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Rapid and complete withdrawal of intratesticular testosterone was achieved via the destruction of all Leydig cells with the specific Leydig cell cytotoxin ethane dimethanesulphonate (EDS). Restoration of testosterone levels was accomplished by administration of a single dose (25 mg) of testosterone esters (T) known to reverse the antispermatogenic effects of androgen withdrawal. Quantitation of the degenerating germ cells in cross sections of seminiferous tubules (ST) at stages IV-V, VII, IX, and X-XI of the spermatogenic cycle was used as a sensitive biological index of the effects of testosterone withdrawal and restoration upon the function of the Sertoli cells. Compared to control testicular tissues, the mean numbers of pyknotic germ cells per ST cross section at stages VII, IX and X-XI increased significantly (P < 0.01-0.001) between 4 to 8 days post-EDS treatment, but only in stage VII tubules was this trend reversed significantly (P < 0.005) within 2 days by T supplementation. In EDS-treated rats, stages VII, VIII, IX, and X-XI also exhibited significant (P < 0.05-0.001) increases (compared to controls) in the volumetric proportions by which intraepithelial vacuoles appeared within the seminiferous tubules. Again, in EDS+T supplemented rats, the appearance of vacuoles was significantly (P < 0.001) suppressed in stage VII and VIII. In contrast to tubules at stages VII-XI, those at stages IV-V were completely unaffected by testosterone withdrawal or replacement. The results show that at selected time intervals after EDS treatment, testosterone supplementation is capable of preventing/reversing these morphological changes within 2 days in stage VII tubules. It is suggested that the induction and subsequent prevention of seminiferous epithelial damage will serve as an important in vivo and in vitro approach for studies on the androgen-mediated changes in Sertoli cell biology during phases of impairment and recovery of their function. Manipulation of adult Sertoli cell function as provided by our model should permit identification of androgen-regulated gene products together with an understanding of their role(s) in normal and abnormal spermatogenesis.
Anat Rec 1993 Apr
PMID:Stage-dependent changes in spermatogenesis and Sertoli cells in relation to the onset of spermatogenic failure following withdrawal of testosterone. 838 23

The male prairie dog (Cynomys ludovicianus) is an annual breeder with complete testicular regression between breeding periods. Knowledge of the seminiferous tubule cycle stages at all phases of the annual cycle is essential for evaluation of testicular effects of endogenous and exogenous hormones. Testis tubule diameter is directly correlated with testicular weight during the annual cycle. Seminiferous tubule stages found during testicular activity start with sperm release and round spermatids in the Golgi stage (I). Then they progress through the cap and acrosome stages (stages II to VI) until elongate spermatids are formed. During these stages preleptotene, leptotene and zygotene cells develop into pachytene cells which mature with the long spermatids (stage VII). Two distinct tubule associations (stages VIII, IX) follow during which the first and second meiotic metaphases occur. These stages are correlated with the middle and late phases of residual lobe retraction and condensation. The last stage (X) has final sperm development and is present with round spermatids that have no Golgi development. During regression changes are initially associated with the seminiferous tubule stages of active testes and end with relocation of Sertoli cell nuclei to a position above the basal layer of spermatogonia. Out of season testes are characterized by few spermatogonial mitoses and absence of viable spermatocytes. In recrudescent testes, Sertoli cell nuclei again become basal, spermatogonia resume mitoses and spermatocytes and spermatids progressively develop. After each cycle of proliferation of germ cells there is sloughing of the most differentiated spermatocytes and spermatids until the final tubule associations of the active testis are present.
Anat Rec 1997 03
PMID:Seminiferous tubule stages in the prairie dog (Cynomys ludovicianus) during the annual breeding cycle. 906 13

