阴道无色素梭形细胞型恶性黑色素瘤1例临床病理分析

目的探讨阴道无色素梭形细胞型恶性黑色素瘤的病理形态学特点、免疫表型、诊断及鉴别诊断。方法回顾性分析1例阴道无色素梭形细胞型恶性黑色素瘤的临床资料、病理组织学及免疫表型特征,并复习相关文献。结果镜下见肿瘤细胞呈弥漫片状分布,大小较一致,未见色素,可见席纹状结构,核呈梭形及短梭形,核仁较明显,可见病理性核分裂,胞质红染,细胞边界不清,肿瘤边缘可见淋巴细胞岛。免疫表型:肿瘤细胞CK、desmin和actin均阴性,S-100、Melan-A和HMB-45均阳性。结论诊断阴道无色素梭形细胞型恶性黑色素瘤需结合形态学及免疫表型特征,其中免疫组化标记HMB-45阳性是确诊的重要依据。     

胆囊原发性恶性黑色素瘤1例及文献复习

目的探讨胆囊原发性恶性黑色素瘤的I临床病理特征、组织发生及鉴别诊断。方法对1例原发于胆囊的恶性黑色素瘤进行光镜观察,并行组织化学及免疫组化染色标记。结果组织学特征为：在上皮和固有层交界处黑色素肿瘤细胞呈巢状或片状分布,肿瘤细胞大小不等,形态多样。瘤细胞内外可见粗大的黑色素颗粒,Masson—Fontana染色阳性,免疫表型HMB45、vimentin及S-100蛋白肿瘤细胞呈阳性表达。结论胆囊原发性恶性黑色素瘤罕见,诊断必须结合病史、全身检查及随访资料,以排除转移性恶性黑色素瘤。     

原发性食管胃交界处恶性黑色素瘤1例及文献复习

目的 分析原发性食管恶性黑色素瘤的临床病理学特征。方 法对1例原发性食管胃交界处恶性黑色素瘤进行组织学观察和免疫组化标记，同时复习相关文献。结果原发性食管胃交界处恶性黑色素瘤的组织学改变类似于皮肤发生的恶性黑色素瘤。免疫表型：肿瘤细胞HMB45、S-100蛋白和vimentin阳性，cytokeratin阴性。同时必须排除皮肤、眼等处的原发病灶。结论 原发性食管胃交界处恶性黑色素瘤(无色素性)是一种罕见的肿瘤，应该与一些食管发生的肿瘤相鉴别如低分化癌、肉瘤和转移性恶性黑色素瘤等。本瘤预后极差，术后平均生存时间仅为10个月。     

儿童甲外恶性血管球瘤1例临床病理分析

目的 探讨儿童甲外恶性血管球瘤临床病理特征、诊断及鉴别诊断.方法 回顾性分析1例儿童甲外恶性血管球瘤病例的临床资料、组织学形态及免疫表型结果.结果 患者女童,13岁,以背部皮肤肿块为主要表现,镜下肿瘤组织由纤维组织或薄壁血管分隔成器官样和结节样结构,与周边组织界限不清,结节中心无大片出血坏死,瘤细胞大小一致,圆形或卵圆形,胞膜界清,胞质丰富透亮,胞核圆形或卵圆形,核深染,核质比增大,小核仁易见,核分裂象10个/10 HPF,可见非典型性核分裂.免疫表型:瘤细胞SMA和CD34均(+)、vimentin和BCL-2均(),而p53、HMB-45、S-100蛋白、Syn、CgA、CK、desmin均(-).肿块扩大切除术后随访至今无复发和转移.结论 甲外恶性血管球瘤临床罕见且缺乏特征性的临床症状体征,结合组织学形态和免疫表型有助诊断和鉴别诊断.治疗方案以肿瘤扩大切除为主.     

单克隆抗体对黑色素瘤特异性反应及黑色素细胞亚群的区分

恶性黑色素瘤约占恶性肿瘤的1%,仅次于肺癌,外检诊断常遇困难,与癌、淋巴瘤和肉瘤难以区别。过去常用嗜银染色或多巴氧化酶组化技术,但不理想。近年来有人用抗S-100蛋白单克隆抗体免疫细胞化学诊断黑色素瘤。这种方法敏感,但无特异性。本文介绍一种单克隆抗体HMB-45,在固定包埋组织中对黑色素瘤和交界痣有高度敏感性及绝对特异性。取含有黑色素瘤转移的腋窝淋巴结作抗原免疫BALB/C小鼠,制作单克隆抗体HMB-45。选取18例原发性皮肤黑色素     

恶性血管周上皮样细胞肿瘤2例并文献复习

目的 探讨恶性血管周上皮样细胞肿瘤(malignant perivascular epitheliod cell tumor,PEComa)的临床、病理特征及鉴别诊断.方法 对2例恶性PEComa进行临床、病理形态学、免疫表型及电镜观察,并复习相关文献.结果 镜下见肿瘤组织由梭形细胞及上皮样细胞构成,细胞异型性明显,细胞胞质透明或嗜酸,细胞核大,有核仁,瘤细胞由纤细的纤维结缔组织及薄壁血管将其分隔成巢状、腺泡状、片状结构,部分区域可见多核瘤巨细胞伴肿瘤坏死,核分裂多见.免疫表型:肿瘤细胞表达HMB-45、S-100、SMA及desmin;电镜下见肿瘤细胞胞质内可见高电子密度核心的内分泌小体和少许不成熟的黑色素小体.结论 恶性PEComa罕见,病理形态多样,熟悉其临床、病理形态、免疫表型及电镜下改变,有助于临床、病理医师对其正确诊断及鉴别诊断.     

