The assessment value of pathological condition of serum adiponectin and amylin in primary osteoporosis and its correlation analysis with bone metabolism indexes.

Background: This paper explores the assessment value of pathological condition of serum adiponectin (APN) and amylin in primary osteoporosis (POP) and their correlation with bone metabolism indexes. Methods: From January 2019 to June 2021, 79 cases of POP patients were selected as the research objects. A test of the patients' bone density was conducted, and clinical grading of POP was via T value (normal, mild, moderate, severe). The analysis of the assessment value of pathological condition of serum APN and amylin for POP and their association with bone metabolism indexes in patients was performed. Results: APN and amylin in patients were declined with POP's aggravation. APN of 5.15 µg/mL or less and amylin of 15.38 pmol/L or less were risk factors influencing the aggravation of pathological condition of POP (P< 0 .0 5). The area under the curve (AUC) of combined detection of APN and amylin to assess the severity of POP was elevated vs. alone test of amylin (P< 0.05). 25-hydroxyvitamin D (25-(OH) D) and total type 1 procollagen amino-terminal propeptide (t-PINP) in patients were descended with the aggravation of pathological condition of osteoporosis (P < 0.05). At the same time, no distinct differences were presented in the three groups of type I collagen hydroxyl terminal peptide b degradation product (ß-CTX) and N-terminal osteocalcin (N-MID) (P> 0.05). APN, amylin, 25-(OH)D, ß-CTX, and t-PINP were negatively linked with POP clinical grade (P< 0.05). APN and amylin were associated with 25-(OH) D, ß-CTX, t-PINP (P< 0.05), and APN and amylin were not linked with N-MID (P> 0.05). Conclusions: Serum APN and amylin are provided with evaluation values for the severity of POP and are associated with bone metabolism in patients.

ROS-induced NLRP3 inflammasome priming and activation mediate PCB 118- induced pyroptosis in endothelial cells.

Growing epidemiological evidence has shown that exposure to polychlorinated biphenyls (PCBs) is harmful to the cardiovascular system. However, how PCB 118-induced oxidative stress mediates endothelial dysfunction is not fully understood. Here, we explored whether and how PCB 118 exposure-induced oxidative stress leads to NLRP3 inflammasome-dependent pyroptosis in endothelial cells. As expected, PCB 118 was cytotoxic to HUVECs and induced caspase-1 activation and cell membrane disruption, which are characteristics of pyroptosis. Moreover, PCB 118-induced pyroptosis may have been due to the activation of the NLRP3 infammasomes. PCB 118 also induced excessive reactive oxygen species (ROS) in HUVECs. The ROS scavenger (±)-α-tocopherol and the NFκB inhibitor BAY11-7082 reversed the upregulation of NLRP3 expression and the increase in NLRP3 inflammasome activation induced by PCB 118 exposure in HUVECs. Additionally, PCB 118-induced oxidative stress and pyroptosis were dependent on Aryl hydrocarbon receptor (AhR) activation and subsequent cytochrome P450 1A1 upregulation, which we confirmed by using the AhR selective antagonist CH 223191. These data suggest that PCB 118 exposure induces NLRP3 inflammasome activation and subsequently leads to pyroptosis in endothelial cells in vitro and in vivo. AhR-mediated ROS production play a central role in PCB 118-induced pyroptosis by priming NFκB-dependent NLRP3 expression and promoting inflammasome activation.

One-pot co-catalysis of corncob with dilute hydrochloric acid and tin-based solid acid for the enhancement of furfural production.

A newly synthesized solid acid catalyst SO42-/SnO2-diatomite was prepared for synthesizing furfural from corncob in the presence of homogeneous Brönsted acid. The relationship between pKa of Brönsted acid and turnover frequency (TOF) of co-catalysis with Brönsted acid plus SO42-/SnO2-diatomite was explored on the conversion of corncob to furfural. HCl (pKa = -7.0) (0.5 wt%) plus SO42-/SnO2-diatomite (3.6 wt%) gave the highest furfural yield (40.1%) with TOF value at 2.98 h-1 in the aqueous media. In the γ-valerolactone-water (6:4, v:v) biphasic media containing 15 g/L ZnCl2, one-pot conversion of corncob with co-catalysts gave a furfural yield of 68.9% at 170 °C for 30 min. Additionally, an efficient SO42-/SnO2-diatomite recycling was achieved with a productivity of 15.6 g furfural/(g solid acid·day) after 5 cycles of repeated use. Clearly, this one-pot co-catalysis process has high potential application for furfural production in future.

ATP2B1 Gene Silencing Increases NO Production Under Basal Conditions Through the Ca2+/calmodulin/eNOS Signaling Pathway in Endothelial Cells.

