晚期腺样囊性癌姑息性放疗的临床分析

目的 探讨晚期腺样囊性癌姑息性放疗的临床意义.方法 回顾性分析我院1990-2000年86例晚期腺样囊性癌患者的临床资料,将患者分为姑息性放疗组50例和未放疗组36例,比较两组5年,10年生存率.结果 姑息性放疗组5年生存率:84%,10年生存率:64%均高于未放疗组(61.1%,36.1%.P值均为:0.01相似文献   

头颈部腺样囊性癌患者的预后及其影响因素分析

目的分析头颈部腺样囊性癌患者的预后及其影响因素。方法回顾性分析2004-2012年我院收治的55例头颈部腺样囊性癌患者的临床资料,其中单纯手术30例,手术加术后放疗22例,放化疗1例,单纯放疗2例,接受化疗15例。接受化疗的15例患者中初治后发生转移行化疗12例,术后同步化放疗2例,同期放化疗1例。采用Kaplan-Meier法和Logrank检验分析其临床疗效和预后情况。结果 55例患者的随访率为96%,中位随访时间46个月。3年、5年总生存率分别为89.8%、77.3%,无远处转移生存率分别为81.8%、35.9%,无局部区域失败生存率分别为79.1%、56.3%。单因素分析显示T分期、术后放疗和手术切缘与总生存率相关(P<0.05),手术切缘和术后放疗与无局部区域失败生存率相关(P<0.05)。多因素分析显示T分期是总生存率的独立影响因素(P=0.005),手术切缘是无局部区域失败生存率的独立影响因素(P=0.047)。结论头颈部腺样囊性癌治疗应尽量手术根治切除,局部晚期推荐手术及放疗综合治疗。     

头颈部腺样囊性癌

天津市肿瘤医院头颈科自1954年5月至1982年3月共收住院治疗并病理证实腺样囊性癌39例,皆来自大、小唾腺。全组的5年生存率为69.3%,健在率为38.5%,10年及20年健在率均为2.5%。作者发现临床期别早晚影响预后,即早期癌的10年生存率为22.2%,晚期癌为0%。能根治性切除者预后好,鼻腔及上额窦的晚期癌宜术前放疗而后再根治性切除。凡淋巴结已有转移者虽行积极治疗预后仍不佳。大唾腺者的预后优于小唾腺者。病理为小管型或筛状型的预后优于实性型。性别、年龄和症状期似与预后无关。治疗失败的主要原因为局部复发,亦有为局部治愈而死于血行转移者。作者对各部位癌的根治术范围作了介绍。     

鼻腔鼻窦腺样囊性癌的CT诊断与病理表现

目的分析和探讨鼻腔鼻窦腺样囊性癌（adenoid cystic carcinoma ACC）的CT表现,提高该病诊断水平。方法对10例经手术和病理证实为腺样囊性癌病例进行回顾性分析,肿瘤原发于上颌窦6例,筛窦3例,鼻腔1例,均侵犯邻近骨壁及窦腔或眼眶。结果 10例患者鼻窦内见软组织影,窦壁骨质呈膨胀性溶骨性破坏或者筛孔样骨质破坏,窦腔轮廓消失。结论腺样囊性癌是一种鼻腔和鼻窦内少见的恶性肿瘤,生长缓慢,症状隐匿,CT平扫和增强具有一定特征性,可以作为与其他鼻窦鼻腔恶性肿瘤鉴别点,但是不具有特异性,需依靠病理确诊。     

颌面部小涎腺腺样囊性癌临床分析

目的 探讨颌面部小涎腺腺样囊性癌(ACC)的治疗及预后.方法 回顾性分析25例颌面部小涎腺ACG的临床资料和随访结果.结果 25例患者均给予手术治疗,随访1～20年,致死因素为局部复发和远处转移,5年生存率为52.0%,10年生存率为28.0%.结论 小涎腺ACC易局部复发和远处转移,临床采用以手术为主的综合治疗可减少复发和转移,提高生存率.     

手术治疗小涎腺肿瘤29例临床观察

目的：探讨口腔小涎腺肿瘤经临床手术治疗效果。方法：收集本院收治的口腔小涎腺肿瘤患者29例的临床资料,分析其病理类型及治疗结果。结果：10例良性小涎腺肿瘤随访5年均存活,未出现复发。19例恶性小涎腺肿瘤患者行单纯手术切除治疗6例,手术切除辅以术后放射治疗13例。随访5年,存活13例,死亡6例,5年生存率为68.42%。结论：手术切除范围及术后是否进行辅助放射性治疗可影响患者预后。     

腭部恶性肿瘤的诊断与治疗

目的探讨腭部恶性肿瘤的临床病理类型、诊断及治疗方法。方法对住院治疗的腭部恶性肿瘤患者84例的临床病理类型、诊断、治疗、预后进行分析及总结。结果 84例恶性肿瘤中,腺源性肿瘤45例（53.6%）,非腺源性肿瘤39例（46.4%）。鳞状细胞癌最多见（31例,36.9%）,其次为腺样囊性癌（22例,26.2%）和黏液表皮样癌（15例,17.9%）。73例患者手术治疗,15例于术后6个月至6年复发。结论腭部恶性肿瘤治疗应采取以手术切除为主的综合治疗,应重视术前组织学诊断,尽量避免术后复发及并发症的发生。     

