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Electroconvulsive therapy (ECT) remains the most acutely effective treatment for severe, often life-threatening episodes of depression [23, 24]. However, its mechanism of action remains unclear . To our knowledge, no study has yet examined telomerase activity in patients with depression undergoing treatment with ECT. Thus, here we examined telomerase activity in PBMCs collected from depressed patients pre- and post-treatment with ECT and from healthy controls at two time-points to approximate a course of ECT. We hypothesized that (1) telomerase activity would be lower in patients with depression compared to healthy controls and (2) telomerase activity would normalize in response to treatment with a course of ECT. We also explored whether there was any relationship between telomerase activity and depression severity or exposure to recent or early life adversity.
Correlations between telomerase activity and HAM-D24 scores in patients with depression. a Correlation between baseline telomerase activity and baseline HAM-D24 score. b Correlation between baseline telomerase activity and the change in HAM-D24 score post ECT. c Correlation between the change in telomerase activity and the change in HAM-D24 score post ECT. d Correlation between baseline telomerase activity and the duration of the current depressive episode in days. HAM-D24, 24-item Hamilton Rating Scale for Depression.
We found no difference in telomerase activity between medicated patients with depression compared to healthy controls, either at baseline/pre-ECT or follow-up/post-ECT. There was no association between telomerase activity and HAM-D24 score or the duration of the current depressive episode in the patient cohort. Our exploratory subgroup analyses found that telomerase activity did not differ between ECT responders and non-responders or remitters and non-remitters. With regard to the association between telomerase activity and exposure to trauma, we found a non-significant difference in telomerase activity in patients who had experienced adverse events during childhood compared to those who had not, though this did not survive adjustment for potential confounders. This trend was not evident in the control group, despite a similar percentage of people in each group having experienced adversity during childhood. While controls who had experienced recent traumatic events had significantly lower telomerase activity compared to those who had not in our unadjusted analysis, this did not survive adjustment for potential confounders.
Malaria parasitaemia and malaria morbidity rates in a cohort of children over a 1 year period. Asymptomatic cases were only detected every 3 months while malaria episodes were detected throughout the year
Although the aetiology of anaemia is complex and multi-factorial, parasitic diseases, including P. falciparum and helminth infections, have long been recognized as major contributors to anaemia in endemic countries. A very high prevalence of anaemia was recorded at baseline (71.5 %) in contrast to the lower prevalences of 30.8, 11.9 and 10.9 % reported by Nkuo-Akenji et al. , Achidi et al.  and Alemu et al. , respectively, but similar to the prevalence reported by Makoge et al. . Children below the age of 5 years were more susceptible to anaemia in accordance with facts that this age group is most vulnerable to malaria and its consequences. Malarial anaemia is more typically associated with the acute clinical state, but there is evidence to suggest that asymptomatic parasitaemia may contribute substantially to anaemia in endemic regions . A greater proportion of participants who were malaria parasitaemia positive were anaemic throughout the study although only a small proportion of the children who were anaemic were actually malaria parasitaemia positive. This implies that despite the fact that malaria parasitaemia was an important cause of anaemia there were obviously other significant contributing factors. Nevertheless, malaria parasitaemia was the major contributor of anaemia as haemoglobin levels of children who experienced malaria episodes were lower compared to those with asymptomatic parasitaemia and those who were malaria parasitaemia negative. In addition, children with malaria episodes as well as those with asymptomatic parasitaemia were associated with susceptibility to anaemia compared to children who were malaria parasitaemia negative.
No significant association of susceptibility to malaria during the study was observed between children positive or negative for helminths. Previous association of helminth infection with an increased risk for malaria incidence has been confirmed in two other studies. The first study reported a positive association between intestinal helminths and infection with P. falciparum in adults in Thailand, whereas the second study on mothers and children in Zaire described a positive association between infection with Ascaris and the occurrence of P. falciparum as reviewed by Hartgers and Yazdanbakhsh, . However, though children positive for helminths seemed to be exposed to the same number of malaria episodes as children who were negative for helminthes, results from a cohort of people on the Thai-Myanmar border have shown that helminth-infected patients had a twofold increase of falciparum malaria incidence (fever + malaria parasites on the blood smear) . In a review, Nacher  reports increased gametocyte carriage in a human study and increased malaria transmission in an animal model of helminth-malaria co-infection. In the absence of disease, patients co-infected with worms and malaria may represent a hub of malaria transmission . A recent meta-analysis of mouse co-infection studies suggests that depending on the existing immune interaction between a given host and malaria parasites, addition of a helminth co-infection may have contrasting effects on malarial disease: co-infection increased mortality and peak parasitaemia in ordinarily resolving Plasmodium infections, but had a far less effect on lethal Plasmodium infections and even tended to delay death in cerebral malaria models .
The global market shock includes a standardized set of risk factor shocks to financial market variables that apply to all banks with significant trading activity. Depending on the type of financial market vulnerability that the global market shock is intended to assess, the market shocks could be based on a single historical episode, multiple historical periods, hypothetical events that are based on salient risks, or a hybrid approach comprising some combination of historical episodes and hypothetical events. A market shock based on hypothetical events may result in changes in risk factors that were not previously observed.11 2b1af7f3a8