Adult Spleen Research Articles

Morphometric Assessment of the Normal Dimensions of the Adult Spleen in North-west Ethiopia Region – A Radiological Study

Morphometric Assessment of the Normal Dimensions of the Adult Spleen in North-west Ethiopia Region – A Radiological Study

Splenocytes from young mice protect immunocompromised mice against death from malaria infection, but they do not proliferate well.

Abstract The immune system plays an essential role in the elimination of malaria parasites. CD4+ T cells are imperative in the immune response to the infection, but immune response to malaria especially in young children is poorly understood, due to a lack of a better young animal model to study the pathogenesis of the disease. We have developed a young mouse (pup) model using day 15 pups to help understand the pathogenesis, and development of protective CD4 T cells in malaria infection. Here, we determined the ability of pup cells to protect immunocompromised RAGKO mice from malaria infection. We infected day 15 old pups with Plasmodium chabudi at 1×105 iRBCs, and transferred splenocytes to RAGKO mice on day 8 post-infection. RAGKO mice were then infected. Mice that received pup cells looked healthier and active throughout the experiment, compared to their counterparts who received adult spleen cells. During the peak of infection, mice that received adult cells lost more weight than the pup cell recipients. On day 60 post-transfer, we observed same numbers of CD4 T cells, central memory and effector memory T cells. There were significantly lower proportions and numbers of IFNγ and TNFα positive cells from pups compared to adult cells. We next determined if there was any difference in the proliferation of CD4 T cells and all splenocytes in pup cells. We purified CD4+ T cells using EasySep kit and cultured them on αCD3/CD28 pre-coated plates, compared to all splenocytes. There was a significant growth in purified CD4 T cells from adult than pup cells. Interestingly, all splenocytes from pups proliferated better than adults. Therefore, our data suggest that pup cells protect RAGKO mice from death, but do not develop into functional memory due to poor proliferation.

Liver atrophy and regeneration in noncirrhotic portal vein thrombosis: Effect of surgical shunts.

The goal of the study is to characterize the relationship between portal vein thrombosis (PVT) and hepatic atrophy in patients without cirrhosis and the effect of various types of surgical shunts on liver regeneration and splenomegaly. Patients without cirrhosis with PVT suffer from presinusoidal portal hypertension, and often hepatic atrophy is a topic that has received little attention. We hypothesized that patients with PVT have decreased liver volumes, and shunts that preserve intrahepatic portal flow enhance liver regeneration. Sixty-four adult and pediatric patients with PVT who underwent surgical shunt placement between 1998 and 2011 were included in a retrospective study. Baseline liver volumes from adult patients were compared with standard liver volume (SLV) as well as a group of healthy controls undergoing evaluation for liver donation. Clinical assessment, liver function tests, and liver and spleen volumes from cross-sectional imaging were compared before and after surgery. A total of 40 patients received portal flow-preserving shunts (32 mesoportal and 8 selective splenorenal), whereas 24 received portal flow-diverting shunts (16 nonselective splenorenal and 8 mesocaval). Baseline adult liver volumes were 26% smaller than SLV (1248 versus 1624 cm3 ; P = 0.02) and 20% smaller than the control volumes (1248 versus 1552 cm3 ; P = 0.02). Baseline adult spleen volumes were larger compared with controls (1258 versus 229 cm3 ; P < 0.001). Preserving shunts were associated with significant increase in liver volumes (886 versus 1131 cm3 ; P = 0.01), whereas diverting shunts were not. Diverting shunts significantly improved splenomegaly. In conclusion, we have demonstrated that patients without cirrhosis with PVT have significant liver atrophy and splenomegaly. Significant liver regeneration was achieved after portal flow-preserving shunts. Liver Transplantation 24 881-887 2018 AASLD.

Inflammatory bone loss associated with MFG-E8 deficiency is rescued by teriparatide.

