interacts_with DB00266?
Structure-activity relationship studies of CNS agents -- XVII . Spiro[piperidine-4',1-(1,2,3,4-tetrahydro-beta-carboline)] as a probe defining the extended topographic model of P08908 receptors . Spiro[piperidine-4',1-(1,2,3,4-tetrahydro-beta-carboline)] ( 10 ) , its derivatives 11-15 and its analogs 16 and 17 were examined as ligands of serotonin P08908 receptors . It was shown that compounds 12 and 14 had essentially the same P08908 affinity as 1-phenylpiperazine and its rigid analog 7 , whereas there were substantial differences in the steric arrangement of their crucial pharmacophores , i.e. aromatic and protonation centers . On the basis of the existing models and using the DB04829 structure as a template , a new , extended three-point topographic model of P08908 receptors has been proposed . Vascular endothelial growth factor signaling is required for the behavioral actions of antidepressant treatment : pharmacological and cellular characterization . This study extends earlier work on the role of vascular endothelial growth factor ( P15692 ) in the actions of antidepressant treatment in two key areas . First , by determining the requirement for P15692 in the actions of a 5-HT selective reuptake inhibitor ( SSRI ) , fluoxetine in behavioral models of depression/antidepressant response ; and second , by examining the role of the P08908 receptor subtype in the regulation of P15692 , and the cellular localization of antidepressant regulation of P15692 expression . The results show that pharmacological inhibition of P15692 receptor signaling blocks the behavioral actions of fluoxetine in rats subjected to chronic unpredictable stress . Infusions of SU5416 or SU1498 , two structurally dissimilar inhibitors of P15692 -Flk-1 receptor signaling , block the antidepressant effects of fluoxetine on sucrose preference , immobility in the forced swim test , and latency to feed in the novelty suppressed feeding paradigm . We also show that activation of P08908 receptors is sufficient to induce P15692 expression and that a P08908 antagonist blocks both the increase in P15692 and behavioral effects induced by fluoxetine . Finally , double labeling studies show that chronic fluoxetine administration increases P15692 expression in both neurons and endothelial cells in the hippocampus . Taken together these studies show that P15692 is necessary for the behavioral effects of the SSRI fluoxetine , as well as norepinephrine selective reuptake inhibitor , and that these effects may be mediated by P08908 receptors located on neurons and endothelial cells . Recent advances relating to the clinical application of naked monoclonal antibodies in solid tumors . This review focuses on the recent advances in clinical data regarding antibody-based therapy in the management of solid tumors . We also discuss perspectives on antibody-based therapy in the future . Thorough understanding of the complex interactions between components of the immunological response has led to interest in the concept of immune-mediated therapy for solid tumors . Over the last few years , several humanized and chimeric monoclonal antibodies ( MAbs ) targeting human epidermal receptor 2 ( P04626 ) , epidermal growth factor receptor ( P00533 ) , and vascular endothelial growth factor ( P15692 ) have been employed in treating solid tumors , including breast , colorectal , lung , head and neck , and gynecologic cancers . DB00072 , bevacizumab , cetuximab , and panitumumab are MAbs that are most widely used in clinical practice with acceptable rates of adverse events . Combination of MAbs with small-molecule inhibitors of the same pathway could potentially increase the efficacy and specificity of antibody-based treatment . Immune-mediated effects may be further exploited with the use of bivalent molecules . Dual ligands targeting dopamine D2 and serotonin P08908 receptors as new antipsychotical or anti-Parkinsonian agents . Psychiatric disorders like schizophrenia and neurodegenerative diseases like Parkinson 's disease are associated with poly-factorial pathogenic mechanisms , with several neurotransmitter systems closely involved . In addition to the cerebral dopaminergic ( DA ) system , the serotoninergic ( 5-HT ) system also plays a crucial role in regulating psychoemotional , cognitive and motor functions in the central nervous system ( CNS ) . Among the large 5-HT receptor family , accumulating data have revealed new insights into the therapeutic benefit of the P08908 receptor in treating various CNS disorders , especially schizophrenia and Parkinson 's disease . The present review discusses the advance of dual agents with mixed actions at the dopamine