Effect of forced-air warming by an underbody blanket on end-of-surgery hypothermia: a propensity score-matched analysis of 5063 patients.

BACKGROUND: Underbody blankets have recently been launched and are used by anesthesiologists for surgical patients. However, the forced-air warming effect of underbody blankets is still controversial. The aim of this study was to determine the effect of forced-air warming by an underbody blanket on body temperature in anesthetized patients. METHODS: We retrospectively analyzed 5063 surgical patients. We used propensity score matching to reduce the bias caused by a lack of randomization. After propensity score matching, the change in body temperature from before to after surgery was compared between patients who used underbody blankets (Under group) and those who used other types of warming blankets (Control group). The incidence of hypothermia (i.e., body temperature < 36.0 °C at the end of surgery) was compared between the two groups. A p value < 0.05 was considered to indicate statistical significance. RESULTS: We obtained 489 propensity score-matched pairs of patients from the two groups, of whom 33 and 63 had hypothermia in the Under and Control groups, respectively (odds ratio: 0.49, 95% confidence interval: 0.31-0.76, p = 0.0013). CONCLUSIONS: The present study suggests that the underbody blanket may help reduce the incidence of intraoperative hypothermia and may be more efficient in warming anesthetized patients compared with other types of warming blankets. TRIAL REGISTRATION: UMIN Clinical Trials Registry (Identifier: UMIN000022909 ; retrospectively registered on June 27, 2016).

Stereoselective Synthesis of Z-α,ß-Unsaturated Sulfones Using Peterson Reagents.

New Peterson reagents were prepared by introducing alkyloxy groups on the silicon atom in order to fix the conformation of the sulfone anion. The reagents 1d and 1e reacted with a variety of aldehydes after the treatment with Li-base to give Z-α,ß-unsaturated sulfones with up to >99:1 selectivity in good to excellent yields. For the reaction with aliphatic aldehydes, CPME (cyclopentyl methyl ether) is the choice of solvent, while DME (1,2-dimethoxyethane) gave higher selectivity for the reaction with aromatic aldehydes.

Formal genesis of the outflow tracts of the heart revisited: previous works in the light of recent observations.

The formal genesis of the great arteries continues to be controversial due to the lack of consensus of septation of the developing outflow tract. In order to make it clear how the great arteries are generated, we have re-examined our previous papers which emphasized the formation of the aorta and pulmonary trunk, concept of the aorticopulmonary septum, formation of the leaflets of semilunar valves, morphogenesis of the crista supraventricularis, programmed cell death and rotation of the outflow tract. In the present paper, we compare outcomes gained from the re-examination of our previous papers with prevalent interpretations of the arterial trunk. We obtained conclusions as follows: (i) The elongation of the fourth and sixth aortic arch arteries, which sprout from the wall of the aortic sac at the expense of the distal truncus, contributes to the formation of the aorta and pulmonary trunk; (ii) Smooth muscle cells of the tunica media of the arterial trunks do not arise from the transformation of the myocardial cells of the truncus wall (not 'arterialization'); (iii) Truncus swellings are divided into two parts: distal and proximal. The former contributes to the separation of the orifices of arterial trunks ('aorticopulmonary septum'). The latter contributes to the formation of the leaflets of the semilunar valves of the aorta and pulmonary trunk; (iv) The origin of the myocardial cells of the crista supraventricularis is a wall of the conus originated from secondary/anterior heart fields; and (v) There has been no acceptable proof that rotation and counterclockwise rotation are involved.

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces disruption of glands of the prostate and fibrosis in rhesus monkeys.

We investigated the effects that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure has on the prostate in rhesus monkey offspring. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and examined histopathologically. Dose-dependent decreases in glands of the prostate and widespread fibrosis were observed in offspring. It is noteworthy that 7 years from the final lactational TCDD exposure, inflammatory cell infiltration and disruption of glands of the prostate were still observed. Differential mRNA expression associated with fibrosis, inflammatory response and disruption of cell components were demonstrated by microarray analysis, with up-regulation of TGM4, TGFB1, COL1A1 and MMP2 confirmed. In conclusion, in utero and lactational exposure to TCDD induced dose-related prostatic fibrosis, indicating prostatic dysfunction and inducible semen quality reduction in second-generation rhesus monkeys.

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces a reduction in epididymal and ejaculated sperm number in rhesus monkeys.

