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Urokinase-type plasminogen activator (uPA) and its receptor (uPAR), plasminogen (Plg), and plasminogen activator inhibitors-1 and -2 (PAI-1 and PAI-2) have been observed in many cancers and may contribute to progression and metastasis. In our study, we examined the expression of the 5 proteins by immunohistochemistry in 59 consecutive primary colorectal cancers (CRC) and correlated the protein expression with patient outcome. In addition, we determined the effect of down-regulation of uPAR on the invasive/metastatic capability of CRC cells, by measuring antisense-uPAR transfected HCT116 and control cell lines, in terms of uPAR expression, uPA-binding activity, invasiveness through Matrigel in vitro and metastasis after cecal orthotopic implantation in nude mice in vivo. We found that higher expression of uPA or uPAR in primary tumor tissues was positively correlated with distant metastasis of CRC (Mann-Whitney, p0.02) and negatively correlated with both patient overall survival (OS) and cancer-specific survival (CSS; Cox model, p0.04). The prognostic value of uPA and uPAR for both OS and CSS was independent of other variables (multivariate Cox model, p0. 007). Antisense-uPAR transfected HCT116 cells, which expressed significantly lower levels of total cellular and cell surface uPAR proteins and uPA-binding activity compared with either wild-type or cells transfected with vector alone (Bonferroni, p0.05/3), consistently showed decreased invasiveness through Matrigel (Bonferroni, p0.05/3) and decreased metastasis formation in nude mice (Fisher, p0.05). Our data suggest that uPAR and uPA are independent prognostic factors in CRC; anti-uPAR treatment, which affects both uPAR and uPA levels, may have potential for new treatment of the disease.

Embryogenic calli were produced from mature zygotic embryos of Picea meyeri Rehd. et Wils. which were cultured on modified LP medium containing 30 g/L sucrose, 2 mg/L 2,4-D and 1 mg/L 6-BA. The growth rate of embryogenic calli could be improved by way of suspension culture in medium MS containing 20 g/L sucrose, 1 mg/L 2,4-D and 1 mg/L KT. The optimum values of initial cell density and shake rate of flask in suspension culture were 3.0% (fresh weight) and 150 r/min respectively. Several parameters which might be correlated with growth were determined over a 10 day period. Maximum growth in terms of fresh weight, dry weight and number of ESM occurred during 6-10 day. pH and conductivity attained the lowest point during 6-8 day. A lot of somatic embryos were obtained following transfer of the suspension cultures to medium MS containing 5 mg/L ABA. Mature somatic embryos grew into plantlets with well developed cotyledons after being cultured on 1/2 MS medium supplemented with 0.5% activated charcoal but without hormone.

In this study we have explored the involvement of oxidative stress in Cr(VI)-induced JNK, p38 and ERK signaling pathways and their effects on Cr(VI) cytotoxicity in human non-small cell lung carcinoma CL3 cells. Exposure to K(2)Cr(2)O(7) markedly activated JNK and p38 and moderately activated ERK in a dose- (10-80 microM) and time-dependent (1-12 h) manner. The activated p38 decreased markedly and rapidly and the activated JNK decreased gradually when Cr(VI) was removed from the medium. Post-incubation of Cr(VI)-treated cells with H(2)O(2) increased the activities of JNK and p38, but not ERK. Co-administering Cr(VI) with 3-amino-1,2, 4-triazole (3AT), a catalase inhibitor, enhanced p38 activation, but did not influence JNK and ERK activation by Cr(VI). Conversely, co-administering Cr(VI) with mannitol, a hydroxyl radical scavenger and a Cr(V) chelator, reduced p38 activation and increased JNK and ERK activation by Cr(VI). These results indicate that p38 activation by Cr(VI) is positively correlated with oxidative stress, while JNK activity can be enhanced by either a quencher (mannitol) or activator (H(2)O(2)) of redox reactions in Cr(VI)-exposed CL3 cells. However, both 3AT and mannitol reduced the cytotoxicity of Cr(VI), but H(2)O(2) did not. The JNK activated by Cr(VI) was decreased (approximately 50%) by expression of a kinase-defective form of MKK7 (MKK7A) but not that of MKK4 (MKK4KR), suggesting that activation of JNK by Cr(VI) is mediated through MKK7. SB202190, a specific inhibitor of p38, markedly decreased JNK but did not change ERK activation by Cr(VI). PD98059, a specific inhibitor of ERK kinases MKK1/2, blocked ERK and p38 but did not alter JNK activation by Cr(VI). Neither the specific kinase inhibitors nor expression of MKK7A altered Cr(VI)-induced cytotoxicity. Together, these results suggest that activation of the JNK, p38 and ERK pathways by Cr(VI) is mediated through diverse redox mechanisms, yet their activation does not correlate with Cr(VI) cytotoxicity.

Cadmium (Cd), a human carcinogen, can induce apoptosis in various cell types. Three major mitogen-activated protein kinases (MAPKs), c-JUN N-terminal kinase (JNK), p38 and extracellular signal-regulated kinase (ERK), have been shown to regulate apoptosis. In this study we explore the ability of Cd to activate JNK, p38 and ERK, including their effects on Cd-mediated growth inhibition and apoptosis in a human non-small cell lung carcinoma cell line, CL3. The kinase activity of JNK was induced dose-dependently by 30-160 microM CdCl(2). High cytotoxic doses of Cd (130-160 microM) markedly activated p38, but low Cd doses did not. Conversely, the activities of ERK1 and ERK2 were decreased by low cytotoxic doses of Cd (/=80 microM) and moderately activated by high Cd doses. Low cytotoxic doses of Cd transiently activated JNK and simultaneously reduced ERK activity, whereas high cytotoxic doses of Cd persistently activated JNK and p38. PD98059, an inhibitor of ERK upstream activators MAPK kinase (MKK) 1 and MKK2, greatly enhanced cytotoxicity and apoptosis in cells treated with low Cd doses. In contrast, SB202190, an inhibitor of p38, decreased the cytotoxicity and apoptosis induced by high Cd doses. Transient expression of a dominant negative form of JNK1, but not that of JNK2, significantly increased the viability and prevented apoptosis of Cd-treated cells. However, expression of wild-type JNK1 did not affect viability and apoptosis of Cd-treated cells. Transfection of wild-type JNK2 or p38 enhanced apoptosis of cells exposed to low Cd doses but did not affect those exposed to high Cd doses. The JNK activity stimulated by low Cd doses was partially suppressed by expression of a dominant negative form of MKK7, but not a dominant negative form of MKK4, indicating that MKK7 is involved in JNK activation by Cd. Together, the results of this study suggest that JNK and p38 cooperatively participate in apoptosis induced by Cd and that the decreased ERK signal induced by low Cd doses contributes to growth inhibition or apoptosis.

