Theoretical studies of the g factors and local structures of the Ni3+ centers in Na2 Zn(SO4 )2 ·4H2 O and K2 Zn(SO4 )2 ·6H2 O crystals.

The local structures and the g factors gi (i = x, y, z) for Ni3+ centers in Na2 Zn(SO4 )2 ·4H2 O (DPPH) and K2 Zn(SO4 )2 ·6H2 O (PHZS) crystals are theoretically studied by using the perturbation formulas of the g factors for a 3d7 ion with low spin (S = 1/2) in orthorhombically compressed octahedra. In these formulas, the contributions to g factors from both the spin-orbit coupling interactions of the central ion and ligands are taken into account, and the required crystal-field parameters are estimated from the superposition model and the local geometry of the systems. Based on the calculations, the Ni-O bonds are found to suffer the axial compression δz (or Δz) of about 0.111 Å (or 0.036 Å) along the z-axis for Ni3+ centers in DPPH (or PHZS) crystals. Meanwhile, the Ni-O bonds may experience additional planar bond length variation δx (≈0.015 Å) along x- and y-axes for the orthorhombic Ni3+ center in DPPH. The theoretical g factors agree well with the experimental data. The obtained local structural parameters for both Ni3+ centers are discussed.

Theoretical studies of the EPR parameters and local structures for the two Cu2+ centers in Cd(HCOO)2 ·2H2 O.

Based on the studies of the electron paramagnetic resonance parameters for two types of the Cu2+ centers in Cd(HCOO)2 ·2H2 O by using the high-order perturbation formulas for a 3d9 ion in a rhombically elongated octahedron, local structure of the doped copper ion is determined. Research suggests that the impurity Cu2+ replaces the host Cd2+ and undergoes the local rhombic elongation distortion, characterized by the axial elongation ratios of 4.1%, and 3.8% along the z-axis and the planar bond length variation ratios of 3.8%, and 3.1% along the x-axis and y-axis, for Cu2+ Centers, I and II, respectively. The above slightly different axial elongation ratios and planar bond length variation ratios may suitably account for the slightly dissimilar axial g anisotropies Δg (≈0.351 and 0.339) and perpendicular g anisotropies δg (≈0.028 and 0.022) of the two centers, respectively.

Comparative analysis of clinicoradiologic characteristics of lung adenocarcinomas with ALK rearrangements or EGFR mutations.

OBJECTIVE: To compare the clinicoradiologic features of tumours with echinoderm anaplastic lymphoma kinase (ALK) rearrangements, epidermal growth factor receptor (EGFR) mutations, or wild type (WT) for both genes in a cohort of patients with lung adenocarcinoma to identify useful characteristics of different gene statuses. METHODS: In 346 lung adenocarcinoma patients, ALK rearrangements were confirmed with fluorescence in situ hybridisation, and EGFR mutations were determined by pyrosequencing assay. Patients were divided into three groups: ALK rearrangement (ALK+ group, n = 48), EGFR mutation (EGFR+ group, n = 166), and WT for both genes (WT group, n = 132). Chest computed tomography (CT) examinations were performed in all patients. The percentages of ground-glass opacity volume (pGGO) and tumour shadow disappearance rate (TDR) were measured using semi-automated nodule assessment software. RESULTS: The pGGO was significantly lower in the ALK+ group (25.1 % ± 24.3) than in the EGFR+ group (37.2 % ± 25.7, p < 0.001) and the WT group (36.1 % ± 24.6, p = 0.001). The TDR in the ALK+ group (17.3 % ± 25.1) was significantly lower than in the EGFR+ group (26.8 % ± 24.9, p = 0.002) and the WT group (25.7 % ± 24.6, p = 0.003). CONCLUSIONS: Solid pattern with lower incidence of lobulated border, finely spiculated margins, pleural retraction, and bubble-like lucency on CT imaging are the main characteristics of ALK rearrangement tumours. KEY POINTS: • EGFR/ALK testing is recommended for lung adenocarcinoma patients for EGFR/ALK-targeted TKI therapy. • EGFR /ALK testing is restricted by limited tissue samples and cost pressures. • Lower pGGO and TDR are the main clinicoradiological characteristics of ALK+ tumours. • pGGO and TDR are predictive factors for selecting patients for ALK/EGFR testing.

CD20-positive T-cell lymphoma with indolent clinical behaviour.

T-cell lymphomas that are positive for CD20 are very rare and most reported cases have demonstrated an aggressive clinical course. An unusual case of a 57-year old female who presented with recurrent enlarged lymph nodes for 12 years is reported. The lymph nodes from both 1995 and 2007 showed effacement of the lymph node architecture by a diffuse and dense infiltrate of small lymphoid cells. In terms of T- and B-cell markers, these small lymphoid cells were immunohistochemically positive for CD2, CD3, CD5, CD43, CD45RO and CD20, and were negative for PAX5, CD79a and cyclin D1. Molecular genetic analysis showed T-cell receptor-gamma chain gene rearrangement. Recognition of this type of CD20-positive T-cell lymphoma is important for ensuring a correct diagnosis so that the patient can be offered the most appropriate therapy. The indolent behaviour of the present case is unusual and awaits further clinical follow-up and laboratory investigation.

