Beneficial effects of Camellia Oil (Camellia oleifera Abel.) on ketoprofen-induced gastrointestinal mucosal damage through upregulation of HO-1 and VEGF.

Nonsteroidal anti-inflammatory drugs, such as ketoprofen, are generally used to treat pain and inflammation and as pyretic agents in clinical medicine. However, the usage of these drugs may lead to oxidative injury to the gastrointestinal mucosa. Camellia oil ( Camellia oleifera Abel.) is commonly used in Taiwan and China as cooking oil. Traditional remedies containing this oil exert beneficial health effects on the bowel, stomach, liver, and lungs. However, the effects of camellia oil on ketoprofen-induced oxidative gastrointestinal mucosal lesions remain unknown. The objective of this study was to evaluate the effect of camellia oil on ketoprofen-induced acute gastrointestinal ulcers. The results showed that treatment of Int-407 cells with camellia oil (50-75 µg/mL) not only increased the levels of heme oxygenase-1 (HO-1), glutathione peroxidase (GPx), and superoxide dismutase (SOD) mRNA expression but also increased vascular endothelial growth factor (VEGF) and prostaglandin E2 (PGE2) protein secretion, which served as a mucosal barrier against gastrointestinal oxidative injury. Moreover, Sprague-Dawley (SD) rats treated with camellia oil (2 mL/kg/day) prior to the administration of ketoprofen (50 mg/kg/day) successfully inhibited COX-2 protein expression, inhibited the production of interleukin-6 (IL-6) and nitrite oxide (NO), reversed the impairment of the antioxidant system, and decreased oxidative damage in the gastrointestinal mucosa. More importantly, pretreatment of SD rats with camellia oil strongly inhibited gastrointestinal mucosal injury induced by ketoprofen, which was proved by the histopathological staining of gastrointestinal tissues. Our data suggest that camellia oil exerts potent antiulcer effects against oxidative damage in the stomach and intestine induced by ketoprofen.

A novel inorganic-organic hybrid borate, poly{[Na(2)(C(4)H(2)O(4))(H(3)BO(3))(H(2)O)(4)]·H(3)BO(3)}.

The structure of the title compound, catena-poly[[[di-µ-aqua-µ-fumarato-µ-(boric acid)-disodium]-di-µ-aqua] boric acid monosolvate], contains two crystallographically independent Na(+) cations, each being six-coordinated by one fumarate O atom, one boric acid O atom and four water O atoms in a distorted octa-hedral geometry. Adjacent [NaO(2)(OH(2))(4)] units share edges and are linked into chains propagating parallel to [100]. The free boric acid mol-ecules are connected to the chains through strong inter-molecular O-H⋯O hydrogen bonds. Additional O-H⋯O hydrogen bonds between the water mol-ecules, the free and coordinated boric acid mol-ecules and the fumarate anion lead to the formation of a three-dimensional supra-molecular structure. With the exception of the two water mol-ecules, all other atoms lie on mirror planes.

A novel metallo-organically templated pentaborate: acetato[N,N'-bis(2-aminoethyl)ethane-1,2-diamine]zinc(II) 4,4',6,6'-tetrahydroxy-2,2'-spirobi[cyclotriboroxane](1-).

The title compound, [Zn(C2H3O2)(C6H18N4)][B5O6(OH)4], contains mixed-ligand [Zn(CH3COO)(teta)]+ complex cations (teta is triethylenetetramine) and pentaborate [B5O6(OH)4]- anions. The [B5O6(OH)4]- anions are connected to one another through hydrogen bonds, forming a three-dimensional supramolecular network, in which the [Zn(CH3COO)(teta)]+ cations are located.

Bis[(m-phenyl-enedimethyl-ene)-diammonium] tetra-deca-borate.

The title compound 2C(8)H(14)N(2) (2+)·[B(14)O(20)(OH)(6)](4-), contains diprotonated C(8)H(14)N(2) (2+) cations and centrosymmetric tetra-deca-borate anions. The crystal structure is stabilized by O-H⋯O and N-H⋯O hydrogen bonds.

Influenza A-associated central nervous system dysfunction in children presenting as transient visual hallucination.

Five children, ages 3 to 6 years, developed visual hallucination and inappropriate behavior within 3 days of the onset of an influenza-like illness. Electroencephalographic examinations showed generalized slow waves in all five cases. Evidence of acute influenza A viral infection was documented in all five cases. Within 8 days all five children were discharged in stable condition. Influenza A-associated central nervous system dysfunction may be more common than previously recognized, and the prognosis is not necessarily poor.