Environmental Chemical Agents Research Articles

Transcription combined metabolic analysis reveals the mechanism of potassium phosphate enhances resistance to walnut anthracnose (Colletotrichum gloeosporioides)

Given the increasingly serious diseases [anthracnose mainly caused by Colletotrichum gloeosporioides (C. gloeosporioides)] of walnut plants in recent years and the environmental pollution caused by chemical pesticides, phosphites had been shown to be new environmental friendly chemical agents for plants. In this study, seven-year-old ‘Xiangling’ and ‘Xifu 4’ walnut trees were treated with different concentrations of potassium phosphite foliar fertilizer. The treatments were T1 (1500-fold dilution fluid of potassium phosphite), T2 (1000-fold dilution fluid of potassium phosphite) and CK (water). The results showed that the disease incidence rates of fruit treated with potassium phosphite were lower than CK. Moreover, the diseased fruit rates of ‘Xiangling’ (4) and ‘Xifu 4’ (14) in T2, lower than they (28 and 38) in CK. Metabolome and transcriptome further analysis revealed that potassium phosphite significantly increased the expression level of genes in the photosynthesis pathway and accumulated terpeniods, phenolic, salicylic acid and other secondary metabolic pathways. In addition, as salicylic acid content significantly increased, the expression level of the gene encoding the disease resistance-related protein (PR1) showed a corresponding trend. In vitro antibacterial tests of six related metabolites on C. gloeosporioides showed that hederagenin, 23-hydroxybetulinic acid, ursolic acid, eriodictyol, and salicylic acid had effect on C. gloeosporioides spores, among which salicylic acid and ursolic acid significantly inhibited the growth of C. gloeosporioides. Further experiments revealed that the minimum inhibitory concentrations of salicylic acid and ursolic acid were 2 and 5 g L−1, respectively. In addition, potassium phosphite could directly inhibit the growth of C. gloeosporioides spores in vitro tests. In conclusion, potassium phosphite enhanced walnut fruit disease resistance through up-regulated the genes related to photosynthetic performance and abundant in secondary metabolites, such as salicylic acid, terpenoids and phenolics, which were antibacterial effects on C. gloeosporioides.

Hydra for 21st Century—A Fine Model in Freshwater Research

Hydra is known for its natural occurrence, anatomical simplicity, intricate physiology, regenerative capacity, and ease of maintenance and manipulation in laboratory environments. It has proven to be a valuable model organism in various disciplines. Its applications range from developmental biology, stem cell research, animal physiology to environmental toxicology including ecotoxicology. The sensitivity of Hydra to a variety of environmental stressors and chemical agents such as metals, nanomaterials, and toxic organic compounds provides valuable insights into physiological mechanisms affected by environmental stressors and pollution, and Hydra can be of great use in environmental monitoring. Furthermore, since green Hydra lives in a symbiotic relationship with unicellular photoautotrophic algae, it is a suitable model organism for symbiosis research. Recently, it has become a popular model in holobiont research. The adaptability and importance of Hydra also extends to aquatic science and aquatic ecology, particularly in the context of monitoring and water pollution. Since the 1980s, Hydra has been increasingly used in various fields of research and has established itself as an important versatile model organism in numerous scientific studies. Hydra also represents an outstanding model in the fields of education and STEM. Hydra continues to be an important model in the 21st century, contributing significantly to our understanding of the biology of water and advancing freshwater research, and possibly finding its way to regenerative medicine and tumor pathobiology research.

Hair cell toxicology: With the help of a little fish.

Hearing or balance loss are disabling conditions that have a serious impact in those suffering them, especially when they appear in children. Their ultimate cause is frequently the loss of function of mechanosensory hair cells in the inner ear. Hair cells can be damaged by environmental insults, like noise or chemical agents, known as ototoxins. Two of the most common ototoxins are life-saving medications: cisplatin against solid tumors, and aminoglycoside antibiotics to treat infections. However, due to their localization inside the temporal bone, hair cells are difficult to study in mammals. As an alternative animal model, zebrafish larvae have hair cells similar to those in mammals, some of which are located in a fish specific organ on the surface of the skin, the lateral line. This makes them easy to observe in vivo and readily accessible for ototoxins or otoprotective substances. These features have made possible advances in the study of the mechanisms mediating ototoxicity or identifying new potential ototoxins. Most importantly, the small size of the zebrafish larvae has allowed screening thousands of molecules searching for otoprotective agents in a scale that would be highly impractical in rodent models. The positive hits found can then start the long road to reach clinical settings to prevent hearing or balance loss.

