Cranial subdural haematoma after spinal anaesthesia

Intracranial subdural haematoma is an exceptionally rare complicationof spinal anaesthesia. A 20-yr-old male underwent appendicectomyunder partial spinal and subsequent general anaesthesia. A weeklater, he presented with severe headache and vomiting not respondingto bed rest and analgesia. Magnetic resonance imaging showeda small acute subdural haematoma in the right temporo-occipitalregion. The patient improved without surgical decompression.The pathogenesis of headache and subdural haematoma formationafter dural puncture is discussed and the literature brieflyreviewed. Severe and prolonged post-dural puncture headacheshould be regarded as a warning sign of an intracranial complication. Br J Anaesth 2001; 86: 893–5     

Retention of ovaries and oxidative stress of surgery.

OBJECTIVE: Surgical menopause results in severe menopausal symptoms due to the sudden withdrawal of estrogen. This study evaluated the impact of surgical menopause on oxidant and antioxidant status. METHODS: Thirty eight women who underwent total hysterectomy with or without bilateral salpingo-oophorectomy were included. Oxidant status was assessed by measuring plasma levels of malondialdehyde (MDA) and antioxidant status by assessing glutathione (GSH) and estrogen levels. RESULTS: The levels of MDA were increased in all women, and GSH levels were significantly decreased in women who underwent hysterectomy alone but significantly increased in those who also had oophorectomy. Estrogen levels were increased if the ovaries were retained even in postmenopausal women, while they were decreased in the women who underwent oophorectomy. CONCLUSION: Oxidative stress of surgery, as assessed by increased MDA levels, occurred in all women. After oophorectomy, estrogen levels decreased and GSH levels increased in both premenopausal and postmenopausal women. The ovaries may therefore respond to oxidative stress of surgery by increasing estrogen production, estrogen being a better antioxidant than GSH.     

Familial Reactive Perforating Collagenosis in a Child: Response to Narrow‐Band UVB

Abstract: A favorable response to narrow‐band ultraviolet B light treatment, a novel option, is illustrated in familial reactive perforating collagenosis, and its use is recommended. Its probable mode of action is outlined.     

Inhibition of growth factor-dependent inositol phosphate Ca2+ signaling by antitumor ether lipid analogues

Cytotoxic ether lipid analogues have been studied for their ability to inhibit growth factor-dependent [Ca2+]i signaling in Swiss 3T3 fibroblasts. 1-Octadecyl-2-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) inhibited 45Ca2+ uptake and inositol(1,4,5)trisphosphate-induced 45Ca2+ release in saponin permeabilized cells with concentration producing 50% inhibition values of 55 and 360 microM, respectively. When cells were exposed to ET-18-OCH3 for 18 h before permeabilization there was selective inhibition of inositol(1,4,5)trisphosphate-induced 45Ca2+ release with a concentration producing 50% inhibition value of 20 microM, but no effect on 45Ca2+ uptake, or on 45Ca2+ release by arachidonic acid. The concentration of ET-18-OCH3 with continuous exposure to inhibit cell growth 50% was 19 microM. The ether lipid analogues 1-hexadecylthio-2-ethyl-rac-glycero-3- phosphocholine and 1-S-octadecyl-2-O-methylthiopropyl-3-N,N-dimethyl-gamma-hydroxy pro pyl ammonium iodide had effects similar to those of ET-18-OCH3 but the noncytotoxic analogue 1-alkyl-2-hydroxy-sn-glycero-3- phosphocholine was without effect. Exposure of cells to 10 microM ET-18-OCH3 produced 81% inhibition of platelet-derived growth factor-stimulated inositol phosphate formation and 66% inhibition of fluoroaluminate anion-stimulated inositol phosphate formation. Addition of ET-18-OCH3 to cells in medium with 10% fetal calf serum gave a transient increase in [Ca2+]i without causing an increase in resting [Ca2+]i, while the addition of ET-18-OCH3 to cells in medium without serum gave a sustained increase in resting [Ca2+]i. Cells exposed to 5 microM ET-18-OCH3 for 18 h showed no increase in resting [Ca2+]i but there was 95% inhibition of the [Ca2+]i response to platelet-derived growth factor, 63% inhibition of the response to bradykinin, and 55% inhibition of the response to vasopressin. The block by ether lipid analogues of inositol phosphate-mediated [Ca2+]i signaling suggests a mechanism for preventing the action of growth factors that could contribute to the inhibition of cell proliferation by the agents.