Laparoscopist's thumb: an occupational hazard.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M W Reed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effect of cryosurgery on normal liver and liver tumour was investigated using 60 adult male rats. Animals were divided into four groups Group A implanted tumour/cryosurgery (n = 19), Group B normal liver/cryosurgery (n = 17), Group C normal liver/sham cryosurgery (n = 10) and Group D implanted tumour/sham cryosurgery (n = 14). At laparotomy animals were injected into the left lateral lobe of the liver with 10(5) HSN fibrosarcoma cells or vehicle. Two weeks after implantation red cell flux was recorded in all animals, the appropriate groups treated with cryosurgery and after thawing red cell flux was monitored over the tumour and at the edge of the cryolesion and over the corresponding normal area in controls. In certain animals red cell flux was measured at hourly intervals for 8 h, and in further groups at 24 h and at 2 weeks after cryosurgery. Results demonstrated that cryosurgery significantly reduced (P < 0.01) red cell flux in both normal and tumour liver, immediately after treatment. Red cell flux remained significantly reduced (P < 0.005) at 8 h after treatment but by 24 h had returned to preoperative levels which was maintained at 2 weeks. The results suggest that microcirculatory shutdown may be a contributing factor to the tumour necrosis occurring after cryosurgery.
The effects of supplemental oxygen therapy on arterial oxygen saturation (SaO2) in unsedated and sedated patients have been studied using pulse oximetry. Hypoxia (minimum SaO2 92% or less) occurred in 41% of unsedated patients breathing room air but in only 11% (p < 0.01) of those receiving supplemental oxygen (41/min) by nasal cannulae. Comparable effects were seen in sedated patients (60% versus 16%, respectively, p < 0.01). Hypoxia during upper alimentary tract endoscopy is common with or without sedation and can be reduced by supplemental oxygen.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The calcium-binding protein calmodulin has been shown to modulate the Ca(2+)-dependent ion channels of Paramecium tetraurelia. Mutations in the calmodulin gene of Paramecium result in an altered pattern of behavioral responses. Antisense oligodeoxyribonucleotides (ODNs), complementary to calmodulin mRNA in Paramecium, were synthesized from a modified solid support that introduced a 3'-hydroxyhexyl phosphate. These 3'-modified ODNs were tested for their ability to alter the behavioral response of Paramecium. The microinjection of antisense ODNs temporarily reduced the backward swimming behavior of the cells in test solutions containing Na+. The injection of sense and random 3'-modified ODNs, or unmodified antisense ODNs, had no effect. The antisense ODN-induced effect was reversed by the injection of calmodulin protein. The pattern of response of the injected cells in various behavioral test solutions indicated that the calmodulin antisense ODNs reduce the Ca(2+)-dependent Na+ current. Antisense ODNs, complementary either to the 5' start site or to an internal sequence of the calmodulin mRNA, were similarly effective in altering behavior. These results show that antisense ODNs may be utilized in ciliated protozoa as a tool for reducing the expression of specific gene products. In addition, Paramecium represents a powerful model system with which to study and develop antisense ODN technology.
Explore the source record for details and available documents.
The effect of dietary copper deficiency on tumour growth, neovascularisation and microvascular integrity was studied in the rat cremaster muscle. Male, weanling Sprague-Dawley rats were fed purified diets which were copper deficient (< 0.5 micrograms g-1 of diet) or copper adequate (5 micrograms g-1 of diet). Seven days after initiation of diets, a chondrosarcoma was implanted in the cremaster muscle of each rat. Five, 10 or 20 days after tumour implantation, rats were anesthetised and their cremasters prepared for observation by intravital microscopy. Intraarterial injection of fluorescein isothiocyanate-conjugated albumin and subsequent observation of fluorescence in the perivascular space indicated no difference in microvascular albumin leakage between the tumour vasculature of copper deficient and copper adequate rats. Neither tumour growth (assessed by wet weight), vascular density (assessed by light microscopy), nor any ultrastructural characteristics of the tumour or its vasculature (assessed by electron microscopy) were affected by copper deficiency. In view of findings by others which indicate changes in tumour characteristics with copper deficiency, we conclude that the copper dependency of tumour growth and vascularisation is a function of the type of tumour, the host tissue, or the conditions of copper depletion.