Since we had subdivided the cell cycle into 11 stages--four for mitosis and seven for the interphase--and since we had experience in detecting DNA in the electron microscope (EN) by the osmium-amine procedure of Cogliati and Gauthier (Compt. Rend. Acad. Sci., 1973;276:3041-3044), we combined the two approaches for the analysis of DNA-containing structures at all stages of the cell cycle. Thin Epon sections of formaldehyde-fixed mouse duodenum were stained by osmium-amine for electron microscopic examination of the stages in the 12.3-hr long cell cycle of mouse duodenal crypt columnar cells. In addition, semi-thin Lowicryl sections of mouse duodenal crypts and cultured rat kidney cells were stained with the DNA-specific Hoechst 33258 dye and examined in the fluorescence microscope. The DNA detected by osmium-amine is in the form of nucleofilaments, seen at high magnification as long rows of 11 nm-wide rings (consisting of stained DNA encircling unstained histones). At all stages of the cycle as well as in nondividing cells, nucleofilaments are of three types: 'free,' 'attached' to chromatin accumulations, and 'compacted' in all chromatin accumulations, the form of dense spirals within. At stage I of the cycle, besides free and attached nucleofilaments, compacted ones are observed in the three heterochromatin forms (peripheral, nucleolus-associated, clumped). Soon after the S phase begins, chromatin 'aggregates' appear, which are small at stage II, mid-sized at stage III, and large at stage IV. Chromatin 'bulges' also appear at stage III and enlarge at stage IV, while heterochromatins disappear. At stage V, aggregates and bulges accrete into 'chromomeres,' a process responsible for the apparent chromosome condensation observed at prophase. The chromomeres gradually line up in rows and, at stage VIa (prometaphase), approach one another within each row and coalesce to build up the metaphase chromosomes which are fully formed at stage VIb (metaphase). Daughter chromosomes arising at stage VII (anaphase) are eventually packed into a chromosomal mass at each pole of the cell. During stage VIII (telophase), the chromosomal mass is split into large chunks. In the course of the G1 phase, the chunks thin out to give rise to irregular 'bands' at stage IX, the bands are then cleaved into central and peripheral fragments at stage X, and finally the central fragments are replaced by free nucleofilaments and clumps at stage XI, while the peripheral fragments are replaced by peripheral heterochromatin. The "nucleoli" at stages I-III are associated with stained heterochromatin but otherwise appear as unstained lucent areas, except for weakly stained patches composed of histone-free DNA filaments. During stage IV, nucleoli lose patches and associated heterochromatin, while weakly lucent, pale vesicles appear within nucleoli and in the nucleoplasm. By the end of substage VIa, nucleoli generally disappear, while pale vesicles persist around the chromosomes appearing at substage VIb. At stages VIII and IX, the vesicles seem to become strongly lucent and, at stages IX and X, they associate and fuse to yield homogeneous lucent areas, the 'prenucleolar bodies,' which include histone-free DNA patches. During stage XI, groups of these bodies associate to give rise to nucleoli. In conclusion, the cell cycle DNA changes can be classified into 4 broad periods (Fig. 6): 1) Stage I is a 2-hr long interphase "pause," during which the stained DNA shows no signs of either chromosome condensation or decondensation, while the overall nuclear pattern is similar to that in nondividing cell nuclei. Nucleoli are fully developed. 2) From stage II to VIa, the "chromosome condensation" period extends over about 7 hr, during which the events are interpreted as follows. Throughout the S phase (stages II-IV), newly-synthesized segments of nucleofilaments approach one another, adhere and thus build aggregates and later bulges on nuclear matrix sites. (ABSTRACT TRUNCATED)
Anat Rec 1998 11
PMID:The eleven stages of the cell cycle, with emphasis on the changes in chromosomes and nucleoli during interphase and mitosis. 981 Dec 21

A two-month-old Appaloosa colt developed neurological signs shortly after birth involving deficits affecting cranial nerves IV, VII, VIII, IX, X and XII, and possibly nerve VI. The most likely differential diagnoses were congenital anomalies, meningoencephalitides, trauma or nutritional causes. The foal was investigated by the analysis of cerebrospinal fluid (CSF), electromyelography (EMG), brain auditory evoked responses, magnetic resonance imaging (MRI), peripheral nerve biopsy, and Western blot analysis for the presence of intrathecal antibodies to Sarcocystis neurona, the causative agent of equine protozoal myeloencephalitis. Significantly abnormal EMG findings included spontaneous electrical activity of the tongue, suggesting denervation. The MRI was useful in ruling out masses, congenital anomalies and focal abscessation. The cytology of CSF revealed mild mononuclear reactivity. Western blot testing of CSF was positive, indicating the intrathecal presence of antibodies to S neurona. The foal was treated with pyrimethamine and trimethoprim-sulphadiazine for two months and returned to nearly normal neurologic status.
Vet Rec 2001 Sep 01
PMID:Suspected protozoal myeloencephalitis in a two-month-old colt. 1155 62

