[Molecular mechanism analysis of a family with hereditary coagulation F â ª deficiency caused by compound heterozygous mutations].

A 34 year old female patient was scheduled to undergo surgical resection due to a "breast nodule". Preoperative examination revealed an activated partial thromboplastin time (APTT) of 66.2 seconds, coagulation factor Ⅺ activity (FⅪ: C) of 2%, and FⅪ antigen (FⅪ: Ag) of 40.3%. The patient and family members showed no abnormal bleeding symptoms. Diagnosed as hereditary coagulation factor Ⅺ deficiency. Genetic testing revealed that the F11 gene had a heterozygous nonsense mutation in exon 10, c.1107C>A (p.Tyr351stop), and a heterozygous missense mutation in exon 13, c.1562A>G (p.Tyr503Cys). The father and son were p Heterozygous carriers of Tyr351stop mutation, while the mother and daughter are p Heterozygous carriers of Tyr503Cys mutations. The in vitro expression results showed that p The Tyr351stop mutation resulted in a significant decrease in the transcription level of F11 gene, while p The Tyr503Cys mutation has no effect on the transcription level and protein expression level of F11 gene, but it leads to a significant decrease in the level of FⅪ:C in the cell culture supernatant.

Cardiac MRI for clinical dilated cardiomyopathy: Improved diagnostic power via combined T1, T2, and ECV.

INTRODUCTION: Early diagnosis of patients with dilated cardiomyopathy (DCM) remains challenging. Cardiac MR can correlate myocardial changes with their pathological basis. There have been some previous studies on the effect of T1 mapping in DCM, but there is limited data on the incremental value of T2 mapping for DCM in routine clinical practice. This study will examine whether the combination of MRI T1 and T2 mapping offers greater advantages in the diagnosis of DCM. METHODS: The study included 28 patients with DCM and 21 healthy controls. CMR evaluation included late gadolinium enhancement (LGE), T1 mapping, extracellular volume (ECV) fraction and T2 mapping. The DCM group was divided into LGE (+) and LGE (-) subgroups. The main modes of LGE are subendocardial, midwall, subepicardial, or transmural. T1 values, T2 values, and ECV in the 16 segments myocardial levels were measured by post-processing software. Student's t-tests or Mann-Whitney U test was used to compare between two groups, and one-way ANOVA or Kruskal-Wallis H test was used to compare between multiple groups, with p values corrected by Bonferroni. The difference was considered statistically significant at P < 0.05. ROC curve analysis was used to compare the area under the curve (AUC) of each index and its combined value, and the cut-off value, sensitivity and specificity were determined by Jordan's index. RESULTS: Mean native myocardial T1, ECV and T2 were significantly higher in the DCM group compared to controls (p ≤ 0.001, respectively). The best cut-off values for T1, T2 and ECV to discriminate DCM from controls were 1184 ms, 40.9 ms and 29.2%, respectively. The AUC of T1, ECV and T2 were 0.87, 0.89, and 0.83, respectively. The combined AUC of the three values was 0.96. CONCLUSION: Native T1 value and ECV overcome some of the limitations of LGE, and the T2 helps to understand the extent of myocardial damage. The combination of T1 and T2 mapping techniques can reveal fibrotic and oedematous changes in the early stages of DCM, providing a more comprehensive assessment of DCM and better guidance for individualised clinical management of patients. IMPLICATIONS FOR PRACTICE: We suggest that the addition of T2 mapping to the routine CMR examination of patients with suspected DCM, and the combined assessment of T1mapping and T2 mapping can provide complementary information about the disease and improve the early diagnosis of DCM.

[Phenotype and genotype analyses of two pedigrees with inherited fibrinogen deficiency].

