Similarities and differences of human and experimental mouse lymphangiomas.

Lymphangioma is a disfiguring malformation of early childhood. A mouse lymphangioma model has been established by injecting Freund's incomplete adjuvant (FIA) intraperitoneally, but has not been compared with the human disease. We show that, in accordance with studies from the 1960s, the mouse model represents an oil-granuloma, made up of CD45-positive leukocytes and invaded by blood and lymph vessels. Several markers of lymphatic endothelial cells are expressed in both mouse and human, like CD31, Prox1, podoplanin, and Lyve-1. However, the human disease affects all parts of the lymphovascular tree. We observed convolutes of lymphatic capillaries, irregularly formed collectors with signs of disintegration, and large lymph cysts. We observed VEGFR-2 and -3 expression in both blood vessels and lymphatics of the patients, whereas in mouse VEGFR-2 was confined to activated blood vessels. The experimental mouse FIA model represents a vascularized oil-granuloma rather than a lymphangioma and reflects the complexity of human lymphangioma only partially.     

Perivascular Drainage of Amyloid-β Peptides from the Brain and Its Failure in Cerebral Amyloid Angiopathy and Alzheimer's Disease

Alzheimer's disease is the commonest dementia. One major characteristic of its pathology is accumulation of amyloid-β (Aβ) as insoluble deposits in brain parenchyma and in blood vessel walls [cerebral amyloid angiopathy (CAA)]. The distribution of Aβ deposits in the basement membranes of cerebral capillaries and arteries corresponds to the perivascular drainage pathways by which interstitial fluid (ISF) and solutes are eliminated from the brain—effectively the lymphatic drainage of the brain. Theoretical models suggest that vessel pulsations supply the motive force for perivascular drainage of ISF and solutes. As arteries stiffen with age, the amplitude of pulsations is reduced and insoluble Aβ is deposited in ISF drainage pathways as CAA, thus, further impeding the drainage of soluble Aβ. Failure of perivascular drainage of Aβ and deposition of Aβ in the walls of arteries has two major consequences: (i) intracerebral hemorrhage associated with rupture of Aβ-laden arteries in CAA; and (ii) Alzheimer's disease in which failure of elimination of ISF, Aβ and other soluble metabolites from the brain alters homeostasis and the neuronal environment resulting in cognitive decline and dementia. Therapeutic strategies that improve elimination of Aβ and other soluble metabolites from the brain may prevent cognitive decline in Alzheimer's disease.     

APC from mice harbouring the filarial nematode, Brugia malayi, prevent cellular proliferation but not cytokine production

Specific T cell hyporesponsiveness and depressed antibody productionis a key feature of human infection with the filarial nematodes,Brugia malayi and Wuchereria bancrofti Despite this immune suppression,responses indicative of T_h2 subset activation are present, includingunusually high levels of specific lgG4. We tested the possibilitythat infection with filarial nematodes causes a reduction inthe co-stimulatory or antigen-presenting capacity of macrophagesresulting in a failure to activate specific T cells. Adherentperitoneal exudate cells (PEC) from mice implanted with adultB. malayi were used to present antigen to the conalbumin-specificT cell clone, D10.G4. Proliferation of the D10 cells at evenbackground levels was completely blocked by the presence ofimplant-derived adherent PEC. However, cytokine production bythese cells in response to antigen was intact, and thus PECfrom implanted mice are capable of functionally processing andpresenting antigen. The elicitation of a suppressive cell populationwas specific for live adults as cells from mice implanted withdead adult parasites effectively stimulated D10 proliferation.The block in cellular proliferation is not due to the productionof factors typically associated with macrophage suppressionsuch as nitric oxide, prostaglandins or catalase. These observationsare consistent with the T cell hyporesponsiveness seen in humancases of patent Brugia infection and may provide a murine modelfor the immune suppression seen in lymphatic filariasis.     

家兔阑尾淋巴管铸型的扫描电镜研究

用淋巴管铸型、冰冻断裂样品及半薄切片样品观察了家兔阑尾巴管及泡周围淋巴窦的立体构筑，可见在阑尾粘膜浅层存在一层毛细淋巴管网，粘膜深层有致密的毛细淋巴管丛，从毛细淋巴管丛发出许多短树枝样毛细淋巴管伸向胸腺依赖区。从粘膜浅层毛细淋忱网及粘膜深层毛细淋巴管丛都发出与腔面垂直的毛细淋巴管，与滤泡周围淋巴窦相连，滤泡周围淋巴窦位于淋巴滤泡的外面和底面从腔面观察，滤泡财要巴窦与粘膜深层的毛细淋巴管丛共同形成茶     

A contribution to the pathogenesis of respiratory disturbances associated with subarachnoid haemorrhage; an experimental approach using an animal model

Summary The present experimental work focuses on the mechanisms involved in respiratory distress observed in the course of subarachnoid haemorrhage. For this purpose, respiratory disturbances were induced in rabbits by injecting fresh autologous blood into the subarachnoid space. For six hours after this artificially induced SAH, blood PO₂ and PCO₂ as well as expiratory air CO₂ were regularly determined, while during the same period cerebral blood flow and cerebrospinal fluid pressure measurements were recorded.The results of this study suggest that pressure effects acting the brain structures that support respiration are principally involved in the pathogenesis of respiratory disturbances following SAH. A decrease in CBF and hypoxia with hypercapnia play a contributing secondary role adding to a vicious cycle phenomenon.     