The effects of copper deficiency on smooth muscle relaxation were studied in the cremaster muscle microcirculation. Male Sprague-Dawley rats were fed either a copper-adequate diet (CuA, 5 micrograms copper/g diet) or copper-deficient diet (CuD, no added copper) for 17-27 d before experimentation. In vivo television microscopy was used to quantify agonist-induced diameter changes in third-order arterioles. Endothelium-dependent relaxation, which is hypothesized to be mediated by nitric oxide, was attenuated by copper deficiency. Both receptor (acetylcholine, 10(-7) to 10(-4) mol/L) and nonreceptor (calcium ionophore A23187, 10(-8) to 10(-7) mol/L) relaxation was decreased. Nitric oxide-mediated dilation, which was endothelium-independent (10(-7) to 10(-5) mol/L sodium nitroprusside), was also attenuated by copper deficiency. Maximal responses were as follows: for acetylcholine, 136 +/- 16% CuA vs. 45 +/- 15% CuD; for A23187, 104 +/- 16% CuA vs. 21 +/- 11% CuD; and for nitroprusside, 125 +/- 12% CuA vs. 46 +/- 13% CuD. There was no difference in microvascular dilation between groups treated with 10(-6) to 10(-4) mol/L of the phosphodiesterase inhibitor papaverine (e.g., CuA 109 +/- 11% vs. CuD 133 +/- 21% with 10(-4) mol/L). These results suggest that copper deficiency inhibits the nitric oxide-mediated mechanism of vascular smooth muscle relaxation without altering the capacity of the smooth muscle to relax. We suggest that copper deficiency either decreases nitric oxide radical availability or disrupts the nitric oxide-guanylate cyclase interaction.
Explore the source record for details and available documents.
A new simulator specifically designed for practising techniques in laparoscopic cholecystectomy is described. The simulator is inexpensive and utilises pig gallbladders. It allows a surgeon to practice without the need for assistance.
A procedure for immobilization of well-defined quantities of oligodeoxyribonucleotides (ODNs) to a versatile nylon support is described. The solid support, a nylon-6/6 bead, is covalently coated with poly(ethyleneimine) to provide a reactive spacer-arm for attachment of ODNs. 5'-Aminohexyl-tailed ODNs are selectively activated using 2,4,6-trichloro-1,3,5-triazine (cyanuric chloride) and then covalently attached to the bead via the triazine moiety. The modified nylon support has a low level of binding of nonspecific nucleic acid and efficiently captures both RNA and DNA targets.
Explore the source record for details and available documents.
Reduced bladder capacity is a major side effect for patients receiving photodynamic therapy (PDT) for bladder cancer. A rat bladder model has been developed to address both the vascular and tissue effects of the photodynamic treatment of the urinary bladder. Bladders were exteriorized and positioned in a plexiglass tissue bath. Effects on microvasculature were assessed during PDT of the bladder by recording luminal diameter changes in arterioles and venules. Animals receiving Photofrin II (10 mg kg-1) 30 min prior to PDT scored a statistically significant reduction in the diameter of the red blood cell column in the vessels, whereas administration of Photofrin II 48 h prior to PDT was ineffective. Morphological changes included significant endothelial and vascular myocyte damage in the 30 min PDT group alone. Among the other tissue components, the mucosal lining was minimally affected and the response of the muscularis was highly variable. Smooth muscle cell changes ranged from mild contraction to frank necrosis with many of the affected cells located near the altered vascular beds. These data suggest that the clinical symptoms of reduced bladder capacity can be accounted for by vascular damage and myocyte sensitivity. Further refinements in the Photofrin II and light doses used in therapy may reduce bladder complications and allow for better management of bladder cancer.
Dilatation of the veins of the broad ligament and ovarian plexi cause a very specific clinical entity called the pelvic congestion or pelvic pain syndrome. The ultrasound and Doppler appearances of this condition are unique and should be easily recognized. We describe these appearances in one patient and review the literature.
Microcirculatory shutdown appears to be of central importance in the mechanisms of action of photodynamic therapy (PDT). Traditionally 24-48 h are allowed between the administration of the photosensitizer and light to allow for tumor localization. However, previous studies have shown that the effects of PDT on the microcirculation are maximal soon after administration of the photosensitizer when serum levels are highest. This study involved the use of television video microscopy of the cremaster muscle microcirculation of male Sprague-Dawley rats to study the involvement of prostanoids in the effects of PDT on the microcirculation 30 min after administration of photofrin II. Pretreatment with topical indomethacin resulted in an altered response to PDT with arteriolar dilation and delay in vessel shutdown. The thromboxane A2 antagonist SQ29548 (100 mg/kg/min iv) resulted in a significant delay in platelet thrombus formation in arterioles and venules. These results indicate that prostanoids are involved in the mediation of the response of the normal microcirculation to PDT.