A prolonged increase in proinflammatory cytokines is associated with osteoporotic and autoimmune bone loss and, conversely, anti-inflammatory pathways are associated with protection against bone loss. Milk fat globule-epidermal growth factor (MFG-E)-8 is a glycoprotein that is proresolving, regulates apoptotic cell clearance, and has been linked to autoimmune disease and skeletal homeostasis. The role of MFG-E8 in the young vs. adult skeleton was determined in mice deficient in MFG-E8 (KO). In vivo, trabecular bone was similar in MFG-E8KO and wild-type (WT) mice at 6 and 16 wk, whereas 22 wk adult MFG-E8KO mice displayed significantly reduced trabecular BV/TV. The number of osteoclasts per bone surface was increased in 22-wk MFG-E8 KO vs. WT mice, and recombinant murine MFG-E8 decreased the number and size of osteoclasts in vitro. Adult MFG-E8KO spleen weight:body weight was increased compared with WT, and flow cytometric analysis showed significantly increased myeloid-derived suppressor cells (CD11bhiGR-1+) and neutrophils (CD11bhiLy6G+) in MFG-E8KO bone marrow, suggesting an inflammatory phenotype. PTH-treated MFG-E8KO mice showed a greater anabolic response (+124% BV/TV) than observed in PTH-treated WT mice (+64% BV/TV). These data give insight into the role of MFG-E8 in the adult skeleton and suggest that anabolic PTH may be a valuable therapeutic approach for autoimmune-associated skeletal disease.-Michalski, M. N., Seydel, A. L., Siismets, E. M., Zweifler, L. E., Koh, A. J., Sinder, B. P., Aguirre, J. I., Atabai, K., Roca, H., McCauley, L. K. Inflammatory bone loss associated with MFG-E8 deficiency is rescued by teriparatide.

Capillary networks and follicular marginal zones in human spleens. Three-dimensional models based on immunostained serial sections.

We have reconstructed small parts of capillary networks in the human splenic white pulp using serial sections immunostained for CD34 alone or for CD34 and CD271. The three-dimensional (3D) models show three types of interconnected networks: a network with very few long capillaries inside the white pulp originating from central arteries, a denser network surrounding follicles plus periarterial T-cell regions and a network in the red pulp. Capillaries of the perifollicular network and the red pulp network have open ends. Perifollicular capillaries form an arrangement similar to a basketball net located in the outer marginal zone. The marginal zone is defined by MAdCAM-1+ marginal reticular stromal cells. Perifollicular capillaries are connected to red pulp capillaries surrounded by CD271+ stromal capillary sheath cells. The scarcity of capillaries inside the splenic white pulp is astonishing, as non-polarised germinal centres with proliferating B-cells occur in adult human spleens. We suggest that specialized stromal marginal reticular cells form a barrier inside the splenic marginal zone, which together with the scarcity of capillaries guarantees the maintenance of gradients necessary for positioning of migratory B- and T-lymphocytes in the human splenic white pulp.

Loss of NRF2 function exacerbates the pathophysiology of sickle cell disease in a transgenic mouse model

AbstractThe basic leucine zipper transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) plays a critical role in the cellular antioxidant response under oxidative stress conditions. In this study, we investigated the role of NRF2 in fetal hemoglobin expression and the pathophysiology of sickle cell disease (SCD) in a NRF2 knockout (SCD/NRF2−/−) transgenic mouse model. NRF2 loss impaired survival of SCD pups during gestation and in the first 2 months of life. Furthermore, fetal hemoglobin expression was inhibited during erythropoiesis in embryonic day 13.5 and embryonic day 18.5 fetal liver and adult spleen and bone marrow cells, respectively. Examination of peripheral red blood cells revealed an increase of reactive oxygen species (ROS) and sickling under hypoxic conditions. Loss of NRF2 function in SCD/NRF2−/− mice produced greater splenomegaly with red pulp expansion and obscured architecture. In addition, NRF2 knockout reduced the expression of its target antioxidant proteins, leading to increased levels of ROS, proinflammatory cytokines, and adhesion molecules in SCD mice. Genetic knockout of NRF2 demonstrates its role in developmentally regulated γ-globin gene expression and the ability to control oxidative stress and the phenotypic severity of SCD.

