Objective To explore the effectiveness of the generative large language model MedGo in nursing decision-making for elderly patients with multimorbidity. Methods A quasi-randomized controlled trial study was conducted involving 6 junior nurses, 6 senior nurses and the MedGo model from January 1, 2025 to March 31, 2025 at the Emergency Internal Medicine Ward of Shanghai East Hospital Affiliated to Tongji University. Clinical data of 120 elderly patients with multimorbidity were analyzed to compare the performance of the three groups in four tasks (nursing diagnosis assessment, nursing intervention formulation, complication identification, and complication prevention) from three evaluation dimensions: decision-making time consumption, decision accuracy, and decision-making quality. Results In terms of decision-making time, the senior nurse group completed all four tasks faster than the junior nurse group (P＜0.01), and the MedGo group completed all four tasks faster than the junior nurse group (P＜0.001) and the senior nurse group (P＜0.001). In terms of decision-making accuracy, senior nurse group scored higher than junior nurse group in all four tasks (P＜0.001), while the MedGo group outperformed the senior nurse group only in complication identification (P＜0.001). In terms of decision-making quality, the MedGo group scored higher than junior nurse group (P＜0.001) and senior nurse group (P＜0.001) in all four tasks. Conclusions The MedGo model demonstrates advantages of high efficiency, accuracy, and quality in nursing decision-making for elderly patients with multimorbidity; senior nurses outperform junior nurses in decision-making, providing diverse references for clinical nursing decision-making.

Cancer remains a leading cause of global mortality, necessitating the development of advanced therapeutic strategies with enhanced efficacy and reduced systemic toxicity. Among promising bioactive agents, lactoferrin (LF)—a multifunctional iron-binding glycoprotein abundantly found in mammalian milk and exocrine secretions—has garnered significant interest for its potent and multifaceted anti-cancer properties. This review provides a comprehensive analysis of the current understanding of LF’s role in oncology, encompassing its structural biology, diverse mechanisms of action, and groundbreaking advancements in its application through nano-engineering. LF exerts anti-tumor effects through multiple pathways, including extracellular action, intracellular action, and immune regulation. It demonstrates a remarkable affinity for cancer cell membranes, binding to overexpressed anionic components such as glycosaminoglycans and sialic acids, as well as to specific receptors including the low-density lipoprotein receptor-related protein-1 (LRP-1). This selective binding facilitates targeted uptake. Upon internalization, LF orchestrates a direct assault by inducing cell-cycle arrest in phases such as G0/G1 or S phase through the modulation of key regulators including cyclins, CDKs, and p53. Furthermore, it promotes programmed cell death via apoptotic pathways, involving caspase activation and downregulation of anti-apoptotic proteins such as survivin. A more recently elucidated mechanism is the induction of ferroptosis, an iron-dependent form of cell death characterized by overwhelming lipid peroxidation. Beyond direct cytotoxicity, LF acts as a potent immunomodulator. It enhances natural killer (NK) cell activity, modulates T-lymphocyte populations, and crucially reprograms tumor-associated macrophages (TAMs) from a pro-tumor M2 state to an anti-tumor M1 state, thereby reversing the immunosuppressive tumor microenvironment (TME). The translation of LF’s potential has been significantly accelerated by nanotechnology. The inherent biocompatibility and natural tumor-targeting capabilities of LF make it an ideal platform for sophisticated drug-delivery systems. This review details various fabrication strategies for LF-based nanoparticles (NPs), including self-assembly, sol-in-oil emulsion, and electrostatic nanocomplexes, among others. Research demonstrates that nano-formulations not only protect LF from degradation but also enhance its bioactivity and anti-cancer potency. More importantly, LF NPs serve as versatile carriers for a wide array of therapeutic agents, including conventional chemotherapeutics, natural compounds, and imaging agents. These engineered systems enable synergistic therapy and facilitate site-specific delivery. Notably, the ability of LF to bind to receptors on the blood-brain barrier (BBB) has been leveraged to develop nano-systems for glioblastoma treatment. Other innovative designs utilize LF to modulate the TME—for instance, by alleviating tumor hypoxia to sensitize cells to radiotherapy and chemotherapy. Despite compelling pre-clinical evidence, the clinical translation of LF and its nano-formulations remains nascent. While early-phase trials have established a favorable safety profile for recombinant human LF, larger Phase III studies have yielded mixed results, underscoring the complexity of its action in humans. Key challenges include enhancing drug targeting, optimizing loading efficiency, ensuring batch-to-batch reproducibility, and achieving deep tumor penetration. Future research must focus on the rational design of next-generation LF-NPs. This entails developing standardized manufacturing protocols, engineering “smart” stimuli-responsive systems for targeted drug release in the TME, and constructing multi-targeting platforms. A concerted interdisciplinary effort is paramount to bridge the gap between bench and bedside. In conclusion, LF, particularly in its nano-engineered forms, represents a highly promising and versatile agent in the oncological arsenal, holding immense potential for precise and effective cancer therapy.

