Young TSPC-derived exosomal circPVT1 ameliorates aging-impaired cell function via SIRT1/NF-κB.

Tendon stem/progenitor cell (TSPC) senescence is often associated with age-dependent tendon diseases and greatly reduces the capacities for tendon repair and replacement. Exosomes contain bioactive molecules and have been increasingly used in regenerative medicine. In the present study, we demonstrated the anti-aging effects of young exosomes from circPVT1-overexpressing TSPCs at early passages (circPVT1-exo). These exosomes attenuated the phenotypes of aged TPSCs at late passages (L-TSPCs) by enhancing self-renewal and proliferation abilities and suppressing cell senescence, maintain their tenogenic capacity, and weaken their osteogenic differentiation. Mechanistically, circPVT1-exo inhibited the NF-κB pathway and increased SIRT1 expression in L-TSPCs. Knockdown of SIRT1 reversed these effects as evidenced by increased senescence, decreased proliferation, and tenogenic differentiation. These results suggest that circPVT1-exo may ameliorate aging-impaired TSPC function by modulating the SIRT1/NF-κB pathway, suggesting that circPVT1-exo has therapeutic potential for age-related diseases.

HPF1 regulates tendon stem/progenitor cell senescence and tendon repair via PARP1-mediated poly-ADP ribosylation of HuR.

BACKGROUND: Tendon stem/progenitor cells (TSPCs) play a vital role in tendon repair, regeneration and homeostasis. However, the specific mechanism of TSPCs aging is still unclear. OBJECTIVE: This study aims to explore the role and molecular mechanism of HPF1 in the aging of TSPCs. METHODS: Young and aged TSPCs (Y-TSPCs and A-TSPCs) were acquired from 3 to 4 and 24-26-month-old Sprague-Dawley male rats, TSPCs (Y-TSPCs and A-TSPCs) were subjected to senescence-associated ß-galactosidase (SA-ß-Gal))staining and telomerase activity detection, p16, p21, Scx, Tnmd, Col1, Col3HPF1 and PAPR1 expression levels were detected by Western blot or Reverse Transcription-quantitative Polymerase Chain Reaction (RT-qPCR), Reciprocal co-immunoprecipitation (co-IP) was used to explore the interaction between HPF1 and PARP1. Ribonucleoprotein immunoprecipitation (RNP-IP) was used to analyze the binding of HuR to the senescence marker gene mRNAs, IP was used to perform HPF1 to the PARylation of HuR, and the half-life of p16 and p21 were detected. Finally, we established an in vivo model, and the tendon tissue was used to perform hematoxylin and eosin (HE) and masson's trichrome staining, as well as the immunohistochemical analysis of Col I and TNMD. RESULTS: Compared with Y-TSPCs, A-TSPCs had significantly enhanced cell senescence and significantly reduced tendon differentiation ability, and significantly increased the expression of HPF1 and PARP1. In addition, HPF1 and PARP1 interacted and coordinated the senescence and differentiation of TSPCs, HPF1 could also regulate the expression of p21 and p21, the interaction of p16 or p21 with HuR, and the poly-ADP ribosylation of PARP1 to HuR. HPF1 overexpression and siHuR co-transfection significantly reduced the half-life of p16 and p21, and HPF1 and PARP1 regulated the mRNA levels of p16 and p21 through HuR. Finally, in vivo experiments have shown that HPF1 or PARP1 overexpression could both inhibit the ability of tendon differentiation and promote cell senescence. CONCLUSIONS: HPF1 promoted the senescence of TSPCs and inhibits the tendon differentiation of TSPCs through PARP1-mediated poly-ADP ribosylation of HuR.

Edge-Cloud Collaborative Defense against Backdoor Attacks in Federated Learning.

