Search

Premature ovarian failure (POF) is characterized by hormonal disorders, amenorrhea, and premature loss of fertility potential in women of reproductive age. Several studies have been conducted on the effectiveness of traditional Chinese medicine (TCM) in treating POF. TCM relied primarily on apoptosis, immunity, and aging to treat POF based on the studies of domestic and foreign literature. Zuogui pills inhibited mitochondrial-dependent apoptosis in the treatment of POF. Huyang Yangkun formula regulated the downstream of the Bcl-2 family to resist apoptosis through the aquaporin-1 protein. Modified Bazhen decoction regulated apoptosis in POF by regulating X-linked inhibitors of apoptosis protein. Bushen Tianjing recipe was effective in treating POF by promoting angiogenesis and preventing apoptosis. As for immunity, Bushen Jianpi prescription and Er-Xian decoction cured autoimmunity POF models and increased follicular development-related protein expression. Bushen Huoxue Tang improved ovarian function and reduced ovarian inflammation by regulating the Nrf2/Keap1 signaling pathway and T lymphocytes. Taohong Siwu decoction promoted the proliferation and differentiation of granulosa cells of POF mice by regulating the TGF-β1/Smads signaling pathway. In addition, ginsenoside Rg1 and Jiajian Guisheng formula treated POF by regulating cell aging-related mechanisms. Si Wu Tang treated POF by activating the angiogenesis-related proteins. The goal of this review is to serve as a reference for in-depth research into the treatment of POF with TCM and provide inspiration for new diagnostic methods and treatment options.

Fibroblast growth factor 21 (FGF21), a known risk factor for atherosclerosis, is readily regulated by exercise, and it can inhibit NOD-like receptor protein 3 (NLRP3)-mediated pyroptosis. However, it is not clear whether aerobic exercise inhibits atherosclerosis via these pathways. Eight-week-old apolipoprotein E-deficient (ApoE-/-) mice on a high-fat diet were randomly divided into 1-h post-exercise (EX-1h), 24-h post-exercise (EX-24h), and sedentary (SED) groups. C57BL/6J wild-type mice fed normal chow served as controls (WT group). Mice in the EX-1h and EX-24h groups were subjected to treadmill exercise training for 12 weeks. Aerobic exercise reduced body weight; blood glucose, lipid, and inflammation levels; and aortic plaque area proportion. Aerobic exercise increased the sensitivity of FGF21 by upregulating the expression of the downstream receptor adiponectin (ApN); the serum FGF21 level after exercise increased initially, and then decreased. Aerobic exercise downregulated the expression of NLRP3 inflammasome-mediated pyroptosis-related markers in the aorta, and FGF21 may participate in the above process. Meanwhile, the liver may be the tissue source of serum FGF21 during aerobic exercise. In conclusion, aerobic exercise may inhibit atherogenesis by regulating FGF21 and NLRP3 inflammasome-mediated pyroptosis. Our study provides new information on the atherosclerosis-preventing mechanism of aerobic exercise.

Long noncoding RNAs play an important role in the occurrence, invasion, as well as metastasis of various human cancers, including hepatocellular carcinoma. Long noncoding RNAs can affect the biological functions of hepatocellular carcinoma cells by regulating various genes; however, only a small fraction of molecular mechanisms of long noncoding RNAs have been elucidated. In the present study, lnc AC010973.1 (lnc-ATG9B-4) was first identified by microarray analysis from 8 patients with hepatocellular carcinoma and confirmed by quantitative PCR in 176 patients with hepatocellular carcinoma. We demonstrated that lnc-ATG9B-4 was tightly relative to the tumorous size, TNM stages, portal vein tumor thrombus (PVTT), the tumor capsule, metastasis, degree of differentiation, and poor prognosis of hepatocellular carcinoma according to long-term follow-up data. In hepatocellular carcinoma cells, overexpression of lnc-ATG9B-4 promoted proliferation, invasion, as well as migration, while inhibiting lnc-ATG9B-4 by siRNA significantly attenuated the proliferation, invasion, as well as migration. Interestingly, lnc-ATG9B-4 increased the expression of cyclin-dependent kinase 5 (CDK5), which was closely related to the development and chemotherapy sensitivity of hepatocellular carcinoma. In summary, our results revealed that lnc-ATG9B-4 suggests an unfavorable prognosis of hepatocellular carcinoma and facilitates the proliferation, invasion, as well as migration of hepatocellular carcinoma cells by upregulating CDK5. This research suggests that lnc-ATG9B-4 may be a new biomarker for predicting the prognosis of hepatocellular carcinoma; meanwhile, targeting lnc-ATG9B-4 might serve as a potential strategy for the treatment hepatocellular carcinoma.

