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Visceral leishmaniasis is a deadly illness caused by Leishmania donovani that provokes liver and spleen inflammation and tissue destruction. In cutaneous leishmaniasis, the protein of L. major named inhibitor of serine peptidases (ISP2) inactivates neutrophil elastase (NE) present at the macrophage surface, resulting in blockade of TLR4 activation, prevention of TNF and IFN production and parasite survival. We report poor intracellular growth of L. donovani in macrophages from knock-out mice for NE (ela-/-), TLR4 or TLR2. NE and TLR4 co-localized with the parasite in the parasitophorous vacuole. Parasite load in the liver and spleen of ela-/- mice were reduced and accompanied by increased nitric oxide and decreased TGF production. Expression of ISP2 was not detected in L. donovani and a transgenic line constitutively expressing ISP2, displayed poor intracellular growth in macrophages and decreased burden in mice. Infected ela-/- macrophages displayed significantly lower IFN mRNA than background mice macrophages and the intracellular growth of was fully restored by exogenous IFN. We propose that L. donovani utilizes the host NE-TLR machinery to induce IFN necessary for parasite survival/growth during early infection. Low or absent expression of parasite ISP2 in L. donovani is necessary to preserve the activation of the NE-TLR pathway.

Breast cancer is one of the most common cancers in women, and rated the second most common cancer and a significant cause of death in females in the Sudan. This study aims to identify tumor protein that elicits humoral immune responses in breast cancer patient in comparison to tissues from healthy individuals as well as from normal tissues of the cancer patient. Serum samples and breast cancer tissue specimens were collected from breast cancer patients (n = 9) and from healthy individuals (n = 5) at Khartoum Teaching Hospital. Breast cancer tissues were homogenized in PBS, centrifuged and the supernatants were lysed in 2X SDS-PAGE sample buffer. The preparation then boiled and the resulting supernatants were subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analysis. Total proteins were separated on SDS-PAGE and transferred to the nitrocellulose paper, then analyzed by immunoblotting for total proteins and serum antibodies using serum from patients with breast cancer and from healthy individuals to enhance humoral immune responses. The SDS-PAGE analysis showed an increase in size of protein bands in the normal control tissues than from breast cancer patients. The Western blot analysis of breast cancer tissues with the serum from breast cancer patients specifically detected major bands than in the normal tissues from the healthy tissues of cancer patients or from healthy individuals. Beside the major bands, additional bands have been detected in breast cancer tissues with the serum from breast cancer patients. The reactive auto-antibodies in patient’s tissues bound to the circulating tumor antigen in patient’s serum and immune complexes would result by Western blotting indication of strong immune response to these proteins. The present study demonstrated that there was a clear decline in the expression of some proteins among breast cancer patients which has been confirmed by strong immune reactions in the Western blotting analysis. Key words: breast cancer , protein expression, SDS-PAGE, Commasie brilliant blue, Western blot.

Tuberculosis (TB) remains a major public health problem worldwide due to its high risk of person-to-person transmission, morbidity and mortality [1]. Sudan has a high burden of tuberculosis. Spoligotyping (spacer oligonucleotide typing) a rapid method for genotyping of Mycobacterium tuberculosis using the principle of reverse hybridization. The ecology of the prevalent mycobacteria strain can vary depending on country and region. The aim of this study was to determine the genotyping of Mycobacterium tuberculosis isolated from Sudan using spoligotyping SPOLDB4. A total of 75 Mycobacterium tuberculosis sputum samples were collected from pulmonary Tuberculosis patients attending references Laboratories and diagnostic centers in Khartoum and Eastern Sudan in (2011–2013). The mycobacteria were genotyped using Spoligotyping technique and data obtained were analyzed and compared to the SPOLDB4 database. Among the 75 isolate analyzed, 57(76%) were identified by SPOLDB4 and 18 (24%) could not be matched to any lineages. The most prevalent genotype cluster was MANU2 38 (50.7%) followed by CASI Delhi 8 (10.7%). In the study SIT54 was the most common pattern 37 (49.3%) followed by SIT25 6(8%).

Background In May 2009, EDCTP supported the establishment of the East African Consortium for Clinical Research (EACCR) involving 35 regional institutions and 6 northern partners to promote capacity development for collaborative multi-site clinical trials and research. EACCR aims to contribute to overcoming a situation of: under-funded, fragmented and uncoordinated regional health research; too few African scientists; inadequate infrastructure; insufficient networking and knowledge-sharing. We present updates on achievements and lessons learnt on increased preparedness to conduct globally-competitive research and clinical trials on poverty-related, neglected and emerging infectious diseases. Methods Retrospectively, we conducted a quasi-purposive summative evaluation through document review, participatory appraisal, direct observation and case studies of the EACCR work packages for governance, research, training and mentoring, infrastructure, and networking between November 2015 and February 2016. Results In the past five years, the Eastern Africa-led consensus-driven consortium has contributed to the following results (at least): 15 new research and capacity-strengthening grants; 150 peer-reviewed publications; 15 trials monitored; 531 scientists and associates mentored; 12 electronic training modules on research and bio-ethics; 2 newly ISO-accredited laboratories; 24 research sites upgraded; 20 partnerships harnessed; 2 knowledge-sharing platforms of the East African Health Research Commission; an interactive website (www. eaccr.org); and an additional 2 million euros leveraged. Conclusions EACCR has increased its capacity and partnerships for on-going and planned multisite clinical trials; we can sustain coordinated collaborative GCP-compliant multisite trials and health research. We can intensify high-level advocacy and resource mobilisation in Eastern Africa in partnership with policy makers, other consortia and development partners. We stand firm on the shoulders of current and promising giants of EACCR, other consortia, EDCTP and other like-minded partners and are thus prepared to conduct and disseminate more African-led health research and capacity-strengthening initiatives on poverty-related, neglected and emerging infectious diseases in Africa during the second programme of EDCTP.