Federated learning has a distributed collaborative training mode, widely used in IoT scenarios of edge computing intelligent services. However, federated learning is vulnerable to malicious attacks, mainly backdoor attacks. Once an edge node implements a backdoor attack, the embedded backdoor mode will rapidly expand to all relevant edge nodes, which poses a considerable challenge to security-sensitive edge computing intelligent services. In the traditional edge collaborative backdoor defense method, only the cloud server is trusted by default. However, edge computing intelligent services have limited bandwidth and unstable network connections, which make it impossible for edge devices to retrain their models or update the global model. Therefore, it is crucial to detect whether the data of edge nodes are polluted in time. This paper proposes a layered defense framework for edge-computing intelligent services. At the edge, we combine the gradient rising strategy and attention self-distillation mechanism to maximize the correlation between edge device data and edge object categories and train a clean model as much as possible. On the server side, we first implement a two-layer backdoor detection mechanism to eliminate backdoor updates and use the attention self-distillation mechanism to restore the model performance. Our results show that the two-stage defense mode is more suitable for the security protection of edge computing intelligent services. It can not only weaken the effectiveness of the backdoor at the edge end but also conduct this defense at the server end, making the model more secure. The precision of our model on the main task is almost the same as that of the clean model.

Gut Microbiota Signatures in Tumor, Para-Cancerous, Normal Mucosa, and Feces in Colorectal Cancer Patients.

Background: Association studies have linked microbiome alterations with colorectal cancer (CRC). However, differences in tumor, para-cancerous, normal mucosal, and fecal microbiota remain to be strengthened. Methods: We performed a study on the ecologically rich and taxonomically diverse of gut microbiota using three types of colorectal mucosa (tumor mucosa, para-cancerous mucosa, normal mucosa) and feces from 98 CRC patients. Additionally, we profiled the microbiota in the fecal occult blood test (FOBT) positive and negative groups at different sampling sites. Results: We found striking variations between tumor mucosal microbiota and normal mucosal microbiota. However, there was no significant difference between tumor and para-cancerous mucosal microbiota, as well as between para-cancerous and normal mucosal microbiota, revealing that the para-cancerous mucosal microbiota was a transitional state between the tumor and normal mucosal microbiota. And the substantial shifts in the fecal microbiota compared to mucosal microbiota indicated the risk of using fecal microbiota to define mucosal microbiota. A strong correlation between FOBT positive and Fusobacterium was discovered, indicating this adherent-invasive genus was closely related to intestinal bleeding. Furthermore, we identified six key genera, including Fusobacterium, Gemella, Campylobacter, Peptostreptococcus, Alloprevotella, and Parvimonas, which appear to be consistently over-represented in tumor mucosa compared to normal mucosa and/or in mucosa compared to feces. Conclusion: Compositional alterations in the microbiota existed in three types of colorectal mucosa and feces in CRC patients. Six key genera may contribute to the topographic variances in the microbiota of tumor-bearing colorectum.

Optimising social conditions to improve autonomy in communication and care for ethnic minority residents in nursing homes: A meta-synthesis of qualitative research.

A large proportion of nursing home residents in developed countries come from ethnic minority groups. Unmet care needs and poor quality of care for this resident population have been widely reported. This systematic review aimed to explore social conditions affecting ethnic minority residents' ability to exercise their autonomy in communication and care while in nursing homes. In total, 19 studies were included in the review. Findings revealed that ethno-specific nursing homes create the ideal social condition for residents to express their care needs and preferences in a language of choice. In nonethno-specific nursing homes, staff cultural competence and nursing home commitment to culturally safe care are crucial social conditions that enable this group of residents to fulfil their autonomy in communicating and in participating in their care. In contrast, social conditions that undermine residents' ability to express their care needs and preferences include low levels of staff cultural awareness and cultural desire, negative attitudes towards residents and limited organisational support for staff to improve culturally responsive and culturally safe care. In conclusion, it is important to optimise the social conditions to support ethnic minority residents to communicate their care needs and preferences.

Circular RNA PVT1 inhibits tendon stem/progenitor cell senescence by sponging microRNA-199a-5p.

