Pathology of a new Toxic Syndrome caused by ingestion of adulterated oil in Spain

Summary The Toxic Syndrome (TS) caused by ingestion of adulterated rapeseed oil in Spain is a new disease of multisystemic character whose aetiology and pathogenesis remains unknown. The most prominent pathological feature is a peculiar non-necrotizing vasculitis, that affects mainly the intima and involves vessels of every type and size in practically every organ. The TS begins with an acute clinical picture with pleuropneumopathy, fever, headaches, exanthems and eosinophilia. In these early clinical phases the main pathological findings were observed in the lungs and consisted of intense pulmonary interstitial oedema with scanty inflammatory mononuclear infiltrates. Ultrastructural study revealed hydropic degeneration of pneumocytes types I and II with desquamation of type I. The patients in this phase died of respiratory failure, later deaths were due to thromboembolic complications. Later still the patients developped a neuromuscular syndrome, sclerodermiform skin lesions and severe weight loss and died predominantly of infectious complications and respiratory failure. The anatomopathological picture in the peripheral nerves was that of inflammatory neuropathy with a lymphocytic perineuritis that led to perineural fibrosis with secondary axonal degeneration. The muscle presented an interstitial inflammatory myopathy at first followed by a neurogenic muscular atrophy. The skin lesions in the late phases consisted in dermal or dermal and subdermal fibrosclerosis, with vasculitis of the small arteries in the lower dermis. The salivary glands and pancreas showed vasculitis and interstitial inflammation which progressed to interstitial fibrosis and parenchymal atrophy.     

碘化钠对人甲状腺上皮细胞TNF-α、IL-1β分泌的影响

为研究碘化钠 (NaI)对人甲状腺上皮细胞 (TEC )分泌细胞因子TNF α和IL 1β的影响 ,以探讨碘在GD病 (GD )发病中的可能机制 ,取手术切除的GD病患者甲状腺组织和甲状腺腺瘤患者瘤旁正常甲状腺组织 ,进行细胞培养。以不同浓度的NaI (10 8～ 10 3 mol/L )刺激单层培养的甲状腺细胞 ,采用放射免疫测定技术测定刺激前后甲状腺细胞培养上清液中细胞因子TNF α和IL 1β的含量。同时以透射电镜观察NaI刺激后甲状腺细胞的形态学改变。结果 :(1)正常甲状腺细胞能分泌少量的TNF α和IL 1β。GD的甲状腺细胞TNF α和IL 1β的分泌量与正常TEC相比显著增加 (P <0 0 1) ;(2 )当NaI浓度为 10 8～10 3 mol/L时 ,正常人甲状腺细胞TNF α、IL 1β的分泌量与 0mol/L组相比无显著性差异 (P >0 0 5 ) ;透射电镜示正常甲状腺细胞无损伤型改变 ;(3)当NaI浓度为 10 6～ 10 3 mol/L时 ,GD甲状腺细胞TNF α的分泌量显著增加 (P <0 0 5 ) ;当NaI浓度为 10 8～ 10 3 mol/L时 ,GD甲状腺细胞IL 1β的分泌量显著增加 (P <0 0 5 )。NaI浓度超过 10 6mol/L时 ,透射电镜示GD甲状腺细胞出现损伤型改变。表明高浓度的碘不仅造成GD甲状腺细胞的直接损伤 ,而且可以增加甲状腺细胞细胞因子TNF α和IL 1β的分泌 ,特别是在GD甲状腺细     

中医药对糖尿病足溃疡相关细胞因子调控作用的研究进展

糖尿病足溃疡是糖尿病严重的破坏性并发症,致残率及致死率逐年增高,严重威胁人类身心健康。中医药治疗糖尿病足溃疡,注重辨证论治与整体观念相结合,不仅能改善中医证候,更能在加速创面愈合的同时减少创面的复发,一定程度上延缓了糖尿病足溃疡的进一步恶化,降低其致残率及致死率。现代研究发现,糖尿病足溃疡难以愈合与各种细胞因子如炎症因子、生长因子、趋化因子等分布异常密切相关;随着现代医学对中医药研究的不断深入,中药单体及复方调控细胞因子治疗糖尿病足溃疡已成为研究热点,该文通过对目前国内外研究现状进行归纳,得出以下总结：(1)芝麻酚、栀子苷、当归补血汤、紫朱软膏等调节肿瘤坏死因子-α(TNF-α)、白细胞介素（IL）-1、IL-6、IL-10等炎症因子,抑制创面炎症。(2)白芷、丹酚酸B、四效散、壮药拔毒生肌膏等调节血管内皮生长因子（VEGF）、血小板衍生生长因子（PDGF）、转化生长因子（TGF）、表皮生长因子（EGF）等生长因子,促进创面胶原沉积及血管新生。(3)芍药苷、隐丹参酮、蜂毒、回阳生肌汤等调节CXC趋化因子配体（CXCL）1、CXCL2、CC趋化因子配体（CCL）2、CCL3、基质细胞衍生...     

