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An environmentally friendly method using the baker's yeast Saccharomyces cerevisiae was developed to recover soluble Au(III) from neutral and acidic solutions at room temperature. Resting cells of S. cerevisiae were able to reduce aqueous Au(III) ions in HAuCl4 solution to metallic Au(0) at pH 7.0 within 120 min when formate was provided as the electron donor under anaerobic conditions. Gold nanoparticles were deposited on the cell surface of S. cerevisiae. The S. cerevisiae cells were also applicable to a bio-material for adsorbing aqueous Au(III) ions from HAuCl4 solution at pH 1.0 under air atmosphere. When processing the aqua regia leachate of electronic waste (Central Processing Units, CPU), the S. cerevisiae cells were able to rapidly and selectively collect aqueous Au(III) ions from the aqua regia leachate at pH 1.2 within 10 min. Our proposed microbial methods enable the rapid and efficient recovery of gold over the pH range 1.0 to 7.0.

Exploration of novel organic luminophores that exhibit thermally activated delayed fluorescence (TADF) in the aggregated state is very crucial for advance of delayed luminescence-based applications such as time-gated bio-sensing and temperature sensing. We report herein that synthesis, photophysical properties, molecular and crystal structures, and theoretical calculations of 2,6-bis(diarylamino)benzophenones. Absorption spectra in solution and calculations using density functional theory (DFT) method revealed that the optical excitation took place through intramolecular charge-transfer from one diarylamino moiety to an aroyl group. While the benzophenones did not luminesce in solution, the solids of the benzophenones emitted green light with moderate-to-good quantum yields. Thus, the benzophenones exhibit aggregation-induced emission. Based on the lifetime measurement, the green emission of the solids was found to include TADF. The emergence of the TADF is supported by the small energy gap between the excited singlet and triplet states, which was estimated by time-dependent DFT calculations. Thin films of poly(methyl methacrylate) doped by the benzophenones also showed green prompt and delayed fluorescence whose lifetimes were in the order of microseconds. Linear correlation between logarithm value of TADF lifetime and temperature was observed with the benzophenone in powder, suggesting that the benzophenones can serve as molecular thermometers workable under aqueous conditions.

We synthesised ten 2-aminoisophthalic acid diesters from commercially available dimethyl 2-bromoisophthalate. The diesters in 2-methyltetrahydrofuran were non-emissive or faintly fluorescent (Φ = 0.04-0.08) at room temperature, while each ester in its powder form exhibited fluorescence in the blue-to-green spectral region with a luminescence efficiency superior to that in solution. Density functional theory (DFT) calculations reveal that luminescence occurs from the lowest singlet excited state generated by intramolecular charge-transfer from an amino moiety to the isophthalate core. Time-dependent DFT calculations suggest that the energy gap between the S1 and T1 states is very small, which allows reverse intersystem crossing allowing delayed fluorescence emission. Indeed, the diesters dispersed in PMMA film exhibit luminescence consisting of two components whose lifetimes are in the order of nano- and microseconds, respectively. The luminescence spectra of the PMMA films in air completely overlapped with those under vacuum, indicating that the long-lived emission was assignable to delayed fluorescence.

Much interest has been paid to cyclic diaryliodonium salts as bis(electrophile)s in transition-metal-catalyzed annulation reactions to produce polycyclic (hetero)aromatic hydrocarbons. Herein, we report that dibenziodolium triflates smoothly react with potassium thioacetate in the presence of CuCl2 in THF or DMSO at 100–110 °C to afford the corresponding dibenzothiophenes in good-to-high yields. The coupling reaction tolerates reactive functional groups such as chloro and cyano and serves as a facile and reliable method for the synthesis of unsymmetrical dibenzothiophenes.

