碱性成纤维细胞生长因子对大鼠脑血肿周围组织和海马bax及bcl-2基因表达的调节

目的:观察碱性成纤维细胞生长因子对大鼠脑出血后出血灶周围脑组织和出血侧海马bax、bcl-2基因表达的影响,探讨神经营养因子对神经细胞调亡的调控。方法:实验于2006-01/10在广西医科大学医学科学实验中心完成。①取成年清洁级Wistar大鼠72只,雌雄各半,体质量250g左右。②采用脑内囊注射胶原酶建立大鼠脑出血模型,动物于苏醒后按Bederson法进行神经病学评分,评分>3分后入选本实验,入选72只大鼠随机抽签法分为3组,每组24只。碱性成纤维细胞生长因子组按8μg/kg剂量肌肉注射,1次/d;生理盐水组肌肉注射等剂量的生理盐水,1次/d;模型组不作任何干预。③每组分别于干预后1,3,7d随机抽取8只大鼠,麻醉状态下取出血灶周围脑组织和出血侧海马,采用半定量反转录-聚合酶链反应检测调亡调控基因bax mRNA,bcl-2mRNA的表达。结果:在建立脑出血模型中共5只大鼠死亡,随后对死亡动物进行解剖,发现脑内血肿量过大,致脑疝形成而导致死亡,后随机补充动物。72只大鼠进入结果分析。①血肿周围脑组织bax mRNA表达:干预后3d,7d,碱性成纤维细胞生长因子组血肿周围脑组织bax mRNA表达比生理盐水组明显减少(3d:0.54±0.19,0.76±0.23,P<0.05;7d:0.45±0.19,0.71±0.16,P<0.01)。②血肿周围脑组织bcl-2mRNA表达:干预后3d,7d,碱性成纤维细胞生长因子组的血肿周围脑组织bcl-2mRNA表达比生理盐水组明显增高(3d:0.68±0.25,0.39±0.19,P<0.05;7d:0.80±0.21,0.48±0.18,P<0.01)。③出血侧海马bax mRNA表达:干预后3d和7d,碱性成纤维细胞生长因子组的出血侧海马bax mRNA表达比生理盐水组均明显减少(3d:0.54±0.18,0.70±0.11;7d:0.43±0.24,0.69±0.18,P均<0.05)。④出血侧海马bcl-2mRNA表达:干预后3d和7d,碱性成纤维细胞生长因子组的出血侧海马bcl-2mRNA表达比生理盐水组均明显增多(3d:0.66±0.11,0.50±0.15;7d:0.72±0.12,0.52±0.22,P均<0.05)。结论:碱性成纤维细胞生长因子能调节凋亡相关基因,提高大鼠脑出血后大脑脑组织和海马bcl-2mRNA的表达,降低bax mRNA的表达。     

Comment on “Structural,electrical, and multiferroic characteristics of lead-free multiferroic: Bi(Co0.5Ti0.5)O3–BiFeO3 solid solution” by N. Kumar,A. Shukla,N. Kumar,R. Choudhary and A. Kumar,RSC Adv., 2018, 8, 36939”

My comments concern the significant errors in the crystallographic part of the commented paper. It was found that the studied crystal is of the sillenite type and the correct formula should be Bi₂₅FeO₃₉ : Co,Ti instead of BiFeO₃. Moreover, the type of unit cell is not correct. Due to the double doping the new type of unit cell, previously unknown, was proposed for such crystals. Furthermore, the authors did not find that the studied sample contains two slightly different phases, both of the sillenite type. The actual chemical composition of the studied crystals is not known.

The significant errors in the crystallographic part of the commented paper are described. The new chemical formula of the studied crystal is proposed: Bi₂₅FeO₃₉ : Co,Ti. The coexistence of two sillenite type phases is evidenced.     

Restriction of cell lysis by homologous complement: II. Protection of erythrocytes against lysis by newly activated complement

Our previous work revealed that homologous complement (C) was ineffective in lysing antibody-sensitized erythrocytes (EA) even at high concentrations. It was also shown that activation of complement on homologous EA resulted in the binding of C9 and the formation of EA bearing complement proteins C1 through C9 (EAC1-9), yet few hemolytic sites were formed. Instead, as shown here, the formation of homologous EAC1-9 caused the cells to become resistant to lysis even by heterologous complement during a second incubation. In contrast, when homologous EAC1-8 were produced by incubating EA with C9-depleted serum, such intermediates were not protected against lysis by heterologous complement during a second incubation. Furthermore, homologous C9 on EAC1-9 was able to reduce the hemolytic efficiency of heterologous complement without blocking C activation and the formation of new C5b-9 complexes. Protection was not modified when homologous EAC1-9 were produced in one step, by incubation of EA with serum, or sequentially by adding C9 to EAC1-8. The minimum number of 9-sites required to confer a protective effect on EAC1-9 was less than 200 per cell. Thus, in addition to its known effect in heterologous cell killing, homologous C9 is capable of protecting homologous cells against inadvertent complement lysis.     

