Insulin Use Is Associated With Improved Outcomes in Critically Ill Patients With Acute Pancreatitis: A Retrospective Matched Cohort Study.

BACKGROUND: Severe acute pancreatitis (SAP) has a mortality of 30% with no current targeted therapy. The potential protective effect of insulin on AP has been reported and needs to be confirmed. Thus, we aim to examine the effect of insulin treatment on the outcome of AP patients. METHODS: A retrospective study was performed using data from the Medical Information Mart for Intensive Care (MIMIC) database. Kruskal-Wallis test, t-tests, and Pearson's chi-squared test were used to compare differences between groups. Propensity score matching and further nearest neighbor matching were used to construct a matched cohort. Cox proportional hazards regression analyses, logistic regression analyses, and the doubly robust estimation method were used to assess the relationship between insulin use and mortality. RESULTS: Nine hundred patients were enrolled in the final analysis. Insulin was associated with better outcomes in AP patients admitted to ICU, and could act as an independent predictor for 30-day mortality (HR = 0.36, 95% CI = 0.24-0.55). Subgroup analysis showed that AP patients with heart failure or without kidney disease or respiratory failure may not benefit from insulin treatment. CONCLUSIONS: Insulin treatment is independently associated with lower 30-day mortality in AP patients, except for those with heart failure or without kidney disease or respiratory failure.

Combining Porous Se@SiO2 Nanocomposites and dECM Enhances the Myogenic Differentiation of Adipose-Derived Stem Cells.

Background: Volumetric Muscle Loss (VML) denotes the traumatic loss of skeletal muscle, a condition that can result in chronic functional impairment and even disability. While the body can naturally repair injured skeletal muscle within a limited scope, patients experiencing local and severe muscle loss due to VML surpass the compensatory capacity of the muscle itself. Currently, clinical treatments for VML are constrained and demonstrate minimal efficacy. Selenium, a recognized antioxidant, plays a crucial role in regulating cell differentiation, anti-inflammatory responses, and various other physiological functions. Methods: We engineered a porous Se@SiO2 nanocomposite (SeNPs) with the purpose of releasing selenium continuously and gradually. This nanocomposite was subsequently combined with a decellularized extracellular matrix (dECM) to explore their collaborative protective and stimulatory effects on the myogenic differentiation of adipose-derived mesenchymal stem cells (ADSCs). The influence of dECM and NPs on the myogenic level, reactive oxygen species (ROS) production, and mitochondrial respiratory chain (MRC) activity of ADSCs was evaluated using Western Blot, ELISA, and Immunofluorescence assay. Results: Our findings demonstrate that the concurrent application of SeNPs and dECM effectively mitigates the apoptosis and intracellular ROS levels in ADSCs. Furthermore, the combination of dECM with SeNPs significantly upregulated the expression of key myogenic markers, including MYOD, MYOG, Desmin, and myosin heavy chain in ADSCs. Notably, this combination also led to an increase in both the number of mitochondria and the respiratory chain activity in ADSCs. Conclusion: The concurrent application of SeNPs and dECM effectively diminishes ROS production, boosts mitochondrial function, and stimulates the myogenic differentiation of ADSCs. This study lays the groundwork for future treatments of VML utilizing the combination of SeNPs and dECM.

Molecular Hydrogen Promotes Adipose-derived Stem Cell Myogenic Differentiation via Regulation of Mitochondria.

BACKGROUND: Acute skeletal muscle injuries are common physical or sports traumas. Cellular therapy has excellent potential for regeneration after skeletal muscle injury. Adipose-derived stem cells (ADSCs) are a more accessible type of stem cell. However, it has a low survival rate and differentiation efficiency in the oxidative stress-rich microenvironment after transplantation. Although molecular hydrogen (H2) possesses anti-inflammatory and antioxidant biological properties, its utility in mitochondrial and stem cell research has not been adequately explored. OBJECTIVE: This study aimed to reveal the role of H2 on adipose-derived stem cells' myogenic differentiation. METHODS: The protective effects of H2 in ADSCs were evaluated by MTT assay, live-dead cell staining, western blot analysis, immunofluorescence staining, confocal imaging, and transmission electron microscopy. RESULTS: An appropriate volume fraction of H2 significantly decreased mitochondrial reactive oxygen species (ROS) levels, increased the number of mitochondria, and promoted mitophagy, thus enhancing the survival and myogenic differentiation of ADSCs. CONCLUSION: This study reveals the application potential of H2 in skeletal muscle diseases or other pathologies related to mitochondrial dysfunction.

