Multivessel revascularisation versus infarct-related artery only revascularisation during the index primary PCI in STEMI patients with multivessel disease: a meta-analysis

Background

There are controversial data regarding infarct-related artery only (IRA-PCI) revascularisation versus multivessel revascularisation (MV-PCI) in ST-elevation myocardial infarction (STEMI) patients with multivessel disease undergoing primary percutaneous coronary intervention (PCI). We performed a meta-analysis comparing outcome in same stage MV-PCI versus IRA-PCI in STEMI patients with multivessel disease.

Methods

Systematic searches of studies comparing MV-PCI with IRA-PCI in the MEDLINE and the Cochrane Database of systematic reviews were conducted. A meta-analysis was performed of all available studies. Primary outcome was all-cause mortality. Secondary endpoints were re-infarction, revascularisation, bleeding and major adverse cardiac events (MACE).

Results

A total of 15 studies were identified with a total number of 35,975 patients. Mortality rate was significantly higher in the MV-PCI group compared with the IRA-PCI group, odds ratio (OR): 1.64 (1.46–1.85). Both the incidence of re-infarction and re-PCI were significantly lower in the MV-PCI group compared with the IRA-PCI group: OR 0.54 (0.34–0.88) and OR 0.67 (0.48–0.93), respectively. Bleeding complications occurred more often in the MV-PCI group as compared with the IRA-PCI group: OR 1.24 (1.08–1.42). Rates of MACE were comparable between the two groups.

Conclusions

MV-PCI during the index of primary PCI in STEMI patients is associated with a higher mortality rate, a higher risk of bleeding complications, but lower risk of re-intervention and re-infarction and comparable rates of MACE.     

Investigation of the VDR gene polymorphisms association with susceptibility to colorectal cancer

The effects of 1,25-dihydroxyvitamin D3 are mediated by binding to a specific intracellular vitamin D receptor (VDR), which has been identified in a variety of tissues. Certain polymorphisms in the VDR gene have been associated with various neoplasms. For this purpose, we studied whether VDR TaqI or FokI genotype are associated with serum 25-hydroxyvitamin D3 in 52 controls and 26 patients with colorectal cancer. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP), and agarose gel electrophoresis tecniques were used to detect these polymorphisms. We measured 25-hydroxyvitamin D3 serum levels by ELISA. The frequencies of the FF, Ff and ff genotypes were 73.1%, 11.5%, 15.4% in colorectal cancer patients and 38.5%, 59.6%, 1.9% in healthy controls, respectively. We observed the T allele in 50% and 58.7%, and the t allele in 50% and 41.3% of colorectal cancer patients and the control group, respectively. In patients with colorectal cancer who have TT genotype, serum 25-hydroxyvitamin D3 level was lower than those with Tt/tt genotype (p:0.016). The frequency of subjects with TTFf or TtFf genotype in colorectal cancer patients was very low compared with all other genotypes (OR = 0.112; 95%CI 0.030-0.419). These data suggest that VDR TtFf or TTFf genotypes may protect against colorectal carcinogenesis. However, further studies are necessary to confirm these findings.     

Apoptosis in raloxifene-treated postmenopausal women

As raloxifene is a mixed estrogen receptor agonist and antagonist, it exerts different effects on apoptosis in different tissues. In this study, we aimed to evaluate apoptosis in the peripheral lymphocytes of postmenopausal women treated with raloxifene and compare it with untreated control subjects. In this way, we expected to deduce some results about the effect of raloxifene on the immune system and to serve as a guide for future studies on this newly proposed effect of a well-known agent. Twenty osteoporotic postmenopausal women treated with raloxifene for 12 months were included in this study. Another 20 osteoporotic postmenopausal women matched for age and postmenopausal years, but without any medication, were chosen as the control group. Apoptosis was evaluated using a morphological and DNA fragmentation assay, in the peripheral lymphocytes of these women. Our results revealed a decrease in the apoptosis percentages of the patients treated with raloxifene (14.6%) with respect to the control subjects (15.8%), but the difference was not statistically significant (p=0.467). This study indicated that raloxifene treatment had no apoptotic effect on peripheral human lymphocytes compared to controls.     

Evaluation of Food Additives and Low-toxicity Compounds for the Control of Bean Rust and Wheat Leaf Rust

The efficacy of low‐toxicity chemicals as possible alternatives to synthetic fungicides for the control of Uromyces appendiculatus and Puccinia triticina was evaluated. A preliminary selection of food additives was performed through in vitro and in vivo preliminary screenings. The ED₅₀ and minimum inhibition concentration (MIC) values showed that most of the food additives used in this study were more toxic to U. appendiculatus than to P. triticina. Acetic acid, potassium carbonate, sodium carbonate and sodium molybdate were the food additives that were more toxic to the urediniospores of P. triticina. Selected compounds and concentrations were tested on bean and wheat plants grown in pots under controlled conditions. Acetic acid, ammonium bicarbonate, potassium acetate, potassium benzoate, potassium bicarbonate, potassium carbonate, sodium acetate and sodium citrate at 0.03, 0.09, 0.03, 0.006, 0.012, 0.012, 0.03 and 0.03 m , respectively, significantly reduced the disease severity of U. appendiculatus without causing any injury to bean leaves. Ammonium bicarbonate, potassium bicarbonate, sodium bicarbonate and sodium citrate at 0.12, 0.03, 0.12 and 0.03 m , respectively, were the most effective in reducing the disease severity caused by P. triticina without causing any injury to wheat leaves.     

