Spleen-derived immune cells are considered to play central role in the progression of ischemic brain damage contributing to both the local and systemic inflammatory response initiated by an ischemic insult in the brain tissue. Brain-spleen communication in acute ischemic brain injury has been studied especially in rodent models of stroke, which mimic the acute focal brain ischemia in humans. Rodent spleens decrease in size after experimentally induced stroke, due mainly by the release of spleen`s immune-cells into the circulation. Splenectomy prior to middle cerebral artery occlusion is protective to the ischemic brain resulting in decreased infarct volume and reduced neuroinflammation. Various therapeutic strategies in clinical use aiming to protect the neural tissue after stroke were found to involve the modulation of splenic activity, altogether indicating that the spleen might be a potential target for therapy in ischemic brain injury. Importantly, the most clinical studies demonstrated that the splenic response in stroke patients is similar to the changes seen in rodent models. Thus, despite the limitations to extrapolate the results of animal experiments to humans, rodent models of stroke represent an important tool for the study and understanding of brain-spleen communication in the pathogenesis of acute brain ischemia.
Introduction: Acute upper extremity ischemia is an uncommon vascular emergency due to a relatively rich collateral network and low workload of the upper limb. Its consequences depend on the site and etiology of the arterial occlusion.
Case presentation: Aiming to emphasize the emerging role of Doppler ultrasound in the diagnosis of acute upper limb ischemia, we report the case of a 70-year-old female, with severe left arm resting pain and digital cyanosis. Due to the patient’s age and the presence of cardiovascular risk factors, cardioembolic or thrombotic arterial occlusion would have been the most likely diagnosis in this case, but the color Doppler ultrasound revealed severe left axillary arterial stenosis with hypoechoic wall swelling, being highly suggestive for arteritis. Temporal artery biopsy was performed, which confirmed giant cell arteritis. An excellent clinical response was obtained after initiation of treatment.
Conclusion: In acute upper limb ischemia, color duplex ultrasound provides quick information about the etiology and localization of arterial lesions, offering characteristic findings in case of large-vessel giant cell arteritis.
Andreea Oltean, Mihaela Ioana Chincesan, Oana Marginean and Emoke Horvath
Myelodysplastic syndromes are a heterogeneous group of clonal disorders characterized by peripheral blood cytopenia and normal or hypercellular bone marrow with dysplasia in more than one blood cell lineage, unfavorable prognosis, and lack of response to treatment. We present the case of a 12-year-old male patient who was referred to the Hematology and Oncology Department of Pediatric Clinic I Târgu- Mures in May 2016, with splenomegaly and pancytopenia. The osteomedullary biopsy revealed myelofibrosis, discrete dysplasia of the myeloid series and megakaryocytes, blasts CD34+ approximately 10%, which led to the diagnosis of myelodysplastic syndrome with myelofibrosis. The myeloid precursors indicated a high risk of transformation into acute myeloid leukemia, so chemotherapy associated with corticosteroids was started, leading to slight improvements. Although myelodysplastic syndrome associated with myelofibrosis is rare at this age, despite the treatment and favorable progression in the case presented, in the absence of hematopoietic stem cell transplantation the prognosis remains unfavorable.
L Dénes, Zsuzsanna Pap, I Fehér, Horváth Emőke, T Mezei, Zsuzsanna Bődi, Klara Brînzaniuc and Z Pávai
The aim of the present study is to establish possible associations between Aquaporin-1, Cyclooxygenase-2 and Apoptosis Protease-Activating Factor-1 expression in breast cancers and pathological and immunohistochemical characteristics of the examined tumors.
For the purpose of this study we used paraffin embedded archived tumor material of 31 breast cancer patients from the Pathology Department of the Odorheiu Secuiesc Municipal Hospital. We performed immunohistochemistry reactions ER, PR, HER2, AQP1, COX2 and APAF1, and following independent evaluation by two pathologists the obtained data was statistically analyzed. The tumors were divided into three groups based on their histological properties, and correlations were made with the examined markers.
AQP1, COX2 and APAF1 immunostaining results produced significant correlations with HER2 status and histological groups. There were no statistical correlations between ER or PR status and the three examined markers.
Lobular carcinomas showed AQP1 and COX2 overexpression, and loss of APAF1 expression, which all correlated with HER2 negative status.
We concluded that AQP1 could be a useful marker for detecting more aggressive subtypes and also for evaluating tumor angiogenesis. COX2 and APAF1 immunoexpression, although somewhat specific to certain histological groups, needs to be further characterized in order to be a useful marker for the clinical setting.