Objective: To analyze the phenotype and genotype of two pedigrees with inherited fibrinogen (Fg) deficiency caused by two heterozygous mutations. We also preliminarily probed the molecular pathogenesis. Methods: The prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT) and plasma fibrinogen activity (Fg∶C) of all family members (nine people across three generations and three people across two generations) were measured by the clotting method. Fibrinogen antigen (Fg:Ag) was measured by immunoturbidimetry. Direct DNA sequencing was performed to analyze all exons, flanking sequences, and mutated sites of FGA, FGB, and FGG for all members. Thrombin-catalyzed fibrinogen polymerization was performed. ClustalX 2.1 software was used to analyze the conservatism of the mutated sites. MutationTaster, PolyPhen-2, PROVEAN, SIFT, and LRT online bioinformatics software were applied to predict pathogenicity. Swiss PDB Viewer 4.0.1 was used to analyze the changes in protein spatial structure and molecular forces before and after mutation. Results: The Fg∶C of two probands decreased (1.28 g/L and 0.98 g/L, respectively). The Fg∶Ag of proband 1 was in the normal range of 2.20 g/L, while it was decreased to 1.01 g/L in proband 2. Through genetic analysis, we identified a heterozygous missense mutation (c.293C>A; p.BßAla98Asp) in exon 2 of proband 1 and a heterozygous nonsense mutation (c.1418C>G; p.BßSer473*) in exon 8 of proband 2. The conservatism analysis revealed that Ala98 and Ser473 presented different conservative states among homologous species. Online bioinformatics software predicted that p.BßAla98Asp and p.BßSer473* were pathogenic. Protein models demonstrated that the p.BßAla98Asp mutation influenced hydrogen bonds between amino acids, and the p.BßSer473* mutation resulted in protein truncation. Conclusion: The dysfibrinogenemia of proband 1 and the hypofibrinogenemia of proband 2 appeared to be related to the p.BßAla98Asp heterozygous missense mutation and the p.BßSer473* heterozygous nonsense mutation, respectively. This is the first ever report of these mutations.

[Development of a Ranking Tool for Scientificity, Transparency and Applicability of Clinical Practice Guidelines].

Objective: To address the limitations of existing methods and tools for evaluating clinical practice guidelines, we aimed to develop a comprehensive instrument focusing on the three main dimensions of guideline development: scientificity, transparency, applicability. We will use it to rank the guidelines according to the scores. We abbreviated it as STAR, and its reliability, validity and usability were also tested. Methods: A multidisciplinary expert working group was set up, including methodologists, statisticians, journal editors, medical professionals, and others. Scoping review, Delphi methods and hierarchical analysis were used to determine the final checklist of STAR. Results: The new instrument contained 11 domains and 39 items. Intrinsic reliability of each domain was indicated by Cronbach's α coefficient, with a average value of 0.646. The Cohen's kappa coefficients for methodological evaluators and clinical evaluators were 0.783 and 0.618. The overall content validity index was 0.905. The R2 for the criterion validity analysis was 0.76. The average score for usability of the items was 4.6, and the mean time spent to evaluate each guideline was 20 minutes. Conclusion: The instrument has good reliability, validity and evaluating efficiency, and can be used for evaluating and ranking guidelines more comprehensively.

Improved tenderness of beef from bulls supplemented with active dry yeast is related to matrix metalloproteinases and reduced oxidative stress.

Supplementing diets with active dry yeast (ADY, Saccharomyces cerevisiae) improves the carcass quality grade of beef cattle and the tenderness of beef. The relevant mechanisms have not been fully elucidated, but may be related to the effect of ADY on oxidative stress and the activity of matrix metalloproteinases (MMPs). To provide further insight into these mechanisms, this study evaluated the influence of ADY supplementation on growth performance, carcass traits, meat quality, concentrations of MMPs in serum (MMP-2, MMP-9 and MMP-13), oxidative stress indices and antioxidant capacity indices in beef cattle. Forty-six crossbred Simmental × Yanbian bulls (∼18 months of age, BW 436 ± 35 kg) participated in a 145-day finishing trial. ADY supplementation significantly improved marbling deposition, intramuscular fat content, and beef tenderness (P < 0.05); altered individual fatty acid proportions in the beef and increased saturated fatty acids while decreasing polyunsaturated fatty acids (P < 0.05); significantly decreased the abundance of reactive oxygen species in serum and meat; significantly increased the level of superoxide dismutase in meat (P < 0.05); tended to increase the level of catalase (P = 0.075) in serum and glutathione reductase (P = 0.066) in meat; and increased the secretion of MMPs. The improvement of beef tenderness following ADY supplementation of finishing bulls is related to the effects of ADY on the secretion of MMPs and the lowering of oxidative stress.

