Substance Abuse Profiles of Patients Admitted to the Alcohol and Drug Addiction Research, Treatment, and Education Center in Turkey.

OBJECTIVES: To determine the substance abuse profiles of patients treated a Drug Addiction Research, Treatment, and Education Center (AMATEM) in association with the percentage of substance use distribution and multiple substance use in their urine samples. For this, we retrospectively evaluated the urine sample analysis reports of 600 male and female patients aged 13 to 65 years who were treated at the AMATEM unit of Istanbul Neuropsychiatry Hospital between January 1st, 2015, and December 12th, 2015. MATERIALS AND METHODS: The urine samples were sent to Üsküdar University Advanced Toxicology Analysis Laboratory and were analyzed using a UPLC tandem mass spectrometer (UPLC-MS/MS). To determine the substance use profiles of the patients applying to AMATEM, statistical assessment was performed on the analysis reports of the patients. RESULTS: When the analysis reports of the 600 urine samples were examined, 293 patients were identified to have used addictive substances. The substances most frequently detected in the urine samples were respectively: cannabis, alcohol, morphine, cocaine, synthetic cannabinoids, 3,4-Methylenedioxymethamphetamine, and amphetamine. CONCLUSION: The findings in our study resemble the rates of cannabis use by the young population throughout the world. Our results show differences to the literature regarding the consumption of synthetic cannabinoids because the variety of synthetic cannabinoids change rapidly around the world each year.

Diversity of killer cell immunoglobulin-like receptor genes in Southern Turkey.

Killer cell immunoglobulin-like receptors (KIRs) are a family of inhibitory and activating receptors expressed by natural killer (NK) cells and regulate NK cells' activity. KIR genes are highly polymorphic markers, characterized by a wide diversity, and can therefore be considered as good population genetic markers. The aim of this study was to determine KIR gene frequencies, ratios of haplotypes and genotypes in Southern Turkey and also to compare the data with other worldwide populations studied previously. The study group consisted of 200 non-related individuals from Southern Turkey. The percentage of each KIR gene in the population group was determined by direct counting. Differences between populations in the distribution of each KIR gene and genotype profile were estimated by two-tailed Fisher Exact test. The most frequent non-framework KIR genes detected in Southern Turkey population were: KIR 2DL1 (97%), KIR 3DL1 (91%), KIR 2DS4 (92%) and the pseudogene 2DP1 (96%). Fourty different genotypes were found in 200 subjects and AA1 genotype was the most frequent (27%). Among 40 different genotypes, ten of these were described for the first time in this study and were added to the database ( http://www.allelefrequencies.net ) numerized as genotype ID from 400 to 409. Gene frequencies and found genotypes demonstrated similarity of Southern Turkey's KIR repertoire with the KIR repertoires of Middle East and European population. High variability seen in KIR genome in this region is thought to be formed as a result of migration and settlement of different civilizations in this region and heterogenity formed in time.

Role of neopterin, C-reactive protein and myeloperoxidase in patients undergoing cardiopulmonary bypass.

OBJECTIVE: The aim of the present study was to investigate the role of neopterin (NP), C-reactive protein (CRP) and myeloperoxidase (MPO) in patients undergoing coronary artery bypass grafting with or without cardiopulmonary bypass (CPB). PATIENTS AND METHODS: Forty patients submitted for elective coronary artery bypass grafting were included in this prospective study. Patients were divided into two groups of 20 individuals, those who did not undergo CPB (group 1), aged 54.1 ± 13.5 years, and those who did (group 2), aged 60.2 ± 11.7 years. In group 1, there were 17 males and 3 females, while in group 2, there were 16 males and 4 females. Serum CRP, serum and urine NP and leukocyte MPO activity were measured preoperatively, at the end of surgery, and 4, 24 and 72 h after surgery using high-performance liquid chromatography, immunoturbidimetry and the reduction in o-dianizidine, respectively. RESULTS: The level of serum NP was higher preoperatively and at the end of surgery (0 h), 4, 24, and 72 h after the operation in those who underwent CPB compared to those who did not. However, there was no significant difference in NP concentrations between the two groups at any time except 24 h after surgery (p = 0.002). Urine NP concentrations showed similar values preoperatively but increased postoperatively in both groups of patients. The only significant difference in urine NP concentration between the two groups occurred at 0 and 24 h after surgery (p = 0.001, p = 0.000). Serum CRP concentrations showed similar values preoperatively, at the end of surgery and 72 h after the operation and increased at 4 and 24 h postoperatively in both groups. The only significant difference in CRP concentration between the two groups occurred 4 and 24 h after surgery (p = 0.024 and p = 0.000, respectively). MPO levels were found to be increased in the CPB patients when compared to those patients who did not undergo CPB. However, the difference between the groups was not statistically significant. CONCLUSION: Our data show that CPB induced a rise in NP and CRP levels.

