An immunohistochemical study of keratin expression in ameloblastoma from a Kenyan population

OBJECTIVES: Ameloblastomas appear to exhibit biological heterogeneity and, except in the case of malignancy, histological appearances that do not always allow their behaviour to be predicted. The aim of this study was to assess keratin expression in African ameloblastomas and to correlate this with their clinical and histological features. MATERIALS AND METHODS: Expression of simple keratins 7, 8, 18 and 19; cornification keratins 1 and 10; basal and differentiation keratins 5 and 14 and hyperproliferation-related keratins 6 and 16 in 14-39 cases of ameloblastoma was assessed by immunohistochemical methods. RESULTS: There was patchy expression of keratin 7 in the suprabasal and stellate reticulum-like cells in some cases. All cases showed similar weak expression for keratins 8 and 18 in suprabasal and stellate reticulum-like cells but none showed keratin 1 or 10 expression. There was intense expression of keratins 5, 14 and 19 by all tumour cells suggesting that they may retain basal cell characteristics with a potential for proliferation. No consistent relationship was seen between histological types and keratin expression pattern. However, keratins 6 and 16, expressed by suprabasal and stellate reticulum-like cells, showed a marked variation within and between cases, with the highest levels of expression in squamous strands. CONCLUSIONS: We propose that squamous strands may represent the sites of most active growth within individual tumours and expression of keratins 6, 16 and 19 may be predictors of rapid growth. There is a need for further investigation of this in longitudinal clinical studies.     

The contribution of activated factor XIII to fibrinolytic resistance in experimental pulmonary embolism

BACKGROUND: The resistance of thrombi to fibrinolysis induced by plasminogen activators remains a major impediment to the successful treatment of thrombotic diseases. This study examines the contribution of activated factor XIII (factor XIIIa) to fibrinolytic resistance in experimental pulmonary embolism. METHODS AND RESULTS: The fibrinolytic effects of specific inhibitors of factor XIIIa-mediated fibrin-fibrin cross-linking and alpha2-antiplasmin-fibrin cross-linking were measured in anesthetized ferrets with pulmonary emboli. Five experimental groups were treated with heparin (100 U/kg) and/or tissue plasminogen activator (TPA, 1 mg/kg) and the percent (mean+/-SD) lysis of emboli was determined: (1) control, normal factor XIIIa activity (14.1+/-4. 8% lysis); (2) inhibited factor XIIIa activity (42.7+/-7.4%); (3) normal factor XIIIa activity+TPA (32.3+/-7.7%); (4) inhibited factor XIIIa activity+TPA (76.0+/-11.9%); and (5) inhibited alpha2-antiplasmin-fibrin cross-linking+TPA (54.7+/-3.9%). Inhibition of factor XIIIa activity increased endogenous lysis markedly (group 1 versus 2; P<0.0001), to a level comparable to that achieved with TPA (group 2 versus 3; P<0.05). Among groups receiving TPA, selective inhibition of factor XIII-mediated alpha2-antiplasmin-fibrin cross-linking enhanced lysis (group 3 versus 5; P<0.0005). Complete inhibition of factor XIIIa also amplified lysis (group 3 versus 4; P<0.0001) and had greater effects than inhibition of alpha2-antiplasmin cross-linking alone (group 4 versus 5; P<0.0005). No significant fibrinogen degradation occurred in any group. CONCLUSIONS: Factor XIIIa-mediated fibrin-fibrin and alpha2-antiplasmin-fibrin cross-linking both caused experimental pulmonary emboli to resist endogenous and TPA-induced fibrinolysis. This suggests that factor XIIIa may play a critical role in regulating fibrinolysis in human thrombosis.     

Punica granatum果实皮甲醇提取物化学成分的分离和标准化(英文)

AIM:The present study was undertaken to isolate and standardize the various active phytochemical constituents present in the fruit rinds of Punica granatum.METHODS:Fruit rinds of Punica granatum were dried and extracted with methanol in a static extractor;the percentage yield of the methanolic extract (MEPG) was found to be 26%;the methanolic extract was partitioned using n-butanol,ethyl acetate and water;the percentage yield of the fractions were found to be 17.16%,26.88% and 47.72% respectively.HPLC was c...     

Cytokine networks in destructive periodontal disease

BACKGROUND Cytokines are important regulatory proteins, produced by activated cells, which act by binding high affinity cell surface receptors. They are involved in almost all aspects of cell biology and form interacting networks, with cascades of sequential cell activation. They often show overlapping activities ( redundancy ) or the same cytokine may have a variety of different effects (pleiotropy). In excess, certain cytokines are damaging and proinflammatory. Tumour necrosis factor a (TNFα) and interleukin-I (IL-I) are markedly proinflammatory, inducing bone resorption, collagenase and prostaglandin E₂ production.
OBJECTIVE: This paper focuses on the role of TNFa and IL-l in the cytokine networks of destructive chronic per-iodontitis; specifically their regulation by T cell cytokines, receptor antagonists and inhibitory soluble forms of the IL-l and TNF receptors.
CONCLUSION: A hypothesis is proposed that destructive periodontal disease may be due to disregulation of these inhibitors, rather than an overproduction of IL-l and TNFα per se.     

