Prevalence of proteinuria and its associated factors in hypertensive diabetic patients.

OBJECTIVE: Hypertensive diabetic patients are at increased risk for chronic kidney disease. Proteinuria is an early sign of kidney damage. Limited research is available on proteinuria and on its associated factors in hypertensive patients with diabetes. This study aimed to assess the prevalence of proteinuria and its associated factors in hypertensive diabetic patients. PATIENTS AND METHODS: The current retrospective study utilized medical records and hospital computers to collect sociodemographic and medical information about the study patients in two major hospitals in Jordan. Binary regression analysis was used to find the factors that are significantly and independently associated with the presence of proteinuria. RESULTS: Data from 522 hypertensive diabetic patients were investigated. Factors including age (OR=0.691; 95% CI: 0.930-0.994; p<0.01), high-density lipoprotein level (OR=0.450; 95% CI: 0.211-0.960; p<0.05), and higher glomerular filtration rate (OR=0.964; 95% CI: 0.950-0.977; p<0.01) were associated with proteinuria among the study patients. In contrast to metformin (OR=0.237; 95% CI: 0.098-0.572; p<0.01), patients who received insulin (OR=1.992; 95% CI: 1.136-3.492; p<0.05), thiazide diuretics (OR=1.848; 95% CI: 1.108-3.083; p<0.05), calcium channel blockers (OR=1.833, 95% CI: 1.110-3.028, p<0.05), or beta-blockers (BBs) (OR=2.199, 95% CI: 1.257-3.848, p<0.01) had a higher likelihood of having proteinuria. CONCLUSIONS: For preserving kidney function, it is deemed necessary to perform regular checkups for proteinuria among hypertensive diabetic patients, particularly in young patients, patients with low levels of high-density lipoprotein, and those with a lower glomerular filtration rate.

Comparison of Effects of Spatial and Non-Spatial Memory Acquisition on the CaMKII Pathway During Hypothyroidism and Nicotine Treatment.

Molecular, cellular, and behavioral studies have shown that hypothyroidism impairs hippocampus-dependent learning and memory in adult rats. In these studies, spatial learning and memory were tested in the radial arm water maze (RAWM), which involved locating a hidden platform. In the present study, we investigated the effects of nicotine and hypothyroidism on the CaMKII pathway during learning and memory processes in both spatial and non-spatial memory forms. We used nicotine as a neuroprotective agent. Hypothyroidism was induced by thyroidectomy in adult rats. Rats were trained on the hidden platform (the RAWM for spatial learning and memory) and compared with age-matched rats that were trained on a clearly visible platform system (2 cm above water with no radial arms for non-spatial learning and memory). Nicotine (1 mg/kg twice/day) was administered subcutaneously for 4 weeks. Immediately after training, the protein levels of memory-related signaling molecules were determined in hippocampal area CA1. Western blot analysis revealed a significant increase in calcineurin levels and decreases in P-CaMKII, PKCγ, and calmodulin protein levels in area CA1 of the hippocampi of hypothyroid rats trained on both the visible and hidden platforms. Nicotine treatment normalizes these levels in hypothyroid rats trained on both the visible and hidden platforms. The results suggest that chronic nicotine treatment prevents hypothyroidism-induced suppression of the CaMKII pathway after spatial and non-spatial learning and memory.

The role of fish oil in attenuating cardiac oxidative stress, inflammation and fibrosis in rat model of thyrotoxicosis.

Hyperthyroidism is associated with cardiovascular complications. Fish oil reduces risk of cardiovascular diseases. This study aims to evaluate the impact of fish oil on myocardial oxidative stress, inflammation and fibrosis in rat model of thyrotoxicosis. Rats were randomized into four groups; control rats, fish oil treated rats (FO, 100mg omega-3/100g body weight/day), hyperthyroid rats (Hyper, i.p levothyroxine 3 mg/kg/day), and hyperthyroid rats treated with fish oil (Hyper + FO) for 8 weeks. Changes in oxidants/antioxidants, inflammatory and fibrotic markers were measured. Thyrotoxicosis increased serum endothelin-1, thiobarbituric acid reactive substances (TBARS) and reduced activities of cardiac catalase and super oxide dismutase (SOD). Cardiac fibrosis paralleled with a decrease of matrix metalloproteinase -2 (MMP2) levels were observed in Hyper group. Use of FO increased activities of SOD and catalase, increased TBARS levels, and attenuated cardiac fibrosis by normalizing MMP-2 levels. Use of FO may attenuate cardiac oxidative stress and fibrosis in hyperthyroid states.