The role of CYP2C9 gene polymorphisms on anticoagulant therapy after heart valve replacement.

OBJECTIVE: The aim of the present study was to investigate the role of CYP2C9 gene polymorphisms after heart valve replacement in a group of patients on warfarin therapy. MATERIALS AND METHODS: The study population consisted of 74 patients with heart valve replacement. Peripheral blood was collected into evacuated tubes containing EDTA, and DNA was extracted from circulating leukocytes by using a high pure PCR template preparation kit. CYP2C9*2, CYP2C9*3 alleles were detected by using real-time PCR. RESULTS: The patients with CYP2C9*1/*3 and CYP2C9*2/*3 genotypes were taking 28.21 and 24.47 mg, respectively, as mean weekly warfarin dose, whereas patients with CYP2C9*1/*1 genotype were taking 33.90 mg. CONCLUSION: The data show that patients with CYP2C9*1/*3 and CYP2C9*2/*3 genotypes needed a lower maintenance dose of warfarin than patients with CYP2C9*1/*1 wild-type genotype.

Effects of peripheral nerve ischemia-reperfusion model on serum cytokine levels.

AIM: Although the neuropathology of ischemic nerve fiber degeneration is relatively well known, its pathogenesis is poorly understood. Local cytokines, which have neuroprotective effects on inflammation and repair, participate in the process by undefined mechanisms. In this study, we evaluated the effects of ischemia and reperfusion on the sciatic nerve of the rat and investigated the probable effects of cytokines on this period. MATERIAL AND METHODS: In the current study, ischemia and reperfusion injury of sciatic nerve was rendered by clamping the femoral artery and vein of the rat for three hours and was followed by varying durations of reperfusion. Activin A, TGF Beta1 and TGF, Beta2 levels were measured in serum samples. RESULTS: TGF Beta1 and Activin A were found to be increased in the ischemic groups compared with the control group (p < 0.05). A significant difference was found between the experimental groups after reperfusion (p < 0.05). There was no statistical significance for TGF Beta2 levels between the study groups (p > 0.05). CONCLUSION: Ischemia causes some important changes in biochemical parameters, and nerve injury continues for a while according to the reperfusion time. Ischemia-reperfusion injury of peripheral nerves caused by various reasons therefore affects the levels of cytokines.

Factor VLeiden and prothrombin G20210A gene polymorphisms in patients with coronary artery disease.

PURPOSE: The precise molecular mechanisms culminating in coronary artery disease (CAD) are not well understood, despite a wealth of knowledge on predisposing risk factors and pathomechanisms. CAD and myocardial infarction (MI) are complex genetic diseases; neither the environment alone, nor a single gene, cause disease, rather, a mix of environmental and genetic factors lead to atherosclerosis of the coronary arteries. MATERIALS AND METHODS: In the present study, our aim was to investigate the roles of prothrombin G20210A mutation and Factor VLeiden mutation in atherosclerotic coronary artery disease. 287 subjects (106 control subjects, who were angiographically normal, and 181 angiographically documented coronary atherosclerotic patients who exhibited coronary artery narrowing to a degree of >or=50%) were included in this study. The mutations were assessed with LightCycler Real-Time PCR mutation detection kits (Roche Diagnostics, GmbH, Germany). RESULTS: 6.6% of control subjects, and 6.1% of patients with (50% coronary artery narrowing were determined to have the Factor VLeiden heterozygote mutation. 6.6% of control subjects had the Prothrombin G20210A heterozygote mutation, while 7.7% of patients with (50% coronary artery narrowing had this mutation. The OR for Factor VLeiden was 1.52 (CI: 0.240-9.602) and for Prothrombin G20210A mutation, the OR was 1.415 (CI: 0.287-6.962). CONCLUSION: Although both the heterozygote Factor VLeiden and Prothrombin gene mutations were more frequent in patients with CAD than in control subjects, there was no statistical relationship found to exist between coronary artery disease and the Factor VLeiden and Prothrombin G20210A mutations.

