[Correlation analysis between prostate imaging report and data system score and pathological results of prostate cancer].

Objective: To explore the correlation between prostate imaging report and data system (PI-RADS) score and international society of uological pathology (ISUP) grade of prostate cancer (PCa) and the role of PI-RADS score in predicting the pathological features of clinically significant PCa (csPCa), positive surgical margin and pathological upgrade. Methods: The pathologically positive patients with multi-parameter magnetic resonance image (mpMRI) were included in this study. The patients with prostate specific antigen (PSA)<100 µg/L were divided into two groups: biopsy group (n=523) and RP group (n=215). The correlation between PI-RADS score and ISUP grade and the accuracy of predicting csPCa in the two groups were evaluated. In the RP group, the correlation between PI-RADS score and postoperative pathological grade or degradation and positive incisal margin was further discussed. The patients with PSA≥100 µg/L (171cases in biopsy group and 6 cases in RP group) were not included in the statistical analysis, and the results were simply described. Results: The age, prostate volume, and PSA level of biopsy group and RP group was (72±8) years vs (68±7) years, 48.3 (32-57) cm(3) vs 47.2 (32-54) cm(3), and 26.3(10.2-34.2)µg/L vs 21.7 (9.24-23.95)µg/L, respectively. The PI-RADS scores ≤ 3,4, and 5 in the biopsy group were 109,97, and 317 respectively, and those in the RP group were 61,55, and 99 respectively. There were significant differences in the composition of ISUP grades of different PI-RADS scores between the two groups (P<0.001), and there was a positive correlation between the two groups (r=0.493 in the biopsy group, r=0.671 in the RP group, both P<0.001). Using PI-RADS score to predict csPCa, biopsy group (AUC=0.764, P<0.001, 95%CI:0.710-0.819) and RP group (AUC=0.807, P<0.001, 95%CI:0.735-0.879) had certain accuracy. The PI-RADS score combined with PSA could improve the accuracy of csPCa prediction in the biopsy group (AUC=0.795,P<0.001, 95% CI:0.746-0.843) and the RP group (AUC=0.852, P<0.001, 95%CI:0.789-0.915). Compared with the pathological results of biopsy in the RP group, 52.6% of the patients showed upgrade and degrade of ISUP, and there was insignificant difference in the composition of PI-RADS scores between upgraded and degraded patients (P>0.05). However, 41.7%(27/65) of the patients with ISUP grade 1 biopsies had pathological upgrades that the patients with PI-RADS ≤ 3 accounted for 33.3%, while the patients with PI-RADS>3 accounted for 66.7%, and there was significant difference between the two groups (P<0.05). After RP, 43.3% of the patients had positive surgical margins, and the patients with PI-RADS score ≤ 3, 4 and 5 were 13 (14%), 24 (25.8%) and 56 (60.2%), respectively, while the PI-RADS scores of patients with negative surgical margin were 48 (39.3%), 31(25.4%) and 43(35.2%), respectively. There was significant difference between the two groups (P<0.001). The higher the PI-RADS score, the greater the possibility of the positive surgical margin. For the patients with PSA ≥ 100 µg/L, 98.8% (169/171) patients in the biopsy group had a PI-RADS score 5. The pathological results of all patients were csPCa, of which 85.4% (146/171) had ISUP grade ≥ 4. Among them, 6 cases underwent RP, 5 cases had ISUP grade ≥ 4, all surgical margin were positive, 5 cases had seminal vesicle invasion, 3 cases had capsule invasion and 3 cases had positive pelvic lymph nodes. Conclusion: ThePI-RADS score is correlated with the ISUP grade of PCa. Combined with PSA can accurately predict csPCa. At the same time, the higher PI-RADS score, the more likely the patients with positive incisal margin after RP and Gleason score of 3+3=6 at the time of puncture will be upgraded pathologically.

Resveratrol Promotes in vitro Differentiation of Osteoblastic MC3T3-E1 Cells via Potentiation of the Calcineurin/NFATc1 Signaling Pathway.