[Clinical phenotype and gene mutation analysis of 12 patients with hereditary protein C deficiency in different families].

Objective: To investigate the molecular pathogenesis and clinical features of unrelated 12 patients with inherited coagulation protein C (PC) deficiency in Chinese population. Methods: The PC activity (PC:A) and PC antigen (PC:Ag) were detected by chromogenic substrate and enzyme linked immunosorbent assay, respectively. The nine exons and flanking sequences of the protein C (PROC) gene were amplified by polymerase chain reaction with direct sequencing, and the suspected mutations were validated by reverse sequencing (clone sequencing for deletion mutations) . Results: The PC:A of the 12 probands decreased significantly, ranging from 18% to 55%, and the PC:Ag of the 10 probands decreased significantly. Eleven mutations were found, out of which four mutations [c.383G>A (p.Gly128Asp) , c.997G>A (p.Ala291Thr) , c.1318C>T (p.Arg398Cys) , and c.532G>C (p.Leu278Pro) ] were discovered for the first time. Six mutations were in the serine protease domain, four mutations were located in epidermal growth factor (EGF) -like domains, and one mutation was located in activation peptide. There were two deletion mutations (p.Met364Trp fsX15 and p.Lys192del) , and the rest were missense mutations. Mutations p.Phe181Val and p.Arg189Trp were identified in three unrelated families. All mutations may be inherited, and consanguineous marriages were reported in two families. Among the probands, nine cases had venous thrombosis, two cases had poor pregnancy manifestations, and one case had purpura. Conclusion: Patients with PC deficiency caused by PROC gene defects are prone to venous thrombosis, especially when there are other thrombotic factors present at the same time.

[Analysis of a pedigree with inherited factor V deficiency caused by compound heterozygous mutation].

Objective: To explore the molecular pathogenesis of a family with hereditary factor Ⅴ (FⅤ) deficiency. Methods: All the exons, flanking sequences, 5' and 3' untranslated regions of the F5 of the proband, and the corresponding mutation sites of the family members were analyzed via direct DNA sequencing. The CAT measurement was used to detect the amount of thrombin produced. The ClustalX software was used to analyze the conservation of mutation sites. The online bioinformatics software, Mutation Taster, PolyPhen-2, PROVEAN, LRT, and SIFT were applied to predict the effects of mutation sites on protein function. The Swiss-PdbViewer software was used to analyze the changes in the protein model and intermolecular force before and after amino acid variation. Results: The proband had a heterozygous missense mutation c.1258G>T (p.Gly392Cys) in exon 8 of the F5, and a heterozygous deletion mutation c.4797delG (p.Glu1572Lys fsX19) in exon 14, which results in a frameshift and produces a truncated protein. Her grandfather and father had p.Gly392Cys heterozygous variation, whereas her maternal grandmother, mother, little aunt, and cousin all had p.Glu1572LysfsX19 heterozygous variation. The ratio of proband's thrombin generation delay to peak time was significantly increased. Conservation analysis results showed that p.Gly392 was located in a conserved region among the 10 homologous species. Five online bioinformatics software predicted that p.Gly392Cys was pathogenic, and Mutation Taster also predicted p.Glu1572Lys fsX19 as a pathogenic variant. Protein model analysis showed that the replacement of Gly392 by Cys392 can lead to the extension of the original hydrogen bond and the formation of a new steric hindrance, which affected the stability of the protein structure. Conclusion: The c.1258G>T heterozygous missense mutation in exon 8 and the c.4797delG heterozygous deletion mutation in exon 14 of the F5 may be responsible for the decrease of FⅤ levels in this family.

