity Questionnaire (IPAQ) (101 men; mean age, 71±11 years); 37 patients (21.4%) were diagnosed with cardiovascular disease (CVD). New events were defined as all-cause death, cerebral stroke, or CVD requiring hospitalization or commencing hemodialysis (HD). Data were analyzed using a multivariate Cox proportional hazard regression model with variables, including sedentary time. There were 34 cases of new events during the observation period, including 4 cases of stroke, 20 cases of CVD, 4 cases of HD implementation, and 6 cases of death. Hazard ratio (HR) calculations for the new event onset group identified sedentary time as a significant independent variable. The independent variable that was identified as a significant predictor of new events was the sedentary time (60 min/day; HR: 1.23, 95% CI: 1.05-1.45, P=0.012). Conclusions Extended sedentary time increased the risk of new cardiovascular or renal events and/or all-cause death in patients with DKD.

Decreased physical activity and activities of daily living (ADL) in patients on hemodialysis (HD) are associated with a poor prognosis. Additionally, comorbid peripheral arterial disease is associated with further deterioration. We conducted a cross-sectional study of ADL difficulty and life-space assessment (LSA) in three groups of patients on hemodialysis according to their ankle-brachial index (ABI) values. The 164 patients were divided into ABI Low (ABI < 0.9), Normal (0.9 ≤ ABI < 1.3), and High (1.3 ≤ ABI) groups, and compared using analysis of covariance with LSA and ADL difficulty adjusted for age. The Kihon checklist (KCL) was used to assess the presence of frailty. The LSA was lower in the Low group than in the High group (F = 3.192, p = 0.044). Similarly, the ADL difficulty was significantly lower in the Low group than in the Normal group (F = 3.659, p = 0.028). In the Low group, the proportion of patients with frailty was 47.1% and KCL physical was significantly lower, indicating that patients on HD with a lower ABI had a higher prevalence of frailty and lower LSA and ADL difficulty. In conclusion, patients on HD with decreased ABI values most likely exhibit decline in physical activity and ADL due to frailty and claudication.

BackgroundReduced lower limb circumference due to sarcopenia in patients with type 2 diabetes mellitus (T2DM) could be a useful screening tool for arteriosclerosis. Hence, the objective of this study was to clarify the relation between lower limb circumference and other body composition factors, muscle strength, and patient characteristics,and the progression of arteriosclerosis in patients with T2DM. MethodsWe included114 patients with T2DM receiving outpatient care, and assessed body composition (lower limb circumferences including tibial rough surface-calf 26% [TRSC%]), muscle strength indicators, patient characteristics, clinical diabetic neuropathy status, and examined their associations with brachial–ankle pulse wave velocity (ba-PWV) using multiple regression analysis. Additionally, the severity of ba-PWV was classified into 1400 cm/s, 1650 cm/s, and 1963 cm/s to investigate their associations using logistic regression analysis. ResultsThe mean age was 63.12±11.96 years and participants had T2DM for 11.25±9.45 years. Body mass index (BMI), HbA1c, abnormal ankle reflex, and TRSC% were adopted in the multiple regression analysis with ba-PWV as the dependent variable. In the logistic regression analysis of ba-PWV divided by 1400 cm/s, an index of arteriosclerosis, BMI was adopted, and when divided by 1963 cm/s, a mortality risk index, BMI, abnormal ankle reflex, and TRSC% were adopted.ConclusionArteriosclerosis in patients with T2DM is associated with a decrease in lower limb circumference; TRSC% was independently associated with severe arteriosclerosis when ba-PWV was ≥1963 cm/s, which is an indicator of mortality risk. Thus, lower limb circumference in the form of TRSC% may reflect the progression of arteriosclerosis.

Hemodialysis patients with diabetic kidney disease (DKD) experience blood glucose fluctuations owing to insulin removal. We evaluated the effects of single and long-term application of neuromuscular electrical stimulation (NMES) during hemodialysis on glycemic control. This trial was conducted in two stages: Stage 1, following a crossover design and 4 week washout period, eleven outpatients with DKD either underwent a single bout of NMES for 30 min (NMES period) or rested (control period) after receiving nutritional support during hemodialysis; Stage 2, following a crossover design and 4 week washout period, each participant received the intervention for 12 weeks. NMES was administered for 30 min at the maximum tolerable intensity. The mean subcutaneous glucose concentration and mean amplitude of glycemic excursion (MAGE) were determined by flash glucose monitoring for 24 h. Changes in glycoalbumin and MAGE before and after NMES initiation were evaluated. The mean blood glucose level and MAGE after a single bout of NMES were significantly lower than those after rest. Glycoalbumin levels and echo intensity of the rectus femoris tended to decrease, but not significantly by ANOVA due to a lack in statistical power after the dropout of three patients. NMES in end-stage DKD decreased blood glucose levels during and after hemodialysis.