Resveratrol has been shown to stimulate differentiation of osteoblastic MC3T3-E1 cells in vitro; however, the mechanisms underlying the anabolic effect of resveratrol on osteoblasts remain largely unknown. Our study was aimed to investigate the molecular mechanism of resveratrol-induced differentiation of MC3T3-E1 cells. MC3T3-E1 cells were treated for 8 days with different concentrations of resveratrol (10-8-10-6 M) and 10-6 M cyclosporine A (CsA), a specific inhibitor of the calcineurin/NFAT pathway. According to the results of pilot studies of cell proliferation and alkaline phosphatase activity, 10-7 M concentration of resveratrol was used in subsequent experiments. The levels of mRNA expression of the osteosis-related genes CaN, NFATc1, and Runx2 were analyzed by real-time RT-PCR; the levels of the corresponding proteins were estimated by Western blot analysis. Resveratrol upregulated expression of the CaN, NFATc1, and Runx2 genes at both mRNA and protein levels compared to the control group (p < 0.05), while CsA reduced the effects of resveratrol (p < 0.05). Using immunohistochemical staining, we showed that resveratrol induced NFATc1 accumulation in the cell nuclei, and treatment with CsA inhibited resveratrol-mediated induction of NFATc1, suggesting that the calcineurin/NFATc1 signaling pathway plays an important role in the regulatory effect of resveratrol on osteoblasts.

Comparative transcriptomic analyses to scrutinize the assumption that genotoxic PAHs exert effects via a common mode of action.

In this study, the accuracy of the assumption that genotoxic, carcinogenic polycyclic aromatic hydrocarbons (PAHs) act via similar mechanisms of action as benzo(a)pyrene (BaP), the reference PAH used in the human health risk assessment of PAH-containing complex mixtures, was investigated. Adult male Muta™Mouse were gavaged for 28 days with seven individual, genotoxic PAHs. Global gene expression profiles in forestomach, liver, and lung (target tissues of exposure) were determined at 3 days post-exposure. The results are compared with our previously published results from mice exposed to BaP via the same exposure regimen. Although all PAHs showed enhanced ethoxyresorufin-O-deethylase activity, DNA adduct formation, and lacZ mutant frequency in the lungs, the unsupervised cluster analysis of differentially expressed genes revealed that the transcriptional changes are both PAH- and tissue-specific, with lung showing the most response. Further bioinformatics-/pathway-based analysis revealed that all PAHs induce expression of genes associated with carcinogenic processes, including DNA damage response, immune/inflammatory response, or cell signaling processes; however, the type of pathways and the magnitude of change varied for each PAH and were not the same as those observed for BaP. Benchmark dose modeling showed transcriptomic data closely reflected the known tumor incidence for the individual PAHs in each tissue. Collectively, the results suggest that the underlying mechanisms of PAH-induced toxicity leading to tumorigenesis are tissue-specific and not the same for all PAHs; based on the tissue type considered, use of BaP as a reference chemical may overestimate or underestimate the carcinogenic potential of PAHs.

Genome-wide identification and characterization of the Dof gene family in Medicago truncatula.

The DNA-binding one zinc finger (Dof) family is a classic plant-specific zinc-finger transcription factor family, which is involved in many important processes, including seed maturation and germination, plant growth and development, and light responses. Investigation of the Medicago truncatula genome revealed 42 putative Dof genes, each of which holds one Dof domain. These genes were classified into four groups based on phylogenetic analysis, which are similar to the groups reported for Arabidopsis and rice. Based on genome duplication analysis, it was found that the MtDof genes were distributed on all chromosomes and had expanded through tandem gene duplication and segmental duplication events. Two main duplication regions were identified, one from tandem duplication and another from segmental duplication. By analyzing high-throughput sequencing data from M. truncatula, we found that most of the MtDof genes showed specific expression patterns in different tissues. According to cis-regulatory element analysis, these MtDof genes are regulated by different cis-acting motifs, which are important for the functional divergence of the MtDof genes in different processes. Thus, using genome-wide identification, evolution, and expression pattern analysis of the Dof genes in M. truncatula, our study provides valuable information for understanding the potential function of the Dof genes in regulating the growth and development of M. truncatula.

