5 Gy全身照射对大鼠伤口巨噬细胞的抑制效应及W11-a12的促愈作用

目的 研究大鼠全身5Gy照射对伤口巨噬细胞（MΦ）功能的影响及W11－a12的促愈作用。方法 采用^60Coγ射线身身照射复合皮肤创伤模型,观察了MΦ酵母－补体复合物玫瑰花环形成试验、吞噬功能和分泌纤维粘连蛋白（FN）、转化生长因子β1（TGFβ1）、碱性成纤维细胞生长因子（bFGF）的功能。结果 大鼠5Gy全身照射复合皮肤创伤后第3、5天伤口内巨噬细胞C3b受体表达、吞噬功能,合成与分泌FN、TGFβ、bFGF的功能均显著受到抑制,但抑制效应的程度不同,MΦ的吞噬功能的抑制重于其分泌功能,分泌TGFβ1功能的抑制重于分泌bFGF的功能,W11-a12能显著逆转辐射对MΦ功能的抑制效应。结论 伤口MΦ功能受抑是合并放射损伤后伤口难愈的主要原因,增强MΦ功能是W11－a12促愈作用的一个途径。     

煤的热解研究III.煤中官能团与热解生成物

借助化学分析和ＦＴＩＲ光谱分析对我国煤化程度不同的１８ 种煤中官能团的研究表明：煤中官能团含量与煤化程度有关;煤中羧基、羟基及醚键等其他含氧官能团的含量与热解生成物ＣＯ２、Ｈ２Ｏ 和ＣＯ 的产率有关,脂肪—ＣＨ 的含量与甲烷和焦油的产率相关联,芳香—ＣＨ 的含量与热解半焦产率有关。煤的热解生成物主要是煤中官能团的断裂所致。     

Epimerization and Hydrolysis of Dalvastatin,a New Hydroxymethylglutaryl Coenzyme A (HMG-CoA) Reductase Inhibitor

In aqueous solutions, dalvastatin (1) undergoes epimerization as well as hydrolysis. The transformation of the drug was studied as a function of pH at 25°C in aqueous solutions containing 20% acetonitrile. At all pH values, first-order plots for the conversion are biphasic, indicating rapid equilibration of 1 with its epimer (2) and slower hydrolysis of 1 to the corresponding -hydroxy acid (3). Apparent first-order rate constants for the biexponential equation are given as a function of pH. The alkyl–oxygen cleavage of the lactone ring results in the epimerization of 1 to 2, whereas the acyl–oxygen cleavage results in the hydrolysis of 1 to 3. The epimerization is an S_N1 reaction reaching an equilibrium of [l] _eq/[2] _eq = 1.27. The epimerization rate is increased with an increase in the water content of the solvent. The hydrolysis of 1 to 3 is acid and base catalyzed. The hydrolysis is reversible in acidic media and irreversible in neutral and basic media. At pH values greater than 9, the hydrolysis reaction proceeds more rapidly than the epimerization.     

Radiology of the orbital apex

The orbital apex, formed by the superior orbital fissure and optic canal, is the cross-road between the orbit and the intracranial structures. Pathological processes may extend intracranially via the superior orbital fissure and vice versa. In addition to intrinsic soft tissue lesions, various pathological processes may involve the surrounding osseous anatomy. Malignant lesions arising from adjacent structures or from haematogeneous metastasis may also infiltrate this region.     

Cation channel control of neurite morphology

The development of neuronal polarity and morphology is essential for a functioning nervous system. The present study was undertaken to explore whether blockade of specific channels alter neuronal morphology. Retinal ganglion cells were cultured in the presence of antagonists to NMDA, AMPA/kainate, L-, N-, P-, and Q-type voltage-dependent calcium channels (VDCCs). Five parameters were measured under these conditions: the number of neurites at the cell body, total neurite length, the length of the longest neurite, the number of branch points per neurite, and the diameter of the cell soma. Antagonists to NMDA and L-type VDCCs reduce the number of neurites at the cell body; antagonists to P- and Q-type VDCCs increase the number of neurites. Antagonists to the N-type VDCCs increase total neurite outgrowth, while antagonists to the NMDA and P-type channels reduce total neurite length. Antagonists to the NMDA and L-type channels increase the length of a single neurite, while decreasing the number of branch points; antagonists to the P- and Q-type VDCCs do essentially the opposite-increase the number of neurites, while decreasing the length of each. Blockade of one or more cation channels in developing retinal ganglion cells significantly perturbs neurite morphology. This study may help elucidate part of the role that cation channel signaling plays in neuritic development.     

Repeated injections of a ciliary neurotrophic factor analogue leading to long-term photoreceptor survival in hereditary retinal degeneration