D2 and serotonin P08908 receptors in the treatment of these diseases . Aripiprazole was the only marketed drug with dual D2 and P08908 profile . It is a partial D2 and P08908 receptor agonist and has been prescribed as an atypical antipsychotical drug . Two other drugs DB06016 and Pardoprunox are being investigated in clinic . Most of the other candidate compounds , including DB04888 , Sarizotan , Mazapertine succinate , PF-217830 , and Adoprazine were discontinued due to either non-optimal pharmacokinetic properties or insufficient therapeutical efficacy . Although much effort has been done to highlight the advantages of the P08908 and D2 dual approach , it has to be pointed out that many of these drugs showed poly-pharmacological profile by targeting many other receptors and/or transporters besides the D2 and P08908 receptors . In this regard , ' pure ' compounds exclusively acting on the D2 and P08908 receptors are highly needed to further validate this approach . Meanwhile , safety concerns and in vivo pharmacokinetic alerts should also be implanted to the drug design art early . Determination of fenofibric acid concentrations by HPLC after anion exchange solid-phase extraction from human serum . Triglycerides are increasingly being recognized as a risk factor for cardiovascular disease . Research efforts to identify sources of variability in triglyceride-lowering response to the lipid-lowering drug fenofibrate require quantification of the active acidic form of this Q07869 agonist . Anion-exchange solid-phase extraction , in combination with reverse-phase high-performance liquid chromatography ( HPLC ) , rapidly and accurately determines steady-state fenofibric acid serum concentrations . Chromatographic separation under isocratic conditions , with use of ultraviolet detection at 285 nm , provides clean baseline and sharp peaks for clofibric acid , 1-napthyl acetic acid ( internal standards ) , and fenofibric acid . Commonly prescribed and over-the-counter nonsteroidal anti-inflammatory drugs ( NSAIDs ) were screened for assay interference , and the assay was employed to quantify fenofibric acid in more than 800 human subject specimens . DB01039 analysis was found to be linear over the range of 0.5 to 40 mg/L and was validated with either internal standard . Accuracies ranged from 98.65 % to 102.4 % , whereas the within- and between-day precisions ranged from 1.0 % to 2.2 % and 2.0 % to 6.2 % , respectively . NSAIDs had minimal interference with the assay , which succeeded in quantifying fenofibric acid in more than 843 of 846 serum samples from human subjects , many taking a variety of coadministered medications . Anion-exchange solid-phase extraction in combination with reverse-phase HPLC accurately determines steady-state fenofibric acid serum concentrations in humans without interference from NSAIDs or commonly administered medications . This method is suitable for quantification of fenofibric acid for clinical pharmacokinetic studies in patients with dyslipidemia . [ Chemotherapy for breast cancer refractory to anthracycline , taxane or trastuzumab ] . Anthracycline , taxane or trastuzumab play a central role in systemic chemotherapy for breast cancer . The standard of subsequent treatment is capecitabine , S-1 , vinorelbine , irinotecan or gemcitabine . DB04845 or nanoparticle paclitaxel is effective for taxane-resistant breast cancer . DB01259 proves effective for trastuzumab-resistant P04626 -overexpressing breast cancer and also for brain metastasis . DB05773 , pertuzumab and neratinib are promising drugs . In terms of antiangiogenic agents , bevacizumab in combination with taxane demonstrates efficacy . DB06626 , sunitinib or pazopanib is under investigation . It is necessary to study the best manner of sequence and combination in these drugs . The design and development of pegfilgrastim ( PEG-rmetHuG- P04141 , Neulasta ) . Recombinant protein technology produces drugs for human therapy in unprecedented quantity and quality . Research is now focusing on the relationship between pharmacokinetic and pharmacodynamic properties of molecules , with the aim of engineering proteins that possess enhanced therapeutic characteristics in contrast to being used as simple replacements for the natural equivalent . The addition of a polyethylene glycol ( PEG ) moiety to filgrastim ( rmetHu- DB00099 , Neupogen ) resulted in the development of pegfilgrastim . DB00019 is a long-acting form of filgrastim that requires only once-per-cycle administration for the management of chemotherapy-induced neutropenia . The covalent attachment of PEG to the N-terminal amine group of the parent molecule was attained using site-directed