Effect of Coenzyme Q10 and green tea on plasma and liver lipids, platelet aggregation, TBARS production and erythrocyte Na leak in simvastatin treated hypercholesterolmic rats

This study was conducted to investigate the hypocholesterolemic effect of simvastatin (30 mg/kg BW) and antioxidant effect of coenzyme Q10 (CoQ10, 15 mg/kg BW) or green tea (5%) on erythrocyte Na leak, platelet aggregation and TBARS production in hypercholesterolemic rats treated with statin. Food efficiency ratio (FER, ADG/ADFI) was decreased in statin group and increased in green tea group, and the difference between these two groups was significant (p<0.05). Plasma total cholesterol was somewhat increased in all groups with statin compared with control. Plasma triglyceride was decreased in statin group and increased in groups of CoQ10 and green tea, and the difference between groups of statin and green tea was significant (p<0.05). Liver total cholesterol was not different between the control and statin group, but was significantly decreased in the group with green tea compared with other groups (p<0.05). Liver triglyceride was decreased in groups of statin and green tea compared with the control, and the difference between groups of the control and green tea was significant (p<0.05). Platelet aggregation of both the initial slope and the maximum was not significantly different, but the group with green tea tended to be higher in initial slope and lower in the maximum. Intracellular Na of group with green tea was significantly higher than the control or statin group (p<0.05). Na leak in intact cells was significantly decreased in the statin group compared with the control (p<0.05). Na leak in AAPH treated cells was also significantly reduced in the statin group compared with groups of the control and CoQ10 (p<0.05). TBARS production in platelet rich plasma was significantly decreased in the groups with CoQ10 and green tea compared with the control and statin groups (p<0.05). TBARS of liver was significantly decreased in the group with green tea compared with the statin group (p<0.05). In the present study, even a high dose of statin did not show a cholesterol lowering effect, therefore depletion of CoQ10 following statin treatment in rats is not clear. More clinical studies are needed for therapeutic use of CoQ10 as an antioxidant in prevention of degenerative diseases independent of statin therapy.     

c-myc is required for osteoclast differentiation.

The role of the receptor activator of nuclear factor kappaB (NF-kappaB) ligand (RANKL)-a tumor necrosis factor (TNF)-related cytokine-in osteoclast formation has been established clearly. However, the downstream signaling pathways activated by this cytokine remain largely unknown. To identify genes that play a role in osteoclastogenesis, we used RAW 264.7 mouse monocytes as a model system for the differentiation of multinucleated osteoclasts from mononucleated precursors. RAW 264.7 cells were induced with RANKL to form multinucleated giant osteoclast-like cells (OCLs) that expressed a number of osteoclast-specific markers and were able to form resorption pits on both calcium phosphate films and bone slices. This system was used to identify genes that are regulated by RANKL and may play a role in osteoclast differentiation. The proto-oncogene c-myc was strongly up-regulated in RANKL-induced OCLs but was absent in undifferentiated cells. Expression of Myc partners Max and Mad, on the other hand, was constant during OCL differentiation. We expressed a dominant negative Myc in RAW 264.7 cells and were able to block RANKL-induced OCL formation. Northern Blot analysis revealed a delay and a significant reduction in the level of messenger RNA (mRNA) for tartrate-resistant acid phosphatase (TRAP) and cathepsin K. We conclude that c-myc is a downstream target of RANKL and its expression is required for RANKL-induced osteoclastogenesis.     

Mesogonadal shunts for extrahepatic portal vein thrombosis and variceal hemorrhage.

