Iron deficiency anaemia influences cognitive functions

Many diseases, different nutritional, metabolic and hormonal changes, ageing and drugs can alter cognitive functions. Anemia via cerebral hypoxia and other possible mechanisms has been suggested to have a great influence on cognition. Iron deficiency anemia, the most common form of anemia, has been suggested to result in cognitive deterioration and alteration of neurological functions. Previous studies resulted in significant discrepancies considering correlation between anemia and cognitive achievement mainly because different or not sensitive enough tests used to measure cognition. We suggest a significant influence of iron deficiency anemia on dynamic properties and functional features of the central nervous system activity. Cognitive achievement is strongly related to hemoglobin level and could be expected in all patients. Higher hemoglobin level results in better CNS function. As a first step in confirming or refuting our hypotheses we suggest standardization of the method used to measure cognition, such as a very sensitive apparatus like Complex reactiometer Drenovac (CRD).     

HIV-1 infection–induced apoptotic microparticles inhibit human DCs via CD44

Acute HIV-1 infection results in dysregulated immunity, which contributes to poor control of viral infection. DCs are key regulators of both adaptive and innate immune responses needed for controlling HIV-1, and we surmised that factors elicited during acute HIV-1 infection might impede DC function. We derived immature DCs from healthy donor peripheral blood monocytes and treated them with plasma from uninfected control donors and donors with acute HIV-1 infections. We found that the plasma from patients with HIV specifically inhibited DC function. This suppression was mediated by elevated apoptotic microparticles derived from dying cells during acute HIV-1 infection. Apoptotic microparticles bound to and inhibited DCs through the hyaluronate receptor CD44. These data suggest that targeting this CD44-mediated inhibition by apoptotic microparticles could be a novel strategy to potentiate DC activation of HIV-specific immunity.     

Frequency of loss of heterozygosity of the NF2 gene in schwannomas from Croatian patients

Aim. To identify gross deletions in the NF2 gene in a panel of schwannomas from Croatian patients in order to establish their frequencies in Croatian population. Methods. Changes of the NF2 gene were tested by polymerase chain reaction/loss of heterozygosity (LOH) using two microsatellite markers, D22S444 and D22S929. Results. The analysis with both markers demonstrated that 43.75% of schwannomas exhibited LOH of the NF2 gene. The D22S444 region exhibited 45.5% of LOHs and the D22S929 region exhibited 14.3% of LOHs. Four LOHs were found in Antoni B, 2 in Antoni A, and 1 in Antoni A and B type tumors. Conclusion. The frequency of changes observed in Croatian patients is broadly similar to that reported in other populations and thus confirms the existing hypothesis regarding the tumorigenesis of schwannomas and contributes to schwannoma genetic profile helping us to better understand its etiology and treatment.     

Prognostic value of cell-free DNA in plasma of out-of-hospital cardiac arrest survivors at ICU admission and 24 h post-admission

Cell-free DNA has been associated with outcome in several acute conditions including two reports concerning the outcomes after cardiac arrest that found association of circulating DNA quantities at admission with mortality. The origins of cell-free DNA are primarily necrosis and apoptosis, which in cardiac arrest occur during ischaemia (“no-flow” and “low-flow” period), during reperfusion injury and as a consequence of post-arrest inflammatory response. Respecting the facts that significant cellular damage may occur during the post-arrest period, and that damage might be reduced by mild therapeutic hypothermia, we investigated the prognostic value of cell free DNA at ICU admission and 24 h after admission.     

Protective effect of urapidil on testicular torsion–detorsion injury in rats

Purpose

The aim of this study was to investigate the effect of urapidil and low-molecular weight heparin (LMWH) on testicular torsion–detorsion injury in rats.

Methods

Thirty-two male Sprague–Dawley rats were used. In the torsion–detorsion (T/D) group, the left testis was twisted at 720° for 3 h. After 3 h of reperfusion, the testis was removed. Urapidil or LMWH was administered intraperitoneally 30 min before detorsion in the treatment groups.

Results

Unilateral testicular torsion–detorsion caused significant increases in the malondialdehyde level and apoptosis and significant decreases in the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in ipsilateral testes (p < 0.001). The rats treated with urapidil had a significant decrease in the malondialdehyde level and apoptosis and significant increases in the SOD and GPx activities in ipsilateral testes compared to the T/D group (p < 0.001). Animals treated with LMWH showed non-significant reductions in malondialdehyde levels and apoptosis compared to the T/D group. In addition, no significant difference in the SOD activities (p = 0.52) between the groups was found. The increase in the GPx activities was significant in the LMWH group compared to the T/D group (p < 0.001).

Conclusion

The administration of urapidil before detorsion prevents ischemia/reperfusion cellular damage in testicular tissue. LMWH was not found to have a beneficial effect on testicular T/D injury in rats.

     

Changes in short-term memory processes in patients with multiple sclerosis

In this study we compared the performance of 39 multiple sclerosis (MS) patients with 28 age-, sex- and education-matched controls on both the Mini-Mental State Examination, a global cognitive assessment tool, and the Sternberg Short-Term memory scanning task, a standardized test of short-term memory (STM) processes. While the STM span of our MS patients did not differ from that of our controls, STM scanning time of the MS group was reliably slower than that of the controls and a significant correlation was observed between STM scanning time and duration but not severity of illness. Our results suggest that processing stages other than the manipulation of data within the STM buffer are also affected by MS.