16例涎腺腺样囊性癌的临床观察

腺样囊性癌好发于涎腺,以小涎腺多见,易于局部复发和远处转移,本院对16例涎腺腺样囊性癌进行了治疗,现总结如下。1临床资料1．1临床资料：自2000年～2005年我院共收治16例涎腺腺样囊性癌。男性10例,女性6例;平均年龄47岁（18～69岁）。原发于小涎腺12例,大涎腺4例。T1、T2、T3及T4期分别为1、4、8及3例。病理类型均为腺样囊性癌。1．2治疗方式：单纯手术5例,手术加放射治疗11例;对于手术切缘不满意及病理切缘阳性者放射剂量达60～70Gy。2结果2．1局部复发：共有5例患者出现局部复发,总的局部复发率为31．2％（5／16）;其中单纯手术者2例,手术加放射治疗者3例。     

乳腺腺样囊性癌免疫组化表型与临床特征探讨

目的探讨乳腺腺样囊性癌免疫组化表型与临床特征。方法对6例乳腺腺样囊性癌患者临床资料进行回顾性分析,内容包括发病部位、治疗方法及结果、随访结果、免疫组化表型等,将上述资料给予统计学分析并得出结论。结果发病部位为外上象限所占比例高达50.00%(P<0.05);均给予乳腺癌根治术并实施术后化学药物辅助治疗;5年无病生存率(83.33%)与死亡率(0)对比差异具有统计学意义(P<0.05);雌激素受体(ER)、孕激素受体(PR)、人表皮生长因子受体2(Her-2)均为(-)表型(P<0.05)。结论乳腺腺样囊性癌免疫组化表型特点为ER、PR、Her-2受体三阴性表达,患者经临床对症治疗后可获得满意疗效及预后,临床医生应准确掌握乳腺腺样囊性癌临床特征及免疫组化表型特点,降低误诊、漏诊记录使患者获得及时救治。     

iNOS及VEGF在人涎腺腺样囊性癌中的表达及意义

目的:研究诱导型一氧化氮合酶(iNOS)和血管内皮生长因子(VEGF)在人涎腺腺样囊性癌中的表达及相关性,探讨两者与人涎腺腺样囊性癌血管生成和临床生物学行为的关系。方法:选取佳木斯大学附属口腔医院颌面外科自2000—03~2007—08确诊的15例腺样囊性癌病例,以10例瘤旁正常涎腺组织做对照。采用免疫组织化学方法(SABC法)检测每例病例中的iNOS和VEGF的表达,并对上述指标用SPSS13.0软件进行统计学分析。结果:iNOS和VEGF在涎腺腺样囊性癌中的表达水平明显高于正常涎腺组织,两组之间有显著性差异(P<0.05)。两种因子之间的相互表达呈正相关。两种因子在腺样囊性癌中的表达与临床分期、淋巴结转移、病理分类密切相关,而与患者的年龄、性别、发病部位以及组织类型均无关。结论:iNOS和VEGF与涎腺肿瘤的发生、发展中有密切关系,随肿瘤恶性程度增高而表达增强。而与患者年龄、性别、发病部位、组织类型均无关。     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

Aquatic Insects and Trace Metals: Bioavailability,Bioaccumulation, and Toxicity

Abstract

The uptake of metals from food and water sources by insects is thought to be additive. For a given metal, the proportions taken up from water and food will depend both on the bioavailable concentration of the metal associated with each source and the mechanism and rate by which the metal enters the insect. Attempts to correlate insect trace metal concentrations with the trophic level of insects should be made with a knowledge of the feeding relationships of the individual taxa concerned. Pathways for the uptake of essential metals, such as copper and zinc, exist at the cellular level, and other nonessential metals, such as cadmium, also appear to enter via these routes. Within cells, trace metals can be bound to proteins or stored in granules. The internal distribution of metals among body tissues is very heterogeneous, and distribution patterns tend to be both metal and taxon specific. Trace metals associated with insects can be both bound on the surface of their chitinous exoskeleton and incorporated into body tissues. The quantities of trace meals accumulated by an individual reflect the net balance between the rate of metal influx from both dissolved and particulate sources and the rate of metal efflux from the organism. The toxicity of metals has been demonstrated at all levels of biological organization: cell, tissue, individual, population, and community. Much of the literature pertaining to the toxic effects of metals on aquatic insects is based on laboratory observations and, as such, it is difficult to extrapolate the data to insects in nature. The few experimental studies in nature suggest that trace metal contaminants can affect both the distribution and the abundance of aquatic insects. Insects have a largely unexploited potential as biomonitors of metal contamination in nature. A better understanding of the physico-chemical and biological mechanisms mediating trace metal bioavailability and exchange will facilitate the development of general predictive models relating trace metal concentrations in insects to those in their environment. Such models will facilitate the use of insects as contaminant biomonitors.     

