Distal radial fractures Injectable calcium phosphate bone cement versus conventional treatment

AMEDLINEsearchwasconductedtoidentifystudiespublishedfromJanuary1999toMarch2004thatcom-paredinjectablecalciumphosphatebone(NorianSRS)cementwithconventionaltreatmentindistalradialfrac-tures.Fromalistof13articlesidentifiedfromthesearchstrategy,fourarticleswe…     

钙剂治疗轻中度妊高征临床应用分析

目的：观察钙剂治疗轻中度妊高征的临床疗效。方法：选择2007年3月-2009年12朋我院产科门诊和住院的轻中度妊高征患者50例,随机分为治疗组和对照组,治疗组给予硝苯地平5-10mg＋碳酸钙、维生素D3合成制剂1片/d;对照组给予硝苯地平5-10mg/次,根据血压变化调整每天硝苯地平用药次数,观察血压、蛋白尿的平均水平,并对结果进行统计学分析。结果：两组患者治疗2周后,平均动脉压、尿蛋白下降,血清钙含量增加,治疗组有效率为92%,对照组为80%,两组疗效比较,差异有统计学意义（P〈0.05）。结论：硝苯地平常用于高血压的治疗,但副作用较大,常需频繁地调整药物剂量,患者尤其妊高征患者对药物的顺应性较差,钙剂几乎没有副作用发生,在联合硝苯地平治疗妊高征的同时为胎儿的发育需要提供了充足的钙源,故应将补充钙剂作为临床轻中度妊高征治疗的首选措施。     

噪声对耳蜗外淋巴中某些离子含量的影响

将１８只豚鼠分为１个对照组和２个暴露组，分别暴露于１１５ｄＢ（ＳＰＬ）、１２５ｄＢ（ＳＰＬ），１．５ｋＨｚ纯音０．５ｈ，以皮层听区诱发电位为检查指标，观察暴露前后动物听力的改变，并测定了耳蜗外淋巴中Ｎａ＋、Ｋ＋、Ｃａ２＋、Ｍｇ２＋离子含量的变化。结果表明，声暴露后各组动物听阈明显提高，且１２５ｄＢ组听力损失明显高于１１５ｄＢ组。１２５ｄＢ声暴露后，耳蜗外淋巴中Ｃａ２＋明显降低，而１１５ｄＢ组与正常对照组相比差异无显著性。声暴露对其它离子的含量没有影响。结果提示Ｃａ２＋可能与声损伤，特别是与永久性听力损失有关。     

HFE codon 63/282 (H63D/C282Y) dimorphism in German patients with genetic hemochromatosis

Abstract: Genetic hemochromatosis (GH) is closely associated with genes of the major histocompatibility complex (MHC) on chromosome 6. Recently, a candidate gene for GH, with structural similarities to MHC class I genes, designated HLA-H and presently named HFE, has been cloned. The HFE gene is localized telomeric to the MHC and several reports have indicated that the HFE gene is mutated in GH patients. In the present study we have analyzed the relationship of HFE gene variants and disease manifestation in GH patients and family members. Fifty-seven patients with GH, 73 family members and 153 healthy blood donors were studied for the amino acid dimorphism at codon 63 (His63Asp=H63D) and codon 282 (Cys282Tyr= C282Y) of the HFE gene. The codon 63 and 282 dimorphism were defined by PCR amplification of genomic DNA samples and restriction enzyme digestion using RsaI/SnaBI for C282Y and Bcll/Mbo 1 for H63D. Ferritin, transferrin serum levels and total iron-binding capacity were determined prior to therapeutic intervention. The Tyr-282 substitution occurred in 53 (93%) of patients compared with 8 (5.2%) of controls (OR=169, P >0.0001). Fifty-one (90%) patients were Tyr-282 homozygous. In contrast, the Asp-63 substitution was present in 5 (8.8%) of the patients compared with 34 (22%) of controls (OR=0.39, P =NS) with none of the patients being homozygous. In Tyr-282 homozygous GH patients serum ferritin levels, transferrin saturation, liver iron and liver iron index were elevated significantly compared to Tyr-282-negative patients, whereas no difference was observed between Tyr/Cys-282 heterozygous and Tyr-282-negative patients.     

Nicardipine improves motor tics

Calcium channel blockers can act on dopaminergic systems, and some reports suggest that they could be useful for the treatment of several movement disorders. In order to assess the efficacy of nicardipine in tics disorders we performed a prospective open non-controlled study which included 10 previously untreated patients. Our results suggest that nicardipine could be a useful and safe treatment for tics.     