Cardiac effects of cigarette tobacco smoking in rat model of diabetes.

AIMS: Tobacco smoking is considered a global health issue, contributing to increased risk of cardiovascular disease (CVD) and diabetes (DM). We aimed to assess effects of cigarette smoking on cardiac inflammation, oxidative stress and fibrosis in rat model of streptozotocin (STZ)-induced diabetes. MAIN METHODS: Adults Wistar rats were assigned into control (fresh air, intraperitoneal injection (i.p) of citrate buffer), cigarette smoking (1 h daily for 4 weeks, i.p citrate buffer), DM (35 STZ mg/kg single i.p, fresh air), and DM + Smoking groups for 4 weeks. Cardiac biomarkers of oxidative stress, inflammation, and fibrosis were evaluated. KEY FINDINGS: STZ-induced diabetes as documented by the persistent increase in blood glucose. Relative to control, a significant decrease in body weight was observed in diabetic groups paralleled with increased heart to body weight ratio and systolic blood pressure in all groups. Levels of total nitrite, thiobarbituric acid substances, endothelin -1, interleukin-6 and myeloperoxidase were increased in the DM, Smoking and DM + Smoking groups without changes in C-reactive protein. Cardiac levels of GSH were increased in Smoking groups whereas activities of catalase and superoxide dismutase increased in DM, Smoking and DM + Smoking groups. DM but not smoking increased cardiac fibrosis with a parallel increase in transforming growth factor beta. Cardiac levels of matrix metalloproteinase-2 were elevated in Smoking groups and decreased in DM. SIGNIFICANCE: Exposure to cigarette smoke may increase risk of CVD in DM by increased cardiac oxidative stress and inflammation. Smoking was associated with increased oxidant enzymes and metalloproteinase-2 probably to prevent cardiac fibrosis.

Cardiac effects of fish oil in a rat model of streptozotocin-induced diabetes.

BACKGROUND AND AIMS: Fish oil (FO) is rich in omega-3 polyunsaturated fatty acids, which have cardio-protective effects. This study aims to evaluate effects of FO in a rat model of streptozotocin (STZ) induced diabetes. METHODS AND RESULTS: Adults male Wistar rats were assigned to control (4 µl corn oil/g corn oil given by oral gavage), FO (4 µl Menhaden FO/g body weight given by oral gavage), diabetes (DM, 35 mg/kg STZ single intraperitoneal injection, corn oil), and DM + FO groups for 8 weeks. Plasma and cardiac biomarkers of oxidative stress, inflammation, and fibrosis were evaluated. STZ-induced diabetes as indicated by the significant increase in serum levels of glucose and percentage of glycated hemoglobins. FO reduced plasma arachidonic acid (AA) percentage and ratio of AA: docosahexaenoic acid (DHA). Plasma and cardiac levels of total nitrite, endothelin -1 (ET-1), and myeloperoxidase (MPO) increased in the DM group, whereas cardiac activities of catalase and superoxide dismutase (SOD) decreased. FO reduced cardiac nitrite and MPO, and plasma ET-1 levels. FO increased cardiac glutathione, catalase and SOD activities. Levels of thiobarbituric acid substances increased in the FO and DM groups with significant synergism in the DM + FO group. FO prevented cardiac fibrosis associated with DM and decreased cardiac transforming growth factor beta-1and p38 MAP kinases. Cardiac levels of matrix metalloproteinase -2 were significantly elevated in FO and DM + FO groups. CONCLUSIONS: FO decreased plasma and cardiac oxidative stress, inflammation and myocardial fibrosis. FO could be used in diabetes to reduce risk and burden of CVDs.

Pentoxifylline increases the level of nitric oxide produced by human spermatozoa.