Effect of a Mixture of Native Iranian Probiotics on Biochemical Factors and Kidney Tissue of Male Rats Exposed to Cadmium Chloride

Introduction: Cadmium (Cd) is an environmental pollutant and chemical agent that destroys cell structure in various tissues. Probiotics are normal flora bacteria that if consumed adequately, will have health benefits in addition to nutritional benefits. The aim of this study was to investigate the effect of a mixture of native Iranian probiotics on biochemical factors and kidney tissue of male rats exposed to cadmium chloride.
 Methods: In this experimental study, 21 male Wistar rats were divided into 3 groups of 7: control, cadmium chloride recipient (3mg/kg) and cadmium chloride recipient (3mg /kg) + mixture of probiotics (CFU/mL109) were divided. Single-dose cadmium chloride was given to rats by intraperitoneal injection and probiotics by gavage for 30 days. At the end of the test, blood samples were taken directly from the heart to study serum creatinine and urea concentrations by autoanalyzer method and kidney tissue was used for microscopic studies of E&H staining. The data were evaluated using SPSS software version 16 and one-way ANOVA and Tukey test.
 Results: The results of Cadmium chloride significantly increased serum creatinine and urea concentrations compared to the control group (P<0.05) while in the group receiving probiotic mixture compared to the cadmium chloride group showed a significant decrease. Damage to kidney tissue was also shown compared to the control group. On the other hand, the structure of kidney tissue in the group treated with a mixture of probiotics compared to the group of cadmium chloride showed improvement.
 Conclusion: It is possible to use as a candidate a mixture of native Iranian probiotics (Lactobacillus rhamnosus, Lactobacillus casei and Lactobacillus holoticus) against cadmium chloride damage to the tissues of male rats.

Abstract D090: Can exposure to environmental chemical and biologic agents increase the risk of prostate cancer and its outcomes?

Abstract Introduction: It is generally believed that the environment plays some role in the development of prostate cancer, but the extent of that role is not understood. The objective of this study is to perform a systematic review of the literature to bring together the best available evidence on the suspected relationship between the environment and prostate cancer. Methods: PubMed, Web of Science, CINAHL, CancerLit, and the Cochrane Library were searched. We examined peer-reviewed English language studies examining the association between the environment and prostate cancer risk between 1990 and May 31, 2019. We further included studies if they met all of the following criteria: (1) considered at least one chemical or biological agents; (2) reported risk for incidence, mortality, serious adverse events, or hospital admissions. We extracted data from each study, including location, health outcome, and risk estimates. Results of the studies were combined using a qualitative synthesis due to the variation across and within outcomes in reported results. Results: We assessed 198 studies, of which we selected 51 for an in-depth review. Thirty-four articles fulfilled our predetermined inclusion criteria and were included in the qualitative synthesis. Of the 34 articles, 16 were prospective cohort studies, and 9 were case-control studies. These 34 articles explored a number of environmental agents including chemicals, ionizing radiation, electromagnetic fields, and infectious agents. Chemical exposures included second-hand exposure to industrial chemicals and to environmental carcinogens. Several of the studies (n=21) were based on ecological comparisons and did not provide a quantitative risk estimate. Exposure to ionizing radiation and electromagnetic fields showed no association with risk of prostate cancer. There is an inconsequential link between pesticides and an increased risk of prostate cancer through a potential endocrine-disrupting mechanism based on androgen imbalance. In most cases the overall evidence was inadequate in number, reported outcomes, quality of study to establish a relationship between a specific environmental agent and risk of prostate cancer; the evidence from chemical exposure studies was not sufficient to draw an inference. Conclusions: Overall, the reviewed epidemiologic evidence provides a weak level of evidence supporting the hypothesis that there is a causal relationship between environmental exposures and increased risk of prostate cancer. Because a large number of individuals are exposed to suspected environmental carcinogens, investigation of the association between prostate cancer and environmental chemical and biological agents deserves to be a high priority. Such investigations do not only have health implications but can also provide a fundamental understanding of the process of prostate carcinogenesis. Citation Format: Oluwabunmi Dada, Hadiza Galadima, John Cyrus, Georges Adunlin. Can exposure to environmental chemical and biologic agents increase the risk of prostate cancer and its outcomes? [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr D090.