Genetic polymorphism of VEGF-1154 (A/G) in laryngeal squamous cell carcinoma.

BACKGROUND: Angiogenesis has been shown to be increased in various human tumors including head and neck squamous cell carcinoma (SCC). Vascular endothelial growth factor (VEGF) is thought to be one of the most important angiogenic factors in tumorigenesis. In this study, we aimed to investigate whether polymorphism of VEGF-1154 (A/G) genotypes are associated with the risk of laryngeal SCC. METHODS: A prospective, randomized, case-control study in a tertiary university hospital was done. The study group consisted of 57 Caucasian patients with laryngeal SCC and 89 control subjects. Blood samples were obtained before surgery or from the patients under follow-up to 5 years after surgery. VEGF-1154 (A/G) genotypes were detected by real-time polymerase chain reaction with thermal cycler system. RESULTS: According to the high-risk (GG) genotype, the difference between the patient and control groups was statistically significant (OR 0.43, 95% CI=0.19-0.95, p=0.037). CONCLUSIONS: GG genotype of the VEGF gene may increase the risk of laryngeal SCC in this population. VEGF gene polymorphism may be an important potential genetic and therapeutic marker of laryngeal SCC.

Are glutathione S-transferase gene polymorphisms linked to neonatal jaundice?

Glutathione S-transferases (GSTs) are a major group of phase II detoxification enzymes involved in the metabolism of both endogenous and xenobiotic compounds. In addition to their catalytic function in detoxification, GSTs participate in binding to nonsubstrate ligands such as bilirubin. Ligandin, which is one of the principal hepatic-binding proteins, is also a member of the GST family. The aim of the present study was to investigate the possible relationship between neonatal jaundice and the GST gene polymorphisms. The study cohort consisted of a patient group of 116 newborns (plasma bilirubin levels > or = 15 mg/dl) and a control group of 54 newborns (plasma bilirubin levels <13 mg/dl). In the patient group, the null genotype frequencies in GSTM1 and GSTT1 were 52.6 and 19%, respectively; in the control group, these were 63 and 27.8%, respectively. The frequencies of GSTM1 and GSTT1 were similar in the patient and control groups (p > 0.05). Total bilirubin levels were found to be significantly higher in patients with the GSTM1 null genotype than in patients with the GSTM1 wild genotype (p = 0.042). There was no statistically significant difference in total bilirubin levels between patients with the null GSTT1 genotype and those with the wild GSTT1 genotype. It is conceivable that there is a relation between GSTM1 gene polymorphism and total bilirubin levels in neonatal jaundice. We suggest that GSTM1 gene polymorphisms may affect ligandin functions in hepatocytes, which are important in bilirubin transportation. Consequently, patients with the GSTM1 null genotype may have higher total levels of bilirubin.

The association between N-acetyltransferase 2 gene polymorphisms and pancreatic cancer.

Pancreatic cancer has been linked with exposure to environmental chemicals, which generally require metabolic activation to highly reactive toxic or carcinogenic intermediates. N-acetyltransferase 1 (NAT1) and N-acetyltransferase 2 (NAT2) are expressed primarily in extrahepatic and hepatic tissues, respectively. Both enzymes catalyze N- and O-acetylation of aromatic and heterocyclic amines. It is believed that these compounds are activated via O-acetylation and detoxified by N-acetylation. Several polymorphisms of these two genes have been associated with an increased risk of cancer. Twenty-seven cases of pancreatic cancer and 104 controls were included in this study. Blood was collected in EDTA-containing tubes, and genomic DNA was extracted from the white blood cells by using a high pure PCR template preparation kit. Genotyping of NAT2 polymorphisms was detected by a real time PCR instrument. There was a significant difference in the distribution of the NAT2*6A acetylators phenotype between cases and the controls. The odds ratio of pancreatic cancer for the NAT2*6A slow phenotype was 5.7 (95% CI = 1.27-25.55; p = 0.023) compared with the fast type. Our results suggest that slow acetylators have higher risk of developing pancreatic cancer than fast acetylators. NAT2 gene polymorphisms may be associated with genetic susceptibility to pancreatic cancer.

