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The trial court, however, did not specify the grounds upon which the motion to set aside was based. It is the function of the trial court to specify grounds upon which a ruling is made, and the reviewing court to then determine if that ruling is supported by the grounds set forth. See First National Bank of Springdale v. Washington, *537 294 Ark. 208, 742 S.W.2d 855 (1988); Cf. Pontoon v. M.G. Oliver & Co., 251 Ark. 695, 473 S.W.2d 876 (1971).
While it is true that a motion to set aside is addressed to the sound discretion of the trial court, a sound discretionary basis exists only when the trial court employs the proper legal criteria. We agree with the insured that the trial court could not have applied a standard that allowed the setting aside of a judgment against an insured under Rule 60(b) if the insurer consented, as it did in this case, to the judgment having been rendered. See Interstate Fire & Casualty Company v. Blagg, 235 Ark. 675, 361 S.W.2d 721 (1962); B & M Rigid v. Parker, 262 Ark. 613, 559 S.W.2d 145 (1977); Christian & Cox v. Frye, 283 Ark. 487, 677 S.W.2d 529 (1984).
The record indicates that the trial court relied on Rule 60(b) in denying the insurer’s motion. There is no indication, however, that the court applied the correct legal standard. Since the trial court’s decision is not supported by the facts that appear in this record, we reverse and remand this case for a new trial.
We want to emphasize, however, that we do not hold, nor do we even intimate that the insurer should prevail at trial. We hold only that, under the facts of this case, it was

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Never Lose your PC Security With Auslogics Registry Cleaner PRO.. Avast Antivirus Pro 2019 Crack. for Windows.Role of paraoxonase 1 genetic polymorphisms (Q192R) in the protection from hypertension and atherogenesis in type 2 diabetes.
The enzyme paraoxonase-1 (PON1) is involved in the protection of the lipidic membrane against oxidative stress. It has been described that the genetic polymorphism -208 G > A contributes to the susceptibility to type 2 diabetes, although the influences on cardiovascular risk have not been well established. Our aim was to verify whether the PON1 polymorphism influences the prevalence of metabolic syndrome components and coronary artery disease in patients with type 2 diabetes. The study included 113 patients (M/F: 68/45, age 58.2 +/- 11.8 years, body mass index 31.3 +/- 6.3 kg/m2). All subjects underwent a study of coronary artery disease, and a review of the medical history to determine the presence of the components of the metabolic syndrome and coronary artery disease. All subjects were genotyped for the PON1-Q192R polymorphism (rs662, position 192). The -208G>A PON1 polymorphism was found in 9.7% of patients with type 2 diabetes, and its frequency was slightly higher among women (10.8%) than men (8.7%), but this difference was not significant. The PON1 -208A allele was found in 5.6% of patients with type 2 diabetes. It was significantly associated with coronary artery disease (OR 3.35, 95% CI 1.23-9.24) and also with the presence of hypertension (OR 3.57, 95% CI 1.10-11.53). The carriers of the -208A allele showed lower PON1 enzymatic activity than those homozygous for the -208G allele. The PON1-Q192R polymorphism does not play a relevant role in type 2 diabetes. This enzyme protects, however, against hypertension and atherogenesis and, therefore, this polymorph
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