Search

Introduction: Work-related stress (WRS) is a highly prevalent and pervasive problem that can result in loss of productivity and deterioration of a lecturer's health. Lecturing work requires coping with some of the stressful situations found in any workplace to have a favourable quality of work life. The study determined the influence of sex, years of teaching experience, and academic rank on work-related stress, coping mechanisms, and quality of work life among lecturers at Nnamdi Azikiwe University (NAU)., Method: This was a cross-sectional survey involving 283 lecturers consecutively recruited from NAU after proportionate randomization of the lecturers in 101 departments. The Health and Safety Executive Work Related stress (HSE-WRS), Work-Related Quality of life (WRQL), and Brief-cope Questionnaires (BCQ) were applied to assess the participant's work-related stress, quality of work life, and coping mechanism (CM) respectively. Data were analyzed using Kruskal Wallis and Mann-Whitney U tests at a 0.05 level of significance., Result: Sex, years of teaching experience, and academic rank had statistically significant influence on 14 subsets of coping mechanism with p-values

Background: Natural spices are commonly used by the people in Nigeria. They may be easily contaminated with heavy metals when they are dried and then pose a health risk for the consumers., Objective: The aim of this study was to determine the levels of heavy metals in some commonly consumed natural spices namely Prosopis Africana, Xylopia aethiopica, Piper gineense, Monodora myristica, Monodora tenuifolia and Capsicum frutescens sold in the local markets of Awka, Anambra state, South East Nigeria to estimate the potential health risk., Results: The range of heavy metal concentration was in the order: Zn (14.09 - 161.04) > Fe (28.15 - 134.59) > Pb (2.61 - 8.97) > Cr (0.001 - 3.81) > Co (0.28 - 3.07) > Ni (0.34 - 2.89). Pb, Fe and Zn exceeded the maximum allowable concentrations for spices. The Target Hazard Quotient (THQ) of the spices varied from 0.06-0.5. Estimated daily intakes (EDI) were all below the tolerable daily intake (TDI). The lead levels in Prosopis africana, Xylopia aethiopica, Piper gineense, Monodora myristica and Capsicum frutescens which are 8-30 times higher than the WHO/FAO permissible limit of 0.3 mg/kg., Conclusions: Lead contamination of spices sold in Awka (south east Nigeria) may add to the body burden of lead. A good quality control for herbal food is important in order to protect consumers from contamination., Key Words: food products, spices, potential toxic metals, risk assessment, public health.

Currently, understanding of physiology and disease patterns is undergoing a fundamental paradigm shift with attendant shift in education of health professionals worldwide towards active learning to encourage exploration of connections and their relationships. We introduced problem-based learning to physiology teaching of medial laboratory students to confirm worldwide reports that active learning environments offer better learning opportunities over the traditional methods which is the predominant teaching method in Nigerian universities. Our findings indicate that problem-based learning increases students' attendance/participation in classes and performance in examination. We recommend the integration of active learning into physiology curriculum of Nigerian Universities.

Background: Proliferative lupus nephritis (PLN) is characterized by increased expression of inducible nitric oxide (NO) synthase (iNOS). Inhibition of iNOS with NG-monomethyl L-arginine (L-NMMA) abrogates renal disease in two models of murine PLN, but the mechanism of this effect is unknown. Reactive oxygen species have both direct and indirect pathogenic effects in inflammatory lesions and are therefore potentially an important therapeutic target in PLN. We hypothesized that inhibition of iNOS activity would reduce ROS production in murine PLN., Methods: A dose escalation of L-NMMA (0, 20, 100, and 500 mg/kg/day) was performed in New Zealand Black x New Zealand White F1 (NZB/W) mice with active renal disease. Twenty-four-hour urine nitrate + nitrite (NOX) was measured with a chemiluminescence NO analyzer. Twenty-four-hour urine 8-isoprostane F2alpha (8-iso-PGF2alpha) was measured by gas chromatography-negative ion chemical ionization mass spectrometry. MRL-MpJFASlpr (MRL/lpr) and NZB/W mice were divided into three groups and given either L-NMMA, L-N6-iminoethyl-lysine (L-NIL), or distilled water for 2 weeks. Urine NOX and 8-iso-PGF2alpha were determined after 2 weeks., Results: L-NMMA reduced both urine NOX and 8-iso-PGF2alpha levels in a dose-dependent fashion in NZB/W and MRL/lpr mice. Urine NOX and 8-iso-PGF2alpha levels were highly correlated. Both specific (L-NIL) and nonspecific (L-NMMA) iNOS inhibition reduced urine NOX and 8-iso-PGF2alpha levels in both models of murine PLN., Conclusion: These findings suggest that iNOS activity is a major source of reactive oxidant stress in these models of murine PLN. Future studies will address the pathogenic role of reactive oxygen stress in PLN.