Cytochrome P450 polymorphisms in patients with Behcet's disease.

OBJECTIVES: Although the etiopathogenesis of Behcet's disease (BD) remains unknown, increased neutrophil functions such as chemotaxis, phagocytosis and excessive production of reactive oxygen species, including superoxide anion, may be responsible for the oxidative tissue damage observed in BD. Cytochrome P-450 are a multigene family of enzymes involved in the detoxification and occasional activation of a wide variety of chemicals. Our aim was to investigate CYP2C9 and CYP2C19 polymorphisms in patients with BD. METHODS: Sixty-two subjects with BD and 107 healthy control subjects were enrolled in the study. Polymorphisms of CYP2C9 and CYP2C19 were performed by real-time PCR with a LightCycler instrument. We researched associations between CYP polymorphisms and BD. RESULTS: The frequencies of wild-type and heterozygous CYP2C19*2 genotypes were 66.1% and 33.9% in the patients and 83.2% and 16.8% in the controls, respectively. There was a 2.53-fold increased risk of Behcet's disease in individuals with the CYP2C19*2 heterozygous genotype (OR = 2.53; 95% CI, 1.22-5.25) when compared with the control group. But the CYP2C9*2, CYP2C9*3 and CYP2C19*3 gene polymorphisms were not related to an increased risk of developing BD. CONCLUSIONS: We observed that patients with BD presented with a higher prevalence of the heterozygous CYP2C19*2 genotype. Hereditary deficiencies of this enzyme activity may lead to an imbalance between pro- and antioxidant systems, resulting in the formation of excessive reactive oxygen species.

Glutathione S-transferase gene polymorphisms in Turkish patients with diabetes mellitus.

Glutathione S-transferases (GSTs) are enzymes involved in the metabolism of many disease-causing electrophilic substrates and protect the cells against oxidative stress. In the present study, we investigated the GSTM1, GSTT1 and GSTP1 gene polymorphisms in diabetic patients and healthy individuals and searched whether polymorphisms in GST genes are associated with diabetes mellitus (DM) in the Turkish population. The study population consisted of 98 unrelated healthy individuals and 98 patients with DM. Genotyping of GSTM1, GSTT1 and GSTP1 genes was performed using real time polymerase chain reaction with a Light Cycler instrument. Patients had a higher frequency of the GSTM1 null genotype than the control group (Odds ratios, OR = 3.7; 95% confidence intervals, CI = 2.05-6.70). However, there was no significant difference in the frequencies of the GSTT1 and GSTP1 gene polymorphisms between the patients and control group. The combined analysis of these three GST genotypes showed a further DM risk increase (OR = 5.7, 95% CI = 1.51-31.07). This is the first study to determine the association of diabetes with GST gene polymorphism in the Turkish population. These results show that GSTM1 null genotype may play a significant role in the aetiopathogeneses of DM and the GSTM1 gene may be a useful marker in the prediction of DM susceptibility of the Turkish population.

N-acetyltransferase 2 polymorphism in patients with diabetes mellitus.

The arylamine N-acetyltransferases (NATs) are a unique family of enzymes that catalyse the transfer of an acetyl group from acetyl-CoA to the terminal nitrogen of hydrazine and arylamine drugs and carcinogens. Human arylamine NATs are known to exist as two isoenzymes, NAT1 and NAT2. The objective of this study was to identify whether the genetic polymorphism of NAT2 plays a role in susceptibility to Diabetes Mellitus (DM). Ninety-seven patients with DM and 104 healthy controls were enrolled in the study. NAT2*5A, NAT2*6A, NAT2*7A/B and NAT2*14A polymorphisms were detected by using real time PCR with LightCycler (Roche Diagnostics GmbH, Mannheim, Germany). According to our data, the NAT2*5A and NAT2*6A mutant genotypes and NAT2*14A heterozygous genotype were associated with an increased risk of development of DM (OR = 47.06; 95%CI: 10.55-209.77 for NAT 2*5A, OR = 18.48; 95%CI: 3.83-89.11 for NAT2*6A and OR = 18.22; 95%CI: 6.29-52.76 for NAT2*14A). However, the NAT2*7A/B gene polymorphism carried no increased risk for developing DM disease. After grouping according to phenotypes as either slow or fast acetylators, NAT2*6A slow acetylator was found to be a significant risk factor for DM (OR = 6.09; 95%CI: 1.99-18.6, p = 0.02). The results indicate that NAT2 slow acetylator genotypes may be an important genetic determinant for DM in the Turkish population.