To correlate conformational rigidity with membranolytic selectivity of antimicrobial activity and cytotoxicity, we prepared six cyclic analogs of protegrin-1 (PG-1), an 18-residue cationic peptide with a broad-spectrum antimicrobial activity. These cyclic protegrins bear end-to-end peptide bonds together with varying numbers (zero to three) of cross-strand disulfide constraints. The most constrained analog is a cyclic tricystine protegrin (ccPG 3) containing three evenly spaced, parallel disulfide bonds. Antimicrobial assays against 10 organisms in low- and high-salt conditions showed that these cyclic protegrins were broadly active with different antimicrobial profiles against Gram-positive and Gram-negative bacteria, fungi and one tested virus, HIV-1. Compared to PG-1, the cyclic tricystine ccPG 3 displayed approximately a 10-fold decrease in hemolytic activity against human cells and 6- to 30-fold improvement of membranolytic selectivity against six of the 10 tested organisms. In contrast, [DeltaSS]cPG 8, a cyclic protegrin with no disulfide bond, and [DeltaCys6,15]cPG 5, a cyclic mimic of PG-1 with one disulfide bond, exhibited activity spectra, potency, and cytotoxicity similar to PG-1. Circular dichroism showed that cyclic protegrins containing with one to three cystine bonds displayed some degree of beta-strand structures in water/trifluoroethanol or phosphate-buffered solutions. Collectively, our results indicate that cyclic structures are useful in the design of antimicrobial peptides and that an increase in the conformational rigidity of protegrins may confer membranolytic selectivity that dissociates antimicrobial activity from hemolytic activity.

This retrospective study was undertaken to investigate the expression of bcl-2 protein and messenger RNA in colorectal cancer (CRC). Immunohistochemical analysis using a monoclonal mouse antibody to the bcl-2 protein and in situ hybridization using a digoxigenin-labelled bcl-2 cRNA probe were carried out on formalin-fixed and paraffin-embedded specimens from 53 colorectal adenocarcinomas, 27 liver secondaries, and 60 adenomas with various degrees of dysplasia. Normal human tonsil sections were used as positive controls. Expression of bcl-2 protein and of messenger RNA was evaluated semiquantitatively. The expression of bcl-2 protein was gradually and significantly lost during the progression from moderately dysplastic adenoma to primary CRC (moderate/severe dysplasia: Mann-Whitney U-test, p=0.0001; severe dysplasia/primary CRC: p=0.027), whereas the cellular expression of bcl-2 mRNA was gradually increased during the dysplasia/adenoma-carcinoma neoplastic sequence. These observations suggest that in a proportion of colorectal cancer cases, the bcl-2 proto-oncogene expression may be down-regulated at a post-transcriptional level.

To investigate DNA damage induced by Pb2+ and its prevention by scavengers, we determined DNA strand breakage and the formation of 8-hydroxydeoxyguanosine (8-OHdG) in DNA using plasmid relaxation assay and HPLC with electrochemical detection, respectively. Lead acetate induced DNA strand breakage in 10 mM of Hepes buffer, pH 6.8, in a time- and dose-dependent manner. Compared with lead, zinc acetate did not significantly induce DNA breakage. The singlet oxygen scavengers NaN3 and 2,2,6,6-tetramethyl-4-piperidone (TEMP) inhibited lead-induced DNA breakage more efficiently than the hydroxyl radical scavengers mannitol and DMPO. Deuterium oxide (D2O), a singlet oxygen enhancer, potentiated lead-induced DNA breakage. At low ratios to Pb2+, NADPH, glutathione, and 2-mercaptoethanol enhanced lead-induced DNA breakage, whereas high ratios of these agents protected it. Catalase and superoxide dismutase (SOD) did not protect DNA breaks induced by Pb2+. Lead-induced DNA breakage was markedly enhanced by H2O2, and this induction was inhibited by NaN3, TEMP, EDTA, catalase, BSA, and glutathione. In contrast, mannitol and SOD potentiated Pb2+/H2O2-induced DNA breaks. The results indicate that singlet oxygen, lead, and H2O2 are all involved in the reaction system, whereas hydroxyl radical and superoxide did not. Lead could cause a small amount of 8-OHdG formation in calf thymus DNA and dose-dependently induced the formation of this adduct in the presence of H2O2. Singlet oxygen scavengers were more effective than hydroxyl radical scavengers in protection from lead/H2O2-induced 8-OHdG adducts. Taken together, these results suggest that lead may induce DNA damage through a Fenton-like reaction and that singlet oxygen is the principal species involved.

We undertook a retrospective study to investigate the correlation between the expression of vascular endothelial growth factor (VEGF) and urokinase-type plasminogen activator (u-PA) proteins with progression of colorectal carcinoma (CRC). Immunohistochemical analyses using antibodies against VEGF and u-PA were carried out on archival specimens of 58 human colon carcinomas, 30 liver secondaries and 20 adenomas. Expression of VEGF was significantly reduced in the metastatic liver tumours compared with primary ones (Wilcoxon test, P = 0.002), suggesting VEGF activity to be secondarily down-regulated once the tumour cells reach the hepatic parenchyma. There was no strong evidence from our data that the level of VEGF or u-PA in the primary tumour could predict risk of liver metastasis or survival duration. VEGF and u-PA expression were positively correlated in primary CRC suggesting that both proteins may interact in vivo (chi-square test, P = 0.019) in tumour progression.

Reports on the histological and biochemical nature of periprosthetic fibrous/granulomatous tissue has, to date, been largely limited to frozen tissue sections. This study reports the cytokine and matrix metalloproteinase profiles found in periprosthetic interface tissues in THA which have failed due to aseptic loosening and in capsular tissues obtained at primary surgery. The study employs immunohistochemistry, in situ hybridization, and color video image analysis on formalin fixed and paraffin embedded sections.

Various grades of portland blast furnace slag cement (PBFC) and normal portland cement (OPC) concrete have been cured under adiabatic and semi-temperature matched curing conditions. Comparisons of the compressive strength between adiabatic, semi-temperature matched and ambient cured concrete have been made. The results indicated that the curing history had significant influence on the compressive strength development and the in-situ early strength of PBFC concrete is comparable to the same grade of OPC concrete after three days. The high curing temperature (above 65 degrees C) reduced the later-age strength both for PBFC and OPC. The durability of the concrete cured under various conditions was also evaluated by rapid chloride permeability test.