Worrisome histologic alterations following fine-needle aspiration of benign parotid lesions

OBJECTIVE: To describe the histologic changes associated with preoperative fine-needle aspiration biopsies of benign parotid lesions and the features that distinguish these changes from malignant neoplasms. MATERIALS AND METHODS: Ten benign parotid lesions with a recent history of preoperative fine-needle aspiration were selected, including pleomorphic adenoma (4 cases), oncocytic adenoma (3 cases), myoepithelioma (1 case), Warthin tumor (1 case), and lymphoepithelial cyst (1 case). RESULTS: A spectrum of histologic alterations were observed. Alterations included squamous cell metaplasia (8 cases), infarction and necrosis (4 cases), subepithelial stromal hyalinization (3 cases), acute and chronic hemorrhage and inflammation with multinucleated giant cells (all cases), granulation tissue with subsequent fibrosis (all cases), cholesterol cleft formation (1 case), pseudoxanthomatous reaction (1 case), pseudocapsular invasion (1 case), and microcystic degeneration (2 cases). In cases with exuberant squamous metaplasia, necrosis, or subepithelial stromal hyalinization, a diagnosis of squamous cell carcinoma or low-grade mucoepidermoid carcinoma was seriously considered. CONCLUSIONS: Knowledge of a previous fine-needle aspiration procedure and awareness of its effects on histology of the subsequent parotidectomy specimens are necessary to avoid potential misdiagnosis.     

Activated protein C decreases plasminogen activator-inhibitor activity in endothelial cell-conditioned medium

Confluent cultures of endothelial cells from human umbilical cord were used to study the effect of activated human protein C (APC) on the production of plasminogen activators, plasminogen activator-inhibitor, and factor VIII-related antigen. Addition of APC to the cells in a serum-free medium did not affect the production of tissue-type plasminogen activator (t-PA) or factor VIII-related antigen; under all measured conditions, no urokinase activity was found. However, less plasminogen activator-inhibitor activity accumulated in the conditioned medium in the presence of APC. This decrease was dose dependent and could be prevented by specific anti-protein C antibodies. No decrease was observed with the zymogen protein C or with diisopropylfluorophosphate-inactivated APC. APC also decreased the t-PA inhibitor activity in endothelial cell-conditioned medium in the absence of cells, which suggests that the effect of APC is at least partly due to a direct effect of APC on the plasminogen activator- inhibitor. High concentrations of thrombin-but not of factor Xa or IXa-- had a similar effect on the t-PA inhibitor activity. The effect of APC on the plasminogen activator-inhibitor provides a new mechanism by which APC may enhance fibrinolysis. The data suggest that activation of the coagulation system may lead to a secondary increase of the fibrinolytic activity by changing the balance between plasminogen activator(s) and its (their) fast-acting inhibitor.     

A Comparison of Skin Interface Temperature Response Between the ProHeat Instant Reusable Hot Pack and the Standard Hydrocollator Steam Pack

The ProHeat^™ reusable hot pack is being used increasingly as a substitute for the standard hydrocollator steam pack. This study evaluated the effects of these two modalities on skin temperature. Seventeen subjects were studied during separate 30-minute applications of a ProHeat pack with a wet barrier, a ProHeat pack with a dry barrier, a hydrocollator pack, and a control pack on their nondominant calf. We measured the skin interface temperature and pack surface temperature during each application with surface thermocouples. The skin interface temperature rise time to the minimum therapeutic temperature (104°F) and the total time at and above the minimum therapeutic temperature, for each application, were analyzed using an analysis of variance (ANOVA) with repeated measures (p<.05). The ProHeat pack application, with one layer of wet toweling as a barrier, was not significantly different from the hydrocollator steam pack application. We conclude that the ProHeat pack, prepared with a wet barrier, can be considered a viable alternative to the standard hydrocollator steam pack.