改良内侧上颌骨切除术治疗21例鼻息肉病

目的:探讨鼻息肉病的可行性手术方法,以提高治疗效果。方法:21例鼻息肉病患者一侧行唇龈沟径路,保留下鼻甲的改良内侧上颌骨切除术(modifiedmedialmaxillectomy,MMM);另侧行单纯鼻息肉摘除和鼻内筛窦切除术,并作为对照组。结果:术后随访12～34个月,平均20个月;改良内侧上颌骨切除术侧未见复发,另侧复发6例,两组复发率差异有显著性(P<0.05)。结论:改良内侧上颌骨切除术使鼻息肉病患者术后复发率显著降低,治疗效果显著,是一种可供选择的有效的治疗手段。     

尿毒症患者的性激素变化及其临床意义探讨

目的 :探讨女性尿毒症患者卵巢功能障碍的发病情况及其临床意义。方法 :应用酶免疫法 (EIA)测定了2 3例更年期前女性尿毒症非透析患者、15例透析患者及 2 9例健康献血者中促卵泡素 (FSH)、泌乳素 (PRL)、促黄体素 (LH)、雌二醇 (E2 )及孕酮 (P)的水平。结果 :尿毒症女患者PRL、FSH及LH均较健康对照组升高 ,而孕酮值显著降低 ,对此均有显著差异 ;且尿毒症女患者PRL升高、孕酮值降低与肾小球滤过率 (GFR)呈明显相关。透析患者较非透析患者PRL升高更为明显 ,孕酮值亦较非透析患者有所升高 ,但无显著意义。结论 :尿毒症女患者的排卵障碍及月经紊乱等都与尿毒症的严重程度相平行。透析并不能改善尿毒症女患者的卵巢功能障碍 ,只有纠正与改善肾功能 ,才能使尿毒症女患者的卵巢功能得以改善     

Ca^＋＋对链霉素抗原—抗体反应的抑制作用

为探讨临床中使用钙制剂抢救链霉素过敏休克病人有良好效果的原因,由被动血凝试验、被动皮肤过敏试验和ELISA法证实,Ca~( )可以抑制链霉素抗原-抗体的反应。这种抑制作用是通过Ca~( )链霉素抗原结合,封闭链霉素抗原决定簇来加以实现的。     

Localization of dystonic muscles with 18F-FDG PET/CT in idiopathic cervical dystonia.

The purpose of this study was to investigate whether (18)F-FDG PET/CT is useful for localizing dystonic cervical muscles in patients with idiopathic cervical dystonia (ICD) by comparing disease severity before and disease severity after botulinum toxin (BT) injection into hypermetabolic muscles. METHODS: Six patients with ICD underwent (18)F-FDG PET/CT. Dystonic muscles suitable for BT injection therapy were defined as those showing diffusely increased (18)F-FDG uptake. RESULTS: Hypermetabolic cervical muscles were identified in all 6 patients. In 2 patients who underwent PET/CT both in a supine position and in a sitting position during (18)F-FDG uptake, abnormal hypermetabolic muscles were observed by PET/CT only when patients were in the sitting position with their heads and necks in the adopted abnormal involuntary posture. Symptoms were significantly improved in 4 patients who underwent BT injection therapy guided by PET/CT and who were clinically monitored. CONCLUSION: (18)F-FDG PET/CT is potentially useful for identifying dystonic cervical muscles for BT therapy in patients with ICD.     

宋《本草图经》草木部所述植物药主要产地及药材集散地考略

1 宋代社会经济、医事制度与历史地理 1.1 宋代的社会经济 宋朝是我国历史上继唐朝之后,社会经济发展、科技文化进步的一个历史时期,后世有"治隆唐宋"之说.公元960年陈桥兵变,赵匡胤(宋太祖)"黄袍加身"以后,遂代周而自立,是为宋朝,史称北宋.当时的社会在经历了五代十国的战乱之后而趋于安定,经济逐渐恢复,科学也日益发达.     

The effects of chymase on matrix metalloproteinase-2 activation in neointimal hyperplasia after balloon injury in dogs.

Chymase is known to generate angiotensin II in the vascular wall. In this study we investigated a novel role for chymase other than angiotensin II production in vascular proliferation after balloon injury. Chymase promoted the migration of vascular smooth muscle cells in the matrix-coated invasion chambers and activated promatrix metalloproteinase-2 obtained from the culture medium of vascular smooth muscle cells. Two weeks after balloon injury, significant neointimal formation was found in dog carotid arteries. After injury, active matrix metalloproteinase-2 was increased in parallel with the augmentation of chymase activity that was seen in the proliferating region of the vascular wall. The oral administration of NK3201 (1 mg/kg per day), a chymase inhibitor, prevented neointimal formation and significantly suppressed both active matrix metalloproteinase-2 and chymase activities 2 weeks after injury. These results suggest that chymase inhibitors can prevent the development of intimal hyperplasia via the inhibition of matrix metalloproteinase-2 activation in balloon-injured arteries.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.     

Association of the GNAS1 gene variant with hypertension is dependent on alcohol consumption.

The beta-adrenoceptor (beta-AR)-stimulatory guanine nucleotide-binding (Gs) protein system has been shown to play important roles in the cardiovascular system. The gene encoding the alpha-subunit of Gs proteins (GNAS1) is a candidate genetic determinant for hypertension. Because alcohol consumption is known to affect blood pressure partly through the beta-AR-Gs protein system, we examined the possible interaction between GNAS1 T393C polymorphism and drinking status in the association with hypertension in the present study. As a result, a non-significant but reasonable trend supporting the presence of an interaction was shown (p = 0.076). In line with this trend, the T393C polymorphism significantly interacted with drinking status in the association with systolic blood pressure (p = 0.028). Moreover, supporting the presence of an interaction, T allele carriers consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than CC homozygotes in non-drinkers and light drinkers. In contrast, CC homozygotes consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than T allele carriers in moderate to heavy drinkers. The present study also showed a significant interaction between the T393C polymorphism and drinking status in the association with pulse pressure (p = 0.026), reflected by a significant association between the T393C polymorphism and pulse pressure in moderate to heavy drinkers (p = 0.026). These findings may be helpful in conducting further molecular and biological studies on the relationship among the effects of alcohol, the beta-AR-Gs protein system, and hypertension.