We have previously shown that c-erbB-2 oncoprotein encoded by the erbB-2 gene is overexpressed in human colorectal cancers that metastasis compared to those that are cured by surgery. To determine whether c-erbB-2 is also differentially expressed in vivo in metastasising and non-metastasising tumours, we developed models of colorectal cancer growth in nude mice. Human colon cancer cell lines, HCT116, KM12SM, LIM1215 and SW480, were injected into the caecum after characterising their morphology, doubling time, DNA flow-cytometry and expression of c-erbB-2. Six weeks later, xenografted tissues were fixed for histological analysis and detection of c-erbB-2 by immunohistochemistry, 78% (21/27) of mice developed caecal cancers. The caecal tumours derived from HCT116, KM12SM or LIM1215 were highly metastatic; 67 to 100% of them had liver metastases and lymph node involvement and 33 to 75% had lung tumours. Most of the tumours were c-erbB-2-positive. In contrast SW480 caecal tumours had only 33% lymph node involvement, but not liver or lung metastases. Only one SW480 caecal tumour and one lymph node metastasis expressed c-erbB-2. C-erB-2 was more frequently expressed in xenografted tissues in colon cancer primaries and secondaries of the highly metastatic cells (HCT116, KM12SM and LIM1215) compared to the cells (SW480) giving predominantly local growth. Our results suggest that c-erbB-2 gene may play an important role in the development of metastasis from colorectal cancer.

Evidence-based health care (EBHC) is a growing movement to integrate healthcare research with healthcare practice. A key element to EBHC is convenient access to relevant high-quality evidence. The Cochrane Collaboration is an international consortium of persons dedicated to producing and maintaining systematic reviews of healthcare practice and is an invaluable resource to the EBHC movement. This article will describe EBHC briefly and will highlight how the Cochrane Collaboration supports the EBHC perspective to create an efficient and effective healthcare system.

The molecular mechanisms responsible for metastasis are not fully understood. Recently, expression of the KAI1 gene on human chromosome 11p11.2 was found to be down-regulated in metastatic prostate cancer cell lines compared with normal human prostate, suggesting that KAI1 may be a metastasis suppressor gene. The aim of this study was to investigate whether there is reduced expression of KAI1 in late-stage bladder cancer. Sixty-six paraffin-embedded bladder tissue sections were analyzed for KAI1 mRNA by in situ hybridization. Nineteen of these were from patients with no histological evidence of bladder cancer, and 47 were from papillary transitional cell carcinomas (TCCs); of these, 16 were highly invasive. KAI1 mRNA was highly expressed in the specimens of normal bladder (11 of 11; 100%), inflammatory bladder (5 of 8; 63%), and noninvasive papillary TCCs of grades 1 and 2 (15 of 24; 63%), compared to grade 3 papillary TCCs (1 of 7; 14%) or invasive TCCs (1 of 16; 6%). The differences in expression between local and invasive disease were statistically significant (P/= 0.01, chi2 test). Our results suggest that down-regulation of KAI1 mRNA is significantly associated with invasive bladder cancer and that KAI1 may represent an invasion/metastasis suppressor gene in bladder cancer.

Studies in epithelial cancer, including colorectal cancer, suggest that c-erbB-2 may be an important gene in metastatic disease. The expression of c-erbB-2 mRNA and c-neu were assessed in 25 human non-metastasising colorectal cancers and 34 primary metastasising colorectal cancer and their liver metastasis by in situ hybridisation and immunohistochemistry respectively. The metastasising colorectal cancers and their liver metastases expressed c-erbB-2 mRNA (76%, 70%) and c-neu (70%, 68%) at significantly higher levels than the nonmetastasising tumours (28% and 36% respectively chi-squared: p0.003 and p0.04). Moreover, c-erbB-2 mRNA predicted the development of liver metastases in tumours that had not metastasised to lymph nodes (p = 0.002). This gene may play an important role in the development of metastasis in colorectal cancer and its mRNA expression may have important implications for deciding which patients with lymph node negative disease require chemotherapy.

The structural and magnetic properties of F16CuPc thin films and powder, including x-ray diffraction (XRD), superconducting quantum interference device (SQUID) magnetometry, and theoretical modelling of exchange interactions are reported. Analysis of XRD from films, with thickness ranging between 100 and 160 nm, deposited onto Kapton and a perylene-3,4,9,10-tetracarboxylic-3,4,9,10-dianhydride (PTCDA) interlayer shows that the stacking angle (defined in the text) of the film is independent of the thickness, but that the texture is modified by both film thickness and substrate chemistry. The SQUID measurements suggest that all samples are paramagnetic, a result that is confirmed by our theoretical modelling including density functional theory calculations of one-dimensional molecular chains and Green's function perturbation theory calculations for a molecular dimer. By investigating theoretically a range of different geometries, we predict that the maximum possible exchange interaction between F16CuPc molecules is twice as large as that in unfluorinated copper-phthalocyanine (CuPc). This difference arises from the smaller intermolecular spacing in F16CuPc. Our density functional theory calculation for isolated F16CuPc molecule also shows that the energy levels of Kohn-Sham orbitals are rigidly shifted similar to 1 eV lower in F16CuPc compared to CuPc without a significant modification of the intramolecular spin physics, and that therefore the two molecules provide a suitable platform for independently varying magnetism and charge transport.

The molecular nature of lead-induced mutations was examined in this study to more thoroughly understand lead mutagenesis. Chinese hamster ovary K1 cells were exposed to 0.5-3 mM lead acetate for 24 h. The median lethal dose (LD50) value was 1.5 mM, and the hypoxanthine guanine phosphoribosyltransferase (HPRT) mutant frequency increased linearly as lead concentrations were raised from 0.5 to 1.5 mM. We also amplified the HPRT cDNAs of 56 independent lead-induced mutants by reverse transcriptase-polymerase chain reaction (PCR). Forty-two mutant cDNAs were successfully amplified: 36 mutants had transcripts of normal or slightly smaller than normal size, and six mutants had large deletions. The other 14 mutants whose HPRT cDNA could not be amplified were subjected to genomic-DNA PCR analysis. All of those mutants had one or more exons missing from their genomic HPRT DNA. DNA sequencing of mutant cDNAs showed that 22 had single-base substitutions, four had small alterations, 10 had single-exon deletions, and six were missing two or three exons. Furthermore, DNA sequencing of the HPRT intron-exon boundaries in eight splice mutants revealed that all of them had single-base substitutions in their genomic DNA. G.C base substitutions occurred 3.3-fold more frequently than A.T base substitutions. Similar frequencies were observed for G.C--A.T, G.C--T.A, and G.C--C.G mutations. These results suggest that G.C base pairs may be the primary target sites for lead mutagenesis.