reductive alkylation . Pegylation increases the size of filgrastim so that it becomes too large for renal clearance . Consequently , neutrophil-mediated clearance predominates in elimination of the drug . This extends the median serum half-life of pegfilgrastim to 42 hours , compared with between 3.5 and 3.8 hours for DB00099 , though in fact the half-life is variable , depending on the absolute neutrophil count , which in turn reflects of the ability of pegfilgrastim to sustain production of those same cells . The clearance of the molecule is thus dominated by a self-regulating mechanism . DB00019 retains the same biological activity as filgrastim , and binds to the same Q99062 , stimulating the proliferation , differentiation and activation of neutrophils . Once-per-chemotherapy cycle administration of pegfilgrastim reduces the duration of severe neutropenia as effectively as daily treatment with filgrastim . In clinical trials , patients receiving pegfilgrastim also had a lower observed incidence of febrile neutropenia than patients receiving filgrastim . Q14703 lyase in thymic perivascular spaces promotes egress of mature thymocytes via up-regulation of P21453 . DB03203 1-phosphate ( Q14703 ) and P21453 ( P21453 ) play an important role in the egress of mature P01730 or CD8 single-positive ( SP ) thymocytes from the thymus . DB08868 hydrochloride ( FTY720 ) , an P21453 functional antagonist , induced significant accumulation of CD62L(high) Q07108 (low) mature SP thymocytes in the thymic medulla . Immunohistochemical staining using anti- P21453 antibody revealed that P21453 is predominantly expressed on thymocytes in the thymic medulla and is strongly down-regulated even at 3h after FTY720 administration . 2-Acetyl-4-tetrahydroxybutylimidazole ( THI ) , an Q14703 lyase inhibitor , also induced accumulation of mature SP thymocytes in the thymic medulla with an enlargement of the perivascular spaces ( P15151 ) . At 6h after THI administration , P21453 -expressing thymocytes reduced partially as if to form clusters and hardly existed in the proximity of CD31-expressing blood vessels in the thymic medulla , suggesting Q14703 lyase expression in the cells constructing thymic medullary P15151 . To determine the cells expressing Q14703 lyase in the thymus , we newly established a mAb ( YK19-2 ) specific for mouse Q14703 lyase . Immunohistochemical staining with YK19-2 revealed that Q14703 lyase is predominantly expressed in non-lymphoid thymic stromal cells in the thymic medulla . In the thymic medullary P15151 , Q14703 lyase was expressed in ER-TR7-positive cells ( reticular fibroblasts and pericytes ) and CD31-positive vascular endothelial cells . Our findings suggest that Q14703 lyase expressed in the thymic medullary P15151 keeps the tissue Q14703 concentration low around the vessels and promotes thymic egress via up-regulation of P21453 . MicroRNA-155 modulates Treg and Th17 cells differentiation and Th17 cell function by targeting O15524 . MicroRNA ( miR ) -155 is a critical player in both innate and adaptive immune responses . It can influence P01730 (+) T cell lineage choice . To clarify the role of miR-155 in P01730 (+) CD25(+) regulatory T ( Treg ) /T helper (Th)17 cell differentiation and function , as well as the mechanism involved , we performed gain-and loss-of-function analysis by transfection pre-miR-155 and anti-miR-155 into purified P01730 (+) T cells . The results showed that miR-155 positively regulated both Treg and Th17 cell differentiation . It also induced the release of interleukin ( IL ) -17A by Th17 cells , but not the release of P22301 and transforming growth factor ( TGF ) -β1 by Treg cells . Furthermore , we found that miR-155 reacted through regulating Janus kinase/signal transducer and activator of transcription ( JAK/ P35610 ) rather than TGF-β/mothers against decapentaplegic homolog ( SMAD ) signaling pathway in the process of Treg and Th17 cells differentiation . This may because suppressors of cytokine signaling ( Q9NSE2 )1 , the important negative regulator of JAK/ P35610 signaling pathway , was the direct target of miR-155 in this process , but Q15796 and Q99717 were not . Therefore , we demonstrated that miR-155 enhanced Treg and Th17 cells differentiation and Q16552 production by targeting O15524 . Elevation of P13500 and P13500 / P15692 ratio in cerebrospinal fluid of amyotrophic lateral sclerosis patients . Amyotrophic lateral sclerosis ( P35858 ) is a neurodegenerative disease with progressive cell death of upper and lower motor neurons . In this study , we measured monocyte chemotactic protein-1 ( P13500 ) and vascular endothelial growth factor ( P15692 ) levels in cerebrospinal fluid ( P04141 ) and serum by enzyme-linked immunosorbent assay ( ELISA ) in 42 P35858 patients , and compared these levels with those of control subjects with other neurodegenerative disorders or with those of normal controls . P13500 levels in P04141 were significantly higher in P35858 patients than in the control group . P15692 levels in P04141 tended to be lower in P35858 patients than in the control group , but not significantly . A positive correlation was found between P13500 levels in P04141 of P35858 patients and the total Norris scale . The elevation of P13500 / P15692 ratio in P04141 was more specific to P35858 patients compared to other neurological diseases such as Parkinson 's disease ( PD ) and spinocerebellar ataxia ( SCA ) and to controls . Our data suggested that both P13500 levels and P13500 / P15692 ratio in P04141 may be useful markers for the clinical diagnosis of P35858 . Distribution of polyamines and their biosynthetic enzymes in intestinal adaptation . P11926 ( ODC ) and the polyamines have been shown to be important for growth processes in the intestinal mucosa . The highest activity of ODC is found in the differentiated , nonproliferating villus-tip cells rather than in the rapidly proliferating undifferentiated crypt cells . During poststarvation refeeding and lactation , we now show that increases in ODC activity paralleled the time course of mucosal hyperplasia and thymidine incorporation . Increases in ODC ( threefold ) were similar in villus and crypt cells , and the villus-crypt gradient of decreasing ODC activity ( 40:1 ) was maintained . The activity of the other polyamine biosynthetic enzyme , S-adenosylmethionine decarboxylase ( P18827 ) , was highest in the crypt cells in the basal state and increased throughout the entire villus-crypt axis during refeeding and lactation , preserving a villus-crypt gradient opposite to that of ODC . During hyperplasia , all three polyamines increased . DB01917 was highest in the villus-tip cells , paralleling ODC activity , whereas spermidine and spermine were highest in the crypt cells and paralleled the distribution of P18827 activity . Thus P18827 activity and spermidine and spermine content may play a more important role than ODC and putrescine in regulation of intestinal mucosal proliferation . It is also possible that the threefold increases in the low levels of ODC in the crypt cells are adequate to trigger cell proliferation , whereas the higher ODC levels in villus cells may represent an association with the differentiation of the enterocytes . Analysis of polymorphism in renin angiotensin system and other related genes in South Indian chronic kidney disease patients . BACKGROUND : Several P00797 Angiotensin System ( DB01367 ) polymorphisms alter the homeostasis to an abnormal state . Similarly , other genes such as O60500 ( O60500 ) and Q9NP85 ( Q9NP85 ) contribute to the loss of renal function during renal diseases . In Indian population , studies in DB01367 and other renal specific gene polymorphisms in Chronic Kidney Disease ( CKD ) patients are scanty . METHODS : We examined 118 CKD patients and 98 control subjects for the occurrence of common polymorphisms in angiotensin converting enzyme insertion/deletion ( P12821 ; I/D ) , angiotensinogen ( AGT ; M235T ) , chymase ( CMA ; -1903G > A ) , angiotensin receptor type-1 ( P30556 -1166A > C ) , methylene DB00116 reductase ( P42898 ; 677C > T ) , nephrin ( O60500 ; R1160X ) and podocin ( Q9NP85 ; R291W and R229Q ) . RESULT : Significant association was observed in AGT-M235T polymorphism between CKD patients and controls . The frequency of TT genotype was higher in CKD patients when compared with controls ( 0.39 vs. 0.14 ; chi(2)=20.3 , P < 0.001 ) . P12821 -DD genotype showed a higher level of systolic pressure with a median of 166 mmHg ( P < 0.05 ) when compared to II and ID genotypes . Two heterozygous conditions of Q9NP85 -R229Q polymorphism were found among 105 CKD patients . No significant associations were found in genotype frequencies in other above polymorphisms between CKD patients and controls . CONCLUSION : Asian Indian population with AGT-TT genotypes may have a higher relative risk towards CKD with odds ratio ( OR ) 3.98 ( 95 % CI=1.92-8.25 ; P=0.0002 ) . Q15796 / P84022 in endothelium is indispensable for vascular stability via P21453 and P19022 expressions . Transforming growth factor-β ( TGF-β ) is involved in vascular formation through activin receptor-like kinase ( Q9UM73 )1 and P36897 . P36897 , which is expressed ubiquitously , phosphorylates Q15796 and P84022 , whereas endothelial cell ( EC ) -specific P37023 activates Q15797 and Q99717 . Because P36897 kinase activity is required