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BACKGROUND: Health Care Workers (HCWs), including medical doctors, played a pivotal role as a first-line defence against the COVID-19 pandemic. Because of high exposure, HCWs are at an increased risk of contracting the disease. AIMS: This study aims to assess the level of precautionary measures, both at home and the workplace, amongst medical doctors who were on duty during the national lockdown in Jordan. METHODS: A cross-sectional study was conducted between March 23 and May 1, 2020, utilising a self-administered web-based questionnaire to examine a sample of medical doctors (n = 270) working at different healthcare institutions in Jordan. Likert scale was used to code the data and generate means and percentages. RESULTS: The most practiced on-duty precautionary measures were cleaning hands with water and disinfectant for more than 20 seconds (47.4%), followed by proper hygiene before and during meals (38.9%). The most practiced off-duty measures were taking off clothes before entering the residential place (65.9%) and prohibiting visitors (58.1%). Overall, the mean work protection percentage score was 73.8% (range: 28%-100%), while the mean home safety percentage score was 71.3% (range: 25%-100%). Work protection score was positively correlated with the home safety score. Female doctors were found to be more precautious at home than males. Doctors with chronic illness(es) were found to be less precautious than their healthier counterparts. Participants who isolated themselves expressed the highest level of home safety practice. Doctors who reported to smoke were found more precautious at home and doctors who preferred to work during lockdowns were more precautious at the workplace. CONCLUSION: The level of precautionary behaviour of medical doctors in Jordan was not optimal. More attention and efforts are needed to enhance the adherence of doctors to precautionary guidance. Strengthening the role of infectious disease and infection control units within healthcare settings remains a necessity.

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In this study we examined enhancement effects of Artemisinin plus Glucantime and shark cartilage extract on promastigotes and amastigotes of L.infantum in in-vitro condition.The toxicity of artemisinin, glucantime, and shark cartilage extract on the L. infantum promastigotes and amastigote-infected macrophages was evaluated using MTT assay. The role of these drugs inducing apoptosis in promastigotes, un- infected, and parasite- infected macrophages was also studied. Using promastigote assay, IC50 values of artemisinin and glucantime as standalone drugs as well as in combination were obtained to be 50, 400, and 100µg/mL respectively. The flow cytometry analysis of apoptotic promastigotes stained with Annexin-V FITC staining showed that artemisinin, glucantime, artemisinin plus glucantime, artemisinin plus shark cartilage extract, and shark cartilage extract alone applied at their IC50 concentrations resulted in 53.5%, 73.92%, 64.46%, 49.9%, and 47.34% apoptosis respectively. The results of MTT assay indicated that cytotoxicity of artemisinin, glucantime, artemisinin plus glucantime, shark cartilage plus artemisinin, and shark cartilage in infected macrophages after 72h was 75%, 84%, 82%, 30%, and 3% respectively. In un- infected macrophages, cytotoxicity of Artemisinin, Glucantime, Artemisinin plus Glucantime and shark cartilage was 15%, 31%, 21%, 2%, and 0% respectively.This study suggests that artemisinin, glucantime, artemisinin plus glucantime, and shark cartilage extract have significant killing effects on promastigotes and amastigotes. Also, it proved that artimisinin alone and in combination with glucantime and shark cartilage extract has little toxic effect on macrophages, but could induce apoptosis in L.infantum promastigotes and amastigote-infected macrophages. Thus, these chemicals can be used as alternative drugs for in-vivo studies.

