The alymphoplasia (aly) mutation of mouse is autosomal recessive and characterized by the systemic absence of lymph nodes (LN) and Peyers patches (PP) and disorganized splenic and thymic structures with immunodeficiency. Although recent reports have shown that the interaction between lymphotoxin (L …

These microRNA 219-2 conditional mutant mice are designed to generate a null allele or a |i|lacZ|/i| tagged null allele when combined with Flp or Cre recombinase expressing strains. This mutant mouse strain may be useful in studies of microRNA biology.

Its been shown that eating materials get excited about immune legislation in the intestine. and VCAM-1) on stromal cells as well as the appearance is controlled by NFB-inducing kinase (NIK). As a result, NIK-mutant aly/aly mice present decreased awareness to FTY720 in the legislation of peritoneal B-cell trafficking because of the impaired appearance of adhesion substances although peritoneal B1 cells in aly/aly mice portrayed comparable degrees of S1P1. 5. Distinct S1P Dependency of Trafficking of Intraepithelial T-Lymphocytes in the Gut Many lymphocytes may also be within the intestinal epithelium and known as as intraepithelial lymphocytes (IELs) [42]. IELs are T cells KU-60019 mainly, but unlike in typical T cells seen in the systemic compartments (e.g., spleen) which mostly exhibit the T-cell receptor (TCR), in the IEL subset now there is an plethora of T cells expressing the T cell receptor (TCR) furthermore to TCR+ T cells [42]. TCR identifies peptide antigen provided via main ...

DISC1 mutant mice exhibit greater responses to an NMDA antagonist, MK-801, and D-serine treatment[a] Locomotor activity in open field of male mice before and af

PHENOTYPE: Homozygous mutant mice show a decreased mean percentage of natural killer cells when compared with controls. Male homozygous mutant mice exhibit impaired sensorimotor gating/attention during prepulse inhibition testing. [provided by MGI curators ...

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The generalized lymphoproliferative disorder (gld) mouse strain is characterized by severe splenomegaly/lymphadenopathy, the production of autoimmune antibodies, and the appearance of CD4/CD8-negative T cells. An additional TNF deficiency of gld/gld mice attenuates the course of the disorder through a yet-unknown mechanism. In this study, we could demonstrate that the reduced splenomegaly and lymphadenopathy in B6.gld/gld.TNF-/- mice were correlated with a decreased peripheral T cell proliferation rate and a delayed polyclonal activation. A comparative analysis of naïve T cells and memory/effector T cells showed an age-dependent difference in the T cell activation pattern in the spleen of B6.gld/gld and B6.gld/gld.TNF-/- mice. T cells from B6.gld/gld.TNF-/- spleens and lymph nodes showed significantly higher levels of CCR7 and CD62 ligand on their surface compared with B6.gld/gld mice when mice of the same age were compared. Additionally, we found an increased titer of the Th1 cytokine ...

Nmu (Neuromedin U) and Nmus (Neuromedin S) gene double knock-out mice. Nmu KO: Exon 9 of the Nmu gene was replaced with a PGK-neo cassette. Homozygous mutant mice show a increased body weight. Nms KO: Exon 8 of the Nms gene was replaced with a neo cassette. Homozygous mutant mice show no obvious abnormality. Nmu gene knockout mice (RBRC04549), Nms gene knockout mice (RBRC04550 ...

The PD1 (programmed cell death 1) gene is an immunoinhibitory receptor that belongs to the CD28 family, and plays a role in the negative control of proliferation, differentiation and class switching of B cells. Homozygous mutant mice exhibit abnormalities in leukopoiesis and the immune system which vary considerably depending on the genetic background. The homozygous mutant mice with BALB/c background exhibit autoimmune dilated cardiomyopathy. The mutant mice of the BALB/c-PD1 (N10 line) show severe dilated cardiomyopathy and start to die as early as 5 weeks of age. Meanwhile, the BALB/c-PD1 (N12) line mutant mice exhibit less severe dilated cardiomyopathy and survive longer than N10 line ...