The design and development of organic phosphors that exhibit efficient emission at room temperature but do not contain precious metals such as iridium and platinum have attracted increasing attention. We report herein highly efficient green phosphorescence-emitting 1,4-dibenzoyl-2,5-bis(siloxy)benzene crystals in air at room temperature. Remarkable luminescence quantum yields of 0.46 to 0.64 and long lifetimes ranging from 76.0 to 98.3 ms were observed. X-ray diffraction analysis of the single crystals revealed that there were several intermolecular interactions causing suppression of intramolecular motion, thereby minimizing nonradiative decay of the triplet excited state. Comparison with the corresponding 2,5-bis(dimethylphenylsilylmethyl) and 2,5-bis(trimethylsilyl) derivatives revealed that the siloxy groups are essential for efficient room temperature phosphorescence. Density functional calculations suggested that σ–n conjugation was operative in the siloxy moieties. Electron spin resonance measureme...

Much interest has been paid to cyclic diaryliodonium salts as bis(electrophile)s in transition-metal-catalyzed annulation reactions to produce polycyclic (hetero)aromatic hydrocarbons. Herein, we report that dibenziodolium triflates smoothly react with potassium thioacetate in the presence of CuCl2 in THF or DMSO at 100–110 °C to afford the corresponding dibenzothiophenes in good-to-high yields. The coupling reaction tolerates reactive functional groups such as chloro and cyano and serves as a facile and reliable method for the synthesis of unsymmetrical dibenzothiophenes.

Background We found in previous work a significant association between schizophrenia and D20S95 on chromosome 20p12.3. In this study, we analyzed 10 microsatellite markers and found an association of schizophrenia with D20S882 and D20S905 that flank D20S95. The chromogranin B gene ( CHGB ) is 30 kb from D20S905. The chromogranin B (secretogranin I) belongs to a series of acidic secretory proteins that are widely expressed in endocrine and neuronal cells, and its cerebrospinal fluid levels have been reported to decrease in patients with chronic schizophrenia. Methods We screened for polymorphisms in CHGB with polymerase chain reaction direct sequencing methods in 24 Japanese schizophrenic patients and identified a total of 22 polymorphisms. Allelic and genotypic distributions of detected polymorphisms were compared between unrelated Japanese schizophrenic patients ( n = 192) and healthy control subjects ( n = 192). Results Statistically significant differences in the allelic distributions were found between schizophrenic patients and control subjects for 1058C/G (A353G) (corrected p = 7.7 × 10 −5 ) and 1104A/G (E368E) (corrected p = 8.1 × 10 −6 ). The 1058C/G and 1104A/G alleles were in almost complete linkage disequilibrium and were in linkage disequilibrium with D20S95. Conclusions Results suggest that the CHGB variations are involved in the susceptibility to schizophrenia in our study population.

Background: Restenosis after coronary intervention remains an unsolved and important clinical problem. We histologically examined the mechanism of restenosis after both balloon injury and stenting. Methods: Coronary arteries of swine were subjected to balloon injury and stenting. Next, just after stenting or at 7, 14, or 28 days, the animals were sacrificed for the evaluation by morphometric analysis, histological observation, and immunostaining. Results: The neointimal area peaked at 14 days in the balloon injury group (BG) and increased linearly up to 28 days in the stent group (SG). At 28 days, the total vascular area in the BG was reduced to 78% of the control values. In the SG, the total vascular area remained enlarged. According to the phenotypic analysis, the vascular smooth muscle cells (VSMCs) in the neointimal area at 28 days were the contractile type in the BG and the synthetic type in the SG. Proliferating cell nuclear antigen (PCNA) and macrophage-positive cells were not observed in neointima in the BG at 28 days, whereas they were observed around the stent struts in the SG. In addition, numerous inflammatory cells, such as neutrophils and eosinophils, were also present in the SG. Conclusions: Restenosis after balloon injury consisted of arterial remodeling and neointimal hyperplasia, whereas that after stenting consisted mostly of neointimal hyperplasia. The neointimal area in the SG lasted longer than that in the BG. Continuous inflammation may be an important factor in the restenosis of stenting.

