Molecular cloning, expression profiling, and yeast complementation of 19 β-tubulin cDNAs from developing cotton ovules

Microtubules are a major structural component of the cytoskeleton and participate in cell division, intracellular transport, and cell morphogenesis. In the present study, 795 cotton tubulin expressed sequence tags were analysed and 19 β-tubulin genes (TUB) cloned from a cotton cDNA library. Among the group, 12 cotton TUBs (GhTUBs) are reported for the first time here. Transcription profiling revealed that nine GhTUBs were highly expressed in elongating fibre cells as compared with fuzzless-lintless mutant ovules. Treating cultured wild-type cotton ovules with exogenous phytohormones showed that individual genes can be induced by different agents. Gibberellin induced expression of GhTUB1 and GhTUB3, ethylene induced expression of GhTUB5, GhTUB9, and GhTUB12, brassinosteroids induced expression of GhTUB1, GhTUB3, GhTUB9, and GhTUB12, and lignoceric acid induced expression of GhTUB1, GhTUB3, and GhTUB12. When GhTUBs were transformed into the Saccharomyces cerevisiae inviable mutant, tub2, which is deficient in β-tubulin, one ovule-specific and eight of nine fibre-preferential GhTUBs rescued this lethality. This study suggests that the proteins encoded by cotton GhTUBs are involved during cotton fibre development

Convergence of generalized AOR iterative method for linear systems with strictly diagonally dominant matrices

AbstractIn this paper, some improvements on Darvishi and Hessari [On convergence of the generalized AOR method for linear systems with diagonally dominant coefficient matrices, Appl. Math. Comput. 176 (2006) 128–133] are presented for bounds of the spectral radius of lω,r, which is the iterative matrix of the generalized AOR (GAOR) method. Subsequently, some new sufficient conditions for convergence of GAOR method will be given, which improve some results of Darvishi and Hessari [On convergence of the generalized AOR method for linear systems with diagonally dominant coefficient matrices, Appl. Math. Comput. 176 (2006) 128–133]

Bis[3-chloro-6-(3,5-dimethyl-1H-pyrazol-1-yl)picolinato]nickel(II) tetra­hydrate

In the title complex, [Ni(C11H9ClN3O2)2]·4H2O, the Ni atom is coordinated by four N atoms and two O atoms derived from two tridentate 3-chloro-6-(3,5-dimethyl-1H-pyrazol-1-yl)picolinate ligands. The cis-N4O2 donor set defines a distorted octa­hedral geometry. In the crystal structure, the complex and water mol­ecules are linked by O—H⋯O hydrogen bonds

Bis[6-(3,5-dimethyl-1H-pyrazol-1-yl)picolinato-κ2 N 1,O 2]cadmium(II) 1.75-hydrate

In the title complex, [Cd(C11H10N3O2)2]·1.75H2O, the Cd atom is coordinated by four N atoms and two O atoms from two tridentate 6-(3,5-dimethyl-1H-pyrazol-1-yl)picolinate ligands in a distorted cis-N4O2 octa­hedral geometry. Three water mol­ecules, with occupancies of 1.0, 0.5 and 0.25, complete the asymmetric unit. The components of the crystal structure are linked via hydrogen bonds, forming a three-dimensional network

[3-Chloro-6-(3,5-dimethyl-1H-pyrazol-1-yl)picolinato](pyridine-2,6-dicarboxyl­ato)nickel(II) dihydrate

In the title compound, [Ni(C11H9ClN3O2)(C7H3NO4)]·2H2O, the NiII atom is coordinated by two N atoms and one O atom of 3-chloro-6-(3,5-dimethyl-1H-pyrazol-1-yl)picolinate and by one N atom and two O atoms of pyridine-2,6-dicarboxyl­ate in a distorted octa­hedral coordination. In the crystal structure, mol­ecules are linked together by inter­molecular O—H⋯O hydrogen bonds. One water mol­ecule is disordered over two positions; the site occupancies are ca 0.53 and 0.47

The Combination of Human Urinary Kallidinogenase and Mild Hypothermia Protects Adult Rats Against Hypoxic-Ischemic Encephalopathy-Induced Injury by Promoting Angiogenesis and Regeneration

Objectives: Human Urinary Kallidinogenase (HUK) is a tissue kallikrein that plays neuroprotective role in ischemic conditions via different mechanisms. Mild hypothermia (MH) is another robust neuroprotectant that reduces mortality but does not profoundly ameliorate the neurological outcome in hypoxic-ischemic encephalopathy (HIE) patients. However, whether the combination of HUK and MH can be used as a promising neuroprotective treatment in HIE is unknown. Methods: One-hundred and forty-four adult Wistar rats were randomly divided into five groups: Sham, HIE, HUK, MH and a combination of HUK and MH treatment. The HIE rat model was established by right carotid dissection followed by hypoxia aspiration. The survival curve was created within 7 days, and the neurological severity scores (NSS) were assessed at days 0, 1, 3, and 7. Nissl staining, Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), immunofluorescent staining and western blotting were used to evaluate neuronal survival, apoptosis and necrosis, tight-junction proteins Claudin-1 and Zonula occludens-1 (ZO-1), vascular endothelial growth factor (VEGF), doublecortex (DCX), bradykinin receptor B1 (BDKRB1), BDKRB2 and Ki67 staining. Results: The combined treatment rescued all HIE rats from death and had a best survival curve compared to HIE. The Combination also reduced the NSS scores after HIE at days 7, better than HUK or MH alone. The combination of HUK and MH reserved more cells in Nissl staining and inhibited neuronal apoptosis and necrosis as well as significantly attenuated HIE-induced decreases in claudin-1, ZO-1, cyclin D1 and BDKRB1/B2 in comparison to HUK or MH treatment alone. Moreover, the combined treatment increased the expression of VEGF and DCX as well as the number of Ki67-labeled cells. Conclusions: This study demonstrates that both HUK and MH are neuroprotective after HIE insult; however, the combined therapy with HUK and MH enhanced the efficiency and efficacy of either therapy alone in the treatment of HIE, at least partially by promoting angiogenesis and regeneration and rescuing tight-junction loss. The combination of HUK and MH seems to be a feasible and promising clinical strategy to alleviate cerebral injury following HIE insult. Highlights: -The combination of HUK and MH distinctly reduces neurological dysfunction in HIE rats.-HUK enhances the neuroprotective effects of MH in HIE.-MH attenuates tight-junction disruption, upregulates the BDKR B1/2, DCX and cyclin D1.-The combination of MH and HUK enhances the expressions of MH/HUK mediated-BDKR B1/2, DCX, cyclin D1 and Ki67 positive cells

Diaqua­bis(1H-1,2,4-triazole-3-carboxyl­ato)cadmium(II)

In the title complex, [Cd(C3H2N3O2)2(H2O)2], the CdII atom is coordinated by two N and two O atoms from two deprotonated 1H-1,2,4-triazole-3-carboxylic acid ligands (TRIA) and two water mol­ecules. The Cd atom is located on an inversion centre. In the crystal structure, mol­ecules are linked together via O—H⋯O and N—H⋯O hydrogen bonds, forming a three-dimensional network

Bis[6-(3,5-dimethyl-1H-pyrazol-1-yl)picolinato]manganese(II) trihydrate

In the title complex, [Mn(C11H10N3O2)2]·3H2O, the MnII atom is coordinated by four N atoms and two O atoms in a distorted octa­hedral geometry. The mol­ecules are linked together via hydrogen bonds involving the water molecules. One of these is disordered equally over two positions