Immunomodulatory effect of bone marrow mesenchymal stem cells on T lymphocytes in patients with decompensated liver cirrhosis.

We explored the immunomodulatory effects of bone marrow mesenchymal stem cells (BMSCs) on peripheral blood T lym-phocytes in patients with decompensation stage, hepatitis B-associated cirrhosis. MSCs from nine patients were analyzed by flow cytometry. Peripheral blood lymphocytes were isolated for fluorescent staining. Following stimulation by phytohemagglutinin (PHA), peripheral blood lymphocytes were co-cultured with BMSCs in serum and divided into four groups: (1) BMSC + lymphocyte + PHA contact culture group; (2) BMSC + lymphocyte + PHA non-contact culture group; (3) lym-phocyte + PHA positive control group; and (4) lymphocyte-only negative control group. Lymphocyte proliferation and frequencies of CD4(+)CD25(+)CD127(-) Tregs and CD4(+)CD8(-)IL-17(+) (Th17) cells were de-tected. Cell proliferation in groups 1 and 2 declined compared with group 3 (P < 0.01), and was notably higher than in group 4 (P < 0.01). CD4(+)CD25(+)CD127(-) Tregs frequencies in groups 1 and 2 were higher than in groups 3 and 4. In an intra-group comparison before and after culture, Th17 cell frequencies in groups 1 and 2 were higher than in group 4 (P < 0.01), but lower than in group 3 (P < 0.01). The Treg/Th17 ratio in groups 1 and 2 increased (P < 0.01), but did not change signifi-cantly in groups 3 and 4 (P > 0.05). In a comparison between groups after culture, the Treg/Th17 ratio in groups 1 and 2 increased more than in groups 3 and 4 (P < 0.01). BMSCs from cirrhotic patients can inhibit the proliferation of peripheral blood T lymphocytes, upregulate the ex-pression of CD4(+)CD25(+)CD127(-) Tregs, and improve Treg/Th17 imbal-ance. The mechanism by which this takes place may be associated with immunomodulatory effects induced by the secretion of soluble factors.

Effects of Forage:Concentrate Ratio on Growth Performance, Ruminal Fermentation and Blood Metabolites in Housing-feeding Yaks.

The objective of this study was to determine the effect of forage: concentrate ratio (F:C) on growth performance, ruminal fermentation and blood metabolites of housing-feeding yaks. Thirty-two Maiwa male yaks (initial body weight = 207.99±3.31 kg) were randomly assigned to four dietary treatments (8 yaks per treatment). Experimental diets were: A, B, C, D which contained 70:30, 60:40, 50:50 and 40:60 F:C ratios, respectively. Dry matter intake and average daily gain in yaks fed the C and D diets were greater (p<0.05) than yaks fed the A and B diets. No differences were found in ruminal NH3-N, total volatile fatty acids, acetate, butyrate, valerate, and isovalerate concentrations. The propionate concentration was increased (p<0.05) in the C and D groups compared with the A and B diets. In contrast, the acetate to propionate ratio was decreased and was lowest (p<0.05) in the C group relative to the A and B diets, but was similar with the D group. For blood metabolites, no differences were found in serum concentrations of urea-N, albumin, triglyceride, cholesterol, low density lipoprotein, alanine aminotransferase, and aspartate aminotransferase (p>0.05) among treatments. Treatment C had a higher concentration of total protein and high density lipoprotein (p<0.05) than A and B groups. In addition, there was a trend that the globulin concentration of A group was lower than other treatments (p = 0.079). Results from this study suggest that increasing the level of concentrate from 30% to 50% exerted a positive effect on growth performance, rumen fermentation and blood metabolites in yaks.

Prognostic relevance and therapeutic implications of centromere protein F expression in patients with esophageal squamous cell carcinoma.