Porous Se@SiO2 nanoparticles improve oxidative injury to promote muscle regeneration via modulating mitochondria.

Background: Acute skeletal muscle injuries are common among physical or sports traumas. The excessive oxidative stress at the site of injury impairs muscle regeneration. The authors have recently developed porous Se@SiO2 nanoparticles (NPs) with antioxidant properties. Methods: The protective effects were evaluated by cell proliferation, myogenic differentiation and mitochondrial activity. Then, the therapeutic effect was investigated in a cardiotoxin-induced muscle injury rat model. Results: Porous Se@SiO2 NPs significantly protected the morphological and functional stability of mitochondria, thus protecting satellite cells from H2O2-induced damage to cell proliferation and myogenic differentiation. In the rat model, intervention with porous Se@SiO2 NPs promoted muscle regeneration. Conclusion: This study reveals the application potential of porous Se@SiO2 NPs in skeletal muscle diseases related to mitochondrial dysfunction.

Muscle injuries are very common in daily life and in sports. When a muscle is injured, the local response inhibits the regeneration and differentiation of stem cells inside the muscle, thus hindering muscle regeneration. The authors have recently developed a nanoparticle with the ability to protect muscle stem cell function, promote stem cell proliferation and differentiation and facilitate muscle regeneration after skeletal muscle injury in rats. Thus, this study reveals the potential of porous Se@SiO₂ nanoparticles in skeletal muscle diseases associated with mitochondrial dysfunction.

Knockdown of RAD51AP1 suppressed cell proliferation and invasion in esophageal squamous cell carcinoma.

BACKGROUND: Esophageal cancer is a common malignant tumor of digestive tract with esophageal squamous cell carcinoma (ESCC) being the main histological subtype. This study aimed to identify potential hub gene associated with the pathophysiology of ESCC through bioinformatics analysis and experiment validation. METHODS: Three microarray datasets were obtained from the Gene Expression Omnibus (GEO) database. The overlapping differentially expressed genes (DEGs) were analyzed by GEO2R tool. Gene Ontology (GO) and Kyoto Encyclopedia of Genes (KEGG) pathway analyses were performed to predict the potential functions of DEGs. Nine hub genes were identified using protein-protein interaction (PPI) network and Cytoscape software. We selected RAD51-associated protein 1 (RAD51AP1) for further research because of its poor prognosis and it has not been sufficiently studied in ESCC. The effects of RAD51AP1 on proliferation, apoptosis, migration and invasion of ESCC cells were determined by in vitro functional assays. RESULTS: RAD51AP1 expression was significantly upregulated in ESCC tissues compared with normal tissues by using The Cancer Genome Atlas (TCGA) database. High expression of RAD51AP1 was associated with worse survival in ESCC patients. RAD51AP1 expression was positively associated with the enrichment of Th2 cells and T helper cells. Furthermore, CCK-8 and colony formation assays showed knockdown of RAD51AP1 inhibited the proliferation of ESCC cells. Flow cytometry analysis indicated knockdown of RAD51AP1 induced cell cycle arrest and apoptosis in ESCC cells. Transwell assay revealed knockdown of RAD51AP1 suppressed the migration and invasion of ESCC cells. CONCLUSIONS: Finally, our results demonstrated that RAD51AP1 silencing significantly inhibited cell proliferation and invasion in ESCC, thereby highlighting its potential as a novel target for ESCC treatment.

Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.