[A homozygous variant in a consanguineous pedigree with inherited protein S deficiency].

Objective: To observe the clinical feature of familiar hereditary protein S deficiency, and to explore the related gene mutation. Methods: The blood samples were obtained from the proband and the family memebers(3 generations,6 persons). PROS1 gene of the proband and the family members was analyzed. The 15 exons and flanking sequence of PROS1 gene were analyzed by PCR and DNA sequencing. Results: Five out of 6 family members were diagnosed as having hereditary protein S deficiency. The proband suffered from pulmonary embolism. The others had no obvious thrombotic event. The gene sequencing revealed that the proband carried a c.-168C>T homozygous variant in the promoter of exon 1. His parents, brother and son all carried c.-168C>T heterozygosis variant at the same position. The gene of his wife was a wild type. Conclusion: A gene variant (c.-168C>T) of PROS1 was discovered in this Chinese family. Gene variant of PROS1 may result in protein S deficiency. Patients with protein S deficiency may suffer from vein thrombosis and(or) pulmonary embolism.

Effect of Lonicera japonica extract on lactation performance, antioxidant status, and endocrine and immune function in heat-stressed mid-lactation dairy cows.

Here, we examined the effects of Lonicera japonica extract (LJE) on lactation performance, antioxidant status, and endocrine and immune function in heat-stressed mid-lactation dairy cows. Twenty-four healthy Chinese Holstein mid-lactation dairy cows, all with similar milk yield (30.0 ± 1.0 kg/d), parity (2.5 ± 0.3), and days in milk (105 ± 5 d) were allocated to 4 groups using a randomized complete block design: a negative control group (without LJE supplementation; CON) and groups that received LJE at 14, 28, and 56 g/d. The experiment lasted 10 wk over a hot summer, with a pre-feeding period of 2 wk. Cows were exposed to heat stress, as the average temperature-humidity index was greater than 72. The results showed that LJE had no effect on respiration rate; however, it reduced the rectal temperature of dairy cows experiencing heat stress in both a linear and quadratic manner; the lowest (39.03°C) was recorded for the LJE-28 group, lower than the CON group. Supplementation with LJE did not affect dry matter intake, milk yield, or milk composition. The majority of biochemical parameters in serum were unaffected by supplementation with different amounts of LJE; the exception was creatinine, which was reduced quadratically. Compared with the CON group, serum triiodothyronine concentrations increased significantly in the LJE-28 group. Addition of LJE to the diet increased thyroxine concentrations quadratically; values peaked at 18.62 ng/mL in the LJE-28 group. Furthermore, supplementation with increasing amounts of LJE quadratically increased the activity of glutathione peroxidase and total antioxidant capacity in serum but decreased concentration of malondialdehyde. Although we detected no differences in the concentrations of IgA, IgM, or cytokines, dairy cows in the LJE-28 group had higher IgG and IL-4 concentrations than did cows in the CON group. Supplementation with LJE increased concentrations of IgG and IL-4 in the serum quadratically but decreased that of IL-2. Finally, heat shock protein 72 concentrations in the serum tended to fall quadratically as the amount of LJE increased. In summary, LJE had no negative effects on lactation performance but helped to alleviate heat stress by improving antioxidant status and promoting endocrine and immune functions. Supplementation with LJE at 28 g/d is recommended for lactating dairy cows experiencing heat stress during hot summers.

Irisin alleviates renal injury caused by sepsis via the NF-κB signaling pathway.

