BACKGROUND: In spite of the clinical introduction of brachytherapy to reduce restenosis, the biologic responses of vascular smooth muscle cells(VSMCs) to radiation have not been well studied. We investigated the effects and mechanisms of gamma-irradiation on the cell cycle of VSMCs using primary cultures of rat aortic VSMCs and 137Cs as a radiation source. METHODS & RESULTS: The cell counts after irradiation with 0, 2, 8, 16 Gray (Gy) (n=, each) were 3.28, 2.34, 1.94 and 1.30 x 105/ml at 24h, and 5.10, 2.00, 1.80 and 1.20 x 105/ml at 48h, respectively. The proportions of cells in the G0/G1, S and G2/M phases, as measured by Fluorescence Activated Cell Sorter, were 61, 9 and 30% at 12 hours after 16Gy radiation (control 61, 34 and 5%), 65, 9 and 26% at 24 hours (control 70, 16 and 14%); and 67, 7 and 26% (control 78, 12 and 10%) at 48 hours, which demonstrated G1 and G2 arrest. By immunoblot analysis and kinase assay, gamma-irradiation with 8 or 16 Gy increased the expression of p21, universal cell cycle inhibitor, and decreased the expression and activity of CDK2, an important kinase during the later stages of G1/S progression, as well as the expression and activity of CDK1, which is important in the G2/M phase transition. In contrast, radiation did not affect the expression or activity of either CDK4 or CDK6. The cell-cycle inhibitors, p27 and p16 were not involved in the radiation-induced cell cycle arrest of VSMCs. CONCLUSION: Gamma-irradiation can effectively inhibit VSMC proliferation because it causes cell cycle arrest at both the G1 phase by enhancing P21 expression and suppressing CDK2, and at the G2/M phase by suppressing CDK1.
Animals ; Brachytherapy ; Cell Count ; Cell Cycle ; Cell Cycle Checkpoints ; Cyclin-Dependent Kinases* ; Fluorescence ; G1 Phase ; Muscle, Smooth, Vascular* ; Phase Transition ; Phosphotransferases ; Rats

No abstract available.
Clostridium difficile* ; Clostridium* ; Diarrhea* ; Humans

No abstract available.
Child* ; Hepatitis B Surface Antigens* ; Hepatitis B Vaccines* ; Hepatitis B* ; Hepatitis B, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Infant* ; T-Lymphocyte Subsets*

No abstract available.

No abstract available.
Child* ; Humans

No Abstract available.
Korea*

Gastric cancer cells express large amounts of galectin-3 on the cell surface. This fact may provide the possibility to use galectin-3 protein as a surface target for delivering cytotoxic anticancer agents. To investigate the possibility of application of galectin-3 protein as a target protein in delivering cytotoxic anticancer agents, we synthesized doxorubicin immunoconjugate by using maleimidocaproic acid and conjugated doxorubicin immunoconjugate to anti-galectin-3 mAb. The anticancer effect of immunotoxin was assayed on NIH3T3, AGS and KATO III cell lines. The anticancer effect of immunotoxin on AGS cell line is highest and that of KATO III is higher than that of NIH3T3. This results relate to that of flow cytometry analysis previously shown and indicate that galectin-3 protein can be used as a target protein on the surface of gastric cancer cell for delivering cytotoxic anticancer agents.
Antineoplastic Agents* ; Cell Line ; Doxorubicin ; Flow Cytometry ; Galectin 3 ; Galectins* ; Immunoconjugates ; Immunotoxins ; Staphylococcal Protein A ; Stomach Neoplasms

No abstract available.
Torticollis*

BACKGROUND: Many studies reported that endothelium-dependent vasodilator response is impaired in patients with congestive heart failure. But the opposite results also were reported. The aim of this study was to determine the presence of endothelial dysfunction and its characteristics. METHODS AND MATERIALS: Forearm blood flow was measured in 12 patients with congestvie heart failure (7 males and 5 females, mean age 53+/-11 years old) and 10 normal control subjects (5 males and 5 females, mean age 41+/-10 years old) using strain-gauge plethysmography. The endothelium-dependent vasodilators were acetylcholine (7.5, 15, and 30 microgram/min), which uses a pertussis toxin-sensitive signal transduction pathway, and bradykinin (100, 200, and 400 ng/min), which uses a pertussis toxin-insensitive signal transduction pathway to activate nitric oxide production. Sodium nitroprusside (0.8, 1.6, and 3.2 microgram/min) was used as an endothelium-independent vasodilator. All drugs were infused into the brachial artery with random order. RESULTS: The basal forearm blood flow was similar between both groups. The maximum flow in response to acetylcholine, bradykinin, and sodium nitroprusside was also similar in two groups. CONCLUSIONS: Patients with congestive heart failure showed normal endothelium-dependent vasodilator responses to both acetylcholine and to bradykinin. This finding indicates that the endothelial vasodilator function is normal in the patients with heart failure.
Acetylcholine ; Brachial Artery ; Bradykinin ; Endothelium ; Endothelium-Dependent Relaxing Factors ; Estrogens, Conjugated (USP)* ; Female ; Forearm ; Heart Failure* ; Humans ; Male ; Nitric Oxide ; Nitroprusside ; Plethysmography ; Signal Transduction ; Vasodilation* ; Whooping Cough

There are numerous drug interactions related to many psychotropic and cardiovascular medications. Firstly, the principles in predicting drug interactions are discussed. Cytochrome P (CYP) 450 plays a significant role in the metabolism of these drugs that are substrates, inhibitors, or inducers of CYP450 enzymes. The two most significant enzymes are CYP2D6 and CYP3A4. The ability of psychotropic drugs to act as inhibitors for the enzymes may lead to altered efficacy or toxicity of co-administered cardiovascular agents as a substrate for the enzymes. The following is also a review of the known interactions between many commonly prescribed cardiovascular agents and psychotropic drugs. Most beta blockers are metabolized by CYP2D6, which may lead to drug toxicity when they use in combination with potent CYP2D6 inhibitors including bupropion, chlorpromazine, haloperidol, selective serotonin reuptake inhibitors, and quinidine. Concomitant administration of lithium with angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and diuretics may increase serum lithium concentrations and toxicity. Calcium channel blockers and cholesterol lowering agents are subject to interactions with potent inhibitors of CYP3A4, such as amiodarone, diltiazem, fluvoxamine, nefazodone, and verapamil. Prescribing antiarrhythmic drugs in conjunction with medications are known to prolong QT interval and/or inhibitors on a relevant CYP450 enzyme is generally not recommended, or needs watchful monitoring. Digoxin and warfarin also have warrant careful monitoring if co-administered with psychotropic drugs.
Amiodarone ; Angiotensin Receptor Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Anti-Arrhythmia Agents ; Bupropion ; Calcium Channel Blockers ; Cardiovascular Agents ; Chlorpromazine ; Cholesterol ; Cytochrome P-450 CYP2D6 ; Cytochrome P-450 Enzyme System ; Cytochromes ; Digoxin ; Diltiazem ; Diuretics ; Drug Interactions ; Drug Toxicity ; Fluvoxamine ; Haloperidol ; Lithium ; Psychotropic Drugs ; Quinidine ; Serotonin Uptake Inhibitors ; Triazoles ; Verapamil ; Warfarin