NIK is widely held as a central mediator of noncanonical NF-κB signaling and the activation of NF-κB2. Indeed, both NF-κB2−/− and NIKaly/aly mice show impaired T and B cell responses, while displaying lymphocyte infiltration into various organs similar to that of Aire−/− mice (Anderson et al., 2002; Liston et al., 2003; Kajiura et al., 2004; Zhu et al., 2006). However, the autoimmune phenotype in NIKaly/aly and NF-κB2−/− mice seems to originate from the stromal compartment, as transplantation of NIKaly/aly or NF-κB2−/− thymi into WT mice was sufficient to induce the breakdown in self-tolerance, which is mediated by the loss of Aire function in mTECs (Kajiura et al., 2004; Zhu et al., 2006). In contrast, the impairment of T cell responses in NIKaly/aly mice resulted from disrupted NIK signaling in hematopoietic cells (Greter et al., 2009). Also, NIKaly/aly mice have a defect in the generation of Treg cells, which is not observed in NF-κB2−/− mice (Zhu et al., 2006). ...

Regional variations in the distribution of small intestinal intraepithelial lymphocytes in alymphoplasia (aly/aly) mice and heterozygous (aly/+) mice.: Regional

Th1 cell differentiation is impaired in these mice. Primary murine embryonic fibroblasts prepared from mutant embryos have decreased viability and increased genomic DNA fragmentation with UV irradiation. This mutant mouse strain represents a model that may be useful in studies related to signal transduction.

So I had purchased a full grown boesemani rainbow from my LFS a couple of weeks ago. The fish looked fine in the store but when I got him home his scales...

TY - JOUR. T1 - Growth hormone-releaser diet attenuates cognitive dysfunction in klotho mutant mice via insulin-like growth factor-1 receptor activation in a genetic aging model. AU - Park, Seok Joo. AU - Chung, Yoon Hee. AU - Lee, Jeong Hyun. AU - Dang, Duy Khanh. AU - Nam, Yunsung. AU - Jeong, Ji Hoon. AU - Kim, Yong Sun. AU - Nabeshima, Toshitaka. AU - Shin, Eun Joo. AU - Kim, Hyoung Chun. N1 - Funding Information: This study was supported by a grant from the Brain Research Center from the 21st Century Frontier Research Program (2012K001115) funded by the Ministry of Science and Technology, Republic of Korea. JHL and DKD were supported by the BK21 PLUS program, National Research Foundation of Korea. Equipment at the Institute of Pharmaceutical Science (Kangwon National University) was used for this study.. PY - 2014. Y1 - 2014. N2 - Background: It has been recognized that a defect in klotho gene expression accelerates the degeneration of multiple age-sensitive traits. Accumulating evidence ...

The patches can appear elsewhere but most patients will describe a long story of patches appearing intermittently on different parts ...

The Nomination Committee assists the Board with oversight of the competence profile and composition of the Board, nomination of members and committees, and other tasks on an ad hoc basis as specifically decided by the Board.

This report describes the development of obesity syndromes in mice caused by two autosomal recessive mutations, fat (fat), located on chromosome 8, and tubby (tub), located on chromosome 7. Both mutations cause slowly developing but ultimately severe obesity conditions. Although hyperinsulinemia, hyperactivity of the beta cell of the islets of Langerhans, and beta-cell degranulation are consistent features, these obesity syndromes do not progress to severe diabetes. The many different single-gene mutations in the mouse that produce obesity-diabetes syndromes of varying degrees of severity make the mutant mouse a powerful tool for analyzing the number and nature of the primary defects than can cause obesity states.