OBJECTIVE: Renal injury caused by sepsis is a difficult point in the field of critical care medicine today, which seriously endangers the health of patients. The aim of our paper was to study the role of irisin in the inflammation and apoptosis of renal injury caused by sepsis and its potential mechanism of action. MATERIALS AND METHODS: Lipopolysaccharide (LPS) was utilized to establish an acute kidney injury model. HK-2 cells were divided into 3 groups: control group, LPS group, LPS+irisin group. The expression of TNF-α, IL-1ß, Bcl-2, and Bax were detected using Western blot. Commercial enzyme-linked immunosorbent assay (ELISA) kits were used to detect the levels of TNF-α, IL-6, and IL-1ß in the cell supernatant. The LDH content was detected to observe cell damage. TUNEL staining and flow cytometry were to investigate the apoptosis in three groups. The viability of HK-2 cells was detected using Cell Counting Kit-8 (CCK-8) assay. RESULTS: After HK-2 cells were treated with LPS, the LDH content in the cell supernatant was greatly increased, and the expression of TNF-α, IL-6, and IL-1ß was also significantly increased. However, after treatment with irisin, LDH content and expression of inflammatory factors were significantly suppressed. Similarly, LPS treatment greatly elevated the levels of TNF-α, IL-1ß, Bax, p65 and IκKα, as well as inhibited the expression of Bcl-2 and IκB-α. However, irisin treatment reversed these situations. In addition, the number of TUNEL-positive cells and the apoptotic rate were also greatly decreased in LPS+irisin group compared with those in LPS group. CONCLUSIONS: Irisin could inhibit inflammation and apoptosis of HK-2 cells treated with LPS via the NF-κB pathway.

[Risk considerations of periodontal tissues reconstructions in the strategies of orthodontic treatment].

With the increase of adult patients seeking for orthodontic treatment, the influence of periodontal tissue on orthodontic treatment has gradually become the focus. For patients with periodontitis, it is essential to controlling the severity of periodontitis prior to orthodontic treatment. Periodontal disease can cause additional bone loss and make the orthodontic treatment complicated. Reducing the risk of orthodontic treatment in this situation is our major concern. In addition to periodontitis, orthodontic treatment may also cause gingival recession. On the other hand, the alveolar bone defects such as bone fenestration and bone dehiscence are common in some patients without periodontitis. For these patients, we should take more care of the interrelationship between bone defects and orthodontic treatment. This article briefly demonstrates the risk considerations of periodontal supporting tissue in orthodontic therapy focusing on the influence of periodontitis, gingival recession and alveolar bone fenestration and dehiscence.

Effect of dexmedetomidine on kidney injury in sepsis rats through TLR4/MyD88/NF-κB/iNOS signaling pathway.

OBJECTIVE: The aim of this study was to investigate the effect of dexmedetomidine (DEX) on kidney injury in sepsis rats through the Toll-like receptor 4 (TLR4)/myeloid differential protein-88 (MyD88)/nuclear factor-κB (NF-κB)/inducible nitric oxide synthase (iNOS) signaling pathway. MATERIALS AND METHODS: A total of 30 Sprague-Dawley (SD) rats were randomly divided into three groups, including the control group (n=10), lipopolysaccharide (LPS)-induced acute kidney injury (AKI) group (model group, n=10) and DEX treatment group (DEX group, n=10). The model of sepsis was successfully established in rats. The levels of serum creatinine (Cr), blood urea nitrogen (BUN), serum interleukin-6 (IL-6), IL-1ß, IL-10 and tumor necrosis factor-α (TNF-α) were detected via enzyme-linked immunosorbent assay (ELISA). The pathological changes in kidney tissues were detected via hematoxylin-eosin (HE) staining. Furthermore, the mRNA and protein expressions of TLR4, MyD88, NF-κB, and iNOS in the kidney were detected via fluorescence quantitative Polymerase Chain Reaction (PCR) and Western blotting, respectively. RESULTS: Compared with the control group, rats in the model group showed significant kidney injury, markedly increased levels of serum Cr, BUN and pro-inflammatory cytokines, remarkably decreased the level of IL-10 (p<0.05), and significantly increased mRNA and protein expressions of TLR4, MyD88, NF-κB, and iNOS. In the DEX group, AKI was markedly improved, while the expressions of inflammatory cytokines were remarkably declined. Furthermore, the mRNA and protein expressions of TLR4, MyD88, NF-κB, and iNOS decreased significantly. CONCLUSIONS: DEX has a protective effect on LPS-induced AKI, whose mechanism may be related to the inhibition of the TLR4/MyD88/NF-κB/iNOS pathway.