Cancer remains a leading cause of global mortality, necessitating the development of advanced therapeutic strategies with enhanced efficacy and reduced systemic toxicity. Among promising bioactive agents, lactoferrin (LF)—a multifunctional iron-binding glycoprotein abundantly found in mammalian milk and exocrine secretions—has garnered significant interest for its potent and multifaceted anti-cancer properties. This review provides a comprehensive analysis of the current understanding of LF’s role in oncology, encompassing its structural biology, diverse mechanisms of action, and groundbreaking advancements in its application through nano-engineering. LF exerts anti-tumor effects through multiple pathways, including extracellular action, intracellular action, and immune regulation. It demonstrates a remarkable affinity for cancer cell membranes, binding to overexpressed anionic components such as glycosaminoglycans and sialic acids, as well as to specific receptors including the low-density lipoprotein receptor-related protein-1 (LRP-1). This selective binding facilitates targeted uptake. Upon internalization, LF orchestrates a direct assault by inducing cell-cycle arrest in phases such as G0/G1 or S phase through the modulation of key regulators including cyclins, CDKs, and p53. Furthermore, it promotes programmed cell death via apoptotic pathways, involving caspase activation and downregulation of anti-apoptotic proteins such as survivin. A more recently elucidated mechanism is the induction of ferroptosis, an iron-dependent form of cell death characterized by overwhelming lipid peroxidation. Beyond direct cytotoxicity, LF acts as a potent immunomodulator. It enhances natural killer (NK) cell activity, modulates T-lymphocyte populations, and crucially reprograms tumor-associated macrophages (TAMs) from a pro-tumor M2 state to an anti-tumor M1 state, thereby reversing the immunosuppressive tumor microenvironment (TME). The translation of LF’s potential has been significantly accelerated by nanotechnology. The inherent biocompatibility and natural tumor-targeting capabilities of LF make it an ideal platform for sophisticated drug-delivery systems. This review details various fabrication strategies for LF-based nanoparticles (NPs), including self-assembly, sol-in-oil emulsion, and electrostatic nanocomplexes, among others. Research demonstrates that nano-formulations not only protect LF from degradation but also enhance its bioactivity and anti-cancer potency. More importantly, LF NPs serve as versatile carriers for a wide array of therapeutic agents, including conventional chemotherapeutics, natural compounds, and imaging agents. These engineered systems enable synergistic therapy and facilitate site-specific delivery. Notably, the ability of LF to bind to receptors on the blood-brain barrier (BBB) has been leveraged to develop nano-systems for glioblastoma treatment. Other innovative designs utilize LF to modulate the TME—for instance, by alleviating tumor hypoxia to sensitize cells to radiotherapy and chemotherapy. Despite compelling pre-clinical evidence, the clinical translation of LF and its nano-formulations remains nascent. While early-phase trials have established a favorable safety profile for recombinant human LF, larger Phase III studies have yielded mixed results, underscoring the complexity of its action in humans. Key challenges include enhancing drug targeting, optimizing loading efficiency, ensuring batch-to-batch reproducibility, and achieving deep tumor penetration. Future research must focus on the rational design of next-generation LF-NPs. This entails developing standardized manufacturing protocols, engineering “smart” stimuli-responsive systems for targeted drug release in the TME, and constructing multi-targeting platforms. A concerted interdisciplinary effort is paramount to bridge the gap between bench and bedside. In conclusion, LF, particularly in its nano-engineered forms, represents a highly promising and versatile agent in the oncological arsenal, holding immense potential for precise and effective cancer therapy.

