Novel compounds effective as xanthine oxidase inhibitors, method for preparing the same, and pharmaceutical composition containing the same TECHNICAL FIELD The present invention relates to novel compounds of formula (1): in which A, D, E, Q Y and Q are as defined below, which are effective as an inhibitor for xanthine oxidase, a process for preparing the same, and a pharmaceutical composition comprising a therapeutically effective amount of the same. BACKGROUND ART Xanthine oxidase is known as an enzyme which converts hypozanthine to xanthine and further converts thus-formed zanthine to uric acid. Although most mammals have uricase, humans and chimpanzees do not, thereby uric acid is known to be the final product of purine metabolism (S. P. Bruce, Ann. Pharm., 2006, 40, 2187-2194). Sustained elevation of blood concentration of uric acid causes various diseases, representatively including gout. As described above, gout is caused by an elevated level of uric acid in the body, indicating the condition in which uric acid crystals accumulated in cartilage, ligament and surrounding tissue induce severe inflammation and pain. Gout is a kind of inflammatory articular disease, and its incidence rate has steadily increased during past 40 years (N. L. Edwards, Arthritis & Rheumatism, 2008, 58, 2587-2590). From the 1960s to the mid-1990s, gout patients in the West exhibited an astonishing increase of about 200-300%, mainly in males. The increased rate of gout patients can be traced to obesity, aging, kidney function decline, hypertension, etc. The incidence rate of gout appears to be a level of about 1.4/1,000 persons, but it also depends on the uric acid level. That is, while the incidence rate of gout is 0.5% in a patient group with a blood uric acid level of 7.0 mg/dl or more, the incidence rate of gout is 5.5%) in a patient group with a uric acid level of 9.0 mg/dl or more (G. Nuki, Medicine, 2006, 34, 417-423). Considering the incidence rate as described above, blood uric acid level is found to be an important causative factor for gout. In addition, dietary habits, alcohol, lipid and obesity can serve as important inducing factors of gout. Recently, the correlation of uric acid with heart failure, hypertension, diabetes, kidney diseases and cardiovascular diseases has been extensively investigated by many researchers, and the importance of uric acid control has been increased (D. I. Feig et al., N. Eng. J. Med, 2008, 23, 1811-1821). In addition, as an inhibitor of xanthine oxidase, allopurinol is known to have an effect on ulcerative colitis (Aliment. Pharmacol. Ther. 2000, 14, 1159-1162 ; WO 2007/043457). Allopurinol was a unique drug for the treatment of gout for 40 years, until febuxostat was approved as an arthrifuge in USA in 2009 (Brain Tomlinson, Current Opin. Invest. Drugs, 2005, 6, 1168-1178). Allopurinol is known to be a non-specific inhibitor for various enzymes that are involved in purine and pyrimidine metabolism, and it has a Ki of 700 nM for xanthine oxidase (Y. Takano et al., Life Sciences, 2005, 76, 1835-1847). Allopurinol is immediately oxidized to oxypurinol by xanthine oxidase, and this metabolite is known to act as a potent inhibitor for xanthine oxidase. However, it is known that allopurinol causes gastrointestinal side effects and skin rash and exhibits poor compliance in the case of long-term administration. Especially among patients receiving allopurinol, the side effect of Stevens-Johnson syndrome is reported, at a low rate but it is unpredictable and lethal (Felix Arellano et al., Ann. Pharm., 1993, 27, 337-43). This serious side effect is known to accompany necrocytosis in the skin and mouth mucosa, and without proper treatment about 25% of patients may die as a result. Thus, in order to develop novel xanthine oxidase inhibitors various researches have been conducted resulting in numerous patent publications (for example, WO 1992/009279, WO 1998/018765, WO 2007/004688, WO 2007/043457, WO 2008/126770, WO 2008/126898, WO 2008/126899). Among these, WO 1998/018765 describes the inhibitory effect of pyrazoles and phenyl derivatives against xanthine oxidase, and WO 2008/126898 reports that indole compounds exhibit an inhibitory effect against xanthine oxidase. SUMMERY OF THE INVENTION One object of the present invention is to provide novel compounds of formula (1) which exhibit very excellent inhibitory effect against xanthine oxidase. Another object of the present invention is to provide a novel process for the preparation of the