The methanolic leaf extract of Costus afer. Ker (family: Zingiberaceae) was investigated for some pharmacological effects in vivo and in vitro. Brine shrimp lethality test showed that the extract was significantly (p < 0.05) cytotoxic with LC50 of 21.3 ppm. The extract showed moderate local anesthetic property, about twice less than lignocaine of the same concentration, on guinea pig wheal test. The extract contracted the guinea pig ileum in a concentration-dependent manner, but had no effect on pleuripara and nullipara non-gravid uteri at progestogenic and estrogenic phases respectively. The contractile effect on the guinea pig ileum was partially inhibited by atropine but completely reversed by adrenaline. The extract induced expulsion of whole fetuses still enveloped within the placental membrane at the 3rd trimester of pregnancy. The extract exhibited a biphasic antihyperglycemic activity. At 200 mg/kg body wt., p.o., it decreased the blood glucose level by 50% in Streptozotocin-induced hyperglycemia in male rats in 60 minutes post dosing. However, doses above 200 mg/kg body wt., p.o., caused increase in blood glucose level, potentiating the action of STZ. At 10 microg/ml the extract induced about 98% glucose uptake in differentiated 3T3-L1 adipocytes when compared with insulin (340 nm).

Equine protozoal myeloencephalitis (EPM) is a serious neurologic disease in the horse most commonly caused by Sarcocystis neurona. The domestic cat (Felis domesticus) is an intermediate host for S. neurona. In the present study, nine farms, known to have prior clinically diagnosed cases of EPM and a resident cat population were identified and sampled accordingly. In addition to the farm cats sampled, samples were also collected from a mobile spay and neuter clinic. Overall, serum samples were collected in 2001 from 310 cats, with samples including barn, feral and inside/outside cats. Of these 310 samples, 35 were from nine horse farms. Horse serum samples were also collected and traps were set for opossums at each of the farms. The S. neurona direct agglutination test (SAT) was used for both the horse and cat serum samples (1:25 dilution). Fourteen of 35 (40%) cats sampled from horse farms had circulating S. neurona agglutinating antibodies. Twenty-seven of the 275 (10%) cats from the spay/neuter clinic also had detectable S. neurona antibodies. Overall, 115 of 123 (93%) horses tested positive for anti-S. neurona antibodies, with each farm having greater than a 75% exposure rate among sampled horses. Twenty-one opossums were trapped on seven of the nine farms. Eleven opossums had Sarcocystis sp. sporocysts, six of them were identified as S. neurona sporocysts based on bioassays in gamma-interferon gene knockout mice with each opossum representing a different farm. Demonstration of S. neurona agglutinating antibodies in domestic and feral cats corroborates previous research demonstrating feral cats to be naturally infected, and also suggests that cats can be frequently infected with S. neurona and serve as one of several natural intermediate hosts for S. neurona.

The effect of inoculation dose of Sarcocystis neurona sporocysts on the development of clinical neurologic disease in horses was investigated. Twenty-four seronegative weanling horses were subjected to the natural stress of transport and then randomly assigned to 6 treatment groups of 4 horses each. Horses were then immediately inoculated with either 10(2), 10(3), 10(4), 10(5), or 10(6) S. neurona sporocysts or placebo using nasogastric tube and housed indoors. Weekly neurologic examinations were performed by a blinded observer. Blood was collected weekly for antibody determination by Western blot analysis. Cerebrospinal fluid was collected before inoculation and before euthanasia for S. neurona antibody determination. Horses were killed and necropsied between 4 and 5 wk after inoculation. Differences were detected among dose groups based on seroconversion times, severity of clinical neurologic signs, and presence of microscopic lesions. Seroconversion of challenged horses was observed as early as 14 days postinfection in the 10(6) sporocyst dose group. Mild to moderate clinical signs of neurologic disease were produced in challenged horses from all groups, with the most consistent signs seen in the 10(6) sporocyst dose group. Histologic lesions suggestive of S. neurona infection were detected in 4 of the 20 horses fed sporocysts. Parasites were not detected in equine tissues by light microscopy, immunohistochemistry, or bioassay in gamma-interferon gene knockout mice. Control horses remained seronegative for the duration of the study and had no histologic evidence of protozoal infection.

