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C40H28N4O10Co, monoclinic, C2/c (no. 15), a = 29.686(3) Å, b = 6.2315(4) Å, c = 21.0994(15) Å, β = 114.727(8)°, V = 3545.3(5) Å3, Z = 4, Rgt(F) = 0.0386, wRref(F2) = 0.0897, T = 293(2) K.

C66H34N4O12F12Er2, triclinic, P1̄ (no. 2), a = 11.8934(5) Å, b = 12.0041(4) Å, c = 12.4578(5) Å, α = 68.718(4)°, β = 64.205(4)°, γ = 87.053(3)°, V = 1480.09(12) Å3, Z = 1, R gt(F) = 0.0326, wR ref(F 2) = 0.0626, T = 293(2) K.

Background: Epilepsy is a chronic, complex, unprovoked, and recurrent disorder of the nervous system that affected several people worldwide. Phyllanthus amarus (PA) has been documented to have neuroprotective potential. Aim: To evaluate the potential of standardized extract of PA and its possible mechanism of action against the Pentylenetetrazol (PTZ)-induced convulsion and kindling associated post-ictal depression in experimental mice. Materials and Methods: Phyllathin was isolated from methanolic extract of PA and well-characterized using HPTLC, ESI-MS/MS, and LC/MS. Phyllathin containing a standardized extract of PA (50, 100, and 200 mg/kg) was administered in convulsed and kindled mice, followed by an assessment of various parameters. Results: The spectral analysis confirmed the molecular formula and weight of phyllanthin as C24H34O6 and 418.2342 Da. PA (100 and 200 mg/kg) significantly ameliorated PTZ-induced ( p < 0.05) duration, onset of tonic-clonic convulsion, and mortality in mice. It also significantly attenuated ( p < 0.05) PTZ-induced kindling in mice. Alteration in brain GABA, dopamine, and glutamate, Na+K+ATPase, Ca+2-ATPase activities, and oxido-nitrosative stress in kindled mice was significantly restored ( p < 0.05) by PA treatment. It also significantly ( p < 0.05) down-regulated brain mRNA expressions of NF-κB, TNF-α, IL-1β, COX-2, and TLR-4. Histological aberrations induced by PTZ in the brain of a kindled rat was significantly ( p < 0.05) ameliorated by PA. Conclusion: Phyllanthin containing a standardized extract of PA exerts its antiepileptic potential via balancing excitatory (glutamate) and inhibitory (GABA) brain monoamines, voltage-gated ion channels (Na+K+/Ca+2-ATPase) and inhibition of NF-κB/TLR-4 pathway to ameliorate neuroinflammation (TNF-α, IL-1β, and COX-2) in experimental mice.

The modeling air-cooled turbine blades specimens of DD6 single crystal superalloy with different distributions of cooling film holes were used to study the high cycle fatigue properties at room temperature. The SEM fracture observation was carried out. The results indicate that the cooling holes have significant effects on the high fatigue life of DD6 single crystal superalloy. The average life of non-hole specimens is four times of that of the three-row holes specimens under the same testing conditions. However, the distribution of cooling film holes has relatively less influence on fatigue life. The fracture of the specimens with non-hole is linear source by SEM analysis, but the cracks are found around the cooling film holes and the fracture of the specimens with single row to three rows is a typical multi-source rupture, and cracks all initiate from near film holes. According to fracture and crystallography theoretical conjecture, the cracks propagate along the {001} slip plane for non-hole, single-row holes and the middle location of the multi-row holes specimens. However, the cracks around the holes grow along the {111} slip plane for upper and lower holes of the specimens with multi-row holes. In addition, the distribution of stress field along cooling holes of four different specimens was analysed by FEM method. The results show that the fracture location and morphology of specimens are consistent well with numerical simulation analysis.

C48H30N4O12F12Cu3, monoclinic, P21/n (no. 14), a = 12.9112(5) Å, b = 28.1127(6) Å, c = 14.2324(5) Å, β = 110.665(4)°, V = 4833.5(3) Å3, Z = 4, R gt(F) = 0.0489, wR ref(F 2) = 0.1108, T = 173(10) K.

C34H24Cu2F8N4O8, monoclinic, P21/n (no. 14), a =13.074(3) Å, b = 20.229(4) Å, c = 14.419(3) Å, β = 108.889(2)°, V = 3608.2(12) Å3, Z = 4, R gt(F) = 0.0512, wR ref(F 2) = 0.1465, T = 296(2) K.

