Placental levels of polycyclic aromatic hydrocarbons (PAHs) and their association with birth weight of infants.

As an alarming group of pollutants, polycyclic aromatic hydrocarbons (PAHs) gather much public health concern not only because of their carcinogenic or co-carcinogenic risk but also by interfering with hormone systems or by causing oxidative damage, henceforth liable to toxic actions on reproduction. Accordingly, the present study was aimed to explore the association between in-utero exposure to PAHs by evaluating their placental levels and infant birth weight among 110 healthy and nonsmoking pregnant women. Placental tissue samples were collected instantly after delivery and were analyzed for the presence of sixteen Environmental Protection Agency (EPA) listed PAHs with the help of Gas chromatography equipped with flame ionization detector (GC-FID). Chrysene and benzo(k)fluoranthene were the predominant PAHs detected in tissue samples. To assess the source of origin of PAHs in placenta tissue samples, the ratio of low molecular weight PAHs to high molecular weight (∑LMW/∑HMW PAHs) was calculated, showing the predominance of pyrogenic sources of PAHs possibly responsible for the exposure of the studied population. Results of regression analysis demonstrated the inverse although not significant association of naphthalene (Nap), acenaphthylene (Acy), anthracene (Anth), pyrene (Pyr), benzo(b)fluoranthene (BbF), benzo(k)Fluoranthene (BkF), benzo(a)pyrene (BaP), indeno (123 cd pyrene (IcdP), dibenzo(ah)anthracene (DahA) and benzo(ghi)Perylene (BghiP) with birth weight of neonates. Additionally, the regression model lay light upon the significant association of fluoranthene (Fla) (coefficient= -1.41 gram, p < 0.05) to the depletion trend of birth weight after adjusting for potential covariates. These findings suggest the possible role of an environmental contaminants like PAHs on impairment of fetal growth.

Environmental toxic metals in placenta and their effects on preterm delivery-current opinion.

Preterm birth is a significant public reproductive health concern globally; Furthermore, preterm birth has long-lasting medical and pecuniary burdens on the society. Moreover, preterm birth is well-established as the underlying cause of low birth weight in infants as well as neonatal mortality. A growing body of literature suggests that the etiology of preterm delivery in women is elusive; however, countless environmental factors are considered responsible for preterm birth. Environmental contaminants that are toxic metals such as lead, cadmium, arsenic, and mercury are familiar confounding factors for preterm birth globally. Recent studies have indicated that these toxic heavy metals induce oxidative stress in the trophoblastic placental tissue by producing reactive oxygen species that alter the mechanism of antioxidants possibly leading to preterm birth. Moreover, no obvious mechanism underlying metal-induced oxidative stress in the placenta has been identified until date. Consequently, this review offers an outline of the currently existing scientific information on the association of toxic metals and redox status of the placental tissue with preterm birth. Furthermore, this study critically recognizes the gaps related to the deleterious effect of metals on the gestation period in scientific literature.

Do paroxysmal hemicrania and hemicrania continua represent different headaches? A retrospective study.

OBJECTIVE: Hemicrania continua and paroxysmal hemicrania are considered different headaches belonging to a group of trigeminal autonomic cephalalgias. However, they share many clinical features. Both headaches also show complete response to indomethacin, which is a mandatory criterion for their diagnosis. Are they really different headaches? To answer this question, we compared the pain characteristics and autonomic features between two headaches. We also determined whether paroxysmal hemicrania transforms into hemicrania continua or vice versa in their natural history. METHODS: The patients with hemicrania continua and paroxysmal hemicrania were compared for severity, location, character, and mean effective indomethacin dose. The number of autonomic features and their severity was also compared. The natural history of headache was looked into to see the evolution of hemicrania continua and paroxysmal hemicrania from episodic and chronic pains, respectively. RESULTS: We included 35 patients with hemicrania continua and 27 patients with paroxysmal hemicrania from July 2015 to March 2017. The mean age of patients with paroxysmal hemicrania was 34.42 years, and hemicrania continua was 37 years. Both groups were similar for majority of pain characteristics and number/severity of autonomic features. However, paroxysmal hemicrania had higher pain severity. Five patients transformed from paroxysmal hemicrania to hemicrania continua, and 3 patients transformed from hemicrania continua to paroxysmal hemicrania. CONCLUSION: Paroxysmal hemicrania and hemicrania continua were similar on majority of pain characteristics and autonomic features. The paroxysmal hemicrania and hemicrania continua are not exclusive headaches and can transform into each other.

Association Between Placental Polycyclic Aromatic Hydrocarbons (PAHS), Oxidative Stress, and Preterm Delivery: A Case-Control Study.