Objective To investigate the related mechanism which metformin inhibited the proliferation of HCT116 colorectal cancer cells via down-regulating the expression of up-frameshift protein 1(UPF1).Methods TCGA and UALCAN databases were utilized to analyze the expression level of UPF1,while Western blotting and Real-time PCR were performed to validate the differences of UPF1 expressions in colon cancer tissues and adjacent normal tissues.Clone formation assay,CCK-8 assay,wound healing assay and Transwell invasion assay were used to examine the effects of knockdown UPF1 on the proliferation,migration and invasion of HCT116 cells respectively.The HCT116 cell dataset with UPF1 knockdown was screened from GEO database for Kyoto Encydopedia of Genes and Genomes(KEGG)pathway analysis,the expression level of differential genes that enriched in Hippo pathway were verified by Real-time PCR.The HCT116 cells were treated with metformin,Western blotting and Real-time PCR were employed to detect the UPF1 expression.Mendelian randomization analysis was performed to explore the causal association between metformin treatment and colorectal cancer.Results Analysis of TCGA and UALCAN databases showed that both UPF1 mRNA and protein were highly expressed in colon cancer tissues and the expression level of UPF1 was closely correlated with clinicopathologic stage and lymph node metastasis.Compared with adjacent normal tissues,the UPF1 protein and mRNA were highly expressed in colon cancer tissues.Knockdown UPF1 expression could inhibit the proliferation,migration and invasive ability of HCT116 cells.There were 8 differential genes affect the Hippo pathway by KEGG enrichment analysis,Real-time PCR experiments confirmed that CTNNB1,BMP4,TEAD2,PARD6G and FZD1 mRNA decreased in HCT116 cells with UPF1 knockdown.Both UPF1 protein and mRNA expressions decreased after metformin treatment in HCT116 cells.Mendelian randomization analysis showed a negative causal association between metformin treatment and colorectal cancer.Conclusion Knockdown of UPF1 expression inhibits the proliferation of HCT116 cells through regulating Hippo pathway.Metformin can reduce the UPF1 expression for further inhibiting the proliferation of colorectal cancer cells.

Type 2 diabetes mellitus(T2DM) is a prevalent metabolic and endocrine disorder. Long-term hyperglycemia can lead to severe chronic complications, imposing substantial economic burdens on both society and patients. Despite the availability of various hypoglycemic agents for clinical use, these agents often fail to meet the therapeutic needs of T2DM and its complications. Consequently, there is an urgent need for novel therapeutic strategies and drugs. Lithocarpus litseifolius(L. litseifolius), commonly referred to as "cordyceps on trees", has a long history of use in traditional medicine and can be applied in tea, sugar, and medicine. Research indicates that L. litseifolius extracts are rich in dihydrochalcones, including trilobatin, phloridzin, and phloretin, which exhibit a range of pharmacological activities, such as anti-inflammatory, antioxidant, hypoglycemic, hypolipidemic, hepatoprotective, and cardioprotective effects. These properties suggest potential applications in the treatment of T2DM and its complications. This review systematically compiled and organized the relevant literature from the past decade on dihydrochalcones(trilobatin, phloridzin, and phloretin) from L. litseifolius extracts. It highlighted recent research progress regarding their role in treating T2DM and its complications through mechanisms such as reducing insulin resistance, regulating glucose transport, improving glucose and lipid metabolism, modulating enzyme activity, regulating gut microbiota, and alleviating inflammation and oxidative damage. The purpose of this review is to provide a reference and basis for future research on the prevention and treatment of T2DM and its complications using dihydrochalcones(trilobatin, phloridzin, and phloretin) from L. litseifolius extracts.