Alzheimer’s disease – current trends in basic and clinical research. Highlights from the 16th ECNP

Advances in the molecular biological knowledge of neuronal nicotinic acetylcholine receptors (nAChRs) have led to a growing interest by the pharmaceutical industry in the development of novel compounds that selectively modulate nAChR function. The ability of (-)-nicotine, an activator of nAChRs, to enhance attentional aspects of cognition in animals and humans, to exert neuroprotective and anxiolytic-like effects, and presumably to mediate the negative correlation between smoking and Alzheimer's (and Parkinson's) Disease, has focused interest on the potential therapeutic utility of modulators of nAChR function for treatment of some of the deficits associated with these progressive, neurodegenerative conditions. Numerous compounds are known which activate nAChRs and which might serve as lead compounds toward the development of such agents. The pharmacologic diversity of neuronal nAChR subtypes suggests the possibility of developing selective compounds which would have more favourable side-effect profiles than existing agents. This broader class of agents, collectively called cholinergic channel modulators (ChCMs), is anticipated to encompass compounds which would have more favourable side-effect profiles than existing agents, which generally exhibit low selectivity. This selectivity may be achieved by preferentially activating some subtypes of nAChRs (i.e., Cholinergic Channel Activators, ChCAs) or inhibiting the function of other subtypes (Cholinergic Channel Inhibitors, ChCIs). An overview of the biology of nAChRs and the rationale for the use of ChCMs for the treatment of dementia related to neurodegenerative diseases are presented, followed by a discussion of lead compounds and compounds under consideration for clinical evaluation.     

2-(Acetoxyphenyl)-(Z)-styryl sulfides as cyclooxygenase inhibitors

2-(Acetoxyphenyl)-(Z)-styryl sulfides are described as selective cyclooxygenase-2 (COX-2) inhibitors, useful for treating inflammation and COX-2-mediated disorders including neoplasia. 2-(Acetoxyphenyl)-(Z)-styryl sulfide is claimed to be the most potent COX inhibitor in the series with a COX-2 selectivity ratio of 33. This compound is also claimed to be superior to celecoxib (Celebrex^®, Pfizer) in inhibiting cell growth of colorectal carcinoma cells. In this evaluation, the COX inhibitory activity of this compound is compared to that previously disclosed for diarylheterocycles and 2-(acetoxyphenyl)alkyl sulfides. The validity of the DLD-1 cell line in the growth inhibition studies is questioned based on recent literature reports indicating the lack of COX-2 expression in this cell line.     

Sleep-disordered breathing with chronic opioid use

Chronic opioid use for pain relief or as substitution therapy for illicit drug abuse is prevalent in our societies. In the US, retail distribution of methadone and oxycodone has increased by 824 and 660%, respectively, between 1997 and 2003. μ-Opioids depress respiration and deaths related to illicit and non illicit chronic opioid use are not uncommon. Since 2001 there has been an emerging literature that suggests that chronic opioid use is related to central sleep apnoea of both periodic and non-periodic breathing types, and occurs in ～ 30% of these subjects. The clinical significance of these sleep-related abnormalities are unknown. This review addresses the present knowledge of control of ventilation mechanisms during wakefulness and sleep, the effects of opioids on ventilatory control mechanisms, the sleep-disordered breathing found with chronic opioid use and a discussion regarding the future research directions in this area.     

Drug targets for cognitive enhancement in neuropsychiatric disorders

The investigation of novel drug targets for treating cognitive impairments associated with neurological and psychiatric disorders remains a primary focus of study in central nervous system (CNS) research. Many promising new therapies are progressing through preclinical and clinical development, and offer the potential of improved treatment options for neurodegenerative diseases such as Alzheimer's disease (AD) as well as other disorders that have not been particularly well treated to date like the cognitive impairments associated with schizophrenia (CIAS). Among targets under investigation, cholinergic receptors have received much attention with several nicotinic agonists (α7 and α4β2) actively in clinical trials for the treatment of AD, CIAS and attention deficit hyperactivity disorder (ADHD). Both glutamatergic and serotonergic (5-HT) agonists and antagonists have profound effects on neurotransmission and improve cognitive function in preclinical experiments with animals; some of these compounds are now in proof-of-concept studies in humans. Several histamine H3 receptor antagonists are in clinical development not only for cognitive enhancement, but also for the treatment of narcolepsy and cognitive deficits due to sleep deprivation because of their expression in brain sleep centers. Compounds that dampen inhibitory tone (e.g., GABA_A α5 inverse agonists) or elevate excitatory tone (e.g., glycine transporter inhibitors) offer novel approaches for treating diseases such as schizophrenia, AD and Down syndrome. In addition to cell surface receptors, intracellular drug targets such as the phosphodiesterases (PDEs) are known to impact signaling pathways that affect long-term memory formation and working memory. Overall, there is a genuine need to treat cognitive deficits associated with many neuropsychiatric conditions as well as an increasingly aging population.