Centromere protein F (CENP-F), a cell cycle-regulated centromere protein, has been shown to affect numerous tumorigenic processes. This study aimed to clarify the prognostic significance of CENP-F expression in patients with esophageal squamous cell carcinoma (ESCC). The levels of CENP-F messenger RNA and protein were higher in ESCC cell lines than in the normal tissues. An immunohistochemical analysis of paired tissue specimens showed that the CENP-F expression was higher in tumorous tissues than in the adjacent non-tumorous tissues (P < 0.001). Moreover, there was a significant correlation between CENP-F expression and gender (P = 0.012), clinical stage (P = 0.039), and T classification (P = 0.026). Patients with higher CENP-F expression had shorter overall survival than those with lower CENP-F expression (P = 0.009). Multivariate Cox analysis indicated that CENP-F expression is an independent prognostic factor for overall survival (hazard ratio = 0.582, 95% confidence interval = 0.397-0.804, P = 0.041). Importantly, it was found that zoledronic acid (ZOL) could significantly enhance the chemotherapeutic sensitivity of ESCC cell lines with high CENP-F expression to cisplatin, although ZOL alone only exhibited a minor inhibitory effect to ESCC cells. In summary, these findings demonstrate that CENP-F may serve as a valuable molecular marker for predicting the prognosis of ESCC patients. In addition, the data indicate a potential benefit of combining ZOL with cisplatin in ESCC, suggesting that CENP-F expression may have therapeutic implications.

Genomic selection of seed weight based on low-density SCAR markers in soybean.

With the development of molecular marker technology, crop breeding has been accelerated by marker-assisted selection for the improvement of quantitative traits. However, due to the traits' polygenic nature, traditional marker-assisted selection methods are ill-suited for identification of quantitative trait loci. Genomic selection (GS) was introduced into crop breeding to achieve more accurate predictions by considering all genes or markers simultaneously. We used dozens of sequence-characterized amplified region (SCAR) markers for genotyping soybean varieties, and we identified markers associated with hundred-seed weight. The best linear unbiased predictor and Bayesian liner regression methods were used to construct GS models to predict the hundred-seed weight trait based upon genotype information for trait selection. Both GS models showed good prediction performance in soybean, as the correlation coefficient between genomic estimated breeding values and true breeding values was as high as 0.904. This indicated that GS was performed effectively based on dozens of SCAR markers in soybean; these markers were of low density but easily detectable. Therefore, the combination of GS modeling and highly effective molecular marker technology involving SCAR markers can facilitate genetic breeding in soybean. This approach may also be suitable for genetic selection in other crops, such as wheat, maize, and rice.

Gametocidal chromosomes enhancing chromosome aberration in common wheat induced by 5-azacytidine.

The gametocidal (Gc) chromosome from Aegilops spp induces chromosome mutation, which is introduced into common wheat as a tool of chromosome manipulation for genetic improvement. The Gc chromosome functions similar to a restriction-modification system in bacteria, in which DNA methylation is an important regulator. We treated root tips of wheat carrying Gc chromosomes with the hypomethylation agent 5-azacytidine; chromosome breakage and micronuclei were observed in these root tips. The frequency of aberrations differed in wheat containing different Gc chromosomes, suggesting different functions inducing chromosome breakage. Gc chromosome 3C caused the greatest degree of chromosome aberration, while Gc chromosome 3C(SAT) and 2C caused only slight chromosome aberration. Gc chromosome 3C induced different degrees of chromosome aberration in wheat varieties Triticum aestivum var. Chinese Spring and Norin 26, demonstrating an inhibition function in common wheat.

RAPD and ISSR-assisted identification and development of three new SCAR markers specific for the Thinopyrum elongatum E (Poaceae) genome.

Diploid Thinopyrum elongatum, a wild relative of wheat, contains many agronomically desirable traits and has potential for increasing genetic variability and introducing desirable characters in this crop. Few molecular markers are available for rapid screening of T. elongatum genome segments in the wheat genetic background. We used 36 RAPD primers and 33 ISSR primers to screen for polymorphisms in the common wheat variety Chinese Spring and in T. elongatum. Two RAPD markers and one ISSR marker, designated OPF03(1407), LW10(1487) and UBC841(701), were identified and were specific for the T. elongatum E genome. Three pairs of primers flanking these specific sequences were designed to produce SCAR markers. All three SCAR markers were T. elongatum E genome-specific. Two of these SCAR markers, SCAR(807) and SCAR(577), were present in all seven T. elongatum chromosomes, while SCAR(839) was specific for T. elongatum chromosomes 2E and 3E. These newly developed SCAR markers should be useful for detecting alien genome chromatin or chromosome segments in the genetic background of common wheat.