OBJECTIVE Postoperative nausea and vomiting (PONV) is an extremely common side effect of general anesthesia that is difficult to manage. We tested a hypothesis that an aggressive prophylactic intervention with additional antiemetic drugs will reduce the incidence of PONV in a high-risk pediatric population undergoing adenotonsillectomy. METHODS In this retrospective study, pediatric patients undergoing adenotonsillectomy were screened for their risk factors for PONV. Patients who had 3 or more risk factors were identified as high risk and received either scopolamine patch preoperatively (for patients over 40 kg body weight) or diphenhydramine immediately postextubation in addition to ondansetron and dexamethasone, which are given routinely. Incidences of PONV within the first 60 minutes of a postanesthesia care unit (PACU) stay were collected and analyzed. RESULTS Overall postoperative vomiting rates during the first hour of a PACU stay were 4.3% for the group that was treated with dexamethasone and ondansetron only and 3.9% for the group that was treated with additional antiemetic drugs. Aggressive prophylactic management of PONV did reduce the rate of nausea and vomiting in a group of high-risk patients (p < 0.0001). The postoperative antiemetic drug usage was also decreased during the first 60 minutes of a PACU stay. However, the approach did not reduce the overall rate of PONV for the entire study population (p = 0.1612 for nausea and p = 0.0678 for vomiting). CONCLUSION Aggressive intraoperative management of PONV with additional antiemetic drugs are beneficial in high-risk pediatric population. Intraoperative diphenhydramine usage decreased the rate of PONV. However, preoperative scopolamine patch prevention did not improve PONV, which may be related to the drug's longer onset of action. Our result suggests that current clinical practice is undertreating PONV in pediatric patients receiving general anesthesia.

Caspase-8 is an initiator of apoptotic signalling, and aberrations in procaspase-8 have been verified to be associated with malignant tumours. In previous studies, various procaspase-8 mutants were identified in AML patients, such as Q482H and M476W/Q482H mutations. The Q482H mutation can abolish caspase-8-mediated apoptosis by attenuating the dimerization of procaspase-8 protein monomers, causing AML patients carrying the Q482H mutation to develop resistance to chemotherapeutics. The patients with the M476W/Q482H mutation were sensitive to chemotherapy. Nevertheless, the underlying molecular mechanism is still unclear in regard to how the M476W/Q482H mutation restored caspase-8-mediated apoptosis. In this study, apoptosis was detected in the cells overexpressing the WT or mutant procaspase-8 with or without TRAIL treatment. Western blotting was devoted to detect the cleavage of procaspase-8 or the expression of proteins downstream in the apoptotic cascade and CO-IP was employed to analyze the dimerization of WT and mutant procaspase-8 proteins. Results demonstrated cells carrying the M476W/Q482H mutation restored caspase-8-mediated and TRAIL-induced apoptosis. The M476W/Q482H mutation recovered the dimerization of procaspase-8. Taken together, the M476W/Q482H mutation have restored caspase-8-mediated apoptosis resulting from the recovery of procaspase-8 dimerization.

