Multiple Causes for Delay in Arrival at Hospital in Acute Stroke Patients in Aydin, Turkey

This descriptive, hospital-based study, performed in western Turkey, was designed to assess the level of pre-hospital delay and reasons for such delay in acute stroke patients, taking into consideration certain factors such as socioeconomic status, availability of transport options at onset of symptoms. Data were collected from hospital records, and a questionnaire was administered that included questions about socio-demographics, self-reported risk factors and questions related to hospital arrival. The rate of patients arriving at the hospital more than 3 hours after symptom onset was found to be 31.6% for this study. Approximately 1/3 of patients delayed going to the hospital because they were waiting for symptoms to go away while 1/3 of patients were not aware of the importance of seeking immediate medical help. There was a significant relationship between the use of ambulance transportation and length of time before arrival at the hospitals, though there was no statistically significantly relationship between the existence of stroke risk factors and hospital arrival delay. These results will likely be helpful to health care decision makers as they develop a model for stroke health care and community based training

Balancing repair and tolerance of DNA damage caused by alkylating agents

Alkylating agents constitute a major class of frontline chemotherapeutic drugs that inflict cytotoxic DNA damage as their main mode of action, in addition to collateral mutagenic damage. Numerous cellular pathways, including direct DNA damage reversal, base excision repair (BER) and mismatch repair (MMR), respond to alkylation damage to defend against alkylation-induced cell death or mutation. However, maintaining a proper balance of activity both within and between these pathways is crucial for a favourable response of an organism to alkylating agents. Furthermore, the response of an individual to alkylating agents can vary considerably from tissue to tissue and from person to person, pointing to genetic and epigenetic mechanisms that modulate alkylating agent toxicity

Syndrome of Inappropriate Secretion of Antidiuretic Hormone Associated with Localized Herpes Zoster Ophthalmicus

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with localized herpes zoster is rarely reported and may be under-appreciated. We describe two diabetic men with herpes zoster ophthalmicus (HZO) who developed hyponatremia (114 and 116 mmol/L) during acute illness. Both were euvolemic and had elevated urine osmolality (435 and 368 mmol/kg.H2O) and sodium (Na+) concentration (61 and 63 mmol/L) along with normal cardiac, renal, liver, and endocrine function consistent with the diagnosis of SIADH. Thorough investigation for other causes of SIADH, including detailed physical examination, laboratory studies, and computed tomography of the brain, chest, and abdomen, were negative. Despite antiviral therapy (acyclovir) for herpes zoster, ophthalmoplegia, keratitis, and post-herpetic neuralgia (PHN) developed. Even with fluid restriction and high salt diet, SIADH lasted for 3 to 4 months and resolved concomitantly with resolution of PHN, suggesting an association between SIADH and HZO. These two cases raise the potential for herpes zoster infection, especially HZO, to involve the regulatory pathway of ADH secretion, contributing to SIADH. The presence of PHN, which reflects greater neural damage may, at least in part, explain the prolonged ADH secretion and hyponatremia