Neurotransmitter release evoked by α-latrotoxin in the smooth muscle of the female pig urethra

Neuronal regulation of smooth muscle tone in the female pig urethra has mainly been studied in vitro using electrical field stimulation (EFS) of nerves. Excitatory control is considered to be exerted by released noradrenaline, whereas inhibitory control is non-adrenergic non-cholinergic (NANC), and mediated by nitric oxide (NO), and an as yet unidentified agent. We investigated the functional and morphological effects of α-latrotoxin (αLTX), a spider neurotoxin believed to cause massive release of vesicle-stored neurotransmitters, on spontaneously developed urethral smooth muscle tone. The effects were compared to those of EFS and high potassium. In the presence of the NO-synthesis inhibitor N^ω-nitro-L-arginine (L-NOARG: 0.3 mM) both αLTX and EFS evoked contractions. After treatment with scopolamine and phentolamine, no contraction was observed, and under these conditions αLTX and EFS induced relaxation. At low frequencies (<12 Hz), the EFS-induced relaxations were rapid, whereas at higher frequencies (>12 Hz), they were biphasic, consisting of a rapid first phase followed by a more long-lasting second phase. L-NOARG abolished the relaxations at low frequencies, as well as the first phase of the biphasic relaxation. The second phase was not affected by treatment with L-NOARG, but 0.1 μM ω-conotoxin GVIA, blocker of N-type voltage-operated calcium- channels (VOCCs), markedly reduced or abolished the response. In the presence of L-NOARG or ω-conotoxin GVIA, the αLTX-induced relaxation was significantly decreased, and the combination of L-NOARG and ω-conotoxin GVIA further reduced or abolished the relaxation. In preparationstreated with tetrodotoxin or scorpion venom, believed to inactivate nerves by acting on sodium channels, αLTX and EFS had no effects. αLTX-induced relaxation was not associated with changes in cyclic GMP or cyclic AMP content. High (80 mM) potassium solution induced a triphasic response of the preparation. A transient relaxation was followed by a restoration of tone, and then by a persistent relaxation. The persistent relaxation was slightly reduced by scorpion venom or L-NOARG, but reduced by 50% by a combination of L-NOARG and ω-conotoxin GVIA. Ultrastructural analysis of the urethral circular smooth muscle layer revealed a moderate amount of nerve profiles supplying the smooth muscle. In control preparations, the nerve profiles contained both small synaptic vesicles and large dense core vesicles. αLTX caused a major loss of both types of vesicle. The present data suggest that αLTX has the ability to release not only adrenergic and cholinergic transmitters, but also NANC mediators of relaxation, including NO, from nerve terminals in the urethra. Received: 13 January 1997 / Accepted: 17 April 1997     

Modulation of bone loss during calcium insufficiency by controlled dynamic loading

Summary Changes in the midshaft cross-sectional area of the ulna were measured in egg-laying turkeys on a diet insufficient in calcium. Left: right comparisons were used to assess the bone loss over a six-week period due to 1) calcium insufficiency, 2) calcium insufficiency plus disuse, and 3) calcium insufficiency and disuse interrupted by a short daily period of intermittent loading applied from an external device. Calcium insufficiency alone in the intact ulna resulted in a 15% reduction in cross-sectional area. In the functionally deprived bones this loss was increased to 32%. In bones where the disuse was interrupted by a single short daily period of loading, the degree of bone loss was significantly modified (P<0.006) to 25%. No significant difference in the modulating effect of loading was achieved by varying the peak strain from 0.0015 to 0.003, the strain rate from 0.01 to 0.05, or the duration of the single loading period from 100 sec per day to 25 minutes. All the loading regimes employed had been demonstrated to be osteogenic in mature male birds on a diet sufficient in calcium.     

Calcium entry blocker: Treatment in acute pain in cluster headache patients

15 chronic cluster headache patients in whom pain was induced by nitroglycerin received acute intravenous treatment with a calcium entry blocker. At the time of peak pain we noted a sudden decrease after the Verapamil injection. The mechanism by which the calcium entry blocker afforded relief is unlikely to have been vasodilatation in patients whose blood vessels had just been dilated by nitroglycerin. A more probable mechanism is blockade of the release of the pain-inducing neurotransmitters. The vasodilatation phase is not a primary factor in the onset of pain.

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Sommario Sono stati studiati 15 soggetti affetti da Cluster cronica inducendo loro la crisi dolorosa con Trinitrina, trattandoli poi con calcio antagonista (Verapamil) per via endovenosa. Al momento dell'apice del dolore, valutato dal paziente con un analogo visivo, la somministrazione di Verapamil endovena, determina una rapida estinzione del dolore. L'azione efficace del Ca-antagonista non può sicuramente essere rapportata alla vasodilatazione poiché la crisi dolorosa insorge già in una fase di vasodilatazione per l'azione della Trinitina. Il meccanismo d'azione più probabile è il blocco del release di neurotrasmettitori inducenti l'attacco doloroso. Si sottolinea che la vasodilatazione non è il fattore primario dell'induzione del dolore.