Pentoxifylline (PF) is a xanthine derivative drug primarily used to treat peripheral vascular disorders. It is currently used in assisted reproductive technologies to enhance human sperm motility. However, the mechanism by which this enhancement occurs is not fully understood. Given that nitric oxide has been identified as a trigger to sperm motion, we asked whether nitric oxide modulates the stimulatory effect of PF on sperm motility. A total of 41 semen samples from infertile males were studied. Nitric oxide production in the presence of 5 mm PF was tested using different bio-analytical methods (spectrophotometry, fluorometry and fluorescence microscopy). The spectrophotometric determination showed higher levels of nitrite, an indirect measure for nitric oxide, in sperm samples supplemented with PF compared to controls. The fluorometric experiment showed higher 4, 5-diaminofluorescein triazole, a product from the reaction between nitric oxide and 4, 5-diaminofluorescein diacetate, after adding PF to spermatozoa. The fluorescence microscopy images of the spermatozoa supplemented with PF showed higher green fluorescence, indicating higher 4, 5-diaminofluorescein triazole levels, compared to controls. It is concluded that PF enhances nitric oxide production in human spermatozoa, which explains, at least in part, the mechanism by which PF stimulates human sperm motility.

Assessment of genotoxicity of vincristine, vinblastine and vinorelbine in human cultured lymphocytes: a comparative study.

Vincristine (VCR), vinblastine (VBL) and vinorelbine (VRL) are anticancer agents from the Vinca alkaloid family that have the potential to induce genotoxic effect. The aim of the present study was to compare the genotoxic effect of VCR, VBL and VRL. Levels of 8-hydroxy-2-deoxy guanosine (8-OHdG) and sister chromatid exchanges (SCEs) were measured in cultured human blood lymphocytes treated with VCR, VBL and VRL at concentrations of 0.01 and 0.1 µg/mL. Results showed that VCR, VBL and VRL significantly increased the 8-OHdG levels (p <0.05), whereas it did not cause a significant increase in the frequencies of SCEs in human blood lymphocytes as compared to controls. On the other hand, all three agents significantly increased cells mitotic index (p <0.05). At both tested concentrations, the magnitude of the increase in 8-OHdG was VBL>VCR>VRL. In conclusion, VCR, VBL and VRL induce DNA damage as indicated by the increase in the 8-OHdG biomarker but with different magnitude.

Assessment of genotoxicity of waterpipe smoking using 8-OHdG biomarker.

Waterpipe tobacco smoking is increasing in popularity, particularly among young adults. This popularity is related to the lack knowledge regarding the health effects of waterpipe smoking. In this study, we examined the genotoxicity of waterpipe smoking using an 8-hydroxy deoxyguanosine (8-OHdG) assay. Genotoxicity was evaluated in the saliva, urine, and serum of 66 waterpipe adult smokers and 46 healthy nonsmokers. The level of addiction to waterpipe smoking was evaluated using the Lebanon Waterpipe Dependence Scale-11. Levels of 8-OHdG in the samples were measured using commercially available enzyme-linked immunosorbent assays. Levels of 8-OHdG in the saliva (52,430 ± 2923 vs 48,430 ± 4189 pg/mL), urine (2815 ± 312 vs 2608 ± 180 pg/mL), and serum (19,720 ± 202 vs 19,670 ± 254 pg/mL) were similar between waterpipe smokers and nonsmokers (P > 0.05). In addition, no correlations were found between dependence score and levels of 8-OHdG in all sample types. In conclusion, 8-OHdG is not a good biomarker for genotoxic effect of waterpipe smoking.

The role of TNF-α G-308A promoter polymorphism in glycemic control in Type 2 diabetes patients.

BACKGROUND: TNF-α polymorphisms were shown to be associated with insulin resistance and diabetes development and complications. AIM: To investigate the association between glycemic control in Type 2 diabetes patients and TNF-α G-308A single nucleotide polymorphism (SNP). METHODS: This was a cross-sectional observational study, where diabetes patients from both genders (170 male and 185 female) were enrolled in the study. Patients were divided into two groups: good glycemic control (n = 158) and poor glycemic control (n = 197). Genotyping of TNF-α G-308A SNP was carried out using restriction fragment length polymorphisms-polymerase chain reaction. RESULTS: The results showed that TNF-α G-308A SNP is strongly associated with glycemic control in type 2 diabetes patients. Patients with the AA and AG genotypes had better glycemic control than those with GG genotype (P < 0.01). Other parameters that impacted glycemic control include duration of the disease (P < 0.01) and response to insulin therapy (P < 0.01). However, no contribution for gender or statins use to glycemic control was observed (P > 0.05). CONCLUSION: TNF-α G-308A SNP might modulate glycemic control among type 2 diabetes patients.

