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12篇 您的检索式：作者名="Lubka"

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		题名	作者	年代	出处	被引量
	1	Risk identification-basic stage in risk management显示文摘	Lubka Tchankova	2002	Environmental Management and Health2002，13，3：	1
	2	Conversion of Cs aromatics and n-pentane over Ga2O3/HZSM-5 mechanically mixed catalysts 显示文摘	Vladislav Kanazirev Veselina Mavrodinova Lubka Kosova	1991	Catalysis Letters1991，9，1：	1
	3	The intestinal trefoil factor(Tff3), also expressed in the inner ear, interacts with peptides contributing to apoptosis显示文摘	Lubka M Shah AA Blin N	2009	J Appl Genet2009，50，2：	1
	4	Cytokineregulation of the trefoil factor family binding proteinGKN2 (GDDR/TFIZl/blottin) in human gastrointestinalepithelial cells显示文摘	Baus-Loncar M Lubka M Pusch CM	2007	Cell Physiol Biochem2007，20，14：	1
	5	Risk identification – basic stage in risk management'显示文摘	Lubka Tchankova		0，，03：	1
	6	Cytokine regulation of the trefoil factor family binding protein GKN2(GDDK/TFIZ1/blottin)in human gastrointestinal epithelial cells显示文摘	Baus-Loncar M Lubka M Pusch CM	2007	Cell Physiol Biochem2007，20，14：	1
	7	Cytokine regulation of the trefoil factor family binding protein GKN2(GDDR/TFIZ1/blottin)in human gastrointestinal epithelial cells显示文摘	Baus-Loncar M Lubka M Pusch CM		0，，：	1
	8	Risk identification - basic stage in risk management 显示文摘	Lubka Tchankova	2002	Environmental Management and Health2002，，13：	1
	9	Cytokine regulation of the trefoil factor family binding protein GKN2 (GDDR/TFIZ1/ blottin) in human gastrointestinal epithelial ceils显示文摘	Bans-Loncar M Lubka M Pusch CM	2007	Cell Physiol Biochem2007，20，14：	1
	10	Cytokine regulation of the trefoil factor family binding protein GKN2 (GDDIL/TFIZI/b\|ottin) in human gastrointestinal epithelial cells 显示文摘	Baus-Loncar M Lubka M Pusch C M	2007	Cell Physiol Bioehem2007，20，14：	1
	11	Lack of Tff3 peptide results in hearing impairment and accelerated presbyacusis显示文摘	Lubka M Müller M Baus-Loncar M		0，，：	1
	12	A role for complement blockade in kidney transplantation显示文摘Kidney transplantation is a life-saving procedure for patients with end-stage renal failure,but unfortunately,only a limited number of patients benefit from this procedure due to organ shortage.Moreover,even after transplantation,the graft can be lost due to antibody-mediated rejection(AMR).A recent study by Schmitz et al.in Nature Communications[1]provides new hope to prevent AMR and prolong renal allograft survival.The authors inhibited the innate immune complement cascade at the level of its central component C3 and successfully prevented the tissue injury mediated by donor-specific antibodies(DSAs)in a primate model.	Diana Karpman Zivile Bekassy Anne Grunenwald Lubka TRoumenina	2022	Cellular & Molecular Immunology2022，19，7：	0

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