This study surveyed wood dust exposure levels and pulmonary hazards among wood mill workers. Dust concentrations as measured by six-stage cascade impactors were high in work areas of grinding and screening. Total dust concentrations for these dusty activities ranged from 4.4 to 22.4 mg/m3, and the respirable proportions were between 2.4% and 50.2%. The dust level in the sawing work was 2.9 mg/m3. Although symptoms of cough and phlegm were higher in smoking workers than in nonsmoking workers, the prevalence of respiratory symptoms in the exposed workers was not significantly higher than in the controls. However, the incidence of symptoms such as chronic phlegm and chronic bronchitis in the nonsmoking high-exposure workers was significantly higher than in nonsmoking controls. The mean values of MMF, PEFR, and FEF25% were significantly lower in the exposed workers than in controls for both smokers and nonsmokers. The pulmonary function deficits, with the exception of FEV1.0/FVC, also showed a significant trend with increasing levels of wood dusts exposure classified by job titles for both smokers and nonsmokers. After adjustment for age, sex, height, and smoking status, all parameters of pulmonary function were significantly lower in exposed workers than in controls and showed a declining trend with increasing exposure levels classified by job titles. These results indicate that high level of wood dust exposure in the wood mill industries may lead to pulmonary hazards. Engineering control and industrial hygiene are mandatory for dusty activities.

A total of 2848 study sites, with about 500 people in each, were randomly sampled for this investigation which covered a total population of 1 477 742. By stool examinations using the Kato-Katz thick-smear and larval-culture techniques, overall prevalences of 47.0%, 18.8%, and 17.2% were obtained for Ascaris lumbricoides, Trichuris trichiura, and hookworm infections, respectively. The number of infections due to Ascaris, Trichuris, and hookworm was estimated as 531 million, 212 million, and 194 million, respectively. Egg counts showed that 75-95% of the subjects had light infections. Higher prevalences of ascariasis and trichuriasis were found in the age group of 5-9, 10-14 and 15-19 years, and among adults for hookworm. Students, farmers (including vegetable growers) and fishermen were the occupational groups with high infection rates. The prevalence of helminthiases was found to be closely associated with climatic and geographical factors. In view of the morbidity and mortality due to these helminthiases, their control, particularly in schoolchildren, is very important.

This paper is concerned with the propagation of Lamb waves in double-layered nanoplates and a nonlocal continuum model is presented. Each layer of the double-layered nanoplates is coupled through the van der Waals interaction. The equations of wave motion are derived and dispersion relations are obtained. The present model predicts some notable features of the dispersion relations in double-layered nanoplates, in comparison with Lamb waves in classic plates in vacuo. By considering the van der Waals interaction, some modes appear in pairs at the same frequency, their phase velocities are very close at a given frequency. Some modes only propagate in a very narrow frequency band and may disappear above certain frequencies. The small-scale has significant influence on the propagation characteristics of Lamb waves. Larger values of the scale coefficient result in lower escape frequencies and phase velocities of Lamb waves.

The effect of human O6-methylguanine-DNA methyltransferase (MGMT) on the cytotoxicity, the mutagenicity, and the specific kinds of base substitutions induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were examined in non-MGMT transfected Chinese hamster ovary cells (CHOM cells) and in those cells which had been transfected with human MGMT complementary DNA (AGT cells). AGT cells containing a high level of human MGMT activity were markedly more resistant to the cytotoxic and mutagenic effects of MNNG than CHOM cells which had no detectable MGMT activity. The dosages of MNNG which reduced to 50% of colony forming ability were estimated to be 0.8 microM for CHOM and 10 microM for AGT cells. The induction frequency of 6-thioguanine-resistant cells was significantly declined in AGT cells. At 4 microM MNNG, this frequency was declined from 273 mutants/10(6) viable CHOM cells to 13 mutants/10(6) viable AGT cells. The entire coding region of the hypoxanthine (guanine) phosphoribosyltransferase (hprt) gene in 37 AGT and 22 CHOM mutants was characterized by direct sequencing of the mRNA-polymerase chain reaction-amplified complementary DNA. Base changes at the intron-exon boundaries of the hprt DNA in the splicing mutants were further examined. Those results indicated that G to A transitions were significantly reduced in MNNG-treated AGT cells (chi 2 test, P0.001), suggesting that O6-methylguanine was repaired error free by human MGMT. In contrast, no difference arose in the frequencies of T to C transitions induced by MNNG in these two populations. All of the G to A transitions induced in AGT cells were located on the nontranscribed strand, assuming that the causative lesion was O6-methylguanine (P0.05). Such a strand specificity was not observed in CHOM mutants. Most of the G to A transitions observed in CHOM mutants were located at the middle guanine of 5'-GGPu sequences. Transitions observed at these sites, particularly 5'-GGG, were significantly reduced in AGT mutants (P0.05). Our results have suggested that human MGMT specifically repairs O6-methylguanine with a preference to remove those located on the transcribed strand and middle guanine of 5'-GGG.

An eight-month-old male infant with corrected transposition of the great arteries and severe systemic atrioventricular valve regurgitation due to "Ebstein-like anomaly" is reported. Through a midline sternotomy and transeptal approach, a 20 mm Medtronic Hall aortic mechanical valve was reversely implanted into the systemic atrioventricular valve. Anti-platelet drugs (acetylsalicylic acid and dipyridamole) were prescribed for prevention of thromboembolism. The patient is doing well three years after operation.

