Localized wall thickening of the gallbladder mimicking a neoplasm

Clinical diagnosis of chronic cholecystitis is made based on diffuse hyperechoic thickening of the gallbladder wall as shown by ultrasonographic examination. We herein report three cases of chronic cholecystitis showing localized hypoechoic thickening of the gallbladder wall that mimicked gallbladder cancer by ultrasonography. Histologically, hypertrophy of the muscularis propria was a common characteristic finding in these three patients. A smooth surface of the inner hypoechoic layer of the thickened wall was considered to be a reliable finding in the differential diagnosis between this type of chronic cholecystitis and gallbladder cancer.     

Morphology of geniculocortical axons in turtles of the genera Pseudemys and Chrysemys

Summary An analysis has been made of the morphology of axons in the geniculocortical pathway of turtles using the anterograde transport of horseradish peroxidase in both in vivo and in vitro preparations. Following injections of HRP into the dorsolateral thalamus, labeled axons could be traced from the dorsal lateral geniculate complex to the telencephalon. They are unbranched and free of varicosities within the diencephalon. They travel in the dorsal peduncle of the lateral forebrain bundle, through the basal telencephalon and dorsally into the pallial thickening. Many axons are situated deep in the pallial thickening and bear numerous varicosities that often appear apposed to the proximal dendrites or somata of neurons retrogradely labeled by thalamic injections of horseradish peroxidase. Individual axons continue from the pallial thickening into the dorsal cortex where they shift dorsally and bear varicosities as they course from lateral to medial in the superficial third of layer 1. These data indicate that the terminal zone of the dorsal lateral geniculate complex within the telencephalon of turtles is more extensive in the mediolateral direction than previously believed. Geniculate axons bear varicosities both within the pallial thickening as well as the dorsal cortex, but have different relationships to potential postsynaptic elements in the two areas. Geniculocortical axons overlie somata and proximal dendrites of neurons in the pallial thickening, but intersect the distal dendrites of neurons in the dorsal cortex.     

Postextrasystolic potentiation does not distinguish ischaemic from stunned myocardium

Myocardial function is impaired by ischaemia, and it remains depressed during reperfusion following short periods of ischaemia (stunned myocardium). We tested whether ischaemic and reperfusion dysfunction, in particular the time course of its recovery, can be distinguished by postextrasystolic potentiation (PESP). In eight open-chest dogs, posterior systolic wall thickening (sonomicrometry) was reduced by graded occlusion of the left circumflex coronary artery (LCX) from 17.4±6.8% (SD) during control conditions to 10.7±1.3% (mild ischaemic dysfunction), 7.2±2.3% (moderate ischaemic dysfunction), 3.6±1.4% (severe ischaemic dysfunction), and -4.4±3.6% (complete coronary occlusion). Extrasystoles with constant prematurity and a fully compensated postextrasystolic interval were induced after at least 4 min steady-state ischaemia. After each ischaemic period full recovery of posterior systolic wall thickening was assured. During 8 h of reperfusion following a 15-min LCX occlusion, extrasystoles were induced when posterior systolic wall thickening was comparable to one degree of the preceding ischaemic dysfunction. The increases in posterior systolic wall thickening induced by PESP were 10.5±5.8% during control conditions, during ischaemia they were 11.5±3.5% (mild dysfunction), 12.3±4.6% (moderate dysfunction), 12.6±4.1% (severe dysfunction) and 10.4±4.4% (complete coronary occlusion), and during reperfusion they were 12.8±8.2% (severe dysfunction), 13.0±9.7% (moderate dysfunction) and 10.7±2.2% (mild dysfunction). These increments in systolic wall thickening as well as those in ejection thickening were not significantly different. PESP can thus not distinguish between ischaemic and reperfusion dysfunction nor between different degrees of myocardial dysfunction.This study was supported by the Deutsche Forschungsge-meinschaft (He 1320/3-2). cand. med. S. Schäfer was involved in some of these experiments and presented part of the data at the 56th Annual Meeting of the Deutsche Gesellschaft für Herz- und Kreislaufforschung in Mannheim (Z Kardiol 79 [Suppl 1]: 24,1990). Part of the data were also presented at the 11th Congress of the European Society of Cardiology in Nice (Eur Heart J 10 [Suppl]: 242, 1989) and at the 73rd Annual Meeting of the Federation of American Societies for Experimental Biology in New Orleans (FASEB J 3: A841, 1989)     

心肌多普勒组织显像与心肌增厚率相关分析

目的：研究脉冲多普勒组织显像评价室壁运动的可行性。方法：对19例研究对象左室基底段心肌进行脉冲多普勒组织显像并测量最大收缩速度及心肌收缩平均加速度和在同一部位的M-mode运动轨迹上测量心肌增厚率,对其进行相关回归分析。结果：心肌脉冲多普勒显像的最大收缩速度与M-Mode测量的心肌增厚率呈中度相关（r=0.55,P＜0.05),脉冲多普勒组织显像的心肌收缩平均加速度与M-mode的心肌增厚率呈中度相关（r=0.56,P＜0.05)。结论：脉冲多普勒组织显像显示的心肌最大收缩速度和心肌收缩平均加速度可作为评价室壁节段运动的指标。     