BACKGROUND: Non-small cell lung cancer (NSCLC) accounts for about 80-85% of total lung cancer cases. Identifying the molecular mechanisms of anti-tumor drugs is essential for improving therapeutic effects. Herein, we aim to investigate the role of thalidomide in the tumorigenicity of NSCLC. METHODS: The A549 xenograft nude mouse model was established to explore therapeutic effects of thalidomide. The expression of FGD5-AS1 was evaluated in carcinomatous and paracarcinomatous tissues from NSCLC patients as well as NSCLC cell lines. CCK-8 assay was performed to assess cell viability. The invasive capacity was examined using transwell assay. The tube formation assay was applied to determine cell angiogenesis. Flow cytometry was subjected to validate CD8+ T cell activity. The FGD5-AS1/miR-454-3p/ZEB1 regulatory network was analyzed using luciferase reporter, RIP and ChIP assays. RESULTS: Thalidomide reduced tumor growth and angiogenesis and increased CD8+ T cell ratio in a mouse model. Enhanced expression of FGD5-AS1 was positively correlated with the poor survival of NSCLC patients. Knockdown of FGD5-AS1 notably suppressed the proliferation, invasion and angiogenesis of cancer cells as well as the apoptosis of CD8+ T cells. Thalidomide targeted FGD5-AS1 to exert its anti-tumor activity in NSCLC. FGD5-AS1 acted as a sponge of miR-454-3p to upregulate ZEB1, thus increasing the expression of PD-L1 and VEGFA. Simultaneous overexpression of FGD5-AS1 and silencing of miR-454-3p reversed thalidomide-mediated anti-tumor effects in NSCLC. CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.

Discovery of novel indole derivatives that inhibit NEDDylation and MAPK pathways against gastric cancer MGC803 cells.

A series of novel indole derivatives were synthesized and evaluated for their antiproliferative activity against three selected cancer cell lines (MGC803, EC-109 and PC-3). Among these analogues, 2-(5-methoxy-1H-indol-1-yl)-N-(4-methoxybenzyl)-N-(3,4,5-trimethoxyphenyl)acetamide (V7) showed the best inhibitory activity against MGC803 cells with an IC50 value of 1.59 µM. Cellular mechanisms elucidated that V7 inhibited colony formation, induced apoptosis and arrested cell cycle at G2/M phase. Importantly, indole analogue V7 inhibited NEDDylation pathway and MAPK pathway against MGC803 cells.

LncRNA SNHG7 Mediates the Chemoresistance and Stemness of Breast Cancer by Sponging miR-34a.

Chemoresistance is considered to be a major cause of the recurrence and metastasis of breast cancer (BC). LncRNA SNHG7 has been reported to be upregulated in breast cancer and to promote tumor progression and metastasis. Nevertheless, the function and potential regulatory mechanism of SNHG7 in BC drug resistance are still largely unclear. This study indicated that SNHG7 was highly expressed in chemoresistant BC tissues and cells. Upregulated SNHG7 might predict a low pCR rate and poor clinical outcome in BC patients. Knockdown of SNHG7 enhanced drug sensitivity and drug-induced apoptosis in chemoresistant BC cells. In terms of the mechanism, miR-34a was found to be a target of SNHG7 and its expression in breast cancer tissues and chemoresistant cell lines was negatively correlated with SNHG7 expression. Importantly, sh-SNHG7 upregulated miR-34a expression, reduced the percentages of CD44+/CD24-cells, and inhibited sphere-formation and stem cell factor (Oct4, Nanog, SOX2) expression. Functional loss experiments showed that the repressive effect of SNHG7 knockdown on BC cell stemness was partially reversed by transfection with miR-34a inhibitors. In summary, this study indicated that SNHG7 contributed to the chemoresistance of BC and mediated chemoresistance and cancer stemness by sponging miR-34a.

Synthesis and Biological Evaluation of Amino Chalcone Derivatives as Antiproliferative Agents.

Chalcone is a common scaffold found in many biologically active compounds. The chalcone scaffold was also frequently utilized to design novel anticancer agents with potent biological efficacy. Aiming to continue the research of effective chalcone derivatives to treat cancers with potent anticancer activity, fourteen amino chalcone derivatives were designed and synthesized. The antiproliferative activity of amino chalcone derivatives was studied in vitro and 5-Fu as a control group. Some of the compounds showed moderate to good activity against three human cancer cells (MGC-803, HCT-116 and MCF-7 cells) and compound 13e displayed the best antiproliferative activity against MGC-803 cells, HCT-116 cells and MCF-7 cells with IC50 values of 1.52 µM (MGC-803), 1.83 µM (HCT-116) and 2.54 µM (MCF-7), respectively which was more potent than the positive control (5-Fu). Further mechanism studies were explored. The results of cell colony formatting assay suggested compound 10e inhibited the colony formation of MGC-803 cells. DAPI fluorescent staining and flow cytometry assay showed compound 13e induced MGC-803 cells apoptosis. Western blotting experiment indicated compound 13e induced cell apoptosis via the extrinsic/intrinsic apoptosis pathway in MGC-803 cells. Therefore, compound 13e might be a valuable lead compound as antiproliferative agents and amino chalcone derivatives worth further effort to improve amino chalcone derivatives' potency.