Background Stent design causes the differences of restenosis rate, but the morphological differences after the various types of stent implantation have not been clarified. Design Seven types of stents were implanted in pig coronary arteries to clarify how the mechanism of restenosis differs with coil stents and tube stents. Methods The left anterior descending coronary arteries (LADs) of pigs were injured using coronary angioplasty balloons (diameter: 3.0 mm; length: 20 mm; balloon/ artery ratio: 1 : 2). Fourteen days after the injury, four types of coil stents (Cordis, Wiktor, GR-I, and GR-II) and three types of tube stents (Palmaz-Schatz, gfx, and Multilink) were implanted, and the LADs were extracted 28 days after the implantation. Results The proliferated neointima was eccentric in the coil stents and concentric in the tube stents. Although there was no significant difference in the area of neointima, the area of the lumen was significantly larger in the tube stents than in the coil stents (P < 0.01) because of the larger area of stent. Cells positive for anti-proliferating cell nuclear antigen antibody were mainly observed around the stent struts, and most of these cells were also positive for either anti-macrophage or anti-smooth muscle actin antibodies. Conclusions Compared to the coil stents, the tube stents induce less negative remodelling including stent recoil, resulting in a wider luminal area. In order to prevent restenosis, it is crucial to implant a stent that will cause less negative remodelling.

To clarify the role of vascular endothelial growth factor (VEGF) in the process of restenosis, a Palmaz-Schatz stent was implanted in the left anterior descending coronary artery of male pigs at 2 weeks after balloon injury (balloon/artery ratio 1.2:1). The animals were euthanized at 1, 2, and 4 weeks after stenting, and western blot and immunohistochemical analysis were performed using VEGF, fms-like tyrosine kinase (flt)-1, and platelet-derived growth factor (PDGF) antibodies. The expressions of VEGF and flt-1 protein in the neointima were observed as early as 1 week after stenting and remained for up to 4 weeks, while re-endothelialization was complete at 2 weeks. These protein expressions were demonstrated in proliferated smooth muscle cells throughout the entire period after stenting and, in addition, they were observed in the macrophages and endothelial cells of microvessels around stent struts at 4 weeks. The expression pattern of VEGF corresponded with that of PDGF, a growth factor well-known to induce neointimal proliferation. The cell proliferative activity, measured by the proliferating cell nuclear antigen index, around the struts remained high until 4 weeks after stenting, while that in the other areas declined at 4 weeks. These results suggest that VEGF is involved in the process of restenosis not only through its angiogenic properties and induction of monocyte chemotaxis, but also by a synergistic effect with PDGF.

Free radicals have been implicated in myocardial reperfusion injury. Hydrogen peroxide (H2O2) is a precursor of highly reactive oxygen intermediates. In this study, we investigated myocardial injury caused by endogenous H2O2 during the early reperfusion period following brief ischemia with electron microscopy and the cerium method. This method involves formation of an electrondense precipitate when H2O2 reacts with cerium chloride (CeCl3). We used isolated, functioning hearts prepared according to the working heart model, which were reperfused with a solution containing 0.5mM CeCl3 for 5 min after 10 min of ischemia. Some hearts were treated with 3-amino-1,2,4-triazole (ATZ) to inhibit catalase; others were treated with ATZ and superoxide dismutase (SOD), which dismutates the superoxide anion to hydrogen peroxide. In the control group (no drugs given) and the ATZ-treated group, the CeCl3−H2O2-dependent reaction products during the reperfusion period appeared in 12% and 28%, respectively, of the microvascular spaces. Treatment with SOD did not produce a decrease in electron-dense precipitates or a decrease in myocardial injury during ischemia-reperfusion. Moreover, in the ATZ group, moderately injured myocytes were seen (swelling of mitocondria, intermyofibrillar edema). Our results indicate that in myocytes, catalase plays an important role in the defense against H2O2 and that the increase in H2O2 is a cause of reperfusion injury. However, SOD does not protect against H2O2 in the absence of catalase.

