Scar tissue at the recipient site reduces the sensory recovery in myocutaneous flaps

In 1993 it was reported that sensory nerve axons enter myocutaneous flaps from all sides of the wound bed through empty perineural tubes, suggesting that small flaps (because less tissue must be reinnervated) and old flaps (because the regenerating process should be completed) would have the best sensation. However, sensory recovery is correlated with neither the flap size nor their age. Since all 16 flaps in this study were placed on significantly traumatized limbs, scar formation should hinder sprouting axons from entering the flap; the present study was performed to test this hypothesis. The sensation of 16 myocutaneous flaps (group A) placed in a nontraumatized wound bed was compared to that of patients in a previous study (group B). All 32 flaps were tested for pin-prick, hot, cold, 30-Hz, 256-Hz vibration, constant touch, moving two-point discrimination, and static two-point discrimination. The results were rated as follows: 2 points for a modality being present all over the flap, 1 for its partial or dull presence, and 0 for no sensation. The elapsed time following surgery was 1.10 –5.40 years in group A and 1.50–8.20 years in group B. Patients in group A scored a mean score of 8.0±2.1 points (4–11) and those in group one of B 5.9± 4.8 (0–13). There was a significant correlation between score and flap age in group A but not in group B; there was no correlation in either group between score and the flap size. Our findings suggest that scar formation is detrimental to the capacity for sensory recovery in myocutaneous flaps. Maximum scar tissue excision is recommended, especially since sensory recovery is not less than in large flaps.     

Effects of preoperative chemoradiotherapy on postsurgical morbidity and mortality in cT3-4 +/- cM1lymph cancer of the oesophagus and gastro-oesophageal junction.

OBJECTIVE: Very few studies have examined post-operative morbidity after resection of oesophageal carcinoma, especially in patients treated with induction chemo- and radiotherapy for locally advanced stages. This study assessed the effects of induction chemoradiotherapy on post-operative course after resection of locally advanced oesophageal carcinoma (cT3-4 + cM1lymph). METHODS: Induction therapy consisted of 5-fluorouracil days 1-5 and days 21-25, cisplatin day 1 + day 21 and concomitant radiotherapy 18-20 fractions of 2Gy (total dose 36-40Gy). Induction chemoradiotherapy was completed in 109 patients. Surgery was performed in 90 patients (operability: 90/109 = 83%): 85 patients underwent resection with curative intent (resectability: 85/109 = 78%), bypass operation was performed in five patients. Nineteen patients could not be operated on. Results were compared to a matched group of pT3M1LYM/pT4 patients (n = 86) who underwent primary surgery in the same period. RESULTS: Resection was complete (R0) in 68 patients (68/90 = 76%). Mean duration of surgery was 428 min (range: 240-690). Peroperative complications were haemorrhage in three patients (3/90 = 3.3%), tracheobronchial perforation in three patients (3/90 = 3.3%). Median total hospital stay was 20.5 days (range: 8-355). Mean duration of intubation was 7 days (range: 1-190); 67 patients (67/90 = 74.4%) were intubated for less than 24 h. Non-tumour related hospital mortality after resection was 8.3% (7/84 patients). Mortality after two-field lymphadenectomy was 5.2 versus 11.7% after three-field lymphadenectomy. After primary surgery (n = 86) overall mortality was 2.3% (P = 0.015) and nil after two- and three-field lymphadenectomy (P = 0.011). Medical morbidity consisted of pneumonia in 43 patients (43/90 = 48%), atelectasis in ten patients (10/90 = 11%), dysrhythmia in 21 patients (21/90 = 23%), sepsis in 11 patients (11/90 = 12%) and adult respiratory distress syndrome in ten patients (10/90 = 11%). Surgical morbidity included pleural effusion in 16 patients (16/90 = 18%), tracheal fistula in two patients (2/90 = 2%), chylothorax in two patients (2/90 = 2%) and acute pancreatitis in one patient (1/90 = 1%). Ten patients (10/90 = 11%) had a radiologically confirmed anastomotic leak; however only in four out of them with clinical manifestation; treatment was conservative in all four patients. Major morbidity occurred in 27 patients (27/90 = 30%). Overall rate of morbidity was significantly higher after three-field lymphadenectomy (85%) as compared to two-field lymphadenectomy (68.7%; P = 0.023). CONCLUSIONS: Chemoradiotherapy followed by resection of cT3-4 +/- cM1lymph oesophageal carcinoma is feasible with acceptable mortality. Mortality, however, seems to be significantly higher when compared to a group of pT3M1LYM/pT4 patients who underwent primary surgery (8.3 versus 2.3%; P = 0.015) in the same period in our department.     

In vivo and in vitro studies on the opioidergic control of the secretion of gonadotrophin-releasing hormone and luteinizing hormone in sexually immature and adult male rats.