Feasibility and efficacy evaluation of metallic biliary stents eluting gemcitabine and cisplatin for extrahepatic cholangiocarcinoma.

BACKGROUND: Effective endoscopic management is fundamental for the treatment of extrahepatic cholangiocarcinoma (ECC). However, current biliary stents that are widely used in clinical practice showed no antitumor effect. Drug-eluting stents (DESs) may achieve a combination of local chemotherapy and biliary drainage to prolong stent patency and improve prognosis. AIM: To develop novel DESs coated with gemcitabine (GEM) and cisplatin (CIS)-coloaded nanofilms that can maintain the continuous and long-term release of antitumor agents in the bile duct to inhibit tumor growth and reduce systemic toxicity. METHODS: Stents coated with different drug-eluting components were prepared by the mixed electrospinning method, with poly-L-lactide-caprolactone (PLCL) as the drug-loaded nanofiber membrane and GEM and/or CIS as the antitumor agents. Four different DESs were manufactured with four drug-loading ratios (5%, 10%, 15%, and 20%), including bare-loaded (PLCL-0), single-drug-loaded (PLCL-GEM and PLCL-CIS), and dual-drug-loaded (PLCL-GC) stents. The drug release property, antitumor activity, and biocompatibility were evaluated in vitro and in vivo to confirm the feasibility and efficacy of this novel DES for ECC. RESULTS: The in vitro drug release study showed the stable, continuous release of both GEM and CIS, which was sustained for over 30 d without an obvious initial burst, and a higher drug-loaded content induced a lower release rate. The drug-loading ratio of 10% was used for further experiments due to its ideal inhibitory efficiency and relatively low toxicity. All drug-loaded nanofilms effectively inhibited the growth of EGI-1 cells in vitro and the tumor xenografts of nude mice in vivo; in addition, the dual-loaded nanofilm (PLCL-GC) had a significantly better effect than the single-drug-loaded nanofilms (P < 0.05). No significant differences in the serological analysis (P > 0.05) or histopathological changes were observed between the single-loaded and drug-loaded nanofilms after stent placement in the normal porcine biliary tract. CONCLUSION: This novel PLCL-GEM and CIS-eluting stent maintains continuous, stable drug release locally and inhibits tumor growth effectively in vitro and in vivo. It can also be used safely in normal porcine bile ducts. We anticipate that it might be considered an alternative strategy for the palliative therapy of ECC patients.

Corpus cavernosum smooth muscle cell dysfunction and phenotype transformation are related to erectile dysfunction in prostatitis rats with chronic prostatitis/chronic pelvic pain syndrome.

BACKGROUND: The relationship between chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and erectile dysfunction (ED) has been shown in many studies. However, the specific mechanism remains unclear. This study was to investigate the corpus cavernosum smooth muscle cell function and phenotype transformation in Experimental autoimmune prostatitis (EAP) rats. METHODS: EAP was induced in rats by using prostate protein supplemented with immuneadjuvant extraction, and the max-ICP and MAP were measured. IHC and Masson staining were done to assess inflammatory infiltration and collagen deposition in the corpus cavernosum, respectively. Subsequently, normal rat and EAP rat CCSMCs were purified by tissue block implantation and differential adherence method. The oxidative stress, smooth muscle phenotype transformation, cell cycle and intracellular calcium ion transport were also evaluated. RESULTS: The ratio of max ICP/MAP in EAP rats significantly reduced, and the TNF-α content and collagen deposition in the corpus cavernosum markedly increased as compared to healthy rats. High-purity rat CCSMCs were obtained. Oxidative stress was evident and the cGMP content decreased in the EAP rat CCSMCs. The expression of Cav1.2, IP3R1 and RyR2 increased, but the SERCA2 expression decreased in EAP rat CCSMCs, which was accompanied by increased intracellular calcium. Increased expression of OPN, collagen and KCa3.1, decreased Calponin expression and increased proportion of cells in the S phase were also observed in the EAP rat CCSMCs. CONCLUSION: CP causes oxidative stress and imbalance of intracellular calcium in CCSMCs and promotes CCSMCs transformation from contractile to synthetic state, which may be involved in the pathogenesis of ED.