Loss of NRF2 Function Worsens the Pathophysiology of Sickle Cell Disease in a Transgenic Mouse Model

The basic leucine zipper transcription factor, nuclear factor (erythroid-derived 2)-like 2 (NRF2) plays a critical role in the cellular antioxidant response to control oxidative stress. We and others previously demonstrated that NRF2 activation enhances γ-globin gene transcription and fetal hemoglobin expression in human primary erythroid progenitors through changes in chromatin structure (Zhu et al., Haematologica 2017). In this study, we investigated the protective role of NRF2 in reversing the pathophysiology of sickle cell disease (SCD) in a SCD/NRF2 knockout (SCD/NRF2KO) transgenic model created in our lab by crossbreeding Townes SCD mice (Ryan et al., Science 1997) and NRF2 knockout mice (Kuroha et al., J Biochem 1998). The NRF2 gene is transmitted through autosomal recessive Mendelian genetics for wild-type, heterozygote and NRF2KO pups. By contrast, the SCD/NRF2KO genotype was present in &amp;lt;2% of pups. In addition, the fertility and litter size of SCD/NRF2KO females were lower than SCDWT mice, suggesting a critical role of NRF2 in the survival of pups during gestation. To determine the hematopoietic effect of NRF2KO in SCD, we monitored the complete blood count with differential and reticulocyte count. There was no significant change in any parameters except higher total white blood cell counts in the SS/NRF2KO mouse suggesting increased inflammation. Examination of globin gene expression patterns in SS/NRF2KO mice showed reduced γ-globin gene expression during erythroid differentiation in the E13.5 and E18.5 fetal liver, adult spleen and bone marrow. In addition, peripheral blood red cells had a 33% increase (p&amp;lt;0.05) in reactive oxygen species and a significant 38% increase in sickling under in vitro hypoxic conditions. We next characterized the effects of NRF2 loss on organ pathology. The SCD/NRF2KO mice displayed greater splenomegaly indicating exaggerated hemolysis most likely due to high levels of reactive oxygen species. By 8-10 weeks of age, the SCD/NRF2KO mouse showed significant inflammation by hematoxylin-eosin staining of the spleen, lung and liver when compared to SCD/NRF2WT mice. Protein expression profiling by western blotting using adult spleen demonstrated downregulation of the antioxidant proteins heme oxygenase 1 (HMOX1), NADPH: quinone oxidoreductase 1 (NQO1) and catalase by 31%, 60%, and 48% respectively (p&amp;lt;0.05). To further support a severe disease phenotype, the expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) were increased by 1.7-fold and 2.3-fold (p&amp;lt;0.05) while vascular endothelial growth factor (VEGF) levels were not changed. Lastly, the expression of interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), monocyte chemoattractant protein (MCP-1) and macrophage migration inhibitory factor (MIF-1) was elevated in SCD/NRF2KO mice compared to SCDWT mice. These data validate a critical role of NRF2 in ameliorating the phenotypic severity of SCD by protecting against red blood cell sickling, oxidative stress and tissue inflammation. Furthermore, the ability of NRF2 to mediate fetal hemoglobin induction provides a rationale for the development of therapeutic agents that activate NRF2 expression. Disclosures No relevant conflicts of interest to declare.

SIRPα+ dendritic cells regulate homeostasis of fibroblastic reticular cells via TNF receptor ligands in the adult spleen

In secondary lymphoid organs, development and homeostasis of stromal cells such as podoplanin (Pdpn)-positive fibroblastic reticular cells (FRCs) are regulated by hematopoietic cells, but the cellular and molecular mechanisms of such regulation have remained unclear. Here we show that ablation of either signal regulatory protein α (SIRPα), an Ig superfamily protein, or its ligand CD47 in conventional dendritic cells (cDCs) markedly reduced the number of CD4+ cDCs as well as that of Pdpn+ FRCs and T cells in the adult mouse spleen. Such ablation also impaired the survival of FRCs as well as the production by CD4+ cDCs of tumor necrosis factor receptor (TNFR) ligands, including TNF-α, which was shown to promote the proliferation and survival of Pdpn+ FRCs. CD4+ cDCs thus regulate the steady-state homeostasis of FRCs in the adult spleen via the production of TNFR ligands, with the CD47-SIRPα interaction in cDCs likely being indispensable for such regulation.