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MicroRNAs (miRNAs) are small non-coding RNAs that function as crucial regulators of gene expression. Recently, dysregulation of miRNA expression in the blood has been demonstrated to be associated with various diseases, including type 2 diabetes mellitus (T2D), suggesting a potential for their use as biomarkers of disease prognosis. The present study examined the expression levels of T2D­associated miR­15a in peripheral whole blood samples from patients with T2D, pre­diabetes individuals exhibiting impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), as well as healthy control subjects, in order to investigate the potential of peripheral blood plasma miR­15a as a biomarker for the prediction of T2D and pre­diabetes. The present study included 24 patients with T2D, 22 IFG/IGT individuals and 24 healthy controls. The expression levels of miR­15a were analyzed by reverse transcription-quantitative polymerase chain reaction. The results indicated that the peripheral blood miR­15a expression levels were significantly decreased in patients with T2D and IFG/IGT individuals, compared with healthy control subjects (P<0.05). As determined by multivariate logistic regression analysis, lower miR­15a expression was significantly associated with T2D (odds ratio [OR]; 95% confidence interval [CI]: 0.51; 0.16­0.73, respectively; P<0.05) and pre­diabetes (OR; 95% CI: 0.56; 0.23­0.79, respectively; P<0.05). This association remained statistically significant following adjustment for age, body mass index and hypertension, as well as other biochemical indicators. Furthermore, a receiver operating characteristic analysis revealed that blood miR­15a distinguished patients with T2D and IFG/IGT individuals from healthy controls (area under the curves; 95% CI: 0.864; 0.751­0.977 and 95% CI: 0.852; 0.752­0.953, respectively). These results demonstrated that peripheral blood miR­15a expression levels were significantly lower in patients with T2D and IFG/IGT individuals, compared with healthy individuals. Thus, miR­15a in peripheral whole blood may serve as a potential biomarker for T2D and pre-diabetes.

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Propofol is a short acting intravenous anesthetic that has been used in the treatment of status epileptics. However, the occurrence of seizures in epileptic and non-epileptic patients during recovery from propofol induced anesthesia suggests that propofol may have proconvulsant effects. We have previously shown that propofol displays anticonvulsant effects against picrotoxin (PTX) induced seizures during its peak sedative effects. The purpose of the present study was to compare the time course of the effect of intravenous administration of various doses (2.5, 5, and 10 mg/kg) of propofol and midazolam on PTX-induced seizures in adult female Sprague-Dawley rats. The latency to onset of clonic seizures induced by intraperitoneal injection of PTX was significantly increased by the highest dose of propofol and all doses of midazolam, suggesting that both agents display anticonvulsant effects. The anticonvulsant effects of propofol (10 mg/kg) lasted about 20 min and PTX-induced clonic seizures were observed thereafter and peaked within 30 min post drug administration. Clonic seizures progressed rapidly to tonic seizures leading to high rate of PTX-induced mortality. In midazolam (10 mg/kg) treated rats, clonic seizures were observed 25 min after drug administration and the number of rats exhibiting clonic seizures was highest within 40 min. However, clonic seizures did not progress into tonic seizures and thus, PTX-induced seizure related mortality was significantly reduced. In conclusion, this study provides further evidence for the anticonvulsant effects of propofol and midazolam against PTX-induced seizures. Furthermore, the data of the current study showed that midazolam was more effective than propofol against PTX-induced tonic seizures.

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Memory and learning are impaired by imbalanced diet consumption. High-fat high-carbohydrate diet (HFCD) induces oxidative stress, which results in neuronal damage and interference with synaptic transmission; hence, a decline in cognitive function. Vitamin E is a fat soluble antioxidant that is believed to have positive effects on learning and memory. In this study, we tested the hypothesis that chronic administration of vitamin E prevents learning and memory impairment induced by HFCD. In addition, possible molecular targets for HFCD, and vitamin E that lead to cognitive effects were examined. Vitamin E and/or HFCD were concurrently administered to animals for 6 weeks. Thereafter, behavioral studies were conducted to test the spatial learning and memory using radial arm water maze (RAWM). Additionally, brain derived neurotrophic factor (BDNF) level and antioxidant markers were assessed in the hippocampus. The results of this project revealed that HFCD impairs both short-term and long-term memories (p<0.05). The administration of vitamin E prevented the memory impairment induced by HFCD consumption (p<0.05). The consumption of HFCD reduced activities of hippocampal superoxide dismutase (SOD) and catalase (p<0.05); whereas the levels of thiobarbituric acid reactive substances (TBARS) and oxidized glutathione (GSSG) were elevated (p<0.05). The administration of vitamin E normalized the effect of HFCD on the oxidative stress markers. None of the treatments induced changes in the levels of BDNF or glutathione peroxidase (GPx). In conclusion, HFCD induces memory impairment, and the administration of vitamin E prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.