Anxiety is often comorbid with depression (Zimmerman et al., 2002). In rodents, some animal models of depression display anxiety-like responses (Bale et al., 2000; Schramm et al., 2001; Ansorge et al., 2004; Heim et al., 2004; Wei et al., 2004), whereas others do not (Overstreet, 1993). To determine whether Vmat2 mice show anxiety-like behaviors, animals were subjected to the open field, zero maze, light-dark exploration, and novelty-suppressed feeding tests. Because behaviors of WT and Vmat2 heterozygotes were indistinguishable among these tests, these findings suggest anxiety is not a comorbid feature of the VMAT2 phenotype. Interestingly, these results are similar to those for reserpine-treated hypertensive patients, where anxiety does not appear to accompany their depressive-like states (Freis, 1954).. A core symptom of depression is anhedonia (American Psychiatric Association, 1994). This behavior is modeled as an endophenotype in Flinders rats, learned helpless mice, the chronic mild ...

In addition to sensory neurons, in rodents and birds (and presumably humans) Brn3a is expressed in multiple sites in the central nervous system, including the spinal cord, midbrain superior colliculus, red nucleus, nucleus ambiguus, inferior olivary nucleus, habenula, and retina.[6] Mice with null mutations (knockouts) in Brn3a die at birth, due to developmental defects in the nucleus ambiguus, which is essential for respiration.[7][8][9] Brn3a is a transcription factor which acts in development by regulating downstream target genes. Microarrays have been used to determine many genes downstream of Brn3a in peripheral sensory neurons.[10][11] In the sensory neurons Brn3a is co-expressed with the LIM domain transcription factor ISL1 or Islet1, and has many downstream targets in common with Isl1.[12] Pou4f1/Isl1 double mutant mice show strong epistatic effects in regulation of many downstream genes in the sensory neurons of double mutant mouse embryos.[13] Although the homozygous Brn3a null ...

Programmed cell death (PCD) in the interdigit region of developing vertebrate limbs generates separated rather than webbed digits. Previous models have proposed that bone morphogenetic proteins (BMPs) directly trigger such PCD; however, they might also act indirectly by regulating fibroblast growth factors (FGFs), which act as cell survival factors. To investigate this question, Mark Lewandoskis group inactivated the BMP receptor gene Bmpr1a specifically in the limb buds apical ectodermal ridge (AER) - a source of FGF activity. They report on p. 2359 that in mice, BMP signalling mediates AER induction. However, it subsequently inhibits the expression of the AER survival factors Fgf4 and Fgf8, leading to interdigit PCD. By generating conditional mutant mice, the authors show that Bmpr1a inactivation induces Fgf4 and Fgf8 upregulation in the AER. Webbing persists in mice where Bmpr1a and Fgf8 are inactivated, but disappears when one copy of Fgf4 is also inactivated. Evolutionary alterations in ...

Ins-TOPGAL and Ctnnb1 C429S mutant mice. Ctnnb1 C429S mutant mice were generated by ENU mutagenesis. C492S homozygous mutant mice are infertile. Ins-TOPGAL transgenic mice are useful for visualizing Wnt signal pathway. The transgene contains the nLacZ gene under the control of a TOPFLASH promoter (6x TCF binding motifs upstream of a TK promoter). The transgene construct was flanked by the insulator core elements ...

Calcium, Calcium Channels, Drugs, Ligands, Role, Therapeutic, Alanine, Anxiety, Anxiety Disorder, Arginine, At 10, Carrying, Conflict, Measure, Mice, Mouse, Mutant Mouse Strains, Mutation, Pharmacology, Phenobarbital

Dung, H, Pathologic changes observed in organs of lethargic mutant mice. Abstr. (1972). Subject Strain Bibliography 1972. 311 ...

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A dye-injection technique has been used to determine the developmental stage at which posterior neuropore (PNP) closure occurs in normal and mutant curly tail mouse embryos. In vivo, the majority of non-mutant embryos undergo PNP closure between 30 and 34 somites whereas approximately 50% of all mutant embryos show delayed closure, and around 20% maintain an open PNP even at advanced stages of development. A similar result has been found for embryos developing in vitro from the headfold stage. Later in development, 50-60% of mutant embryos in vivo develop tail flexion defects, and 15-20% lumbosacral myeloschisis. This supports the view that delayed PNP closure is the main developmental lesion leading to the appearance of caudal neural tube defects in curly tail mice. The neural tube is closed in the region of tail flexion defects, but it is locally overexpanded and abnormal in position. The significance of these observations is discussed in relation to possible mechanisms of development of ...

