Zoledronic acid

Gorham-Stout disease is a rare bone resorption disease, the etiology and prognosis of which is uncertain but it is thought to be benign. It can involve one or more bones and can cause pain, swelling, deformity and fractures in affected bones. Diagnosis is made with a combination of clinical, radiological and histopathological examinations once other causes of osteolysis have been excluded. Due to its rarity, there is no standard therapeutic approach.     

棕榈酸及亚油酸对人成骨肉瘤细胞MG63作用的研究

目的探讨棕榈酸及亚油酸对人成骨肉瘤细胞MG63的作用。方法取对数生长期的MG63细胞分5组进行干预,分别是：①对照（CON）组;②棕榈酸1.0×10^-4mol·L^-1组;③棕榈酸5.0×10^-4mol·L^-1组;④棕榈酸10.0×10^-4mol·L^-1组;⑤棕榈酸5.0×10^-4mol·L^-1＋亚油酸1.0×10^-5mol·L^-1组。干预24h后用AO/PI荧光双染和TUNEL法观察细胞凋亡的形态学改变;用Annexin-V/FITC流式细胞技术检测早期细胞凋亡;用单细胞凝胶电泳评估细胞损伤和凋亡情况。结果随着棕榈酸浓度的增加,细胞凋亡比例增加,呈浓度梯度效应。棕榈酸组细胞凋亡百分比明显高于对照组及同时给予亚油酸组（P均〈0.05）。结论棕榈酸能引起成MG63细胞凋亡,亚油酸则对其有保护作用。     

Uric acid nephrolithiasis

Uric acid nephrolithiasis may be the final manifestation of various pathophysiological processes. Recent advances in renal urate transport have elucidated mechanisms by which hyperuricosuria occurs. However, in most uric acid stone formers the primary pathophysiologic defect is an excessively acidic urine pH rather than hyperuricosuria. Insulin resistance may contribute to the development of acidic urine by augmenting endogenous acid production and decreasing renal ammonium excretion. Medical management strategies focus primarily on alkali treatment or decreasing hyperuricosuria.     

Hydrofluoric acid burns

OBJECTIVE: The purpose of this article is to report our experience with hydrofluoric acid (HF) burns and to present our management guidelines for these burns, which include a novel way of delivering calcium combined with dimethyl sulphoxide (DMSO) for cutaneous burns. METHOD: We reviewed our institutional experience from 1977 to 1999 for patients presenting with burns caused by hydrofluoric acid and collected data on age, sex, burn size, anatomical site, method of contact, surgical procedure, and outcome. RESULTS: Of a total of 2310 admissions, 42 HF burns patients were identified during the study period. The average age was 34 years. There were 35 males and 7 females. Seventy-four percent of cases received burns to the upper limb. Median burn size was 1% of the total body surface area. Seventeen percent of patients required a surgical procedure. In 24% of cases, the method of contact was work related and 40% were injured using cleaning products at home or on boats. No deaths were recorded. CONCLUSION: HF injury is uncommon but problematic burns often requiring surgery. RECOMMENDED MANAGEMENT: In cases of cutaneous exposure, treatment should commence immediately with 30 min lavage followed by application dimethyl sulphoxide 50% + calcium gluconate 10% in surgical jelly. If hand or forearm is affected, regional intravenous calcium 'Bier's block' using 40 ml 10% calcium gluconate with 5000 U heparin in total final volume of 40 ml may be indicated. Subcutaneous infiltration may be indicated for elsewhere at 0.5 ml/cm(2) burn of 10% calcium gluconate. Persisting pain may require nail removal or arterial calcium infusion.     

gamma-Aminobutyric acid and gastric acid secretion: a physiologic role?

The purpose of this study was to examine the effect of endogenous brain GABA levels or GABAergic tone on gastric acid secretion. Experiments were performed with Sprague-Dawley rats under urethane anesthesia. Continuous acid secretion was measured in vivo using a gastric luminal perfusion system. Initial experiments studied the effects on basal acid secretion of (aminooxy)acetic acid (AOAA), a substance which increases brain GABA levels, and flumazenil, a substance which decreases central GABAergic neurotransmission. After basal acid secretion was measured for 30 min, AOAA (15 mg/kg), flumazenil (10 mg/kg), or saline was given by intravenous infusion and acid secretion was measured for 120 min. There was no significant difference in acid secretion between groups (n = 8/group). A second series of experiments measured the effects of AOAA, flumazenil, or saline on gastric secretion during submaximal stimulation by bethanechol (180 micrograms/kg/hr) in normal and vagotomized rats. Total acid secretions (mean +/- SE) after saline, AOAA, or flumazenil were 78.7 +/- 11.8, 51.0 +/- 5.9, and 109.3 +/- 1.5 mumole/90 min, respectively (P less than 0.01). In vagotomized rats, there were no significant differences in rates of acid secretion between groups. In summary, GABAergic tone did not effect basal acid secretion in anesthetized rats. However, during submaximal acid secretion, acid secretion decreased when brain GABA levels increased, and acid secretion increased when GABAergic neurotransmission was inhibited. We conclude that endogenous brain GABA levels may effect gastric acid secretion in rats, perhaps via inhibition of central-vagal tone.