The aim of this study was to clarify the role of the adenosine triphosphate (ATP)-sensitive potassium channel on the mechanism of ischemic preconditioning (IP). Thirty-five anesthetized dogs were divided into 5 groups: (1) Control (C), (2) IP, (3) intravenous infusion of nicorandil (Ni) prior to IP, (4) glibenclamide (Gl) pretreated with IP (Gl+IP), and (5) Gl pretreated with Ni (Gl+Ni). All groups had 60 min ischemia followed by 60 min reperfusion, and were analyzed by biochemical and morphological procedures. At the end of the 60-min reperfusion, %segment shortening in C indicated paradoxical bulging. This value had significantly recovered in IP and Ni groups, but it was still negative in the Gl+IP and Gl+Ni groups. Ca++-ATPase activity of the sarcoplasmic reticulum (SR) was significantly decreased in C. In the IP and Ni groups, this activity was significantly maintained; however, in the Gl+IP and Gl+Ni groups it was similar to that in C. State 3 respiration of mitochondria showed similar changes in the SR. In the ultrastructural observations, severely damaged cells were not observed in the IP and Ni groups. These results indicated that an ATP-sensitive potassium channel opener enhanced the effects of IP and its blockade abolished these phenomena. It was conclude that the ATP-sensitive potassium channel may play a key role in the mechanism of IP. (Jpn Circ J 1998; 62: 915 - 924)

This paper reports on the experience of using vaccination in the treatment of recurrent tonsillitis. All of the 82 patients, who were aged between 5 and 67 years and who suffered from recurrent tonsillitis, were given an injection of a bacterial vaccine (Broncasma Berna, Swiss Serum Institute, Berne) that has been used in many countries for three decades. A dose of 0.05 ml was given once every 4 to 14 days (average once a week) on 3 to 20 occasions (average 8). The treatment prevented 75 of the 82 patients (91%) from having attacks of recurrent tonsillitis for extended periods. These 75 patients included three who relapsed into recurrent tonsillitis in spite of having tonsillectomies. As the dose used was relatively small, none of the patients complained of spontaneous pain or fever although three complained of slight tenderness at the injection point on the following day. The effect on recurrent tonsillitis of the Paspat intracutaneous injection (Luitpold Werk, Munich) has also been investigated recently. It was effective in two patients who did not respond to Broncasma Berna. In this retrospective study, low doses of bacterial vaccine reduced the incidence of recurrent tonsillitis and were well tolerated.

The effect of preconditioning (PC) on acute ischemic myocardial injury was investigated in an openchest dog model. Preconditioned dogs received four 5-min occlusions of the left anterior descending coronary artery (LAD), each separated by 10 min of reperfusion. Four groups were used to assess the effect: non-PC group (G-1), PC group (G-2), 8-phenyltheophylline-(adenosine receptor blocker) infused PC group (G-3), and nicorandil- (ATP-sensitive K-channel opener) infused PC group (G-4). The LAD was occluded for 60 min, followed by 60 min of reperfusion in all dogs. The rate of ultrastructural myocardial severe injury was 26% in G-1, 0% in G-2, 5% in G-3, and 0% in G-4. Biochemical analayses also indicated higher values of myocardial contractile function in G-2 and G-4 than G-1 and G-3. These data suggest that the adenosine receptor and K channel may play a key role in PC.

Active oxygen species, including hydrogen peroxide (H2O2), have been implicated in myocardial reperfusion injury. Recently, spin-trap agents and biochemical techniques applied to intact hearts have shown that H2O2 is generated by leukocytes, by endothelial cells, and by mitochondria in myocytes. In this study, we used electron microscopy and the cerium (Ce) method to histologically investigate H2O2 formation during hypoxia—reoxygenation and its toxic effects on myocardium. This Ce method involves the formation of an electron-dense precipitate when H2O2 reacts with cerium chloride (CeCl3). Single myocytes were obtained from rat hearts by the collagenase method. Isolated myocytes were reoxygenated for 15 minutes after 30 minutes of hypoxia. Digitonin and CeCl3, were added to make cell membranes permeable and to detect intracellular H2O2 by electron microscopy. In the control group, the ultrastructure was well preserved and no dense deposits were found in myocytes. However, in the hypoxia—reoxygenation group, precipitates, which were cerium—H2O2 reaction products, were found along swollen mitochondria. Moreover, in the hypoxia-reoxygenation group, cell viability was reduced to 72% of control. These results indicate that H2O2 is generated by mitochondria and that its relese into cytosol may lead to myocyte death during hypoxia—reperfusion.

