The effects of high hydrostatic pressure treatment on the flavor and color of grated ginger.

High hydrostatic pressure (HHP) was applied to grated ginger in order to inactivate quality-degrading enzymes in a non-thermal manner. The effects of HHP treatment on the flavor and the color of the grated ginger were investigated just after treatment and during storage. After HHP treatment (400 MPa, 5 min), geraniol dehydrogenase (GeDH) was inactivated to less than 5%, but the activity of polyphenol oxidase (PPO) was reduced only to 37%. Heat treatment (100 °C, 10 min) inactivated GeDH to 43% and PPO to about 10%. In storage, the reduction of geranial, neral, and citronellal to the corresponding alcohols was observed in the untreated and the heat-treated ginger, while it was not in the HHP-treated grated ginger. In the HHP-treated sample, terpene aldehydes almost disappeared without the formation of the corresponding alcohols. Browning was not observed immediately after HHP treatment, while it was complete in the heat-treated sample. The color change during storage appeared to reflect the residual activity of PPO.

Gene expression profiling of the effect of high-dose intravenous Ig in patients with Kawasaki disease.

Kawasaki disease (KD) is an acute vasculitis of infants and young children, preferentially affecting the coronary arteries. Intravenous infusion of high dose Ig (IVIG) effectively reduces systemic inflammation and prevents coronary artery lesions in KD. To investigate the mechanisms underlying the therapeutic effects of IVIG, we examined gene expression profiles of PBMC and purified monocytes obtained from acute patients before and after IVIG therapy. The results suggest that IVIG suppresses activated monocytes and macrophages by altering various functional aspects of the genes of KD patients. Among the 18 commonly decreased transcripts in both PBMC and purified monocytes, we selected six genes, FCGR1A, FCGR3A, CCR2, ADM, S100A9, and S100A12, and confirmed the microarray results by real-time RT-PCR. Moreover, the expressions of FcgammaRI and FcgammaRIII on monocytes were reduced after IVIG. Plasma S100A8/A9 heterocomplex, but not S100A9, levels were elevated in patients with acute KD compared with those in febrile controls. Furthermore, S100A8/A9 was rapidly down-regulated in response to IVIG therapy. Persistent elevation of S100A8/A9 after IVIG was found in patients who later developed coronary aneurysms. These results indicate that the effects of IVIG in KD may be mediated by suppression of an array of immune activation genes in monocytes, including those activating FcgammaRs and the S100A8/A9 heterocomplex.

Oral high-dose phenobarbital therapy for early infantile epileptic encephalopathy.

We report oral high-dose phenobarbital therapy for a patient with early infantile epileptic encephalopathy with suppression bursts (Ohtahara syndrome). At 1 month of age, many series of tonic spasms, with raising limbs and crying lasting for a few minutes, developed and increased up to approximately 300 times per day. Initially intravenous midazolam (0.5 mg/kg/hour) slightly decreased the seizures, although oral vitamin B6, valproic acid, clonazepam, and zonisamide had little effect. Oral high-dose phenobarbital therapy was begun at a dosage of 15 mg/kg/day, and the seizures markedly decreased to 5-10 times per day and the epileptic discharges on electroencephalogram greatly decreased. Serum phenobarbital levels ranged between 60 and 100 mg/dL. High-dose phenobarbital therapy should be considered for the treatment of early infantile epileptic encephalopathy with suppression bursts.