Suppose that we are given a positive integer k, and a k-(vertex-)coloring \(f_0\) of a given graph G. Then we are asked to find a coloring of G using the minimum number of colors among colorings that are reachable from \(f_0\) by iteratively changing a color assignment of exactly one vertex while maintaining the property of k-colorings. In this paper, we give linear-time algorithms to solve the problem for graphs of degeneracy at most two and for the case where \(k \le 3\). These results imply linear-time algorithms for series-parallel graphs and grid graphs. In addition, we give linear-time algorithms for chordal graphs and cographs. On the other hand, we show that, for any \(k \ge 4\), this problem remains NP-hard for planar graphs with degeneracy three and maximum degree four. Thus, we obtain a complexity dichotomy for this problem with respect to degeneracy of a graph and the number k of colors.

Water deprivation activates the renin-angiotensin system. We have hypothesized that the renal expression of (pro)renin receptor ((P)RR), a specific receptor for renin and prorenin, could be changed under dehydration. Moreover, plasma levels of soluble (P)RR (s(P)RR) comprising of the extracellular domain of (P)RR may reflect the renal (P)RR expression. In the present study, we therefore aimed to clarify changes of plasma s(P)RR concentrations and kidney tissue (P)RR levels using rats with dehydration. Male Wister-Kyoto rats were divided into two groups; dehydrated (DH) rats deprived of water for 72 hours with free access to food, and control rats. Plasma s(P)RR concentrations measured by enzyme-linked immunosorbent assay were significantly lower in DH rats (6.94 ± 2.08 ng/mL, mean ± SD, n = 5) than in control (12.54 ± 2.00 ng/mL, n = 5) (p < 0.05). Western blot analysis confirmed lower expression levels of s(P)RR in plasma in DH rats than in control. By contrast, western blot analysis showed higher levels of full-length (P)RR and lower levels of furin (an enzyme responsible for generation of s(P)RR from full-length (P)RR) in the kidney tissues obtained from DH rats compared to control. There was no significant difference in the renal (P)RR mRNA levels between DH rats and control. These findings suggest that water deprivation may elevate the renal full-length (P)RR levels via reducing the expression of furin. Increased full-length (P)RR may contribute to the up-regulation of the renal renin-angiotensin system and the production of concentrated urine under dehydration.

A feedback vertex set F of an undirected graph G is a vertex subset of G whose removal results in a forest. Such a set F is said to be independent if F forms an independent set of G. In this paper, we study the problem of finding an independent feedback vertex set of a given graph with the minimum number of vertices, from the viewpoint of graph classes. This problem is NP-hard even for planar bipartite graphs of maximum degree four. However, we show that the problem is solvable in linear time for graphs having tree-like structures, more specifically, for bounded treewidth graphs, chordal graphs and cographs. We then give a fixed-parameter algorithm for planar graphs when parameterized by the solution size. Such a fixed-parameter algorithm is already known for general graphs, but our algorithm is exponentially faster than the known one.

A functional receptor for renin and prorenin ((P)RR) was identified as a new component of the renin–angiotensin system. The precise localization of (P)RR in the kidney has not been clarified. The present study was designed to determine the localization of (P)RR in the rat nephron and to investigate the regulation of renal (P)RR expression by high salt (HS) intake. (P)RR mRNA levels in the kidney sections and isolated nephron segments were examined using reverse transcription and polymerase chain reaction (RT-PCR), and (P)RR protein levels were examined by immunoblot and immunohistochemical analyses. Renal (P)RR mRNA and protein levels in rats fed a HS diet for 4 weeks were also compared with those fed a normal salt diet. (P)RR mRNA was expressed in various nephron segments of the cortex and medulla; glomeruli (Glm), proximal tubules (PT), thick ascending limbs (TAL) and collecting ducts (CD). (P)RR protein was highly expressed in the PT, medullary TAL (MTAL) and inner medullary CD (IMCD), and lowly in the preglomerular arterioles (Art) and Glm. HS intake increased (P)RR protein levels in the Glm, PT and tubules of medullary rays. These results indicated that (P)RR is expressed throughout various nephron segments and Art, and that (P)RR protein is expressed predominantly in the PT, MTAL and IMCD. HS intake appears to upregulate the (P)RR expression in the Glm, PT and tubules of medullary rays, suggesting that (P)RR may be involved in the regulation of renal function and HS-induced disorders.

