恶性肿瘤合并头颈部真菌感染的临床与病理学观察

目的 探讨恶性肿瘤合并头颈部真菌感染的临床与病理特点.方法回顾分析21例恶性肿瘤合并头颈部真菌感染患者的临床和病理资料;用HE染色、过碘酸-雪夫(PAS)染色和环六亚甲基四胺银(GMS)染色显示组织病变特点及真菌的形态特征,用黏蛋白5B(MUC5B)抗体免疫组织化学EnVision法染色标记真菌;13例组织标本进行了真菌培养.结果患者发病年龄12～72岁(中位年龄48岁),男性17例,女性4例.病理学检查证实合并侵袭性真菌性鼻窦炎(IFS)有8例(38.1%),其中波及眶内者6例(28.6%),侵入颅内1例;原发疾病为白血病(7例)及鼻咽癌(1例);病原真菌为接合菌(5例)和曲霉菌(3例),均有化疗或放疗及使用抗生素的病史.其余13例真菌感染发生于鼻腔鼻窦、咽喉及腭部原发肿瘤的坏死组织内,病原真菌主要为曲霉菌(6例)和念珠菌(4例),7例有放疗等治疗史.真菌培养结果9例阳性(9/13).随访病例14例,死亡6例.结论 恶性肿瘤可合并头颈部真菌感染,以IFS最为多见,好发于白血病化疗后,易累及眼眶,预后较差;病原真菌的类别在IFS以接合菌和曲霉菌多见;病理学检查仍然是尽快确定诊断及初步鉴别常见接合菌和曲霉菌类别的一个重要手段.     

肝衰竭合并细菌和真菌感染的回顾性研究

目的研究肝衰竭患者并发细菌与真菌双重感染的临床特点。方法以我院1986年1月至2006年6月收治的肝衰竭患者合并细菌和真菌双重感染者为研究对象,细菌感染需有临床表现和病原学阳性,统计分析相关资料。结果真菌感染者共507例,合并细菌和真菌双重感染者132例。132例中慢性重型肝炎85例(64.39%),失代偿期活动性肝硬化40例(30.3%)。细菌感染153例次,医院感染发生率为54.90%。分离出细菌204株,G-杆菌143株(70.10%)、G 球菌61株(29.90%)。腹腔感染占首位,共122例次,其次为肺部30例次。真菌感染143例次,医院感染发生率为86.71%。分离出真菌155株,其中白色念珠菌90株(58.06%),烟曲霉菌17株(10.97%),非白色念珠菌25株(16.13%)。肺部感染占首位(94例次),其次为口腔(53例次)。治疗后无效和死亡84例(63.64%)。结论失代偿期活动性肝硬化和慢性重型肝炎是继发细菌和真菌感染的主要人群。真菌的医院感染发生率高于细菌。继发真菌感染的患者预后差。     

少数民族地区血培养中病原菌的分布及耐药性分析

目的：分析少数民族地区血培养阳性标本中的病原菌分布的特点及耐药状况。方法回顾性分析2013年1月~12月180例血流感染的临床资料。结果2000人次血培养共分离病原菌180株,阳性率(9%),其中革兰阳性菌96株(53%),革兰阴性菌84株(47%),真菌2株(1%),阳性菌中(真菌除外)所有菌株对万古霉素和替考拉宁敏感,对红霉素和青霉素耐药。阴性菌中对亚胺培南,美罗培南,头孢哌酮/舒巴坦敏感,对安苄西林,头孢唑啉,头孢呋辛等耐药较高。结论临床医生应根据药敏结果合理使用抗生素,达到抗感染的目的。     

气管切开术后呼吸道获得性感染的临床观察

目的 研究气管切开术后患者呼吸道获得性感染的发生率,致病菌的药敏与耐药情况以便指导临床治疗.方法 分析我院耳鼻喉科、肿瘤科、神经外科监护室2003年5月-2009年4月间,43例昏迷患者气管切开术后对其呼吸道的分泌物作细菌培养,药敏资料及临床使用抗生素的情况.结果 43例121次痰培养阳性114次,阳性率94.2%,其中细菌96株,占84%,共19个菌种;霉菌18株,占16%,均为真菌,9例怀疑厌氧菌感染,送检阳性3例,细菌与真菌混合感染12例,二重感染率达27.9%.革兰阴性(G-)杆菌主要是绿脓杆菌(34%)、不动杆菌(16%)、大肠杆菌(5.6%),三者共占55.6%;革兰阳性(G+)菌球主要是表皮样葡萄球菌(15%)、金黄色葡萄球菌(7.2%)、粪链球菌(3.2%),三者共占25.496.药敏试验结果为:对青霉素类、三代头孢、喹诺酮、氨基糖苷类、碳青霉烯类,G-杆菌分别为20%～30%、40%～65%、90%、90%和93%.G+杆菌分别为80%、30%～50%、85%、85%、95%.结论 危重病人气管切开术后呼吸道获得性感染率较高,病原菌的耐药与交叉耐药日趋严重,广谱抗生素的滥用导致霉菌感染,时刻危及病人生命,必须采取有效措施,防止感染.     

