Dendritic cells cross-talk with tumour antigen-specific CD8+ T cells, Vγ9γδT cells and Vα24NKT cells in patients with glioblastoma multiforme and in healthy donors.

The finding that dendritic cells (DCs) orchestrate innate and adaptive immune responses has stimulated research on harnessing DCs for developing more effective vaccines for DC therapy. The expression of cytomegalovirus (CMV) antigens in glioblastoma multiforme (GBM) presents a unique opportunity to target these viral proteins for tumour immunotherapy. Here, we demonstrate that Vγ9γδT cells, innate immune cells activated by zoledronate (Z) and Vα24 natural killer (Vα24NK) cells, innate/adaptive immune cells activated by α-galactosylceramide (G) can link innate and adaptive immunities through cross-talk with interferon (IFN) DCs from patients with glioblastoma multiforme (GBM) and healthy donors in a manner that can amplify the activation and proliferation of CMVpp65-specific CD8+ T cells. The IFN DCs derived from patients with GBM used in this study express lower levels of programmed cell death ligand (PD)-L1 and PD-L2 and higher levels of C-C receptor 7 (CCR7) than the most commonly used mature interleukin (IL)-4 DCs. The expression level of programmed cell death 1 (PD-1) on CD8+ T cells, including CMVpp65-specific CD8+ T cells, expanded by IFN DCs pulsed with the CMVpp65-peptide and Z plus G (IFN DCs/P+Z+G), was lower than that expanded by IFN DCs pulsed with the peptide alone (IFN DCs/P). Multi-functional T cells, including human leucocyte antigen (HLA)-A*0201-restricted CMVpp65-specific CD8+ T cells, Vγ9γδT cells and Vα24NKT cells, efficiently kill the HLA-A*0201-positive GBM cell line expressing CMVpp65 protein (T98G). These findings indicate that DC therapy using IFN DCs/P+Z+G and/or CTL therapy using CMVpp65-specific CD8+ T cells expanded by IFN DCs/P+Z+G may lead to a good clinical outcome for patients with GBM.

Teriparatide improves volumetric bone mineral density and fine bone structure in the UIV+1 vertebra, and reduces bone failure type PJK after surgery for adult spinal deformity.

We conducted a prospective comparative study of the effect of teriparatide therapy for preventing vertebral-failure-type PJK after reconstructive surgery for adult spinal deformity. Prophylactic teriparatide improved the volumetric bone mineral density and fine bone structure of the vertebra above the upper-instrumented vertebra and reduced the incidence of vertebral-failure-type PJK. INTRODUCTION: Proximal junctional kyphosis (PJK) is a complication after corrective surgery for spinal deformity. This study sought to determine whether teriparatide (TP) is an effective prophylactic against PJK type 2 (vertebral fracture) in surgically treated patients with adult spinal deformity (ASD). METHODS: Forty-three patients who started TP therapy immediately after surgery and 33 patients who did not receive TP were enrolled in this prospective case series. These patients were female, over 50, surgically treated for ASD, and followed for at least 2 years. Preoperative and postoperative standing whole-spine X-rays and dual-energy X-ray absorptiometry scans, and multidetector CT images obtained before and 6 months after surgery were used to analyze the bone strength in the vertebra above the upper-instrumented vertebra (UIV+1). RESULTS: Mean age was 67.9 years. After 6 months of treatment, mean hip-bone mineral density (BMD) increased from 0.721 to 0.771 g/cm2 in the TP group and decreased from 0.759 to 0.729 g/cm2 in the control group. This percent BMD change between groups was significant (p < 0.05). The volumetric BMD (326 to 366 mg/cm3) and bone mineral content (BMC) (553 to 622 mg) at UIV+1 were also significantly increased in TP group. The bone volume/tissue volume ratio increased from 46 to 54 % in the TP group, and the trabecular bone thickness and number increased by 14 and 5 %, respectively. At the 2-year follow-up, the PJK type 2 incidence was significantly lower in the TP group (4.6 %) than in the control group (15.2 %; p = .02). CONCLUSIONS: Prophylactic TP treatment improved the volumetric BMD and fine bone structure at UIV+1 and reduced the PJK-type 2 incidence.

Characteristics of neuropathic pain and its relationship with quality of life in 72 patients with spinal cord injury.