Chalcones/chemistry* ; Diabetes Mellitus, Type 2/metabolism* ; Humans ; Animals ; Elaeocarpaceae/chemistry* ; Drugs, Chinese Herbal/therapeutic use* ; Hypoglycemic Agents/chemistry* ; Plant Extracts/chemistry*

This study aimed to characterize and identify the non-volatile components in aqueous and ethanolic extracts of the stems and leaves of Rhododendron tomentosum by using sensitive and efficient ultra-performance liquid chromatography-quadrupole-time of flight mass spectrometry(UHPLC-Q-TOF-MS) combined with a self-built information database. By comparing with reference compounds, analyzing fragment ion information, searching relevant literature, and using a self-built information database, 118 compounds were identified from the aqueous and ethanolic extracts of R. tomentosum, including 35 flavonoid glycosides, 15 phenolic glycosides, 12 flavonoids, 7 phenolic acids, 7 phenylethanol glycosides, 6 tannins, 6 phospholipids, 5 coumarins, 5 monoterpene glycosides, 6 triterpenes, 3 fatty acids, and 11 other types of compounds. Among them, 102 compounds were reported in R. tomentosum for the first time, and 36 compounds were identified by comparing them with reference compounds. The chemical components in the ethanolic and aqueous extracts of R. tomentosum leaves and stems showed slight differences, with 84 common chemical components accounting for 71.2% of the total 118 compounds. This study systematically characterized and identified the non-volatile chemical components in the ethanolic and aqueous extracts of R. tomentosum for the first time. The findings provide a reference for active ingredient research, quality control, and product development of R. tomentosum.
Rhododendron/chemistry* ; Chromatography, High Pressure Liquid/methods* ; Drugs, Chinese Herbal/chemistry* ; Mass Spectrometry/methods* ; Plant Leaves/chemistry*

Objective : To investigate the effects of sinapine on lung tissue inflammation and mucus hypersecretion in asthmatic mice. Methods: Eight-week-old female C57BL/6J mice were randomly divided into Control group, ovalbumin(OVA) group, Sinapine group, and Sinapine+OVA group. The asthmatic mice model were established by intraperitoneal injection of OVA combined with aluminum hydroxide [Al(OH)3] suspension and OVA nasal stimulation. One hour before OVA nasal stimulation, the mice in Sinapine+OVA group and Sinapine group were intraperitoneally injected with sinapine solution, and the mice in OVA group and Control group were treated with the same dose of 0.9% sodium chloride solution. 24 hours after the last OVA stimulation, the inflammation of lung tissue of mice were observed by HE staining; the mucus secretion were evaluated by PAS staining; the mRNA expression levels of Interleukin-4(IL-4), Interleukin-5(IL-5), Interleukin-13(IL-13), tumor necrosis factor-alpha(TNF-α), Mucin 5ac(Muc5ac), and the mRNA of the key genes of Notch pathway such as Notch receptor 1(Notch1), Notch receptor 2(Notch2), Notch receptor 3(Notch3), and hes family bHLH transcription factor 1(Hes1) in lung tissues were detected by real-time fluorescent quantitative PCR(RT-qPCR); the expression levels of Notch1, Notch2, Notch3 and Hes1 proteins were determined by Western blot. Results : Compared with Control group, the inflammation score and PAS score of lung tissues of mice in OVA group increased(P<0.001); the mRNA expression levels of IL-4, IL-5, IL-13, TNF-α, and Muc5ac of mice in OVA group were enhanced(P<0.05); the mRNA and protein expression levels of Notch2, Notch3, and Hes1 of mice in OVA group significantly increased(P<0.001), while there was no significant difference in the mRNA and protein expression levels of Notch1. Compared with OVA group, the inflammation score and PAS score of lung tissues of mice in Sinapine+OVA group decreased(P<0.001); the mRNA expression levels of IL-4, IL-5, IL-13, TNF-α, and Muc5ac of mice in Sinapine+OVA group were reduced(P<0.05); the mRNA and protein expression levels of Notch2, Notch3, and Hes1 of mice in Sinapine+OVA group were downregulated(P<0.05), while there was no significant difference in the mRNA and protein expression levels of Notch1. Conclusion Sinapine can alleviate the lung tissue inflammation and mucus hypersecretion in asthmatic mice, and its mechanism may be related to the inhibition of Notch2/Notch3-Hes1 signal pathway.