[Transurethral bipolar plasmakinetic prostatectomy for benign prostatic hyperplasia in high-risk and senior patients in China: a systematic review and meta-analysis].

Objective: To evaluate the effectiveness and safety of transurethral bipolar plasmakinetic prostatectomy in the treatment of benign prostatic hyperplasia in high-risk and senior patients in China. Methods: The PubMed, Cochrane Library, CBM, CNKI and WanFang databases were searched with computer for collecting relevant interventional case series from establishment dates to September 14, 2018. After quality evaluation and data extraction independently conducted by two authors, the Meta-analysis was performed using the Comprehensive Meta-analysis V2 software. Results: Eighteen studies involving 1 899 patients are included. Maximum flow rate increased to 12.28 ml/s (95%CI: 8.42-16.14), 12.88 ml/s (95%CI: 9.85-15.92) ,14.32 ml/s (95%CI: 10.47-18.18), 14.93 ml/s (95%CI: 10.19-19.67) and 20.00 ml/s (95%CI: 19.08-20.92) in 1, 3, 6, 12 and 24 months after surgery, respectively. International prostate symptom score decreased to -18.60 (95%CI: -23.20--14.00), -17.62 (95%CI: -20.21--15.03), -19.14 (95%CI: -20.70--17.59), -19.06 (95%CI: -21.53--16.60) and -22.90 (95%CI: -24.26--21.54), respectively. Quality of life decreased to -2.38 (95%CI: -4.26--0.50), -3.39 (95%CI: -4.57--2.21),-3.75 (95%CI: -4.14--3.36), -3.36(95%CI: -4.56--2.16), and -4.58(95%CI: -4.75--4.41). Post void residual decreased to -231.16 ml (95%CI: -288.30--174.01), -76.10 ml (95%CI: -116.71--35.50), -159.90 ml(95%CI: -207.21--112.59) and -87.70 ml (95%CI: -91.91--83.48). The event rate of postoperative adverse reactions all were not high. Conclusion: Transurethral bipolar plasmakinetic prostatectomy has better clinical efficacy and no obvious side effects in the treatment of benign prostatic hyperplasia in high-risk and senior patients in China.

Expression pattern of nanos, piwil, dnd, vasa and pum genes during ontogenic development in Nile tilapia Oreochromis niloticus.

Primordial germ cells (PGCs) are specified by maternally provided determinants in fish. PGCs migrate then into prospective gonadal sites during early development and give rise to germ cell lineage. PGC disrupted animals do not sexually mature which has a range of commercial as well as environmental benefits. To find potential target genes for sterilisation of Nile tilapia, relative mRNA abundance patterns and tissue distribution of four nanos, two piwil, dnd1, vasa and three pum genes were investigated during ontogenic development from unfertilised eggs to newly hatched larvae and in adult tissues, respectively. The ontogenic pattern of RNA abundance revealed that all the investigated gene transcripts are maternally deposited to varying degrees, except for nanos2 which is not expressed in eggs. The ontogenic patterns of relative RNA abundance could be grouped into three categories. The first one, including nanos3, piwil1, piwil2, dnd1 and vasa, showed abundant transcript levels during early developmental stages which are then degraded during the period of maternal to zygotic transition between blastula and gastrula stages with a reduction in expression of four to five orders of magnitude by hatching stage. Another, including pum2 and pum3, showed similar patterns to the first group, but the transcript levels are reduced by only two orders of magnitude. The third group, including nanos1a, nanos1b and pum1, was characterised by a zygotic increase. nanos2 had no detectable transcripts until hatching stage. The tissue screening of nanos1a, nanos1b, pum1, pum2 and pum3 showed that they are expressed in various tissues, implying their potential pleiotropic effects in these tissues apart from gonads. In contrast, nanos3, piwil1, piwil2, dnd1 and vasa appeared to be exclusively expressed in gonads (both ovary and testis), and nanos2 showed testis-specific expression. Based on these results nanos3, piwil1, piwil2, dnd1 and vasa were prioritised among the 11 selected genes as potential target genes for sterilisation in Nile tilapia as they have no significant zygotic expression during embryogenesis, they are expressed exclusively in gonads and maternally deposited. These features suggest a potential role of these genes in the specification and maintenance of PGCs during the ontogenic development of Nile tilapia.

