Effects of nerve compression on fast axonal transport in streptozotocin-induced diabetes mellitus

Summary The hypothesis that nerves in diabetes mellitus exhibit an increased susceptibility to compression was experimentally tested. Inhibition of fast axonal transport was induced by local compression in sciatic nerves of rats with streptozotocin-induced diabetes mellitus. Fast anterograde axonal transport was measured after application of³H-leucine to the motor neurone cell bodies in the spinal cord. The sciatic nerve as subjected to local, graded compression in vivo by a small compression chamber. The amount of accumulation of proteins was quantified by calculation of a transport block ratio. Compression at 30 mm Hg for 3 h induced a significantly greater (p<0.05) accumulation of axonally transported proteins at the site of compression in nerves of diabetic animals (transport block ratio: 1.01±0.35; n=7) than in nerves of controls (0.67±0.16;n=7). Accumulation was significantly higher in ligature experiments of both control (1.34±0.44;n=8;p< 0.01) and diabetic animals (1.45±0.30;n=8 ;p< 0.05), indicating that the block of transport in compressed nerves was incomplete. Neither sham compressed diabetic (0.50±0.09;n=6) nor control (0.49±0.11;n=6) nerves showed any block of axonal transport. The possible causes of the increased inhibition of fast axonal transport in diabetic rats are discussed. The results indicate that diabetes may lead to an increased susceptibility of peripheral nerves to compression.     

The COVID PIVOT – Re-orienting Child and Youth Mental Health Care in the Light of Pandemic Restrictions

Psychiatric Quarterly - The COVID pandemic required significant changes in the provision of youth mental health services during the period of lockdown/stay at home orders. Things which were...     

Mutations in protein N-arginine methyltransferases are not the cause of FTLD-FUS

The nuclear protein fused in sarcoma (FUS) is found in cytoplasmic inclusions in a subset of patients with the neurodegenerative disorder frontotemporal lobar degeneration (FTLD-FUS). FUS contains a methylated arginine–glycine–glycine domain that is required for transport into the nucleus. Recent findings have shown that this domain is hypomethylated in patients with FTLD-FUS. To determine whether the cause of hypomethylation is the result of mutations in protein N-arginine methyltransferases (PRMTs), we selected 3 candidate genes (PRMT1, PRMT3, and PRMT8) and performed complete sequencing analysis and real-time polymerase chain reaction mRNA expression analysis in 20 FTLD-FUS cases. No mutations or statistically significant changes in expression were observed in our patient samples, suggesting that defects in PRMTs are not the cause of FTLD-FUS.     

Angioplasty Guidewire Velocity: A New Simple Method to Calculate Absolute Coronary Blood Velocity and Flow

The Thrombolysis In Myocardial Infarction (TIMI) frame count is a relative index of coronary flow that measures time by counting the number of frames required for dye to travel from the ostium to a standardized coronary landmark in a cineangiogram filmed at a known speed (frames/s). We describe a new method to measure distance along arteries so that absolute velocity (length ÷ time) and absolute flow (area × velocity) may be calculated in patients undergoing percutaneous transluminal coronary angiography (PTCA). After PTCA, the guidewire tip is placed at the coronary landmark and a Kelly clamp is placed on the guidewire where it exits the Y-adapter. The guidewire tip is then withdrawn to the catheter tip and a second Kelly clamp is placed on the wire where it exits the Y-adapter. The distance between the 2 Kelly clamps outside the body is the distance between the catheter tip and the anatomic landmark inside the body. Velocity (cm/s) may be calculated as this distance (cm) ÷ TIMI frame count (frames) × film frame speed (frames/s). Flow (ml/s) may be calculated by multiplying this velocity (cm/s) and the mean cross-sectional lumen area (cm²) along the length of the artery to the TIMI landmark. In 30 patients, velocity increased from 13.9 ± 8.5 cm/s before to 22.8 ± 9.3 cm/s after PTCA (p <0.001). Despite TIMI grade 3 flow both before and after PTCA in 18 patients, velocity actually increased 38%, from 17.0 ± 5.4 to 23.5 ± 9.0 cm/s (p = 0.01). For all 30 patients, flow doubled from 0.6 ± 0.4 ml/s before to 1.2 ± 0.6 ml/s after PTCA (p <0.001). In the 18 patients with TIMI grade 3 flow both before and after PTCA, flow increased 86%, from 0.7 ± 0.3 to 1.3 ± 0.6 ml/s (p = 0.001). Distance along coronary arteries (length) can be simply measured using a PTCA guidewire. This length may be combined with the TIMI frame count to calculate measures of absolute velocity and flow that are sensitive to changes in perfusion. TIMI grade 3 flow is composed of a range of velocities and flows.     

Postoperative hemorrhage

Summary The mechanism of clotting and its concomitant anticoagulant reaction is considered. Tests for the detection of bleeding tendencies are recommended. Coagulation defects in disease conditions of interest to the proctologist are discussed. Read at the meeting of the American Proctologic Society, Atlantic City, New Jersey, June 15 to 17, 1959.