Autoimmune mechanisms may be involved in the pathogenesis of insulin dependent diabetes mellitus (IDDM). Multiple autoantibodies have been detected in patients with IDDM. Islet cell antibodies (ICA), complent-fixing islet cell antibodies (CF-ICA) and antibodies to an islet cell protein 64000 M(r) (64K antibodies) have been regarded as immunological markers in IDDM. ICA detection with immunohistochemistry requires fresh normal human pancreas (blood group O) which provides an antigen for measuring ICA in serum samples. In the present study ICA detection was first carried out by using avidin-biotin-peroxidase complex technique (ABC) method and paraffin sections of human pancreas (blood group O), Serum samples were obtained from 17 patients with IDDM, 20 with NIDDM and 20 without diabetes mellitus. In patients with IDDM, ICA were detected in 9 of the 17 (52.94%) while none of the patients with NIDDM and without diabetes mellitus were ICA positive. In comparison with other methods, the present one is more reliable, sensitive, specific and simple. Therefore, it may be widely used for ICA detection in clinical practice.

Background Identifying molecular determinants underpinning response and resistance to anti-cancer therapies is essential to selecting optimal treatment for patients (pts). The PI3K pathway is frequently deregulated in cancer. In preclinical models deregulated PI3K has been shown to enhance the survival of breast cancer cells and confer resistance to chemotherapy and HER2−directed agents. This exploratory study evaluated the impact PIK3CA mutations and PTEN loss had on the efficacy of paclitaxel alone (P) and in combination with lapatinib (L+P) in HER2−positive metastatic breast cancer (MBC) pts enrolled in study EGF104535, results of which demonstrated that pts treated with the combination of L+P derived an absolute improvement in median overall survival (OS) of 7.3.months (median OS=27.8 months in L+P compared with 20.5 months in P). Method Baseline tissue from primary breast tumor or metastatic site was obtained in the form of formalin-fixed, paraffin-embedded material. Of the total study population (n=444), 389 pts had tissue available for biomarker analyses, 277 of whom provided written informed consent for optional tumor genetics (i.e., PIK3CA analysis). PTEN was evaluated on whole sections by immunohistochemistry (rabbit monoclonal antibody); pathology review and image analysis were performed, producing an ordinal score and optical density (OD). Qiagen/DxS assay was used in assessing PIK3CA mutation status. Logistic regression and Cox-proportional hazard models were used in analyses of biomarkers with efficacy endpoints. Results Evaluable results for PTEN and PIK3CA were available for 91% (354/389) and 62% (171/274) of pts, respectively. In the overall population, 24% (65/274) had tumors harboring PIK3CA mutations (E542K, E545K/D, H1047R); 13% (49/389) had absence of PTEN expression. Survival outcome appeared to be independent of PTEN expression (P >0.2). PIK3CA mutations were significantly associated with worse OS (HR=1.88; 95% CI=1.26, 2.80; P=0.002). PFS was significantly improved in pts treated with L+P compared with P in both PTEN strata (loss/expression; P Conclusions In this exploratory study, PTEN was not prognostic whereas PIK3CA mutations appear to be an adverse prognostic feature in HER2+ MBC. PTEN expression may not be predictive as both strata derived significant benefit with L+P treatment. PFS benefit from L+P was significant in pts with PIK3CA wildtype tumors whereas the PFS benefit was not significant in the PIK3CA mutation strata. Additional analyses are ongoing and will be presented. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr S3-3.

To investigate the effect of DNA replication on the mutation spectrum induced in diploid human fibroblasts by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), cells were synchronized and exposed to MNNG either at the G1-S border or in late S phase, and the mutations in the hypoxanthine (guanine) phosphoribosyltransferase (hprt) gene were examined. The coding regions of 92 independent mutants were characterized by direct sequencing of mRNA-polymerase chain reaction-amplified complementary DNA. While there was little difference in the sensitivity of the two populations to the cytotoxic effects of MNNG, the frequency of mutants induced in late S populations was significantly lower than that induced in G1-S populations. The majority of induced complementary DNA mutations were single base substitutions (54%) and splice site mutations (43%). Analysis of the intron-exon boundaries of more than one-half of the splicing mutants showed that almost all contained base substitutions in the hprt gene. A broad mutational spectrum was observed in low-dose (4, 6, or 8 microM) treatments; only 27% were G to A transitions, whereas 80% of base substitutions derived from the high-dose (10 or 12 microM) treatments were G to A transitions in G1-S populations. An intermediate frequency (64%) of G to A transitions was observed in late S populations exposed to MNNG. When the causative premutation lesion was O6-methylguanine, 75% of G to A transitions that were observed in G1-S populations clustered on both the transcribed and the nontranscribed strands of the 5' half of the hprt gene. In contrast, 50% of G to A transitions were located only on the nontranscribed strand of this region in late S populations. The results indicate that O(6)-alkylguanine-DNA-alkyltransferase may not efficiently remove O(6)-methylguanine from the 5' half of the gene but can repair lesions far away from this region during initiation of replication. Our results are consistent with the notion that the putative origin of replication is located at intron 1 of the hprt gene.

Desmosomes were isolated first from fresh cow nose epidermis. Desmoplakin I (DP I) was purified from desmosome preparations by SDS-polyacrylamide gel electrophoresis and anti-DP I McAb was obtained via hybridoma technique. The tissue specificity showed that all the normal epithelia, different kinds of epithelial tumors and meningioma were positive, whereas non-epithelial tissues and their corresponding tumors gave a negative result. Positive staining showed a series of punctate reaction locating along the cell-cell borders, each spot representing a desmosome or a cluster of closely spaced desmosomes. It is suggested that McAb of DP I is a reliable immunohistochemical probe for epithelial tumor and meningioma diagnosis.

Chinese versions of Conners' Teacher's Rating Scale (CTRS) and the Werry-Weiss-Peters Activity Scale (WWPAS) were applied to 4,290 randomly selected primary school children in Kaohsiung. Using relative operational characteristic analysis to determine the best cut-off points, the validity of the WWPAS and CTRS for estimating the prevalence of attention deficit hyperactivity disorder (ADHD) was established. It was found that CTRS had satisfactory results, but the WWPAS did not have an optimal cut-off score. Using CTRS as a screening tool, the estimated overall prevalence rate of ADHD among Kaohsiung primary school children was found to be 9.9%, while the rate in boys (14.9%) was 3.3 times higher than in girls (4.5%). The assumption that hyperactivity is uncommon among Chinese children was proven to be unreliable.