Efficacy and Safety of Once-Weekly versus Twice-Weekly Bortezomib in Patients with Hematologic Malignancies: A Meta-analysis with Trial Sequential Analysis.

STUDY OBJECTIVE: To compare the efficacy and safety of once-weekly and twice-weekly bortezomib therapy in patients with hematologic malignancies. DESIGN: Meta-analysis of 13 clinical or randomized controlled trials, with trial sequential analysis (TSA). PATIENTS: A total of 1567 patients with hematologic malignancies who received either once-weekly or twice-weekly bortezomib therapy. MEASUREMENTS AND MAIN RESULTS: We conducted a comprehensive literature search of the PubMed, EMBASE, and Cochrane Library databases. A meta-analysis was conducted to calculate the pooled effect size; TSA was performed to assess the reliability of the pooled results. The pooled risk ratio (RR) for the overall response rate (ORR) was 1.00 (95% confidence interval [CI] 0.77-1.29, p=0.99), indicating no significant differences between patients who received once-weekly bortezomib and those who received twice-weekly bortezomib. TSA showed that the cumulative Z-curve of the ORR entered the futility area, implying that reliable evidence was obtained for this pooled result. The pooled RR for any grade of peripheral neuropathy was 0.48 (95% CI 0.26-0.88, p=0.02); however, the TSA plot revealed that there was insufficient evidence for this result. The pooled RR for peripheral neuropathy grade 3 or higher was 0.21 (95% CI 0.13-0.34, p<0.00001), and reliable evidence was obtained according to TSA. Regarding the other toxicities, including anemia, thrombocytopenia, neutropenia, infection, diarrhea, constipation, nausea, vomiting, and fatigue, we did not find any significant differences between patients who received once-weekly bortezomib and those who received twice-weekly bortezomib. CONCLUSION: Compared with twice-weekly bortezomib, once-weekly bortezomib had a comparable ORR and a probable lower incidence of peripheral neuropathy. More clinical trials are needed to draw a conclusion regarding the difference in peripheral neuropathy between the two groups because of the insufficient evidence detected by TSA and the inconsistent results among subgroups.

The role of Cdk5-mediated Drp1 phosphorylation in Aß1-42 induced mitochondrial fission and neuronal apoptosis.

Alzheimer's disease, one of the most common neurodegenerative diseases, is pathologically characterized by Amyloid beta containing plaques and neurofibrillary tangles. Amyloid beta (Aß) induces neuronal apoptosis through the intracellular Ca2+ increase, subsequent hyperactivation of cyclin-dependent kinase 5 (Cdk5) and mitochondrial abnormality. Recently, Cdk5 was identified as an upstream regulator of mitochondrial fission during neuronal apoptosis, but the underlying mechanism remains unclear. Here, in vitro phosphorylation assays showed that Cdk5 could phosphorylate the recombinant Drp1 at Serine 579. Aß1-42 stimulation increased the phosphorylation level of Drp1 at Serine 579 in mouse cortical neurons. Cdk5 inhibitor roscovitine and knockdown of Cdk5 by a lentiviral vector expressing shRNA targeting Cdk5 (Lenti-Cdk5-shRNA) efficiently prevented Aß1-42 induced Drp1 phosphorylation in neurons. In addition, Aß1-42 stimulation induced markedly mitochondrial fission in neurons. Roscovitine, Lenti-Cdk5-shRNA and expression of phospho-defect mutatant GFP-Drp1-S579A in neurons attenuated Aß1-42 induced mitochondrial fission, whereas expression of phospho-mimetic mutant GFP-Drp1-S579D alone resulted in mitochondiral fission similar to Aß1-42 stimulation. Moreover, Roscovitine and Lenti-Cdk5-shRNA suppressed the cleavage of caspase-3 and protected neurons against Aß1-42 induced neuronal apoptosis.Thus, our data indicate that Drp1 is a direct target of Cdk5, and Cdk5-mediated phosphorylation of Drp1 at Serine 579 regulates Aß1-42 induced mitochondrial fission and neuronal toxicity.

Amyloid ß-42 induces neuronal apoptosis by targeting mitochondria.