Tendon stem/progenitor cell (TSPC) senescence can lead to age-dependent tendon maladies and undermines both tendon repair and replacement capacity in humans. The mechanisms underlying TSPC senescence and sensitivity to adverse factors are complicated. In this study, we analyzed involvement of the circular RNA (circRNA) PVT1 (circPVT1) in TSPC senescence. circPVT1 expression was found to be significantly diminished in human TSPCs under prolonged in vitro culture. Accordingly, circPVT1 knockdown promoted senescence progression and suppressed self renewal, migration, and tenogenic differentiation of TSPCs. Furthermore, we found that circPVT1 directly targets microRNA (miR)-199a-5p thereby attenuating its negative regulation of SIRT1 expression. Either miR-199a-5p inhibition or SIRT1 overexpression attenuated the senescence-boosting effect of circPVT1 knockdown, implying that circPVT1 suppresses TSPC senescence in part by upregulating the miR-199a-5p-SIRT1 signaling axis. Our findings conclusively explain the major roles of circPVT1 in TSPC senescence regulation; circPVT1 is a novel potential therapeutic target for reducing tendon senescence.

Overexpression of AMPD2 indicates poor prognosis in colorectal cancer patients via the Notch3 signaling pathway.

BACKGROUND: AMPD2 is a critical enzyme catalyzing smooth muscle energy supply and metabolism; however, its cellular biological function and clinical implication in colorectal cancer (CRC) are largely unknown. AIM: To clarify the role of AMPD2 in CRC and study the pathway and prognostic value of its role. METHODS: AMPD2 expression was analyzed by integrated bioinformatics analysis based on TCGA data sets and immunohistochemistry in tissue microarrays, and the correlation between AMPD2 expression and clinicopathological parameters, Notch3 expression, and prognostic features was assessed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis were then performed to investigate the regulatory pathway involved. The effects of AMPD2 expression on CRC cells and Notch3 protein expression were investigated by downregulation and overexpression of AMPD2. RESULTS: AMPD2 mRNA was significantly overexpressed in tumor tissue when compared with normal tissue in a cohort of the TCGA-COAD data set. Biological function enrichment analysis indicated that the Notch pathway strongly correlated with AMPD2 expression, and that the expression of Notch3 and JAG2 mRNA was positively associated with AMPD2 in CRC tissues. In vitro, AMPD2 overexpression markedly reduced Notch3 protein expression in CRC cells, while knockdown of AMPD2 showed the opposite findings. In addition, protein expression was significantly up-regulated in our CRC cohort as indicated by tissue microarray analysis. High expression of AMPD2 protein correlated with advanced depth of tumor and poor differentiation. Furthermore, high AMPD2 expression in CRC tissues was an indicator of poor outcome for CRC patients. CONCLUSION: AMPD2 is commonly overexpressed in CRC, and acts as a metabolism oncogene to induce CRC progression through the Notch signaling pathway. Thus, AMPD2 may be a novel prognostic biomarker for CRC.

Challenges and opportunities for the multicultural aged care workforce: A systematic review and meta-synthesis.

AIMS: To identify (a) the challenges for multicultural aged care teams; (b) the opportunities to facilitate teamwork; and (c) the strategies to assist team members in a multicultural work environment. BACKGROUND: High-income countries have an increasingly culturally diverse aged care workforce. Fostering teamwork in such an environment is challenging. METHODS: This systematic review of qualitative studies followed the Joanna Briggs Institute (JBI) meta-aggregation approach. Six databases were searched. Retrieved articles were screened by two reviewers. This review identified 111 findings that were aggregated into 15 categories and five themes. FINDINGS: Aged care workers' awareness of cultural diversity varies, and their knowledge of each other's cultural background is limited. However, cultural skills are demonstrated, contributing to teamwork. Their experience in cross-cultural encounters is broad, and enhanced team cohesion is desired. CONCLUSIONS: The cultural competence of the aged care workforce shapes team building, peer support opportunities and positive cross-cultural experiences. IMPLICATIONS FOR NURSING MANAGEMENT: Recommendations are provided for the adaptation of aged care workers to culturally diverse teams, fostering teamwork to enhance care outcomes for clients. Interventions for improvements in cross-cultural leadership and management, and staff experience of cross-cultural encounters are much needed.

LncRNA-FEZF1-AS1 Promotes Tumor Proliferation and Metastasis in Colorectal Cancer by Regulating PKM2 Signaling.

