Zika and travel in the news: a content analysis of US news stories during the outbreak in 2016-2017.

OBJECTIVES: This study aimed to understand what information the US media communicated about Zika virus (ZIKV) and travel in 2016 and 2017. STUDY DESIGN: We conducted a content analysis of news coverage about ZIKV and travel from April 5, 2016 to March 31, 2017. METHODS: We obtained a stratified, random sample of English language, US print newspaper and television news coverage about ZIKV and travel. We developed a coding scheme to assess key messages in the news, including how ZIKV is transmitted, the symptoms and outcomes of ZIKV infection, and recommended prevention behaviors. RESULTS: Almost all news stories mentioned mosquito-borne transmission (96.8%) and just over half mentioned sexual transmission (55.3%). News stories were more likely to talk about ZIKV outcomes (78.8%) than ZIKV symptoms (40.6%). However, outcomes affecting babies were mentioned more frequently than outcomes affecting adults. Recommendations included a wide array of protective behaviors, such as delaying or avoiding travel (77.6%) and using mosquito repellent (41.0%). However, few studies (10.9%) mentioned barriers to practicing ZIKV prevention behaviors. CONCLUSIONS: Public health organizations and professionals can use these findings to help improve communication about future outbreaks of mosquito-borne illnesses. We also recommend conducting real-time monitoring of news media and frequent content analysis of news stories to ensure coverage provides the information the public needs.

Attention-deficit hyperactivity disorder (ADHD) as a pyridoxine-dependent condition: urinary diagnostic biomarkers.

The data obtained in children with different forms of epilepsy allowed us to consider epilepsy as an inborn error of pyridoxine (vitamin B6) metabolism (Dolina et al., 2012). Mutual interconnections between ADHD and epilepsy indicate that such an approach is reasonable for ADHD. To check such an assumption we analyzed in ADHD patients the same parameters of pyridoxal phosphate (PLP)-dependent tryptophan (TRP) degradation, which were analyzed in epileptic children. The level of TRP and concentrations of compounds formed or metabolized by TRP degradation, the ratios between some of them, and the level of 4-pyridoxic acid were HPLC detected in ADHD children and healthy controls. The data obtained, including low values of 4PA/TRP, IND/TRP and IND/KYN ratios, have evidenced dramatically impaired activity of pyridoxine-dependent enzymes in ADHD patients. Ritalin treatment did not change the general pattern of TRP degradation, but still created a kind of balance between some of detected metabolites. However, the 4PA/TRP, IND/TRP and IND/KYN ratios remained as low as in untreated patients, keeping the importance of diagnostic markers. Almost identical parameters of TRP degradation in untreated ADHD and epileptic patients allow to assume that inborn disorders of vitamin B6 metabolism are the common biochemical background of both diseases. The disturbed activity of PLP dependent enzymes apparently forms those profound disturbances of neurotransmitter systems, which are inherent in ADHD: low concentrations of monoamines and disordered amino acid metabolism. If vitamin B6 disorders are the core biochemical disturbances inherent in ADHD, then the long-term pyridoxine treatment is pathogenetically based replacement therapy of the disease. According to our data, multi-year pyridoxine treatment normalizes completely the pattern of ADHD behavior, without causing any serious side effects.

Preoperative open field behavior predicts levels of neuropathic pain-related behavior in mice.

Exploratory open field (OF) activity was assessed in seven different mouse strains and selection lines. We counted the number of beam interruptions made by three cagemate mice at a time. This assay tests reactivity to aversive stimuli, anxiety and emotionality. One hindlimb was then totally denervated by transecting the sciatic and saphenous nerves on one side, and autotomy, a behavior thought to be related to neuropathic pain, was quantified over 35 days. We report that OF activity and autotomy are highly variable across different strains/lines. These results reaffirm the genetic control of these behaviors. We also found that these behaviors are inversely and significantly correlated. We suggest that common genetically-determined neural mechanisms may underlie anxiety, emotionality and neuropathic pain in mice.

Genomic imprinting and audiogenic seizures in mice.

Audiogenic seizure (AGS) susceptibility in mice is a multifactorial behavioral disorder that involves severe generalized convulsions in response to loud, high-frequency sound. The inheritance of AGS susceptibility was examined in crosses between AGS-susceptible DBA/2J (D2) mice and epilepsy-prone (EP) mice. The EP mice were selected for high AGS susceptibility in a BALB/c-derived line. The AGS phenotype was similar in the EP and D2 mice at 30 days of age. The frequency of generalized clonic-tonic AGS was high in both the D2 and the EP mice (53 and 83%, respectively) but was low in the reciprocal EPD2F1 and D2EPF1 hybrids (14 and 19%, respectively). In the backcross to the EP parent, no significant associations were found between AGS susceptibility and microsatellite markers linked to Asp1 or Asp2, AGS genes located on Chromosomes 12 and 4, respectively. Significant associations were found for markers linked to Asp3, which is located in the proximal region of Chromosome 7. The influence of Asp3 on AGS susceptibility was seen in the EP x EPD2F1 backcross but not in the reciprocal EPD2F1 x EP backcross, suggesting that Asp3 expression is influenced by genomic imprinting. A model is proposed where genomic imprinting represses the maternal Asp3 allele, providing an influence largely from the paternal allele.