All-optically controllable random laser based on a dye-doped polymer-dispersed liquid crystal with nano-sized droplets.

This study elucidates for the first time an all-optically controllable random laser in a dye-doped polymer-dispersed liquid crystal (DDPDLC) with nano-sized LC droplets. Experimental results demonstrate that the lasing intensity of the random laser can be controlled to decrease by increasing irradiation time/intensity of one green beam, and increase by increasing the irradiation time of one red beam. The all-optical controllability of the random laser is attributed to the green (red)-beaminduced isothermal nematic-->isotropic (isotropic-->nematic) phase transition in LC droplets by trans-->cis (cis-->trans back) isomerization of azo dyes. This isomerization may decrease (increase) the difference between the refractive indices of the LC droplets and the polymer, thereby increasing (decreasing) the diffusion constant (or transport mean free path), subsequently decreasing the scattering strength and, thus, random lasing intensity.

[A new mediation analysis method for multiple mediators].

Mediation analysis is mainly used to explore the causal mechanism between independent variable X and dependent variable Y. It determines whether mediator M plays a role and evaluate the role's degree in the causal path by decomposing the causal path between the independent variable X and the dependent variable Y. However, the classical mediation analysis is generally used for single mediator. This paper introduces a new mediation analysis method for multiple mediators.

[Application of parametric g-formula in causal analysis].

At present, traditional methods on statistics have limitations in controlling time- varying confounding. This paper introduces an analysis method, parametric g-formula, which would adjust time-varying confounding, and also exemplifies the steps of its implementation for purpose to provide a new reference for researchers to deal with long-term observational data.

Expression of 2',3'-cyclic nucleotide 3'-phosphodiesterase in the amoeboid microglial cells in the developing rat brain.

Expression of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) in amoeboid microglial cells (AMC) in developing rat brain from prenatal day 18 (E18) to postnatal day 10 (P10) was demonstrated by immunohistochemistry/immunofluorescence and immunoelectron microscopy both in vivo and in vitro, respectively. Furthermore, real time-polymerase chain reaction (PCR) was performed to determine the expression of CNPase at mRNA level in cultured microglial cells in control conditions and following lipopolysaccharide stimulation. CNPase immunoreactive amoeboid microglia occurred in large numbers in the corpus callosum, subventricular zone and cavum septum pellucidum at P0 but were progressively reduced with age and were undetectable at P14. By immunoelectron microscopy, immunoreaction product was associated primarily with the plasma membrane, filopodial projections and mitochondria in AMC. Real time-PCR analysis revealed that CNPase mRNA was expressed by cultured amoeboid microglia and was significantly up-regulated in microglial activation induced in vitro by lipopolysaccharide. The functional role of CNPase in AMC remains speculative. Given its expression in AMC transiently occurring in the perinatal brain and that it is markedly elevated in activated microglia, it is suggested that the enzyme may be linked to the major functions of the cell type such as release of chemokines and cytokines. In relation to this, CNPase may play a key role associated with transportation of cytoplasmic materials.

Transient transfection of GGH3-1' cells [GH3 cells stably transfected with the gonadotropin-releasing hormone (GnRH) receptor complementary deoxyribonucleic acid] with the carboxyl-terminal of beta-adrenergic receptor kinase 1 blocks prolactin release: evidence for a role of the G protein beta gamma-subunit complex in GnRH signal transduction.