Purpose: Long non-coding RNAs (lncRNAs) play key roles in human cancers. Here, FEZF1-AS1, a highly overexpressed lncRNA in colorectal cancer, was identified by lncRNA microarrays. We aimed to explore the roles and possible molecular mechanisms of FEZF1-AS1 in colorectal cancer.Experimental Design: LncRNA expression in colorectal cancer tissues was measured by lncRNA microarray and qRT-PCR. The functional roles of FEZF1-AS1 in colorectal cancer were demonstrated by a series of in vitro and in vivo experiments. RNA pull-down, RNA immunoprecipitation and luciferase analyses were used to demonstrate the potential mechanisms of FEZF1-AS1.Results: We identified a series of differentially expressed lncRNAs in colorectal cancer using lncRNA microarrays, and revealed that FEZF1-AS1 is one of the most overexpressed. Further validation in two expanded colorectal cancer cohorts confirmed the upregulation of FEZF1-AS1 in colorectal cancer, and revealed that increased FEZF1-AS1 expression is associated with poor survival. Functional assays revealed that FEZF1-AS1 promotes colorectal cancer cell proliferation and metastasis. Mechanistically, FEZF1-AS1 could bind and increase the stability of the pyruvate kinase 2 (PKM2) protein, resulting in increased cytoplasmic and nuclear PKM2 levels. Increased cytoplasmic PKM2 promoted pyruvate kinase activity and lactate production (aerobic glycolysis), whereas FEZF1-AS1-induced nuclear PKM2 upregulation further activated STAT3 signaling. In addition, PKM2 was upregulated in colorectal cancer tissues and correlated with FEZF1-AS1 expression and patient survival.Conclusions: Together, these data provide mechanistic insights into the regulation of FEZF1-AS1 on both STAT3 signaling and glycolysis by binding PKM2 and increasing its stability. Clin Cancer Res; 24(19); 4808-19. ©2018 AACR.

Role of male genetic factors in recurrent pregnancy loss in Northeast China.

OBJECTIVE: This study aimed to investigate the roles of male genetic factors, including Y chromosome microdeletions and chromosomal heteromorphism, in recurrent pregnancy loss (RPL) in Northeast China. STUDY DESIGN: We evaluated 1072 male patients from Northeast China whose wives had a history of two or more consecutive miscarriages. We also selected 971 infertile and 200 fertile men as control groups. Semen analysis was carried out by computer-assisted sperm analysis. Y chromosome microdeletions were detected by polymerase chain reaction and chromosomes were evaluated by karyotype analysis. RESULTS: There were no microdeletions in the RPL and fertile control groups, but 112 of the infertile men had Y chromosome microdeletions. Chromosomal heteromorphism was detected in all the groups. Patients in the infertile control group had a significantly higher percentage (2.16%) of Y variation (Yqh±) heteromorphism compared with the RPL group, but there were no significant differences in the incidences of chromosomal heteromorphism among the other groups. CONCLUSION: Y chromosome microdeletions and chromosomal heteromorphism are not associated with RPL in Northeast China. Some RPL males had structural chromosome anomalies, all of which were reciprocal translocations. We suggest that it may not be necessary to detect Y chromosome microdeletions in RPL males with Yqh±.

LncRNA-p21 inhibited the proliferation of osteosarcoma cells via the miR-130b/PTEN/AKT signaling pathway.

Osteosarcoma (OS) is the most common type of malignant bone tumor in children and adolescents. However, the molecular mechanism underlying OS development is unclear. Here, we investigated the contribution of lncRNA-p21, a novel long non-coding RNA, on OS cell proliferation. Our results demonstrated that the expression of lncRNA-p21 was repressed in OS tissue. Growth curves and the cell colony formation assay showed that lncRNA-p21 significantly inhibited the proliferation of OS cell lines. In addition, the expression of lncRNA-p21 increased the protein levels of proliferation markers, such as Ki-67 and cyclin D1. Subsequently, lncRNA-p21 overexpression up-regulated the protein level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), a well-known inhibitor of AKT signaling. Moreover, our gain and loss function assay showed that the promotion of PTEN by lncRNA-p21 was mediated by miR-130b, an oncogene overexpressed in OS tissue. Our findings may provide a novel lncRNA-targeted therapy for patients with OS.