Double-fluorescence staining was combined with confocal laser scanning microscopy to localize fetal liver kinase-1 (Flk-1) and fms-like tyrosine kinase-1 (Flt-1) in the neonatal rat brain. The results showed that Flk-1 and Flt-1 immunostaining was observed in the cells with neuron-specific enolase, a neuronal marker, and with factor VIII (F VIII), an endothelium marker, but not in cells with glial fibrillary acidic protein (GFAP), a glial marker, of brain sections from rats on postnatal day 7 (P7). This indicates that both vascular endothelial growth factor (VEGF) receptors were distributed in the neurons and the vascular endothelium. A regional analysis showed that Flt-1 was distributed most densely in the hippocampus, followed by the retrosplenial agranular cortex and the striatum, and Flk-1 was evenly distributed throughout the brain. In a comparison of the density of immunopositive staining neurons, Flt-1 was much higher than Flk-1 in most of the brain regions. A time-course analysis showed that both Flt-1 and Flk-1 were highly expressed in the cerebral vessel of rats on P1, P7, and P14, and then declined in adults, consistent with the development of angiogenesis in neonates. In the neurons, Flt-1 was highest in the cerebral cortex and hippocampus of P1-P14 rats, and then gradually decreased, whereas Flk-1 abruptly increased and reached its highest level in adults. The results suggest that Flt-1 and Flk-1 are expressed in the neurons with their individual time-dependent manners and regional distribution in the brain. However, the significance of the neuronal distribution of Flt-1 and Flk-1 remains to be determined.
Anat Rec A Discov Mol Cell Evol Biol 2003 Sep
PMID:Distribution of Flk-1 and Flt-1 receptors in neonatal and adult rat brains. 1292 95

Venous thromboembolic disease is a major cause of morbidity and mortality, necessitating antithrombotic therapy. A human monoclonal anti-factor (F)VIII antibody, LCL-mAb-LE2E9, produced by a lymphoblastoid cell line derived from a hemophilia A patient with inhibitor to wild-type but not mutant self FVIII, was previously reported to achieve efficient inhibition of thrombosis in an experimental vena cava thrombosis model in mice. Here, the antithrombotic efficacy of a recombinant DNA-derived version of this anti-FVIII antibody (rec-mAb-LE2E9) was tested in mice which carry a type II heparin binding site antithrombin deficiency mutation and display spontaneous chronic thrombosis in several sites including the penile vein of sexually active males. The recombinant anti-FVIII antibody (100 microg, repeated after 3 days) prevented thrombotic priapism in all treated males, whereas all control animals treated with saline (group of four animals) developed priapism within 6 days after mating (P < 0.05 for treated vs. saline). The rec-mAb-LE2E9 and the original LCL-mAb-LE2E9 were equally effective (five and seven males/group, respectively). These results confirm that FVIII inhibition represents a potent antithrombotic strategy, and show that both LCL-mAb-LE2E9 and rec-mAb-LE2E9 efficiently prevent thrombosis in a physiological model representative of thrombosis in patients with a severe prothrombotic risk.
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PMID:Inhibition of factor VIII with a partially inhibitory human recombinant monoclonal antibody prevents thrombotic events in a transgenic model of type II HBS antithrombin deficiency in mice. 1471 70

We evaluated the relationship among proliferation, death and migration of granule cells in lobules VI-VIII of vermis, in comparison with lobule III, during cerebellar development. To this aim, a single injection of cisplatin, i.e., a cytostatic agent that is known to induce death of proliferating granule cells, was given to 10-day-old rats. Histochemical markers of proliferating (PCNA immunoreaction) and apoptotic (TUNEL staining) cells were used; the variations of the external granular layer (EGL) thickness were evaluated in parallel. After PCNA and TUNEL reactions, evident changes of the whole EGL were found on PD11 (1 day after treatment), when a reduction of the thickness of this layer was found in treated rats, mainly in consequence of the high number of apoptotic cells in all the cerebellar lobules. On PD17 (7 days after treatment), a thick layer of proliferating cells was observed in lobules VI-VIII of treated rats, while the peculiar pattern of the normal development showed a thin EGL. At the same time, in treated rats, the number of apoptotic cells in EGL was low. In all developmental stages of treated rats, after GFAP immunoreaction, glial fibers appeared twisted, thickened, and with an irregular course; intensely labeled end-feet were present. The damage of radial glia suggests an alteration of migratory processes of granule cells, which is also evidenced by the decreased thickness of the premigratory zone of the EGL. Injured radial glia fibers were restricted to lobules VI-VIII and they persisted at PD30, leading to the presence of ectopic granule cells in the molecular layer, as we previously described.
Anat Rec A Discov Mol Cell Evol Biol 2005 Dec
PMID:Proliferation and migration of granule cells in the developing rat cerebellum: cisplatin effects. 1624 1