Bisphenol A exposure disrupts aspartate transport in HepG2 cells.

The liver is the organ responsible for bisphenol A (BPA) metabolism, an environmental chemical agent. Exposure to this toxin is associated with liver abnormalities and dysfunction. An important role played by excitatory amino acid transporters (EAATs) of the slc1 gene family has been reported in liver injuries. To gain insight into a plausible effect of BPA exposure in the liver glutamate/aspartate transport, using the human hepatoblastoma cell line HepG2, we report a BPA-dependent dynamic regulation of SLC1A3 and SLC1A2. Through the use of radioactive [3 H]- d-aspartate uptake experiments and immunochemical approaches, we characterized time and dose-dependent regulation of the protein levels and function of these transporters after acute exposure to BPA. An increase in nuclear Yin Yang 1 was found. These results suggest an important involvement of the EAATs in liver physiology and its disruption after acute BPA exposure.

Drug-induced Hepatotoxicity and Hepatoprotective Medicinal Plants: A Review

Abstract: The Liver, a paramount organ is the Chief site for metabolism of nutrients and energy production in the human body. It is also necessary for metabolism and elimination of exogenous drugs and harmful substances via kidney. Hepatotoxicity caused by a variety of environmental pollutants, pathogenic microorganism, viruses, drugs and chemical agents may account for various hepatic diseases such as jaundice, necrosis, hepatitis, fibrosis and cirrhosis etc. Ayurveda is a traditional medicinal system of India and is being practiced continuously since ancient times and at present for the treatment of various human diseases. Medicinal plants as a significant source of therapeutic compounds used for the development of effective drugs against a variety of human diseases include liver ailments. Hence, therapeutic plants are becoming popular in the pharmaceutical industry to develop a safe and effective medicine for the treatment of the emerging new human diseases. Therefore, the present review is aimed to compiling data on hepatoprotective medicinal plants which have been investigated against drug-induced hepatotoxicity. Key words: Medicinal Plants, Carbon tetrachloride, Paracetamol, Alcohol, Hepatotoxicity, Hepatoprotection.

Phân tích mối liên quan giữa bệnh ung thư và thức ăn

There are increasing number of cancer deaths worldwide, motivating more studies to find solutions for the prevention of cancer. Although some of cancer diseases are attributed to gene inherited from parents, most of other cancers are formed from an interaction between gene and environmental factors, including physical, chemical and biological agents. Food is accounted to 30% of risk factors that cause cancer. Food can contribute to the formation of cancer through three mechanisms: epigenetic factors, DNA damage-caused by oxidative stress and mutagenesis. In contrast, some of food containing bioactive compounds are able to prevent or minimize above cancer-induced mechanisms. This paper is to analyze molecular mechanisms of food driving cancer and summarize some food components that can support or prevent the process of cancer development. From such analysis, some notifications to maintain healthy diets and lifestyle in the prevention of cancer thread are also suggested.