Role of norepinephrine in suppressed IgG production in epilepsy-prone mice.

The responses of two substrains of Balb/c mice (Epilepsy Prone and Epilepsy Resistant) to immunization with sheep red blood cells (SRBC) were examined to determine whether chronic neurochemical differences between the two strains could influence B cell function. Anti-SRBC IgG production in the Epilepsy Prone (EP) strain was reduced relative to the Epilepsy Resistant (ER) strain, while anti-SRBC IgM production was unaffected. No differences were found in in vitro antibody (Ab) production or T lymphocyte function between the EP and ER strains, suggesting that in vivo conditions rather than an intrinsic cellular defect are responsible for reduced IgG production by EP mice. Basal splenic norepinephrine (NE) levels were significantly higher in EP mice than those in ER mice, and remained significantly higher following immunization. ER mice treated with the beta 2 adrenergic agonist terbutaline on days 4, 5 and 6 after immunization produced significantly lower numbers of IgG PFC than did saline treated controls. Addition of NE during later stages of in vitro immunization suppressed both anti-SRBC IgM and IgG production by splenic lymphocytes from Balb/c mice, and NE was found to decrease IFN gamma production. These observations suggest that dysregulation of splenic NE can have an impact on the immune response.

An inbred epilepsy-prone substrain of BALB/c mice shows absence of the corpus callosum, an abnormal projection to the basal forebrain, and bilateral projections to the thalamus.

BALB/c mice lack a corpus callosum in about 11% of the population. Two inbred substrains of BALB/c mice, epilepsy-prone (EP) and epilepsy-resistant (ER), have been examined to determine whether these substrains differ in regard to corpus callosum morphology. Further, this study addressed the issue of whether misrouted cortical axons form an aberrant pathway instead of the corpus callosum. Initial studies that examined fresh brain tissue of adult animals revealed normal corpora callosa in all ER mice but deficient or absent corpora callosa in all EP mice. Subsequently, Dil crystals were placed in the motor cortices of aldehyde-fixed brains of 2-week-old animals to investigate cortical projections in both inbred substrains of mice. Fluorescent microscopy revealed that all of the ER animals had normal corpora callosa, whereas all EP animals exhibited either reduced corpora callosa (partially callosal) or an absence (acallosal) of this structure. Both acallosal and partially callosal EP mice displayed an extensive, aberrant projection to the basal forebrain as well as bilateral projections to midline and intralaminar thalamic nuclei. The fibers projecting to the basal forebrain arose from the cortex, coursed toward the midline before turning ventrally along the midline, and appeared to terminate in the medial septal nucleus and the nucleus of the diagonal band. ER animals lacked this aberrant cortical projection to the basal forebrain. Electron microscopic results obtained from EP mice indicated that labeled axons in this aberrant pathway formed axosomatic, axodendritic, and axospinous synapses with the neurons in the medial septal/diagonal band complex. The function of the aberrant projection to the basal forebrain remains unknown but it may provide an abnormal excitatory input to a region that provides cholinergic and GABAergic input to the cerebral cortex and hippocampus. The additional projections to midline and contralateral intralaminar thalamic nuclei in EP mice may function to intensify the synchronization of bilateral discharges.

Effect of sustained pyridoxine treatment on seizure susceptibility and regional brain amino acid levels in genetically epilepsy-prone BALB/c mice.

Epilepsy-prone and epilepsy-resistant substrains were selectively bred from a strain of BALB/c mice; audiogenic-sensitive epilepsy-prone animals showed enhanced sensitivity to chemical convulsants. Treatment with pyridoxine (100 mg/L in drinking water) initiated at mating and continued throughout pregnancy and the life of the offspring abolished the enhanced sensitivity to chemical convulsants and reduced the severity of audiogenic seizures. Withdrawal of pyridoxine restored the enhanced seizure sensitivity. [1H] Nuclear magnetic resonance (NMR) spectroscopy of perchloric acid extracts of tissue was used to determine the concentrations of several compounds [N-acetylaspartate (NAA), GABA, glutamate, aspartate, alanine, taurine, creatine, cholines, inositol] in the hippocampus, neocortex, brainstem, and cerebellum of untreated and pyridoxine-treated 6-week-old female animals. The ratios of the concentrations of excitatory to inhibitory putative neurotransmitter amino acids tended to be higher in epilepsy-prone animals, with the most pronounced difference being a significantly elevated glutamate/GABA ratio in every brain region examined. Pyridoxine treatment abolished this imbalance in the hippocampus, brainstem, and cerebellum, but not in the neocortex. Treatment of epilepsy-resistant animals with pyridoxine using the same protocol decreased the glutamate/GABA concentration ratio in the hippocampus, brainstem, and neocortex and resulted in impaired development of the animals. The amino acid imbalance and the accompanying seizure susceptibility in these genetically epilepsy prone mice may originate from an inborn error in pyridoxine metabolism or in a pyridoxine-dependent enzyme system.

