• Korean Journal of Microbiology
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• v.39 no.3
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• pp.166-174
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• 2003

Microcystin produced by cyanobacteria in surface waters, such as eutrophic lake and river, is a kind of serious environmental problems due to its toxicity to human and wild animals. Microcystin is synthesized nonribosomally by the large modular multi-functional enzyme complex known as microcystin synthetase encoded by the mcy gene cluster. Amplification of mcy genes by PCR from cultures and environmental samples is a simple and efficient method to detect the toxigenic Microcystis. In order to evaluate primers designed to detect toxic microcystin-producing strains, 17 cyanobacterial strains and 20 environmental samples were examined by PCR with 7 pairs of primers. Some microcystin-producing cyanobacteria were not detected with FAA-RAA, TOX4F-TOX4R and FP-RP primers. The fragment of unexpected size was amplified with NSZW2-NSZW1 primers in Microcystis strains isolated from the lakes in Korea. TOX1P-TOX1F primers failed in amplification of toxin-producing strains. Only MSF-MSR and TOX2P- TOX2F primers amplified the fragments of mcy genes from 11 strains of microcystin-producing Microcystis. The water samples taken from 20 lakes in Korea were analyzed by PCR using each of the primers. In all the water samples, cyanobacteria capable of producing microcystin were detected by the PCR with TOX2P-TOX2F primers. These results indicate that TOX2P-TOX2F primers are better than the other primers for detection of microcystin-producing Microcystis strains in Korea. The nucleotide sequences of mcy gene in Microcystis aeruginosa NIER10010 suggest genetic diversity of Korean isolates.

• Journal of Chest Surgery
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• v.32 no.3
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• pp.224-236
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• 1999

Background: To evaluate the short-term effect of dynamic cardiomyoplasty on circulatory function and detect the related factors that can affect it, experimental cardiomyoplasties were performed under the state of normal cardiac function and heart failure. Material and Method: A total of 10 mongrel dogs weighing 20 to 30kg were divided arbitrarily into two groups. Five dogs of group A underwent cardiomyoplasty with latissimus dorsi(LD) muscle mobilization followed by a 2-week vascular delay and 6-week muscle training. Then, hemodynamic studies were conducted. In group B, doxorubicin was given to 5 dogs in an IV dose of 1 mg/kg once a week for 8 weeks to induce chronic heart failure, and simultaneous muscle training was given for preconditioning during this period. Then, cardiomyoplasties were performed and hemodynamic studies were conducted immediately after these cardiomyoplasties in group B. Result: In group A, under the state of normal cardiac function, only mean right atrial pressure significantly increased with the pacer-on(p<0.05) and the left ventricular hemodynamic parameters did not change significantly. However, with pacer-on in group B, cardiac output(CO), rate of left ventricular pressure development(dp/dt), stroke volume(SV), and left ventricular stroke work(SW) increased by 16.7${\pm}$7.2%, 9.3${\pm}$3.2%, 16.8${\pm}$8.6%, and 23.1${\pm}$9.7%, respectively, whereas left ventricular end-diastole pressure(LVEDP) and mean pulmonary capillary wedge pressure(mPCWP) decreased by 32.1${\pm}$4.6% and 17.7${\pm}$9.1%, respectively(p<0.05). In group A, imipramine was infused at the rate of 7.5mg/kg/hour for 34${\pm}$2.6 minutes to induce acute heart failure, which resulted in the reduction of cardiac output by 17.5${\pm}$2.7%, systolic left ventricular pressure by 15.8${\pm}$2.5% and the elevation of left ventricular end-diastole pressure by 54.3${\pm}$15.2%(p<0.05). With pacer-on under this state of acute heart failu e, CO, dp/dt, SV, and SW increased by 4.5${\pm}$1.8% and 3.1${\pm}$1.1%, 5.7${\pm}$3.6%, and 6.9${\pm}$4.4%, respectively, whereas LVEDP decreased by 11.7${\pm}$4.7%(p<0.05). Comparing CO, dp/dt, SV, SW and LVEDP that changed significantly with pacer-on, both under the state of acute and chronic heart failure, augmentation widths of these left ventricular hemodynamic parameters were significantly larger under the state of chronic heart failure(group B) than acute heart failure(group A)(p<0.05). On gross inspection, variable degrees of adhesion and inflammation were present in all 5 dogs of group A, including 2 dogs that showed no muscle contraction. No adhesion and inflammation were, however, present in all 5 dogs of group B, which showed vivid muscle contractions. Considering these differences in gross findings along with the following premise that the acute heart failure state was not statistically different from the chronic one in terms of left ventricular parameters(p>0.05), the larger augmentation effect seen in group B is presumed to be mainly attributed to the viability and contractility of the LD muscle. Conclusion: These results indicate that the positive circulatory augmentation effect of cardiomyoplasty is apparent only under the state of heart failure and the preservation of muscle contractility is important to maximize this effect.