After coronary stent implantation, the unfavorable in-stent restenosis often occurs by the formation of neointima due to the proliferation of smooth muscle cells. Platelet-derived growth factor (PDGF) and other peptide growth factors contribute to this process, but little is known about the role of non-peptide factors in this process. In the present study, the role of histamine, a non-peptide factor, in the formation of neointima was investigated using a pig coronary model of in-stent restenosis and a culture system of coronary smooth muscle cells. A Palmaz-Schatz stent was implanted in the left anterior descending coronary artery of male pigs. At 1, 2 and 4 weeks after stenting, the histamine content of neointima was determined to be 326 +/- 82, 1427 +/- 280 and 440 +/- 69 pmol/mg protein, respectively, by HPLC fluorometry. In contrast, the histamine content of arterial media from the untreated control arteries was only 15.3 +/- 1.6 pmol/mg protein. These results demonstrate that the histamine content of neointima is about 20 to 90-fold that of the normal media. In vitro, histamine by itself did not stimulate the proliferation of cultured smooth muscle cells, but potentiated the PDGF-stimulated proliferation of the cultured cells via a mechanism independent of H1 and H2 histamine receptors. Thus, histamine may be an important non-peptide factor in the pathogenesis of in-stent restenosis.

Legal and ethical conflicts arise in building a community network for mental health workers with confidentiality. Another ethical problem is encountered by involving mental health volunteers who are not obliged to be confidential. The authors made a questionnaire from the following six points of view: 1) the current attitudes of mental health professionals and workers toward confidentiality, 2) the degree of disclosure of individual information, 3) the relation between collaboration with family and confidentiality, 4) the range of extended confidence, 5) the extent of sharing individual information with volunteers, 6) the guidelines of confidentiality. The questionnaire was delivered to the following objects: 1,471 mental health professionals, 3,400 mentally disabled people and 3,400 of their family members. The returned questionnaires were analyzed and led to the following conclusions. The authors also conducted a bibliographical investigation on this subject. 1) Attitudes toward confidentiality varied among mental health professionals and also among mental health facilities. This created difficulties and confusion among them. 2) Transmission of individual information to the caregiving family members is important to help the mentally disabled, however, mental health professionals varied in the extent to which they informed them. 3) Mental health professionals in the same institute were regarded as an extent of extended confidence by 67.5% of the mentally disabled and 80.5% of family members. The caregiving family members were also regarded as such by 58.4% of the mentally disabled and 69.5% of family members. 4) The methods of transmission of individual information within a facility and/or with other facilities varied among mental health professionals. 5) A contract of confidentiality with volunteers was made only by 8.1% of mental health professionals. However, 34.1% of the mentally disabled and 24.0% of family members refused to transmit individual information to such volunteers. 6) Disclosure of individual information to the mentally disabled or their representatives is inevitable for them to authorize transmission of their individual information to others. Authorization of transmission of their individual information without knowing the content of such records is not valid authorization. 7) It is necessary to establish guidelines on confidentiality, according to 42.1% of the mentally disabled and 44.2% of their family members.

Free radicals have been implicated in myocardial reperfusion injury. Hydrogen peroxide (H(2)O(2)) is one possible source of reactive oxygen intermediates. We studied the formation and toxicity of H(2)O(2) in isolated myocytes during hypoxia-reoxygenation with the use of cerium. This method involves formation of an electron-dense precipitate when H(2)O(2) reacts with cerium chloride (CeCl(3)). Single myocytes were obtained from rat hearts by collagenase digestion. Isolated myocytes were reoxygenated for 15 min after 30 min of hypoxia. The cells were treated with digitonin to increase the permeability of the plasma membrane, and CeCl(3) was added to detect intracellular H(2)O(2) on electron microscopy. In the nonhypoxia control group, the ultrastructure of cells was well preserved, and no dense deposits were found in myocytes. In the hypoxia-reoxygenation group, precipitates, i.e., Ce-H(2)O(2) reaction products, were found inside and along swollen mitochondria, and cell viability was reduced to 72.3% of control. These results indicate that endogenous H(2)O(2) is generated by mitochondria and that its release into the cytosol may lead to myocyte death under pathological situations such as hypoxia-reoxygenation.

