Kimura病和上皮样血管瘤的临床病理学观察

目的探讨Kimura病和上皮样血管瘤的临床病理学特征、免疫学表型及两者的鉴别诊断。方法分析和观察9例Kimura病和3例上皮样血管瘤的临床资料和组织学形态,应用免疫组织化学(SP法)研究其免疫表型,所用抗体包括CD43、CD3、CD45RO(UCHL-1)、CD20、CD79α、Ki-67、CD31、CD34、第Ⅷ因子相关抗原(FⅧRAg)、CD68(KP-1)和细胞角蛋白(AE1／AE3)。结果临床上,Kimura病多见于男性患者,而上皮样血管瘤多见于女性。两者均好发于头颈部,但Kimura病多表现为皮下多发性结节或局部肿胀,部分病例伴有区域淋巴结肿大,而上皮样血管瘤则多表现为皮肤单发的小结节或丘疹样病变。组织学上,两者均可位于真皮内或皮下,但Kimura病均以增生的淋巴组织为主,其中7例可见淋巴滤泡形成,内含活跃的生发中心,滤泡问可见大量增生的毛细血管后微静脉型血管,其内皮呈肿胀状或扁平状,血管周围和滤泡旁可见大量的嗜酸性粒细胞浸润,3例内可见嗜酸性微脓疡形成。3例上皮样血管瘤均以成簇增生的血管为主,其中2例为毛细血管型,1例为小至中等大的血管型。血管内衬胞质丰富、深嗜伊红染的上皮样内皮细胞。除内衬管腔外,内皮细胞还可在血管腔内生长或在血管周围呈实性片状增生或排列成条索状,部分细胞的胞质内含有空泡,拟形成原始血管腔。2例的问质内可见多少不等的慢性炎症细胞反应,但不见淋巴滤泡形成,嗜酸性粒细胞浸润也远不如Kimura病明显。免疫组织化学显示,Kimura病中的淋巴滤泡表达B细胞抗原,滤泡间的淋巴细胞多表达T细胞标记,而上皮样血管瘤中的内皮细胞强阳性表达CD31和FⅧRAg等内皮标记。结论Kimura病和上皮样血管瘤是两种完全不同的病种,前者是一种淋巴组织的增生,而后者则是一种良性的血管瘤,掌握两者的临床特点和组织学形态对避免将两者相互混淆具有十分重要的意义。     

胃血管内乳头状内皮细胞增生1例

血管内乳头状内皮细胞增生(intravascular papillary endothelial hyperplasia, IPEH), 又称Masson瘤, 是一种局限于血管内的内皮细胞反应性增生, 通常是由于血管损伤继发血栓机化引起。病变好发于手指、头颈部、躯干等皮肤黏膜的浅表部位, 而发生于胃的IPEH极为罕见, 胃镜表现为黏膜下隆起性病变, 患者通常有不明原因的黑便、大便隐血试验阳性等消化道出血症状。术前病理活检难以明确诊断, 临床上易误诊为胃肠道间质瘤、异位胰腺、黏膜下血管瘤等黏膜下病变, 确诊依赖于组织病理学检查。认识其存在并熟悉相关组织形态学特征有助于其诊断与鉴别诊断, 防止误诊、漏诊。     

耳鼻咽喉头颈部结外Rosai-Dorfman病临床病理特征

目的探讨耳鼻咽喉头颈部结外Rosai-Dorfman病的临床病理学特征、诊断及鉴别诊断。方法收集北京同仁医院5例耳鼻咽喉头颈部结外Rosai-Dorfman病例,并行常规HE、组织化学和免疫组化染色。结果患者年龄37～72岁,平均49岁。5例中原发于喉2例,原发于鼻腔2例,原发于鼻翼皮肤1例。组织病理学特征:①低倍镜下为上呼吸道黏膜下或皮肤真皮内肿瘤细胞弥漫浸润,呈不同程度淡染区和深染区相间交错;②高倍镜下窦组织细胞增生,伴有不同程度其它慢性炎症细胞浸润,可见"伸入现象",病变特征不如结内病变明显;③免疫组化染色结果显示窦组织细胞S-100和CD68阳性,CD1a、CD20、CD45RO阴性。结论耳鼻咽喉头颈部发生的结外Rosai-Dorfman病是一种少见的组织细胞增生性疾病,有特定的组织病理学特征,在诊断上需要和该部位的其他肿瘤和炎性病变鉴别。     

淋巴结Kikuchi病与结核病的病理鉴别诊断

目的 探讨Kikuchi病(KD)病理诊断和鉴别诊断的重要意义.方法 复习31例原病理诊断KD的HE切片,并对其中的20例进行结核病相关的病原学榆测.结果 31例原病理诊断为KD的病例中,13例(41.94%)改诊为结核病,12例仍诊断为KD.结论 淋巴结碎屑性坏死并非KD特有病变,诊断KD需先除外有明显碎屑性坏死的淋巴结结核病,后者主要表现:①碎屑性坏死虽明显,但趋于干酪样坏死;②坏死区内或同时在淋巴窦(主要边缘窦)内,组织细胞、巨噬细胞和泡沫细胞增生,并演变为上皮样细胞和趋于肉芽肿形成;③坏死灶内、外可有数量不等的中性粒细胞浸润;④抗酸杆菌/结核杆菌病原学检测阳性;⑤缺乏KD的典型临床过程.     