TY - JOUR. T1 - Hereditary emphysema in the tight-skin mouse. Evaluation of pathogenesis. AU - Rossi, G. A.. AU - Hunninghake, G. W.. AU - Gadek, J. E.. AU - Szapiel, S. V.. AU - Kawanami, O.. AU - Ferrans, V. J.. AU - Crystal, Ronald. PY - 1984/7/19. Y1 - 1984/7/19. N2 - The tight-skin (Tsk/+) mouse is a genetically determined model characterized by alveolar enlargement and physiologic evidence of emphysema. Morphologic evaluation of the lungs of these animals demonstrated increased numbers of potential protease-secreting cells (alveolar macrophages and neutrophils) in the lower respiratory tract prior to development of the emphysematous lesions. Quantitation of the neutrophils in the lungs of these animals was carried out by bronchoalveolar lavage. In the Tsk/+ mice, neutrophils constituted 3.5 ± 2% of all inflammatory and immune effector cells present compared with 0.4 ± 0.1% in control (+/+) mice (p , 0.01). The Tsk/+ animals had no evidence of infection to explain the presence of the ...

Question - Dark, itchy and flaky skin after blunt force injury. What is it and how can I get rid of it?. Ask a Doctor about diagnosis, treatment and medication for Hypertrophic scar, Ask a Dermatologist

Although the underlying causes of autism spectrum disorders (ASD) are complex, two aspects have emerged from studies over the years: 1) there is a large genetic component to ASD, and 2) ASD is a disorder of brain development.

TY - JOUR. T1 - FoxM1 insufficiency hyperactivates Ect2-RhoA-mDia1 signaling to drive cancer. AU - Limzerwala, Jazeel F.. AU - Jeganathan, Karthik B.. AU - Kloeber, Jake A.. AU - Davies, Brian A.. AU - Zhang, Cheng. AU - Sturmlechner, Ines. AU - Zhong, Jian. AU - Fierro Velasco, Raul. AU - Fields, Alan P.. AU - Yuan, Yaxia. AU - Baker, Darren J.. AU - Zhou, Daohong. AU - Li, Hu. AU - Katzmann, David J.. AU - van Deursen, Jan M.. N1 - Funding Information: We thank B. Childs, R. Naylor and C. Sieben for helpful discussions, and G. Nelson for managing the mouse colony. We thank the transgenic and gene knockout core at Mayo Clinic for generation of all mutant mouse strains, D. Billadeau (Mayo Clinic, Rochester) for the Cofilin 1 antibody, G. Razidlo (Mayo Clinic, Rochester) for Cytochalasin D and GST-PBD construct, S. Kaufmann (Mayo Clinic, Rochester) for H1299 and A549 cell lines and R. Thaler for assistance with the in vitro GEF activity assay. The human tumor results shown here are in whole or ...

Such Knockin mice have an inserted exogenous gene that is regulated under the native promoter, providing a physiologically relevant and secure expression.

Even though FLASH mutant mice have been claimed to die in the early embryonic stage , FLASH KO ES cells was revealed to proliferate and differentiate commonly

When Fidos flaky skin is disrupting his day with itching and chewing, and yours with questions and concerns, its time to plan a visit to your vet. In the meantime, narrowing the possibilities for the source of your pups problems can help you find ways to relieve his dermatological misery.

Soothes irritations, treats flaky skin and moderates sebum levels. Protects against environmental factors, revealing a relaxed, replenished and smooth skin.

Homozygous mutants have a white belt across the back in the midtrunk region and a white belly patch that coalesces to form a white belt ...