上皮样恶性周围性神经鞘瘤临床病理分析

目的 探讨上皮样恶性周围性神经鞘瘤(epithelioid malignant peripheral nerye sheath tumor,EMPNST)的临床病理特征及鉴别诊断.方法 收集9例EMPNST的临床病理资料,行光镜和EnVision法免疫组化观察,并复习文献.结果 9例EMPNST,女性4例;年龄20～67岁,中位年龄37.5岁;病变主要位于四肢,上肢3例,下肢4例,右季肋部和咽隐窝各1例;>5 cm 7例,其中1例>10 cm;<5 cm 2例,平均6.2 cm,无包膜.深在型8例,浅在型1例,组织学,纯上皮样型5例,其中2例见节细胞样或横纹肌样瘤样区域,4例混合型伴有梭形细胞区.免疫表型S-100蛋白及NSE 9例均呈阳性反应,纯上皮样型5例S-100蛋白呈强阳性,4例混合型呈灶性阳性,8例PGP 9.5阳性,7例MBP阳性,5例EMA灶性或弱阳性,4例vimentin阳性,3例CD57灶性阳性,而HMB-45、desmin、CD34、CK阴性.结论 EMPNST是恶性周围性神经鞘瘤的一种少见亚型,形态学上缺乏特征性,易与其他软组织上皮样肿瘤混淆.S-100蛋白及PGP9.5阳性是诊断EMPNST有价值的指标,但缺乏特异性,因此诊断时必须结合临床、组织形态和免疫表型的结果,综合判断以免引起误诊.     

鼻腔恶性黑色素瘤10例临床病理分析

目的 探讨鼻腔恶性黑色素瘤的临床病理特征,并对其诊断和鉴别诊断进行讨论.方法 结合组织形态学结构和免疫组化,对10例鼻腔恶性黑色素瘤进行临床病理分析.结果 10例鼻腔恶性黑色素瘤中男性3例,女性7例,年龄52～83岁,平均年龄59.8岁.肿瘤由上皮样,梭形及未分化小细胞等多种类型的细胞组成.免疫组化标记瘤细胞均表达HMB-45、S-100蛋白、vimentin.结论 鼻腔黏膜恶性黑色素瘤易误诊为其它鼻腔原发性肿瘤,导致临床处理不当,延误治疗,与皮肤恶性黑色素瘤相比,鼻腔黏膜恶性黑色素瘤更具有侵袭性、预后差等特点.     

婴儿色素性神经外胚瘤1例报道并文献复习

目的 探讨婴儿色素性神经外胚瘤的临床病理特征、免疫组化、诊断和鉴别诊断要点。方法 对1例婴儿色素性神经外胚瘤进行组织学和免疫组化观察和文献复习。结果 婴儿色素性神经外胚瘤好发于1岁以内的婴儿，肿瘤多见于上颌骨和颅骨，表现为浸润性和溶骨性破坏。组织学上显示大的并含不等量色素颗粒的上皮样细胞和小的神经母细胞样细胞。免疫组化显示CK、HMB-45、S-100蛋白、NSE在上皮样细胞呈阳性表达，小圆形瘤细胞S-100蛋白、NSE阳性或部分阳性。肿瘤彻底切除，随访3年未发现转移和复发。结论 婴儿色素性神经外胚瘤是一种少见的起源于神经嵴细胞的肿瘤，具有特征性的临床病理改变，需要和神经母细胞瘤、恶性黑色素瘤及其它小圆细胞肿瘤鉴别，生物学行为属于潜在恶性或低度恶性肿瘤，彻底切除预后良好。     

原发性宫颈恶性黑色素瘤临床病理观察

目的探讨原发性宫颈恶性黑色素瘤的临床病理特征、鉴别诊断及预后。方法对5例宫颈恶性黑色素瘤通过光镜、免疫组化进行观察和分析,并随访。结果5例平均43．4岁,临床表现为不规则阴道出血或排液,妇检示宫颈菜花状或黑色结节状肿物;镜检示肿瘤细胞异型性大,细胞形态多样,表现为痣样细胞、上皮细胞、梭形细胞或混合细胞。免疫表型：HMB45、Melan—A（MART-1）、tyrosinase、S-100蛋白、vimentin均阳性表达。结论原发性宫颈恶性黑色素瘤恶性程度高,预后差。HMB45、Melan—A（MART-1）、S-100蛋白对恶性黑色素瘤有着重要意义,需要注意与癌、癌肉瘤、淋巴瘤或绒癌相鉴别。     

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.     

即早基因c-fos与脑血管病及学习记忆

即早基因c-fos是广泛存在于原核细胞和真核细胞的高度保守基因.在正常情况下,c-fos基因参与细胞生长、分化、信息传递、学习和记忆等生理过程,而在病理情况下c-fos基因表达及调控变化与多种疾病的发生和发展有关.C-fos在中枢神经系统的某些部位可有基础水平的表达,但表达很低,当受到如脑缺血、脑出血、痫性发作、应激等刺激后,其在数十分钟内做出反应,在对外界刺激-转录耦联的信忠传递过程中起着核内第三信使的重要作用.     

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.