Stress Erythropoiesis Model Systems.

Bone marrow steady-state erythropoiesis maintains erythroid homeostasis throughout life. This process constantly generates new erythrocytes to replace the senescent erythrocytes that are removed by macrophages in the spleen. In contrast, anemic or hypoxic stress induces a physiological response designed to increase oxygen delivery to the tissues. Stress erythropoiesis is a key component of this response. It is best understood in mice where it is extramedullary occurring in the adult spleen and liver and in the fetal liver during development. Stress erythropoiesis utilizes progenitor cells and signals that are distinct from bone marrow steady-state erythropoiesis. Because of that observation many genes may play a role in stress erythropoiesis despite having no effect on steady-state erythropoiesis. In this chapter, we will discuss in vivo and in vitro techniques to study stress erythropoiesis in mice and how the in vitro culture system can be extended to study human stress erythropoiesis.

Effect of sodium metabisulfite on lipid peroxidation and enzyme activities in adult rat stomach and spleen

Sodium metabisulfite (NaMBS) has been used as an antioxidant and antimicrobial agent in a variety of drugs and foods. The aim of our study was to evaluate the effect of subchronic ingestion of NaMBS on lipid peroxidation, protein and enzymatic antioxidants in the gastric tissue and splenic Wistar rat. The rats were divided into four groups (n = 06 rats/group) as follows; Control (C), rats treated with 0.25% NaMBS (S0.25%), rats treated with 1% NaMBS (S1%) and rats treated with 4% NaMBS (S4%). NaMBS was administered to animals via drinking water. At the end of the experimental period, Malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxi-dase (GPx), catalase (CAT) and thiols were determined. Redox status assess-ment revealed that 1% and 4% NaMBS doses induced gastric and spleen lipid peroxidation in animals compared to the control group. On the other hand, activities of SOD, GPx, CAT and thiols were reduced in the S1% and S4% groups in the stomach and spleen compared to the controls. Slight changes were detected in the GPx and CAT in the stomach of S0.25% group compared to the control group. In conclusion, the subchronic consumption of NaMBS has an adverse effect on the spleen and stomach by inducing oxidative damage leading to an increase in lipid peroxidation, protein oxidation and alteration of enzyme activity antioxidant.

Embryo derived macrophages regulate dendritic cell pool size in the adult spleen

Dendritic cells (DCs) are potent antigen presenting cells that depend on Flk2-mediated signals for their differentiation in vivo. However, in Flk2-deficient mice a small but functionally active fraction of DCs remains. We show here that the combined deficiency for Flk2 and Csf1r, another member of the same family of receptor tyrosine kinases, results in natural DC null mice. In contrast to Flk2, Csf1r-mediated signals affect DC differentiation by a cell extrinsic, non-hematopoietic mechanism that does not require Csf1r signaling within the entire adult mouse. During embryonic development Csf1r activation is crucial for the generation of macrophages, which emerge from erythro-myeloid progenitors in the yolk sac before the presence of definitive hematopoietic stem cells (dHSCs). Tissue-resident red pulp macrophages (RPMp) in the spleen are such embryonic macrophages, and we show here that Csf1r signaling is required for their differentiation. In the absence of Flk2-mediated signals, loss of Csf1r expression results in complete ablation of spleen DCs in vivo due to the lack of embryonic macrophages. RPMps have been implicated in the maintenance of tissue hemostasis, removal of pathogens and clearance of cellular debris. We assign here a novel important role to RPMps in the maintenance of tissue homeostasis by regulating the pool size of dHSC-derived myeloid cells in the spleen.