STUDY DESIGN: A cross-sectional study. OBJECTIVES: Neuropathic pain (NP) after spinal cord injury (SCI) tends to be hard to treat, and its heterogeneous properties make it difficult to identify and characterize. This study was conducted to assess the characteristics of SCI-related NP in detail. SETTING: A single hospital for SCI rehabilitation. METHODS: This study included 72 patients who were seen at our hospital in 2012 and 2013 and who had sustained SCI at least 3 months before enrollment. The patients completed the Neuropathic Pain Symptom Inventory (NPSI) and the Short Form (SF)-36 Health Inventory. The NPSI score was analyzed for correlations with clinical presentations of SCI and SF-36 subitems. RESULTS: Paresthesia/dysesthesia was the most common subtype of NP after SCI. With regard to location, below-level superficial NP was significantly more intense than at-level pain. Patients who underwent surgery showed significantly less evoked pain compared with patients with non-surgery. Patients reported significantly more severe pain if >1 year had elapsed after the SCI. Patients with an American Spinal Injury Association Impairment Scale grade of B for completeness of injury reported more intense NP than those with other grades. Among the SF-36 subitems, NP correlated significantly with bodily pain, general health and mental health. CONCLUSION: NP in SCI patients was significantly associated with the location of pain, the time period since the injury, surgery and quality-of-life factors. A more detailed understanding of the characteristics of NP may contribute to better strategies for relieving the pain associated with SCI.

Cross-Scale Interactions between Electron and Ion Scale Turbulence in a Tokamak Plasma.

Multiscale gyrokinetic turbulence simulations with the real ion-to-electron mass ratio and ß value are realized for the first time, where the ß value is given by the ratio of plasma pressure to magnetic pressure and characterizes electromagnetic effects on microinstabilities. Numerical analysis at both the electron scale and the ion scale is used to reveal the mechanism of their cross-scale interactions. Even with the real-mass scale separation, ion-scale turbulence eliminates electron-scale streamers and dominates heat transport, not only of ions but also of electrons. Suppression of electron-scale turbulence by ion-scale eddies, rather than by long-wavelength zonal flows, is also demonstrated by means of direct measurement of nonlinear mode-to-mode coupling. When the ion-scale modes are stabilized by finite-ß effects, the contribution of the electron-scale dynamics to the turbulent transport becomes non-negligible and turns out to enhance ion-scale turbulent transport. Damping of the ion-scale zonal flows by electron-scale turbulence is responsible for the enhancement of ion-scale transport.

Twenty-year trends in neonatal surgery based on a nationwide Japanese surveillance program.

AIM: To discuss the chronological changes observed in a national survey of neonatal surgery in Japan performed every 5 years by the Committee in the Japanese Society of Pediatric Surgeons. METHODS: We analyzed the data obtained for 20 years from 1993 to 2013 and herein report the chronological changes. RESULTS: The number of summarized cases was least in 1993, with 2806 cases, and subsequently increased to 3753 cases in 2013. The mortality rate among the patients with maternal transport linearly decreased (p = 0.0386). Although the proportion of extremely low birth weight infants linearly increased (p = 0.0014), with an annual rate of +0.39 %, the mortality rate linearly decreased (p = 0.0010), with an annual rate of -1.68 %. Moreover, the overall mortality rate linearly decreased (p = 0.0002), with an annual rate of -0.26 %. Most diseases were observed to exhibit a decline in the mortality rate with the same trend as overall mortality. The decline in the mortality rate was most robust with respect to congenital diaphragmatic hernia (CDH). The mortality rates, except for that of CDH, omphalocele, esophageal atresia, and intestinal perforation, declined to 5 % or lower by 2013. CONCLUSIONS: The present findings may be the result of remarkable progress in perinatal management.

Detailed features of palisade vessels as a marker of the esophageal mucosa revealed by magnifying endoscopy with narrow band imaging.