EFFECTS OF INTRANASAL BACTERIAL ENDOTOXIN ADMINISTRATION ON EXPRESSION OF ALPHA-SYNUCLEIN IN PERIPHERAL STRUCTURES OF THE OLFACTORY SYSTEM

The involvement of olfactory dysfunction led to the proposal of ‘the olfactory vector hypothesis’ to explain both olfactory losses and the etiology of idiopathic Parkinson disease (PD) as a result of the transit of an environmental virus or chemical agent that enters the central nervous system (CNS) via the nose, activating the glial response of the brain that may lead to dopamine neuronal damage. Previously created chronic, progressive a mouse model of PD by intranasal instillation of a LPS displayed several key features of early-stage PD: a progressive hypokinesia, selective loss of dopamine neurons, a reduction in striatal dopamine content, and α-synuclein (α-syn) accumulation and aggregation in the substance nigra. Other PD model based on nasal inoculation with α-syn aggregates also expressed parkinsonian-like behavioral and immunological features.We suggested that intranasal administration of LPS might cause an increase in expression and misfolding of a-syn in olfactory receptor cells that are projected into olfactory bulbs. We observed an increase in the expression of the native and phosphorylated forms of immunoreactive a-syn in olfactory cells, olfactory nerve and olfactory bulbs where, in addition, activated glial cells were observed. The findings suggest that bacterial antigens can cause parkinsonian-like features both by inducing a glial neuroinflammatory response and by increasing the production of phosphorylated a-syn in peripheral structures of the olfactory system.

Vascular Cells and Tissue Constructs Derived from Human Pluripotent Stem Cells for Toxicological Screening.

The ability of human stem cells to generate somatic cell lineages makes them ideal candidates for use in toxicological testing and eventually, preclinical drug development. Such resources would support an evolution away from human primary cells or research animal models, which suffer from variability and poor predictability, toward off-the-shelf assays of chemical toxicity and drug efficacy using human cells and tissues. To this end, we generated vascular cell populations (smooth muscle cells and endothelial cells) from human pluripotent stem cells (hPSCs), arranged them into 3D co-cultures within supportive gel matrices, and directed their propensity for self-organization resembling microvasculature. The resulting vascular cell populations and co-cultured constructs were then arrayed in high throughput and used for screening a library of environmental and clinical chemical agents for immunological and toxicological responses. The screen effectively stratified the chemicals into various levels of toxicity, with both cell type-specific and co-culture-dependent responses observed. Thus, hPSC-derived vascular cells and constructs could be progressed further toward use in toxicant and drug screening.

Aflatoxin M1 Contamination in Raw Cow Milk of Dairy Farms in Behbahan area, Khuzestan province, Iran

Introduction: Mycotoxins are among the environmental chemical agents with toxic effects on animals and humans. Aflatoxins (AF) are a major group of mycotoxins produced following the growth of some species of Aspergillus flavus and Aspergillus parasiticus, particularly in agricultural products. Aflatoxin M1 (AFM1) is secreted to milk and remains there since the process of pasteurization and sterilization has little effect on this metabolite. The aim of this study was to investigate the natural occurrence of AFM1 in raw milk in Behbahan area, which is an area of high-density livestock production in southwest of Iran. The other aim was to compare these obtained levels with the accepted level recommended by the European community (50 ng/L). Methods: In the present study, 90 samples of raw milk were collected from five dairy farms in Behbahan region, Khuzestan province, Iran. The AFM1 was analyzed using the Enzyme Linked Immune Sorbent Assay (ELISA) method by ELISA kits from Euro Clone, Italy. Data were analyzed by ANOVA and the results were reported as mean ± SE. The significant level was set at p ≤ 0.05. Results: The concentration of aflatoxin M1 in (15)16.54% of raw milk was higher than maximum tolerance limit accepted by European Union /Codex Alimentarius Commission (50 ng/l). The results of this study showed that all 90 investigated raw milk samples were contaminated with AFM1 (100%). Conclusion: A significant difference was observed between concentration means of AFM1 in various studied farms at P < 0.05. Consequently, high occurrence of AFM1 in raw milk samples was considered as a possible hazard for human health. However, further longitudinal studies are required on milk samples and other dairy products in Behbahan as well as other regions of Iran to estimate the representative intake of AFM1 in Iran.

Development of Fluorescent Assay for Monitoring of Dehalogenase Activity.