蛤蚧皮质加厚区的形态解剖及三维重建

目的明确蛤蚧皮质加厚区的位置、核团的形态及与比邻结构的关系,为研究皮质加厚区的功能提供依据。方法对蛤蚧脑行冷冻冠状连续切片(厚60μm),Nissl染色,对每张含有皮质加厚区的切片进行摄片和测量,选取其中1套用于三维重建,重组软件为3D MAX。结果1.皮质加厚区位于端脑吻侧端,前背侧室嵴外侧,外侧皮层内侧和背侧皮层腹侧。皮质加厚区的吻尾长(912.67±110.96)μm(n=10),体积(0.1430±0.0414)μm3(n=10)。2.皮质加厚区从吻侧端到尾侧端大约可分为前段、中段、后段和末段。后段的背腹径最长,可分为背侧部和腹侧部,两部分的细胞分界清晰。结论皮质加厚区为一吻尾径长于内外径的狭长片状结构,背侧缘较腹侧缘平滑;加厚区的尾侧端比吻侧端大,且尾端的后段分离成背侧和腹侧两个细胞群。     

Cytokines and fibrinolytic enzymes in tuberculous and parapneumonic effusions

Tuberculous (TB) pleurisy and parapneumonic effusion (PPE) are common causes of pleural fibrosis. The mechanisms underlying fibrin deposition may be different since involved inflammatory cells are distinct. In this study, we measured various cytokines and fibrinolytic enzymes and compared the differences between the two effusions. PPE was further divided into noncomplicated PPE and complicated PPE/empyema subgroups. Tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, macrophage inflammatory protein (MIP)-1beta, monocyte chemoattractant protein (MCP)-1, plasminogen activator inhibitor type 1 (PAI-1) and tissue type plasminogen activator (tPA) were measured using enzyme-linked immunosorbent assays. Significantly higher values of PAI-1, PAI-1/tPA ratio, IL-1beta, IL-8 and MIP-1beta and significantly lower values of TNF-alpha, IL-6 and MCP-1 were observed in PPE/empyema than in TB effusions. Compared to noncomplicated PPE, complicated PPE/empyema had significantly higher levels of TNF-alpha, IL-1beta, IL-8 and MIP-1beta. TB pleurisy patients who had higher effusion levels of TNF-alpha, IL-1beta and IL-8 were predisposing to residual pleural thickening. The underlying mechanisms of fibrin formation and deposition between the two effusions studied (PPE/empyema and TB pleurisy) could not be fully explained by the results of the present study. More studies are needed to explore this further.     

Suppression of neointimal thickening by a newly developed HMG-CoA reductase inhibitor,BAYw6228, and its inhibitory effect on vascular smooth muscle cell growth

1. The aim of this study was to determine whether BAYw6228 (BAYw), a newly developed 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitor, could suppress an atherogenic process such as intimal thickening by a mechanism other than lowering the level of serum cholesterol.
2. First, we evaluated the in vitro effect of BAYw on the proliferation of vascular smooth muscle cells (SMC) from various species: Sprague-Dawley (SD) rats, New Zealand (NZ) white rabbits, intimal cells from Watanabe hereditary hyperlipidemic (WHHL) rabbit and SMC from the new-born human aorta. The increasing rate of total protein content of these cells was inhibited by the addition of BAYw in a dose-dependent fashion. In the presence of 2% foetal calf serum (FCS), the value of IC₅₀ was 1.0 μM in SD rats. 2.1 μM in NZ white rabbits, and 0.3 μM in WHHL rabbits. With human SMC, the value was 0.02 μM in the presence of 10% FCS and 0.2 μM with a mixture of growth factors.
3. Based on these above in vitro findings, we next examined the in vivo effect of the agent to determine whether it could suppress rabbit intimal thickening induced by balloon catheterization. A balloon catheter was inserted from a peripheral branch of the left external carotid artery to the aorta to denude the endothelium of the left common carotid artery in Japanese white rabbits. After 12 days they were divided into control and BAYw groups. The former were subcutaneously injected with saline and the latter with BAYw 1 mg kg⁻¹ day⁻¹. Two days after the beginning of treatment, a second balloon injury was performed to the previously injured left common carotid artery in both groups. After another two weeks, the left common carotid artery was removed and variously stained. Although the total serum cholesterol in the BAYw group was significantly lower than in the control (P<0.05), the difference was not enough to affect intimal thickening. In addition, the BAYw group had a smaller intima/media ratio than the control group, decreasing to 45% of control (P<0.05). By anti-α smooth muscle actin antibody staining, these intimal thickening areas were entirely occupied by SMCs, and their amount was attenuated by BAYw. By anti-rabbit macrophage antibody (RAM 11) staining, the number of positive cells in the intimal thickening was markedly decreased in the BAYw group compared to control (P<0.01).
4. These results indicate that BAYw has an inhibitory effect on intimal thickening by attenuating intimal SMC proliferation and infiltration of macrophages, suggesting that BAYw could be effective in the prevention of the progression of atherosclerotic plaque-like restenosis after angioplasty.