The frequency of UDP-glucuronosyltransferase 1A1 promoter region (TA)7 polymorphism in newborns and it's relation with jaundice.

Increased bilirubin formation and decreased bilirubin conjugation play an important role in the pathogenesis of the newborn jaundice. Although physiologic jaundice is seen in most of the newborns, there are many risk factors that affect the severity and duration of hyperbilirubinemia. The latest studies showed that the frequency and severity of neonatal jaundice have been increased when mutations of the gene coding UDP-glucuronosyltransferase(UGT)1A1 coexist with other risk factors. Healthy term newborns weighing over 2500 g. were included in this study. The patient group consisted of 107 newborns either with total bilirubin level over 15 mg dl(-1) within 7 days or 5 mg dl(-1) after 15 days of age. The control group consisted of 55 newborns with bilirubin levels in physiological ranges. We investigated the frequency of promoter region [thymine-adenine(TA)]7 polymorphism in UGT1A1 gene. Factors which might cause pathologic and prolonged jaundice with coexisting polymorphism were also investigated. UGT1A1 6/7 genotype was found to be 11% in patient group and 13% in the control group. The difference between patient and control groups was not statistically significant. (TA)7 allele frequency was 0.069 and it is concluded that UGT1A1 promoter region polymorphism was not a risk factor for neonatal jaundice.

Relationship between N-acetyl transferase-2 gene polymorphism and risk of bronchial asthma.

There are still uncertainties as to the mechanism of many pathological conditions, among them allergic diseases. It has been suggest that acetylation rate may be a factor that influences the development of allergic diseases. The aim of the present study was to investigate further whether the genetic polymorphism of the NAT2 plays a role in susceptibility to bronchial asthma disease. Ninety-seven patients with bronchial asthma (atopic n= 62; non-atopic n= 35) and 104 healthy individuals were participated in this study. DNA was extracted from the leucocyte by high pure template preparation kit. NAT2*5A, NAT2*6A, NAT2*7A/B and NAT2*14A polymorphisms of NAT2 were detected by using LightCycler-NAT2 mutation detection kit by real time PCR with LightCycler instrument. We found that mutant NAT2*5A (OR= 3.84, 95% CI= 1.08-13.6) and NAT2*6A (OR= 5.27, 95% CI= 1.06-26.05) genotype could be associated with a high risk for the development of bronchial asthma according to the genotype. After grouping phenotype, the risk for bronchial asthma was more than two times higher (OR= 2.7, 95% CI= 1.07-6.97) in individuals with the slow NAT2*5A acetylator phenotype compared to the fast phenotype. Our study suggests that the NAT2 slow acetylators may be a determinant in susceptibility to asthma disease. This finding may have implications for the theories for the pathogenesis of the disease as well as for therapeutic aspects.

Roles of nitric oxide, malondialdehyde, and fibronectin in an experimental peripheral nerve ischemia-reperfusion model.