术前孤立性CRP升高与体外循环术后并发症的相关性

目的探讨无感染的、术前孤立性C-反应蛋白(CRP)增加,对于体外循环心脏术后的结果,是否有预测性价值。方法分术前孤立性CRP升高(10.5～70.2mg／L)50例(A组)与CRP正常(＜10mg／L)50例对照(B组),B组匹配A组在年龄、性别和疾病种类,两组均进行体外循环心脏手术。结果A组脓毒性并发症(20％)比对照组(2％)多(P＜0.01)。这些病人微生物学阳性仅10％。A组中需要儿茶酚胺支持的占28％,而B组仅12％(P＜0.05)。A组较B组术后需呼吸机支持的时间明显延长(25.2±6.2h比6.6±0.5h)(P＜0.01)、ICU滞留时间也较B组长(4.6±0.8d比2.6±0.3d)(P＜0.05)。结论术前孤立性CRP升高的病人,体外循环术后,发生脓毒性并发症的可能性明显增加。且大多数病例微生物学实验阴性,推测大多数脓毒性并发症是由于全身炎症反应综合征的原因。     

Clinical significance and assessment of cytokines in various stages of ulcerative colitis

Summary In order to study the clinical significance and change of interleukin (IL)-1β and IL-10 concentration in intestinal mucosal tissues in various stage of ulcerative colitis (UC), IL-1β and IL10 levels were measured by enzyme linked immunosorbent assays (ELISA). Our results showed that IL-β level caused by spontaneous secretion in the intestinal mucous tissues in active stage of ulcerative colitis was significantly higher than that in normal controls and in remission stage of ulcerative colitis (P <0. 01,P<0. 001). IL-10 level in various stage of UC was relatively lower in controls, but there was no significantly difference between the two groups. Our study suggested that higher IL-1β level in active might play an important role in pathogenesis of UC, and IL-10, as an anti-inflammatory cytokine, was low in active UC, suggesting that it may be a important factor contributing to the development of higher IL-1β level. This project was supported by the grant of the Scientific Research Fund of the Ministry of Health (No. 98-2-387).     

Familial Mediterranean fever (FMF)-response to TNF-blockers used for treatment of FMF patients with concurrent inflammatory diseases

ObjectiveFamilial Mediterranean fever (FMF) is the most common interleukin 1 (IL-1)-driven monogenic autoinflammatory disease. Yet published data also suggest that tumor necrosis factor (TNF) may have a role in the pathogenesis of FMF and may serve as a target for treatment. In the present study we evaluate this hypothesis.MethodsTo this goal, we studied the incidental effect on FMF of TNF-directed treatment, administered to colchicine-refractory FMF patients for the management of a concurrent inflammatory disease. The rates of FMF patients and of treatments with complete or nearly complete FMF response were determined, based on the number of FMF attacks during TNF-blocker exposures. The possible effect of various FMF and non-FMF features on the outcome was determined using comparative analysis. Patients were identified and data were retrieved using electronic files from the FMF clinic.ResultsTwenty-six patients were identified, each receiving ≥ 1 of four TNF-blockers for a mean duration of 27.6 ± 16.4 months. The TNF-blockers were found to induce complete or nearly complete FMF response in 10 (38.5%) of the patients, and in 13 of 50 (26%) exposures. No clinical, genetic, demographic, or therapeutic feature could predict which FMF patient would respond favorably to TNF-blocker therapy.ConclusionThis study suggests that TNF-blockers may be beneficial for a small proportion of colchicine-resistant FMF patients.     

Involvement of leukocytes and cytokines in the ovulatory process and corpus luteum function

The role of leukocytes and cytokines in ovarian physiology isnow established, although the function of each cell type andcytokine remains to be determined in detail. Current knowledgeof these effects on follicle development, ovulation, luteinizationand luteotrophic process and luteolysis is reviewed. It is possiblethat further research will help to unravel some of the clinicalmysteries in ovarian function, including polycystic ovary syndrome,premature menopause, ovulatory disorders, and luteal phase defect.Furthermore, the increasing use of cytokines and their antagonistsin clinical practice may have significant effects upon reproductivefunction.     

Non-adenomatous colorectal polyposis syndromes

Gastrointestinal polyps are common lesions that usually present singly or in small numbers. Although the term ‘multiple colorectal polyposis’ was originally applied to patients carrying at least 100 large intestinal adenomas, it has subsequently become broadened to include patients carrying multiple polyps regardless of their nature. Most of the non-adenomatous polyposis syndromes are hereditary. They can be classified according to the dominant type of polyp, their distribution in the gastrointestinal tract and their potential for the development of gastrointestinal cancers. This review summarises their main clinical, genetic and histopathological features.     

Interleukin-3-dependent potentiation of IgE responsiveness in mouse basophils

Basophils produce interleukins (IL)-4 in response to various stimuli and may contribute to type 2 immune responses to various infections and allergens. We found that resting basophils freshly isolated from mice produce IL-4 in response to IL-3 but not to high-affinity Fc receptor (FcεRI) cross-linking (CL), yet both required the immunoreceptor tyrosine-based activation motif (ITAM) containing adaptor Fc receptor γ-chain (FcRγ), while basophils activated in vitro by IL-3 become responsive to FcεRI CL. Acquisition of responsiveness to FcεRI CL occurred upon infection with Trichinella spiralis or administration of superantigen. Because cultured basophils return to a quiescent state upon starvation with IL-3 with surface FcεRI levels unchanged, this acquisition is reversible and probably reflects intracellular events requiring protein synthesis. Interestingly, similar activation-associated acquisition was observed for responsiveness to other stimuli, including CD200R3 CL, which is known to signal via DAP-12, and the allergen protease papain. This acquisition of responsiveness to FcεRI CL was inhibited by Jak inhibitor. Thus, the IL-3 signal bifurcates downstream of Jak, into two distinct pathway, one leading to IL-4 production and the other to render basophils competent to respond to stimuli dependent on ITAM-containing adaptors DAP12 and FcRγ for IL-4 production.