     

Evaluation of regional haemodynamics and alterations of vascular wall of the lower limbs in hypertensive subjects

This study was designed to analyse the relationship betweenarterial hypertension and changes in arterial blood flow andvascular wall damage of the lower limbs in hypertensive patientswith various degrees of hypertension. Six hundred and fifty-four hypertensive patients (421 malesand 233 females) aged 35 to 70 years and 88 healthy subjects(63 males and 25 females) aged 39 to 60 years were studied.Strain-gauge plethysmography of the lower limbs was used tocalculate arterial calf blood flow (RF), arterial calf bloodflow after post-ischaemic hyperaemia (PF), basal and minimalvascular resistances (BVR and MVR), time to reach peak flow(tPF), time until 50% reduction of peak flow (tT) and totalrecovery time (tT). In 108 (67 males and 41 females) of the hypertensive patients,a morphological study by echo-Doppler duplex scanning of thepopliteal artery was performed to measure medial-intimal thickeningand popliteal lumen diameter. Our results indicate that regional haemodynamics of the lowerlimbs worsened in hypertensives in comparison with control subjects.In addition, the change in peripheral haemodynamics was relatedto the degree of hypertension. Moreover, medial-intimal thickeningwas significantly (P<0.05) higher in severe hypertensivesthan mild hypertensives. Popliteal lumen diameter was significantly(P<0.05) lower in severe hypertensives than moderate andmild hypertensives. In all these subjects mean blood pressurewas correlated directly (r=0.31; P<0.001) with medial-intimalthickening and inversely (r= – 0.37; P<0.001) withpopliteal lumen diameter. Multiple regression analysis indicatedthat mean blood pressure, age and serum cholesterol were independentlycorrelated to medial-intimal thickening. This relationship wasnot influenced by the diabetic patients and smokers among thegroups. Our results indicate that hypertension impairs peripheral flowand encourages the development of medial-intimal thickening.     

Penile elongation and thickening—a myth? Is there a cosmetic or medical indication?

Penile lengthening and thickening techniques can be performed in different ways for treatment of congenital penile hypoplasia and dysmorphophobia in terms of aesthetics or function. Particularly for penile lengthening, a combination of surgery and stretcher device is suggested. Surgery for lengthening comprises three different stages: suture with plane alternating edges of the pubo-penile skin, infrapubic lipectomy, and section of the suspensory ligament. Our approach to penile thickening differs depending on whether dysmorphophobia is related to aesthetics or function. While pericavernosal apposition of autografts is suggested in the first case, a technique developed by the authors is performed in the latter, which comprises bilateral longitudinal incision of the corpora cavernosa and enlargement of the tunica albuginea by means of saphenous grafts. The endothelial lining, which constitutes the internal surface of the veins, is highly compatible with the endothelium of the corpora cavernosa; therefore, the incidence of postoperative subareolar fibrosis and occlusive vein pathology is lower than after surgery performed with techniques using grafts of other material. The described procedure did not cause postoperative complications in terms of infection, wound healing and cosmetic appearance. All subjects resumed regular sexual activity after 4 months without any disturbance or functional limitation. Diametrical measurements at the 9-month follow-up revealed an increase of 1.1-2.1 cm. The reliability and efficiency of these procedures are strongly influenced by factors other than technical problems; however, expert diagnosis and psychological consultation in the case of dysmorphophobia will confirm and specify the indications.     

COX基因多态性与缺血性卒中的相关性研究

【摘要】 目的 探讨环氧合酶(COX)代谢通路基因多态性及其与缺血性卒中发病率的关系。方法 将2013年2月~2015年11月在德阳市人民医院和温州医科大学第三附属医院神经内科住院经头颅CT和MRI检查确诊的299例急性缺血性卒中患者,根据彩超结果分为颈动脉易损斑块组（VP）94例、稳定斑块组（SP）74例和无斑块组（NP）131例;同时再分为颈动脉内膜增厚组（IT）108例和非内膜增厚组（NT）191例。使用聚合酶链反应和质谱分析测定基因多态性,包括前列腺素合酶1(PTGS1 rs1236913)、前列腺素H合酶2(PTGS2 rs689466)、血栓素A2合酶(TBXAS1 rs2267679、rs41708、rs194149)、前列腺素E合酶(PTGES2 rs6478818)、环前列腺素合成酶(PTGIS rs5602、rs5629)。结果 在易损斑块组和无斑块组之间TBXAS1 rs194149 GG基因型(P=00281),PTGIS rs5602 CT基因型(P=00319)存在显著差异。内膜增厚组和非内膜增厚组之间PTGS2 rs689466 GG基因型(P=00216)显示显著差异。多元回归分析显示,PTGIS的AA基因型(P=00308,OR:0275,95%CI:0079～0955)和PTGS2的AG+ GG基因型(P=00065,OR:2162,95%CI:1232～3795)是内膜增厚的破坏性因素。结论 COX的单核苷酸多态性(SNP)与脑梗死的发病率存在相关性,PTGIS和PTGS2基因多态性与内膜增厚脑卒中患者相关。