Alzheimer's disease (AD), with a typical pathological hallmark of amyloid­beta (Aß)­containing plaques and neurofibrillary tangles, is one of the most common types of chronic neurodegenerative diseases. Aß oligomers serve a crucial role in the pathogenesis of AD, and lead to neuronal loss. However, the precise mechanism of Aß oligomers in AD remains to be elucidated. The present study demonstrated that 10 µM Aß­42 activated the caspase signaling pathway, and induced significant apoptosis in primary cultured mouse cerebral cortical neurons. The results of reverse transcription­quantitative polymerase chain reaction and western blotting demonstrated that Aß­42 (10 µM) also significantly upregulated the transcription and expression of the mitochondrial fission protein dynamin­related protein 1 (Drp1), and downregulated the transcription and expression of mitochondrial fusion proteins, including mitofusin 1/2 (Mfn1/2) and mitochondrial dynamin like GTPase (OPA­1). Neurons were transfected with pDsRed2­Mito for mitochondrial imaging, which revealed that 10 µM Aß­42 induced mitochondrial fission in cortical neurons. In addition, 2',7'­dichlorodihydrofluorescein diacetate and tetramethylrhodamine ethyl ester staining indicated that Aß­42 increased the reactive oxygen species (ROS) level and reduced mitochondrial membrane potential in neurons. Inhibition of Drp1 activity by Mdivi­1 efficiently prevented Aß­42­induced ROS production and disruption of mitochondrial membrane potential. Loss of mitochondrial membrane potential may activate PTEN­induced putative kinase 1 (Pink1), the prominent sensor for mitochondrial damage, and trigger the process of mitophagy to remove the damaged mitochondria. In the present study, western blotting revealed that the levels of autophagy marker microtubule­associated proteins 1A/1B light chain 3B (LC3B) and Pink1 were upregulated after Aß­42 stimulation. In conclusion, these data indicated that Aß­42 induces neuronal apoptosis by targeting mitochondria, including promotion of mitochondrial fission, disruption of mitochondrial membrane potential, increasing intracellular ROS level and activation of the process of mitophagy. Therefore, mitochondria may represent a potential therapeutic target for AD in the future.

[Impacts of different procedures of testicular sperm retrieval on testicular function and antisperm antibodies in azoospermia patients].

OBJECTIVE: To investigate the influence of different procedures of testicular sperm retrieval on the levels of serum inhibin B (INHB), antisperm antibodies (AsAb), follicle-stimulating hormone (FSH), and testosterone (T) in patients with azoospermia. METHODS: We randomly assigned 210 azoospermia patients to receive testicular sperm extraction (TESE, n = 50), testicular sperm aspiration (TESA, n = 56), testicular fine needle aspiration (TEFNA, n = 64), or microscopic TESE (micro-TESE, n = 40). We measured the levels of serum INHB, FSH, and T and the positive rate of AsAb before and at 1 and 3 months after surgery. RESULTS: Compared with the baseline, the levels of serum FSH at 1 and 3 months after surgery showed no statistically significant differences in the TESE (ï¼»8.51 ± 4.34ï¼½ vs ï¼»8.76 ± 3.07ï¼½ and ï¼»7.24 ± 3.32ï¼½ IU/L, P >0.05), TESA (ï¼»7.70 ± 2.72ï¼½ vs ï¼»7.90 ± 4.57ï¼½ and ï¼»8.04 ± 3.65ï¼½ IU/L, P >0.05), TEFNA (ï¼»6.04 ± 3.17ï¼½ vs ï¼»6.08 ± 2.70ï¼½ and ï¼»6.10 ± 3.32ï¼½ IU/L, P >0.05), or micro-TESE group (ï¼»6.59 ± 2.74ï¼½ vs ï¼»6.89 ± 1.78ï¼½ and ï¼»6.75 ± 2.57ï¼½ IU/L, P >0.05); the positive rate of AsAb (IgM) was significantly increased at 1 month in the TESE (0.00 vs 14.00%, P <0.05) and micro-TESE groups (2.50% vs 15.00%, P <0.05), while the serum T level markedly decreased in the two groups (ï¼»16.52 ± 6.25ï¼½ vs ï¼»9.25 ± 5.76ï¼½ nmol/L and ï¼»14.16 ± 5.45ï¼½ vs ï¼»8.23 ± 4.12ï¼½ nmol/L, P <0.05); the levels of serum INHB were remarkably reduced at 1 and 3 months in the TESE (ï¼»70.56 ± 23.17ï¼½ vs ï¼»42.63 ± 15.34ï¼½ and ï¼»44.05 ± 18.47ï¼½ pg/ml, P <0.05), TESA (ï¼»68.71 ± 14.74ï¼½ vs ï¼»40.55 ± 20.51ï¼½ and ï¼»42.11 ± 19.34ï¼½ pg/ml, P <0.05), TEFNA (ï¼»76.81 ± 27.04ï¼½ vs ï¼»46.31 ± 19.28ï¼½ and ï¼»48.32 ± 20.54ï¼½ pg/ml, P <0.05), and micro-TESE groups (ï¼»74.74 ± 28.35ï¼½ vs ï¼»45.27 ± 18.83ï¼½ and ï¼»47.64 ± 28.34ï¼½ pg/ml, P <0.05), but with no statistically significant differences among the four groups (P >0.05). CONCLUSIONS: Different procedures of testicular sperm retrieval have different impacts on the testicular function and AsAb in patients with azoospermia.