Emőke Horváth, Adina Huțanu, Alex Orădan, Liviu Chiriac, Daniela Lucia Muntean, Előd-Ernő Nagy and Minodora Dobreanu
Introduction: Experimental acute cerebral ischemia quickly triggers circulating inflammatory cells, provoking infiltration of neutrophils and macrophages in the damaged brain region. N-3 polyunsaturated fatty acids alleviate the ischemic deterioration, however, their potential effect on bone marrow cell mobilization is less known.
Materials and methods: healthy male Wistar rats were submitted to intraperitoneal saline injection (n=10, sham Group), transient middle cerebral artery occlusion (tMCAO) and saline injection (n=10, placebo Group), tMCAO and highly purified fish-oil administration (n=10, T Group). At the two latter groups, twenty-four hours after tMCAO, MRI scans were performed to identify the ischemic regions; the eligible animals were sacrificed, the left parietal bones being removed and subjected to qualitative and quantitative histological and immunohistochemical analysis.
Results: The active hematopoietic surface was maximal at the T-Group, being significantly lower in the P- and S-Groups (p=0.006 and p= 0.017). The MPO positive surface increased significantly in the T-compared to the S-Group (22.57± 0.86 % vs. 18.87± 0.68%, p= 0.004). Arg1 expression was significantly higher (p=0.001), while iNOS expression was lower (p=0.004) in the T- than in the P-Group, but similar to the S-group. The Arg1/iNOS2 ratio was higher in the FO-treated than in the P-group (p<0.001).
Conclusion: the ischemic conditions triggered granulopoiesis and the increase of iNOS2 positive, type M1 macrophage in the rat bone marrow. Fish-oil treatment generated the expansion of overall hematopoietic surface along with normalization of iNOS2, up-regulating the potentially protective Arg1 positive M2 type macrophages and causing a significant shift in the M2/M1 ratio.
Annamária Szántó, Zsuzsanna Pap, Z Pávai, I Benedek, Judit Beáta Köpeczi, Aliz- Beáta Tunyogi, Emőke Horváth and Benedek Erzsébet Lázár
Background: The elucidation of the genetic background of the myeloproliferative neoplasms completely changed the management of these disorders: the presence of the Philadelphia chromosome and/or the BCR-ABL oncogene is pathognomonic for chronic myeloid leukemia and identification of JAK2 gene mutations are useful in polycytemia vera (PV), essential thrombocytemia (ET) and myelofibrosis (PMF). The aim of this study was to investigate the role of molecular biology tests in the management of myeloproliferative neoplasms.
Materials and methods: We tested the blood samples of 117 patients between April 2008 and February 2013 at the Molecular Biology of UMF Târgu Mureș using RQ-PCR (for M-BCR-ABL oncogene) and/or allele-specific PCR (for JAK2V617F mutation).
Results: Thirty-two patients presented the M-BCR-ABL oncogene, 16 of them were regularly tested as a follow-up of the administered therapy: the majority of chronic phase patients presented decreasing or stable values, while in case of accelerated phase and blast phase the M-BCR-ABL values increased or remained at the same level. Twenty patients were identified with the JAK2V617F mutation: 8 patients with PV, 4 with ET, 3 with PMF, 4 with unclassifiable chronic myeloproliferative disease and 1 patient with chronic myelomonocytic leukemia. There was no case of concomitant occurance of both molecular markers.
Conclusions: Molecular biology testing plays an important role in the management of myeloproliferative neoplasms: identification of the molecular markers confirms the final diagnosis, excluding secondary causes of abnormal blood count parameters. Regular monitoring of MBCR- ABL expression level is useful in the follow-up of therapeutic efficiency.
Adriana-Stela Cosma, Cristina Radu, Alexandra Moldovan, Alina Bogliș, George Andrei Crauciuc, Emőke Horváth, Marcela Cândea and Florin Tripon
Objective: The aim of the current study was to investigate possible associations between catalase C262T (CAT C262T), glutathione peroxidase 1 Pro198Leu (GPX1 Pro198Leu), manganese superoxide dismutase Ala16Val (MnSOD Ala16Val) gene polymorphisms and non-Hodgkin Lymphoma risk (NHL) in a Romanian population and the five-year overall survival rate of the NHL patients.
Methods: We included in this case-control study 406 individuals, divided into two groups: the control group (n=315) and the patients group (n=91). The DNA was extracted from peripheral blood and amplified using specific techniques.
Results: The variant homozygous genotype of GPX1 Pro198Leu represents a risk factor for NHL development and no associations regarding the risk for NHL were found for MnSOD Ala16Val and CAT C262T gene polymorphisms. Two of the studied polymorphisms were associated with the overall survival rate thus: negative association regarding MnSOD Ala16Val, associated with higher overall survival rate and a positive one regarding CAT C262T, associated with lower overall survival rate.
Conclusions: According to our results, the mentioned polymorphisms may be considered as susceptible markers of the five-year overall survival rate for NHL patients. Future studies with a larger number of patients are needed to confirm our results.