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BACKGROUND: Thyroid gland dysfunction and echocardiographic cardiac abnormalities are well-documented in patients with transfusion dependent beta-thalassemia major (ß-TM). AIM: This cross-sectional analytic study was conducted to investigate left ventricle (LV) diastolic and systolic function using pulsed Doppler (PD) and tissue Doppler (TD) echocardiography and correlate that with serum level thyroid stimulating hormone in patients with ß-TM. METHODS: The study was conducted on patients with ß-TM (n = 110, age 15.9 ± 8.9 years) and compared with a control group (n = 109, age 15.8 ± 8.9 years). In all participants, echocardiographic indices of PD and TD were performed and blood samples were withdrawn for measuring the serum level of TSH, free T4, and ferritin. A linear regression analysis was performed on TSH level as the dependent variable and serum ferritin as independent. Stepwise multiple regression analysis was used to determine the odds ratio of different biochemical and echo variables on the risk of developing hypothyroidism. RESULTS: Patients with ß-TM compared with controls had thicker LV septal wall index (0.65 ± 0.26 vs. 0.44 ± 0.21 cm/M(2), P < 0.001), posterior wall index (0.65 ± 0.23 vs. 0.43 ± 0.21 cm/m(2), P < 0.01) and larger LVEDD index (4.35 ± 0.69 vs.3.88 ± 0.153 mm/m(2), P < 0.001). In addition, ß-TM patients had higher transmitral E wave velocity (E) (70.81 ± 10.13 vs. 57.53 ± 10.13 cm/s, P = 0.02) and E/A ratio (1.54 ± 0.18 vs. 1.23 ± 0.17, P < 0.01) and shorter deceleration time (DT) (170.53 ± 13.3 vs. 210.50 ± 19.20 m sec, P < 0.01). Furthermore, the ratio of transmitral E wave velocity to the tissue Doppler E wave at the basal septal mitral annulus (E/Em) was significantly higher in the ß-TM group (19.68 ± 2.81 vs. 13.86 ± 1.41, P < 0.05). The tissue Doppler systolic wave (Sm) velocity and the early diastolic wave (Em) were significantly lower in the ß-TM group compared with controls with Sm, 4.82 ± 1.2 vs. 6.22 ± 2.1 mm/sec, P < 0.05 and (Em), 3.51 ± 2.7 vs. 4.12 ± 2.5 mm/sec. P < 0.05, respectively). The tricuspid valve velocity was significantly higher in ß-TM patients compared with controls 2.85 ± 0.56 vs. 1.743 ± 0.47 m sec, respectively, P < 0.01). The prevalence of subclinical hypothyroidism in patients with ß-TM was 15.4%, with significantly higher mean serum TSH compared with controls (6.78 ± 1.5 vs. 3.10 ± 1.02 µIU/mL, P < 0.01) and positively correlated with the serum ferritin level (r = 0.34, P = 0.014). On multiple regression analysis, the LV mass, LVEF%, and E/A ratio were not positive predictors of hypothyroidism in patients with ß-TM. CONCLUSION: We conclude that patients with ß-TM had a high prevalence of subclinical hypothyroidism of 15.4%. Thyroid stimulating hormone was significantly high and positively correlated with the serum ferritin level. Echo cardiographic pulsed Doppler showed a restrictive LV diastolic pattern suggestive of severe diastolic dysfunction with preserved left ventricle systolic function.