Interactions between products of the mouse W locus, which encodes the c-kit tyrosine kinase receptor, and the Sl locus, which encodes a ligand for c-kit receptor, which we have designated stem cell factor (SCF), have a critical role in the development of mast cells. Mice homozygous for mutations at either locus exhibit several phenotypic abnormalities including a virtual absence of mast cells. Moreover, the c-kit ligand SCF can induce the proliferation and maturation of normal mast cells in vitro or in vivo, and also can result in repair of the mast cell deficiency of Sl/Sld mice in vivo. We now report that administration of SCF intradermally in vivo results in dermal mast cell activation and a mast cell-dependent acute inflammatory response. This effect is c-kit receptor dependent, in that it is not observed when SCF is administered to mice containing dermal mast cells expressing functionally inactive c-kit receptors, is observed with both glycosylated and nonglycosylated forms of SCF, and ...

Mice. Rnf8-/- mice (AS0574 strain) were previously reported (11). Trp53fl/fl conditional mutant mice (37) (NCI Mouse Repository) were intercrossed with WapCre transgenic mice (The Jackson Laboratory) to obtain WapCre Trp53fl/fl mice. Subsequent crosses of Rnf8-/- mice with WapCre Trp53fl/fl mice generated Rnf8-/- WapCre Trp53fl/fl females. Mice in this study were on a mixed 129/J × C57BL/6 genetic background and were genotyped by PCR for Rnf8WT (forward 5′-TGATGACACCTGGGCATGT-3′; reverse 5′-TCTTTGAGACAGCGCCTGG-3′), Rnf8 mutant (forward 5′-TCAAAGGTTTGCCCTCTGAT-3′; reverse 5′-CGGAGCGGATCTCAAACTCT-3′), Trp53fl (forward 5′-CAGCCTCTGTTCCACATACACT-3′; common 5′-TGGATGGTGGTATACTCAGAGC-3′), Trp53WT (forward 5′-AGGCTTAGAGGTGCAAGCTG-3′; common 5′-TGGATGGTGGTATACTCAGAGC-3′), and Cre (forward 5′-CCATCTGCCACCAGCCAG-3′; reverse 5′-TCGCCATCTTCCAGCAGG-3′). All mice were housed in a pathogen-free mouse facility at the Princess Margaret Cancer Centre. Ten- to 12-week-old ...

The role of MC in non-allergic inflammatory responses has been a subject of many recent investigations. Although in vitro evidence of T cell-MC interactions exists, as does proof that MC are normally present in secondary lymphoid organs, little is known about the in vivo contribution of these cells to adaptive immune responses 28-31. The availability of the W/Wv mouse model has been pivotal in definitively establishing a role for MC in innate immune responses that confer, for example, resistance to bacterial infection 32. However, because the c-kit mutations present in this mouse can affect the development of other hematopoietic cell lineages, the use of this model requires stringent proof that MC are responsible for any phenotypic differences observed between W/Wv mice and their WT counterparts. This is particularly true in instances such as the present study of EAE where MC effects on T cell function are being investigated. Despite the widespread use of W/Wv mice, a careful analysis of ...

Sigma-Aldrich offers abstracts and full-text articles by [Madoka Kato, Akira Shimizu, Yoko Yokoyama, Kyoichi Kaira, Yutaka Shimomura, Akemi Ishida-Yamamoto, Kiyoko Kamei, Fuminori Tokunaga, Osamu Ishikawa].

This animation of early neural development from week 3 onward shows the neural groove fusing to form the neural tube. View - Dorsolateral of the whole early embryo and yolk sac. Cranial (head) to top and caudal (tail) to bottom. Yolk sac is shown to the left. Beginning with the neural groove initially fusing at the level of the 4th somite to form the neural tube and closing in both directions to leave 2 openings or neuropores: a cranial neuropore (anterior neuropore) and a caudal neuropore (posterior neuropore). The animation also shows as the embryo grows and folds it increases in size relative to the initial yolk sac. Note also the increasing number of somites over time. ...