Background Hospice care is a multidisciplinary approach that focused on patients’ quality of life, and nurses allocate more of their time with patients and patients’ families than those nurses working in other disciplines. Nurses’ knowledge of and attitudes toward hospice care can affect the quality of hospice care. At present, China’s hospice care institutions are suffering from an obvious shortage of nursing staff. Since clinical nurses are the main force behind the future provision of hospice care, their knowledge of, attitudes and willingness to practice can greatly promoted the growth of hospice care, however, available data on clinical nurses’ willingness to practice hospice care are limited. Methods A cross-sectional descriptive study design was employed to collect data from 1833 nurses working in tertiary or secondary general hospitals in Guangxi, China. We examined nurses’ demographic characteristics and scores on the Chinese version of the hospice care knowledge scale, the Chinese version of the Bradley Attitude Assessment Questionnaire, and a brief quiz concerning their willingness to practice hospice care in the future. Descriptive, single factor, multiple regression analyses and logistic regression analyses were used for data analysis. Results Nurses displayed moderate mean scores for both knowledge of and attitudes, and only 505 (27.5%) nurses expressed their willingness to practice hospice care, 1329 (72.5%) of nurses sampled expressed their unwillingness or uncertainty. Multivariate regression analyses showed that education, professional qualification, monthly income, whether they had been trained in hospice care, and willingness to practice hospice care were the main influencing factors of knowledge; education, whether they lived with someone aged >60 years, and whether they had been trained in hospice care were main factors influencing attitudes. Additionally, logistic regression analyses showed that hospice care knowledge, whether they had been trained in hospice care, and whether they had clinical experience affected the nurses’ willingness to practice hospice care. Conclusion This study highlighted a knowledge gap and moderate attitudes toward hospice care among nurses, and most nurses did not prefer to practice hospice care. Having been trained in hospice care was the main common factor of nurses’ knowledge of, attitudes toward, and willingness to practice hospice care in the future, indicating the necessity to provide nurses with more targeted hospice care training.

Background The downregulation of miRNA-485-5-p was related to prognosis of various cancers, including hepatocellular carcinoma (HCC), while MUC1 was aberrantly expressed in many cancers and could be a biomarker for prognosis and diagnosis of cancers. The aim of the study was to investigate whether the miRNA-485-5p inhibited proliferation and promoted apoptosis by targeting MUC1 in HCC cells.Methods The expression of miRNA-485-5p in patients with HCC was measured by qPCR, and the epxression of MUC1 was detected by qPCR, western blot and immunohistochemistry. Bioinformatics and dual luciferase assay verified the targeting relationship between miRNA-485-5p and MUC1 in HCC cells. Cell proliferation was detected by CCK-8 assay. Cell apoptosis was detected by flow cytometry.Results The expression of miRNA-485-5p in HCC tissues is downregulated than that in adjacent tissue. However, the exprssion of MUC1 is opposite to the expression of miRNA-485-5p in the patients with HCC. Silencing MUC1 and overexpression miRNA-485-5p both inhibit proliferation and promote apoptosis in HCC cells. MiRNA-485-5p directly targete to the binding site of the MUC1 3’UTR and downregulated the expression of MUC1. Overexpression of MUC1 and miRNA-485-5p reverse the effect of miRNA-485-5p on the cell proliferation and apoptosis.Conclusion MiRNA-485-5p inhibits the proliferation and facilitates the apoptosis by negatively regulating the expression of MUC1 in HCC cells.

Primary hypobetalipoproteinemia (pHBL) is characterized by plasma cholesterol levels ApoB48, and FHBL harbouring as yet unknown molecular defects. Not linked FHBL kindred are not homogeneous in terms of plasma NCS levels. NCS cannot replace genetic HBL analysis.

We sequenced all protein-coding regions of the genome (the "exome") in two family members with combined hypolipidemia, marked by extremely low plasma levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides. These two participants were compound heterozygotes for two distinct nonsense mutations in ANGPTL3 (encoding the angiopoietin-like 3 protein). ANGPTL3 has been reported to inhibit lipoprotein lipase and endothelial lipase, thereby increasing plasma triglyceride and HDL cholesterol levels in rodents. Our finding of ANGPTL3 mutations highlights a role for the gene in LDL cholesterol metabolism in humans and shows the usefulness of exome sequencing for identification of novel genetic causes of inherited disorders. (Funded by the National Human Genome Research Institute and others.).

Hepatic steatosis is associated with insulin resistance, but it is not clear whether increased intrahepatic triglyceride (IHTG) content causes the resistance or is a marker. Subjects with familial hypobetalipoproteinemia (FHBL) have high levels of IHTG because of a genetic defect in hepatic export of triglycerides, and provide a unique cohort to study the relationship between steatosis and insulin sensitivity.One group of lean subjects with normal IHTG content (2.2% +/- 0.6% of liver volume) (n = 6), and 3 groups of overweight and obese subjects matched for body mass index, were studied: (1) normal IHTG content (3.3% +/- 0.5%; n = 6), (2) high IHTG content (21.4% +/- 2.6%) due to nonalcoholic fatty liver disease (NAFLD; n = 6), and (3) high IHTG content (18.1% +/- 2.2%) due to FHBL (n = 3). A hyperinsulinemic-euglycemic clamp procedure, in conjunction with glucose tracer infusion, was used to determine multiorgan insulin sensitivity.Hepatic insulin sensitivity (reciprocal of glucose rate of appearance [micromol x kg fat-free mass(-1) x min(-1)] x insulin [mU/L]) was greatest in the Lean group (2.0 +/- 0.4); it was the same among subjects with FHBL (0.8 +/- 0.1) and the group with normal IHTG content, matched for body mass index (0.7 +/- 0.1), but greater than the NAFLD group (0.3 +/- 0.1) (P