2007年秋冬季北京地区成人发热就诊患者中人冠状病毒229E感染状况分析

目的 了解北京地区成人发热就诊患者中人冠状病毒HCoV-229E感染病原学、临床表现和流行病学特点.方法 2007年10月至12月从北京地区发热且有呼吸道症状的就诊成人中采集158份鼻咽拭子标本,利用荧光定量RT-PCR法进行HCoV-229E筛查;利用常规PCR方法扩增HCoV-229E基因片段测序;对感染阳性患者进行HCoV-NL63、HCoV-HKU1及HMPV的共感染筛查、临床表现描述和流行病学特点分析.结果 158份鼻咽拭子标本中荧光定量RT-PCR检测出103(65.2%)例HCoV-229E阳性;其中26例存在与HCoV-NL63(3例)、HCoV-HKU1(3例)及HMPV(20例)的混合感染;HCoV-229E阳性标本的临床表现以头痛(70.9%)、咽红(70.9%)、咽痛(69%)、寒颤(68%)、咳嗽(33%)、有痰(21.3%)、流涕(21.4%)和鼻塞(16.5%)为主,少量可见呕吐(6.8%)、呼吸困难(3.9%)和腹泻(1.9%);统计学分析表明其感染与性别、年龄无关.结论 人冠状病毒HCoV-229E感染在秋冬季成人发热就诊患者中为常见病原,可合并感染其他病毒.其临床表现呈上呼吸道感染特征.2007年秋冬季在北京地区成人中可能存在HCoV-229E局部流行.     

肿瘤患者放、化疗期间发热反应的护理

总结了93例肿瘤患者放、化疗出现发热反应的观察及护理.通过对放化疗前、放化疗期间及发热反应的观察予以一系列护理措施,有效的控制肿瘤患者放、化疗后感染发热,以减少放、化疗的并发症,提高放、化疗的有效率.     

87例培养阳性解脲脲原体的药敏分析

目的了解泌尿生殖道标本中解脲脲原体对不同抗生素的敏感性差异.方法用法国生物梅里埃生产的支原体IST试剂盒对泌尿生殖道分泌物等标本进行培养鉴定和药敏试验.结果其中有87例解脲支原体培养阳性,药敏结果分析发现解脲脲原体分别对6种抗生素敏感如下:四环素60例(69.00%)、强力霉素68例(78.16%)、交沙霉素82例(94.25)、原始霉素全部敏感率(100%)、红霉素只有7例(8.05%)、氧氟沙星28例(32.18%).结论应将原始霉素、交沙霉素、强力霉素、四环素列为临床治疗解脲支原体感染首先药物.     

头颈部肿瘤放疗患者创伤后成长的相关因素

目的:探讨头颈部肿瘤放射治疗患者创伤后成长水平及相关因素。方法:选取天津市某三级甲等医院放射治疗科接受放射治疗的150例头颈部肿瘤患者,采用一般情况调查表、创伤后成长量表(PTGI)、疾病不确定感量表(MUIS)、Herth希望量表(HHI)和癌症应对问卷(CCMQ)对研究对象进行横断面研究。结果:头颈部肿瘤放射治疗患者PTGI总分为(62.8±12.3)分。多重线性回归分析显示,已婚(β=0.37)、未接受同步放化疗(β=0.13)、放疗次数≥30次(β=0.13)、Herth希望水平高(β=0.45)、采取积极癌症应对方式(β=0.24)者的创伤后成长水平较高。结论:本研究提示,已婚、未接受同步放化疗、放疗次数≥30次、较高希望水平、积极癌症应对方式可能有助于头颈部肿瘤放射治疗患者的创伤后成长。     

2426例泌尿生殖道支原体培养及药敏检测结果分析

目的 对2426例泌尿生殖道支原体培养和药敏检测结果分析.方法 选取我院2426例泌尿生殖道感染患者,对其实施支原体培养和药敏实验,分析其培养结果和检测结果.结果 支原体培养结果:共检测出1186例支原体阳性,其中972例Un阳性、55例Mh阳性以及159例Un+Mh阳性.药敏检测结果:排在前四位的分别是美满霉素(MIN)89.53％、强力霉素(DOX)85.47％、克拉霉素(CLA)81.98％以及交沙霉素(TOS)79.07％.结论 在泌尿生殖道支原体感染患者临床治疗中,支原体培养和药敏检测结果有助于其选择合理药物实施治疗.     

466例成年女性宫颈支原体感染现状及药敏分析

目的：为了解本地区成年女性子宫颈解脲支原体（Uu）及人型支原体（Mh）的分布及抗生素的药敏现状,为临床诊断和合理用药提供依据。方法：应用支原体培养、鉴定、药敏一体化试剂盒,对919例疑为支原体感染患者的宫颈分泌物进行培养、鉴定与分型,并测定其对10种常用抗生素的敏感性。结果：919例可疑病例中支原体培养阳性466例（50．70%）,其中单纯解脲支原体（Uu）阳性395例（43．0％）,单纯人型支原体（Mh）阳性20倒（2．2%）,Uu＋Mh阳性混合感染51例（5．5％）;药敏结果显示,支原体对10种抗生素敏感率排名：交沙霉素96,78％、克拉霉素93．13％、阿奇霉素92．92％。耐药率排名：司帕沙星51．29％、氧氟沙星40．99必、左氧氟沙星36．91％。结论：本地区成年妇女生殖道临床感染支原体主要为解脲支原体（Uu）．交沙霉素等新一代大环内醅类抗生素为首选药物,喹诺酮类抗生素耐药率高。     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

类赖氨酰氧化酶2与肿瘤转移和发生

类赖氨酰氧化酶2(lysyl oxidase-like 2,LOXL2)是赖氨酰氧化酶(lysyl oxidase,LOX)基因家族的成员之一,其表达产物能促进胶原沉积.LOXL2的过表达能促进纤维化,并与肿瘤侵袭、转移及不良预后有关.目前大部分学者认为LOXL2是一种转移促进基因,也有实验支持其是一种肿瘤抑制基因.研究发现LOXL2可以通过激活Snail/Ecadherin通路或Src/FAK通路促进转移.LOXL2有望作为肿瘤生物标志物,用于预后判断,成为一个新的治疗靶点.