Responses to prolonged low-temperature treatment of imbibed seeds (vernalization) were examined in barley (Hordeum vulgare). These occurred in two phases: the perception of prolonged cold, which occurred gradually at low temperatures, and the acceleration of reproductive development, which occurred after vernalization. Expression of the VERNALIZATION1 gene (HvVRN1) increased gradually in germinating seedlings during vernalization, both at the shoot apex and in the developing leaves. This occurred in darkness, independently of VERNALIZATION2 (HvVRN2), consistent with the hypothesis that expression of HvVRN1 is induced by prolonged cold independently of daylength flowering-response pathways. After vernalization, expression of HvVRN1 was maintained in the shoot apex and leaves. This was associated with accelerated inflorescence initiation and with down-regulation of HvVRN2 in the leaves. The largest determinant of HvVRN1 expression levels in vernalized plants was the length of seed vernalization treatment. Daylength did not influence HvVRN1 expression levels in shoot apices and typically did not affect expression in leaves. In the leaves of plants that had experienced a saturating seed vernalization treatment, expression of HvVRN1 was higher in long days, however. HvFT1 was expressed in the leaves of these plants in long days, which might account for the elevated HvVRN1 expression. Long-day up-regulation of HvVRN1 was not required for inflorescence initiation, but might accelerate subsequent stages of inflorescence development. Similar responses to seed vernalization were also observed in wheat (Triticum aestivum). These data support the hypothesis that VRN1 is induced by cold during winter to promote spring flowering in vernalization-responsive cereals.

Drugs and chemicals are almost easily available in Iran. Natural toxins as poisonous plants and animals also exist in most parts of the country. Therefore, acute poisonings, either intentional or accidental and also drug abuse/addiction are common in Iran. In spite of these difficulties there is no center for poison control and surveillance in this country to gather information and analyse data. The files of a systematic randomised ten percent of all hospital-referred poisoned patients from 21 March 1993 to 20 March 2000 in Imam Reza (p) University Hospital of Mashhad (71589 cases) were screened retrospectively. Young adults (40.3%) and school children (22.9%) were the most vulnerable group. Mean age was 22.3 (S.D. 14.38) years with a minimum of less than one and a maximum of 98 years old. A female predominance was found (53.4%). Intentional poisoning was more common (54.4%) than accidental exposures (45.2%). Fourteen cases were classified as criminal poisoning. 79.7% of exposures were via ingestion, followed by dermal exposures (14.1%), and inhalation (6.2%). The majority (83.7%) of patients were from urban areas. Most patients (68.6%) were treated in the Emergency Toxicology Clinic and discharged, 19.2% were temporarily hospitalized and 11.3% were hospitalized for 24 hr. Main groups of poisons were pharmaceuticals (61.4%), chemicals (22.8%), and natural toxins (16.6%). The overall number of poisoned patients was higher in spring and summer (62.8%). In conclusion, acute poisonings, particularly self-poisonings, are common in Iran. Since medical documentation is not routinely provided in this country the results of this retrospective study can be used for surveillance. Establishment of fluent data gathering and analysis within the local health system are challenges for the future.

This study examines the relation between seizure and plasma tramadol concentration in patients with tramadol poisoning, as a novel centrally acting analgesic used for the treatment of mild to severe pain. All patients admitted with a history of tramadol overdose accompanied by unconsciousness or seizures referred to