The rapid accumulation of sequence data and powerful protein engineering techniques providing large mutant libraries have greatly heightened interest in efficient methods for biochemical characterization of proteins. Herein is reported a continuous assay for screening of enzymatic activity. The assay is developed and tested with the model enzymes haloalkane dehalogenases and relies upon a fluorescent change of a derivative of 8-hydroxypyrene-1,3,6-trisulphonic acid due to the pH drop associated with the dehalogenation reactions. The assay is performed in a microplate format using a purified enzyme, cell-free extract or intact cells, making the analysis quick and simple. The method exhibits high sensitivity with a limit of detection of 0.06 mM. The assay is successfully validated with gas chromatography and then applied for screening of 12 haloalkane dehalogenases with the environmental pollutant bis(2-chloroethyl) ether and chemical warfare agent sulfur mustard. Six enzymes exhibited detectable activity with both substrates. The within-day variability of the assay for five replicates (n = 5) was 21%.

Estimation of graphene surface stability against the adsorption of environmental and technological chemical agents

The ability of graphene to resist the chemical transformations caused by chemisorption of several environmental and technological chemical agents (H2, O2, H2O, H2O2) was studied using DFT ab initio calculations of potential energy surfaces of adsorption on perfect and defect (single vacancy and Stone–Wales defect) graphene with zero and finite curvature. Beside the evident result that structural imperfections such as curvature and atomic defects make graphene chemically vulnerable, it was found that the two kinds of impact of vacancies and Stone–Wales defects on the chemical stability of a sp2‐hybridized carbon lattice are essentially different. In the latter case, chemisorption barriers for any kind of chemical agents decrease with increasing curvature but, in the case of single vacancies the finite curvature lowers the adsorption probability for oxygen‐based molecules. In general, it was shown that single‐layered graphene could be used as an effective protecting coating against environmental and technological chemical agents.

Environmental Contaminants and Pancreatic Beta-Cells.

Despite health policies as well as clinical and research efforts, diabetes prevalence is still rising around the world. A multitude of causes have been suggested for this increase, mostly related to familial background, the occidental diet which is rich in fat/carbohydrates, and sedentary life style. Type 2 diabetes involves malfunctions of the primary pancreatic beta-cells, usually attributed to local damage; however, it can be associated with other stressful environmental agents, such as chemical contaminants from food, plastic and air, among others. Indeed, exposure to these chemical agents during perinatal and adolescent life can increase the risk of developing cardiometabolic diseases later in life. This review explores data showing which environmental chemical agents may produce injury in beta-cells and further impair the insulinotropic process of type 2 diabetes. Additionally, it points the need to also consider unusual causes of metabolic diseases, such as environmental contaminants.

Assessment of perception and intention in pesticide purchase in Taiwan.

Environmental chemical agents such as pesticides can be purchased easily at a relatively low price, and this has resulted in high concern of environmental toxicity to human health, due to their persistence in various environmental bodies. Hence, this study aims to propose important factors influencing pesticide purchase intentions, including consumers' perceptions of the brand image and the ecological health risk. Since consumers are primary users, the seller knows the product's features but not the psychology of those who purchase it. Therefore, we attempted to clarify purchase intentions and perceptions using structural equation modeling techniques to empirically analyze survey data from 324 pesticide consumers in Taiwan. Our results demonstrate that perceived brand image positively affects perceived quality of a product, whereas perceived risk negatively affects perceived quality and purchase intentions. Furthermore, this study provides evidence that perceived quality positively affects purchase intentions. These relationships suggest that perceived quality mediates both the positive association between brand image and purchase intentions and the negative association between perceived risk and purchase intentions. Based on such outcomes, we propose that consumers need to be informed of pesticides related to costs and environmental benefits.

Nonalcoholic fatty liver disease and type 2 diabetes: common pathophysiologic mechanisms.

Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for advanced liver disease, type 2 diabetes (T2DM), and cardiovascular diseases. The prevalence of NAFLD in the general population is around 30 %, but it is up to three times higher in those with T2DM. Among people with obesity and T2DM, the NAFLD epidemic also is worsening. Therefore, it is important to identify early metabolic alterations and to prevent these diseases and their progression. In this review, we analyze the pathophysiologic mechanisms leading to NAFLD, particularly, those common to T2DM, such as liver and muscle insulin resistance. However, it is mainly adipose tissue insulin resistance that results in increased hepatic de novo lipogenesis, inflammation, and lipotoxicity. Although genetics predispose to NAFLD, an unhealthy lifestyle, including high-fat/high-sugar diets and low physical activity, increases the risk. In addition, alterations in gut microbiota and environmental chemical agents, acting as endocrine disruptors, may play a role.