[Orchidopexy increases the levels of serum anti-Müllerian hormone and inhibin B in cryptorchidism patients].

OBJECTIVE: To investigate the levels of serum anti-Müllerian hormone (AMH) and inhibin B (INHB) in patients with unilateral cryptorchidism before and after orchidopexy. METHODS: This study included 58 cases of unilateral cryptorchidism treated by orchidopexy and 32 healthy controls. Before and at 6 months after surgery, we measured the length and circumference of the penis, the volume of the undescended testis, and levels of serum AMH and INHB. RESULTS: There were statistically significant differences between the unilateral cryptorchidism and healthy control groups in the levels of serum AMH (ï¼»102.80 ± 17.35 vs 108.76 ± 13.64ï¼½ ng/ml, P<0.05) and INHB (ï¼»70.24 ± 5.73ï¼½ vs ï¼» 77.72 ± 5.94ï¼½ pg/ml, P<0.05) at the baseline, but not at 6 months after orchidopexy (AMH: ï¼»109.76 ± 17.25ï¼½ vs ï¼»108.03 ± 14.13ï¼½ ng/ml, P>0.05; INHB: ï¼»75.76 ± 5.94ï¼½ vs ï¼»77.63 ± 5.99ï¼½ pg/ml, P>0.05). No remarkable differences were observed between the unilateral cryptorchidism and healthy control groups in the preoperative penile length (ï¼»2.05 ± 0.23ï¼½ vs ï¼»2.11 ± 0.22ï¼½ cm, P>0.05), penile circumference (ï¼»3.91 ± 0.23ï¼½ vs ï¼»3.99 ± 0.20ï¼½ cm, P>0.05) and volume of the undescended testis (ï¼»0.45 ± 0.02ï¼½ vs ï¼»0.46 ± 0.02ï¼½ ml, P>0.05), or in the postoperative penile length (ï¼»2.09 ± 0.23ï¼½ vs ï¼»2.16 ± 0.22ï¼½ cm, P>0.05), penile circumference (ï¼»4.00 ± 0.25ï¼½ vs ï¼»3.98 ± 0.19ï¼½ cm, P>0.05) and volume of the undescended testis (ï¼»0.45 ± 0.02ï¼½ vs ï¼»0.45 ± 0.02ï¼½ ml, P>0.05). Compared with the baseline, the cryptorchidism patients showed markedly increased levels of serum AMH (ï¼»102.80 ± 17.35ï¼½ vs ï¼»109.76 ± 17.25ï¼½ ng/ml, P<0.05) and INHB (ï¼»70.24 ± 5.73ï¼½ vs ï¼»75.76 ± 5.94ï¼½ pg/ml, P<0.05) after orchidopexy. CONCLUSIONS: Orchidopexy can elevate the levels of serum AMH and INHB and protect the testicular function of cryptorchidism patients.

New organic-inorganic hybrid compounds constructed from polyoxometalates and transition metal mixed-organic-ligand complexes.