Objective:To evaluate the role of exosomes in propofol-induced elimination of cardioprotective effect of remote ischemic preconditioning (RIPC) in rats.Methods:This experiment was performed in 2 parts. In vivo experiment Forty-eight healthy SPF male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-300 g, were divided into 5 groups using the random number table method: sham operation group (Sham group, n=12), ischemia-reperfusion (I/R) group ( n=12), RIPC group ( n=8), RIPC+ propofol group (RIPC+ P group, n=8), and propofol+ I/R group (P+ I/R group, n=8). The model of myocardial I/R injury was developed by ligating the left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion in anesthetized animals. Four cycles of 5-min ischemia induced by occlusion of the bilateral hind limbs with a tourniquet/5-min reperfusion served as the RIPC stimulus. Propofol was intravenously infused at a rate of 12 mg·kg -1·h -1 in RIPC+ P group (during RIPC) and in P+ I/R group (for 40 min). Exosomes from RIPC-treated and RIPC+ propofol-treated rats were extracted (RIPC-EXO and RIPC+ P-EXO respectively) for determination of the expression of surface markers of exosomes CD9 and HSP70. Another 24 rats were randomly selected, and the aforementioned exosomes were injected at 15 min before myocardial ischemia, resulting in RIPC-EXO+ I/R group ( n=12) and RIPC+ P-EXO+ I/R group ( n=12). At the end of reperfusion, the area of myocardial infarction was determined, the concentration of serum cardiac troponin I (cTnI) was measured by the enzyme-linked immunosorbent assay, and the expression of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) in myocardial tissues was detected by Western blot. Cell experiment H9c2 cells were cultured in vitro and divided into 4 groups ( n=6 each) using a random number table method: control group (C group), hypoxia-reoxygenation group (H/R group), RIPC-EXOc group and RIPC+ P-EXOc group. The cells were exposed to hypoxia for 4 h followed by reoxygenation for 16 h in H/R group. RIPC-EXO and RIPC+ P-EXO were added at a final concentration of 300 μg/ml before hypoxia in RIPC-EXOc group and RIPC+ P-EXOc group, respectively. The cell viability was determined using a cell counting kit-8 assay and the expression of Bax and Bcl-2 expression was detected by Western blot. Results:In vivo experiment Compared with RIPC-EXO group, the expression of CD9 and HSP70 was significantly down-regulated in RIPC+ P-EXO group ( P<0.05). Compared with Sham group, the percentage of the area of myocardial infarction was significantly increased, and the serum cTnI concentration and Bax/Bcl-2 ratio in myocardial tissues were increased in I/R group ( P<0.05). Compared with I/R group, the percentage of the area of myocardial infarction was significantly decreased in RIPC group and RIPC-EXO+ I/R group, the serum cTnI concentration and Bax/Bcl-2 ratio in myocardial tissues were significantly decreased in RIPC-EXO+ I/R group ( P<0.05), and no significant change was found in the percentage of the area of myocardial infarction in RIPC+ P group ( P>0.05). The percentage of the area of myocardial infarction was significantly larger in RIPC+ P group than in RIPC group ( P<0.05). Compared with RIPC-EXO+ I/R group, the percentage of the area of myocardial infarction was significantly increased, and the serum cTnI concentration and Bax/Bcl-2 ratio were increased in RIPC+ P-EXO+ I/R group ( P<0.05). Cell experiment Compared with C group, the cell viability was significantly decreased, and the Bax/Bcl-2 ratio was increased in H/R group ( P<0.05). Compared with H/R group, the cell viability was significantly increased, and the Bax/Bcl-2 ratio was decreased in RIPC-EXOc group ( P<0.05). Compared with RIPC+ EXOc group, the cell viability was significantly decreased, and the Bax/Bcl-2 ratio was increased in RIPC+ P-EXOc group ( P<0.05). Conclusions:Propofol may abolish the myocardial protective effect of RIPC by decreasing the production and release of serum exosomes in rats.