A long-term developmental toxicity study of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure was performed in rhesus monkeys and the effect on male reproductive organs was determined in the second generation. Dams received 0, 30 or 300 ng/kg TCDD subcutaneously on Day 20 of gestation, and then 5% of the initial dose was injected every 30 days until Day 90 after delivery. The offspring were maintained until reaching sexual maturity, and evaluated by semen analysis, and histopathology of the testes and epididymides. Ejaculated sperm concentration was severely reduced at 300 ng/kg, and sperm viability and activity were dose-proportionally reduced, although effects on spermatogenesis were slight. Histomorphometry revealed markedly reduced area of the ductus epididymis accompanying decreased reserved sperm in the 30 and 300 ng/kg groups. In conclusion, in utero and lactational exposure to TCDD induced a reduction of sperm quality in rhesus monkeys.

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects bone tissue in rhesus monkeys.

Bone tissue is one of the target tissues for dioxins and dioxin-like compounds. Therefore, the aim of this study was to investigate effects of in utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), on bone tissue in rhesus monkey, the most human-like experimental model available. Pregnant rhesus monkeys (Macaca mulatta; age 4-10 years) were exposed to TCDD with a total dose of 40.5-42.0 or 405-420ng/kg bodyweight by repeated subcutaneous injections starting at gestational day 20 and followed by injections every 30 days until 90 days after delivery. At a mean age of 7 years the offspring were sacrificed and the femur bone dissected. Results from peripheral Quantitative Computed Tomography (pQCT) analyses of the metaphyseal part of the femur bones in female offspring showed significant increases in trabecular bone mineral content (BMC; +84.6%, p<0.05, F-value (F)=5.9) in the low-dose treatment group compared with the controls. In the same animals, analysis of the mid-diaphyseal part revealed increases in total BMC (+21.3%, p<0.05, F=5.2) and cortical cross-sectional area (CSA; +16.4%, p<0.01, F=7.4) compared with the controls. In males, changes in biomechanical properties indicating more fragile bone were observed. Displacement at failure were significantly increased in the male low-dose group compared to the controls (+38.0%, p<0.05, F=11). The high dose of TCDD did not induce any significant changes in bone morphology. In conclusion, in utero and lactational low-dose, but not high-dose exposure to 2,3,7,8-TCDD induced disruption of bone tissue development in rhesus monkey, a result suggesting that similar effects might occur in humans also.

In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects tooth development in rhesus monkeys.

We thought to validate the current tolerable daily intake (TDI) value for dioxin (4 pg/kg) in Japan. Pregnant rhesus monkeys received an initial dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 0, 30, or 300 ng/kg subcutaneously) on day 20 of gestation; the dams received additional injection of 5% of the initial dose every 30 days until day 90 after delivery. The teeth of stillborn, postnatally dead, and surviving offspring (now approximately 4 years old) were evaluated. None of the offspring in the 0 and 30 ng/kg groups (n=17 and 15, respectively) had tooth abnormalities, whereas 10 of 17 in the 300 ng/kg had them. These findings suggest the lowest-observed adverse-effect level (LOAEL) for TCDD in the rhesus monkey is between 30 and 300 ng/kg, and probably is close to that for rodents (86 ng/kg) on which the current TDI was based. It is reasonable to conclude that the current TDI needs no immediate modification.

Erythemas caused by electrodes while monitoring neuromuscular blockade: three cases.

Skin erythemas formed in three patients during surgery at the sites where negative electrodes had been attached to stimulate the ulnar nerve for a neuromuscular transmission monitor (Relaxograph). The patients were all women, aged 52, 62, and 74 years, and general anesthesia lasted 8 h 20 min, 4 h 50 min, and 8 h 45 min, respectively. The electrodes used were disposable ECG electrodes in the first two patients and one designed for a neuromuscular monitor in the third; all were carbon-coated and then covered with gel. However, when the electrodes were detached from the lesion, they all showed loss or damage of the carbon coating under the gel. We recommend balancing the merit of monitoring with the risk of complications, even when applying an apparently safe, noninvasive monitor.

[Perioperative failure of hemodialysis shunts: analysis of risk factors].