High plasma apolipoprotein B (apoB) and LDL cholesterol levels increase cardiovascular disease risk. These highly correlated measures may be partially controlled by common genetic polymorphisms. To identify chromosomal regionsthatcontain genes causing low plasmalevelsofone or bothparametersinCaucasianfamiliesascertainedforfamilial hypobetalipoproteinemia (FHBL), we conducted a whole- genome scan using 443 microsatellite markers typed in nine multigenerational families with at least two members with FHBL. Both variance components and regression-based link- age methods were used to identify regions of interest. Com- mon linkage regions were identified for both measures on chromosomes 10q25.1-10q26.11 (maximum log of the odds (LOD) 5 4.2 for LDL and 3.5 for apoB) and 6q24.3 (maxi- mum LOD 5 1.46 for LDL and 1.84 for apoB). There was also evidence for linkage to apoB on chromosome 13q13.2 (LOD 5 1.97) and to LDL on chromosome 3p14.1 at 94 cen- timorgan (LOD 5 1.52). Bivariate linkage analysis provided further evidence for loci contributing to both traits (6q24.3, LOD 5 1.43; 10q25.1, LOD 5 1.74). We evaluated single nu- cleotide polymorphisms (SNPs) in genes within our linkage regions to identify variants associated with apoB or LDL levels. The most significant finding was for rs2277205 in the 5¶ untranslated region of acyl-coenzyme A dehydrogenase short/branched chain and LDL (P 5 10 27 ). Three additional SNPs were associated with apoB and/or LDL (P , 0.01). Although only the linkage signal on chromosome 10 reached genome-wide statistical significance, there are likely multiple chromosomal regions with variants that contributeto low levels of apoB and LDL and that may protect against coronary heart disease.—Sherva, R., P. Yue, G. Schonfeld, and R. J. Neuman. Evidence for a quantitative trait locus affecting low levels of apolipoprotein B and low density lipoprotein on chromosome 10 in Caucasian families. J. Lipid Res. 2007. 48: 2632-2639.

This article is relied on the market price monitoring system in the cloud platform of the Government Procurement in Tianjin and using the Copula model to establish the dependency relationship between the market reference price, the actual bid price and maximum likelihood method to estimate the unknown parameters. Through comparing fitting effect between the Empirical function and five kinds of Copula defined by different distributions containing Gaussian, t, Clayton, Gumbel and Frank, we can draw a conclusion that the two price series have a high level of dependency, and the Gaussian-Copula fit to the data most. However, any change in one price could not cause significant fluctuations to the other price by examining the tail of the correlation coefficient. From the model research applied in the dynamic changes of the procurement price, the government is able to monitor the reasonableness and accuracy of bids, and a certain preventive mechanism is established for inflated prices.

Fatty liver is prevalent in apolipoprotein B (apoB)-defective familial hypobetalipoproteinemia (FHBL). Similar to humans, mouse models of FHBL produced by gene targeting ( apob+/38.9) manifest low plasma cholesterol and increased hepatic triglycerides (TG) even on a chow diet due to impaired hepatic VLDL-TG secretive capacity. Because apoB truncations shorter than apoB48 are expressed in the intestine, we examined whether FHBL mice may have limited capacity for intestinal dietary TG absorption. In addition, we investigated whether FHBL mice are more susceptible to diet-induced hepatic TG accumulation. Fat absorption capacity was impaired in apoB38.9 mice in a gene dose-dependent manner. Relative fractional fat absorption coefficients for apob+/+, apob+/38.9, and apob38.9/38.9were 1.00, 0.96, and 0.71, respectively. To raise hepatic TG, we fed high-fat (HF) and low-fat (LF) pellets. Hepatic TG level was observed in rank order: HF > LF > chow. On both LF and HF, liver TG level was higher in the apob+/38.9than in apob+/+. Hepatic TG secretion remained impaired in the apob+/38.9on the HF diet. Thus the FHBL mice are more susceptible to diet-induced fatty liver despite relatively reduced intestinal TG absorption capacity on a HF diet.

