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Optic nerve demyelination is one of the clinical features of combined central and peripheral demyelination (CCPD), an entity with heterogenous immunopathogenesis and clinical characteristics, overlapping between multiple sclerosis (MS) and chronic inflammatory demyelinating polyneuropathy (CIDP). Of interest, earlier studies among patients with CIDP prior to discovery of antibodies against paranodal protein neurofascin 155 (anti–NF 155) also reported optic nerve dysfunction. We aimed to evaluate optic nerve demyelination among anti–NF 155 CIDP patients. We studied 2 patients with anti–NF 155 CIDP using visual-evoked potentials (VEP) and optical coherence tomography (OCT). Both patients had distal acquired demyelinating symmetric (DADS) subtype CIDP. Other common features were prominent sensory ataxia, hand tremors, significantly elevated cerebral spinal fluid protein, high titre anti–NF 155 antibodies and poor response to corticosteroid and intravenous immunoglobulin (IVIg). No central nervous system neuroradiological abnormality detected. Both had normal visual acuity and colour vision, but one had subclinical right relative afferent pupillary defect (RAPD). VEP of both showed bilateral prolonged P100 latencies. OCT for patient with RAPD demonstrated moderate to severe retinal nerve fibre layer (RNFL) thinning. Identification of optic nerve demyelination among subclinical CIDP with anti–NF 155 antibodies expanded the spectrum of demyelination within the subset of CCPD.

Both HIV-1 infection and iron overload are independently associated with infection by Mycobacterium tuberculosis due to impaired macrophage function. A prospective study of in vitro assessment of macrophage function was undertaken in a group of asymptomatic HIV-1 infected remunerated (professional) blood donors with (n = 54) or without (n = 54) prevalent practice of oral iron intake (subgroups I and II respectively). The assessment was carried out at enrolment as well as at the point of development of AIDS related illness (ARI). The subgroup I showed higher levels of pro-inflammatory cytokines viz. IL-1β, IL-6 and IL-8, but lowered levels of IL-12p70 in serum as well as in supernatant of monocyte derived macrophage (MDM) cultures both at enrolment and at the point of development of ARI in the subset of cases that developed pulmonary tuberculosis (PT) on follow up compared to the subset that developed categories of ARI other than pulmonary tuberculosis (non-PT) on follow up. The subgroup II of HIV-1 positive donors did not show any such alterations at enrolment or at the point of development of PT or non-PT categories of ARI on follow up. There was significant depression of nitrite level in serum as well as that produced by MDM culture at enrolment in subgroup I regardless of category of ARI developed on follow up while in subgroup II there was significant elevation in these levels at enrolment, more among cases developing PT than those developing non-PT category of ARI. The subgroup I demonstrated increased production of superoxide at enrolment. The present study suggested that depressed production of nitrite and IL-12p70 by macrophages induced by iron overload may be responsible for greater susceptibility of HIV-1 positive donors to M. tuberculosis while superoxide may be a less powerful anti-mycobacterial tool.

Imbalance of essential trace elements viz. Zinc, Selenium, Iron, Copper and Magnesium has been reported to influence disease course in HIV-1, HBV and HCV infections by altering immune status. A study was taken up to examine plasma levels of Th1 (IFN-γ and IL-2) and Th2 (IL-4 and IL-10) categories of cytokines and immune activation markers (TNF-α, TNFR I and TNFR II) in an asymptomatic group of HIV-1, HBV and HCV infected blood donors in relation to trace elements. Plasma levels of Zn, Se and Mg were depressed in all the three groups of blood donors (P γ were depressed in all the three groups of blood donors (P γ, and in HBV infection while positive correlations were found between Mg and TNFR I and TNFR II and Se with TNFR II. HCV infection showed a positive correlation between Se and IFN-γ (P < 0.001), Mg and IL-4 (P = 0.02), Fe and IL-10 (P < 0.01). The present study reveals possible relationship between trace element level alterations and alterations in cytokine and immune activation levels in HIV-1, HBV and HCV infection.