Restenosis after coronary intervention remains an unsolved and important clinical problem. We histologically examined the mechanism of restenosis after both balloon injury and stenting.Coronary arteries of swine were subjected to balloon injury and stenting. Next, just after stenting or at 7, 14, or 28 days, the animals were sacrificed for the evaluation by morphometric analysis, histological observation, and immunostaining.The neointimal area peaked at 14 days in the balloon injury group (BG) and increased linearly up to 28 days in the stent group (SG). At 28 days, the total vascular area in the BG was reduced to 78% of the control values. In the SG, the total vascular area remained enlarged. According to the phenotypic analysis, the vascular smooth muscle cells (VSMCs) in the neointimal area at 28 days were the contractile type in the BG and the synthetic type in the SG. Proliferating cell nuclear antigen (PCNA) and macrophage-positive cells were not observed in neointima in the BG at 28 days, whereas they were observed around the stent struts in the SG. In addition, numerous inflammatory cells, such as neutrophils and eosinophils, were also present in the SG.Restenosis after balloon injury consisted of arterial remodeling and neointimal hyperplasia, whereas that after stenting consisted mostly of neointimal hyperplasia. The neointimal area in the SG lasted longer than that in the BG. Continuous inflammation may be an important factor in the restenosis of stenting.

Broncasma Berna, an inactivated bacterial vaccine, has been safely used throughout the world for 30 years for the prevention or treatment of various infectious processes. Until now, there has been no published report regarding its use as a treatment for chronic suppurative otitis media. In this small study, five such patients (median age: 57 years) underwent a series of seven 0.05-ml injections of Broncasma Berna. In all cases, their otorrhea diminished markedly and their tympanic membranes were almost completely dry. The cost of treatment was extremely low.

We clarified the role of K(ATP) channels in the mechanism of ischemic preconditioning by using K(ATP) channel opener, nicorandil, and K(ATP) channel inhibitor, glibenclamide. Forty anesthetized dogs were divided into five groups: (a) control (C), (b) ischemic preconditioning (PC), (c) intravenous infusion of nicorandil before PC (Ni), (d) glibenclamide pretreated with PC (Gl + PC), and (e) glibenclamide pretreated with Ni (Gl + Ni). All groups were followed by 60-min ischemia and 60-min reperfusion and analyzed by the biochemical procedures. At the end of 60-min reperfusion, percentage of segment shortening in C indicated paradoxic bulging. This value was significantly recovered in PC and Ni, but it was still negative in Gl + PC and Gl + Ni. Ca2+ -adenosine triphosphatase (ATPase) activity of sarcoplasmic reticulum (SR) was significantly decreased in C. In PC and Ni, this activity was significantly maintained; however, in Gl + PC and Gl + Ni, it was similar to that in C. State III respiration of mitochondria showed similarity to the changes in SR. These results indicated that the K(ATP) channel opener enhanced the effects of ischemic preconditioning, and its blockade abolished these phenomena. We conclude that the ATP-sensitive potassium channel may play one of key roles in the mechanisms of ischemic preconditioning in the dog model.