(Pro)renin receptor ((P)RR) was newly identified as a member of the renin-angiotensin system (RAS). (P)RR exists in two forms; full-length form (f(P)RR) and soluble form (s(P)RR). The truncated hydrophilic s(P)RR is generated by furin cleavage in the trans-Golgi network and is secreted into the extracellular space. Compared with Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR) demonstrated low urine concentration ability and resistance to vasopressin in a state of dehydration (DH). RAS system contributes to the regulation of body fluid balance, but roles of (P)RR in a state of dehydration (DH) are not clarified. The purpose of this study was to examine the effects of DH on the (P)RR expression in the kidney of WKY and SHR. Twelve week-old, male WKY and SHR were randomly divided into two groups (n=5 in each group); control and DH groups. DH was induced by water restriction for 72 hours in metabolic cage. After 72 hours, rats were killed, and (P)RR protein levels in plasma, urine and kidney were examined by using Western blot. (P)RR mRNA levels were examined by using competitive RT-PCR methods. In addition, furin protein levels were also investigated. DH increased urine osmolarity in WKY and SHR (4090±451 and 3796±429 mOsm/kg). DH significantly decreased the s(P)RR levels in the plasma of WKY and SHR (0.3- and 0.7-fold, P

The (pro)renin receptor ((P)RR)-bound (pro)renin not only causes the generation of angiotensin II via the increased enzymatic activity, it also activates the receptor’s own intracellular signaling pathways up-regulating the expression of the profibrotic proteins. To clarify the regulation of (P)RR expression, the present study examined the effects of high salt diet and nitric oxide synthase (NOS) inhibition on the (P)RR expression in the kidney. The nephron segments were isolated from male Sprague-Dawley (SD) rats by microdissection and bulk isolation technique, and the (P)RR mRNA and protein expressions were examined by using reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. In adiition, 5 week-old, male SD rats were randomly divided into 3 groups: a control group, a high salt diet (HS) group and a Nω-Nitro-L-arginine (L-NAME) group, and each group was treated with vehicle, high salt diet (8%, NaCl), or L-NAME (600mg/ml in drinking water), respectively. After 4 weeks, the (P)RR expression in the kidney was compared among these groups. The (P)RR mRNA was expressed in the glomerulus (Glm), the proximal convoluted and straight tubule, the cortical and medullary thick ascending limb (TAL) and collecting duct. The (P)RR protein as well as mRNA was expressed widely in the nephron segments; the preglomerular arteriole, the Glm, the proximal tubules (PT), the medullary TAL (mTAL) and inner medullary collecting duct (IMCD). Compared with the control group, the (P)RR protein levels significantly increased in the kidney cortex of both HS group and L-NAME group by 96% (p

Recently, (pro)renin receptor ((P)RR), a specific receptor for renin and prorenin, was newly identified as a member of the renin angiotensin system (RAS). (P)RR binding to the prorenin, causes the generation of angiotensin II via the increased enzymatic activity. (P)RR exists in two forms, one is full-length form (f(P)RR), and the other is soluble form (s(P)RR). RAS as well as vasopressin system contributes to the regulation of body fluid balance in a state of dehydration, but roles of (P)RR are unidentified. The purpose of this study was to examine the effects of dehydration on (P)RR expression in the plasma, the urine and kidney. Twelve week-old, male Wister Kyoto rats (n=10) were randomly divided into two groups, and the dehydration was induced by water restriction for 72 h in metabolic cage. Food intake and urinary output were measured. After 72h, rats were killed, and the protein expression of (P)RR in the plasma, the urine and kidney was investigated by using Western blotting. Compared with control rats, dehydration significantly increased osmotic pressure in the plasma and urine (286.8±2.9 vs 305.6±16.8 mOsm/L, p