Our aim was to ascertain whether fatty liver may be present in the genetic form of familial hypobetalipoproteinemia (FHBL) linked to a susceptibility locus on chromosome 3p21. Three genetic forms of FHBL exist: (a) FHBL caused by truncation-specifying mutations of apolipoprotein B (apoB), (b) FHBL linked to chr3p21, and (c) FHBL not linked either to APOB or to chr3p21. Fatty liver is common in apoB-defective FHBL. Hepatic fat contents were quantified by magnetic resonance spectroscopy in 16 subjects with 3p21-linked FHBL, 32 subjects with apoB-defective FHBL, and 39 sex- and age-matched controls. Mean liver fat of 3p21 subjects was similar to controls and approximately 60% lower than apoB-defective FHBL subjects ( P = .0012). Indices of adiposity (body mass index, waist/hip ratio) and masses of abdominal subcutaneous, retroperitoneal, and intraperitoneal adipose tissue (IPAT) were quantified by MR imaging. Mean measures of adiposity were similar in the 3 groups, suggesting that adiposity per se was not responsible for differences in liver fat. Liver fat content was positively correlated with IPAT. The intercepts of regression lines of IPAT on liver fat content were similar in controls and 3p21, but higher in apoB-defective FHBL subjects. The slopes of the lines were steepest in apoB-defective, intermediate in 3p21, and flattest in controls. Lipoprotein profiles and very low density lipoprotein-apoB100 kinetics of 3p21 and apoB-defective groups also differed. Thus, 2 genetic subtypes of FHBL also differ in several phenotypic features.

We report two novel APOB mutations causing short apolipoprotein B (apoB) truncations undetectable in plasma and familial hypobetalipoproteinemia (FHBL). In Family 56, a 5 bp deletion in APOB exon 7 (870_874del5) causes a frame shift, converting tyrosine to a stop codon (Y220X) and producing an apoB-5 truncation. In Family 59, a point mutation (1941G>T) in APOB exon 13 converts glutamic acid to stop codon (E578X), specifying apoB-13. A recurrent mutation in exon 26 (4432delT) produces apoB-30.9 in Family 58. In some members of these families, we observed that plasma low-density lipoprotein (LDL) cholesterol and apoB levels were unusually low even for subjects heterozygous for FHBL. To ascertain whether genetic variations in apolipoprotein E (apoE) would explain some of the variations of apoB and LDL cholesterol levels, apoE genotypes were assessed in affected subjects from a total of eight FHBL families with short apoB truncations. Heterozygous FHBL with the epsilon3/epsilon4 genotype had 10-1 5mg/dL higher plasma LDL cholesterol and apoB levels compared to subjects with the epsilon2/epsilon3 and epsilon3/epsilon3 genotypes. The apoE genotype has been reported to account for approximately 10% of the variation of LDL cholesterol in the general population. It accounted for 15-60% of the variability of plasma LDL cholesterol or apoB levels in our FHBL subjects. The physiologic bases for the greater effects of apoE in FHBL remain to be determined.

Familial hypobetalipoproteinemia (FHBL) subjects may develop fatty liver. Liver fat was assessed in 21 FHBL with six different apolipoprotein B (apoB) truncations (apoB-4 to apoB-89) and 14 controls by magnetic resonance spectroscopy (MRS). Liver fat percentages were 16.7 +/- 11.5 and 3.3 +/- 2.9 (mean +/- SD) (P = 0.001). Liver fat percentage was positively correlated with body mass index, waist circumference, and areas under the insulin curves of 2 h glucose tolerance tests, suggesting that obesity may affect the severity of liver fat accumulation in both groups. Despite 5-fold differences in liver fat percentage, mean values for obesity and insulin indexes were similar. Thus, for similar degrees of obesity, FHBL subjects have more hepatic fat. VLDL-triglyceride (TG)-fatty acids arise from plasma and nonplasma sources (liver and splanchnic tissues). To assess the relative contributions of each, [2H2]palmitate was infused over 12 h in 13 FHBL subjects and 11 controls. Isotopic enrichment of plasma free palmitate and VLDL-TG-palmitate was determined by mass spectrometry. Non-plasma sources contributed 51 +/- 15% in FHBL and 37 +/- 13% in controls (P = 0.02). Correlations of liver fat percentage and percent VLDL-TG-palmitate from liver were r = 0.89 (P = 0.0001) for FHBL subjects and r = 0.69 (P = 0.01) for controls. Thus, apoB truncation-producing mutations result in fatty liver and in altered assembly of VLDL-TG.