The palisade vessels present at the distal end of the esophagus are considered to be a landmark of the esophagogastric junction and indispensable for diagnosis of columnar-lined esophagus on the basis of the Japanese criteria. Here we clarified the features of normal palisade vessels at the esophagogastric junction using magnifying endoscopy. We prospectively studied palisade vessels in 15 patients undergoing upper gastrointestinal endoscopy using a GIF-H260Z instrument (Olympus Medical Systems Co., Tokyo, Japan). All views of the palisade vessels were obtained at the maximum magnification power in the narrow band imaging mode. We divided the area in which palisade vessels were present into three sections: the area from the squamocolumnar junction (SCJ) to about 1 cm orad within the esophagus (Section 1); the area between sections 1 and 3 (Section 2); and the area from the upper limit of the palisade vessels to about 1 cm distal within the esophagus (Section 3). In each section, we analyzed the vessel density, caliber of the palisade vessels, and their branching pattern. The vessel density in Sections 1, 2, and 3 was 9.1 ± 2.1, 8.0 ± 2.6, and 3.3 ± 1.3 per high-power field (mean ± standard deviation [SD]), respectively, and the differences were significant between Sections 1 and 2 (P= 0.0086) and between Sections 2 and 3 (P < 0.0001). The palisade vessel caliber in Sections 1, 2, and 3 was 127.6 ± 52.4 µm, 149.6 ± 58.6 µm, and 199.5 ± 75.1 µm (mean ± SD), respectively, and the differences between Sections 1 and 2, and between Sections 2 and 3, were significant (P < 0.0001). With regard to branching form, the frequency of branching was highest in Section 1, and the 'normal Y' shape was observed more frequently than in Sections 2 and 3. Toward the oral side, the frequency of branching diminished, and the frequency of the 'upside down Y' shape increased. The differences in branching form were significant among the three sections (P < 0.0001). These results indicate that the density of palisade vessels is highest near the SCJ, and that towards their upper limit they gradually become more confluent and show an increase of thickness. Within a limited area near the SCJ, observations of branching form suggest that palisade vessels merge abruptly on the distal side. We have demonstrated that palisade vessels are a useful marker for endoscopic recognition of the lower esophagus.

Energy-selective confinement of fusion-born alpha particles during internal relaxations in a tokamak plasma.

Long-pulse operation of a self-sustained fusion reactor using toroidal magnetic containment requires control over the content of alpha particles produced by D-T fusion reactions. On the one hand, MeV-class alpha particles must stay confined to heat the plasma. On the other hand, decelerated helium ash must be expelled before diluting the fusion fuel. Here, we report results of kinetic-magnetohydrodynamic hybrid simulations of a large tokamak plasma that confirm the existence of a parameter window where such energy-selective confinement can be accomplished by exploiting internal relaxation events known as sawtooth crashes. The physical picture - a synergy between magnetic geometry, optimal crash duration and rapid particle motion - is completed by clarifying the role of magnetic drifts. Besides causing asymmetry between co- and counter-going particle populations, magnetic drifts determine the size of the confinement window by dictating where and how much reconnection occurs in particle orbit topology.

Generation and amplification of magnetic islands by drift interchange turbulence.

We investigate the multiscale nonlinear dynamics of a linearly stable or unstable tearing mode with small-scale interchange turbulence using 2D MHD numerical simulations. For a stable tearing mode, the nonlinear beating of the fastest growing small-scale interchange modes drives a magnetic island with an enhanced growth rate to a saturated size that is proportional to the turbulence generated anomalous diffusion. For a linearly unstable tearing mode the island saturation size scales inversely as one-fourth power of the linear tearing growth rate in accordance with weak turbulence theory predictions. Turbulence is also seen to introduce significant modifications in the flow patterns surrounding the magnetic island.

J chain is encoded by a single gene unlinked to other immunoglobulin structural genes.

Immunoglobulin J chain mediates the polymerization of both IgM and IgA immunoglobulins. Its synthesis is closely regulated in B lymphocytes, apparently at the level of RNA transcription. To define the genetic bases of this regulation, we have determined the location and number of J chain genes in the mouse. Analysis of DNA from a group of somatic cell hybrids containing various mouse chromosomes on a constant background of Chinese hamster chromosomes indicated that this gene is located on mouse chromosome 5, unlinked to immunoglobulin heavy and light chain structural genes. Restriction mapping experiments further suggested the existence of a single J chain gene per haploid genome. This result was confirmed by quantitative analyses of band intensities yielded by Southern blots of mouse genomic DNA and J gene-containing plasmid DNA.

Observation of quasi-two-dimensional nonlinear interactions in a drift-wave streamer.

A streamer, which is a bunching of drift-wave fluctuations, and its mediator, which generates the streamer by coupling with other fluctuations, have been observed in a cylindrical magnetized plasma. Their radial structures were investigated in detail by using the biphase analysis. Their quasi-two-dimensional structures were revealed to be equivalent with a pair of fast and slow modes predicted by a nonlinear Schrödinger equation based on the Hasegawa-Mima model.

