骨髓基质细胞立体定向移植治疗大鼠脑缺血损伤的实验研究

目的:观察骨髓基质细胞立体定向移植对大鼠脑缺血损伤后神经功能恢复的作用并探讨其作用机制。方法:制作SD大鼠大脑中动脉缺血模型(MCAO);体外培养骨髓基质细胞,观察其生物学特性以及立体定向移植后对脑缺血损伤后神经功能改善情况。结果:骨髓基质细胞体外可以长期传代、扩增,分泌NGF、VEGF等多种神经保护性因子;立体定向移植后,骨髓基质细胞在脑内存活、迁徙,小部分分化成具有神经元表面标志的细胞,与对照组相比,骨髓基质细胞移植组神经功能改善情况好于对照组。结论:骨髓基质细胞具有多向分化潜能,表达并分泌多种神经保护性营养因子。立体定向移植MSCs,对改善脑缺血损伤后的神经功能状况具有积极作用。     

长期培养起始细胞在不同的基质细胞层上的培养

长期培养起始细胞（ＬＴＣ－ＩＣ）是一群迄今为止经体外培养所获得的最幼稚的造血祖细胞。作者用正常人类骨髓基质细胞以及５株人或鼠的骨髓外纤维细胞作基底层，移种上ＣＤ／ＳＢＡ￣－细胞，进行持续８周的长期培养，获得了人类正常骨髓中的长期培养起始细胞；同时筛选出ＭＲＣ－５细胞株作为支持血细胞生成、分化的理想细胞株。     

CTLA-4Ig对复发性单纯疱疹性角膜基质炎的抑制作用

目的：研究CTLA-4Ig对复发性单纯疱疹性角膜基质炎（HSK）的抑制作用。方法：采用复发性HSK的BALB/c鼠模型，经紫外线B光照射角膜诱导HSK复发；使用CTLA-4Ig作为负性调节因子，观察其对复发性HSK的影响。结果：注射CTLA-4Ig的小鼠，复发性HSK的角膜混浊程度及角膜炎性细胞浸润明显减轻，迟发型超敏反应明显减弱，外周血中CT4^ T细胞减少了92.8％。结论：CTLA-4Ig通过阻断B7:CD28/CTLA-4协同刺激途径，抑制了CD4^ T细胞的增殖，阻止了复发性HSK的发展。     

Isolation of murine cementoblasts: unique cells or uniquely-positioned osteoblasts?

While cementoblasts express a number of mineral-related proteins, including bone sialoprotein (BSP), osteopontin (OPN) and osteocalcin (OC), these proteins do not appear to be expressed by cells of the intermediate dental follicle/periodontal ligament (PDL). This information was utilized in an experimental strategy to isolate presumptive cementoblasts from the root surface of day 24 murine mandibular first molars. Using microscopic dissection techniques, molars were carefully extracted from their alveolar crypts and subjected to trypsin-collagenase digestion to remove adherent cells. Primary cultures were established and assayed for expression of proteins known to be expressed by cementoblasts at this timepoint in vivo (i.e. BSP, OPN, OC) and also an odontoblast-specific protein (i.e. DSP) to rule out contamination by pulpal cells. A subgroup of cells were found to express Type I collagen (89% of cells), BSP (46%), OPN (23%) and OC (30%); DSP was not detected within these cultures. We propose that cells within this heterogeneous population, which express this profile of osteogenic proteins, represent cementoblasts. The availability of a cementoblast cell line will make possible rigorous and controlled in vitro analysis of these cells and allow for determination of the unique characteristics of these cells not shared with other cells, particularly osteoblasts.     

Bone alkaline phosphatase and prostate-specific antigen in the monitoring of prostate cancer

A retrospective study has been made on the interrelationship of serum bone alkaline phosphatase (BAP), measured by the Ostase-RIA, and prostate-specific antigen (PSA) in 156 patients with M0 and M1 prostate cancer. BAP is a more sensitive and more specific method of determining osteoblast activity than total alkaline phosphatase (TAP). The main difference between these two assays is seen when the TAP is in the range of normal to twice-normal. BAP shows a low intraindividual variation in M0 disease, and was within normal limits in 18 patients following radical prostatectomy with a PSA < 0.1 ng/ml. A raised BAP was observed in 86.4% of M1 disease at diagnosis before treatment. The change of BAP was concordant with PSA in 69% of 49 cases of M1 disease, although there are marked differences in the rates of change of the two markers. A nadir of PSA ? 10 ng/ml after androgen blockade in M1 disease was associated with a high probability of a normal BAP. © 1994 Wiley-Liss, Inc.     

Stem cells in prostatic epithelia

The normal prostate is, structurally and functionally, a highly complex glandular tissue in which populations of epithelial and stromal cells interact, one with the other, and are under a constant state of proliferation, differentiation, elimination and selective secondary replenishment so that functional integrity of the tissue is maintained. The ability of normal prostatic tissue to maintain its structure and function is dependent upon retention of cells, generally regarded as 'stem cells', which are able to respond by proliferation and selective differentiation within a wide range of phenotypic alternatives. With respect to cells in the epithelial compartment, replenishment is possible at several levels from within distinct pathways of normal cellular differentiation. It is now appreciated that fully differentiated prostatic epithelial cells retain a far greater degree of phenotypic 'plasticity' than was earlier apparent from morphological examination of the intact tissue. This inherent plasticity, coupled with the ability of the intact tissue to respond to diverse environmental (particularly humoral) stimuli by regenerating a wide and divergent spectrum of functional prostatic epithelial phenotypes is its strength — but also its weakness. Disturbance and distortion of the homeostatic regulatory mechanisms, whether physical or humoral, which control the normal sequence of epithelial proliferation, differentiation and elimination exposes these cells, particularly multipotent 'stem cells', to an increased probability of genetic change, thus resulting in either transient, or permanent, neoplastic transformation.     

Corneal and Other Ocular Changes in Progressive Systemic Scleroderma

The ocular and systemic complications are reported of two patients having progressive systemic scleroderma. Although ocular complications and particularly those affecting the cornea are said to be uncommon one patient had corneal marginal furrowing with neovascularisation and the other a bilateral diffuse opacification of the anterior corneal stroma. The ocular and systemic complications of scleroderma are reviewed.     

Corneal dystrophies. I. Dystrophies of the epithelium,Bowman's layer and stroma

Most corneal dystrophies are autosomal dominant, bilateral disorders that primarily affect one layer of an otherwise normal cornea, progress slowly after their appearance in the first or second decade, and are not associated with a systemic disease. Epithelial basement membrane dystrophy and Fuchs' endothelial dystrophy are seen commonly by the general ophthalmologist; fleck, posterior polymorphous, granular or lattice dystrophies are seen more rarely, and others may never be seen in general office practice. While the distinctive clinical appearance of most corneal dystrophies allows accurate diagnosis, the integration of slitlamp findings with histopathologic and biochemical findings aids in the understanding of the clinical observations and provides a more rational basis for therapy. Transmission electron microscopy is the most accurate method of histopathologic diagnosis. Epithelial dystrophies usually manifest intraepithelial cysts and abnormal basement membrane. In stromal dystrophies, an abnormal substance accumulates within the keratocytes or among the collagen fibrils; it may be an excess normal metabolite (like glycosaminoglycans in macular dystrophy), a material not usually present (like amyloid in lattice dystrophy), or a substance of unknown composition (like hyaline in granular dystrophy). Each dystrophy is illustrated with a composite drawing. Endothelial dystrophies will be reviewed separately in a second article.