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Better vaccines and new therapeutic drugs could be a successful breakthrough against intracellular bacteria. M. tuberculosis ABC transporter ATPase (Rv0986) plays a role in mycobacterial virulence by inhibiting phagosome-lysosome fusion. Thus, it could be a potential vaccine candidate. C. pneumoniae another important intracellular bacterium possesses a protein named CpB0255, which is homologous with the mycobacterial Rv0986. The aim of this study was the cloning, over-expression and purification of CpB0255 ABC transporter ATPase protein to study its biological properties. The immunogenicity and protective effect of recombinant chlamydial ATPase protein combined with Alum adjuvant were investigated in mice. The immunization resulted in the reduction of the number of viable C. pneumoniae in the lungs after challenge. Our results confirm that chlamydial ATPase induces protective immunity in mice.

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Acta Microbiologica et Immunologica Hungarica
Authors: Ildikó Faludi, Ágnes Csanádi, Ágnes Szabó, Katalin Burián, Valéria Endrész, and A. Miczák

Chlamydophila pneumoniae possesses a type III secretion system (TTSS), which allows the bacteria to secrete effector molecules into the inclusion membrane and into the cytosol of the host cell. Low calcium response protein H (LcrH), as a part of the TTSS, is a chaperone protein expressed from the middle to late stages of the chlamydial developmental cycle. Gene of LcrH (CPn0811) in a 6His-tagged form was cloned from C. pneumoniae CWL029, expressed and purified from Escherichia coli using the HIS-select TALON CellThru Resin. The purity was checked with mass spectrometry. The samples were used for immunization of BALB/c mice. The inducible E. coli clone, which over-expresses the chlamydial LcrH, permits the study of the biological properties of this protein.

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It remains difficult to distinguish adenoid cystic carcinoma (ACC) from polymorphous low-grade adenocarcinoma (PLGA). Although these neoplasms exhibit nearly similar histologic patterns, their biologic behavior is significantly different. This study was carried out in an attempt to overcome the histological overlap between these tumors using immunohistochemical method for c-kit and galectin-3 proteins on twenty cases of salivary gland tumors including twelve ACC and eight PLGA. Results revealed positive cytoplasmic reactivity for c-kit in 100% of ACC cases and only in 25% of PLGA. On the other hand, galectin-3 expression was observed in 100% of both ACC and PLGA cases. Moreover, solid variant of ACC showed overexpression of both proteins than cribriform and tubular subtypes. Significant positive correlation between the two studied proteins in ACC and PLGA was also observed (p < 0.05). Upon these results, over expression of c-kit and galectin-3 in ACC cases supports the concept of solid variant as a high-grade tumor. Moreover, c-kit may be used as a helpful marker to distinguish ACC from PLGA in cases where the diagnosis can be challenging.

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Matrix metalloproteinases (MMPs) constitute a large family of enzymes that degrade extracellular matrix proteins (ECM). MMPs are implicated in different pathological conditions such as cancer. Bcl-2 and P53 are key controllers of programmed cell death (PCD) or apoptosis. The aim of the present study was to determine the MMP-9, P53 and Bcl-2 levels in Egyptian patients with Mycobacterium tuberculosis (MTB) (Group I) compared with healthy control individuals (Group II). The concentrations of serum MMP-9 were determined quantitatively using enzyme immunoassay (EIA). P53 and Bcl-2 levels were assayed by flow cytometric analysis using specific monoclones. MMP-9 level was significantly higher in MTB patients compared with healthy control. Similarly, P53 and Bcl-2 levels were increased in MTB patients compared with healthy ones. These data reflect the alteration of MMP-9 level during the course of MTB infection, accompanied with apparent dysregulation of cellular apoptosis as indicated by P53 and Bcl-2 over-expression.

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Absztrakt:

Az inzulinszerű növekedési faktorok (IGF-ek) létezését a porcba történő szulfátbeépítés stimulálása kapcsán ismerték fel. Az IGF-ek a növekedési hormonnal (GH) kölcsönhatásban részt vesznek az embrionális fejlődésben és a születés utáni növekedésben. Az IGF1-ek fiziológiai hatása a szövetek növekedése és fejlődése, lipid- és szénhidrát-metabolizmus, túlélés/’anti-aging’, gyulladáscsökkentő, anabolikus antioxidáns, neuro- és hepatoprotektív tulajdonságok. A GH–IGF-tengelyről szóló ismereteink szerteágazóak, részben ellentmondásosak, kutatásuk napjainkban is intenzíven folyik. Ezért tartottuk érdemesnek e hatalmas ismeretanyag áttekintését és interpretálását. A GH–IGF-szisztéma működésével kapcsolatos közlemények tanulmányozása, különös tekintettel a kevésbé ismert anyagcsere-szabályozásra. A növekedési faktorok 75%-ban a májban keletkeznek GH- és inzulinstimulációra, hatásaikat specifikus receptoraikon fejtik ki, és kötőfehérjék módosítják. Az IGF1 növeli az izomtömeget és a csontsűrűséget. A mikrobióta indukálja az IGF1-et, ami elősegíti a csontnövekedést és -átépülést. A rövid láncú zsírsavak, melyek a mikrobióták által fermentált rostokban keletkeznek, IGF1-et indukálnak, ami arra utal, hogy a mikrobióta a csont egészségét is befolyásolja. Az IGF1-nek direkt és indirekt glükózszintcsökkentő hatása is van, fokozza az izomban a szabadzsírsav-oxidációt; ez csökkenti a szabadzsírsav-beáramlást a májba, így az inzulin-jelátvitel javul, csökken a máj glükózkibocsátása. Az inzulinszerű peptidek bioaktivitását az agyban a neuronalis túlélés, az izgalmi és gátló neurotranszmisszió, a normális szabadzsírsav-szint fenntartása, a kognitív funkció javítása, a sejtkárosodás elleni védelem, neurogenezis, angiogenezis jellemzik. Az IGF1 közvetlenül befolyásolja a cirkadián BMAL1-gén expresszióját a hypothalamicus sejtekben. Ez a szabályozás az IGF1 újonnan felismert ’zeitgeber’ szerepére utal. Az IGF2 hatásai kevésbé tisztázottak, bár releváns szerepe van a fetus fejlődésében, és protektíven hat az agyra. Az IGF-ek hiánya vagy éppen túlzott jelenléte számos betegségben kimutatható, illetve ezekkel oki összefüggésbe hozható. E felismerés hasznosítása a klinikai orvostudomány legközelebbi feladatai közé tartozik. Orv Hetil. 2019; 160(45): 1774–1783.

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Orvosi Hetilap
Authors: József Kas, Attila Csekeő, Csaba Fehér, Attila Vágvölgyi, Gábor Grmela, Judit Varga, Zsolt Rozgonyi, Ibolya Soltész, János Fillinger, Zsuzsanna Pápai, Erika Lahm, and Pál Vadász

insulin-like growth factor-II producing non-islet-cell tumor hypoglycemia. Growth Horm IGF Res. 2006; 16: 211–216. 7 Hajdu M, Singer S, Maki RG, et al. IGF2 over-expression in solitary

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-Gallego J : Quercetin decreases oxidative stress, NF-kappaB activation, and iNOS over expression in liver of streptozotocin-induced diabetic rats. J. Nutr. 135 , 2299 – 2304 ( 2005 ) 12. Eleazu CO , Eleazu KC , Chukwuma S , Essien UN

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The present study was designed to reveal possible common and specific neuroendocrine mechanisms of depressionand anxiety-like states in rodents. Animal models of depression and anxiety (in particular, posttraumatic stress disorder, PTSD) were applied including the learned helplessness and the stress-restress paradigms, respectively. Immunocytochemical staining revealed that depressive- and anxiety-like states in animals were accompanied by the rise in corticotropin-releasing hormone (CRH) immunoreactivity in the parvocellular division of the hypothalamic paraventricular nucleus (PVN). Decrease in vasopressin-immunoreactivity in early period of depressive-like state development was followed by the normalization of vasopressin content in the hypothalamic PVN in delayed period. Increased CRH and vasopressin immunoreactivity in the magnocellular part of the PVN in delayed period of anxiety-like state development was detected only in the stress-restress paradigm. These results suggest that CRH hyperdrive in the parvocellular PVN appears to be a common neuroendocrine abnormality for depressive- and anxiety-like states in animals, while over-expression of CRH and vasopressin in the magnocellular PVN represents a specific feature of anxiety/PTSD-like state.

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Mikhail KA Serry N Hatem 2002 AML1 gene over-expression in childhood acute lymphoblastic leukemia

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Amplification and over-expression of the MDM2 gene in a subset of human malignant gliomas without p53 mutations Cancer Res 54 2736 2739 . 37

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