In vitro splicing analysis showed that availability of a cryptic splice site is not a determinant for alternative splicing patterns caused by +1G-->A mutations in introns of the dystrophin gene.

BACKGROUND: Splicing patterns are critical for assessing clinical phenotype of mutations in the dystrophin gene. However, it is still unclear how to predict alternative splicing pathways in such cases of splice-site mutation in the dystrophin gene. OBJECTIVE: To identify elements determining alternative splicing pathways in intron +1G-->A mutations of the dystrophin gene. RESULTS: We found that exon 25 is spliced out in the +1G-->A mutation in intron 25, resulting in mild Becker muscular dystrophy, and that a cryptic splice site within exon 45 was activated in severe Duchenne muscular dystrophy with a mutation of +1G-->A mutation in 45. Furthermore, in vitro splicing analysis using a pre-constructed expression vector showed that the mutant intron 25 produced one transcript that lacked exon 25. In contrast, the same splice-site mutation in intron 45 produced three splicing products. One product used the same cryptic donor splice site within exon 45 as the in vivo donor site and another product used a cryptic splice site within the vector sequence. Notably, the available cryptic splice site was not activated by the same G-->A mutation of intron 25. CONCLUSION: It was concluded that sequences inserted into the in vitro splicing assay minigene contain cis-elements that determine splicing pathways. By taking other +1G-->A mutations in the introns of the dystrophin gene reported in the literature into consideration, it seems that cryptic splice-site activation is seen only in strong exons. This finding will help to elucidate the molecular pathogenesis of dystrophinopathy and to predict efficiency of induction of exon skipping with antisense oligonucleotides for treatment of Duchenne muscular dystrophy.

Effects of ABCB1 3435C>T genotype on serum levels of cortisol and aldosterone in women with normal menstrual cycles.

ABCB1, also known as MDR1/P-glycoprotein, can transport cortisol and aldosterone. We examined the effects of ABCB1 polymorphisms on serum levels of cortisol and aldosterone among different phases of the normal menstrual cycle in 51 non-pregnant healthy Japanese female volunteers (22 +/- 1 years old). The menstrual cycle was divided into three phases: premenstrual phase (14 days preceding the onset of menstruation, N = 22; menstrual phase, N = 11, and postmenstrual phase, N = 18). ABCB1 -129T>C, 1236C>T, 2677G>A/T, and 3435C>T genotypes were determined. Serum levels of cortisol, aldosterone, estradiol, progesterone, and testosterone were measured. The serum levels of estradiol in the pre- and post-menstrual phases and of progesterone in the premenstrual phase were significantly increased when compared to their serum levels in the menstrual phase (P < 0.005). In the postmenstrual phase, the mean serum cortisol level in subjects with the 3435CT and 3435TT genotype was 7.6 +/- 3.4 microg/dL (mean +/- SD, N = 7), which was significantly lower than in women with the 3435CC genotype (9.9 +/- 1.8 microg/dL, N = 11) (P = 0.037). The opposite effect was observed in the serum aldosterone level during the postmenstrual phase (97.2 +/- 23.4 and 141.2 +/- 48.5 pg/mL for 3435CC and 3435CT + 3435TT, respectively; P = 0.041). These findings suggest that ABCB1 3435C>T genotype can influence serum levels of cortisol and aldosterone during the postmenstrual phase of the normal menstrual cycle.

Dystrophin nonsense mutations can generate alternative rescue transcripts in lymphocytes.

Secondary alterations in splicing have been reported to produce semi-functional mRNA from several nonsense mutations in the dystrophin gene. Disruptions of exonic splicing enhancers by single nucleotide changes are thought to underlie such alterations. The precise frequencies of such nonsense mutation-dependent splicing alterations, however, remain unknown. Here we analyzed the splicing patterns of dystrophin mRNA in lymphocytes from 38 patients with dystrophinopathies due to nonsense mutations in the dystrophin gene. In seven of the cases (18%), we observed partial skipping of the nonsense-encoding exon. Two of the seven cases, however, exhibited complex activation of a nonsense mutation-created splice site, which resulted in the generation of novel transcripts. Examination of cis-regulatory splicing elements through calculation of splicing probability scores and identification of potential splicing enhancer or silencer sequences failed to disclose a single cause for exon skipping. Remarkably, individual differences in splicing patterns were observed for cells from patients with identical nonsense mutations (C.5899C>T). Although five cases produced semi-functional dystrophin mRNAs, only one of these exhibited a mild clinical course. These results provide important insights about targets for exon skipping induced by candidate antisense oligonucleotides and for ribosomal read-through of nonsense mutations.