Using a stringent statistical methodology, 593 of the 6190 proteins identified in our current study displayed significantly different levels between the wild-type and R9C hearts. (Another ∼1000 proteins were tentatively identified, albeit with less confidence, primarily as a result of lower spectral counts.) The identification of proteins comprising the altered profiles allowed us to interrogate more carefully the mechanisms underlying the progression of cardiac disease at least for the R9C mouse.. These proteomic changes, when analyzed for functional enrichment in GO terms, largely confirmed previous studies highlighting changes in the organization of the cytoskeleton and contractile apparatus together with systematic perturbations of energy metabolism. Other proteins and original categories found to be up-regulated in the R9C mouse include protein degradation and ubiquitination, protein folding and processing, proteins involved in ER stress responses, activation of apoptosis, cellular ...

Caspr3-Deficient Mice Exhibit Low Motor Learning during the Early Phase of the Accelerated Rotarod Task. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

EMMA is short for the European Mouse Mutant Archive. It is a repository and distributor of mutant mouse strains in the form of frozen sperm and embryos or live animals. Together with similar organisations worldwide it forms the Federation of International Mouse Resources FIMRe. ...

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There are many reasons that flak skin can form on the face, but how do you solve the problem? This hub will try to help you control this often embarrassing problem.

D: The skeleton of a wild-type mouse (right) and Wwtr1tm1Whun/Wwtr1tm1Whun mouse (left) embryos stained with Alizarin red and Alcian blue to stain bone (red) and cartilage (blue), respectively. Note the slightly shorter skeleton of the homozygous mouse embryo. G & H: Hematoxylin and eosin staining of longitudinal kidney sections from 8 week old wild-type (G) and homozygous mutant mouse (H), showing numerous cysts in the corticomedullary region of the homozygous mouse kidney. Magnification: x20 ...

Factor XII Knockout Mice - Mutant mice are from an ongoing colony made in-house at our state of the art facility in the U.S.A and available immediately. No waiting for cryo recovery or costly breeding. Complete absence of FXII protein confirmed by Western Blot. Useful for cardiovascular and neurological studies.

A Novel N-ethyl-N-nitrosourea-Induced Mutation in Phospholipase C gamma 2 Causes Inflammatory Arthritis, Metabolic Defects, and Male Infertility In Vitro in a Murine Model ...

Filagra lowest prices 2 FFilagra Tafra The Breast Center at Anne Arundel Medical Center Annapolis, Maryland. (1992) TAP1 mutant mice are deficient in antigen presentation, surface class I molecules, and CD4в8 T cells. Y.

For a while now [way before I started the DKR] Ive had really dry, flaky skin in my eyebrows. By in, I mean that its underneath the actual hairs [is that what you call them? haha] Ive tried rubbing moisturizer on but it hasnt helped a whole lot. For a week or so Ive been using the baby brush on them but it doesnt really get down to my skin, I think. Has anyone else had this problem?? I think that it may have gotten a lot worse when I started using the AcneFree system at the beginning ...

[1848 1846 via Curbed Flickr Pool/Jeremy Brooks] · Drunken, mutant mice chillin at UCSF [SF Weekly]· Theres a crazy dangerous fence about to fall over in SoMa [Live SoMa]· Weird art at Hayes...

Mice are identical with dirty condition. Mice usually live in moist and dirty area. We know that dirty area contains bacteria. Finally, mice bring bacteria to a house where they live. Bacteria from mice will cause various diseases. When mice urinate or defecate in our home, their feces and urine contain bacteria, even virus. When virus or bacteria contaminate water and food in our home, finally it makes us get risk to experience diseases caused by mice.. There are so many diseases caused by mice. The best way to avoid disease caused by mice is getting rid of mice as soon as possible. You can ask exterminator to get rid of mice. You can also use mice trap to trap mice. Finally, your home will be free of mice.. ...

Expression of ELC mRNA is decreased in the LNs and spleens of plt mice. Tissues from +/+ (A and C) and plt (B and D) mice were analyzed as described in the

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