BACKGROUND: Because vascular access dysfunction results in substantial morbidity in patients undergoing chronic hemodialysis, this complication should be avoided. However, we experienced four patients whose hemodialysis shunts failed within 24 hours postoperatively. METHODS: We retrospectively analyzed operations performed under general anesthesia in our hospital for patients receiving hemodialysis shunts between May 2001 and October 2002. Comparisons between cases with and without perioperative shunt failures were performed using Mann-Whitney and Fishers exact tests. RESULTS: Spinal surgery (P<0.01) and surgery placed in prone or knee-chest positions (P<0.05) were significantly more frequent, and the operation times (P<0.01) and blood losses (P<0.05) were significantly greater, in the occluded group (n=4) than in the non-occluded group (n=12). CONCLUSIONS: Prone position might have impaired venous backflow from the shunt, thus promoting thrombogenesis. Additionally, moderate hemorrhage, with or without blood transfusion, may have induced a transient hypercoagulable state during the operation, which thus contributed to the acute shunt failure.

Life span shortening of normal fibroblasts by overexpression of BCL-2: a result of potent increase in cell death.

It is well known that BCL-2 protects against cell death by both apoptosis and necrosis. The culture of bcl-2-transfected normal fibroblasts showed a shorter life span by about 12 population doubling levels compared to that of vector transfectants (64 vs 76 population doubling levels, respectively). An MTT assay revealed that BCL-2-overexpressing cells (HCA2/bcl-2) showed more severe growth suppression due to hydrogen peroxide or doxorubicin treatment than vector control cells (HCA2/vector). We observed a significant number of dead cells in the HCA2/bcl-2 culture, but not in the HCA2/vector culture. Other BCL-2 family proteins with both antiapoptotic and proapoptotic activity and other apoptosis-related factors were maintained at similar levels, indicating that overexpression of BCL-2 is the major reason that normal fibroblasts are sensitized to cell death. A broad caspase inhibitor (z-Val-Ala-Asp-fmk) and inhibitors of specific caspases (acetyl-Asp-Glu-Val-Asp-CHO, acetyl-Ile-Glu-Thr-Asp-CHO, and acetyl-Leu-Glu-His-Asp-CHO) suppressed cell death of HCA2/bcl-2 effectively, suggesting involvement of caspase 3-, 8-, and 9-dependent pathways in cell death and that the form of death is apoptosis. Unexpectedly, involvement of active MEK in cell death was shown by the use of its inhibitor, suggesting that crosstalk between BCL-2 and the MAP kinase cascade regulates death as well as life span.

[Airway management in tracheal stenosis caused by malignant goiter].

We report a case of malignant goiter with severe tracheal stenosis. The patient was a 61-year-old female, who had orthopnea on admission. Radiological examinations revealed a tracheal stenosis extending from 4.5 cm to 8 cm below the glottis; the smallest caliber being 5 mm. On the seventh day after admission, the patient complained of dyspnea even while sitting. An emergency tracheotomy was scheduled. While the patient was awake in a sitting position, a fiberscope was inserted endotracheally to confirm the intact inner surface of the trachea, and then an armored endotracheal tube (outer diameter 9.2 mm, inner diameter 6.5 mm) was inserted. Unexpectedly, the tube could be advanced through the stenosis without resistance. After induction of general anesthesia, the patient was placed in a supine position, and a tracheotomy was performed. This case demonstrates that, while intubation of the trachea through a stenosis is sometimes dangerous, it may be indicated when the inner surface of the trachea is intact and a tube with an inner diameter greater than 5 mm can then be placed.

Effect of BCL-2 down-regulation on cellular life span.

Reactive oxygen species (ROS) are toxic for cells. BCL-2 is known as the anti-death protein and acts as an antioxidant. When the BCL-2 level of normal fibroblasts was suppressed by antisense bcl-2 oligodeoxynucleotide or antisense bcl-2 RNA expression, the life span of the culture was shortened by about 11 population doublings (approx. 15% of the total life span) in comparison to the control culture. Since about twice as many cell deaths were observed in the antisense culture than in the vector culture, the life span shortening was probably caused by ROS-induced death. Acceleration of telomere shortening was not evident in the antisense culture. Other BCL-2 family proteins showed no significant change in expression. Cell death was suppressed by N-acetyl-L-cysteine, an antioxidant, suggesting that ROS were the major cause of cell death. In conclusion, reduction of BCL-2 makes cells more sensitive to death induced by ROS and leads to shortening of the culture's life span.