Emerging epidemiological and experimental evidence has shown that the ATP2B1 gene is associated with blood pressure control. Impaired eNOS activity and NO production may be among the mechanisms involved. However, little is known about how PMCA1, which is encoded by the ATP2B1 gene, regulates the activity of eNOS and NO production. In the present study, we investigated the role of the ATP2B1 gene in regulating eNOS activity and NO production under basal conditions in HUVECs and explored the mechanisms involved. Silencing ATP2B1 gene expression resulted in higher NO production and eNOS activity under basal conditions in HUVECs. Additionally, ATP2B1 gene silencing resulted in enhanced intracellular calcium concentrations compared to that in the negative siRNA-transfected HUVECs. The enhanced eNOS activity mediated by ATP2B1 gene silencing was Ca2+/calmodulin dependent, as verified by the administration of the calcium chelator BAPTA-AM or the calmodulin-specific antagonist W7. Taken together, silencing ATP2B1 gene expression results in higher NO production and eNOS activity under basal conditions in HUVECs. Furthermore, the enhanced eNOS activity induced by ATP2B1 gene silencing may be mediated via higher levels of intracellular Ca2+, and the effect was confirmed to be dependent on the eNOS-calmodulin interaction.

Biological synthesis of 2,5-bis(hydroxymethyl)furan from biomass-derived 5-hydroxymethylfurfural by E. coli CCZU-K14 whole cells.

Biocatalytic upgrading of bio-based platform chemical 5-hydroxymethylfurfural (5-HMF) to 2,5-bis(hydroxymethyl)furan (BHMF) is currently of great interest due to the product specificity, mild reaction and high efficiency. In this work, 200mM 5-HMF could be effectively biotransformed to BHMF at 90.6% with highly 5-HMF-tolerant recombinant E. coli CCZU-K14 whole cells at pH 6.5 and 30°C under the optimum reaction conditions (cosubstrate glucose 1.0mol glucose/(mol 5-HMF), D-xylose 400mM, l-glutamic acid 250mM, Mg2+ 1.5mM, 0.2mol ß-cyclodextrin/(mol 5-HMF), CTAB (cetyltrimethyl ammonium bromide) 12.5mM, and 0.1g wet cells/mL). It was found that E. coli CCZU-K14 was highly tolerant to 5-HMF (up to 400mM). Effective bioreduction of biomass-derived 5-HMF (≤200) to BHMF was successfully demonstrated in this study. In conclusion, this strategy showed high potential application for the synthesis of BHMF.

ATP2B1 gene Silencing Increases Insulin Sensitivity through Facilitating Akt Activation via the Ca2+/calmodulin Signaling Pathway and Ca2+-associated eNOS Activation in Endothelial Cells.

Endothelial cell insulin resistance may be partially responsible for the higher risk of atherosclerosis and cardiovascular disease in populations with insulin resistance and type 2 diabetes mellitus (T2DM). A genome-wide association study revealed a significant association between the ATPase plasma membrane Ca2+ transporting 1 (ATP2B1) gene and T2DM in two community-based cohorts from the Korea Association Resource Project. However, little is known about the implication of the ATP2B1 gene on T2DM. In the present study, we investigated the role of the ATP2B1 gene in endothelial cell insulin sensitivity. ATP2B1 gene silencing resulted in enhanced intracellular calcium concentrations and increased insulin-induced Akt activation compared to that in the negative siRNA-transfected HUVECs (Human Umbilical Vein Endothelial Cells). The elevated insulin sensitivity mediated by ATP2B1 gene silencing was Ca2+/calmodulin-dependent, as verified by administration of the calcium chelator BAPTA-AM or the calmodulin-specific antagonist W7. Moreover, higher levels of phosphorylation of eNOS (Ser1177) were observed in ATP2B1-silenced HUVECs. In addition to BAPTA-AM and W7, L-NAME, an eNOS antagonist, abolished insulin-induced Akt phosphorylation at Ser473 in both si-Neg and si-ATP2B1-transfected endothelial cells. These results indicate that the enhanced insulin sensitivity in ATP2B1-silenced endothelial cells is alternatively dependent on an increase in intracellular Ca2+ and the subsequent activation of the Ca2+/calmodulin/eNOS/Akt signaling pathway. In summary, ATP2B1 gene silencing increased insulin sensitivity in endothelial cells by directly modulating the Ca2+/calmodulin signaling pathway and via the Ca2+/calmodulin/eNOS/Akt signaling pathway alternatively.

Chemical-enzymatic conversion of corncob-derived xylose to furfuralcohol by the tandem catalysis with SO42-/SnO2-kaoline and E. coli CCZU-T15 cells in toluene-water media.