Chronic nicotine treatment reverses hypothyroidism-induced impairment of L-LTP induction phase: critical role of CREB.

We have previously shown that adult onset hypothyroidism impairs late-phase long-term potentiation (L-LTP) and reduces basal protein levels of cyclic-AMP response element binding protein (CREB), mutagen-activated protein kinase (MAPKp42/44), and calcium calmodulin kinase IV (CaMKIV) in area Cornu Ammonis 1 (CA1) of the hippocampus. These changes were reversed by chronic nicotine treatment. In the present study, levels of signaling molecules important for L-LTP were determined in CA1 area of the hippocampus during the induction phase. Standard multiple high-frequency stimulation (MHFS) was used to evoke L-LTP in the CA1 area of the hippocampus of hypothyroid, nicotine-treated hypothyroid, nicotine, and sham control anaesthetized adult rats. Chronic nicotine treatment reversed hypothyroidism-induced impairment of L-LTP at the induction phase. Five minutes after MHFS, Western blotting showed an increase in the levels of P-CREB, and P-MAPKp42/44 in sham-operated control, nicotine, and nicotine-treated hypothyroid animals, but not in hypothyroid animals. The protein levels of total CREB, total MAPK p42/44, BDNF, and CaMKIV were not altered in all groups 5 min after MHFS. Therefore, normalized phosphorylation of essential kinases such as P-CREB and P-MAPK p42/44 in the CA1 area of nicotine-treated hypothyroid animals plays a crucial role in nicotine-induced rescue of L-LTP induction during hypothyroidism.

Levothyroxin replacement therapy restores hypothyroidism induced impairment of L-LTP induction: critical role of CREB.

Cyclic-AMP response element binding protein (CREB) is a transcription factor crucial for late phase long-term potentiation (L-LTP) induction and maintenance. Upon multiple high frequency stimulation (MHFS), large Ca(2+) influx activates adenylyl cyclase. This, in turn, activates PKA, which by itself or through MAPK p42/p44 can activate (phosphorylate) CREB. Upon phosphorylation, P-CREB activates multiple genes essential for L-LTP generation. Calcium calmodulin kinase IV (CaMKIV) is also activated by calcium and can directly activate CREB. We have shown previously that hypothyroidism impairs L-LTP and reduces the basal protein levels of CREB, MAPK p42/p44, and CaMKIV in area CA1 of the hippocampus. In the present study, levels of these signaling molecules were determined in area CA1 during the induction and maintenance phases of L-LTP. Standard MHFS was used to evoke L-LTP in the CA1 area of hypothyroid, levothyroxin treated hypothyroid and sham control anesthetized adult rats. Chronic levothyroxin treatment reversed hypothyroidism-induced L-LTP impairment. Five minutes after MHFS, western blotting showed an increase in the levels of P-CREB, and P-MAPK p42/p44 in sham-operated control, and levothyroxin treated hypothyroid animals, but not in hypothyroid animals. The protein levels of total CREB, total MAPK p42/p44, BDNF and CaMKIV were not altered in all groups five minutes after MHFS. Four hours after MHFS, the levels of P-CREB, and P-MAPK p42/p44 remained unchanged in hypothyroid animals, while they were elevated in sham-operated control, and levothyroxin treated hypothyroid animals. We conclude that respective normalized phosphorylation of essential kinases such as P-CREB and P-MAPK p42/p44 is correlated with restoration of normal L-LTP induction and maintenance in the CA1 area of levothyroxin-treated hypothyroid animals.

Diabetes impairs synaptic plasticity in the superior cervical ganglion: possible role for BDNF and oxidative stress.