Extrahepatic portal vein thrombosis (EHPVT) may occur in children or adults and usually comes to clinical attention due to complications of portal hypertension such as variceal hemorrhage. A variety of standard surgical techniques exist to manage these patients, but when these fail surgical options are limited. We describe two novel portosystemic shunts that utilize the gonadal vein as an autologous conduit. Four patients were evaluated for EHPVT with variceal bleeding. None of the patients were candidates for a standard splenorenal shunt due to prior surgical procedures. The first patient underwent a left mesogonadal shunt and the remaining 3 patients underwent a right mesogonadal shunt. Postoperative ultrasound or computed tomography (CT) scan confirmed early patency of the shunt in each patient. There have been no further episodes of variceal hemorrhage with follow-up of 3.5 years in the child who underwent the left mesogonadal shunt, and 17, 19, and 20 months in the patients who underwent the right mesogonadal shunt. Three of the 4 shunts remain patent. One shunt thrombosis occurred in a patient homozygous for the Factor V Leiden mutation despite anticoagulation with coumadin. This is the first report of the successful use of the gonadal vein as an in situ conduit for constructing a portosystemic shunt. In conclusion, the right and left mesogonadal shunts may be useful as salvage operations for patients with EHPVT who have failed standard surgical shunt procedures.     

Critical size defect in the canine mandible.

OBJECTIVE: The purpose of this study was to determine the minimum size defect in a canine mandible that would not spontaneously heal during the dog's natural life (the critical size defect). STUDY DESIGN: Sixteen adult female mongrel dogs underwent continuity resection on both sides of the mandible to create bilateral defects. In 8 dogs, mandibular defects ranging from 5 to 20 mm were created with periosteal resection. In the other 8 dogs, mandibular defects ranging from 30 to 60 mm were created preserving the periosteum. The dogs were then killed at 6 months and the defects examined using radiographs and histologic analysis. RESULTS: When the periosteum was removed, mandibular defects greater than 15 mm failed to heal across the entire defect. However, when the periosteum was preserved, mandibular defects needed to be greater than 50 mm in order to fail to heal. CONCLUSION: The critical size defect in a canine mandible model is 15 mm when the periosteum is removed and 50 mm when the periosteum is preserved.     

Surface properties of endosseous dental implants after NdYAG and CO2 laser treatment at various energies.

OBJECTIVES: Dental lasers have been used for uncovering submerged implants as well as decontaminating implant surfaces when treating peri-implantitis. The objective of this study was to compare the possible alterations of the smooth surface and resorbable blast material (RBM) surface implants after using NdYAG and CO(2) lasers at various energies. MATERIALS AND METHODS: Ten smooth surface implants and 10 RBM surface implants were used. Two smooth surface implants and 2 RBM surface implants served as a control group that was not lased. The remaining implants were treated using NdYAG and CO(2) lasers. The surface of each implant was treated for 10 seconds on the second and third threads. The smooth surface implants (group 1) were treated using a pulsed contact NdYAG laser at power settings of 1, 2, 3.5, and 5 W, which are commonly used for soft tissue surgery; the corresponding energy and frequency were 50 mJ and 20 Hz, 100 mJ and 20 Hz, 350 mJ and 10 Hz, and 250 mJ and 20 Hz, respectively. The group 2 RBM implants were treated using a pulsed contact NdYAG laser. The group 3 smooth surface implants were treated using a pulsed wave non-contact CO(2) laser at 1, 2, 3.5, and 5 W, and the group 4 RBM implants were treated using a pulsed wave non-contact CO(2) laser. Data were analyzed using scanning electron microscopy. RESULTS: The control surface was very regular and smooth. After NdYAG laser treatment, the implant surface showed alterations of all the surfaces. The amount of damage was proportional to the power. A remarkable finding was the similarity of the lased areas on the smooth and RBM surfaces. CO(2) laser at power settings of 1.0 or 2.0 W did not alter the implant surface, regardless of implant type. At settings of 3.5 and 5 W, there was destruction of the micromachined groove and gas formation. CONCLUSION: This study supports that CO(2) laser treatment appears more useful than NdYAG laser treatment and CO(2) laser does not damage titanium implant surface, which should be of value when uncovering submerged implants and treating peri-implantitis.     