One-pot synthesis of furfuralcohol from corncob-derived xylose was attempted by the tandem catalysis with solid acid SO42-/SnO2-kaoline and recombination Escherichia coli CCZU-T15 whole-cells in the toluene-water media. Using SO42-/SnO2-kaoline (3.5wt%) as catalyst, the furfural yield of 74.3% was obtained from corncob-derived xylose in the toluene-water (1:2, v:v) containing 10mM OP-10 at 170°C for 30min. After furfural liquor was mixed with corncob-hydrolysate from the enzymatic hydrolysis of oxalic acid-pretreated corncob residue, furfural (50.5mM) could be completely biotransformed to furfuralcohol with Escherichia coli CCZU-T15 whole-cells harboring an NADH-dependent reductase (ClCR) in the toluene-water (1:3, v:v) containing 12.5mM OP-10 and 1.6mM glucose/mM furfural at 30°C and pH 6.5. Furfuralcohol was obtained at 13.0% yield based on starting material corncob (100% furfuralcohol yield for bioreduction of furfural step). Clearly, this one-pot synthesis of furfuralcohol strategy shows high potential application for the effective utilization of corncob.

Enzymatic in situ saccharification of sugarcane bagasse pretreated with low loading of alkalic salts Na2SO3/Na3PO4 by autoclaving.

Sugarcane bagasse (SCB) is an abundant, renewable and inexpensive agricultural byproduct for the production of biofuel and other biobased products. To effectively saccharify SCB with cellulases, combination with dilute alkali salts Na2SO3/Na3PO4 (0.4% Na3PO4, 0.03% Na2SO3) at 7.5% sulfidity and hot water (DASHW) in "one-pot" pretreatment media by autoclaving at 110°C for 40min was attempted to pretreat SCB in this study. Furthermore, FT-IR, XRD and SEM were employed to characterize the changes in the cellulose structural characteristics (porosity, morphology, and crystallinity) of the pretreated Na2SO3/Na3PO4-SCB solid residue, which indicated that combination pretreatment could effectively remove lignin and hemicellulose for enhancing enzymatic saccharification. After 72h, the reducing sugars and glucose from the enzymatic in situ hydrolysis of 50g/L Na2SO3/Na3PO4-SCB in dilute Na2SO3/Na3PO4 (0.27% Na3PO4, 0.02% Na2SO3) media were obtained at 33.8 and 21.8g/L, respectively. Finally, the SCB-hydrolysates containing 20g/L glucose were used for ethanol fermentation in the presence of dilute alkali salts. After 48h, the ethanol yield was 0.42g ethanol/g glucose, which represents 82.1% of the theoretical yield. In conclusion, this study provided an effective pretreatment strategy for enhancing SCB's saccharification, which has potential application of other lignocellulosic materials.

2,3',4,4',5-Pentachlorobiphenyl impairs insulin-induced NO production partly through excessive ROS production in endothelial cells.

Polychlorinated biphenyls (PCBs) have been reported to be associated with increased risk to hypertension, atherosclerosis, cardiovascular disease, etc. 2,3',4,4',5-Pentachlorobiphenyl, known as PCB-118, is a member of coplanar PCBs which renders their structure similar to polychlorinated dibenzo-p-dioxins (PCDDs) and has dioxin-like activity. In our current study, we investigated the effect of PCB-118 exposure on nitric oxide (NO) production and the underlying mechanisms in vitro. Exposure of PCB-118 impaired insulin-induced NO production and endothelial nitric oxide synthase (eNOS) activity in human umbilical vein endothelial cells (HUVECs) with no significant effect on cell viability. Furthermore, PCB-118 treatment induced oxidative stress. In addition, scavenging of reactive oxygen species (ROS) by 10 µM N-acetyl-l-cysteine (NAC) partly rescued impaired insulin-induced eNOS activities and NO productions induced by PCB-118 in HUVECs. Taken together, these results indicate that PCB-118 mediates lower eNOS activity and impairs insulin-induced NO production partly through excessive ROS production in endothelial cells.

One-pot chemo-enzymatic synthesis of furfuralcohol from xylose.

Furfuralcohol (FOL) is an important intermediate for the production of lysine, ascorbic acid, and lubricants. It can be used as a hypergolic fuel in rocketry. In this study, it was attempted to synthesize FOL from xylose by tandem catalysis with solid acid SO42-/SnO2-Montmorillonite and recombination Escherichia coli CCZU-K14 whole cells. Using SO42-/SnO2-Montmorillonite (3.0wt% dosage) as catalyst, a highest furfural yield of 41.9% was achieved from xylose at 170°C for 20min. Furthermore, Escherichia coli CCZU-K14 whole cells were used for bioconverting furfural to FOL. The optimum biocatalytic reaction temperature, reaction pH, cosubstrate concentration, and substrate concentration were 30°C, 6.5, 1.5mol glucose/mol furfural, and 200mM, respectively. Finally, the yield of FOL from 200mM furfural was achieved to 100% by Escherichia coli CCZU-K14 whole cells after 24h. In conclusion, this strategy show high potential application for the effective synthesis of FOL.