Indications for partial parotidectomy using retrograde dissection of the marginal mandibular branch of the facial nerve for benign tumours of the parotid gland.

The aims of this study were to evaluate the efficacy of partial parotidectomy using retrograde dissection of the marginal mandibular branch of the facial nerve for benign tumours of the parotid gland and to establish the indications for its use. We examined 106 consecutive patients with previously untreated benign tumours in the lower portion of the parotid gland who were treated by parotidectomy. The first group (anterograde group, n=52) consisted of those who had standard anterograde parotidectomy. The remaining patients, who underwent retrograde parotidectomy, were further divided into two groups: those in whom the upper edge of the tumour was located below the mastoid tip (below mastoid group, n=46) or those in whom it was above the mastoid tip (above mastoid group, n=8). The operating time was significantly shorter in the below mastoid group (141.2, 127.5, and 98.1minutes, respectively) as was intraoperative blood loss (41.1, 53.0, and 24.4ml, respectively), compared with the other two groups. There was a higher incidence of facial nerve dysfunction in the above mastoid group postoperatively (4/8) than in the other two groups. The results suggested that the presence of a tumour of any size located below the mastoid tip is a good indication for parotidectomy using retrograde dissection of the marginal mandibular branch of the facial nerve.

Immunosuppressant FK506 induces interleukin-6 production through the activation of transcription factor nuclear factor (NF)-kappa(B). Implications for FK506 nephropathy.

FK506 is a powerful immunosuppressive drug currently in use that inhibits the activation of several transcription factors (nuclear factor (NF)-AT and NF-kappaB) critical for T cell activation. We show here that, contrary to the situation in T cells, FK506 activates transcription factor NF-kappaB in nonlymphoid cells such as fibroblasts and renal mesangial cells. We further show that FK506 induces NF-kappaB-regulated IL-6 production in vitro and in vivo, in particular in kidney. IL-6 has been shown previously to produce renal abnormalities in vivo, such as mesangioproliferative glomerulonephritis. Similar renal abnormalities were also observed in FK506-treated animals. These results thus suggest a causal relationship between FK506-induced NF-kappaB activation/IL-6 production and some of FK506-induced renal abnormalities.

Chromatin structure and developmental expression of the human alpha-globin cluster.

The human alpha-like globins undergo a switch from the embryonic zeta-chain to the alpha-chain early in human development, at approximately the same time as the beta-like globins switch from the embryonic epsilon-to the fetal gamma-chains. We investigated the chromatin structure of the human alpha-globin gene cluster in fetal and adult erythroid cells. Our results indicate that DNase I-hypersensitive sites exist at the 5' ends of the alpha 1- and alpha 2-globin genes as well as at several other sites in the cluster in all erythroid cells examined. In addition, early and late fetal liver erythroid cells and adult bone marrow cells contain hypersensitive sites at the 5' end of the zeta gene, and in a purified population of 130-day-old fetal erythroid cells, the entire zeta-to alpha-globin region is sensitive to DNase I digestion. The presence of features of active chromatin in the zeta-globin region in fetal liver and adult bone marrow cells led us to investigate the transcription of zeta in these cells. By nuclear runoff transcription studies, we showed that initiated polymerases are present on the zeta-globin gene in these normal erythroid cells. Immunofluorescence with anti-zeta-globin antibodies also showed that late fetal liver cells contain zeta-globin. These findings demonstrate that expression of the embryonic zeta-globin continues at a low level in normal cells beyond the embryonic to fetal globin switch.

Fine positioning of a poloidal probe array.

Multipoint detection is an essential requirement for investigating plasma turbulence which is a highly nonlinear phenomenon in space and time. We have fabricated an array of 64-channel poloidal probes surrounding the linear cylindrical plasma named LMD-U in order to study turbulence properties, particularly the nonlinear mode couplings, in the domain of poloidal wave number and frequency. However, misalignments of probe tips produce spurious modes, which do not exist in the real plasma, to distort the precise wave number measurements. The paper presents the description of the 64-channel poloidal probe array with means to adjust the probe positions, with discussion on the effects of the misalignments on the wave number measurements.