The spleen

The spleen

Developmental differences between newborn and adult mice in response to romiplostim

Thrombocytopenia is frequent among sick neonates. While most cases are transient, some neonates experience prolonged and severe thrombocytopenia. These infants often pose diagnostic and therapeutic challenges, and may receive large numbers of platelet transfusions. Romiplostim (ROM) is a thrombopoietin (TPO)-receptor-agonist approved for treatment of adults with chronic immune thrombocytopenia (ITP). The immature platelet fraction (IPF) is a novel measure of newly produced platelets, which could aid with the diagnostic evaluation of thrombocytopenic neonates. This study had the following two objectives: (1) compare the response of newborn and adult mice to escalating doses of ROM in vivo and (2) assess the correlation between IPF and megakaryocyte (MK) mass in newborn and adult treated and untreated mice. In the first set of studies, newborn (day 1) and adult mice received a single subcutaneous (SC) dose of ROM ranging from 0 to 300 ng/g, and platelet counts were followed every other day for 14 days. Both sets of mice responded with dose-dependent platelet and IPF increases, peaking on days 5–7 post-treatment, but neonates had a blunted response (2.1-fold compared to 4.2-fold maximal increase in platelet counts, respectively). On day 5 post-treatment with 300 ng/g ROM, MKs in the bone marrow (BM) and spleen of adult mice were significantly increased in numbers and size (p < 0.0001 for both) compared to controls. MKs in the spleen and BM (but not liver) of treated neonates also increased in number, but not in size. The immature platelet count (IPC, calculated as IPF x platelet count) was highly correlated with the MK number and size in neonatal and adult BM and spleen, but not neonatal liver. The lack of response of neonatal liver MKs was not due to a cell-intrinsic reduced responsiveness to TPO, since neonatal liver progenitors were more sensitive to murine TPO (mTPO) in vitro than adult BM progenitor. In vivo treatment of newborn mice with high mTPO doses or with higher doses of ROM (900 ng/g) resulted in peak platelet counts approaching 3-fold of controls. Taken together, our data indicate that newborn mice are less responsive to ROM than adult mice in vivo, due to a combination of likely pharmacokinetic differences and developmental differences in the response of MKs to thrombopoietic stimulation, evidenced by neonatal MKs increasing in numbers but not in size. PK/PD studies in human infants treated with ROM are warranted.

Regulation of Human CD27+IgM+ B Cell Activation by Cis-Binding of the Inhibitory Molecule CD22 to CD22 Ligand (CD22L)

Background: ABO-incompatible (ABOi) heart transplantation (HTx) can be performed safely in infants and results in B cell tolerance to donor ABO antigens by mechanisms that remain unclear. We showed that the inhibitory molecule CD22 is more highly expressed on splenic CD27+IgM+ B cells, which contain the vast majority of ABO-specific antibody secreting cell precursors, compared to other splenic B cell subsets. CD22 expression was highest on infant CD27+IgM+ B cells and decreased with age. Binding of CD22 to sialic acids (CD22L) on the same cell (cis-binding) or different cells (trans-binding) regulates B cell activation and may lead to B cell tolerance. Here, we studied whether CD22-CD22L cis-binding affects activation of CD27+IgM+ and CD27-IgM+ B cells from pediatric and adult spleen. Methods: CD27+IgM+ and CD27-IgM+ B cells were isolated via fluorescence-activated cell sorting from pediatric (n=3; age range: 0–2.5 yr) and adult (n=3; age range: 21–46 yr) spleen obtained from organ donors. To ‘break’ CD22-CD22L cis-binding, sorted B cells were treated with neuraminidase (NEU) to cleave surface sialic acids. Activation of B cells was defined by analyzing intracellular phosphorylation of PLCγ2 (pY759) after stimulation with anti-IgM antibodies using ‘phospho-flow’ cytometry. Results: Kinetics of pY759 signaling after stimulation were similar between untreated CD27+IgM+ and CD27-IgM+ B cells as well as pediatric and adult samples. At peak response (1–3 min after stimulation), the median fluorescence intensity (MFI) of pY759 in pediatric CD27+IgM+ B cells was comparable to that in pediatric CD27-IgM+ B cells (350–614 vs. 259–565), whereas in adult cells the MFI was higher in CD27+IgM+ B cells than in CD27-IgM+ B cells (540–912 vs. 248–328). NEU treatment had a strong effect on kinetics and magnitude of pY759 signaling in both pediatric and adult CD27+IgM+ B cells: the MFI of pY759 increased to 506–2023 and 1086–2051, respectively, at peak response (4–8 min after stimulation). In contrast, treatment had minimal effect on pY759 signaling in CD27-IgM+ B cells. Conclusion: NEU treatment increased the magnitude of pY759 signaling in stimulated CD27+IgM+ B cells, but not CD27-IgM+ B cells, suggesting that CD22-CD22L cis-binding may play a role in control of activation of CD27+IgM+ B cells. This finding may contribute to unraveling mechanisms of B cell tolerance in ABOi HTx in children. Canadian National Transplant Research Program (CNTRP) investigator.

