[Relation between intraoperative salvaged blood transfusion and postoperative infection after cardiac surgery].

In cardiac surgery, several studies have shown bacterial contamination rates of intraoperative salvaged blood ranging from 12.7 to 96.8%. We evaluated the relation between intraoperative salvaged blood transfusion produced by the Cell Saver 5 device (Haemonetics Corp., Braintree, MA, USA) and postoperative infection determined by bacteriological study and the postoperative clinical course after cardiac surgery. Seven cases of cardiac surgery were investigated by bacteriological study. Although bacteria were cultured from all salvaged blood, no bacteria were cultured from the patients' blood 24 hours after salvaged blood infusion. Another 26 patients who underwent cardiac surgery, were divided into groups: group CS (n = 15) with salvaged blood transfusion after operation and group N (n = 11) without salvaged blood transfusion, and were evaluated in relation to the postoperative clinical course. There were no statistically significant differences between group CS and group N in the data of WBC, CRP and maximum body temperature. One case of deep sternal wound infection and 2 cases of local wound infection were observed in group CS, but none in group N (p = 0.18). These complications were treated by primary closure without muscle flaps. We conclude that salvaged blood autotransfusion was not related to postoperative infections in cardiac surgery.

[Bacterial contamination of salvaged blood in open heart surgery: is that an airborne contamination or a normal skin flora contamination?].

We investigated sources of bacterial contamination of intraoperative salvaged blood producted by autologous transfusions device (CS; CELL SAVER 5, Heamonetics Corp., Braintree, MA). Eleven patients undergone open heart surgeries including 2 emergency operations with a median sternotomy enrolled in this study. Blood samples were drawn from salvaged blood bags. Airborne contaminants (AB) were collected by a blood agar plate put besides the operation bed for 30 minutes. The median wounds samples were collected by a swab. Bacterial growth was detected in 81.8% of salvaged blood samples. Twenty-nine bacterium were isolated from CS, 72.4% of those were Staphylococci. 9.1% of sample was positive in wound swabs. Forty bacterium were isolated from plate cultures. 65% of them were Staphylococci. Staphylococcus epidermidis and coagulase negative Staphylococcus isolated both CS and AB in the 2 cases had the same identify codes, and incubated from several AB cultures. Corynebacterium sp. is also isolated from both CS and AB cultures in other 2 same cases. In 7 out of 8 cases (87.5%), from which Staphylococci isolated in CS, the Staphylococci were cultured from AB in not the same but the other cases. In conclusion, highly incidence of the identification in identical code of Staphylococci indicated that the main source of CS contamination was highly suspected to AB.

Inhibition of mucosal lipid hyperoxidation by green tea extract in 1,2-dimethylhydrazine-induced rat colonic carcinogenesis.

Phosphatidylcholine hydroperoxide (PCOOH) measured using a chemiluminescence detector to examine colonic mucosal lipid hyperoxidation increased after injection of 1,2-dimethylhydrazine and green tea extract (GTE), which we previously showed inhibited carcinogenesis and oxidative DNA damage in the gastrointestinal tract. Therefore, the hyperoxidation of membrane phospholipids reflected well the degree of DNA damage and carcinogenic alteration, and may be a useful intermediate biomarker for initiation of carcinogenesis.

Inhibitory effects and toxicity of green tea polyphenols for gastrointestinal carcinogenesis.

BACKGROUND: Recently, and epidemiologic study showed a lower risk of gastrointestinal carcinogenesis in green tea drinkers. An experiment on two-stage skin carcinogenesis in mice showed that (-)-epigallocatechin gallate (EGCG), one of the main constituents of green tea, inhibited tumor formation. METHODS: The inhibitory effects of EGCG and green tea extract (GTE) on N-ethyl-N'-nitro-N-nitroguanidine (ENNG)-induced duodenal carcinogenesis in the mouse, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced carcinogenesis of the glandular stomach in the rat, and azoxymethane-induced colon carcinogenesis in the rat were examined. The toxicity of GTE was assessed experimentally and GTE was applied clinically in normal volunteers to determine the effective dose and to assess its harmful effects. RESULTS: EGCG and GRE inhibited chemical carcinogenesis of the gastrointestinal tract in rodents. Judging from the epidemiologic and experimental findings, it was determined that 1 g per day of GTE might be an effective dose. GTE was not toxic and no harmful effect was found during its clinical use. CONCLUSIONS: These findings suggest that EGCG and GTE are useful in preventing gastrointestinal carcinogenesis, and the clinical usefulness of GTE, which has no harmful effects and is inexpensive, should be studied further.

Inhibition of 1,2-dimethylhydrazine-induced oxidative DNA damage by green tea extract in rat.

Following subcutaneous injection of 1,2-dimethylhydrazine (DMH), which is carcinogenic to rat colon and liver, to Sprague-Dawley rats, a significant increase of 8-hydroxydeoxyguanosine (8-OHdG) was observed in the DNA of colonic mucosa and liver. The 8-OHdG formation reached the maximal level at about 24 h after the DMII injection. On the other hand, no increase of 8-OHdG was observed in the DNA of the kidney. Drinking green tea extract (GTE) for ten days prior to the DMH injection significantly inhibited the formation of 8-OHdG in the colon. These findings demonstrate that DMH causes oxidative damage to the DNA of its target organ, and that GTE protects colonic mucosa from this oxidative damage.