for P37023 to transduce TGF-β signaling via Q15797 /5 in ECs , P36897 knockout ( KO ) mice were not able to give us the precise mechanisms by which TGF-β/ P36897 / Q15796 /3 signaling is implicated in angiogenesis . To delineate the role of Q15796 /3 signaling in endothelium , the Q15796 gene in P84022 KO mice was selectively deleted in ECs using Tie2-Cre transgenic mice , termed EC-specific Q15796 /3 double KO ( EC- Q15796 /3KO ) mice . EC- Q15796 /3KO embryos revealed hemorrhage leading to embryonic lethality around Q96BH3 .5 . EC- Q15796 /3KO embryos exhibited no abnormality of vasculogenesis and angiogenesis in both the yolk sac and the whole embryo , whereas vascular maturation was incomplete because of inadequate assembly of mural cells in the vasculature . Wide gaps between ECs and mural cells could be observed in the vasculature of EC- Q15796 /3KO mice because of reduced expression of P19022 and sphingosine-1-phosphate receptor-1 ( P21453 ) in ECs from those mice . These results indicated that Q15796 /3 signaling in ECs is indispensable for maintenance of vascular integrity via the fine-tuning of P19022 , P33151 , and P21453 expressions in the vasculature . Targeting eIF4GI translation initiation factor affords an attractive therapeutic strategy in multiple myeloma . BACKGROUND : Deregulation of protein synthesis is integral to the malignant phenotype and translation initiation is the rate limiting stage . Therefore , eIF4F translation initiation complex components are attractive therapeutic targets . METHODS : Protein lysates of myeloma cells ( cell lines/patients ' bone marrow samples ) untreated/treated with bevacizumab were assayed for eIF4GI expression , regulation ( P15559 /proteosome dependent fragmentation ) ( WB , DB00266 , qPCR ) and targets (WB). eIF4GI was inhibited by knockdown and 4EGI-1 . Cells were tested for viability ( ELISA ) , death ( FACS ) and eIF4GI targets ( WB ) . RESULTS : Previously , we have shown that manipulation of P15692 in myeloma cells attenuated P06730 dependent translation initiation . Here we assessed the significance of eIF4GI to MM cells . We demonstrated increased expression of eIF4GI in myeloma cells and its attenuation upon P15692 inhibition attributed to elevated P15559 /proteasome dependent fragmentation and diminished mRNA levels . Knockdown of eIF4GI was deleterious to myeloma cells phenotype and expression of specific molecular targets ( Q99717 /ERα/HIF1α/c-Myc ) . Finally , we showed that the small molecule 4EGI-1 inhibits eIF4GI and causes a reduction in expression of its molecular targets in myeloma . CONCLUSION : Our findings substantiate that translation initiation of particular targets in MM is contingent on the function of eIF4GI , critical to cell phenotype , and mark it as a viable target for pharmacological intervention . Peroxisome proliferator-activated receptor-gamma agonists increase vascular endothelial growth factor expression in human vascular smooth muscle cells . Vascular endothelial growth factor ( P15692 ) , expressed in a variety of mesenchymal cells including vascular smooth muscle cells ( VSMC ) , is a potent mitogen for endothelial cells , and is used clinically applied for ischemic disease of peripheral vessels . To determine whether peroxisome proliferator-activated receptor gamma ( PPARgamma ) regulates P15692 production in VSMC , we examined P15692 secretion from VSMC treated with Q07869 agonists . DB00197 increased P15692 secretion in a time- and dose-dependent manner ( 261 +/- 35 % with 25 mM of troglitazone for 24 h ) , and also increased levels of P15692 mRNA . P15692 secretion was also increased by other PPARgamma agonists , pioglitazone , LY171883 , and 15d-PGJ2 ( 224 +/- 17.1 % , 247 +/- 36.8 % and 171 +/- 7.8 % , respectively ) , but not the PPARgamma agonists bezafibrate and Wy14643 ( 85.2 +/- 1.5 % , 94.6 +/- 3.2 , respectively ) . Our findings suggest that thiazolidinediones might be useful for the therapeutic angiogenesis for ischemic artery disease . DB08868 : direct CNS effects of sphingosine 1-phosphate ( Q14703 ) receptor modulation and implications in multiple sclerosis therapy . DB08868 is the first oral disease-modifying therapy approved for relapsing forms of multiple sclerosis ( MS ) . Following phosphorylation in vivo , the active agent , fingolimod phosphate ( fingolimod-P ) , acts as a sphingosine 1-phosphate ( Q14703 ) receptor modulator , binding with high affinity to four of the five known Q14703 receptors ( P21453 , Q99500 , O95977 and Q9H228 ) . The mechanism of action of fingolimod in MS has primarily been considered as immunomodulatory , whereby fingolimod-P modulates P21453 on lymphocytes , selectively retaining