A study of a method for distribution analysis of skin color

Background/aims: The objective and quantitative assessment of the skin is important in medical and cosmeceutical research. Assessment of color is an important element for analyzing the surface of the skin, which is usually determined subjectively by a doctor or using color analysis devices. These devices, however, cannot provide correct color information because color is construed from the mean value of the observation region, and analysis of color distribution is impossible. The purpose of this paper is to develop an objective analysis method to permit skin color measurement of each pixel unit of an image and analyze the distribution of skin surface color. Methods: The Skin Color Distribution Analyzer (SCDA) is an analysis method newly developed at the Research Institute for Skin Image at Korea University. The SCDA system presented in this paper performed a novel form of quantitative and objective analysis of skin color distribution using each pixel color model parameter found in image wavelength information. In this paper, distribution analysis was conducted on normal skin and skin lesions and skin affected by artificially induced irritant contact dermatitis and pigmented nevous. The method selected a grade using a color model parameter. Twenty healthy Korean males participated in this study. A comparative study of the eight anatomical areas was performed, including the exposure and non‐exposure parts and the medial aspect and the lateral aspect of the forearm. A reliability test for the SCDA system was also conducted with a spectrometer (SPEC) using the color analysis method. Results: Each skin lesion was precisely segmented by grade and each parameter hada different statistical significance for results of analysis of distribution in pigmented nevous and the artificially induced irritant contact dermatitis. Parameters L^*, b^*, a^*, and EI showed salient traits. Showed resemble measured result in the SCDA system and the SPEC of normal skin. The exposed site, in comparison with the non‐exposed site, showed a notable difference in the L^* parameter and a significant statistical difference in the x and z parameters, except b^*. The comparison of the medial and lateral aspects of the forearm showed a notable difference in the L^* parameter and a significant statistical difference in the parameters except y and b^*. In the reliability test result using the SCDA system and the SPEC, the SCDA system was highly reliabile in terms of the CV value in all color model parameters. Conclusions: The color distribution analysis method using the SCDA system has revealed an aspect that the existent method of medical research has not shown, and is considered to be more reliable than other methods. This method can provide better study findings because it can be applied to other fields in addition to the medical science field and the ripple effect is thought to be bigger in other science field too.     

Increased lymphocyte beta-adrenergic receptor density in progressive multiple sclerosis is specific for the CD8+, CD28- suppressor cell.

Beta-adrenergic receptor density on T cells from healthy humans is greatest on suppressor cells (CD8+, CD28-) and the effect of catecholamines, secreted by the sympathetic nervous system, predominates on this subset. The sympathetic skin response, a measure of sympathetic nervous system function, is absent in most patients with chronic progressive multiple sclerosis (MS). We measured beta-adrenergic receptor density on suppressor cells, cytotoxic cells, and monocytes from patients with chronic progressive MS and healthy control subjects. Control receptor density on suppressor cells was 2.8 +/- 0.3 fmol/10(6) cells versus a density of 5.1 +/- 0.7 fmol/10(6) cells for patients. Cytotoxic cell (CD8+, CD28+) receptor density was 1.4 +/- 0.4 fmol/10(6) cells in control subjects and 0.9 +/- 0.3 fmol/10(6) cells in the patients. Monocytes displayed beta-adrenergic receptor densities of 2.6 +/- 0.4 fmol/10(6) cells in normal individuals and 2.7 +/- 0.4 fmol/10(6) cells in the patient group. CD8 lymphocyte beta-adrenergic receptor densities in patients with relapsing-remitting and those with stable MS were not different from control values, yet were significantly less than the values for patients with chronic progressive MS. We find that mononuclear cells from healthy control subjects and patients with chronic progressive MS proliferate in response to 200 units/ml of recombinant human interleukin-2 (IL-2) similarly. However, IL-2 treatment increased beta-adrenergic receptor density on normal mononuclear cells, but failed to increase it on mononuclear cells from patients with chronic progressive MS.(ABSTRACT TRUNCATED AT 250 WORDS)