Objective:To evaluate the role of exosomes in reduction of myocardial ischemia-reperfusion (I/R) injury (MIRI) by remote preconditioning of trauma (RPCT) in rats.Methods:This experiment was performed in 2 parts. In vivo experiment Adult male Sprague-Dawley rats, aged 8 weeks, weighing 250-300 g, were used. Six rats were selected and randomly divided into 2 groups ( n=3 each): control group and RPCT group. Rats in control group underwent thoracotomy only, while rats in RPCT group were subjected to an additional 4 cm transverse skin incision along the abdominal midline after thoracotomy. Blood samples were collected, and serum exosomes were isolated from blood samples and labeled as control exosomes and RPCT exosomes. The expression of exosomal surface marker proteins CD9 and heat shock protein 70 (HSP70) was determined by Western blot, and the serum exosome concentration was measured. Another 30 rats were selected and randomly assigned to 5 groups ( n=6 each): sham operation group (Sham group), I/R group, I/R+ RPCT group, I/R+ control exosomes group (I/R+ EXO-CON group), and I/R+ RPCT exosomes group (I/R+ EXO-RPCT group). The MIRI model was established by ligating the left anterior descending coronary artery for 30 min followed by 120 min of reperfusion in anesthetized animals. In I/R+ RPCT group, the MIRI model was prepared at 15 min after the end of RPCT. In I/R+ EXO-CON and I/R+ EXO-RPCT groups, control exosomes and RPCT exosomes 100 μg were administered via the jugular vein at 15 min before ischemia respectively. At the end of reperfusion, the myocardial infarct size was measured, serum concentrations of cardiac troponin T (cTnT) and lactate dehydrogenase (LDH) were determined, and the contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardial tissues were measured. The expression of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase-3 and cleaved caspase-3 was detected. In vitro experiment H9c2 cells were cultured in vitro and randomly divided into 4 groups ( n=6 each): control group (Con group), hypoxia/reoxygenation (H/R) group, H/R+ control exosomes group (H/R+ EXO-CON group), and H/R+ RPCT exosomes group (H/R+ EXO-RPCT group). The rats were subjected to 4 h of hypoxia followed by 16 h of reoxygenation to establish the H/R injury model. In H/R+ EXO-CON and H/R+ EXO-RPCT groups, control exosomes and RPCT exosomes 4 μg were added at 15 min before hypoxia respectively. The cell survival rate and concentration of lactate dehydrogenase (LDH) in the supernatant were measured, and the expression of Bax, Bcl-2, cleaved caspase-3 and caspase-3 was detected. Results:In vivo experiment Compared with control group, the expression of serum CD9 and HSP70 was significantly up-regulated, and the exosome concentration was increased in RPCT group ( P<0.05). Compared with Sham group, the serum concentrations of cTnT and LDH, percentage of myocardial infarct size, content of MDA in myocardial tissues, Bax/Bcl-2 ratio, and cleaved caspase-3/caspase-3 ratio were significantly increased, and the activity of SOD was decreased in I/R group ( P<0.05). Compared with I/R group, the serum cTnT and LDH concentrations, percentage of myocardial infarct size, content of MDA in myocardial tissues, Bax/Bcl-2 ratio and cleaved caspase-3/caspase-3 ratio were significantly decreased, and the activity of SOD was increased in I/R+ RPCT group ( P<0.05), and no significant changes were observed in the aforementioned parameters in I/R+ EXO-CON group ( P>0.05). There were no significant differences in the aforementioned parameters between I/R+ RPCT group and I/R+ EXO-RPCT group ( P>0.05). In vitro experiment Compared with Con group, the cell survival rate was significantly decreased, and the LDH concentration in the supernatant and Bax/Bcl-2 and cleaved caspase-3/caspase-3 ratios were increased in H/R group ( P<0.05). Compared with H/R group, the cell survival rate was significantly increased, the LDH concentration in the supernatant, and Bax/Bcl-2 and cleaved caspase-3/caspase-3 ratios were decreased in H/R+ EXO-CON group ( P<0.05), and no significant changes were found in the aforementioned parameters in H/R+ EXO-RPCT group ( P>0.05). Conclusions:The mechanism by which RPCT reduces MIRI may be related to the increased release of serum exosomes in rats.