The p16/miR-217/EGR1 pathway modulates age-related tenogenic differentiation in tendon stem/progenitor cells.

Previous studies have shown that the differentiation potential declines with the age of progenitor cells and is linked to altered levels of senescence markers. The purpose of this study was to test whether senescence marker p16 affects age-related tenogenic differentiation in tendon stem/progenitor cells (TSPCs). Young and aged TSPCs were isolated from young/healthy and aged/degenerated human Achilles tendons, respectively. Cellular aging and capacity for tenogenic differentiation were examined. The results showed that the tenogenic differentiation capacity of TSPCs significantly decreases with advancing age. TSPCs from elderly donors showed upregulation of senescence-associated ß-galactosidase and p16 and concurrently a decrease in Type I collagen concentration and in the expressions of tendon-related markers: Scx, Tnmd, Bgn, Dcn, Col1, and Col3. Overexpression of p16 significantly inhibited tenogenic differentiation of young TSPCs. Analysis of the mechanism revealed that this effect is mediated by microRNA-217 and its target EGR1. These results indicated that p16 inhibits tenogenic differentiation of TSPCs via microRNA signaling pathways, which may serve as a potential target for the prevention or treatment in the future.

Epigenetic silencing of the Wnt antagonist APCDD1 by promoter DNA hyper-methylation contributes to osteosarcoma cell invasion and metastasis.

Osteosarcoma (OS) is the most common type of bone tumor in children and adults. However, the molecular mechanism underlying OS tumorigenesis remains unclear. Here, we report that the expression of APCDD1, a Wnt antagonist, was reduced in OS tissues and cells compared to adjacent normal tissue and osteoblast cells, respectively. Mechanistically, this was due to increased levels of methylation in the promoter region of the APCDD1 gene. Consistently, the DNA methyltransferase inhibitor 5-AZA-dC, reduced DNA methylation in the APCDD1 promoter, and restored APCDD1 expression in OS tissue and cells. Moreover, DNMT3a, but not DNMT1 or DNMT3b, was the major DNA methyltransferase that facilitated hyper-methylation of DNA in the APCDD1 promoter, thus reducing APCDD1 mRNA levels in OS tissues. Importantly, ectopic expression of APCDD1 suppressed activity of the Wnt/ß-Catenin signaling pathway in OS cells and inhibited their invasion and reversed their EMT-like properties, while depletion of APCDD1 promoted invasion and metastasis of osteosarcoma cells in vitro and in vivo. Thus, we have provided the first evidence that APCDD1 expression is epigenetically silenced in OS, which may facilitate invasion and metastasis of OS cells.

Induced membrane technique: Advances in the management of bone defects.

Management of bone defects caused by trauma, osteomyelitis, and tumors is challenging, with many controversies over the optimal reconstruction method. Masquelet discovered induced membrane in management of large diaphyseal defects accidentally, and developed this technique with a concept of induced membrane. Induced membrane technique holds great potential for the reconstruction of bone defects, alternatively to manage this clinical challenge quiet easily. Induced membrane has unique structural characteristics and biological properties, which render this technique has an advantage of the time to bone healing is relatively independent of the length of bone defect. Herein, we reviewed the latest advances made in induced membrane technique and highlighted the concept of induced membrane in the management of bone defects.

Enhanced tenogenic differentiation and tendon-like tissue formation by CHIP overexpression in tendon-derived stem cells.

The carboxyl terminus of Hsc70-interacting protein (CHIP, also known as STUB1) plays critical roles in the proliferation and differentiation of many types of cells. The potential function of CHIP in tendon-derived stem cells (TDSCs) remains largely unknown at present. Here, we investigated the effects of CHIP on tenogenic differentiation of TDSCs via lentivirus-mediated overexpression. Forced expression of CHIP induced morphological changes and significantly enhanced cell proliferation, as well as tendon differentiation in vitro. Upon stimulation with differentiation induction medium, CHIP-overexpressing TDSCs displayed significant inhibition of differentiation into osteogenic and adipogenic lineages. Subsequent implantation of TDSCs overexpressing CHIP with collagen sponges into nude mice induced a marked increase in ectopic tendon formation in vivo, compared with the control group. Our findings collectively suggest that CHIP is an important contributory factor to tenogenic tissue formation.