The majority of diabetics develop serious disorders of the autonomic nervous system; however, there is no clear understanding on the causes of these complications. In this study, we examined the effect of streptozocin (STZ)-induced diabetes on activity-dependent synaptic plasticity, associated levels of brain-derived neurotrophic factor (BDNF) and antioxidant biomarkers in the rat sympathetic superior cervical ganglion. Diabetes (STZ-induced) was achieved by a single intraperitoneal injection of streptozocin (55 mg/kg).Compound action potentials were recorded from isolated ganglia before (basal) and after repetitive stimulation, or trains of paired pulses to express ganglionic long-term potentiation (gLTP) or long-term depression (gLTD). The input/output curves of ganglia from STZ-treated animals showed a marked rightward shift along most stimulus intensities, compared to those of ganglia from control animals, indicating impaired basal synaptic transmission in ganglia from STZ-induced diabetic animals. Repetitive stimulation induced robust gLTP and gLTD in ganglia isolated from control animals; the same protocols failed to induce gLTP or gLTD in ganglia from STZ-induced diabetic animals, indicating impairment of activity-dependent synaptic plasticity in these animals. Molecular analysis revealed significant reduction in the levels of BDNF and the ratio of glutathione/oxidized glutathione. Additionally, the activity of glutathione peroxidase, glutathione reductase, catalase, and the levels of thiobarbituric acid-reactive substances were increased in ganglia from STZ-treated animals. In conclusion, impaired basal synaptic transmission and synaptic plasticity are associated with reduced BDNF and altered oxidative stress biomarkers in the sympathetic ganglia from STZ-induced diabetic animals, suggesting a possible correlation of these factors with the manifestations of STZ-induced diabetes in the peripheral nervous system.

Frequency of MDR1 single nucleotide polymorphisms in a Jordanian population, including a novel variant.

The multidrug resistance gene (MDR1 or ABCB1) codes for P-glycoprotein, which plays an important role in regulating absorption, distribution, and elimination of drugs. We examined MDR1 gene variants in 100 unrelated subjects from various regions of Jordan. The MDR1 gene was scanned using direct sequencing. Six rare variants in MDR1 were detected, including a new variant, T3075A. This variant did not affect the protein sequence (synonym for threonine). Among the common SNPs, the frequencies of rs1128503 (C1236T) genotypes were: 0.23 (CC), 0.41 (CT) and 0.36 (TT). For the rs2032582 (G2677T) SNP, genotype frequencies were 0.38 for GG, 0.45 for GT, 0.13 for TT, 0.03 for GA, and 0.01 for TA, whereas for rs1045642 (C3435T), genotype frequencies were 0.17 for CC, 0.5 for CT and 0.33 for TT. The observed distribution of the common variants in the Jordanian population was within the range detected in other populations. These data on MDR1 gene variants in the Jordanian population will be useful for investigations on response to P-glycoprotein substrate drugs.

The role of type II deiodinase polymorphisms in clinical management of hypothyroid patients treated with levothyroxine.

STUDY OBJECTIVE: Several factors can affect achieving the goals with levothyroxine (L-T4) therapy. This study investigates the clinical and biochemical response to L-T4 replacement therapy in hypothyroid patients in correlation with genetic variation in Deiodinase type || (DIO2) gene. DESIGN AND SETTING: This is a cross-sectional correlation study. The setting was the diabetes and endocrinology clinics at 2 Jordanian Hospitals. METHODOLOGY: Patients with primary hypothyroidism who are controlled on stable L-T4 replacement therapy were recruited and thyroid function test was performed. Genetic analysis to detect 4 single nucleotide polymorphisms (SNPs) rs225011, rs7140952, rs225012 and rs2839858 in DIO2 gene was carried out using the polymerase chain reaction-based restriction fragment length polymorphism assay (PCR-RFLP). RESULTS: There was no correlation between the 4 SNPs in DIO2 gene and replacement doses of L-T4, whereas a statistical significance was found between rs7140952 and central obesity (P<0.05), and systolic and diastolic blood pressure (P<0.05). The dose of L-T4 was associated with lower levels of TSH, fT4, central obesity, body mass index and waist circumference. CONCLUSION: While L-T4 dose is associated with several positive effects on hypothyroid patients, none of the examined SNPs in DIO2 is correlated with replacement doses of the drug. However, rs7140952 polymorphism is associated with components of metabolic syndrome including blood pressure and central obesity.

Caffeine prevents cognitive impairment induced by chronic psychosocial stress and/or high fat-high carbohydrate diet.

