Relationship of transforming growth factor beta 1 to angiogenesis in gastric carcinoma.

Transforming growth factor-beta (TGF-beta) comprises a group of multifunctional regulatory proteins, whose effects include angiogenesis. The expression of TGF-beta 1 in gastric carcinomas (70 cases) has been determined and related to pathological features and microvessel count by immunohistochemical staining for TGF-beta 1 and Factor VIII related antigen. Prominent reactivity for TGF-beta 1 was associated with the depth of invasion (r = 0.2; p < 0.05) and increased microvessel count (r = 0.5; p < 0.05). Also, the microvessel count had a significant correlation with invasiveness (r = 0.34; p < 0.05) and lymph node metastasis (r = 0.28; p < 0.05). These findings indicate that TGF-beta 1 may have a role in tumor invasion and angiogenesis.     

CT analysis and histopathology of bone remodeling in patients with chronic rhinosinusitis.

OBJECTIVE: To evaluate the findings of computed tomography (CT) and histopathology of the bulla ethmoidalis as objective markers of bone remodeling in chronic rhinosinusitis (CRS). METHODS: Preoperative ostiomeatal unit (OMU) scans and histopathologic findings of the bulla ethmoidalis were performed on 23 patients (39 sides) undergoing endoscopic sinus surgery for CRS. Lund-Mackay scores and Hounsfield units (HU) of the bulla were checked in coronal CT scans. The pathologist graded the severities of the mucosal and bony changes in histopathology. Statistical analysis was performed using Mann-Whitney U test and Spearman correlation coefficient (r). RESULTS: The HU values of the bulla were significantly increased with higher Lund-Mackay scores in OMU CT (r = 0.405, P = 0.01). The bony grades in histopathology were significantly increased with higher mucosal grades (r = 0.821, P = 0.0001). These findings in CT scans and histopathology were well correlated with each other (r > 0.3, P < 0.05). CONCLUSION: HU may be a useful objective marker of bone remodeling in chronic rhinosinusitis.     

Flavonoids from the leaves ofRhododendron brachycarpum

The flavonoids isolated from the leaves ofRhododendron brachycarpum, were identified as quercetin, avicularin, quercitrin and hyperin.     

前列腺癌及其癌前病变的细胞核形态特征与DNA含量的定量研究

应用计算机图像分析技术，对３０例前列腺癌（ＰＣ）和３０例前列腺非典型增生（ＰＤ）的石蜡包埋标本进行了核形态定量参数、ＤＮＡ含量的定量测定。结果显示：ＰＤ的核面积明显高于正常细胞而低于ＰＣ（Ｐ＜０．０１）。三级ＰＤ之间，两两相比有非常显著性差异（Ｐ＜０．０１）。ＰＤ３与ＰＣ１的核面积有明显交叉，说明ＰＤ３具有ＰＣ的某些特征。正常前列腺上皮细胞与ＰＤ细胞核ＤＮＡ含量及倍体分布近似。ＰＤ１～ＰＤ３细胞核ＤＮＡ含量均值呈递增现象。ＰＣ组织分化程度越低，细胞核ＤＮＡ含量增高越显著，２Ｃ和４Ｃ细胞越少，呈明显相关关系。提示ＤＮＡ含量变化与前列腺癌和癌前病变的细胞分化异常密切相关。     

A novel cycloartane glycoside fromThalictrum uchiyamai

A new cycloartane glycoside (1) was isolated from the aerial part ofThalictrum uchiyamai Nakai (Ranunculaceae). On the basis of chemical and physicochemical evidence, the aglycone structure of this compound was characterized as 16,25-dihydroxy-3,24-diacetoxy-9, 19-cycloartane-29-oic acid, a new derivative of cycloartane triterpene. Also, the oligosaccharide moiety of this glycoside were determined as 29-O-α-L-rhanmnopyranosyl-(1→2)-[β-D-xylofuranosyl-(1→6)]-β-D-glucopyranosy by application of HMBC technique. Consequently, the structure of compound 1 was elucidated as 29-O-α-L-rhanmnopyranosyl-(1→2)-[β-D-xylofuranosyl-(1→6)]-β-D-glucopyranosyl-16, 25-dihydroxy-3,24-diacetoxy-9,19-cycloartane-29-oic acid ester.     

Extensive Aberrant Mongolian Spot

A 9-month-old male infant had generalized diffuse blue-gray pigmentation over most of his body, sparing the scalp, face, neck, palms, soles, periumbilical area, genital area, and nipples. Within the lesion, there were several conspicuous macules of considerably darker hue. Histologic examination revealed numerous dermal melanocytes. By 16 months of age, the child's blue-gray pigmentation had decreased substantially.     

Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists

The antagonist pharmacology of glutamate neurotoxicity was quantitatively examined in murine cortical cell cultures. Addition of 1-3 mM DL-2-amino-5-phosphonovalerate (APV), or its active isomer D-APV, acutely to the exposure solution selectively blocked the neuroexcitation and neuronal cell selectively blocked the neuroexcitation and neuronal cell loss produced by N-methyl-D-aspartate (NMDA), with relatively little effect on that produced by either kainate or quisqualate. As expected, this selective NMDA receptor blockade only partially reduced the neuroexcitation or acute neuronal swelling produced by the broad-spectrum agonist glutamate; surprisingly, however, this blockade was sufficient to reduce glutamate-induced neuronal cell loss markedly. Lower concentrations of APV or D-APV had much less protective effect, suggesting that the blockade of a large number of NMDA receptors was required to acutely antagonize glutamate neurotoxicity. This requirement may be caused by the amplification of small amounts of acute glutamate-induced injury by subsequent release of endogenous NMDA agonists from injured neurons, as the "late" addition of 10-1000 microM APV or D-APV (after termination of glutamate exposure) also reduced resultant neuronal damage. If APV or D-APV were present both during and after glutamate exposure, a summation dose-protection relationship was obtained, showing substantial protective efficacy at low micromolar antagonist concentrations. Screening of several other excitatory amino acid antagonists confirmed that the ability to antagonize glutamate neurotoxicity might correlate with ability to block NMDA-induced neuroexcitation: The reported NMDA antagonists ketamine and DL-2-amino-7-phosphono-heptanoate, as well as the broad-spectrum antagonist kynurenate, were all found to attenuate glutamate neurotoxicity substantially; whereas gamma-D-glutamylaminomethyl sulfonate and L-glutamate diethyl ester, compounds reported to block predominantly quisqualate or kainate receptors, did not affect glutamate neurotoxicity. The present study suggests that glutamate neurotoxicity may be predominantly mediated by the activation of the NMDA subclass of glutamate receptors--occurring both directly, during exposure to exogenous compound, and indirectly, due to the subsequent release of endogenous NMDA agonists. Given other studies linking NMDA receptors to channels with unusually high calcium permeability, this suggestion is consistent with previous data showing that glutamate neurotoxicity depends heavily on extracellular calcium.