Mechanism of osteogenic and adipogenic differentiation of tendon stem cells induced by sirtuin 1.

The aim of the present study was to assess the expression of sirtuin (Sirt)1 in tendon stem cells (TSCs) and to elucidate its association with osteogenic and adipogenic differentiation of TSCs. Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analyses were performed to detect Sirt1 mRNA and protein levels in TSCs, respectively. TSCs were positive for Sirt1 expression, which was elevated by Sirt1 activator SRT1720 in a time- and concentration- dependent manner, and decreased by Sirt1 inhibitor EX527. TSCs were treated with SRT1720 and EX527 for various time periods and resulting changes in osteogenic and adipogenic protein markers were analyzed using alizarin red and oil red O staining. According to RT-qPCR and western blot analyses, the associated factors ß­catenin, Runt-related transcription factor 2 (Runx2) and bone morphogenetic protein 2 were elevated following increases of Sirt1 levels, while CCAAT/enhancer binding protein (CEBP)α and peroxisome proliferator-activated receptor (PPAR)γ were decreased. These results suggested that osteogenic differentiation capacity was enhanced, while adipogenic differentiation capacity declined. Further mechanistic study revealed that phosphoinositide­3 kinase (PI3K) and AKT were decreased following activation of Sirt1. In conclusion, the present study suggested that Sirt1 promotes the osteogenic differentiation of TSCs through upregulating ß­catenin and Runx2 and inhibits the adipogenic differentiation of TSCs through the PI3K/AKT pathway with downregulation of CEBPα and PPARγ.

Redefining 'Chinese' L1 in SLP: Considerations for the assessment of Chinese bilingual/bidialectal language skills.

PURPOSE: Language assessment of bilingual/bidialectal children can be complex. This is particularly true for speakers from China, who are likely to be bilingual and bidialectal at the same time. There has been, however, a lack of understanding of the diversity of Chinese languages as well as data on bidialectal children's L1 syntactic development and the development of L1 bidialectal children's L2 acquisition. METHOD: This paper provides information on the complexity of the language system for people from China. It will present illustrative examples of the expressive language outputs of bilingual and bidialectal children from the perspective of bilingual, bidialectal linguists and speech-language pathologists. Then it will outline why appropriate assessment tools and practices for identification of language impairment in bilingual Chinese children need to be developed. RESULT: Considerations include that Chinese bilingual children may differ in L2 performance because of lack of exposure in the target language or because of their varied L1 dialectal backgrounds, but not necessarily because of language impairment. CONCLUSION: When evaluating morphosyntactic performance of bilingual children, a series of reliable threshold indicators for possible language impairment is urgently needed for SLPs to facilitate accurate diagnosis of language impairment.

CTGF positively regulates BMP12 induced tenogenic differentiation of tendon stem cells and signaling.

BACKGROUND/AIMS: Disordered differentiation of tendon stem cells (TSCs) during repair of injured tendon can result in the pathogenesis of chronic tendinopathy. Understanding tenocyte differentiation may provide new therapeutic insights for the prevention and treatment of chronic tendinopathy. The aim of our study was to determine if CTGF exerts a similar effect on BMP12-driven differentiation of rat TSCs. METHODS: In overexpressing and RNA interference CTGF TSCs, tenogenic differentitation and the expression of related genes were determined by immunofluorescence staining, quantitative PCR, and western blotting, with or without BMP12 treatment. The interaction in vitro between CTGF and BMP12 was detected by Chemical crosslinking assay. RESULTS: Our results showed that BMP12 effectively increased the expression of the tenocyte lineage markers scleraxis (Scx) and tenomodulin (Tnmd) at both mRNA and protein levels. Over-expression of CTGF from a lentiviral vector increased the expression of Scx and Tnmd as well as tendon proteins type I collagen (ColI) and tenascin-C (Tn-C) in TSCs compared to non-treated control cells with or without simultaneous BMP12 stimulation. Knockdown of CTGF expression decreased the expression of Scx, Tnmd, ColI and Tn-C compared to control cells. Chemical crosslinking experiments demonstrated a direct interaction between CTGF and BMP12. CONCLUSION: In conclusion, BMP12 plays a crucial role in tenogenesis via the Smad1/5/8 pathway, and CTGF positively promotes this effect.