Impact of Cu and Fe concentrations on oxidative damage in male infertility

Oxidative stress in the reproductive system is thought to have an effect on the fertilizing ability of sperm. The purpose of this study was to assess the interaction of iron (Fe) and copper (Cu) ions in suspected subfertile and fertile male groups and to find out the relationships of the semen parameters (sperm count, motility, and abnormal morphology), glutathione, malondialdehyde, and reactive oxygen species with these variables. Semen and blood obtained from 60 subfertile men and from 40 fertile volunteers were examined. The sperm count and motility in the subfertile male group were found lower than those in fertile male group (p<0.001). Cu levels in serum and seminal plasma in the subfertile male group were significantly higher than those in the fertile male group (p<0.001 and p<0.05, respectively). There was also a significant increase in the Fe level of seminal plasma in the subfertile male group (p<0.001). However, there was no significant difference in the Fe level of serum in the subfertile male group. In conclusion, these findings suggest that Cu and Fe might be mediators of the effects of oxidative damage and play an essential role in spermatogenesis and male infertility; the determination of Fe and Cu levels in serum and seminal plasma during infertility investigation is recommended.     

Changes of nitric oxide synthase-containing nerve fibers and parameters for oxidative stress after unilateral cavernous nerve resection or manuplation in rat penis

After pelvic surgeries such as radical prostatectomy, two major complications--urinary incontinence and erectile dysfunction (ED) may occur. Etiologies for ED are multiple pathologic mediators/systems. Oxidative stress, which is known to be induced after surgical trauma, could be a cause of ED. The purposes of in this study are to investigate the effect of unilateral manipulation/ dissection and resection of the cavernous nerve (neurotomy) to NOS (nitric oxide synthase)-containing nerve fibers and pressure after electro stimulation in rat corpus cavernosum, and to determine whether these procedures would produce oxidative stress within rat cavernous tissue 3 weeks and 6 months after the operation. Male rats were divided into 5 groups. Rats in groups 1 and 2 underwent unilateral cavernous nerve manipulation and sacrificed 3 weeks and 6 months after the operation, respectively. Rats in groups 3 and 4 underwent unilateral neurotomy of a 5-mm. segment of the cavernous nerve, and they were sacrificed 3 weeks and 6 months after nerve ablation, respectively. Group 5 rats were control animals for biochemical analysis. Intracavernous pressure following electro stimulation reduced is significantly 3 weeks after unilateral resection, as compared to that of the manipulated nerve (P < 0.05), and it recovered 6 months after neurotomy. The recovery was also confirmed by NADPH (nicotinamide adenine dinucleotide phosphate) diaphorase staining in neurotomy groups. Lipid peroxidation, which is an indicater of oxidative stress, was determined by measuring thiobarbituric acid reacting substance (TBARS) levels and superoxide dismutase (SOD) activity. These markers indicated that unilateral cavernous nerve manipulation or resection produced oxidative stress within rat corpus cavernosum. Oxidative stress was more prominent 3 weeks after unilateral neurotomy (P < 0.05). Also, compared to the control animal group, oxidative stress was observed three weeks after manipulation of unilateral cavernous nerve (P < 0.05). Resection of the cavernous nerve caused more prominent oxidative stress than in the manipulation group. This study suggested, that unilateral cavernous neurotomy caused a decrease of intra cavernous pressure and NOS fibers in rat corpus cavernosum, and they recovered 6 months after neurotomy. Our data also provided evidence that neurotomy and manipulation of the cavernous nerve caused oxidative stress in rat corpus cavernosum and that oxidative stress was more prominent in the nerve resection group.     

Inhibition of inducible nitric oxide synthase in murine visceral larva migrans: effects on lung and liver damage

The roles of nitric oxide production and oxidative process were studied in mice infected with Toxocara canis and treated with aminoguanidine which is a specific inhibitor of inducible nitric oxide synthase (iNOS). Relations of nitric oxide synthase inhibition and tissue pathology were assessed by biochemical, histological and immunohistochemical methods. In experiments, Balb/c albino mice were inoculated with T. canis eggs either with or without aminoguanidine treatment or alone, at 24th, 48th hours and on 7th days. LPx and SOD values in liver tissue and plasma were measured. Liver and lung tissues were evaluated for the pathological lesions. The expression of eNOS and iNOS in both tissues were studied with immunohistochemistry in the same intervals. We observed significant differences between T. canis infected and aminoguanidine treated animals. Larval toxocarosis led to oxidative stress elevation in plasma. Microscopic examination of the liver histological sections revealed pathological lesions in the hepatic parenchyma in infected mice. In the mice received T. canis eggs plus aminoguanidine, the sinusoidal areas were enlarged. Histological lesions were more severe at 48 hours after infection. Numbers of eNOS and iNOS expressing epithelial cells were increased in the T. canis infected mice. The activities of eNOS and iNOS were also observed in the body of the larvae which have migrated to lung and liver. As a result, we have demonstrated that in vivo production of eNO and iNO during T. canis infection cause direct host damages and it is strongly related to the oxidative stress. We propose that larval NO can also be effective in larval migration, but it needs further investigation on distribution of NO in larvae.