Selective inhibition of histidine-modified pancreatic alpha-amylase by proteinaceous inhibitor from Phaseolus vulgaris.

Chemical modification of two histidine residues of porcine pancreatic alpha-amylase (EC 3.2.1.1) by diethyl pyrocarbonate in the presence of a high concentration of maltotriose caused a decrease of amylase activity and an increase of maltosidase activity (hydrolysis of p-nitrophenyl-alpha-maltoside). By binding a proteinaceous inhibitor from Phaseolus vulgaris (white kidney bean) with the modified enzyme, the amylase activity was further decreased but the maltosidase activity was retained to about 100% that of the native enzyme. Both amylase and maltosidase activities of the native enzyme were almost completely inhibited by the proteinaceous inhibitor. The increase of maltosidase activity by histidine modification was due to an increase of kcat, whereas the Km value was not changed; but binding of the proteinous inhibitor affected mainly the Km value of the modified enzyme.

[Synchronized hemifacial spasm induced by sound stimulation].

A 42-year-old woman whose hemifacial spasm develops not only involuntarily but also synchronously to the sound stimulation to the left ear is presented. She had about 10 years history of left hemifacial spasm which occurred only involuntarily, and she was treated successfully by microvascular decompression method on June 1982. She had been uneventful and free from facial spasm until around January 1983, about 7 months after the first surgery, when her hemifacial spasm recurred and interestingly enough, this spasm started to occur not only involuntary but also synchronously to stimulation of the sound. On her electromyography (EMG) of the face, high amplitude discharge were noted sporadically during her facial muscle twitching, but more constant and regular high amplitude discharge on EMG were also evoked invariably and synchronously with the sound stimulation which was induced by 90 dB click sound and once this sound stimulation discontinued her facial muscle twitching ceased and abnormal discharge of EMG which appeared with sound stimulation disappeared instantly. On March 18, 1983, her left posterior fossa was explored and another angled artery was found compressing the facial nerve just at the root entry zone, more proximally than the previous site where the nerve was found compressed and decompressed at the first surgery. After complete replacement of this offending artery from the nerve, her facial spasm disappeared completely and was never evoked by the sound stimulation. Her postoperative EMG revealed no abnormal discharges at all after the sound stimulation by click sound in the ear.(ABSTRACT TRUNCATED AT 250 WORDS)

The origin of the long-wavelength fluorescence emission band (77 degrees K) from photosystem I.

Isolated photosystem I (PSI)-110 particles, prepared using a minimal concentration of Triton X-100 [J. E. Mullet, J. J. Burke, and C. J. Arntzen (1980) Plant Physiol. 65, 814-822] and further subjected to short-term solubilization with sodium dodecyl sulfate (SDS), were resolved into four pigment-containing bands on polyacrylamide gel electrophoresis (PAGE). We have identified these in order of increasing electrophoretic mobility as being (a) CPIa, (b) CPI, (c) the light-harvesting complex of photosystem I (LHC-I), and (d) a free pigment-zone. LHC-I had an absorption maximum in the red at 668-669 nm and a shoulder at 650 nm, which was resolved by its first-derivative spectrum to indicate the presence of chlorophyll b. LHC-I exhibited a 77 degrees K fluorescence emission maximum at 729-730 nm. The 77 degrees K fluorescence emission maxima of CPIa and CPI, excised from the gel, were at 729 and 722 nm, respectively. The LHC-I band, excised from the gel and rerun on dissociating SDS-PAGE, was resolved into two polypeptide doublets of 24-22.5 and 21-20.5 kDa. The CPIa band under similar conditions was resolved into polypeptides of 68, 24, 22.5, 21, 20.5, 19, 15, and 14 kDa; on the contrary, CPI contained only the 68-kDa polypeptide. When intact thylakoids were subjected to "nondenaturing" SDS-PAGE, LHC-I comigrated with an oligomeric form (dimer) of the light-harvesting chlorophyll a/b pigment-protein that preferentially serves photosystem II (LHCP-II). When this combined LHC-I/LHCP-II pigment-protein band was prepared by SDS-PAGE from isolated stroma lamellae, it exhibited a long-wavelength fluorescence band near 730 nm at 77 degrees K. When a similar preparation was obtained from sucrose density gradients containing SDS [J. Argyroudi-Akoyunoglou and H. Thomou (1981) FEBS Lett. 135, 171-181], it was found to be enriched in a 21-kDa polypeptide. The data suggest that the 21-kDa polypeptide of LHC-I is the chlorophyll-containing polypeptide responsible for the long-wavelength fluorescence of LHC-I; other polypeptides in the complex (20.5, 22.5, and 24 kDa) presumably bind chlorophyll and also serve an antennae function.