This study primarily aimed to investigate the prevalence of human papillomavirus (HPV) and other common pathogens of sexually transmitted infections (STIs) in spermatozoa of infertile men and their effects on semen parameters. These pathogens included Ureaplasma urealyticum, Ureaplasma parvum, Chlamydia trachomatis, Mycoplasma genitalium , herpes simplex virus 2, Neisseria gonorrhoeae, Enterococcus faecalis, Streptococcus agalactiae, Pseudomonas aeruginosa , and Staphylococcus aureus . A total of 1951 men of infertile couples were recruited between 23 March 2023, and 17 May 2023, at the Department of Reproductive Medicine of The First People's Hospital of Yunnan Province (Kunming, China). Multiplex polymerase chain reaction and capillary electrophoresis were used for HPV genotyping. Polymerase chain reaction and electrophoresis were also used to detect the presence of other STIs. The overall prevalence of HPV infection was 12.4%. The top five prevalent HPV subtypes were types 56, 52, 43, 16, and 53 among those tested positive for HPV. Other common infections with high prevalence rates were Ureaplasma urealyticum (28.3%), Ureaplasma parvum (20.4%), and Enterococcus faecalis (9.5%). The prevalence rates of HPV coinfection with Ureaplasma urealyticum, Ureaplasma parvum, Chlamydia trachomatis, Mycoplasma genitalium , herpes simplex virus 2, Neisseria gonorrhoeae, Enterococcus faecalis, Streptococcus agalactiae , and Staphylococcus aureus were 24.8%, 25.4%, 10.6%, 6.4%, 2.4%, 7.9%, 5.9%, 0.9%, and 1.3%, respectively. The semen volume and total sperm count were greatly decreased by HPV infection alone. Coinfection with HPV and Ureaplasma urealyticum significantly reduced sperm motility and viability. Our study shows that coinfection with STIs is highly prevalent in the semen of infertile men and that coinfection with pathogens can seriously affect semen parameters, emphasizing the necessity of semen screening for STIs.
Humans ; Male ; Infertility, Male/epidemiology* ; Coinfection/microbiology* ; Papillomavirus Infections/virology* ; Adult ; Sexually Transmitted Diseases/complications* ; China/epidemiology* ; Staphylococcus aureus/isolation & purification* ; Chlamydia trachomatis/isolation & purification* ; Prevalence ; Mycoplasma genitalium/isolation & purification* ; Ureaplasma urealyticum/isolation & purification* ; Neisseria gonorrhoeae/isolation & purification* ; Enterococcus faecalis/isolation & purification* ; Streptococcus agalactiae/isolation & purification* ; Herpesvirus 2, Human/genetics* ; Pseudomonas aeruginosa/isolation & purification* ; Semen/virology* ; Sperm Motility ; Spermatozoa/microbiology* ; Human Papillomavirus Viruses