Although there are many studies of the neuropathology of the ischemic degeneration of peripheral nerves, the pathogenesis is not well-understood. The roles of several biomolecules on this process were previously reported. An adhesion molecule, fibronectin, which is applied locally (as a conduit material), is very effective in nerve recovery. This study was carried out to evaluate the roles of fibronectin, lipid peroxidation, and nitric oxide (NO) in an experimental model of peripheral nerves. Ischemia and reperfusion injury of sciatic nerves was rendered by clamping the femoral artery and vein. Rats were divided into nine groups. Ischemia and reperfusion were not applied to group 1. In group 2, only ischemia was performed, but reperfusion was not accomplished. For groups 3-9, 1, 2, and 24 h and 1, 2, 3, and 4 weeks of reperfusion were applied following 3 h of ischemia. Then NO, malondialdehyde (MDA), and fibronectin levels were observed in serum samples of rats. Colorimetric and nephelometric assays were used for determination of the levels of these parameters. In this study, all biochemical parameters were found to be increased in the ischemia groups when compared with the control group 1 (P < 0.05). A significant difference was observed between study groups with respect to MDA, NO, and fibronectin levels (P < 0.05). Also, some correlations were established between biochemical parameters in the same group, depending on the varying reperfusion time (r > 0.50). Ischemia causes some important changes in biochemical parameters, and depending on the reperfusion time, nerve injury continues for a while. In our study, we observed that serum levels of MDA decreased in the periods when NO and fibronectin simultaneously increased. Such increases may contribute to neural recovery, and there may be interactions among them.

In vitro re-mineralization of demineralized bone matrix in human serum.

The aim of this study was to develop an in vitro re-mineralization model in human serum. For this purpose a commercially produced demineralized human bone matrix (DBM) was incubated in samples of human serum pools obtained from two physiologically different groups. The first group consisted of young males and the second of older females. After incubation periods of 4 and 7 days at 37 degrees C, changes in the levels of calcium and inorganic phosphate content of the serum and DBM samples were measured. The results of the study showed that the change in mineral content of serum and DBM samples in both study groups was statistically significant. The decrease in serum calcium content and increase in DBM inorganic phosphate content were significant in the young group for longer incubation times. In the older group, both serum calcium and inorganic phosphate decreased and DBM mineral content increased for the same incubation time. When the two physiological groups were compared, statistically significant differences were identified for changes in mineral levels in both serum and the DBM samples. These data indicate that the mineral content of human serum decreases and that of DBM increases when these two materials are incubated together. These changes provide evidence for the re-mineralization of DBM. The model described here could also detect a difference in re-mineralization capability between two different groups of human sera.

N-acetyltransferase 2 gene polymorphism in patients with colorectal carcinoma.

The acetylation polymorphism is a common inherited variation in human drug and carcinogen metabolism. Because N- acetyltransferase (NAT2) is important for the detoxification and/or bioactivation of drugs and carcinogens, polymorphisms of this gene have important implications in therapeutics of and susceptibility to cancer. In this study, NAT2 genotype (NAT2*5A (C(481)T), NAT2*6A (G(590)A), NAT2*7A/B (G(857)A)) and NAT2*14A (G(191)A) and phenotype were determined in 125 patients with colorectal carcinoma and 82 healthy control in Mersin, a city located in the southern region of Turkey. Isolation of the subjects' DNA was performed by using a highly purified PCR template preparation kit/(Roche Diagnostics cat. no: 1 796 828) and the NAT2 polymorphism was detected using real-time PCR (Roche Diagnostics, GmbH, Mannheim, Germany). According to this study high protein intake is associated with the increased risk for the development of colon cancer (OR = 1.73; 95% CI, 1.10-3.07). Although only NAT2*14A fast type was associated with increased risk in patients with colorectal carcinoma (OR = 3.03; 95% CI, 1.56-5.86), when a high protein diet was considered, NAT2*7A/B fast genotype was also found to be associated with an increased risk (OR = 2.06, 95% CI for NAT2*7A/B, 1.10-3.86; OR = 2.65; 95% CI, 1.29-5.46 for NAT2*14A). Smoking status did not differ between the control and patient groups. Our data suggest that exposure to carcinogens through consumption of a high-protein diet may increase the risk of colorectal carcinoma only in genetically-susceptible individuals.

N-acetyltransferase 2 phenotype may be associated with susceptibility to age-related cataract.