[Effects of 7-methoxy-4'-hydroxyl-3'-diethylaminomethylisoflavone (MHDF) on hemodynamics and aorta in rats].

MHDF is a synthetic isoflavone derivative with anti-ischemic effect. In this paper, the effects of MHDF on in vivo hemodynamics and in vitro contraction of rat aorta were reported. MHDF (3-12.8 mg/kg) was found to decrease +/- dP/dtmax, Vmax, Vpm and LVSP, prolong T-dP/dtmax of left ventricle and slow the HR in rats. It was also shown to inhibit the changes of heart performance induced by CaCl2 in rats. In isolated rat aorta, MHDF caused a noncompetitive antagonism of noradrenaline-and CaCl2-induced contraction with the pD2' of 3.11 +/- 0.21 and 3.73 +/- 0.07. The high K(+)-evoked contraction with IC50 of 17.6 mu mol/L was also found to be inhibited. The results suggest that the effect of MHDF on vascular muscle is different from that of an alpha-blocker and may be attributable to inhibition of extracellular calcium influx or intracellular calcium release.

Effects of lisinopril and captopril on calcium in rat heart.

We studied the effects of lisinopril (Lis) and captopril (Cap), two angiotensin-converting enzyme inhibitors, on calcium in ischemia/reperfusion and normal rat hearts. Ischemia/reperfusion hearts were subjected to 15 min ischemia followed by 1 or 30 min reperfusion. Lis 0.1 mumol.L-1 and Cap 200 mumol.L-1 decreased the concentration of calcium in ischemia/reperfusion hearts (the content of calcium in reperfusion 1 min heart were reduced from 4.0 +/- 0.6 to 2.7 +/- 0.5 and 3.0 +/- 0.9 mumol/g dry wt respectively). In cultured cell of neonatal rat heart, both drugs inhibited the uptake of 45Ca2+. The activity of Na+,K(+)-ATPase prepared from rat heart was increased (activity increased from 15.7 +/- 2.3 in control group to 21.2 +/- 2.0 and 22.0 +/- 3.1 mumol/h mg protein in Lis and Cap groups, respectively). This calcium lowering effects of Lis and Cap may be important in protecting the ischemia/reperfusion damage of myocardium.

Effect of in vivo microdialysis of 1,2,3,4-tetrahydro-9-aminoacridine (THA) on the extracellular concentration of acetylcholine in the striatum of anesthetized rats.

1,2,3,4-Tetrahydro-9-aminoacridine (THA, tacrine) is a potent cholinesterase (ChE) inhibitor which is under consideration for the treatment of Alzheimer's disease. This paper examines the effect of in vivo microdialysis of THA, THB-013 (an analog of THA) and physostigmine on the extracellular concentration of acetylcholine (ACh) in the striatum of anesthetized rat, as well as their effects on in vitro striatal ChE activity. In addition, the interaction of THA and physostigmine with cholinergic receptors in rat striatum has been investigated. All three drugs inhibited ChE activity and increased the extracellular concentration of ACh in a concentration-dependent manner. In the presence of THA, atropine induced a smaller increase in extracellular ACh concentrations than it did in the presence of physostigmine, under experimental conditions in which THA (100 microM) and physostigmine (10 microM) produced an equivalent effect on ChE activity. THA bound significantly to both muscarinic and nicotinic receptors in rat striatum, whereas physostigmine did not show significant binding. THA (100 microM) and physostigmine (10 microM) produced an additive effect on the extracellular concentration of ACh, and the addition of THA (10 microM) to physostigmine (1 microM) produced further inhibition of in vitro ChE activity. 4-Aminopyridine (100 microM), a K+ channel blocker, showed no detectable effect by itself on the extracellular concentration of ACh, however, it significantly increased the extracellular concentration of ACh in the presence of physostigmine (10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hypoxia on angiotensin II content and its receptor in guinea pig aorta.

AIM: To study the effects of hypoxia on the vasoconstrictive response and the angiotensin II (Ang II) content and its receptor. METHODS: Hypoxia was induced in isolated aorta of guinea pig by gassing N2. The vasoconstrictive response of aorta to Ang II was recorded. Ang II content and its receptor were measured by radioimmuoassay. RESULTS: Ang 3-3000 nmol L-1 increased the contractile response of aorta. Hypoxia amplified the vasoconstrictive effect of Ang II. The concentration of Ang II were 44 +/- 24 and 50 +/- 17 pg/g wet wt (n = 10), respectively in non-hypoxic and hypoxic aortae. The receptor density in non-hypoxic aorta was 17 +/- 3 fmol mg-1, and that in hypoxia was 33 +/- 5 fmol mg-1 (P < 0.01). CONCLUSION: The enhancement of the vasoconstrictive action of Ang II by hypoxia is due to the increase in the angiotensin receptor density, but not associated with the changes in the Ang II content in hypoxic aorta of guinea pig.