PURPOSE: To determine whether ciliary neurotrophic factor (CNTF) or brain-derived neurotrophic factor (BDNF) treatment leads to long-term photoreceptor survival in hereditary retinal degeneration. METHODS: An autosomal dominant feline model of rod-cone dystrophy was used throughout the study with two normal animals. In the first experiment, intravitreal injections of a human CNTF analogue (Axokine; Regeneron Pharmaceuticals, Tarrytown, NY) were administered to one eye of each animal (n = 10) beginning on postnatal day 10 and were repeated every 4 weeks. Clinical and histopathologic examinations were performed at 5.5, 9.5, and 13.5 weeks. In the second experiment, animals (n = 17) were randomly assigned to receive intravitreal injections of either Axokine (at half the initial dose), human BDNF, or the vehicle for Axokine to one eye at 5.5 weeks. The same therapy was repeated every 4 weeks in each group. Clinical and histopathologic examinations were performed at 9.5, 13.5, and 17.5 weeks. Photoreceptor survival was assessed by cell counting. Apoptotic cells were identified by morphology and a modified TdT-dUTP terminal nick-end labeling (TUNEL) technique. In the third experiment, two normal animals were treated with Axokine as in the first experiment. Glial fibrillary acidic protein ((GFAP) immunohistochemistry was performed to assess glial cell reaction. RESULTS: In the first two experiments, Axokine significantly prolonged photoreceptor survival (P < 0.01) and reduced the presence of apoptotic cells (P < 0.05) and TUNEL-positive cells (P < 0.05). In the second experiment, results in the the BDNF- and sham-injected eyes were not significantly different from those in the untreated eyes. Minimal posterior subcapsular cataract and mild retinal folds were found in all Axokine-treated eyes in both dystrophic and normal animals. These complications were milder in the second experiment when injections were started later and at a reduced dose. GFAP immunolabeling was also increased in all Axokine-treated eyes. CONCLUSIONS: Axokine, but not BDNF, delays photoreceptor loss in this hereditary retinal degeneration. Repeated injections maintain the protective effect.     

Visual-evoked potential evidence of chiasmal hypoplasia

PURPOSE: To show that chiasmal hypoplasia or aplasia need not be an isolated developmental anomaly and to examine the spectrum of associated clinical findings to explore the possibility that these patients may represent a phenotypic manifestation of a developmental gene anomaly. DESIGN: An observational case series. PARTICIPANTS: Five infants, between several weeks and 7 months of age, in whom the electrophysiologic characteristic of chiasmal hypoplasia had been noted were included. METHODS: Flash electroretinography and flash and pattern visual-evoked potentials (VEPs) were elicited from all patients. Clinical ophthalmologic examinations, including funduscopy, were performed, and all patients had magnetic resonance imaging (MRI) brain scans. MAIN OUTCOME MEASURES: The occipital distribution of monocular VEP response peaks was studied. The symmetry of lateral channel responses was compared for monocular stimulation. RESULTS: All five patients had a crossed asymmetry in the monocular VEP occipital distribution, which is consistent with a paucity of fibers crossing at the chiasm. The MRI findings supported this electrophysiologic observation, illustrating degrees of chiasmal hypoplasia and variable coincidence of other midline abnormalities of the brain. Optic disc appearances varied from normal to hypoplastic and colobomatous. CONCLUSIONS: The ophthalmologic and MRI findings of five patients who showed a crossed asymmetry in monocular flash VEPs are consistent with a paucity of axons crossing at the chiasm. The similarities between achiasmia in humans and mice due to a Pax2 gene anomaly are discussed.     

Contact lens wear after photorefractive keratectomy: comparison between rigid gas permeable and soft contact lenses.

PURPOSE: To determine if rigid gas permeable (RGP) or soft contact lenses can be successfully worn after photorefractive keratectomy (PRK) to correct residual refractive errors. METHODS: Patients with residual stable ametropia after PRK were fit with RGP or soft lenses. Manifest refraction, corneal topography, and keratometry were performed, and post-PRK corneal haze was graded during the study visits. Contact lens fit characteristics and comfort were assessed. Lens centration, visual quality, and ocular surface status were graded, and visual acuity with contact lenses was charted. RESULTS: Eighteen patients were recruited for RGP lens fitting. The mean refractive error post-PRK was +0.80 D +/- 2.03 (range: -3.50 to+3.00 D). The mean contact lens power was -3.90 D +/- 2.03 (range: 0 to -7.00 D), and the mean contact lens base curve was 7.88 mm +/-0.16. A significant positive tear film at the site of the central ablation was noted, contributing to excessive minus lens power in all cases. Despite mild to moderate lens instability and de-centration, 14 patients reported excellent visual quality with the lenses, and pre-PRK best-corrected acuity was achieved in all patients. Twenty-five percent (4 of 16) of the patients were able to wear the lenses all day. Eleven patients were recruited for soft contact lens fitting-five from the RGP trial. The mean refractive error post-PRK was -0.64 D +/- 2.01 (range: -3.50 to +1.75D). The mean contact lens power was -0.60 D +/- 2.07 (range: -3.75 to +2.5 D), and the mean contact lens base curve was 8.33 mm +/- 0.42. Eight patients were corrected with lenses to their pre-PRK best-corrected acuity, and nine patients reported excellent visual quality with the lenses. All the patients had excellent lens centration. Thirty-six percent (four of 11) of patients were wearing the lenses all day. CONCLUSIONS: Fitting RGP lenses after PRK results in good visual acuity but may be associated with mild to moderate lens instability and decentration. Soft contact lens fitting also results in good visual acuity. Soft lenses were better tolerated by the subjects in our study because of improved lens centration and stability.     

Primary intramedullary spinal cord primitive neuroectodermal tumor with intracranial seeding in an infant

Primary spinal cord primitive neuroectodermal tumor (PNET) is a rare entity. In all, 13 cases have been reported in the literature, including 3 with intracranial seeding. A 3-month-old girl with involvement of the spinal cord below the mid-thoracic level is described. The brain MRI revealed findings indicative of seeding along the intracranial subarachnoid space. Biopsy, duraplasty and removal of laminotomy flap were done. In spite of a good response to the first cycle of postoperative 8-drugs-in-a-day chemotherapy, further treatment was refused. She died 21 days after the onset of leg weakness, which reveals the rapid progression of untreated cases. To our knowledge, this is the first case of spinal cord PNET with parenchymal involvement that has been described in an infant.