Activation of transcription factors in a mouse lung following exposure to environmental chemical and biological agents.

Environmental biological and chemical agents can modulate innate and acquired immunity in the lung via the stimulation of Toll-like receptors (TLRs). To investigate the effect of environmental chemical agents on the activation of NF-κB and activator protein (AP)-1 subunits and the role of TLR4 signaling in the lung, C3H/HeN and C3H/HeJ (TLR4-defective) mice were exposed to 0 or 50 ppm of toluene for 6 hr/day, 5 days/week for 6 weeks. Some groups of mice were also stimulated with OVA or LPS as a biological agent. The DNA-binding activities of the NF-κB subunits (p50, p52, p65 and RelB) and AP-1 family members (FosB, c-Fos, +c-Jun, JunD) were compared using TransAM ELISA kits. Exposure to toluene alone produced no significant changes in both mice. Although stimulation with OVA or LPS alone significantly increased the DNA binding activities of p50 and p52 in C3H/HeN mice, there were no interactions between biological factors and toluene. In the C3H/HeJ mice, stimulation with OVA or LPS increased p65 and p52 binding activity and the combination of exposure to toluene and OVA significantly increased the DNA binding activities of the p65 and p52 in the lung. During AP-1 activation, co-exposure to toluene and OVA increased JunD binding activity in C3H/HeJ mice, while co-exposure to toluene and LPS influenced c-Fos binding activity in C3H/HeN mice. These results indicate that TLR4 may play an important role in activation of NF-κB or AP-1 family following exposure to environmental biological and chemical agents.

Human contamination by persistent toxic substances: the rationale to improve exposure assessment.

We know quite a lot about the generalized human contamination by environmental chemical agents; this statement is fully compatible with the view that most countries lack the necessary monitoring systems. We also know quite a lot about the toxic effects of environmental pollutants; this statement is fully compatible with the proposal that we need both more research and more energetic policies to decrease human contamination by such pollutants. Unsurprisingly, we know too little about the (environmental and social) causes and the etiopathogenesis (mechanisms) of the most prevalent diseases, and we will continue to miss relevant causes and mechanisms if we neglect the toxic chemicals that commonly contaminate humans, worldwide. Basic, clinical end environmental-epidemiological research on human health should more often consider integrating biomarkers of internal dose of environmental chemical pollutants. When we act in more responsible, rational, and scientific ways; when we become less dismissive towards environmental hazards; and when we thus neglect less the generalized human contamination by environmental chemical agents and their toxic effects, we will expand mechanistic biologic knowledge, and we shall as well increase the effectiveness of interventions and policies that enable the primary prevention of human diseases which cause huge amounts of economic burden and human suffering.

Clinical and epidemiologic characteristics of nodding syndrome in Mundri County, southern Sudan

Nodding syndrome (repetitive nodding and progressive generalized seizures) is assuming epidemic proportions in South Sudan, Tanzania and Uganda. To describe clinical and epidemiological features of nodding syndrome in southern Sudan based on preliminary investigations conducted in 2001 and 2002. Household surveys, clinical, electrophysiological (EEG) assessments, informant interviews and case-control studies were conducted in the town of Lui and the village of Amadi in southern Sudan. Nodding syndrome is characterized by involuntary repetitive nodding of the head, progressing to generalized seizures; mental and physical deterioration. The EEGs were consistent with progressive epileptic encephalopathy. Prevalence of Nodding syndrome in Lui and Amadi was 2.3% and 6.7% respectively. All case control studies showed a positive association between cases and Onchocerca volvulus. A history of measles was negatively associated with being a case: 2/13 of cases and 11/19 of controls had had measles: odds ratio 0.13 (95% CI 0.02, 0.76). Environmental assessment did not reveal any naturally occurring or manmade neurotoxic factors to explain Nodding Syndrome, although fungal contamination of food could not be ruled out. Nodding Syndrome was strongly associated with Onchocerca volvulus. There was no evidence to suggest an environmental pollutant, chemical agent, or other toxic factor.