autoreactive lymphocytes in lymph nodes to reduce damaging infiltration into the central nervous system ( CNS ) . However , emerging evidence indicates that fingolimod has direct effects in the CNS in MS . For example , in the MS animal model of experimental autoimmune encephalomyelitis ( EAE ) , fingolimod is highly efficacious in both a prophylactic and therapeutic setting , yet becomes ineffective in animals selectively deficient for P21453 on astrocytes , despite maintained normal immunologic receptor expression and functions , and Q14703 -mediated immune activities . Here we review Q14703 signaling effects relevant to MS in neural cell types expressing Q14703 receptors , including astrocytes , oligodendrocytes , neurons , microglia and dendritic cells . The direct effects of fingolimod on these CNS cells observed in preclinical studies are discussed in view of the functional consequences of reducing neurodegenerative processes and promoting myelin preservation and repair . The therapeutic implications of Q14703 modulation in the CNS are considered in terms of the clinical outcomes of MS , such as reducing MS-related brain atrophy , and other CNS disorders . Additionally , we briefly outline other existing and investigational MS therapies that may also have effects in the CNS . A multi-analyte assay for the non-invasive detection of bladder cancer . Accurate urinary assays for bladder cancer ( BCa ) detection would benefit both patients and healthcare systems . Through genomic and proteomic profiling of urine components , we have previously identified a panel of biomarkers that can outperform current urine-based biomarkers for the non-invasive detection of BCa . Herein , we report the diagnostic utility of various multivariate combinations of these biomarkers . We performed a case-controlled validation study in which voided urines from 127 patients ( 64 tumor bearing subjects ) were analyzed . The urinary concentrations of 14 biomarkers ( P10145 , P14780 , P09238 , P18827 , P55774 , P05121 , P16070 , P15692 , P03950 , Q16790 , A1AT , P10451 , PTX3 , and P02649 ) were assessed by enzyme-linked immunosorbent assay ( ELISA ) . Diagnostic performance of each biomarker and multivariate models were compared using receiver operating characteristic curves and the chi-square test . An 8-biomarker model achieved the most accurate BCa diagnosis ( sensitivity 92 % , specificity 97 % ) , but a combination of 3 of the 8 biomarkers ( P10145 , P15692 , and P02649 ) was also highly accurate ( sensitivity 90 % , specificity 97 % ) . For comparison , the commercial BTA-Trak ELISA test achieved a sensitivity of 79 % and a specificity of 83 % , and voided urine cytology detected only 33 % of BCa cases in the same cohort . These data show that a multivariate urine-based assay can markedly improve the accuracy of non-invasive BCa detection . Further validation studies are under way to investigate the clinical utility of this panel of biomarkers for BCa diagnosis and disease monitoring . Immunohistochemical studies of the epididymal duct in Egyptian water buffalo ( Bubalus bubalis ) . Using immunohistochemistry ( IHC ) , this study aimed to evaluate the regional distribution pattern of some biologically active proteins in the epididymis of Egyptian water buffalo and to determine the structural-functional relationships of the different epididymal structures . Wax-embedded sections from different regions of the epididymal duct from adult , clinically healthy , buffalo bulls were used . Primary antibodies against angiotensin converting enzyme ( P12821 ) , S-100 , galactosyltransferase ( GalTase ) , alpha smooth muscle actin ( α-SMA ) , connexin 43 ( P17302 ) and vascular endothelial growth factor ( P15692 ) were used for immunohistochemical studies . The results showed that , in addition to the well-known principal and basal cells , the epididymal epithelium , similar to that of other species , possessed apical cells and intraepithelial leukocytes . IHC showed that , with the exception of P15692 which reacted negatively , all antibodies used displayed variable reactivity in the different epididymal structures . Apical cells expressed a strong reaction with P12821 along the entire length of the duct . The principal cells in the caput epididymis exhibited a distinct reactivity with S-100 and GalTase . The peritubular muscular coat displayed a marked immunostaining for α-SMA and for P17302 . In conclusion these findings showed a regional-specific distribution pattern , distinct from that in bovine bulls . Some potential functional capacities , especially absorptive and secretory ones , are discussed in relation to the different epididymal regions .