Sarcocystis neurona causes encephalomyelitis in many species of mammals and is the most important cause of neurologic disease in the horse. Its complete life cycle is unknown, particularly its development and localization in the intermediate host. Recently, the raccoon (Procyon lotor) was recognized as a natural intermediate host of S. neurona. In the present study, migration and development of S. neurona was studied in 10 raccoons that were fed S. neurona sporocysts from experimentally infected opossums; 4 raccoons served as controls. Raccoons were examined at necropsy 1, 3, 5, 7, 10, 14, 15, 22, 37, and 77 days after feeding on sporocysts (DAFS). Tissue sections of most of the organs were studied histologically and reacted with anti-S. neurona-specific polyclonal rabbit serum in an immunohistochemical test. Parasitemia was demonstrated in peripheral blood of raccoons 3 and 5 DAFS. Individual zoites were seen in histologic sections of intestines of raccoons euthanized 1, 3, and 5 DAFS. Schizonts and merozoites were seen in many tissues 7 to 22 DAFS, particularly in the brain. Sarcocysts were seen in raccoons killed 22 DAFS. Sarcocysts at 22 DAFS were immature and seen only in skeletal muscle. Mature sarcocysts were seen in all skeletal samples, particularly in the tongue of the raccoon 77 DAFS; these sarcocysts were infective to laboratory-raised opossums. This is the first report of the complete development of S. neurona schizonts and sarcocysts in a natural intermediate host.

Equine protozoal myeloencephalitis (EPM) is a disease of horses that is primarily associated with infection with the apicomplexan Sarcocystis neurona. Infection with this parasite alone is not sufficient to induce the disease, and the mechanism of neuropathogenesis associated with EPM has not been reported. Nitric oxide (NO) functions as a neurotransmitter, a vasodilator, and an immune effector and is produced in response to several parasitic protozoa. The purpose of this work was to determine if the concentration of NO metabolites (NO(x)(-)) in the cerebrospinal fluid (CSF) is correlated with the development of EPM. CSF NO(x)(-) levels were measured before and after transport-stressed, acclimated, or dexamethasone-treated horses (n = 3 per group) were experimentally infected with S. neurona sporocysts. CSF NO(x)(-) levels were also compared between horses that were diagnosed with EPM after natural infection with S. neurona and horses that did not have clinical signs of disease or that showed no evidence of infection with the parasite (n = 105). Among the experimentally infected animals, the mean CSF NO(x)(-) levels of the transport-stressed group, which had the most severe clinical signs, was reduced after infection, while these values were found to increase after infection in the remaining groups that had less severe signs of EPM. Under natural conditions, horses with EPM (n = 65) had a lower mean CSF NO(x)(-) concentration than clinically normal horses with antibodies (Abs) against S. neurona (n = 15) in CSF, and horses that developed ataxia (n = 81) had a significantly lower mean CSF NO(x)(-) concentration than horses that did not have neurologic signs (n = 24). In conclusion, lower CSF NO(x)(-) levels were associated with clinical EPM, suggesting that measurement of CSF NO(x)(-) levels could improve the accuracy of diagnostic tests that are based upon detection of S. neurona-specific Abs in CSF alone and that reduced NO levels could be causally related to the development of EPM.

Equine protozoal myeloencephalitis (EPM) is a serious neurologic disease of horses in the Americas and Sarcocystis neurona is the most common etiologic agent. The distribution of S. neurona infections follows the geographical distributions of its definitive hosts, opossums (Didelphis virginiana, Didelphis albiventris). Recently, cats and skunks were reported as experimental and armadillos as natural intermediate hosts of S. neurona. In the present report, raccoons (Procyon lotor) were identified as a natural intermediate host of S. neurona. Two laboratory-raised opossums were found to shed S. neurona-like sporocysts after ingesting tongues of naturally-infected raccoons. Interferon-gamma gene knockout (KO) mice fed raccoon-opossum-derived sporocysts developed neurologic signs. S. neurona was identified immunohistochemically in tissues of KO mice fed sporocysts and the parasite was isolated in cell cultures inoculated with infected KO mouse tissues. The DNA obtained from the tongue of a naturally-infected raccoon, brains of KO mice that had neurological signs, and from the organisms recovered in cell cultures inoculated with brains of neurologic KO mice, corresponded to that of S. neurona. Two raccoons fed mature S. neurona sarcocysts did not shed sporocysts in their feces, indicating raccoons are not likely to be its definitive host. Two raccoons fed sporocysts from opossum feces developed clinical illness and S. neurona-associated encephalomyelitis was found in raccoons killed 14 and 22 days after feeding sporocysts; schizonts and merozoites were seen in encephalitic lesions.