Nora病的临床病理分析

目的探讨Nora病(Nora’s lesion,NL)的临床、病理学特征及鉴别诊断。方法对2例NL的临床、病理组织学、影像学特点进行观察分析,并复习相关文献。结果本组2例NL均表现为指骨中节骨旁境界清楚的高密度病变,与附着骨骨髓腔不连续。组织学上病变由分化成熟的软骨、骨和纤维组织3种成分混合而成,并可见特征性的"蓝骨"。结论 NL是一种罕见的具有独特临床、病理学特征且有复发倾向的良性增生性病变。     

成人肠道淋巴样息肉病临床病理分析及文献复习

目的：探讨成人肠道淋巴样息肉病的临床及病理学特征。方法：应用光镜及免疫组织化学方法观察4例成人肠道淋巴样息肉病的组织学特点及免疫学表型,并复习相关文献。结果：4例中3例为男性,1例为女性,年龄分别为75、75、46及70岁。4例病例均因其他疾病切除末端回肠及回盲部时,偶然发现末端回肠多发息肉样隆起,直径0.1~0.5 cm。镜下见回肠粘膜淋巴组织显著增生,淋巴滤泡增生并形成息肉样小结节,淋巴滤泡的生发中心明显增大,围绕生发中心的套区境界清楚。免疫组织化学显示大部分呈滤泡样增生的淋巴细胞CD20强阳性表达,不表达Cyclin D1,生发中心细胞不表达Bcl-2。结论：成人淋巴样息肉病是一种罕见的良性病变,具有独特的临床病理特点,临床上易于同部分恶性肿瘤相混淆,诊断依靠病理组织学及部分辅助方法。     

子宫颈淋巴瘤样病变6例临床病理观察

目的 探讨子宫颈淋巴瘤样病变的临床病理特征及鉴别诊断要点。方法 收集6例子宫颈淋巴瘤样病变，观察其临床病理特点，进行免疫组化染色及随访。结果 6例平均年龄47岁，临床表现不规则阴道出血，妇检示宫颈重度糜烂或息肉。镜检示致密的大淋巴细胞与多量成熟的小淋巴细胞、浆细胞以及分叶核白细胞混合存在，核分裂象活跃。免疫组化染色显示淋巴组织为多克隆性增生，大淋巴细胞CD30和CD20呈不同程度的阳性表达。结论 子宫颈淋巴瘤样病变是一种反应性淋巴组织增生性病变，需要注意与恶性淋巴瘤鉴别。病变特有的组织学表现及免疫组化染色有助于鉴别诊断。     

组织细胞坏死性淋巴结炎的诊断和鉴别诊断

目的 探讨组织细胞坏死性淋巴结炎(KD)的诊断与鉴别诊断。方法 选择46例KD,5例非特异性淋巴结炎(NLD),5例非霍奇金淋巴瘤(NHL),5例霍奇金淋巴瘤(HD),5例猫抓病(CSD)和5例结核性淋巴结炎(TBL),做了组织学、免疫组织化学EnVision法观察,其中6例KD和2例NHL做了电镜观察。结果 KD可有增殖,坏死和黄色瘤样三种病理组织学图像,但其基本的组织学特点为：淋巴结边缘契形淡染病灶和副皮质区融合性淡染病灶,病灶内单核样组织细胞明显增生,出现新月体样组织细胞,凋亡细胞或核碎片增多,无或很少见中性粒细胞等。免疫组织化学标记,灶性的组织细胞CD68和MPO阳性。电镜下可见病灶内增生的单核样组织细胞、新月体样组织细胞、凋亡小体和周围散在T淋巴细胞。结论 典型的KD由于其形态变化多样,有时需与其他淋巴结病仔细鉴别。这时仔细寻找KD的形态学特点,结合组织学、免疫组织化学和电镜观察,有助于确定KD的诊断。     

足趾穿掘性癌1例

穿掘性癌是一种罕见的鳞状细胞癌, 该病发展缓慢, 很少转移, 但常侵犯邻近软组织, 在临床中常表现为感染性病变症状, 因此临床常漏诊。本文报道1例43岁女性患者, 主要表现为双足皮肤反复破溃、流脓, 因临床初步诊断为慢性骨髓炎就诊, 后经过病理检查, 确诊为穿掘性癌。该病罕见, 在形态上易与疣状癌、乳头状鳞状细胞癌、表皮囊肿和假上皮瘤样增生等病变混淆。     

应用MG7观察胃癌相关抗原在胃粘膜异型增生组织中的表达

本文报道59例胃粘膜异型增生、44例胃癌及30例非癌性粘膜对照组,以PAP法引胃癌单克隆抗体MG_7对比染色的结果,并着重分析了10例胃粘膜重度异型增生及3例可疑癌与胃癌之间的关系。实验结果表明重度异型增生及可疑癌病例不仅在病理形态上与癌近似,在肿瘤抗原表达方面也存在相似之处。MG_7染色全部呈现阳性,其组织分布也与癌基本一致,具有癌组织的功能。文中探讨了中、轻度异型增生与重度异型增生的区别。作者认为中、轻度异型增生属良性病变,应称为单纯性不典型增生;而重度异型增生属恶性病变,称为异型增生似更为合理。     

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.