King's Variceal Prediction Score

Variceal haemorrhage can be a life-threatening complication of chronic liver disease in children. There is limited evidence about the optimal prophylactic management and selection criteria of children who will benefit from upper gastrointestinal endoscopy. Children presenting in our centre with suspected portal hypertension or gastrointestinal bleeding and undergoing their first oesophagogastroduodenoscopy between 2005 and 2012 were included. Clinical, biochemical, and radiological data were collected. A separate validation cohort from May 2013 to October 2014 was obtained. Data on 124 treatment-naïve patients were collected; 50% had biliary atresia. Thirty-five (28%) children presented with gastrointestinal bleeding and overall 79 (64%) had clinically significant (grade II-III) varices. Clinical prediction rule, aspartate aminotransferase-platelet ratio index, and varices prediction rule had at optimal cut-off sensitivity and specificity of 76% and 59%, 60% and 55%, and 80% and 59%, respectively. Logistic regression yielded a new prediction rule of (3 × albumin ([g/dL]) - (2 - equivalent adult spleen size [cm]). This King's variceal prediction score had a favourable areas under the curve of 0.772 (0.677-0.867) compared to clinical prediction rule 0.732 (0.632-0.832). At the optimal cut-off of 76 this yielded a sensitivity and specificity of 72% and 73% and a positive and negative predictive value of 82% and 60%, respectively. In the validation cohort areas under the curve was 0.818 (0.654-0.995) with sensitivity and specificity of 78% and 73%, respectively. Our new prediction score may be a useful tool in the selection of children with clinically significant varices eligible for a screening endoscopy.

Long-Term Tissue Culture of Adult Brain and Spleen Slices on Nanostructured Scaffolds.

Long-term tissue culture of adult mammalian organs is a highly promising approach to bridge the gap between single cell cultures and animal experiments, and bears the potential to reduce in vivo studies. Novel biomimetic materials open up new possibilities to maintain the complex tissue structure in vitro; however, survival times of adult tissues ex vivo are still limited to a few days with established state-of-the-art techniques. Here, it is demonstrated that TiO2 nanotube scaffolds with specific tissue-tailored characteristics can serve as superior substrates for long-term adult brain and spleen tissue culture. High viability of the explants for at least two weeks is achieved and compared to tissues cultured on standard polytetrafluoroethylene (PTFE) membranes. Histological and immunohistochemical staining and live imaging are used to investigate tissue condition after 5 and 14 d in vitro, while environmental scanning electron microscopy qualifies the interaction with the underlying scaffold. In contrast to tissues cultured on PTFE membranes, enhanced tissue morphology is detected in spleen slices, as well as minor cell death in neuronal tissue, both cultured on nanotube scaffolds. This novel biomimetic tissue model will prove to be useful to address fundamental biological and medical questions from tissue regeneration up to tumor progression and therapeutic approaches.

