Visible Light Induced Copper-Catalyzed Enantioselective Deaminative Arylation of Amino Acid Derivatives Assisted by Phenol.

The exploration of value-added conversions of naturally abundant amino acids has received considerable attention from the synthetic community. Compared with the well-established asymmetric decarboxylative transformation, the asymmetric deaminative transformation of amino acids still remains a formidable challenge, mainly due to the lack of effective strategies for the C-N bond activation and the potential incompatibility with chiral catalysts. Here, we disclose a photoinduced Cu-catalyzed asymmetric deaminative coupling reaction of amino acids with arylboronic acids.

Thiol-oxidation reduces the release of amylase induced by β-adrenergic receptor activation in rat parotid acinar cells.

In parotid acinar cells, the activation of β-adrenergic receptors induces the accumulation of intracellular cAMP, and consequently provokes the exocytotic release of amylase, a digestive enzyme. The cellular redox status plays a pivotal role in regulating various cellular functions. Cellular redox imbalance caused by the oxidation of cellular antioxidants, as a result of oxidative stress, induces significant biological damage.

Maintenance of paracellular barrier function by insulin-like growth factor-I in submandibular gland cells.

Insulin-like growth factor-I (IGF-I) is expressed in salivary glands. We examined the effects of IGF-I on cell number, the expression and distribution of tight junction proteins and the paracellular barrier function in cells derived from rat submandibular glands. When those cells were cultured in medium containing 10% foetal bovine serum (FBS) or IGF-I, the number of cells was comparable at 10 days.

Characteristics of neurokinin A-induced salivary fluid secretion in perfused rat submandibular gland.

Tachykinins such as neurokinin A (NKA) and substance P have been demonstrated to induce salivary fluid secretion in vivo. However, characteristics of salivary fluid secretion induced by tachykinins in salivary glands have not been well elucidated. In this study, the effects of the tachykinin NKA on salivary fluid secretion were investigated in isolated, perfused rat submandibular gland.

C2-ceramide inhibits the prostaglandin E2-induced accumulation of cAMP in human gingival fibroblasts.

Ceramide is generated by the hydrolysis of membrane sphingomyelin by sphingomyelinase and is implicated in multiple signaling pathways, including those regulating differentiation, inflammation and immune responses. Excess formation of prostaglandin E(2) (PGE(2)) is thought to increase susceptibility to infection, rheumatoid arthritis and inflammation, including periodontal diseases. We investigated the inhibitory effect of C(2)-ceramide, a short-chain ceramide analog, on the PGE(2)-stimulated accumulation of cAMP in human gingival fibroblasts.

Involvement of phosphodiesterase 4 in beta-adrenoceptor agonist-induced amylase release in parotid acinar cells.

beta-Adrenoceptor activation increases intracellular cAMP levels and consequently induces exocytotic amylase release in parotid acinar cells. Phosphodiesterase (PDE) catalyses the hydrolysis of cAMP, which terminates the downstream signaling of this second messenger. We investigated the involvement of PDE4, a cAMP-PDE, in beta-adrenoceptor agonist-induced amylase release in mouse, rat and rabbit parotid acinar cells by using the specific PDE4 inhibitor rolipram.

Phosphorylation of myristoylated alanine-rich C kinase substrate is involved in the cAMP-dependent amylase release in parotid acinar cells.

Myristoylated alanine-rich C kinase substrate (MARCKS) is known as a major cellular substrate for protein kinase C (PKC). MARCKS has been implicated in the regulation of brain development and postnatal survival, cellular migration and adhesion, as well as phagocytosis, endocytosis, and exocytosis. The involvement of MARCKS phosphorylation in secretory function has been reported in Ca(2+)-mediated exocytosis.

Role of protein kinase C-delta in isoproterenol-induced amylase release in rat parotid acinar cells.

In parotid acinar cells, beta-adrenergic receptor activation results in accumulation of intracellular cAMP. Subsequently, cAMP-dependent protein kinase (PKA) is activated and consequently amylase release is provoked. In this paper, we investigated involvement of protein kinase C-delta (PKC delta), a novel isoform of PKC, in amylase release induced by beta-adrenergic receptor stimulation.

The thiol-oxidizing agent diamide reduces isoproterenol-stimulated amylase release in rat parotid acinar cells.

In parotid acinar cells, activation of beta-adrenergic receptors provokes exocytotic amylase release via the accumulation of intracellular cAMP. Cellular redox status plays a pivotal role in the regulation of various cellular functions. Cellular redox imbalance caused by the oxidation of cellular antioxidants, as a result of oxidative stress, induces significant biological damages.

[Experimental study of DNA synthesis in the airway cells and airway remodeling in asthmatic rats].

Objective: To study the DNA synthesis in the airway cells of asthmatic rats after allergen stimulation in association with airway remodeling.

Methods: Double staining immunohistochemical techniques was used to determine DNA synthesis of the airway cells of 12 asthmatic and 12 normal rats. BrdU incorporation into the airway smooth muscle (ASM) and epithelium was quantified by employment of computer-assisted image analysis.