compounds of formula (1). Still another object of the present invention is to provide a pharmaceutical composition for the inhibition of xanthine oxidase, which comprises a therapeutically effective amount of the compounds of formula (1) as an active ingredient. Still another object of the present invention is to provide a method for the treatment and/or prevention of the diseases associated with xanthine oxidase such as hyperuricemia, gout, heart failure, cardiovascular disease, hypertension, diabetes, kidney disease, inflammation and articular disease, and inflammatory bowel disease, which comprises using the compounds of formula (1) as an active ingredient. DISCLOSURE OF THE INVENTION In order to solve the above stated technical subject, the present invention provides the compounds of the following formula (1): in the above formula (1) A is selected from the following substituents A-i, A-ii, A-iii, A-iv, A-v, A-vi, A-vii and A-viii: wherein represents hydrogen, halogen, or halogen- substituted or unsubstituted C1-C6-alkyl, preferably C1-C4-alkyl, X represents O or S, Z represents C or N, E represents hydrogen, halogen, cyano, nitro, substituted or unsubstituted C1-C6-alkyl, or substituted or unsubstituted C1-C6-alkoxy, D represents hydrogen, halogen, cyano, nitro, halogen-substituted or unsubstituted C1-C6-alkyl, -CHO, or -CH=N-OH, Q is selected from the following substituents Q-i, Q-ii and Q-iii-1 to Q-iii-9: (Q-i) hydrogen; (Q-ii) substituted or unsubstituted, saturated or unsaturated, and straight-chain, branched or cyclic alkyl; (Q-iii-1) (wherein W represents O or S, R7 represents hydrogen, or substituted or unsubstituted lower alkyl, and n denotes an integer of 0-3); (Q-iii-2) (wherein W represents O or S, R8 and R9 each represent hydrogen or lower alkyl, and m denotes an integer of 1-3); (Q-iii-3) (wherein R8 and R9 each represent hydrogen or lower alkyl, and m denotes an integer of 1-3); (Q-iii-4) (wherein RIO and Rll each represent hydrogen, halogen, lower alkoxy or lower alkyl, and m denotes an integer of 1-3); (Q-iii-5) (wherein R12 represents substituted or unsubstituted lower alkyl or aromatic group, and n denotes an integer of 0-3); (Q-iii-6) (wherein R13 and R14 each represent substituted or unsubstituted lower alkyl, or together with N to which they are attached may form a 3-7 membered heterocycle, and n denotes an integer of 0-3); (Q-iii-7) (wherein R15 represents substituted or unsubstituted lower alkyl, and m denotes an integer of 1-3); (Q-iii-8) (wherein m denotes an integer of 1-3); (Q-iii-9) (wherein R15 represents substituted or unsubstituted lower alkyl, and m denotes an integer of 1-3); Y represents hydrogen, halogen, substituted or unsubstituted, saturated or unsaturated, and straight-chain, branched or cyclic alkyl, substituted or unsubstituted C1-C6-alkoxy, or substituted or unsubstituted aromatic or heteroaromatic group, and G represents hydrogen, or represents substituted or unsubstituted, saturated or unsaturated, and straight-chain, branched or cyclic alkyl. Hereinafter, unless specially restricted, the compounds of formula (1) as an active ingredient of the therapeutic agent include all their pharmaceutically acceptable salts and isomers, and they should be instrued to fall under the scope of the present invention. For the convenience of explanation only, they are simply referred to as 'compounds of formula (1)' in the present specification. The above compounds of formula (1) according to the present invention have a quite different chemical structure from the earlier known xanthine oxidase inhibitors. As shown in the following experiments, they exhibit an excellent inhibitory effect against xanthine oxidase associated with gout. Thus, they can be used for the prevention and treatment of diseases associated with xanthine oxidase, such as, for example, hyperuricemia, heart failure, cardiovascular disease, hypertension, diabetes, kidney disease, inflammation, articular disease, etc. The terms as used herein will be briefly explained below. If there is no special mention in the present specification, the term "substituted or unsubstituted" means to include both the cases of being substituted and unsubstituted. In the case of "substituted," the radical may be substituted individually and independently by one or more groups selected from alkyl, cycloalkyl, hydroxy, alkoxy, mercapto, alkylthio, cyano, halogen, carbonyl, thiocarbonyl, nitro and their protective derivatives. If appropriate, these groups may be furthermore