Humans and genetically engineered mice with hypobetalipoproteinemia due to truncation-producing mutations of the apolipoprotein B (apoB) gene frequently have fatty livers, because the apoB defect impairs the capacity of livers to export triglycerides (TGs). We assessed the adaptation of hepatic lipid metabolism in our apoB-38.9-bearing mice. Hepatic TG contents were 2- and 4-fold higher in heterozygous and homozygous mice, respectively, compared with wild-type mice. Respective in vivo hepatic fatty acid synthetic rates were reduced to 40% and 15% of the wild-type rate. Hepatic mRNAs for sterol regulatory element-binding protein (SREBP)-1c, fatty acid synthase (FAS), and stearoyl coenzyme A desaturase-1 were coordinately decreased. FAS and SREBP-1c mRNA levels were strongly and positively correlated with each other and inversely correlated with hepatic TGs, suggesting that impaired TG export is a potent inhibitor of fatty acid synthesis. In contrast, levels of plasma β-hydroxybutyrate and of hepatic carnitine palmitoyl transferase and peroxisome proliferator-activated receptor-α mRNAs were not altered, implying that β-oxidation was not affected. Fasting followed by refeeding increased hepatic fatty acid synthesis 56-fold over fasting in normal and heterozygous mice but only 24-fold in homozygous mice. Parallel changes occurred in FAS and SREBP-1c mRNAs. Thus, impairment of very low density lipoprotein export downregulates hepatic fatty acid synthesis, but the adaptation is incomplete, resulting in fatty livers. The signals mediating suppression of FAS and SREBP-1c levels remain to be identified.

Breeding soybean [Glycine max (L.) Merr.] cultivars for resistance to soybean cyst nematode (SCN) [Heterodera glycines Ichinohe] is the most efficient means to control this pest. Evaluating and developing new resistance germplasm sources for soybean breeding is very important to prevent SCN from race shifts and provide durable resistance in soybean. We evaluated a newly found germplasm, soybean plant introduction (PI) 89772, which is resistant to SCN Races 1, 2, 3, 5, and moderately resistant to Race 14. The objectives were to identify molecular markers associated with SCN resistance, investigate resistant allelic relationships, and evaluate marker-assisted selection efficiency. The F 2 and F 2:3 populations were produced by crossing PI 89772 with the susceptible soybean cultivar Hamilton. Thirty-nine restriction fragment length polymorphism (RFLP) and 54 simple sequence repeat (SSR) markers found to be polymorphic were used to anchor loci conferring resistance to SCN Races 1, 2, 3, and 5. Two to three loci were found to give resistance to each SCN race. We found that resistance loci for different races could be anchored within the same region on linkage group (LG) G. A region on LG Bl was also shared by loci providing resistance to SCN Races 1, 2, and 5. Our results indicated that no single locus could provide complete resistance to any one SCN race. The major loci combinations provided high levels of resistance. We conclude that these markers could be highly useful in marker-assisted selection.

Soybean (Glycine max L. Merr.) plant introduction (PI) 438489B is a newly found germplasm source that has resistance to multiple soybean cyst nematode (Heterodera glycines Ichinohe, SCN) races. We studied the inheritance of resistance to SCN races 1, 2, 3, 5 and 14 in PI 438489B using F2 and F2:3 families, which were generated by crossing to the susceptible cultivar ’Hamilton.’ The objectives of this study were to investigate the inheritance for resistance to SCN races in PI 438489B, to find molecular markers associated with resistances, and to study the allelic relationships among resistance loci for different SCN races. The results showed that the responses to SCN races were approximately normally distributed with large environmental effects, and were also highly correlated, which implied that genes giving resistance to different races were similar. The narrow-sense heritabilities of resistance to all five SCN races ranged from 0.55 to 0.88. Fifty one restriction fragment length polymorphism (RFLP) markers and 64 simple sequence repeat (SSR) markers were found to be polymorphic in the F2 population. Quantitative trait loci (QTLs) associated with resistance to SCN races were anchored on soybean linkage groups (LGs) A1, A2, B1, B2, C1, C2, D1a, E and G. These QTLs explained 47.3%, 45.8%, 51.5%, 34.5% and 37.2% of the total phenotypic variances, respectively, for each race we investigated. Some QTLs for different races encompassed the same region of flanking markers; therefore, QTLs for multiple races may be linked or pleiotropic effects may be involved. Some loci provided resistance in a race-specific manner. Resistance to SCN race 14 had a different pattern compared to other races. Our results indicated that resistance to race 14 did not include loci on LGs A2 and G. These flanking markers associated with QTLs could be used to select for resistance to multiple SCN races in soybean breeding programs.