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OBJECTIVE: To determine the incidence and trends of gestational diabetes mellitus (GDM) in Bahrain from 2002 to 2010, and to investigate 2 possible risk factors within the affected population. METHODS: In a retrospective survey, data on maternal body weight and age were collected from women who gave birth in government maternity units in Bahrain and who were screened for GDM during pregnancy using the 2-step approach and criteria of the US Expert Committee on the diagnosis and classification of diabetes. RESULTS: Among 49 552 pregnant women, 4982 (10.1%) were diagnosed with gestational diabetes. The Cox-Stuart test for trend analysis suggested that there was an increase in the incidence of gestational diabetes from 7.2% in 2002 to 12.5% in 2010 (P<0.01). For the period 2006-2010, maternal age, and weight at onset of pregnancy and at time of delivery were positively associated with risk of GDM with an odds ratio (95% confidence interval) of 1.094 (1.081-1.107), 1.081 (1.001-1.104), and 1.027 (1.013-1.040), respectively. CONCLUSION: A combination of increasing maternal weight, maternal age, and incidence of GDM among women in Bahrain indicates a significant future burden on health services.

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The transformation of a traditional discipline-based medical curriculum into a system-based integrated curriculum often poses dilemmas to faculty involved in teaching basic medical sciences. This paper examines the challenges of teaching physiology to medical students in a system-based curriculum. Some of these challenges include: defining the core curriculum, curriculum links, sequencing curriculum content, interdisciplinary integration, and student assessment. A number of relevant issues including defining the core physiology content, faculty expertise, and coping and adapting to curriculum transitions are discussed from a personal perspective. For successful implementation of a system-based curriculum and to overcome the challenges, educational issues should be debated in regional and international forums.

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We have previously evaluated veratridine as an in vitro model of seizure using conventional electrophysiological recordings in rat hippocampal CA1 pyramidal neurones. The aim of this investigation is to further characterize this convulsant as an in vivo model of seizure. Veratridine was administered intraperitoneally to male Fisher rats in a dose range of 100-400 mug/kg. Within 5 min. after the injections, the animals entered a quiescent period which was followed 10-15 min. later by facial automatism (washing), grooming, masticatory jaw movement and profuse salivation. This phenomenon was followed by the development of wet dog shake and forelimb clonus. The time (mean+/-S.E.M.) for the onset of induction of these shakes for all tested doses was 31.65+/-2.85 min. and the number of shakes (mean+/-S.E.M.) 30 min. after the onset was 17.2+/-2.85. The onset and number of wet dog shakes induced by veratridine was dose-dependent. No rat death was recorded until 2 weeks after the experiments. Histopathological studies of animals 2 weeks after veratridine administration showed evidence of apoptosis in the hippocampus. Our results indicate that veratridine produced a behavioural pattern of a limbic seizure which mimics temporal lobe epilepsy in man. Based on our previous findings in vitro and of this investigation in vivo, veratridine can be used as an experimental tool to evaluate potential antiepileptic drugs effective against this type of limbic behaviour.

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Propofol was reported to exhibit an antiepileptic activity. This study was performed to investigate the effect of propofol on evoked and spontaneous seizure-like activity induced by the convulsant veratridine. Studies were performed on rat brain slices using conventional electrophysiological intracellular techniques. The alteration of sodium channel function by veratridine (0.3 microM) induced an evoked and spontaneous seizure-like activity in the hippocampal CA1 pyramidal neurons. Therapeutic concentrations of propofol (10 microM) were ineffective in inhibiting veratridine-induced seizure-like activity. However, higher concentrations (50-100 microM, n=6) inhibited both evoked and spontaneous bursting, induced by veratridine. The inhibitory effect of propofol (100 microM) was associated with membrane hyperpolarization [after veratridine, -66+/-0.71 mV (mean+/-S.E.M.), and after propofol, -77+/-2.15 mV] and with an increase in input resistance [after veratridine (37.8+/-1.2 MOmega) and after propofol (43+/-1.3 MOmega)]. The drug also produced an increase in current threshold. Results from this study are valuable in solving critical questions regarding the antiepileptic activity of propofol and strengthen the validity of the veratridine model in testing for potential antiepileptic drugs.

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