[Effects of an endogenous GABA receptor binding inhibitor on rat blood pressure].

The GABA receptor agonists GABA (400 micrograms icv) and muscimol (1 microgram icv) induced hypotension in urethane-anesthetized rats, while the GABA receptor antagonist bicuculline (2 micrograms icv) elicited hypertension. An endogenous GABA receptor binding inhibitor (1 mg), prepared from bovine cerebellum, showed bicuculline-like hypertensive action in a dose-dependent manner. It was antagonized by icv muscimol, but not by the alpha 2-adrenoceptor agonist clonidine. These in vivo results agree quite well with our previous in vitro receptor binding assay experiments.

Relationship between adenosine-induced vascular effects and ATP-sensitive K+ channels.

AIM: To study the relationship between adenosine (Ade) receptors and adenosine 5'-triphosphate (ATP)-sensitive potassium (KATP) channels in rat aorta. METHODS: Isolated rat aorta rings were suspended for isometric force recording. The vascular effects of Ade were assessed in the presence or absence of functional endothelium. The interactions of Ade and pinacidil (Pin) or glibenclamide (Gli) were investigated. RESULTS: In isolated aorta preconstricted with KCl 20 mmol.L-1, Ade 3-300 mumol.L-1 induced relaxation in a concentration-dependent manner; and in 48/99 preparations from 32 rats, Ade induced initial transient constriction followed by sustained relaxation. When the functions of KATP channels were blocked with Gli 1 or 100 mumol.L-1, effects of Ade were characterized by vasoconstriction rather than vasorelaxation. The combination of Pin 1 mumol.L-1 with Ade 100 mumol.L-1 showed no synergic vasodilatory effects and did not affect Ade-induced vasoconstriction. After the removal of endothelium, Ade still induced vasoconstriction and vasorelaxation, and the constrictive effects showed no difference from those in the presence of endothelium, but the potency of vasodilatory effects became weaker with slower decrease in tension. CONCLUSION: The activation of KATP channels is involved in Ade receptor-induced vasodilation.

[Effects of 7-methoxy-4'-hydroxyl-3'-diethylaminomethylisoflavone on heart atrium and ventricular papillary muscles of guinea pig].

In isolated guinea pig right atria, 7-methoxy-4'-hydroxyl-3'-diethylaminomethylisoflavone (MHDF), a new synthetic isoflavone produced noncompetitive antagonisms to isoproterenol- and histamine-induced positive chronotropic actions with pD'2 values of 5.04 +/- 0.10 and 4.90 +/- 0.18, respectively. MHDF inhibited the positive chronotropic response to CaCl2. In isolated left atria, the negative inotropic action of MHDF increased as the frequency increased. In papillary muscles, MHDF 3 mumol/L reduced the contractile force, while Vmax was decreased and APD and ERP were prolonged. These results indicated that the mechanism of MHDF on myocardium is related to inhibition of Ca2+ influx, Na+ influx and K+ efflux, not by blocking beta or H2 receptors.

Modulation by nucleotides of binding sites for [3H]glibenclamide in rat aorta and cardiac ventricular membranes.

Radioligand binding techniques were employed to determine the modulation by nucleotides of the specific [3H]glibenclamide (Gli) binding to rat aortic and cardiac ventricular preparations. Saturation analysis revealed a single binding site with K(D) value of 31.3 nM and Bmax of 180 fmol/mg wet weight in aortic preparations. We also observed that [3H]Gli bound reversibly and specifically to cardiac membranes. Unlabeled glibenclamide displaced [3H]Gli-specific binding of cardiac membranes completely with K(I) of 54.4 nM. In cardiac membranes, adenosine triphosphate (ATP), adenosine diphosphate (ADP), and uridine diphosphate (UDP) (from 0.01-5 mM) concentration dependently inhibited [3H]Gli binding independent of Mg2+. The values of K(I) were 0.47, 0.22, and 0.58 mM, respectively. However, in aortic preparations, [3H]Gli-specific binding was increased by ATP of 5 and 10 mM and showed a biphasic response to ADP. At concentrations to 1 mM, ADP inhibited binding; above 5 mM, the specific [3H]Gli binding was increased. UDP did not alter the binding up to 5 mM. In the presence of Mg2+ (20 mM), the inhibitory effects of ATP (0.01-1 mM) or ADP (0.01-5 mM) on the binding in cardiac membranes were abolished, whereas the facilitatory effects of ATP or ADP in aortic preparations were strengthened. Analysis of kinetics showed that the time of [3H]Gli association and dissociation in cardiac and aortic preparations was monophasic. The association was delayed with dissociation unchanged by ATP, ADP, and UDP of 1 mM, respectively, in cardiac membranes. In aorta, however, at the same concentration ATP accelerated association and retarded dissociation and vice versa for ADP. Association and dissociation were not changed by UDP of 5 mM. We conclude that ATP, ADP, and UDP are all major allosteric modulators of K(ATP) channels and they affect the antagonist binding to heart (sulfonylurea receptor 2A) and aorta (sulfonylurea receptor 2B) differently.