In vivo and in vitro methods have been used to compare the effects of opioid receptor blockade on the functional activity of the hypothalamo-pituitary-gonadal axis in adult (200 g) and sexually immature (50 g) male rats. In the adult, a single injection of the mu-receptor antagonist, naloxone (500 micrograms/100 g body weight, s.c.), produced hypersecretions of luteinizing hormone (LH) and testosterone. Maximal serum concentrations of the two hormones were attained within 20 and 60 min respectively. In contrast, neither ICI 174864 (100 micrograms/100 g body weight, s.c.) nor MR2266 (150 micrograms/100 g body weight, s.c.), which block delta- and kappa-receptors respectively, stimulated pituitary-gonadal activity; indeed, like the saline vehicle, both tended to depress the serum LH concentration. The injection procedure was sufficient to activate the hypothalamo-pituitary-adrenal axis and, thus, the vehicle-treated controls exhibited significant increases in the plasma adrenocorticotrophin and serum corticosterone concentrations. These effects were enhanced by naloxone (500 micrograms/100 g body weight, s.c.) and by the kappa-opioid receptor (MR2266, 150 micrograms/100 g body weight, s.c.) but not by the delta-opioid receptor antagonist (ICI 174864, 30-100 micrograms/100 g body weight, s.c.). The increases in serum corticosterone and LH concentration induced by naloxone in adult rats were not apparent in the sexually immature (50 g) animals. To the contrary, in the young rats naloxone (250 and 500 micrograms/100 micrograms body weight, s.c.) attenuated, in a dose-dependent manner, the pronounced hypersecretion of corticosterone induced by the vehicle injection. The higher dose of the antagonist (500 micrograms/100 g body weight, s.c.) also overcame the significant reductions in serum LH evident 20 (p less than 0.05) and 40 (p less than 0.01) min after the saline injection but the lower dose (250 micrograms/100 g body weight, s.c.) was ineffective in this respect. In vitro, hypothalami from both adult and sexually immature rats responded to the addition of naloxone (10(-8)-10(-6) M) to the incubation medium with significant (p less than 0.01) concentration-dependent increases in the release of gonadotrophin-releasing hormone (GnRH). In contrast, ICI 174864 (10(-7)-10(-6) M) and MR2266 (10(-7)-10(-6) M) had little effect on the secretion of the releasing hormone by hypothalami from rats of either group although, at the highest concentration tested, MR2266 (10(-6) M) precipitated a small increase in GnRH release from hypothalami from adult rats.(ABSTRACT TRUNCATED AT 400 WORDS)     

Antidiuretic-hormone-induced morphological changes in the ampullary epithelium of the frog semicircular canal

Summary Morphological changes induced by in vitro treatment with arginine-vasotocin, the frog antidiuretic hormone, were studied in the ampullary epithelium of the frog semicircular canal. Morphological changes appeared only in the apical side of the dark cells, while the basal part of these cells and the other cells lining the semicircular canal did not show any change. Changes consisted of the appearance of numerous small vesicles in the apical cytoplasm and the development of microvilli on the apical plasma membrane of the dark cells. These results suggest that arginine-vasotocin could play a role in the regulation of endolymph section.     

反坦克武器击中坦克时舱室内有害气体测试方法的探讨

为探讨在模拟实验条件下，坦克受到反我武器攻击后舱室内有害气体的取样方法和分析方法，用3种武器发射3种弹药攻击坦克，在远距离控制取样设备，取样后在实验室进行坦克舱室内有害气体浓度分析，结果取样成功，坦克被击中后，一氧化碳气体含量有明显的增高，氮氧化物、二氧化硫增高幅度不大，氧含量无明显变化，说明对坦克舱室进行远距离现场控制气体采样是可行的；坦克的受反坦克武器打击后，除弹片和冲击波等致伤因素外，还会造成坦克内乘员一氧化碳中毒。     

A non-azole inhibitor of lanosterol 14 alpha-methyl demethylase in Candida albicans.

6-Hydroxy-N-methyl-N-(2-[4-phenylphenyl] ethyl)-1,2,3,4-tetrahydro-1- napthalene methanamine (A60586), a new non-azole inhibitor of ergosterol biosynthesis in Candida albicans ATCC62376 has been identified. In whole cells A60586 produced a dose related reduction of [14C]acetate incorporation into ergosterol and a concurrent increase in the radiolabelling of 4,4-dimethylated sterols. Similar observations were made with [14C]mevalonic acid lactone labelled cell free extracts. The IC50s for inhibition of ergosterol in the whole cell and cell free systems were 22 microM (10 mg/L) and 7.8 microM (3.5 mg/L), respectively. Analysis by gas chromatography of sterols from cells previously incubated at 37 degrees C for 24 h with A60586 (200 mg/L) confirmed the presence of lanosterol and 14 alpha-methyl fecosterol. These data indicate that A60586, inhibits the demethylation of the C-14 methyl group of lanosterol. The MIC of A60586 for several candida strains ranged from 12.5 to 50 mg/L, and against Cryptococcus albidus and Aspergillus niger ranged from 50 to 100 mg/L. The best in-vitro activity of A60586 was against Torulopsis glabrata (MIC range = 3.12 to 50 mg/L). The membrane permeabilizing effect of this compound (50% leakage of [14C]aminoisobutyric acid at 70 mg/L A60586) may have contributed to its in-vitro antifungal activity.