Documentation of torture is a multidisciplinary, multistage scientific procedure evolved over the past decades through the experience of various strata in medical and related fields. It plays a key role in effective corroboration of facts, providing redress to victims and also has a long term regulatory impact on prevention of torture in a society. The UN endorsed Istanbul protocol serves as the model for effective documentation of torture in the present context and there were many attempts in the recent years to create a systematic and uniform approach among professional bodies to document torture by adopting it to the local medico-legal and legal systems in some less resourced countries. The post independent Sri Lanka is widely known in international human rights forums for the prevalence of torture and its endemicity since 1970s. The long term struggle to ensure justice to torture victims in Sri Lanka has been greatly enhanced by the submission of detailed medico-legal reports on them to relevant courts. As strengthening of medico-legal and legal reporting strategies were more focused towards the end of twentieth century the medico-legal and legal professionals in consensus attempted to use Istanbul Protocol for documentation of torture since 2004. However Sri Lankan experience on application of Istanbul protocol for documentation of torture signifies that unless and until a political commitment is shown by the government to internalize Istanbul Protocol into legal and medico-legal systems locally the expected outcome of effective documentation would not be evident.

Despite common incidence of GB virus C/Hepatitis G virus (GBV-C/HGV) and Torque Teno Virus (TTV) co-infections in subjects with Hepatitis C virus (HCV) infection, pathogenic role of these co-infections in HCV infected subjects has not been clear since studies have mostly been based on liver enzyme profile yielding variable results. Pro-inflammatory cytokines that participate in host immune response against viruses are generated as a consequence of triggering of related genes by Nuclear Factor Kappa B (NF-kB) that is a member of transcription family. Study of three pro-inflammatory cytokines e.g. interleukin 1 beta (IL-1β), Interleukin-6 (IL-6), interleukin-8 (IL-8) in a group of multi-transfused thalassemic subjects in relation to positivity for HCV, HGV and TTV infections showed elevated levels of these cytokines in serum as well as in supernatant of peripheral blood mononuclear cell (PBMCs) cultures in HCV-GBV-C/HGV co-infected subgroup compared to HCV mono-infected subgroup (p

The structure and functioning of poor families have been deeply changed by processes of globalization. The concentration of capital in core areas of the world economy, for example, has spurred massive migrations, as many poor families in the Global South are faced with the decision of sinking further into poverty together or sending a member North in search of survival wages (Sassen, 1998). In places in the Global South where migration is not a viable response to economic crisis, families find other creative ways to make do (Moser, 1993). Compounding poverty, political instability in many areas threatens family safety and health (Lentin, 1997; Davies, 1994). In all situations of marginality and vulnerability, family survival and well-being depend on creative means of survival. This survival is often gendered.

To undertake analysis of hepatitis A viral load, alanine aminotransferase (ALT), and viral genotypes with duration of viremia, and to correlate these parameters with CD4(+)/ CD8(+) lymphocyte populations that control cell-mediated immunity.Cell counts were carried out using fresh whole blood collected in EDTA vials using a fluorescence activated cell sorter. Hepatitis A virus (HAV) RNA was extracted from blood serum, reverse transcribed into cDNA and quantified by Real-Time polymerase chain reaction and was genotyped.Among 11 patients, 10 could be analyzed completely. Of these, 3 had severe acute hepatitis (s-AH) and the remainder had a self-limited acute hepatitis A (AHA), with one patient with fulminant disease (encephalopathy Grade IV) dying on the 4th d. The ALT level was significantly higher both in AHA (1070.9 +/- 894.3; P = 0.0014) and s-AH (1713.9 +/- 886.3; P = 0.001) compared to normal controls (23.6 +/- 7.2). The prothrombin time in s-AH patients (21.0 +/- 2.0; P = 0.02) was significantly higher than in AHA (14.3 +/- 1.1; P = 0.44). The CD4(+)/CD8(+) ratio in AHA patients (1.17 +/- 0.11; P = 0.22) and s-AH (0.83 +/- 0.12; P = 0.0002) were lower than seen in normal healthy controls (1.52). Self-limited cases had peak viral load at the beginning of analysis while in s-AH patients this occurred at the 15th or 30th d. In acute and severe groups, one patient each belonged to genotype IA, with the remaining 8 cases belonging to genotype IIIA. The only fulminant hepatic failure case belonged to genotype IA. HAV viral load and ALT values collected during the entire course of the self-limited infection were directly correlated but this was not the case for s-AH patients.Based on a small-scale study, the persistently higher viral load of s-AH might be due to diminished cellular immunity and hemolysis. The duration of viremia was dependent on the host, as the viral genotype had no apparent role in clinical outcome of AVH and s-AH cases.