Polycyclic aromatic hydrocarbons are known to disturb the antioxidant defense system, which may indirectly contribute to induction of early pregnancy in women. Therefore, the present investigation was designed to offer preliminary information about exposure to PAHs by estimating their placental levels and its association with oxidative stress as well as with preterm birth. Placenta tissue samples were drawn after delivery from 84 healthy pregnant women, recruited at a local nursing home of Agra, India, and levels of PAHs were quantified by gas chromatograph equipped with flame ionization detector. To evaluate redox status biomarkers, malondialdehyde (MDA) and glutathione (GSH) were determined in placenta tissue. Significantly elevated levels of benzo(a)pyrene and MDA while decreasing trend of GSH was found in women with preterm delivery group (study) than women with a full-term delivery group (control). Results demonstrated higher, but statistically insignificant (p > 0.05), levels of naphthalene, anthracene, fluorene, pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene, indeno[1,2,3-cd]pyrene, dibenzo(ah)anthracene, and benzo(ghi)perylene in the study group than the control group. However, higher and lower molecular weight PAHs showed significant correlation for the depletion trend of GSH sights upon an example of oxidative stress mechanism. Because of limited statistical power and absence of controlled confounders, this study does not provide an ample involvement of PAHs with preterm delivery but increased MDA and decreased GSH in cases than controls gives the possible contribution of PAHs to early delivery.

Why do neurologists miss catatonia in neurology emergency? A case series and brief literature review.

Catatonia is a well-described clinical syndrome characterized by features that range from mutism, negativism and stupor to agitation, mannerisms and stereotype. Causes of catatonia may range from organic brain disorders to psychiatric conditions. Despite a characteristic syndrome, catatonia is grossly under diagnosed. The reason for missed diagnosis of catatonia in neurology setting is not clear. Poor awareness is an unlikely cause because catatonia is taught among conditions with deregulated consciousness like vegetative state, locked-in state and akinetic mutism. We determined the proportion of catatonia patients correctly identified by neurology residents in neurology emergency. We also looked at the alternate diagnosis they received to identify catatonia mimics. Twelve patients (age 22-55 years, 7 females) of catatonia were discharged from a single unit of neurology department from 2007 to 2017. In the emergency department, neurology residents diagnosed none of the patients as catatonia. They offered diagnosis of extrapyramidal syndrome in 7, meningitis in 2, and conversion reaction, acute psychosis/encephalopathy and non-convulsive status epilepticus in one each. Their final diagnosis at discharge was catatonia due to general medical condition in 6 (progressive supranuclear palsy in 2, post-status epilepticus, uremic encephalopathy, glioblastoma multiforme and tuberculous meningitis in one each), catatonia due to major depression in 4, schizophrenia and idiopathic catatonia in one each. Extrapyramidal syndrome appeared as common mimic of catatonia. The literature reviewed also revealed the majority of organic catatonia secondary to causes that are usually associated with extrapyramidal features. Therefore, we suggest that neurologists should consider catatonia in patients presenting with extrapyramidal syndromes.

Oxidative stress in status epilepticus: A clinical-radiological correlation.

PURPOSE: To report oxidative stress in the patients with status epilepticus (SE), and correlate these with severity, MRI and outcome. METHODS: Thirty-five patients with SE and 34 controls were included. Blood sample was collected at admission for measuring superoxide dismutase (SOD), catalase, protein carbonyl, glutathione, total antioxidant capacity (TAC), malondialdehyde (MDA) and nitric oxide (NO). The type of SE, duration and Status Epilepticus Severity Score (STESS) at admission and refractoriness to treatment were noted. Cranial magnetic resonance imaging (MRI) findings, in-hospital deaths and disability at discharge were noted. RESULTS: The median age of the patients was 35 and 14 were females. The median STESS was 3 (0-5), and the score was unfavorable in 21(60%) patients. MRI was abnormal in 27(77%) patients. The patients with SE had significantly lower concentrations of SOD, catalase, protein carbonyl, GSH and TAC and higher concentrations of MDA and NO compared to the controls. These levels did not differ between refractory and non-refractory SE. Glutathione level inversely correlated with age. Malondialdehyde and NO levels positively correlated with age and inversely with GSH level. Five (14.3%) patients died in hospital. At discharge, 14 patients had good and 16 had poor outcome. The oxidative stress markers did not correlate with death or disability. CONCLUSION: Oxidative stress is increased in the patients with SE. Further study is needed in larger sample size to explore probable adjunctive treatment option.

Heat stress-induced neuroinflammation and aberration in monoamine levels in hypothalamus are associated with temperature dysregulation.