Our previous studies suggested that a direct hippocampo-cerebellar projection might exist in the chicken. To confirm such a presumption of hippocampo-cerebellar interactions, horseradish peroxidase (HRP) was used as a retrograde tracer to be injected into the white matter of the folia VI-VIII of the cerebellum in young and adult chickens. In another set of experiments, young chickens were subjected to electrolytic lesions of the hippocampal formation (HF), especially the ventromedial portion, and the cerebellum was observed with the electron microscope to find neuronal degeneration in the HF. Following injections of HRP into the cerebellum, a large number of labeled neurons were found in the area APHm-APHim of the HF in the young and adult chickens. As a result of the electrolytic lesions of the APHm-APHim in the HF, many large degenerated nerve fibers were found in the white matter in the vicinity of the lateral nucleus of the cerebellum, and some small degenerated fibers were found in the white matter of the folia VI-VIII. In the cerebellar cortex of folia VI-VIII, degenerated axonal terminals occurred in both the molecular and Purkinje layers, but not in the granular layer. In the lateral nucleus, some dark degenerating axonal terminals were recognized to connect with the perikarya of neurons of this nucleus. The present experiments demonstrate that the APHm-APHim of the HF directly projected to the cortex of folia VI-VIII and the lateral nucleus of the cerebellum in young chickens.
Anat Rec (Hoboken) 2012 Aug
PMID:A direct hippocampo-cerebellar projection in chicken. 2269 31

In the mammalian ovary both gonadotropins and local cytokines, acting through G-protein coupled receptors, govern the physiology of the ovary in part by regulating the cyclic adenosine 3',5'-monophosphate via adenylyl cyclases. The nine transmembrane adenylyl cyclases and a soluble adenylyl cyclase are regulated by a diversity of ligands. In this study we have examined the rat ovaries, prior to and subsequent to gonadotropin treatment, for the presence of different transmembrane adenylyl cyclases by indirect immunofluorescence microscopy. Adenylyl cyclase I immunoreactivity was observed in the nuclei of oocytes in preantral and antral follicles along with some staining in granulosa cells. Equine chorionic gonadotropin injection increased adenylyl cyclase I staining in granulosa cells. Adenylyl cyclase I staining was also observed in luteal and endothelial cells. Adenylyl cyclase II was observed throughout the ovary, including granulosa cells and the ovarian surface epithelium. Adenylyl cyclase II staining was also found to increase in granulosa cells after equine chorionic gonadotropin injection. Adenylyl cyclase III was distributed primarily in theca and smooth muscle cells of arterioles, with faint staining in the oocytes of equine chorionic gonadotropin-injected ovaries. Adenylyl cyclase IV staining was present throughout the ovary, including the nuclei of oocytes. Adenylyl cyclase VIII staining in granulosa cells increased subsequent to equine chorionic gonadotropin injection and remained in luteal cells. Our study reveals the redundancy of adenylyl cyclases present in the rat ovary and, therefore, implies potential regulation of follicular and corpus luteum physiology by cyclic adenosine 3',5'-monophosphate generated through distinct adenylyl cyclases.
Anat Rec (Hoboken) 2012 Oct
PMID:Distribution of adenylyl cyclases in the rat ovary by immunofluorescence microscopy. 2289 45

This review covers the design, structure, and function of auditory brainstem implants. Auditory brainstem implants (ABIs) are auditory prostheses initially designed to treat deafness in patients with neurofibromatosis type 2 (NF2). NF2 typically results in deafness due to disruption of the cochlear nerves. When the tumors are removed the auditory nerve is usually cut or nonfunctional anymore. In these cases, patients cannot benefit from peripheral devices such as cochlear implants (CI). Another cause of VIII nerve loss is bilateral temporal bone fracture. Worldwide, more than 500 persons have received an ABI after removal of the tumors that occur with NF2. More recently, some extensions of indications have been proposed to include subjects who would not benefit enough from a cochlear implant (i.e. cochlear ossification). The ABI is similar in design and function to a CI, except that the electrode is placed on the first auditory relay station in the brainstem, the cochlear nucleus (CN). The ABI electrode array is a small paddle that contains plate electrode contacts. The CN has not a single linear tonotopic organization from base to apex like the cochlea but different tonotopic subunits. The CN comprises multiple neuron types that are characterized by specific properties (morphology, regional distribution and cell-membrane characteristics), synaptic input and responses to acoustic stimuli. As the ABI electrode array is placed along the surface of the CN, each electrode likely activates a variety of neuron types, possibly with different characteristic frequencies. Patients undergoing ABI have variable benefit with regard to sound and speech comprehension. For the majority of patients, this improvement is essentially obtained by an augmentation of lip reading performances. Speech comprehension without lip-reading is not as good as with cochlear implants.
Anat Rec (Hoboken) 2012 Nov
PMID:Auditory brainstem implants: how do they work? 2304 1


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