Editorial: Nodding Disease or syndrome: What is the way forward?

Nodding disease or syndrome is one of those conditions that recently appeared to be of public health concern in some countries in Africa. The disease has been reported to occur in South Sudan, Tanzania, northern Uganda and Liberia. In South Sudan the disease is mainly concentrated along Yei River1, 2. Nodding syndrome is a mentally and physically disabling disease that affects children3, typically between the ages of 5 and 15. The disease is characterized by episodes of repetitive nodding of the head, with progression to generalized tonic-clonic seizures, mental deterioration and physical incapacity1, 3. During seizures the children lose consciousness and they may fall into fire or hurt themselves. They usually drop out of school because of deterioration in cognitive function and inability to cope with the school environment. A disease similar to nodding syndrome was first reported in Uganda by Raper 4 in 1950. This disease was called ‘nakalanga’ because of the pathological dwarfism and the affected persons were incapable of procreation. It occurred among the dwellers of Mabira forest near the source of the Nile in Uganda. The forest was heavily infested by the black fly. The disease occurred among any of the tribes living in the area provided they had lived in the forested area for a sufficient number of years. The children born by uneventful pregnancies became thin, weak and listless around the time of weaning with progressive mental and physical retardation with maximal severity occurring around 8 to 15 years. The local inhabitants, who had long recognized the disease, had incriminated the bites of the black fly. Similarly, a high number of patients with epilepsy and retarded growth was reported in an endemic area for onchocerciasis in western Uganda5. However, a study that evaluated the role of Onchocerca volvulus in the development of epilepsy in rural Tanzania reported no difference in microfilaria density between participants with epilepsy and those without6. Since 2009, about 4000 cases of nodding disease have been reported in northern Uganda. For over 20 years northern Uganda was a conflict area and most people lived in camps for the internally displaced. Following a cease-fire in 2006, most of the people have returned to their villages and this period has coincided with increased numbers of nodding disease, with some families reporting more than two cases7. In this issue of African Health Sciences, Tumwine and others8 report clinical and epidemiological characteristics of nodding syndrome in Mundri county, South Sudan. The study was carried out in poor rural communities that had been characterised by several displacements between 1994 and 1997. The prevalence of Nodding Syndrome in the study areas was 2.1% and 4.6% in the endemic communities. Similar to the epidemic in northern Uganda, some families have more than one affected child. The ratio of male to female cases was 1.2. The age at onset of suspected cases ranged from 2 to 18 years, with a median of 12 years, and the mean duration of illness had been reported to be 3.0 years. Previous case-control studies had shown a positive association between cases and infestation with Onchocerca volvulus microfilaria, evidenced by positive skin snips. The nodding was reported to be worse during meals or upon walking up in the morning, and on the traditional carbohydrate based diet compared to the western style diet. For some children, head nodding did not disrupt eating or the ability to follow commands. Episodes of abnormal behaviour associated with shouting, screaming or running were reported. Physical examination revealed stunting of growth, dwarfism, mental retardation, and poor development of secondary sexual characteristics. Electroencephalographic examination was consistent with progressive epileptic encephalopathy. The authors concluded that Nodding Syndrome was strongly associated with Onchocerca volvulus. There was no evidence to suggest an environmental pollutant, chemical agent, or other toxic factor. The authors recommend larger studies to elucidate the etiology and optimal treatment for these children. It has been proven that symptomatic treatment with anticonvulsants and other supportive measures such as nutrition rehabilitation improves the quality of life, though not a cure. On going studies in northern Uganda speculate that the disease is associated with vitamin B6 deficiency and probably high doses of vitamin B6 may be beneficial to these children. The disease seems to be more prevalent in the poor communities. Improved social economic status, environmental control measures for microfilaria will go along way to reduce morbidity due to nodding syndrome.