氟化钠、单氟磷酸钠漱口后2 h菌斑液、菌斑及唾液氟离子的测定

氟化钠(NaF)和单氟磷酸钠(NaMFP)是目前市售最常见的含氟牙粉。以前一致认为氟的抗龋效能取决于牙所处液体环境中Fˉ浓度,但其临床抗龋效果却与二者的Fˉ浓度出现较大差异。本研究定量分析NaF和NaMFP液漱口后,唾液、全菌斑及菌斑液中Fˉ、MFPˉ浓度的变化,揭示其不同的抗龋特性。 标本取自12位自愿受试者。每个象限各选一颗磨牙或前磨牙取菌斑。测前48h不刷牙,当晚禁食,次日上午收集龈下菌斑和唾液标本作为基线水     

Induction Of Endothelin-1 Expression By Glucose: An Effect Of Protein Kinase C Activation

Enhanced actions or levels of endothelin-1 (ET-1), a potent vasoconstrictor, have been associated with decreased blood flow in the retina and peripheral nerves of diabetic animals and may be related to the development of pathologies in these tissues. Hyperglycemia has been postulated to increase ET-1 secretion in endothelial cells. We have characterized the mechanism by which elevation of glucose is increasing ET-1 mRNA expression in capillary bovine retinal endothelial cells (BREC) and bovine retinal pericytes (BRPC). Elevation of glucose, but not mannitol, from 5.5 to 25 mmol/l for 3 days increased membranous protein kinase C (PKC) activities and ET-1 mRNA in parallel levels by 2-fold in BREC and BRPC. These effects were reversed by decreasing glucose levels to 5.5 mmol/l for an additional 2 days. Glucose-induced ET-1 overexpression was inhibited by a general PKC inhibitor, GF109203X, and a mitogen-activated protein kinase kinase inhibitor, PD98059, but not by wortmannin, a phosphatidylinositol 3-kinase inhibitor. By immunoblot analysis, PKC-beta 2 and -delta isoforms in BREC were significantly increased relative to other isoforms in the membranous fractions when glucose level was increased. Overexpression of PKC-beta 1 and -delta isoforms but not PKC-zeta isoform by adenovirus vectors containing the respective cDNA enhanced in parallel PKC activities, proteins, and basal and glucose-induced ET-1 mRNA expression by at least 2-fold. These results showed that enhanced ET-1 expression induced by hyperglycemia in diabetes is partly due to activation of PKC-beta and -delta isoforms, suggesting that inhibition of these PKC isoforms may prevent early changes in diabetic retinopathy and neuropathy.     

Early Electrophysiological Changes In Transgenic Rat Model Of Charcot-Marie-Tooth

Recently, a reliable transgenic rat model of human Charcot-Marie-Tooth type 1 A has been developed. So far, neurophysiological studies have been performed only in advanced stages of rat disease. Moreover, axonal involvement, which is known to occur in human CMT1A, has never been observed in this rat model. Affected rats show overexpression of Peripheral Myelin Protein (PMP-22) and a peripheral hypomyelinating neuropathy. We perfomed an electrophysiological study in two heterozygous PMP-22 transgenic rats and in one normal control, matched for age (3 weeks) and weight (average: 60 g). Recordings were performed in vivo by stimulating the sciatic nerve at both sciatic notch and ankle sites and recording the Hoffman reflex and direct muscle responses (CMAP). The H-reflex related SNCV and MNCV were calculated by measuring the distance between the sciatic notch and the ankle sites and the respective latencies. The two transgenic rats showed different levels of PMP-22 overexpression, as judged by quantitative PCR. The rat with a lower PMP-22 gene level showed a 30% reduction of MNCV compared to the normal control, while SNCV was not reduced. The CMAP was sized approximately 45% of the normal rat while the ratio between H wave amplitude and CMAP was 30% of the normal, the H wave amplitude being more affected than the CMAP. The action potentials in the rat with a higher transgene level were not recordable. Our data demonstrate that slowing of MNCV is an early finding in the CMT1A rat model. The marked reduction of H wave amplitude in front of a normal SNCV suggests a possible early axonal damage of sensory fibers. The entity of electrophysiological compromission positively correlated with the number of copies for PMP-22 gene. All together these considerations prove the sensitivity of this method, however further studies are needed to confirm these results and to prove that this model may be suitable to investigate the effects of therapeutic approaches.