Model research on repairing meniscus injury in rabbits using bone marrow mesenchymal stem cells and silk fibroin meniscus porous scaffold.

OBJECTIVE: The purpose of this study is to evaluate the histocompatibility and feasibility of structure and function of bone marrow mesenchymal stem cells (BMSCs) and silk fibroin meniscus porous scaffolds in repairing meniscus injury in rabbits. MATERIALS AND METHODS: BMSCs were cultured and identified in vitro, silk fibroin meniscus porous scaffolds were prepared and the histocompatibility of porous scaffolds was evaluated via in vitro culture. Silk fibroin-BMSCs porous scaffolds were implanted into the meniscus defect area of New Zealand white rabbits as the experimental group, the blank scaffold group without BMSCs, pure BMSCs group and blank control group were set up with 10 rabbits in each group. Joint capsules were opened for general observation at 6 weeks and 12 weeks after operation. The specimens received the HE staining, alkaline toluidine blue staining, and immunohistochemical staining of Type I and Type II collagen and S100 protein. RESULTS: In vitro HE staining and SEM observation showed that the scaffolds showed the sponge-like structure with abundant microporous structure on the surface and inside, which had a good histocompatibility with BMSCs. At 6 and 12 weeks after operation in experimental group, meniscus-like tissues were found in the meniscus defect area. HE staining showed the fibrous cartilage-like structure and obvious collagenous fiber structure around arranged in an orderly manner. Alkaline toluidine blue staining showed the cartilage-specific glycosaminoglycan (GAG); Type I and Type II collagen and S100 protein staining were strongly positive. However, the above changes were not seen in other groups. CONCLUSIONS: BMSCs and silk fibroin meniscus porous scaffolds have a better histocompatibility and feasibility of structure and function in repairing meniscus injury in rabbits.

Effects of dietary energy levels on physiological parameters and reproductive performance of gestating sows over three consecutive parities.

OBJECTIVE: This experiment was to evaluate the effects of the dietary energy levels on the physiological parameters and reproductive performance during gestation over three parities in sows. METHODS: A total of 52 F1 gilts (Yorkshire×Landrace) were allotted to one of four dietary treatments using a completely randomized design. The treatments contained 3,100, 3,200, 3,300, or 3,400 kcal of metabolizable energy (ME)/kg diet but feed was provided at 2.0, 2.2, and 2.4 kg/d in the first, second and third parity, respectively. RESULTS: The body weight and body weight gain during gestation increased as the dietary energy level increased (p<0.05, and p<0.01) in the first parity. In the second parity, the body weight of sows was the lowest (p<0.05) when 3,100 kcal of ME/kg treatment diet was provided. The body weight was higher as the dietary energy level increased (p<0.05) during the gestation period in the third parity. During lactation, the voluntary feed intake of lactating sows tended to decrease when gilts were fed higher energy treatment diet (p = 0.08) and the body weight, body weight gain were increased by dietary energy level during gestation (p< 0.05). Backfat thickness was not affected by dietary treatment during the gestation period in three parities, interestingly backfat change from breeding to d 110 of gestation was higher as the dietary energy level increased at the first parity (p<0.05). When gilts were fed 3,400 kcal of ME/kg treatment diet a higher number of weaning piglets was observed in the first parity (p<0.05). The highest culling rate (69%) was seen when gestating sows were fed 3,100 kcal/kg ME treatment diet during three parities. CONCLUSION: In conclusion, the adequate energy intake of gestating sows should be 6,400 or 6,600 kcal of ME/d, 7,040 or 7,260 kcal of ME/d, and 7,680 or 7,920 kcal of ME/d for parity 1, 2, and 3, respectively.