Tehran University Medical Journal

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Background: Hypomagnesemia is commonly encountered in patients with a wide variety of diseases including subarachnoid hemorrhage (SAH), cardiovascular emergencies, head trauma, migraine attacks, seizure and preeclampsia. It seems to be associated with a poor clinical outcome. This study considers the prevalence and temporal distribution of hypomagnesemia after aneurysmal SAH and its correlation with the severity of SAH, delayed cerebral ischemia (DCI) as well as the neurological outcome after a period of three months.

Methods: Between 2003 and 2008, 60 patients were admitted to the emergency ward of Imam Khomeini Hospital with acute SAH. Serum magnesium levels were measured during the first 72 hours, days 4-7, and second and third weeks after SAH. The three-month outcome was assessed according to the Glasgow Outcome Scale (GOS). Clinical SAH grading was performed according to the criteria of the World Federation of Neurological Surgeons (WFNS) and the patients were allocated to "Good" (GOS = 4, 5) and "Poor" (GOS= 1-3) outcome groups. The prevalence of hypomagnesemia was assessed in both patient groups. Fisher exact test was used to analyze data.

Results: Hypomagnesemia occurred in 22% of patients during the first 72 hours after SAH. It was associated with more prevalent DCI (p<0.05), whereas low serum magnesium levels during days 4-7 17% of patients) and the second week (22% of patients) after SAH were correlated with poor clinical outcome (p<0.05). No correlation was found between first 72 hour-hypomagnesemia and poor clinical outcome at three months.

Conclusion: Hypomagnesemia occurs after aneurysmal SAH and it may predict the occurrence of DCI, while low serum magnesium levels during days 4-7 and within the second week of event predict poor clinical outcome at three months. Treatment of this electrolyte disturbance may have a favourable effect on the clinical outcome of patients with aneurysmal SAH.

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Background: Numerous evidences indicate that various environmental stresses during pregnancy affect physiological behavior of the offspring. This experimental study was designed to investigate the effect of noise stress during prenatal period of rats on spatial learning and memory and plasma corticostrone level in postnatal life.
Methods: Three groups of pregnant rats were given daily noise stress with durations of two and/ or four hours in last week of pregnancy period. The fourth group was left unstressed. The male offspring from the unstressed and different stressed groups were assigned as controls and stressed groups. The animals were introduced to a spatial task in Morris water maze 4 trials/day for five consecutive days. The probe test was performed on the 5^th day of the experiment. The delay in findings and the distance passed to locate the target platform were assessed as the spatial learning.
Results: Our results showed that prenatal exposure to noise stress for two and/ or four hours a day, leads to impaired acquisition of spatial learning in the postnatal animals. The plasma level of corticostrone in the two stressed groups of rats markedly matched with their behavioral function. Prenatal exposure to 1- hour noise stress revealed no effects on the offsprings' behavior and plasma corticostrone level.
Conclusion: Based on our study results, it seems that applied range of stress which is executed through the noise stress could increase the plasma corticostrone level and could decrease spatial learning and memory of adult male offspring.

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Thymoglobulin is a purified polyclonal immunoglobulin that has been used widely over the last decades in the prevention and treatment of rejection following renal transplantation. This immunoglobulin works against human thymocytes. Since thymoglobulin does not contain the nephrotoxic properties therefore it can be used in induction therapy especially in patients with higher risk of graft rejection such as patients who receive graft from cadavers. Recent research showed also its beneficial role in cross-match-positive transplantation, a role that is mediated through conjunction with inhibitors of terminal complement activation. This immunoglobulin has also been used for treatment of rejection following renal transplantation. Thymoglobulin can have various effects on various Immune system cells including T cells, B cells and also plasma cells. Thymoglobulin also affects the Tcell surface antigens, natural killer-cell antigens, B cell antigens, plasma cell antigens, adhesion molecules and chemokine receptors. Diverse effects of thymoglobulin on the immune system includes: T cell depletion, induce apoptosis in B cell lineage and interference with dendritic cell functional properties. Thymoglobulin can cause acute complications, delayed complications as well as infectious complications. Acute reaction events includes: anaphylaxis, fever, chills, dyspnea, nausea, vomiting and diarrhea. Thymoglobulin also induces cytokine release syndrome manifested by high grade fevers and chills and treated by steroid therapy. Delayed reactions events usually present as serum sickness and infections. Infectious complications are more important and include cytomegalovirus (CMV) infection, sepsis, candidiasis, herpes simplex and urinary infections. Thymoglobulin can also induce cytokine release syndrome. It has been thought that thymoglobulin increases the risk of post-transplant lymphoproliferative disorder (PTLD), however, debate still exists whether such an association is present when lower dosing regimens are used. In this review, we aimed to present first a brief history of thymoglobulin development and its mechanism of action and then assess the most recent published data regarding the role of thymoglobulin in following issues: immunological tolerance, ischemia-reperfusion injury, delayed graft function, prevention and treatment of acute allograft rejection, live donor transplantation, graft and patient survival and posttrans-plant lymphoproliferative disorder. This review can help specialist in transplant domain to appropriately used thymoglobulin in transplant patients.