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Dieckol, a phlorotannin from Ecklonia cava, has shown potential for use as an anticancer agent that selectively kills cancer cells. However, it is necessary to amplify its potency without damaging its inherent safety in order to develop it as a competitive chemotherapeutic. Here, we explored the controlled O-acylations of dieckol. Acyl groups could be consistently introduced to the 6-O position of dieckol with a high regioselectivity, which was confirmed by NOESY, HMBC and HSQC spectroscopies. In cytotoxicity studies on the newly synthesized 6-O-acetyl, 6-O-benzoyl dieckols and previously synthesized 6-O-alkyl dieckols against A549 vs. normal cells, all of the derivatives showed low cytotoxicity in normal cells with an IC50 of 481–719 μM, and highly structure-dependent cytotoxicity in A549 cells with an IC50 of 7.02 (acetyl)−842.26 (benzyl) μM. The selectivity index also showed a large structure dependency in the range of 0.67 (benzyl)–68.58 (acetyl). An analysis of the structure–activity relationship indicated that the activity was dramatically reduced in the presence of a benzene ring and was highly increased in the presence of small polar substituents. Conclusions: Controlled mono-O-modifications of dieckol could be a powerful tool to enhance the anticancer activity of dieckol, thus contributing to the development strategy for dieckol-based chemotherapeutics.

Purpose: To investigate risk factors of coronary arterial calcification in chronic kidney disease (CKD) patients who did not undergo hemodialysis or peritoneal dialysis. Materials and Methods: We enrolled 83 patients of normal renal function (Group I) and 112 patients of CKD [Group II (CKD stage 1–2) and Group III (CKD stage 3–5)], who were assessed coronary artery calcium score (CACS) with cardiac CT. CACS between the groups were compared. Risk factors for coronary artery calcification in patients with CKD including diabetes, hypertension, and smoking were identified as relevant to CACS using logistic regression analysis. Serologic data of electrolytes were analyzed to evaluate effect for coronary calcification in patients with CKD. Results: Group III showed significant increment of CACS compared to Group I at the CACS level over 400 [odds ratio (OR) = 7.581, p = 0.01]. The OR were decreased in non-diabetic patients group, increased in non-hypertensive patients group, no significant differences in non-current smoker group. Serum phosphorous level was the only factor which showed significant effect for increased CACS (OR of 2.649, p = 0.02). Conclusion: In CKD patients, higher stage of CKD was associated with increased CACS. Diabetes mellitus and increased serum phosphorous level would be considered as factors influencing coronary arterial calcification in CKD patients.

Patients with corticospinal tract dysfunction have slow voluntary movements with brisk stretch reflexes and spasticity. Previous studies reported reduced firing rates of motor units during voluntary contraction. To assess whether this firing behavior occurs because motor neurons do not respond normally to excitatory inputs, we studied motor units in patients with primary lateral sclerosis, a degenerative syndrome of progressive spasticity. Firing rates were measured from motor units in the wrist extensor muscles at varying levels of voluntary contraction < or =10% maximal force. At each force level, the firing rate was measured with and without added muscle vibration, a maneuver that repetitively activates muscle spindles. In motor units from age-matched control subjects, the firing rate increased with successively stronger contractions as well as with the addition of vibration at each force level. In patients with primary lateral sclerosis, motor-unit firing rates remained stable, or in some cases declined, with progressively stronger contractions or with muscle vibration. We conclude that excitatory inputs produce a blunted response in motor neurons in patients with primary lateral sclerosis compared with age-matched controls. The potential explanations include abnormal activation of voltage-activated channels that produce stable membrane plateaus at low voltages, abnormal recruitment of the motor pool, or tonic inhibition of motor neurons. [ABSTRACT FROM AUTHOR]