BVES is novel adhesion protein that functions as a modulator of tight junction (TJ) formation with TJs level directly correlating with BVES expression. TJs, in addition to regulating paracellular passage of molecules, can also directly regulate Rho activity and transcriptional activation of cell cycle regulatory genes (ERBB2, PCNA, CDK4, and Cyclin-D1). Hence, alteration in BVES expression also modulates TJ associated signaling. Interestingly, overexpressing a dominant negative BVES induced human corneal epithelial cells to exhibit increased mesenchymal characteristics. Together, these observations led us to hypothesize that increasing BVES expression in carcinoma cells would induce an epithelial-like phenotype. To evaluate the function of BVES in carcinoma, a semi-adherent LIM2405 human colorectal cancer cell line was stably transfected with wild type BVES (WT-LIM2405) or empty vector (V-LIM2405) as control. Multiple stably transfected clonal isolates of LIM2405 overexpressing BVES exhibited increased epithelial features as evidenced by: i) uniform monolayer formation, ii) decreased vimentin and increased cytokeratin, Zo-1, and occludin expression, iii) decreased cellular motility (66% reduction, p Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3076.

The sera from 86 patients with autoimmune diseases, 31 atopic and 65 healthy blood donors were detected for IgE type rheumatoid factor (IgE-RF) by using anti-human IgE monoclonal antibody and dot immunobinding assay. The positive frequency and mean value of IgE-RF in patients with autoimmune diseases were significantly higher than those in the other groups. IgE-RF was positive in 19/37 cases of rheumatoid arthritis (RA), 6/18 systemic lupus erythematosus and 13/31 primary Sjogren's syndrome, with mean values of 23.1, 12.1 and 26.9 ng/ml respectively. 75% RA patients with IgM-RF (+) had IgE-RF, with a mean value of 27.0 ng/ml, whereas 33% of those with IgM-RF (-) had IgE-RF with a mean value of 16.5 ng/ml. In contrast, only 2/31 atopic and 6/65 healthy blood donors had positive IgE-RF with mean values of 3.7 and 6.1 ng/ml respectively. Hence, IgE-RF is helpful not only in raising the sensitivity of RA diagnosis, but also in distinguishing autoimmune diseases from allergy.

We reported 9 cases of primary Sjogren syndrome (SS) who were complicated with nervous system involvement. All were women. Age between 24 to 58 years old. Their clinical symptoms of the nervous system varied widely, 7 of them manifested with the involvement of central nervous system, the main features were in case 1 bouts of seizures, case 2 multi-level damage of the brain and spinal cord which was similar to multiple sclerosis, case 3 recurrent hemiplegia caused by cerebral thrombosis then fatal vascular hemorrhage, case 4 sudden hemiplegia, case 5 persistent psychological disturbance, case 6 cranial neuropathy of V and VII, case 9 multi-focal symptoms of ataxia, myelopathy and transient blindness. 5 of the 9, case 3, 6-9 all appeared with the symptoms of peripheral neuropathy, case 7 also complicated with carpal tunnel syndrome. 4 of the 9 cases also complicated with renal tubular acidosis and/or chronic active hepatitis and/or fibrosing alveolitis and/or thrombocytopenic purpura and/or myositis. No differences of the positivity of autoantibodies was observed between those with or without nervous system involvement.

It is shown that the superconductivity in Ce1−xGdxFeAsO0.84F0.16 compounds can be modulated by internal (chemical) pressure. The internal pressure is induced by Gd substitution for Ce in CeFeAsO0.84F0.16, which compresses the crystal lattice. The temperature dependences of resistivity and magnetization show that the superconducting-transition temperature Tc is enhanced from 40 K for CeFeAsO0.84F0.16 to 47.5 K for Ce0.6Gd0.4FeAsO0.84F0.16. The increase and subsequent decrease of Tc upon application of external pressure, as observed previously in LaFeAsO0.89F0.11, is entirely confirmed by the modulation of Tc of the Ce1−xGdxFeAsO0.84F0.16 superconductors by internal pressure.

The American Rheumatism Association (ARA) 1958 and 1987 criteria for the classification of rheumatoid arthritis (RA) were applied to 111 consecutive RA patients and 54 patients with non-RA connective tissue diseases from three hospitals of tertiary level in Beijing. Comparison of the two criteria showed that the specificity was the same, being 88% for both, whereas the sensitivity varied from 94% of the 1958 criteria to 91% of the 1987 criteria. Factors affecting the sensitivity were morning stiffness for more than one hour and increase of number of swollen joints from one to three in the 1987 revised criteria.

To explore the possible etiological associations between the infection of Epstein-Barr Virus (EBV) and the occurrence of renal tubular acidosis (RTA) of primary Sjogren's syndrome (SS), renal biopsies from both primary SS with clinical or subclinical RTA and controls were detected by using a monoclonal antibody against EBV early antigen P138 and a 32P-labelled EBV Bam W probe. As a result, cytoplasmic fluorescence staining of epithelial cells with the monoclonal antibody as described above was noted in all the seven renal biopsies from primary SS, and one out of two renal samples among them contained EBV DNA detectable by dot blot hybridization with Bam W probe. Whereas five control renal biopsies were all negative on the same methods of detection. Our study suggested that EBV has been of a lytic fate leading to active replication in the kidneys of patients with RTA of primary SS. Therefore, EBV may play an important role in the renal damage, especially resulting in RTA, of primary SS.

We are comparing the kinds and spectra of mutations induced when DNA containing covalently bound carcinogen residues (adducts) replicates in human cells. A shuttle vector, pZ189, carrying the supF gene coding for a bacterial tyrosine suppressor tRNA as the target was treated with tritiated polycyclic aromatic carcinogens and the number of adducts per plasmid was determined. The plasmids were trarsfected into human cells, and after replication had occurred, the progeny plasmids were rescued and assayed for the frequency of supF mutants. The carcinogens studied included the 7,8-diol-9,10-epoxide of benzo[a]pyrene (BPDE), 1nitrosopyrene (1-NOP), N-acetoxy-2-acetylaminofluorene (N-AcO-AAF), and its trifluoroacetyl derivative (N-AcO-TFA-AF). BPDE binds principally to the N2 position of guanine. The other three carcinogens bind to the C8 position of guanine. Each agent caused a linear increase in the frequency of supF mutants as a function of the number of DNA adducts formed, reaching frequencies as high as 20 x 10-4 to 40 x 10-4, above a background frequency of 1.4 x 10-4. When compared on the basis of adducts formed, BPDE was approximately four times more mutagenic than the other three carcinogens. This difference may reflect intrinsic differences in the nature of the adducts and their location in the DNA molecule, but it may also reflect differences in the rate of removal of particular adducts by nucleotide excision repair since we showed that the host cells excise BPDE induced adducts from genomic DNA at least three times slower than they excise 1-NOP induced adducts. Agarose gel electrophoresis and DNA sequencing analysis of mutants derived from untreated plasmids showed that the majority (70%) involved deletions, insertions, or altered gel mobility (gross rearrangements). In contrast, the majority of those from carcinogen treated plasmids were base substitutions. DNA sequencing of 86 unequivocally independent mutants derived from BPDE treated plasmids and 60 from 1-NOP treated plasmids indicated that 70% to 80% contained a single base substitution, 5%-10% had two base substitutions, and 4%-10% had small insertions or deletions (one or two base pairs). The majority (83%) of the base substitutions were transversions, predominantly G•C→T•A.These two carcinogens produced their own spectrum of mutations. Studies to date with the N-AcO-TFA-AF have shown that the AF adduct induces predominantly base subsitutions and all of these involve guanine.