Five new organic-inorganic hybrid compounds based on different polyoxoanions [HxGeW12O40](n-) or [H3As2W18O62](3-) (x = 0, 2; n = 4, 2), namely [Cu3(2,2'-bpy)3(inic)(OH)(H2O)][GeW12O40]·1.5H2O (1), [Cu2(phen)2(µ2-Cl)2(inic)]2[H2GeW12O40]·2H2O (2), [Cu2(phen)2(µ2-Cl)Cl(nic)]2[H2GeW12O40] (3), [Cu2(2,2'-bpy)2(hnic)Cl]2[H2GeW12O40] (4), [Cu(phen)(inic)H2O][Cu2(phen)2(inic)2(H2O)][H3As2W18O62]·3H2O (5) (inic = isonicotinic acid, nic = nicotinic acid, hnic = 2-hydroxy-nicotinic acid, 2,2'-bpy = 2,2'-bipyridine, phen = 1,10-phenanthroline), have been synthesized and characterized by IR, UV-Vis, XRD, cyclic voltammetric measurements and single crystal X-ray diffraction analysis. Single crystal X-ray analysis reveals that compound 1 is isomorphous and isostructural with a compound reported by us recently, the main difference between the two is the heteroatom of the polyoxoanions in the two compounds. Compound 2 is a supramolecular structure constructed from polyoxoanions and transition metal mixed-organic-ligand complexes. Compound 3 is a novel polyoxoanion bi-supported transition metal mixed-organic-ligand complex. Compound 4 is a 1-D chain structure constructed from polyoxoanions and transition metal mixed-organic-ligand complexes. The photodegradation properties of compounds 1-5 have been analyzed.

[Impact of unilateral cryptorchidism on the levels of serum anti-müllerian hormone and inhibin B].

OBJECTIVE: To investigate the influence of unilateral cryptorchidism on the levels of serum anti-müllerian hormone (AMH) and inhibin B in children. METHODS: We enrolled 65 patients with unilateral cryptorchidism and 45 healthy children in this study. We measured the length and circumference of the penis, the testis volume in the cryptorchidism side, and the levels of serum AMH and inhibin B at the age of 6 and 12 months, respectively. RESULTS: Compared with the healthy controls, the patients with unilateral cryptorchidism showed significant decreases at 12 months in serum AMH (ï¼»108.06±12.40ï¼½ vs ï¼»103.26±17.57ï¼½ ng/ml, P<0.05) and inhibin B (ï¼»77.43±5.66ï¼½ vs ï¼»70.21±5.69ï¼½ pg/ml, P<0.05). No statistically significant differences were found in the length and circumference of the penis and the testis volume in the cryptorchidism side at 6 and 12 months (P>0.05), or in the levels of serum AMH and inhibin B at 6 months (P>0.05). CONCLUSIONS: Unilateral cryptorchidism affects the gonadal function of the patient, and orchiopexy should be timely performed in order to reduce its impact.

Tuning the structures based on polyoxometalates from 1-D to 2-D by using different secondary organic ligands.

Six new organic-inorganic hybrid compounds based on [XM12O40](4-) (X = heteroatom, M = metal atom), namely [Cu(pic)2][H2XM12O40]·2Hapy·2apy (X = Si, M = W for , X = Ge, M = W for and X = Si, M = Mo for ), [Cu(2,2'-bpy)2][Cu(2,2'-bpy)(H2O)][Cu(pic)2]0.5[XM12O40]·nH2O (X = Si, M = Mo, n = 0.5 for , X = Ge, M = W, n = 1 for ) and [Cu(phen)(H2O)]2[Cu(pic)2][GeW12O40]·2.5H2O () (pic = deprotonated picolinic acid, apy = 2-aminopyridine, 2,2'-bpy = 2,2'-bipyridine, phen = phenanthroline), have been synthesized and characterized by IR, UV-Vis, XRD, cyclic voltammetric measurements and single crystal X-ray diffraction analysis. Single crystal X-ray analysis reveals that compounds are isomorphous and isostructural, in which each is based on [H2XM12O40](2-) and [Cu(pic)2]. Compounds and are also isomorphous and isostructural, of which the structures are more interesting than those of compounds . Both structures are constructed from [XM12O40](4-) and metal mixed-organic-ligand complexes. Compound is also constructed from Keggin ions and metal mixed-organic-ligand complexes, which are, however, thoroughly different from those of compounds and . The photodegradation properties of compounds have been analyzed. Compounds also exhibit rapid absorption properties for RhB (Rhodamine B). Detailed analysis of the photodegradation properties of compounds reveals that the molybdate POM has stronger degradation ability for RhB than the tungstate one.