Caffeine alleviates cognitive impairment associated with a variety of health conditions. In this study, we examined the effect of caffeine treatment on chronic stress- and/or high fat-high carbohydrate Western diet (WD)-induced impairment of learning and memory in rats. Chronic psychosocial stress, WD and caffeine (0.3 g/L in drinking water) were simultaneously administered for 3 months to adult male Wistar rats. At the conclusion of the 3 months, and while the previous treatments continued, rats were tested in the radial arm water maze (RAWM) for learning, short-term and long-term memory. This procedure was applied on a daily basis to all animals for 5 consecutive days or until the animal reaches days to criterion (DTC) in the 12th learning trial and memory tests. DTC is the number of days that the animal takes to make zero error in two consecutive days. Chronic stress and/or WD groups caused impaired learning, which was prevented by chronic caffeine administration. In the memory tests, chronic caffeine administration also prevented memory impairment during chronic stress conditions and/or WD. Furthermore, DTC value for caffeine treated stress, WD, and stress/WD groups indicated that caffeine normalizes memory impairment in these groups. These results showed that chronic caffeine administration prevented stress and/or WD-induced impairment of spatial learning and memory.

Chronic caffeine treatment prevents stress-induced LTP impairment: the critical role of phosphorylated CaMKII and BDNF.

Caffeine has been reported to enhance cognition in animal and humans. Additionally, caffeine alleviates cognitive impairment associated with a number of disorders including Alzheimer's disease. The lipophilic nature of caffeine allows for rapid absorption into the bloodstream where it freely crosses the blood-brain barrier. Caffeine promotes dendritic spine growth in cultured hippocampal neurons, which suggests a neuroprotective effect. We examined the effect of chronic caffeine treatment on stress-induced suppression of long-term potentiation (LTP) and impairment of molecules of its signaling cascade. Rats were subjected to daily stress using the psychosocial stress paradigm (intruder model), in vivo recordings from area CA1 of the hippocampus of adult rat, and immunoblot analysis of essential signaling molecules. Caffeine prevented stress-induced LTP impairment. Western blot analysis showed reduction of the basal levels of the phosphorylated calcium calmodulin kinase II (P-CAMKII), total CaMKII, and brain-derived neurotrophic factor (BDNF) in area CA1 of stressed rats. These reductions were prevented by chronic caffeine treatment (0.33 mg/L in drinking water). In addition, caffeine prevented the upregulation of calcineurin levels in stressed rats. High-frequency stimulation (HFS) normally increased P-CaMKII, total CaMKII, and calcineurin levels in control as well as in caffeine-treated stressed rats. However, in stressed rats, the same HFS induced increases in the levels of total CaMKII and calcineurin, but not those of P-CaMKII. The levels of signaling molecules may not reflect activities of these molecules. It appears that the neuroprotective effect of caffeine involves preservation of the levels of essential kinases and phosphatases in stressed rats. This may include preservation of basal levels of BDNF by chronic caffeine treatment in stressed animals. These findings highlight the critical role of P-CaMKII and BDNF in caffeine-induced prevention of stress-induced LTP impairment.

Waterpipe tobacco and cigarette smoking among university students in Jordan.

SETTING: While waterpipe and cigarette smoking have been well studied in Syria and Lebanon, data from Jordan are limited. OBJECTIVES: To characterize the relative prevalence of waterpipe tobacco and cigarette smoking among university students in Jordan, and to compare the demographic and environmental factors associated with each form of tobacco use. DESIGN: We surveyed 1845 students randomly recruited from four universities in Jordan. We used multivariable logistic regression controlling for clustering of individuals within universities to determine associations between demographic and environmental covariates and waterpipe tobacco and cigarette use. RESULTS: Waterpipe tobacco smoking rates were 30% in the past 30 days and 56% ever, while cigarette smoking rates were 29% in the past 30 days and 57% ever. Past 30-day waterpipe tobacco smoking rates were 59% for males and 13% for females. Females had substantially lower odds than males of being current waterpipe (OR 0.12, 95%CI 0.10-0.15) or cigarette (OR 0.08, 95%CI 0.05-0.14) smokers. Current cigarette smoking was more significantly associated with markers of high socio-economic status (SES) than waterpipe tobacco smoking. CONCLUSION: Waterpipe tobacco smoking is as common as cigarette smoking among Jordanian university students. While cigarette smoking is consistently associated with high SES, waterpipe tobacco smoking is more evenly distributed across various populations.