High resolution methylation analysis of the HoxA5 regulatory region in different somatic tissues of laboratory mouse during development

Homeobox genes encode a group of DNA binding regulatory proteins whose key function occurs in the spatial-temporal organization of genome during embryonic development and differentiation. The role of these Hox genes during ontogenesis makes it an important model for research. HoxA5 is a member of Hox gene family playing a central role during axial body patterning and morphogenesis. DNA modification studies have shown that the function of Hox genes is partly governed by the methylation-mediated gene expression regulation. Therefore the study aimed to investigate the role of epigenetic events in regulation of tissue-specific expression pattern of HoxA5 gene during mammalian development. The methodology adopted were sodium bisulfite genomic DNA sequencing, quantitative real-time PCR and chromatin-immunoprecipitation (ChIP). Methylation profiling of HoxA5 gene promoter shows higher methylation in adult as compared to fetus in various somatic tissues of mouse being highest in adult spleen. However q-PCR results show higher expression during fetal stages being highest in fetal intestine followed by brain, liver and spleen. These results clearly indicate a strict correlation between DNA methylation and tissue-specific gene expression. The findings of chromatin-immunoprecipitation (ChIP) have also reinforced that epigenetic event like DNA methylation plays important role in the regulation of tissue specific expression of HoxA5.

A Cadaveric Study of Human Spleen and its Clinical Significance

Abstract Background &amp; Aim: Spleen is an important lymphatic organ that is connected to the blood vascular system. It is important component of the reticulo-endothelial system. The aim of study was to find out the morphological variations in spleen &amp; compare it with previous studies. Material and Methods: The present study was done on 66 human adult spleens belonging to both sexes. Various morphological features of spleen like length, breadth, width and weight were measured. Shape, borders, poles and surfaces of spleen were observed. Results: The weight of spleens was between 30 Gms to 390 Gms, with an average of 139.5 Gms. 40.91% of the spleens were wedge shaped followed by tetrahedral (27.27%), triangular (18.18%), oval (9.1%) and irregular (4.55%). The length of the spleens varied between 5.10 cm to 14.8 cm with average of 9.41 cms. Their breadths were between 4.3 cms to 11 cms with average of 6.4 cms and width was between 2 cms to 5.5 cms with an average of 3.3 cms. In most of the cases, splenic notches were present on the superior border (50%) followed by on both borders (21.21%). Ten spleens had no notches on either of its borders. Conclusions: The findings of this study are useful for physicians, surgeons, radiologists and anatomists.

A cadaveric study of human spleen and its clinical significance

Background & Aim: Spleen is an important lymphatic organ that is connected to the blood vascular system. It is important component of the reticuloendothelial system. The aim of study was to find out the morphological variations in spleen & compare it with previous studies. Material and Methods: The present study was done on 66 human adult spleens belonging to both sexes. Various morphological features of spleen like length, breadth, width and weight were measured. Shape, borders, poles and surfaces of spleen were observed. Results The weight of spleens was between 30 Gms to 390 Gms, with an average of 139.5 Gms. 40.91% of the spleens were wedge shaped followed by tetrahedral (27.27%), triangular (18.18%), oval (9.1%) and irregular (4.55%). The length of the spleens varied between 5.10 cm to 14.8 cm with average of 9.41 cms. Their breadths were between 4.3 cms to 11 cms with average of 6.4 cms and width was between 2 cms to 5.5 cms with an average of 3.3 cms. In most of the cases, splenic notches were present on the superior border (50%) followed by on both borders (21.21%). Ten spleens had no notches on either of its borders. Conclusions: The findings of this study are useful for physicians, surgeons, radiologists and anatomists.

Cloning and expression of cold-inducible RNA binding protein in domestic yak (Bos grunniens).

Cold-inducible RNA binding protein (CIRP) is over-expressed during cold and many other stresses, and could regulate the adaptation to hypothermia. In the present investigation, the objective was to determine the expression of CIRP in adult yak heart, liver, spleen, lung, kidney, brain, ovary, testis and skin by relative quantitative real time polymerase chain reaction (RT-PCR), Western blot and immunohistochemistry from mRNA and protein levels. The CIRP open reading frame encoding was cloned from the domestic yak brain. Results of RT-PCR and Western blot showed the high expression level of CIRP in the heart, kidney, brain, testis and skin, and the lower expression level of CIRP in the lung. Immunohistochemical staining showed CIRP was expressed in the nucleus of neuronal cells, spermatogonia, primary spermatocytes and epidermal cells, and in the cytoplasm of the residual tissues. These observations may provide new data to understand and further study the important role of CIRP protein in the plateau adaptation of the domestic yak on long-term evolution.