G proteins consist of heterotrimeric alpha-, beta-, and gamma-subunits. To assess the role of the beta gamma-subunit complex in GnRH receptor-mediated signal transduction, GGH3-1' cells were transfected with plasmids PRK5-beta ARK1 (495-689) containing complementary DNA (cDNA) of the carboxyl-terminal (Gly495-Leu689) of beta-adrenergic receptor kinase 1 (beta ARK1). GGH3-1' cells are GH3 cells that have been stably transfected with rat GnRH receptor cDNA. The carboxyl region of beta ARK1 (Gly495-Leu689) binds to the beta gamma complex and thereby inhibits its action. Twenty-four hours after stimulation, PRL release, cAMP release, and inositol phosphate (IP) production were measured in these cells and in control cells transfected with vector PRK5 cDNA alone. In cells expressing the beta ARK1-(495-689) sequence there was inhibition of basal PRL release (69.3%), cAMP release (61.2%), and IP production (75.5%) compared to cells containing vector only. When cells expressing the beta ARK1 fragment were stimulated with a GnRH analog (Buserelin; 10(-7) M), maximal responses were inhibited (66.1% for PRL release, 52.3% for cAMP release, and 79.1% for IP production). Scatchard analysis of GnRH analog binding was also performed in the two groups of transfected cells. No significant differences in Kd or receptor numbers were found between beta ARK1-(495-689)-transfected cells and control cells containing the vector alone. These data suggest a role for the beta gamma complex in mediation of cAMP release, IP production, and hormone release in response to agonist occupancy of the GnRH receptor.

Effects of Asn318 and Asp87Asn318 mutations on signal transduction by the gonadotropin-releasing hormone receptor and receptor regulation.

GnRH receptor (GnRH-R) contains Asn87 and Asp318 instead of the more frequently observed Asp87 and Asn318 found in other G protein-coupled receptors. In the present study, site-directed mutagenesis was used to introduce Asn318 and Asp87Asn318 into GnRH-R. The effect on coupling and regulation of GnRH-R was studied by stable expression of wild and mutant mouse GnRH-R in the lactotropic GH3 cells; these normally release PRL in response to TRH stimulation. The responses to Buserelin (a metabolically stable GnRH analog) in three different cell lines, M1, N8, and ND1 (expressing wild-type, Asn318 mutant, and Asp87Asn318 mutant mouse GnRH-R, respectively) were compared with that observed in the previously characterized GGH3-1' cells, which stably express rat GnRH-R. The Asn318 and Asp87Asn318 mutations had no measurable effect on ligand binding, but abolished the initial down-regulation of receptor that was observed in M1 and GGH3-1' cells, suggesting that the normal location of Asn87 and Asp318 in GnRH-R is involved in the regulation of GnRH-R. In N8 and ND1 cells, Buserelin-stimulated inositol phosphate (IP) production was attenuated, but the release of both cAMP and PRL was stimulated in a dose- and time-dependent manner. These mutations apparently impaired the coupling between GnRH-R and G proteins involved in IP production, but not those involved in cAMP release. In M1 cells, Buserelin stimulation produced a significant increase in IP production, but neither cAMP nor PRL release was significantly stimulated. These findings are consistent with the previous suggestion that GnRH-stimulated PRL release is mediated by a cAMP second messenger system in transfected GGH3 cells.

GSTT1 and GSTM1 null genotypes and the risk of gastric cancer: a case-control study in a Chinese population.

Glutathione S-transferase (GST) enzymes are involved in detoxification of many potentially carcinogenic compounds. The homozygous deletions or null genotypes of GSTT1 (theta class) and GSTM1 (mu class) genes may be associated with an increased risk of cancer. Few studies have evaluated the relationship between GSTT1, GSTM1 and the risk of gastric cancer, as well as the potential interactions between these genetic markers and other risk factors of gastric cancer in the Chinese population. We conducted a case-control study with 143 cases with gastric cancer, 166 chronic gastritis (CG) cases and 433 cancer-free population controls from Yangzhong County, China. The epidemiological data were collected by a standard questionnaire for all of the subjects, and blood samples were obtained from 91 gastric cancer cases, 146 CG cases, and 429 controls. GSTT1 and GSTM1 genotypes were assayed by the PCR method, and Helicobacter pylori infection was measured by the ELISA method. Using logistic regression model in SAS, we assessed the independent effects of GSTT1 and GSTM1 null genotypes on the risk of gastric cancer and their potential interactions with other factors. The prevalence of GSTM1 null genotype was 48% in gastric cancer cases, 60% in CG patients, and 51% in controls. The prevalence of GSTT1 null genotype was 54% in gastric cancer cases, 48% in CG patients, and 46% in controls. After controlling for age, gender, education, pack-years of smoking, alcohol drinking, body mass index, H. pylori infection, and fruit and salt intake, the adjusted odds ratio (OR) for GSTT1 and gastric cancer was 2.50 (95% confidence interval (CI), 1.01-6.22). When gastric cancer cases were compared with CG patients, the adjusted OR for GSTT1 was 2.33 (95% CI, 0.75-7.25). However, GSTT1 null genotype was not associated with the risk of CG when using population controls. No obvious association was found between GSTM1 and the risk of both gastric cancer and CG. Our results suggest that GSTT1 null genotype may be associated with an increased risk of gastric cancer in a Chinese population.