No correlation exists between vitamin B12 and quality of life in healthy young adult population.

BACKGROUND AND OBJECTIVES: Vitamin B12 (B12) is essential for well-being and healthy life, since it plays a critical role in DNA synthesis, hematopoiesis and neurologic function. B12 deficiency remains one of the most common nutrition deficiencies in the world and is associated with increasing risk of cardiovascular disease, cancer, mental health problem, osteoporosis, and defect-birth outcomes. The main objective of this study is to determine the impact of B12 levels on quality of life (QOL) among healthy university students. MATERIALS AND METHODS: This cross-sectional study involved 359 healthy university students (age 18-30 years) of both genders. Their QOL was as vitamin B12 level was measured using the IMx system (Abbott laboratories IMX, USA). RESULTS: No correlation was detected between B12 levels and the two major QOL subscales: the Physical Component Summary (PCS) and Mental Component Summary (MCS). Additionally, none of the other eight subscale of the SF-36 was significantly correlated with b12 levels. CONCLUSION: We conclude that no correlation exists between B12 levels and QOL scores among young adult healthy populations. Further investigations are required to confirm the impact of B12 status on QOL among healthy populations.

Post-learning REM sleep deprivation impairs long-term memory: reversal by acute nicotine treatment.

Rapid eye movement sleep deprivation (REM-SD) is associated with spatial learning and memory impairment. During REM-SD, an increase in nicotine consumption among habitual smokers and initiation of tobacco use by non-smokers have been reported. We have shown recently that nicotine treatment prevented learning and memory impairments associated with REM-SD. We now report the interactive effects of post-learning REM-SD and/or nicotine. The animals were first trained on the radial arm water maze (RAWM) task, then they were REM-sleep deprived using the modified multiple platform paradigm for 24h. During REM-SD period, the rats were injected with saline or nicotine (1mg/kg s.c. every 12h: a total of 3 injections). The animals were tested for long-term memory in the RAWM at the end of the REM-SD period. The 24h post-learning REM-SD significantly impaired long-term memory. However, nicotine treatment reversed the post-learning REM-SD-induced impairment of long-term memory. On the other hand, post-learning treatment of normal rats with nicotine for 24h enhanced long-term memory. These results indicate that post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities.

Impaired neural transmission and synaptic plasticity in superior cervical ganglia from ß-amyloid rat model of Alzheimer's disease.

Basal synaptic transmission and activity-dependent synaptic plasticity were evaluated in superior cervical sympathetic ganglia (SCG) of amyloid-ß rat model of Alzheimer's disease (Aß rat) using electrophysiological and molecular techniques. Rats were administered Aß peptides (a mixture of 1:1 Aß1-40 and Aß1-42) by chronic intracerebroventricular infusion via 14-day mini-osmotic pumps (300 pmol/day). Control rats received Aß40-1 (inactive reverse peptide: 300 pmol/day). Ganglionic compound action potentials were recorded before (basal) and after repetitive stimulation. In isolated SCG, ganglionic long-term potentiation (gLTP) was generated by a brief train of stimuli (20Hz for 20s) and ganglionic long-term depression (gLTD) was produced with trains of paired pulses. The input/output (I/O) curves of ganglia from Aß rats showed a marked downward shift along all stimulus intensities, compared to those of ganglia from control animals, indicating impaired basal synaptic transmission. In addition, repetitive stimulation induced robust gLTP and gLTD in ganglia isolated from control animals, but, the same protocols failed to induce gLTP or gLTD in ganglia from Aß rats indicating impairment of activity-dependent synaptic plasticity in these animals. Western blotting of SCG homogenate from Aß rats revealed reduction in the ratio of phosphorylated-/total-CaMKII and in calcineurin protein levels. Although other mechanisms could be involved, these changes in signaling molecules could represent an important molecular mechanism linked to the failure to express synaptic plasticity in Aß rat ganglia. Results of the current study could explain some of the peripheral nervous system manifestations of Alzheimer's disease.