substituted. As used herein, "pharmaceutically acceptable salts" means the salt forms of a compound, which neither give any serious irritation to the organism to which the compound is administered nor damage the biological activities and properties of the compound. Such a "pharmaceutically acceptable salt" includes a non-toxic acid addition salt containing a pharmaceutically acceptable anion, for example, a salt with inorganic acids such as hydrochloric acid, sulfuric acid, nitric acid, phosphoric acid, hydrobromic acid, hydriodic acid, etc.; a salt with organic carboxylic acids such as tartaric acid, formic acid, citric acid, acetic acid, trichloroacetic acid, trifluoroacetic acid, gluconic acid, benzoic acid, lactic acid, fumaric acid, maleic acid, salicylic acid, etc.; or a salt with sulfonic acids such as methanesulfonic acid, ethanesulfonic acid, benzenesulfonic acid, p-toluenesulfonic acid, etc. The compounds of formula (1) can also form a pharmaceutically acceptable salt, for example, a salt with alkali metals or alkaline earth metals such as lithium, sodium, potassium, calcium, magnesium, etc.; a salt with amino acids such as lysine, arginine, guanidine, etc.; or an organic salt with dicyclohexylamine, N-methyl-D-glucamine, tris(hydroxymethyl)methylamine, diethanolamine, choline, triethylamine, etc. The compounds of formula (1) of the present invention may be converted to their salts according to any of the conventional methods. As used herein, "isomer" means those having the same chemical or molecular formula as, but optically or sterically different from, the compounds of formula (1), or salts thereof. The compounds of formula (1) of the present invention may have an oxime structure, and so may exist in the form of geometrical isomers, trans and cis. All the isomers, their salts, and their mixtures (including racemic mixture) are also covered by the present invention. As used herein, "aromatic" means a carbocyclic aryl (e.g., phenyl, naphthyl,etc.) group having a covalent TT electronic system and at least one ring. This term also includes monocyclic or fused-ring polycyclic (i.e., rings sharing the adjacent carbon pairs) groups. As used herein, "heteroaromatic" means a heterocyclic aryl group having a covalent TT electronic system and at least one ring. It includes but is not limited to furan, thiophene, pyrrole, oxazole, thiazole, imidazole, pyrazole, isothiazole, triazole, thiadiazole, pyridine, pyridazine, pyrimidine, pyrazine, triazine, etc. As used herein, "alkyl" means an aliphatic hydrocarbon group. The alkyl group may be "a saturated alkyl" not containing alkene or alkine moiety at all, or "an unsaturated alkyl" containing at least one alkene or alkine moiety. The term "alkene" means a group having at least one carbon-carbon double bond, and "alkine" means a group having at least one carbon-carbon triple bond. Regardless of being saturated or unsaturated, the alkyl group may be branched, linear or cyclic. Unless otherwise stated, the alkyl group may contain 1 to 20 carbon atoms, and the lower alkyl group may contain 1 to 7 carbon atoms. As typical examples thereof, methyl, ethyl, propyl, isopropyl, butyl, isobutyl, t-butyl, pentyl, hexyl, ethenyl, propenyl, butenyl, ethinyl, propinyl, butinyl, cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, etc. can be mentioned. The alkyl group may be substituted or unsubstituted. In the case of "substituted," the radical may be substituted individually and independently by one or more groups selected from cycloalkyl, hydroxy, alkoxy, mercapto, alkylthio, cyano, halogen, carbonyl, thiocarbonyl, nitro and their protective derivatives. As used herein, "heterocycle" means a group wherein the ring carbon atom is replaced by oxygen, nitrogen, sulfur, etc. It may optionally include a double bond. The typical examples thereof may include but are not limited to pyrroline, pyrrolidine, imidazoline, imidazolidine, pyrazoline, pyrazolidine, pyran, piperidine, morpholine, thiomorpholine, piperazine, etc. As used herein, "halogen (or halo)" means F (or -F), CI (or -CI), Br (or -Br) and I (or -I). Other terms in the present specification may be construed to have the meaning conventionally understood in this field by a skilled artisan. Preferred compounds among the compounds of formula (1) above are those wherein Q is selected from the following substituents Q-i to Q-iii-8: (Q-i) hydrogen; (Q-ii) C1-Cg-alkyl which is unsubstituted or substituted by a group selected from halogen, hydroxy, C3-C7-cycloalkyl and 0-R