The aim of this study is to evaluate the role of non-selective endothelin blockade (TAK-044) in ischemic myocardial injury. Forty anesthetized rats were separated into four groups: 1) TAK-I group, after preinjection of TAK-044 (3 mg/kg), LAD was ligated for 60 min and reperfused for 60 min; 2) Saline (SAL)-I group, LAD ligation and reperfusion without TAK-044; 3) TAK-C group, sham operated TAK group; 4) SAL-C group, sham-operated SAL group. Myocardium from each group was separated and analyzed by biochemical and ultrastructural procedures. Reperfusion arrhythmia (VT) was observed in 88% of the SAL-I group, in contrast to only 36% of the TAK-I group. At the end of reperfusion, hemodynamics indicated no significant differences between these two groups. The Ca(++)-ATPase activity of sarcoplasmic reticulum (SR) was 3.9 mumoles Pi/mg protein/h (39% of SAL-C group) in the SAL-I group, while that in the TAK-I group was significantly higher at 6.1 (54%). The ratio of infarct/risk area was 58% in the SAL-I group and 36% in the TAK-I group. In the ultrastructural observations, irreversibly injured cells of the ischemic portion were reduced significantly from 35% (SAL-I group) to 14% (TAK-I group). Thus, our results indicated that endothelin blockade reduced ischemic cellular injury. The mechanism of this reduction was speculated to be a resistance to ischemic injury in the subcellular levels of the myocardium conferred by a reduction of vascular constriction and improvement of imbalance in the energy supply and demand.

The purpose of this study was to examine mitochondrial respiratory impairment in the diabetic heart. Diabetes mellitus was induced in male Wistar rats by intravenous injection of streptozotocin (STZ) for 2 to 16 weeks (Group D). In some of the diabetic rats, insulin was injected for 2 or 3 weeks prior to sacrifice (Group I). Fasting blood glucose was markedly elevated to greater than 300 mg/dl in Group D and was similar to normal glucose levels in Group I. At 2 weeks after STZ injection, state 3 was only 59.1% of that in the control. Complex I and complex V activities were also significantly reduced to 43.4% and 71.7% of those in the control, respectively. These reductions recovered with insulin treatment. This phenomenon persisted for 16 weeks. Morphological studies revealed swelling of the mitochondria and an increase in lipid droplets in diabetic cardiomyocytes, and these were also improved with insulin treatment. We conclude that in the diabetic heart, disturbance of energy production in cardiac mitochondria is generated by the impairment of oxidative phosphorylation due to depression of complex I and complex V. These changes may contribute the cardiac dysfunction that is a complication of diabetes mellitus. (Jpn Circ J 1996; 60: 673 - 682)

To the Editor. —Tonsillectomy is one of the most common operations performed in the world. However, tonsillectomy involves various risks, eg, shock, bleeding, post-tonsillectomy pain, infection, asthma or allergic rhinitis after tonsillectomy, and anesthetic accidents. I have found a simple method for preventing attacks of recurrent tonsillitis. Each of the 72 patients between the ages of 5 and 67 years who suffered from recurrent tonsillitis between 1979 and 1990 was given a 0.05-mL injection of Broncasma Berna once in a 4-to 14-day period subcutaneously or intramuscularly, from three to 20 times in total. This method prevented 68 of the 72 patients from having attacks of recurrent tonsillitis. Most of the cases were followed up for a long time; the longest case was for 10 years. Three patients who relapsed into recurrent tonsillitis in spite of tonsillectomy were cured by Broncasma Berna completely. I presume that general immune systems produce stronger

Kynurenine transaminase activity in rat liver was found in both the mitochondrial and supernatant fractions. The mitochondrial and supernatant fractions contained (a) kynurenine–pyruvate transaminase, which showed a preference for pyruvate as amino acceptor and a pH optimum between 8.0 and 8.5, and (b) kynurenine–α-oxoglutarate transaminase, with a preference for α-oxoglutarate and a pH optimum between 6.0 and 6.5. Possible roles of these enzymes in tryptophan metabolism in the liver are discussed.

Kynurenine transaminase activity in rat kidney was found in both the mitochondrial and supernatant fractions. These fractions contained (a) kynurenine pyruvate transaminase, which showed a preference for pyruvate as amino acceptor, and had a pH optimum between 8.0 and 8.5, and (b) kynurenine 2-oxoglutarate transaminase, with a preference for 2-oxoglutarate and a pH optimum between 6.0 and 6.5. The apparent Km value of the former enzyme for L-kynurenine was much lower than that of the latter enzyme.