INTRODUCTION. Thorough prognostic and metabolic studies of methanol poisonings are scarce. Our aims were to evaluate the factors associated with sequelae and death from methanol poisoning, to develop a simple risk-assessment chart to evaluate factors associated with sequelae and death from methanol poisoning, and to compare the antidotes ethanol and fomepizole. PATIENTS AND METHODS. We present a retrospective observational case series of methanol-poisoned patients from Norway (1979 and 2002-2005), Estonia (2001) and Tunisia (2003/2004), and patients from two different centers in Iran (Teheran 2004-2009 and Mashhad 2009-2010) who were identified by a positive serum methanol and had a blood acid-base status drawn on admission. The patients were divided into different groups according to their outcome: Survived, survived with sequelae, and died. RESULTS. A total of 320 patients were identified and 117 were excluded. Of the remaining 203 patients, 48 died, and 34 were discharged with neurological sequelae. A pH < 7.00 was found to be the strongest risk factor for poor outcome, along with coma (Glasgow Coma Scale (GCS) < 8) and a pCO(2) ≥ 3.1 kPa in spite of a pH < 7.00. More patients died despite hyperventilation (low pCO(2)) in the ethanol group. CONCLUSIONS. Low pH (pH < 7.00), coma (GCS < 8), and inadequate hyperventilation (pCO(2) ≥ 3.1 kPa in spite of a pH < 7.00) on admission were the strongest predictors of poor outcome after methanol poisoning. A simple flow-chart may help identify the patients associated with a poor outcome.

In tramadol overdose, mydriasis or tachycardia appears to indicate a higher risk for seizure. Management may need to be focused on both mu-opioid agonism and potential mild serotonin syndrome.

Background Chemical exposures have been associated with a variety of health effects; however, little is known about the global disease burden from foodborne chemicals. Food can be a major pathway for the general population’s exposure to chemicals, and for some chemicals, it accounts for almost 100% of exposure.  Methods and Findings Groups of foodborne chemicals, both natural and anthropogenic, were evaluated for their ability to contribute to the burden of disease.  The results of the analyses on four chemicals are presented here - cyanide in cassava, peanut allergen, aflatoxin, and dioxin.  Systematic reviews of the literature were conducted to develop age- and sex-specific disease incidence and mortality estimates due to these chemicals.  From these estimates, the numbers of cases, deaths and disability adjusted life years (DALYs) were calculated.  For these four chemicals combined, the total number of illnesses, deaths, and DALYs in 2010 is estimated to be 339,000 (95% uncertainty interval [UI]: 186,000-1,239,000); 20,000 (95% UI: 8,000-52,000); and 1,012,000 (95% UI: 562,000-2,822,000), respectively.  Both cyanide in cassava and aflatoxin are associated with diseases with high case-fatality ratios.  Virtually all human exposure to these four chemicals is through the food supply.  Conclusion Chemicals in the food supply, as evidenced by the results for only four chemicals, can have a significant impact on the global burden of disease. The case-fatality rates for these four chemicals range from low (e.g., peanut allergen) to extremely high (aflatoxin and liver cancer).  The effects associated with these four chemicals are neurologic (cyanide in cassava), cancer (aflatoxin), allergic response (peanut allergen), endocrine (dioxin), and reproductive (dioxin).

Worldwide, lung cancer is the most common form of cancer. Saffron has been used in folk medicine for centuries. We investigated the potential of saffron to induce cytotoxic and apoptotic effects in lung cancer cells (A549). We also examined the caspase-dependent pathways activation of saffron-induced apoptosis against the A549 cells. A549 cells were incubated with different concentrations of saffron extract; then cell morphological changes, cell viability, and apoptosis were determined by the normal invertmicroscope, MTT assay, Annexin V and propidium iodide, and flow cytometric analysis, respectively. Activated caspases were detected by treatment of saffron in lung cancer cells using fluorescein-labeled inhibitors of polycaspases. The proliferation of the A549 cells were decreased after treatment with saffron in a dose- and time-dependent manner. The percentage of apoptotic cells increased with saffron concentrations. Saffron induced morphological changes, decreased percentage of viable cells, and induced apoptosis. Saffron could induce apoptosis in the A549 cells and activate caspase pathways. The levels of caspases involved in saffron-induced apoptosis in the A549 cells indicating caspase-dependent pathway were induced by saffron. The anticancer activity of the aqueous extract of saffron could be attributed partly to its inhibition of the cell proliferation and induction of apoptosis in cancer cells through caspase-dependent pathways activation.

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