An SV40-based shuttle vector, pZ189, carrying a bacterial suppressor tRNA target gene (supF), was treated with radiolabeled polycyclic aromatic carcinogens and the number of covalently bound residues (adducts) per plasmid was determined. The plasmids were transfected into human cell line 293, allowed to replicate, and the progeny plasmids rescued and assayed for the frequency of supF mutants. The agents tested were the 7,8-diol-9,10-epoxide of benzo(a)pyrene (BPDE) and 1-nitrosopyrene (1-NOP). With each agent there was a linear increase in the frequency of supF mutants as a function of the number of DNA adducts formed, reaching frequencies 15 to 25 times higher than the background frequency of 1.4 x 10(-4). When compared on the basis of adducts formed per plasmid BPDE, which forms its principal DNA adduct at the N2 position of guanine, was approximately four times more mutagenic than 1-NOP, which binds principally at the C8 position of guanine. This difference in mutagenic effectiveness may reflect intrinsic differences in the nature of the adducts and their location in the DNA molecule, but it could also reflect a difference in the rate of removal of particular adducts by nucleotide excision repair since the 293 host cell line excised BPDE-induced adducts from genomic DNA at least three times slower than 1-NOP-induced adducts. Agarose gel electrophoresis and DNA sequencing analysis of mutants derived from untreated plasmids showed that the majority (70%) involved deletions, insertions, or altered gel mobility (gross rearrangements). In contrast, the majority of those derived from carcinogen-treated plasmids were base substitutions. DNA sequencing of 86 unequivocally independent mutants derived from BPDE-treated plasmid and 60 from 1-NOP-treated plasmid indicated that 70% to 80% contained a single base substitution, 5%-10% had two base substitutions, and 4%-10% had small insertions or deletions (one or two basepairs). The majority (83%) of the base substitutions in mutants from BPDE- or 1-NOP-treated plasmid were transversions, mainly G.C----T.A. Each carcinogen produced its own spectrum of mutations.

Strong evidence points to mutation induction as one mechanism by which changes are introduced into normal cells to convert them into cancer cells. To understand the mechanisms by which mutations are induced in human cells by carcinogens, we are determining the kinds and spectra of mutations induced in the coding region of the hypoxanthine(guanine)phosphoribosyltransferase (hprt) gene. This region, composed of 654 bp, represents nine exons from a 44 kbp gene. To be able to analyze a large number of independent mutants rapidly and economically, we have optimized the conditions for copying mRNA directly from lysates of a small number of cells (e.g., 100) from a 6-thioguanine-resistant clone using reverse transcriptase and oligo(dT)12-18 primers. Then two 20-mer primers, specific for the cDNA of the hprt gene, are used to amplify the first and second strand cDNA 5 x 10(7)-fold during 30 cycles of polymerase chain reaction (PCR). The product (2 to 10 ng) is then purified by ultrafiltration, diluted 1:10, and subjected to an additional 30 cycles of PCR, using two 20-mer primers located just interior to the first set. The amplification product, 5 to 10 ug, is sequenced directly using three other end-labeled primers and Sequenase. To date, we have analyzed 26 mutants induced by (+-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha,epoxy-7,8,9,10-tetrahydrobenzo [a]pyrene and found that 24/26 involved base substitutions. 97% of these involved G.C, predominantly G.C----T.A, distributed over seven exons, with many of the substitutions located in exon 3.

Kengyilia guidenensis, a new species from western China, is described and illustrated. Cytological observations are provided, and comparisons with similar species are made. During an expedition to western China, a new species of Kengyilia was found. It was growing on a mountain slope close to the highway from Guide to Guomaying, between the 150 and 151 Km road poles. When collected it was identified as K. nana J. L. Yang, Yen & Baum; however, the habitat of K. nana is alpine steppes above 4000 m, whereas the Guide population was found just below 3100 m altitude and in stony slopes. The habitat of the Guide population is similar to that of K. kokonorica (Keng) J. L. Yang, Yen & Baum, but differs by being dwarf in appearance and by having ovate, dense, small spikes. In the same site another species of Kengyilia was found. This was K. mutica (Keng ex Keng & S. L. Chen) J. L. Yang, Yen & Baum, from which it readily differs in gross morphology by its dwarf habit and by its short ovate spike with long lemma awn. Kengyilia mutica does not have awns, and its spike is long and cylindrical. These preliminary observations led to the suspicion that a new species was on hand. The purpose of the present paper is to describe this species and to detail differences from the species most similar to it. MATERIALS AND METHODS Herbarium specimens and seeds were collected in 1993 in Guide County, Qinghai Province, China, and compared with specimens of Kengyilia nana and K. kokonorica (including their types) in N and SAUTI. Cytological observations were made using the methods detailed in Yen and Yang (1990). DESCRIPTION Kengyilia guidenensis Yen, J. L. Yang & Baum, sp. nov. TYPE: China. Qinghai Province: Guide County, Guide to Guomaying highway between markers 150 and 151 Km, alt. 3100 m, 35089'N, 100026'E, 11 Sep. 1993, C. Yen, J. L. Yang & G. L. Sun 930001 (holotype, SAUTI; isotype, DAO). Figure 1. Kengyiliae kokonoricae (Keng) J. L. Yang, Yen & Baum affinis, sed laminis superioribus albo-villosis; spicis brevioribus, 3-3.5 cm, et angustioribus, 5 mm; spiculis brevioribus, 7 mm, et plurifloribus, 5-7; glumis longioribus, 4-7 mm, lanceolatis; aristis lemmatum brevioribus, 1.54 mm; carinis palearum ominino ciliatis; antheris longioribus, 3 mm, differt. Kengyiliae nanae J. L. Yang, Yen & Baum affinis, sed culmis longioribus, 35-50 cm longis; foliorum vaginis glabris, laminis longioribus, 8.5-9 cm longis; spicis angustioribus, 5 mm latis; glumis lanceolatis; aristis lemmatum brevioribus, 1.5-4 mm longis; paleis ominino ciliatis differt. Caespitose perennial, with fibrous roots (Fig. lA). Culms caespitose, erect, 35-50 cm tall, 1.5 mm diam., 2-3-noded, pubescent just below the spike for 1-3 cm, geniculate at the base. Leaf sheaths glabrous, rarely pubescent in the lowermost sheaths; ligules scarious, membranous, truncate, premorse, ca. 0.5 mm long; leaf blades flat or slightly involute, narrowly lanceolate, 8.5-9 cm long, 3 mm wide, their adaxial surface with dense 1-mm-long white hairs emerging from the lateral nerves, their abaxial surface glabrous; leaf blades of the tillers densely pubescent, up to 12 cm long. Spikes erect, short and dense, ovate, 3-3.5 cm long, 5 mm wide; rachis internodes 1.5-2 mm long, densely white-pilose; spikelets oblong-ovate (Fig. 1J), greenish purple, with 5-7 florets 7 mm long (excluding awns); rachilla internodes 1-1.2 mm long, densely hirtulous; glumes unequal, wide lanceolate, w th herbaceous membranous margins (Fig. 1B, C), 1(-3)-nerved, with midrib pronounced and NOVON 5: 395-397. 1995. This content downloaded from 157.55.39.156 on Wed, 14 Jun 2017 18:06:19 UTC All use subject to http://about.jstor.org/terms