Soybean (Glycine max L. Merr.) plant introduction PI 438489B is a unique source that has resistance to all known populations of soybean cyst nematode (Heterodera glycines Ichinohe, SCN). This PI line also has many desirable agronomic characteristics, which makes it an attractive source of SCN resistance for use in a soybean breeding program. However, characterization of SCN resistance genes in this PI line have not been fully researched. In this study, we investigated the inheritance of resistance to populations of SCN races 1, 2, 3, 5, and 14 in PI 438489B. PI 438489B was crossed to the susceptible cultivar ‘Hamilton’ to generate F1 hybrids. The random F2 plants and F3 lines were evaluated in the greenhouse for reaction to these five populations of SCN races. Resistance to SCN races 1, 3, and 5 were mostly conditioned by three genes (Rhg Rhg rhg). Resistance to race 2 was controlled by four genes (Rhg rhg rgh rgh). Three recessive genes were most likely involved in giving resistance to race 14. We further concluded that resistance to different populations of SCN races may share some common genes or pleiotropic effects may be involved.

Objective— Mutations of the ANGPTL3 gene have been associated with a novel form of primary hypobetalipoproteinemia, the combined hypolipidemia (cHLP), characterized by low total cholesterol and low HDL-cholesterol levels. The aim of this work is to define the role of ANGPTL3 gene as determinant of the combined hypolipidemia phenotype in 2 large cohorts of 913 among American and Italian subjects with primary hypobetalipoproteinemia (total cholesterol Methods and Results— The combined hypolipidemia cut-offs were chosen according to total cholesterol and HDL-cholesterol levels reported in the ANGPTL3 kindred described to date: total cholesterol levels, ANGPTL3 and APOB genes. We identified nonsense and/or missense mutations in ANGPTL3 gene in 8 subjects; no mutations of the APOB gene were found. Mutated ANGPTL3 homozygous/compound heterozygous subjects showed a more severe biochemical phenotype compared to heterozygous or ANGPTL3 negative subjects, although ANGPTL3 heterozygotes did not differ from ANGPTL3 negative subjects. Conclusion— These results demonstrated that in a cohort of subjects with severe primary hypobetalipoproteinemia the prevalence of ANGPTL3 gene mutations responsible for a combined hypolipidemia phenotype is about 10%, whereas mutations of APOB gene are absent.

Soybean cyst nematode (SON, Heterodera glycines lchinohe) is a serious pest of soybean [Glycine max (L.) Merr.] in the USA and worldwide. A current classification system has designated 16 different races of SON populations. In the Southern USA, SCN Races 1 and 2 are becoming more prevalent. It is important to identify soybean accessions with resistance to these races. The objective of this study was to bioassay 32 soybean plant introductions (PIs) for resistance to SCN Races 1 and 2 together with standard host differentials and a susceptible control. The bioassays were performed for each of the two races during 1997 to 1998 in thermoregulated water baths in the greenhouse. The results indicated that 25 PIs had resistance to Race 1 and 24 PIs had resistance to Race 2. PIs which were resistant to Race 1 and either moderately resistant or moderately susceptible to Race 2 included PIs 468915, 494182, 507354, 507422, and 509100. PIs 467327, 468903, and 507471 were resistant to Race 2 and additionally were either moderately susceptible or moderately resistant to Race 1. Soybean PIs that were yellow seeded and had various levels of resistance to both races included PIs 494182, 507354, 507422, and 507471. These are the most desirable sources for development of soybean cultivars with resistance to SCN Races 1 and 2. These soybean lines are being fingerprinted by means of microsatellites to identify unique types to allow broadening the diversity of resistance gene introgression.