Heat Stress (HS) induces diverse pathophysiological changes, which include brain ischemia, oxidative stress and neuronal damage. The present study was undertaken with the objective to ascertain whether neuroinflammation in Hypothalamus (HTH) caused under HS affects monoamine levels and hence, its physiological role in thermoregulation. Rats were exposed to HS in a heat simulation environmental chamber (Ambient temperature, Ta=45±0.5°C and Relative Humidity, RH=30±10%) with real-time measurement of core temperature (Tc) and skin temperature (Ts). Animals were divided into two subgroups: Moderate HS (MHS) (Tc=40°C) and Severe HS (SHS)/Heat stroke (Tc=42°C). Rats with MHS showed an increase in Mean Arterial Pressure (MAP) and Heart Rate (HR) while fall in MAP and rise in HR was observed in rats with SHS. In addition, oxidative stress and an increase in pyknotic neurons were observed in HTH. High levels of Adrenocorticotropic-hormone (ACTH), Epinephrine (EPI), Norepinephrine (NE) and Dopamine (DA) in the systemic circulation and progressive increase in EPI and DA levels in HTH were recorded after the thermal insult. Moreover, a substantial increase in Glutamate (Glu) level was observed in HTH as well as in systemic circulation of heat stroke rats. We found a rise in NE whereas a fall in Serotonin (5-HT) level in HTH at MHS, without perturbing inflammatory mediators. However, rats with SHS exhibited significant elevations in NF-kB, IL-1ß, COX2, GFAP and Iba1 protein expression in HTH. In conclusion, the data suggest that SHS induces neuroinflammation in HTH, which is associated with monoamines and Glu imbalances, leading to thermoregulatory disruption.

Early osmotic, antioxidant, ionic, and redox responses to salinity in leaves and roots of Indian mustard (Brassica juncea L.).

Salt-stress-induced alterations in osmotic, ionic, and redox responses were studied in the early period of treatment (30 min to 5 days) in seedlings of Brassica juncea L. Roots and shoots under mild (50 mM) and severe (250 mM) NaCl stress were analyzed for growth, oxidative stress, osmolyte accumulation, antioxidant defense, and redox state. Growth reduction was less pronounced in the early time period of salt stress while oxidative damage increased linearly and in a sustained manner under severe stress up to 6 h. An early and transient reactive oxygen species (ROS) burst, as evidenced by superoxide and hydrogen peroxide level was observed, followed by activation of enzymatic antioxidant system (GPX, SOD, CAT, and GR) in both root and shoot. The enzymatic activity was not affected much under mild stress particularly at early phase; however, severe stress induced a significant increase in the activity of antioxidant enzymes. Root ascorbate was progressively accumulated, and its redox state maintained in the early time phase of treatment under mild stress while increase in root and shoot glutathione content was recorded under mild stress at 5 days when the active ascorbate pool decreased. While early period of salt stress showed significant Na(+) accumulation over control, plants subjected to mild stress measured less Na(+) accumulation up to 5 days compared to severely stressed plants. The results showed an early induction of differential responses to salt stress in roots and shoots of Brassica which include growth limitations, reduced relative water content, increased osmolytes, redox state, and antioxidant system, and a significant Na(+) increase. The results also indicate that roots and shoots may have distinct mechanisms of responses to salt stress.

Heat: not black, not white. It's gray!!!

Heat-related illness (HRI) is a broad term that includes clinical conditions ranging from heat cramps and syncope to heat exhaustion and heatstroke, which may result in death. HRIs are one of the major causes of death worldwide and continue to increase in severity with the rise in global temperature. The identification and estimation of heat-related morbidity and mortality is a major challenge. Heat stress manifests itself into respiratory, cardiovascular, and cerebrovascular disorders, leading to the attribution of the deaths caused by heat stress to these disorders. Although HRIs affect mankind in general, certain occupational workers such as soldiers and athletes are more prone. Various pharmacological and nonpharmacological strategies have been employed to combat HRIs. Despite this, heat exposure results in significant morbidity and mortality. Hence, complete understanding of HRIs at physiological as well as molecular level is required to facilitate design of more efficient preventive and treatment strategies. The impact of heat on mankind is not just restricted to HRIs. Heat treatment, i.e., thermotherapy, has been used extensively since ancient times for relieving pain, making heat a two-edged sword. This review attempts to summarize various HRIs, their physiological and molecular basis, and the state-of-the-art techniques/research initiatives to combat the same. It also illustrates the application of thermotherapy as a means for improving quality of life and morbidity associated with several disease conditions such as fibromyalgia syndrome, heart diseases, cancer, chronic pain, and depression.