Roegneria tridentata is described and illustrated, and its karyotype is characterized. Roegneria tridentata was discovered during our fieldwork in 1992 in the Qi-lain Mt. on the northern border of Qinghai province, China. A few weeks later, it was collected in the A'Nyemaqen Mt. The two localities are more than 400 km apart. Roegneria tridentata Yen & J. L. Yang, sp. nov. TYPE: China. Qinghai: Wenquan, Xinhai, km 337 on highway 214, rocky slope, 3,750 m, 19 Sep. 1992, J. L. Yang et al. no. 9202014 (holotype, Sichuan Agricultural University Triticeae Institute; isotype, MO). Figure 1. Herba perennis caespitosa. Culmi 42-65 cm alti. Laminae 5-7 cm longae, ca. 2 mm latae, inferne glabrae, superne adpressae dense pubescentibus in projectis nervis. Spicae 5-11.5 cm longae, spiculae solitariae, 10-13 mm longae, 4vel 5-florae; glumae oblongae vel oblongoellipticae, primae 4-5 mm longae, secundae 5-6.5 mm longae, glabrae; lemmata oblongo-lanceolata, (7-)8-9 mm longa, primo 9 mm longo, 5-nervia, apicies truncati et tridentati, dentes ca. 0.5 mm longi, saepe nervo medio prominente in 0.5-1 mm longo mucronem producta; paleae apice truncatae, inter carinas scabrae, ad carinas '//2 superiore setuloso-ciliata. Herbs perennial. Culms caespitose, erect or slightly procumbent, geniculate at base, 42-65 cm tall, ca. 1.5-2 mm diam., with 2 or 3 nodes, smooth, glabrous. Leaf sheaths glabrous, persistent basal ones 2-4 cm long; ligule scarious, truncate premorse, ca. 0.5 mm long; blades involute or subinvolute, 57 cm long, ca. 2 mm broad; tillers narrowly linear, usually to 20 cm long, glabrous beneath, appressed densely pubescent on projecting veins of upper surface. Spikes erect, purple or greenish purple, 511.5 cm long, ca. 5 mm broad, with 6-14 spikelets; upper rachis internodes 5-10 mm long, the lower 15-20 mm, both glabrous, hirsute on angles; spikelets solitary, 10-13 mm long, ca. 2 mm broad, with 4 or 5 florets; rachilla internodes appressed puberulent, 1.5-2 mm long; glumes oblong or oblongelliptic, unequal, apically rounded-obtuse, rarely acute, slightly oblique; first glume 4-5 mm long; second glume 5-6.5 mm long, with 3(-5) projected veins, glabrous, sometimes sparsely short spinulose on veins; lemmas oblong-lanceolate, (7-)8-9 mm long, 5-veined, appressed white pubescent on lateral and lower parts, apically truncate and 3-toothed, the teeth ca. 0.5 mm long, sometimes midvein extending into a mucro to 0.5-1 mm long; callus obtuse, puberulent on the sides; paleas shorter to longer than lemmas, apically truncate, scabrous between keels, setulous-ciliate on upper '/3 -l/ of keel; anthers black, ca. 2 mm long. Chromosome number: 2n = 6x = 42 (Fig. 2). The characteristic awnless, 3-toothed lemmas (Fig. Ic) readily distinguish the species from other members of Roegneria C. Koch and from members of related genera. Root tips of young seedlings (ca. 2.5 cm long) were collected at 10:00 A.M. and placed in water at 3-40C for 24 hours. They were transferred to 20 ml 0.01% colchicine solution with 5 drops of dimethyl-sulfoxide and kept for 3 hours before fixation in Carnoy's fluid for 24 hours. Root tip cells were dissociated by 1N HCl for 8 minutes at 60?C, and slides were prepared by the standard acetocarmine squash method. Chromosomes were studied at diakinesis, photographs were taken by computerFigure 1. Roegneria tridentata Yen & J. L. Yang (holotype). -A. Plant. -B. Dorsal view of a floret showing 3-toothed apex of lemma and tip of longer palea. -C. Dorsal view of lemma. -D. Ventral view of floret. -E. Lodicule. -F. Dorsal view of caryopsis. -G. Ovary and stigma. -H. Stamen. -I. First glume. -J. Second glume. -K. Spikelet. NOVON 4: 310-313. 1994. This content downloaded from 207.46.13.127 on Fri, 14 Oct 2016 04:18:32 UTC All use subject to http://about.jstor.org/terms

The interspecific diploid hybrid between Psathyrostachys juncea (2x = 14) and the Chinese endemic species P. huashanica (2x = 14) was obtained and although completely sterile, developed normally. Chromosome pairing observed at MI in the hybrid was high, i.e. 6.57 chiasmata per cell. The average number of bivalents was 4.04 ranging from 2–7. These results indicate a close relationship between the genome of P. huashanica and that of P. juncea.