A baseline impedance analysis in neurologically impaired children: A potent parameter for estimating the condition of the esophageal mucosa.

BACKGROUND: The aim of the present study was to investigate whether the baseline impedance (BI) value is a useful parameter to evaluate the condition of the esophageal mucosa in neurologically impaired (NI) children undergoing multichannel intraluminal impedance pH measurements (pH/MII). METHODS: The retrospective study included 55 NI patients ≤15 years. The patients were divided into acid gastroesophageal reflux disease (GERD), non-acid GERD and GERD (-) groups. Furthermore, the patients in the acid GERD group were subdivided into erosive reflux disease (ERD) and non-erosive reflux disease (NERD) groups. pH/MII parameters and BI values (Z1-6) were compared among three groups or between two groups, respectively. A Spearman's correlation analysis was used for the correlation analysis of pH/MII parameters and BI values. A receiver operator characteristic curve analysis was used to evaluate the optimum cut-off values of BI to discriminate ERD patients. KEY RESULTS: The BI values of the proximal and the distal channels in ERD group were significantly lower than those in NERD group. The BI values of the distal channels demonstrated significant negative correlations with acid exposure related pH/MII parameters. The optimal cut off value of BI in the most distal channel was determined to be 1500 Ω. CONCLUSIONS & INFERENCES: The present study suggested that NI children with reflux esophagitis were likely to suffer mucosal damage up to the proximal esophagus and cut-off BI values may help estimate the presence of reflux esophagitis. Baseline impedance is a potent parameter, reflecting the esophageal mucosal damage in NI children who have difficulty in undergoing endoscopic examinations.

Megakaryocyte polyploidization is associated with decreased expression of polo-like kinase (PLK).

BACKGROUND: During differentiation, megakaryocytes (MK), the bone marrow precursors of circulating blood platelets, undergo polyploidization, repeated rounds of DNA replication without cell division. Mature normal MK may contain a DNA content of up to 128N, in contrast to normal diploid (2N) cells. The extent of polyploidy may influence the number of platelets produced by the MK. Therefore, understanding the molecular mechanisms regulating polyploidization could identify events involved in controlling both cell division and thrombopoiesis. OBJECTIVE: We investigated the expression of several proteins involved in mitosis in cultured mouse MK, and tested the effect of expression on polyploidization. METHODS: Western blot and immunofluorescent analyses were used to assess expression of cell cycle proteins in cultured MK. Populations of polyploidizing MK were separated on the basis of DNA content by flow cytometry. The gene encoding mouse polo-like kinase 1 (PLK-1) was introduced into MK by retroviral transduction, and its effects measured by flow cytometry. RESULTS: Polyploid mouse MK expressed lower levels of two proteins, p55CDC and PLK-1, whose activity is necessary for cell cycle progression and completion of mitosis. Comparison of sorted 2N/4N and polyploid MK indicated that PLK-1 expression was absent in polyploid MK, while expression of other cell cycle proteins was similar in both populations. Forced expression of PLK-1 during MK differentiation was associated with decreased polyploidization. CONCLUSION: These experiments suggest that PLK-1 is an important regulator of polyploidization in differentiating MK.

Reversible suppression of mouse mammary tumor virus replication by prolonged glucocorticoid exposure.

Expression of mouse mammary tumor virus (MuMTV) in MJY-alpha mammary tumor cells was only transiently stimulated by exposure to 14 microM hydrocortisone (HC). Short-term HC treatment for 24-48 hours resulted in twofold-to-fivefold increases in levels of MuMTV polypeptide synthesis, MuMTV surface antigen expression, and MuMTV production. HC treatment also induced quantitative alterations in glycosylation of MuMTV precursors Pr79env and Pr76env. In contrast, prolonged exposure to 14 microM HC for 14-21 days decreased MuMTV polypeptide synthesis, surface antigen expression, and virion production to levels similar to untreated MJY-alpha cells. The pattern of MuMTV precursor glycosylation following prolonged HC treatment was identical to that detected in unexposed control cultures. Attenuation of glucocorticoid-mediated MuMTV stimulation was reversed either by exposure of treated cells to elevated (28 or 60 microM) concentrations of HC or by intermediate passage of treated cells in HC-free medium, suggesting additional levels of control of MuMTV replication.