[Correlation between chromosomal polymorphisms and male sperm quality in population of Jilin Province].

OBJECTIVE: To evaluate the correlation between chromosomal polymorphisms and male sperm quality in Jilin Province. METHODS: A total of 2 584 male patients with infertility in Center for Reproductive Medicine, First Bethune Hospital of Jilin University from 2008 to 2013 were enrolled, which semen analysis, chromosomal analysis, Y chromosome microdeletion analysis and serum hormone levels analysis were performed. A total of 602 healthy individuals, 50 fertile individuals with normal kayrotypes, 50 azoospermia patients with normal kayrotypes and 50 oligospermia patients with normal kayrotypes were selected as control groups. RESULTS: There was no significant difference in the frequency of chromosome polymorphisms between infertile patients and normal control individuals (3.91% (101/2 584) vs 3.16% (19/602), P > 0.05). And there was no significant difference in the frequency of autosomal polymorphisms between infertile patients and normal control individuals (all P > 0.05). The frequency of Yqh-variant was increased by the decrease of sperm count and it appeared a significantly high frequency in azoospermia patients compared with oligospermia patients and sperm count normal patients in the infertile group (57.14% (21/42) vs 24.32% (9/37), 0 (0/13), both P < 0.05). There was no significant difference in the testis volume and serum hormone levels between the infertile patients with chromosomal polymorphisms and patients in control groups with normal kayrotypes (all P > 0.05). The results of PCR amplication indicated that 32.14% (9/28) patients with Yqh ± had Y chromosome microdeletion. CONCLUSIONS: There is no significant correlation between autosomal polymorphisms and male infertility. But Yqh ± may be responsible for Y chromosome microdeletion and male infertility.

[Application of preoperative nutritional risk screening in perioperative nutrition support for colorectal cancer patients].

OBJECTIVE: To investigate the guidance role of preoperative nutritional risk screening in perioperative nutrition support for colorectal cancer patients in order to provide evidence for the rational clinical application of nutrition support. METHODS: Nutritional risk screening was carried out in 290 hospitalized colorectal cancer patients from The Fourth People's Hospital of Wuxi City, Tongji Hospital of Tongji University and The Second Hospital of Soochow University with the nutritional risk screening(NSR) 2002 score summary table. Postoperative bowel function recovery and associated nutritional indices were compared between patients who received preoperative nutrition support according to the risk screening results and those who did not. RESULTS: Among 110 patients at nutritional risk, 65 received perioperative nutrition support and had faster recovery of intestinal function [time to first flatus (2.3±0.5) d vs. (3.3±0.5) d, time to first defecation (3.5±0.5) d vs. (4.6±0.6) d, semi-fluid intake (10.1±1.2) d vs. (12.4±2.2) d], shorter postoperative stay [(15.7±1.1) d vs. (18.8±1.4) d], and higher albumin, prealbumin and transferrin [(33.2±4.5) g/L vs. (26.0±4.0) g/L, (0.28±0.05) g/L vs. (0.16±0.04) g/L, (1.92±0.33) g/L vs. (1.75±0.45) g/L] at 7-day postoperatively (all P<0.05) as compared to those without perioperative nutrition support(n=45). While among 180 cases without nutritional risk, there were no significant differences in the above indices between patients who received preoperative nutrition support and those who did not (all P>0.05). CONCLUSION: It is important to evaluate the nutritional risk in hospitalized patients with colorectal cancer, and to carry out nutrition support actively for those at nutritional risk.