Free radicals and oxidative damage play roles in aging and age-related ocular diseases such as cataracts, so defensive mechanisms become important factors for protection. Because N-acetylation is involved in a wide variety of detoxification processes, this study was conducted to examine the relationship between the acetylator phenotypes and genotypes in a group of patients with age-related cataract. Sixty-one cases of age-related cataract and 104 controls were included in this study. Blood was collected in EDTA-containing tubes, and genomic DNA was extracted from the white blood cells by high pure PCR template preparation kit. Genotyping of NAT2 polymorphisms were detected by using a LightCycler-NAT2 mutation detection kit in real-time PCR. There was a significant difference in the distribution of the NAT2*6A acetylator phenotype between cases and the controls. The odds ratio of cataract for the NAT2*6A slow phenotype was 3.8 (95% CI = 1.08 to 13.11, p = 0.032) compared with the fast type. Our results suggest that slow acetylators are at higher risk of developing age-related cataracts than fast acetylators. As NAT2 is an important xenobiotic-metabolizing enzyme and theoretically xenobiotics such as ultraviolet B radiation, smoking, and alcohol use may induce cataract formation, NAT2 gene polymorphisms may be associated with genetic susceptibility of cataract.

Apolipoprotein E polymorphism in diabetic and non-diabetic patients: does it really contribute to atherosclerosis?

OBJECTIVE: The exact mechanism of the increased cardiovascular morbidity and mortality in type-2 diabetes is still undefined. The aim of our study was to assess the impact of apolipoprotein E (apo E) polymorphism and other factors on atherosclerotic vascular disease in type-2 diabetic patients. We also examined the association between apo E polymorphism and lipid profile in diabetic patients. METHODS AND RESULTS: We assessed the apo E polymorphism in 295 atherosclerotic patients (124 of them had diabetes (according to WHO criteria) and 171 of them had coronary artery narrowing > 50). The detection of apo E polymorphism was made by Real-Time PCR using a Light-Cycler (Roche diagnostics, GmbH, Mannheim, Germany). Serum triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), lipoprotein (a) [Lp(a)], apolipoprotein A (Apo A) and apolipoprotein B (Apo B) levels were determined by biochemical analyser. Genotypic distribution of apo E polymorphism did not differ between diabetic and non-diabetic atherosclerotic patients. The distributions of apo E2/2, E2/3, E2/4, E3/3, E3/4 and E4/4 genotypes in diabetic and non-diabetic atherosclerotic patients were 7.3%: 8.2%, 15.3%: 15.8%, 4.0%: 5.3%, 50.8%: 56.7%, 16.9%: 11.1% and 5.6%: 2.9%, respectively. Participants were grouped as apo E2 (E2/2 or E2/3), apo E3 (E3/3), or apo E4 (E4/4 or E4/3). The distributions of apo E2, E3 and E4 alleles were 23.5%, 52.9%, 23.5%, for diabetic patients, and 25.3%, 59.9%, 14.8% for non-diabetic patients, respectively. The apolipoprotein E genotype was not associated with the lipid levels in diabetic patients. CONCLUSIONS: Our findings imply that apo E polymorphism is not related to the development of atherosclerosis in patients with type-2 diabetes.

Effects of caffeic acid phenethyl ester on endotoxin-induced uveitis in rats.

PURPOSE: Caffeic acid phenethyl ester (CAPE) has antimicrobial, anti-inflammatory, antioxidant, immunomodulatory, and carcinostatic properties. In this study, the efficacy of CAPE in endotoxin-induced uveitis (EIU) in rats is investigated. METHODS: EIU was induced by a footpad injection of lipopolysaccharide (LPS). In the treatment group, 10 micromol/kg CAPE was injected intraperitoneally immediately after LPS injection. At 24 hr after LPS injection, the number of infiltrating cells, protein concentration, and levels of myeloperoxidase (MPO) in aqueous humor; malondialdehyde (MDA), MPO, and total antioxidant levels in serum were determined. Eyes were enucleated for histopathologic evaluation, and, counting inflammatory cells in iris-ciliary body (ICB), the efficacy of treatment was determined. RESULTS: CAPE significantly suppressed LPS-induced increase in the number of inflammatory cells (p = 0.0001), protein concentration (p = 0.0001), and MPO levels (p = 0.0001) in aqueous humor as well as MDA (p = 0.001) and MPO (p = 0.0001) levels in serum. Histopathologic evaluation of ICB showed significant reduction in the inflammatory cell counts in the treatment group (p = 0.0001). CONCLUSIONS: CAPE was found efficient in suppressing inflammation and ocular tissue damage induced by LPS in rats.