[Linkage analysis and mutation detection of GRIA3 in Smith--Fineman--Myers syndrome].

To determine the role of GRIA3 in the etiology of Smith--Fineman--Myers syndrome (SFMS), polymorphic short tandem repeats within GRIA3 gene were genotyped by PCR and denaturing polyacrylamide gel electrophoresis to test linkage between GRIA3 and the gene responsible for SFMS. The open reading frame of GRIA3 was detected for mutation by PCR amplification and direct sequencing in affected and normal males from SFMS family. One of the two short tandem repeats was informative in SFMS family. Tight linkage between SFMS locus and GRIA3 gene was established by STR3 within GRIA3 gene. No disease--causing mutation was found within the open reading frame of GRIA3 gene. The disease in SFMS family from Shandong (China) is not caused by the mutation within open reading frame of GRIA3 gene.

[Pancreatic polypeptide in the control of beta-endorphin and prolactin release from rat anterior pituitary in vivo and in vitro].

This study was designed to examine the possible effects of pancreatic polypeptide (PP) on beta-endorphin (beta-EP) and prolactin (PRL) release from rat anterior pituitary in vivo and in vitro. Injection of 0.5 microgram or 2.0 micrograms PP into the third ventricle of the brain (3rd v.i.) produced a significant decrease of the beta-EP and PRL resting secretion. 0.5 microgram PP (3rd v.i.) did not affect restraint stress-induced release of beta-EP, but partially lowered stress induced release of PRL. 2.0 micrograms PP (3rd v.i.) partially reduced restraint stress-induced release of beta-EP and completely suppressed stress-induced release of PRL. In order to investigate a possible direct action of PP on beta-EP and PRL secretion from the anterior pituitary gland, we incubated dispersed anterior pituitary cells with synthetic PP (0.05, 0.625 and 1.00 micrograms) for 1 n, the secretion of beta-EP was not affected at any dosage tested, but 0.625 and 1.00 micrograms PP significantly decreased the PRL secretion. These data indicate that PP may have an inhibitory role in the control of beta-EP secretion at the level of the hypothalamus, and an inhibitory role in the control of PRL secretion at the level of either hypothalamus or anterior pituitary.

[Regulatory role of galanin on prolactin and beta-endorphin release from anterior pituitary lobe of rat].

The role of brain-gut peptide galanin in the regulation of prolactin (PRL) and beta-endorphin (beta-EP) release from anterior pituitary lobe was studied in vivo in conscious male rats and in vitro with cultured anterior pituitary cells of the rat. Galanin (1 microgram or 3 micrograms/rat) injected into the third cerebral ventricle of rats produced highly significant, dose-related increases of PRL resting secretion, but did not alter resting secretion of beta-EP and restraint stress-induced release of PRL and beta-EP. However, galanin (0.05, 0.5 and 1.0 micrograms/5 x 10(5) cells.ml-1) induced highly significant, dose-related increase of beta-EP secretion from dispersed anterior pituitary cells, but failed to alter significantly PRL secretion from the cultured cells. These results indicate that central galanin has a stimulatory role in pituitary PRL resting secretion via the hypothalamus, whereas peripheral galanin stimulates beta-EP secretion only via direct action of this peptide in anterior pituitary cells.