Thoracic duct lymph and PEEP studies in anaesthetized dogs

PEEP impedes thoracic duct drainage (LF). This can be counteracted by a thoracic duct fistula. Consequently, lung oedema (LOE) should develop during PEEP more slowly with LF at atmospheric pressure (LF_AP) than with LF against jugular venous pressure (LF_JVP). In 12 anaesthetized dogs LOE was produced by Ringer's solution i.v. (2.5 ml/min per kg) for 6 h during PEEP (10 mmHg) with either LF_AP or LF_JVP. Ringer's+PEEP greatly increased aortic, pulmonary artery and wedge pressures, JVP, and cardiac output. Colloid osmotic pressures in plasma and lymph were drastically reduced, pulmonary effective filtration pressure (EFP) rose by about 20 mmHg. LF_JVP increased 7-fold, LF_AP about 19-fold, the respective loss of plasma proteins was 1.83 and 1.06 g/kg during 6 h. Thermal-dye extravascular lung water showed an increment of 68 with LF_JVP versus 43 l/h/g per mmHg with LF_AP. Final lung water content was at any EFP (12.8–31.9 mmHg) lower with LF_AP than with LF_JVP amounting 512 with LF_JVP versus 377 l/g/per mmHg with LF_AP. LF_AP decreased the development of LOE during PEEP by bypassing the PEEP-induced high JVP and thus facilitating the removal of interstitial fluid. It is hypothesized that a thoracic duct fistula might aid the treatment of patients with LOE due to ARDS and therefore requiring high levels of PEEP.     

肝脓肿治疗模式的临床研究

目的探讨肝脓肿的治疗方式和减少并发症的途径。方法对117例肝脓肿的各种治疗方法进行回顾性总结。结果非手术治疗12例,经腹切开引流46列,B超引导下经皮穿刺抽脓或置管引流59例,全部治愈。介入超声治疗组术后平均住院日比手术引流组少6.2d(P<0.01),并发症明显减少(P<0.01)。结论经皮穿刺抽脓或置管引流术简便、安全、住院时间短、费用少,并发症和病死率低,可用于治疗大多数肝脓肿。     

胫骨交锁髓内钉术后感染分析

目的：探讨胫腌骨骨折交锁髓内钉术后感染的预防与治疗方法。方法;对12例术后感染的病例进行回顾性分析。3例经过抗菌素治疗,9例经过闭式滴不引流加抗菌素治疗,结果;全部病例获随访,随访时间10个月－2年,感染控制,骨折愈合,结论：对胫骨交锁髓内钉术后感染的病人,不必急于取出内固定,采用闭式滴注引流加抗菌素治疗可获得满意效果。     

脑室出血的治疗

目的探讨脑室出血的治疗方法。方法选择原发性脑室出血19例,继发性脑室出血21例,其原发出血灶血肿量严格限制在30ml以下,全部病人均采用双侧侧脑室双腔管引流,尿激酶脑室灌注及间断腰穿放液。结果死亡7例,死亡率17．5％,明显低于内科治疗80％的死亡率。结论双腔管双侧脑室引流尿激酶脑室灌注和间断腰穿放液等为目前治疗脑室出血的较为有效的方法。     

CD44v6和nm23-H_1的表达对大肠癌淋巴结转移的影响

目的　探讨CD44v6和nm2 3-H1基因产物表达与大肠癌淋巴结转移的关系。方法　应用SP免疫组化染色法 ,对 76例大肠癌标本进行CD44v6和nm2 3-H1基因产物测定。结果　CD44v6基因产物的高表达和nm2 3-H1基因产物的低表达与大肠癌淋巴结转移有关 (P <0 .0 1)。大肠癌CD44v6和nm2 3-H1表达无相关性 (P >0 .0 5 ) ,但CD44v6阳性表达伴nm2 3-H1阴性表达的患者发生淋巴结转移的可能性大。结论　CD44v6和nm2 3-H1与大肠癌淋巴结转移密切相关 ,两者在淋巴结转移中起协同作用 ,联合检测对判断大肠癌淋巴结转移是一个有用的指标。