Carboxylate-containing polyamides were synthesized from 2,6-di(amino)benzoic acid and dimethylmalonyl dichloride, isophthaloyl dichloride, and fumaryl dichloride. These polymers, {NHC6H3-(COO)NHCOC(CH3)2CO}n, {NHC6H3(COO)NHCO-m-C6H4CO}n, and {NHC6H3(COO)NHCO-trans-CHd CHCO}n, have seven to eight carboxylate units in a polymer chain, and their Ca(II) complexes possess NH‚‚‚O hydrogen bonds, which prevents the Ca-O dissociation by hydrolysis. CaCO3 was obtained from aqueous Ca 2+ and CO3 2-in the presence of the polyamide or the Na salt of these polyamides ([Ca 2+ ]/ [monomer unit] ) 100) to give calcite, vaterite, and/or their mixture. We were able to observe polymers in CaCO3 utilizing the 13 C cross-polarization/magic angle spinning solid-state NMR. The binding of Ca(II) by carboxylate appears to be an important factor in these studies and may be relevant to biomineralization of CaCO3.

To investigate how cardiomyocytes change their length, echocardiographic and morphological studies were performed on rabbit hearts that were subjected to volume overload, overload removal, and repeated cycles of overload and overload removal. These conditions were created by arterio-venous fistula between the carotid artery and jugular vein, closure of the fistula, and cycles of repeatedly forming and closing fistula, respectively. After overload, hearts dilated and myocytes elongated. Intercalated disks repeatedly broadened and narrowed with a 2-day cycle, which continued for 8 weeks in many animals. The cycle consisted of shifts between five modes characterized by two interdigitation elongation-and-shortenings as follows: (I) flat with short (ϳ1/4 to ϳ1/3 sarcomere long) interdigitations; (II) flat with long (one sarcomere long) interdigitations; (III) grooved with short interdigitations; (IV) grooved with long interdigitations; (V) flat with short interdigitations intermingled by sporadic long interdigitations; and return to (I). After overload removal, hearts contracted and myocytes shortened with similar 2-day broadening and narrowing cycle of intercalated disks, in which the five modes were reversed. Repeated overload and overload removal resulted in the repetition of myocyte elongation and shortening. We hypothesize that a single elongation-and-shortening event creates or disposes one sarcomere layer, and the two consecutive elongation-and-shortenings occur complementarily to each other so that the disks return to their original state after each cycle. Our hypothesis predicts that intercalated disks weave and unravel one sarcomere per myocyte per day. (Am J

SummaryAldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) γ. Stimulation of PPAR γ has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin.Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48.A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9 ± 5.6 to 58.1 ± 5.4 pg/mL) and perindopril (74.1 ± 4.7 to 64.7 ± 5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9 ± 4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group.Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR γ stimulating activity is equivalent to ACE-I for the treatment of hypertension. (Int Heart J 2009; 50: 501-512)

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Background Cervical anastomotic stricture after esophagectomy is a serious complication that adversely affects postoperative recovery, nutritional status and quality of life. Cervical anastomosis by a circular stapler (CS) has been widely accepted as a simple and convenient method, but anastomotic strictures are likely to occur. The aim of this study was to investigate an association between CS size and the incidence of anastomotic stricture after cervical esophagogastric anastomosis performed by a CS. Methods Between April 2011 and March 2016, 236 consecutive patients underwent cervical esophagogastric anastomosis by a CS via a retrosternal route after esophagectomy for esophageal cancer. These patients were divided into according to CS size for the procedure as follows: small-sized (25 mm) CS group (SG, n = 116) and large-sized (28 or 29 mm) CS group (LG, n = 120). The clinical data of patients were analyzed retrospectively to compare the two groups. Results Overall, anastomotic strictures were observed in 90 patients (38%). The incidence of anastomotic stricture was significantly lower in the LG than the SG (23% vs. 53%, p \ 0.001) (Table 3). Chronic obstructive pulmonary disease (COPD: FEV1.0% \70%) (OR 2.35, 95% CI = 1.09-5.14; p = 0.029), anastomotic leakage (OR 8.97, 95% CI = 2.69-41.30; p \ 0.001), and a small-sized CS (OR 3.42, 95% CI = 1.82-6.62; p \ 0.001) were independent risk factors for anastomotic stricture in the multivariate analysis. Conclusions If possible, a large-sized CS should be used to prevent cervical anastomotic strictures when performing cervical anastomoses by CS.