Objective Acute kidney injury (AKI) frequently occurs after catheter-based interventional procedures and increases mortality. However, the implications of AKI before thoracic endovascular aneurysm repair (TEVAR) of type B acute aortic dissection (AAD) remain unclear. This study evaluated the incidence, predictors, and in-hospital outcomes of AKI before TEVAR in patients with type B AAD. Methods Between 2009 and 2013, 76 patients were retrospectively evaluated who received TEVAR for type B AAD within 36 h from symptom onset. The patients were classified into no-AKI vs. AKI groups, and the severity of AKI was further staged according to kidney disease: improving global outcomes criteria before TEVAR. Results The incidence of preoperative AKI was 36.8%. In-hospital complications was significantly higher in patients with preoperative AKI compared with no-AKI (50.0% vs. 4.2%, respectively; P < 0.001), including acute renal failure (21.4% vs. 0, respectively; P < 0.001), and they increased with severity of AKI (P < 0.001). The maximum levels of body temperature and white blood cell count were significantly related to maximum serum creatinine level before TEVAR. Multivariate analysis showed that systolic blood pressure on admission (OR: 1.023; 95% CI: 1.003–1.044; P = 0.0238) and bilateral renal artery involvement (OR: 19.076; 95% CI: 1.914–190.164; P = 0.0120) were strong predictors of preoperative AKI. Conclusions Preoperative AKI frequently occurred in patients with type B AAD, and correlated with higher in-hospital complications and enhanced inflammatory reaction. Systolic blood pressure on admission and bilateral renal artery involvement were major risk factors for AKI before TEVAR.

C28H30F4N2O8Ni, Monoclinic, P2 1/n, a = 10.164(7) Å, b = 13.927(9) Å, c = 11.409(8) Å, β = 111.863(10) V = 1498.9(18) Å3, Z = 2, R gt (F) = 0.0389, wR ref (F 2 ) = 0.0957, T = 296(2) K.

C16H18N4O8, monoclinic, C2/m (no. 12), a = 14.517(4) Å, b = 18.006(7) Å, c = 6.916(3) Å, β = 116.97(3)°, V = 1611.2(11) Å3, Z = 4, R gt(F) = 0.0497, wR ref(F 2) = 0.1387, T = 296(2) K.

C26H28N8Br2O12Zn, monoclinic, P21/n (no. 14), a =7.8948(10) Å, b = 17.404(2) Å, c = 11.9437(15) Å, β = 98.719(2)°, V = 1622.1(4) Å3, Z = 2, R gt(F) = 0.0269, wR ref(F 2) = 0.0680, T = 296(2) K.

C14H12O7Cd, orthorhombic, Ima2 (no. 46), a = 30.715(3) Å, b = 7.8833(8) Å, c = 5.8202(6) Å, V = 1409.3(2) Å3, Z = 4, R gt(F) = 0.0159, wR ref(F 2) = 0.0400, T = 296(2) K.

To explore the effects of total flavonoids of Hippophae rhamnoides L. (TFH), quercetin (Que) and isorhamnetin (Isor) on the intracellular free calcium ([Ca(2+)](i)) in vascular smooth muscle cells (VSMC) of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).Fluo 3-acetoxymethylester (Fluo-3/AM) was used to observe the effects of TFH (100 mg/L) and its essential monomers, namely Que (10(-4) mol/L) and Isor (10(-4) mol/L) on changes of [Ca(2+)](i) in cultured SHR and WKY VSMC (abbr. to Ca-SHRCa-WKY) following exposure to high K(+), norepinephrine (NE) and angiotensin II (Ang II), and to compare with the effects of verapamil (Ver).(1) TFH, Que and Isor had inhibitory effects on resting Ca-SHR (P0.05), but had no significant effects on Ca-WKY (P0.05). (2) High K(+) could increase Ca-SHR more significantly than Ca-WKY (P0.05); TFH, Que and Isor could inhibit the elevation of [Ca(2+)](i) induced by high K(+)-depolarization, with the effects similar to that of Ver, and the effect on Ca-SHR was more significant than that on Ca-WKY (P0.05). (3) NE and Ang II could increase Ca-SHR more significantly than Ca-WKY (P0.05), TFH, Que and Isor had remarkably inhibitory effect on the elevation of Ca-SHR and Ca-WKY induced by NE or Ang II. (4) In the absence of extracellular Ca(2+), TFH, Que and Isor also had certain inhibitory effect on Ca-SHR and Ca-WKY induced by NE, and the effect on the former was more significant than that on the latter (P0.05).TFH, Que and Isor might decrease the levels of [Ca(2+)](i) in VSMCs by blocking both voltage-dependent calcium channels (VDC) and receptor-operated calcium channels (ROC) in physiological or pathological state, which may be one of the important mechanisms of their hypotensive and protective effects on target organs in patients with hypertension.