Genetically determined predisposition to convulsions as the result of a generalized defect in the metabolism of catecholamines in the central nervous system.

The author compared the functional properties of the striatal system in KM rats sensitive to the convulsive effects of sound with those in Wistar rats, which are insensitive to these effects. It was shown that bulbocapnine (an antagonist of dopamine) administered to the Wistar rats at a dose of 40 mg/kg body weight caused catalepsy, depressed the motor cortex excitability, and raised the threshold of the generalized Jacksonian-type convulsions. The KM rats showed neither catalepsy nor a rise in the generalized convulsion threshold, and the depression of the motor cortex excitability in them was only slight. Examinations of the apomorphine-induced stereotypy (dose 1.0-10 mg/kg) showed that in the KM rats the sensitivity of the receptors to dopamine was changed. The hyperproduction of catecholamines in the striatum, the hypothalamus, and adrenals in the KM rats suggests that the predisposition to epileptiform states correlates with the generalized defect in the metabolism of catecholamines. It is suggested that the hypersensitivity of KM rats to epileptogenic effects is due to a deficiency (caused by an excess of dopamine) in the depressing function of the striatum.

[Modeling different regimes of bioelectrical activity in the brain in normal subjects and in "increased readiness" in a network of neuron-like elements]. / Modelirovanie razlichnykh rezhimov bioélektricheskoi aktivnosti mozga v norme i pri povyshennoi "sudorozhnoi gotovnosti" na seti iz neironopodobnykh élementov.

Desynchronous (low voltage fast activity), synchronous (high voltage slow waves) as well as convulsive brain activities were stimulated by a computer model of neuronal population. Network excitatory and inhibitory elements possessed fundamental dynamic properties of real neurones. Being independent both of the excitability of elements and of external influence efficacy, synchronous (desynchronous) network activity resulted from the increase (decrease) of the average power of "neuronal" interconnections which imitated mutual and recurrent excitation and inhibition. The inhibition efficacy being reduced as compared with excitation, synchronization of elements became intensified. As a consequence, the rhythmic activity amplitude increased and the appearance of self-sustained oscillations simulating convulsive activity was facilitated. The probable mechanism of EEG activation by virtue of the reduction of mutual and recurrent excitation and inhibition efficacy as well as the significance of inhibitory mechanism deficiency for epileptogenesis are discussed.

[Catecholamine levels in the striatum, hypothalamus, and adrenals of rats with genetic predisposition to epileptic seizures]. / Soderzhanie katekholaminov v striatume, gipotalamyse i nadpochechnikakh krys, geneticheski predraspolozhennykh k sudorozhnym pripadkam.

The content of catecholamines (CA) was studied in the basal ganglia, hypothalamus and adrenals of Krushinsky-Molodkina (KM) rats exhibiting the increased sensitivity to convulsants, and of non-audiogenic Wistar rats. It was found that in all the structures under test the content of CA was considerably higher in KM than in Wistar rats. At the same time the concentration of dopamine in the basal ganglia and hypothalamus was far greater than that of the subsequent reaction products (noradrenaline, homovanillic and dioxyphenyl acetic acids), and the concentration of dopamine in the adrenals exceeded that of noradrenaline and adrenaline. Excess dopamine in the basal ganglia seems likely to be the reason for the failure of caudate nucleus inhibitory function in KM rats, thereby contributing to the increased sensitivity of the animals to convulsants. The relationship between the sensitivity to stressors and the initial level of CA metabolism is discussed.

[Genetically determined predisposition to convulsive seizures as a result of a generalized defect in catecholamine metabolism in the central nervous system]. / Geneticheski determinirovannaia predraspolozhennost' k sudorozhnym pripadkam kak sledstvie generalizovannogo defekta metabolizma katekholaminov v tsentral'noi nervnoi sisteme.

The author compared the functional properties of the strial system in KM rats sensitive to the convulsive effects of sound and in Wistar rats which are insensitive to those effects. It was shown that bulbocapnine (an antagonist of dopamine) administered to the Wistar rats in a dose of 40 mg/kg body weight caused catalepsy, depressed the motor cortex excitability and raised the threshold of the generalized Jacksonian-type convulsions. The KM rats showed neither catalepsy, nor the rise of the generalized convulsion threshold, and the depression of the motor cortex excitability in them was but slight. Examinations of the apomorphine-induced stereotypy (dose 1.0 to 10 mg/kg) showed that in the KM rats the sensitivity of the receptors to dopamine was changed. The hyperproduction of catecholamines in the striatum, the hypothalamus, and the adrenals in the KM rats suggests that the predisposition to epileptimorph states correlates with a generalized defect in the metabolism of catecholamines. It is supposed that the hypersensitivity of the KM rats to epileptogenic effects is due to a deficit (caused by the excess of dopamine) of striatum depressing function.