Neurologic disease in horses caused by Sarcocystis neurona is difficult to diagnose, treat, or prevent, due to the lack of knowledge about the pathogenesis of the disease. This in turn is confounded by the lack of a reliable equine model of equine protozoal myeloencephalitis (EPM). Epidemiologic studies have implicated stress as a risk factor for this disease, thus, the role of transport stress was evaluated for incorporation into an equine model for EPM. Sporocysts from feral opossums were bioassayed in interferon-gamma gene knockout (KO) mice to determine minimum number of viable S. neurona sporocysts in the inoculum. A minimum of 80,000 viable S. neurona sporocysts were fed to each of the nine horses. A total of 12 S. neurona antibody negative horses were divided into four groups (1-4). Three horses (group 1) were fed sporocysts on the day of arrival at the study site, three horses were fed sporocysts 14 days after acclimatization (group 2), three horses were given sporocysts and dexamethasone 14 days after acclimatization (group 3) and three horses were controls (group 4). All horses fed sporocysts in the study developed antibodies to S. neurona in serum and cerebrospinal fluid (CSF) and developed clinical signs of neurologic disease. The most severe clinical signs were in horses in group 1 subjected to transport stress. The least severe neurologic signs were in horses treated with dexamethasone (group 3). Clinical signs improved in four horses from two treatment groups by the time of euthanasia (group 1, day 44; group 3, day 47). Post-mortem examinations, and tissues that were collected for light microscopy, immunohistochemistry, tissue cultures, and bioassay in KO mice, revealed no direct evidence of S. neurona infection. However, there were lesions compatible with S. neurona infection in horses. The results of this investigation suggest that stress can play a role in the pathogenesis of EPM. There is also evidence to suggest that horses in nature may clear the organism routinely, which may explain the relatively high number of normal horses with CSF antibodies to S. neurona compared to the prevalence of EPM.

Sarcocystis neurona is the most important cause of a neurologic disease in horses, equine protozoal myeloencephalitis (EPM). The complete life cycle of S. neurona, including the description of sarcocysts and intermediate hosts, has not been completed until now. Opossums (Didelphis spp.) are definitive hosts, and horses and other mammals are aberrant hosts. In the present study, laboratory-raised domestic cats (Felis domesticus) were fed sporocysts from the intestine of a naturally infected opossum (Didelphis virginiana). Microscopic sarcocysts, with a maximum size of 700 x 50 microm, developed in the muscles of the cats. The DNA of bradyzoites released from sarcocysts was confirmed as S. neurona. Laboratory-raised opossums (D. virginiana) fed cat muscles containing the sarcocysts shed sporocysts in their feces. The sporocysts were approximately 10(-12) x 6.5-8.0 microm in size. Gamma interferon knockout mice fed sporocysts from experimentally infected opossums developed clinical sarcocystosis, and S. neurona was identified in their tissues using S. neurona-specific polyclonal rabbit serum. Two seronegative ponies fed sporocysts from an experimentally-infected opossum developed S. neurona-specific antibodies within 14 days.

The leaf extract (F005) of Ocimum gratissimum was isolated by a bioassay-guided chromatographic separation technique using the brine shrimp lethality test assay. The effects of various concentrations (0.5, 1.0, 2.0, 4.0, and 8.0 mg/ml) of F005 were tested in vitro on infective larvae (L(3)) of Haemonchus contortus and Heligmosomoides polygyrus. Cockerels experimentally infected with Ascaridia galli infective eggs were also treated with various doses (500, 1000, and 1500 mg/kg) of F005 in vivo. F005 produced 15% and 16.6% paralysis of H. contortus and H. polygyrus larvae, respectively, at 8 mg/ml. It induced significant anthelmintic effect in chicks infected with A. galli in a dose-dependent manner with 1,500 mg/kg producing the highest effect (55.8%)., (Copyright © 1998 Gustav Fischer Verlag. Published by Elsevier GmbH.. All rights reserved.)