PCB 118-induced endothelial cell apoptosis is partially mediated by excessive ROS production.

Endothelial cell apoptosis, which may alter the integrity of the endothelium and lead to plaque instability, plays a critical role in the development and pathogenesis of atherosclerosis. Exposure of polychlorinated biphenyls (PCBs) is associated with increased risk of atherosclerosis and cardiovascular disease. In our present study, we explored whether exposure to PCB 118 influences endothelial cell apoptosis in vitro and the underlying mechanisms involved. As expected, exposure to PCB 118 increased the intracellular reactive oxygen species (ROS) levels in HUVECs. Increases in apoptosis and Bax/Bcl-2 ratios were observed in PCB 118-treated HUVECs. N-acetyl-l-cysteine (NAC), a ROS scavenger, partially reduced PCB 118-induced apoptosis and Bax/Bcl-2 ratios in HUVECs. Taken together, PCB 118-induced endothelial cell apoptosis was partially initiated by excessive ROS production.

Effective asymmetric bioreduction of ethyl 4-chloro-3-oxobutanoate to ethyl (R)-4-chloro-3-hydroxybutanoate by recombinant E. coli CCZU-A13 in [Bmim]PF6-hydrolyzate media.

It was the first report that the concentrated hydrolyzates from the enzymatic hydrolysis of dilute NaOH (3wt%)-soaking rice straw at 30°C was used to form [Bmim]PF6-hydrolyzate (50:50, v/v) media for bioconverting ethyl 4-chloro-3-oxobutanoate (COBE) into ethyl (R)-4-chloro-3-hydroxybutanoate [(R)-CHBE] (>99% e.e.) with recombinant E. coli CCZU-A13. Compared with pure glucose, the hydrolyzates could promote both initial reaction rate and the intracellular NADH content. Furthermore, emulsifier OP-10 (20mM) was employed to improve the reductase activity. Moreover, Hp-ß-cyclodextrin (0.01mol Hp-ß-cyclodextrin/mol COBE) was also added into this bioreaction system for enhancing the biosynthesis of (R)-CHBE from COBE by E. coli CCZU-A13 whole-cells. The yield of (R)-CHBE (>99% e.e.) from 800mM COBE was obtained at 100% in the [Bmim]PF6-hydrolyzate (50:50, v/v) media by supplementation of OP-10 (20mM) and Hp-ß-CD (8mM). In conclusion, an effective strategy for the biosynthesis of (R)-CHBE was successfully demonstrated.

[High-dose daidzein affects growth and development of reproductive organs in male rats].

OBJECTIVE: To explore the effect of the phytoestrogen daidzein on the growth and development of the testis and epididymis in male SD rats. METHODS: Thirty 10-week old (early adult) and 30 4-week old (pubertal) male SD rats were included in the study, each age group equally divided into 5 subgroups: normal control, positive control, low-dose, medium-dose and high-dose. The normal and positive control groups were given 1 ml distilled water and the same amount of distilled water containing diethylstilbestrol (DES) at the dose of 0.1 mg/kg, and the low-, medium- and high-dose groups administered daidzein in the dose of 2mg/kg, 20 mg/ kg and 100 mg/kg, respectively, all by gavage for 90 days. Observations were made on the changes in body weight and testicular and epididymal indexes, as well as on the structural changes of the testis and epididymis by H&E staining. RESULTS: The early adult rats showed no significant differences in body weight and testicular and epididymal indexes between the claiclzein groups and the control (P > 0.05), nor did the pubertal rats in epididymal index (P > 0.05). The testicular index differed significantly between the high-dose group (3.21 +/- 0.07) and the normal control (3.71 +/- 0.45) (P < 0.05). The body weight reduced markedly in the high-dose group (P < 0.05), but with no significant differences between the normal control and the other two dose groups (P > 0.05). No obvious changes were observed in epididymal morphology in all the daidzein groups of the early adult and pubertal rats, but high-dose daidzein resulted in smaller testes and impaired spermatogenesis. CONCLUSION: The phytoestrogen daidzein, administered in a high dose, could delay the growth and development of the testis and induce structural changes of testicular tissues in pubertal SD rats.

[Distribution and effects of estrogen receptors in male reproductive system].

Estrogen plays an important role in the regulation of male reproduction. Through binding with the estrogen receptor (ER), estrogen produces genomic and non-genomic effects. Estrogen receptors include ERalpha and ERbeta which distribute in the male reproductive system including the testis, epididymis, prostate and penis. The spermatogenesis is impaired in mice with ERalpha gene knockout; however, it remains normal in mice with ERbeta gene knockout. This phenomenon suggests that the two subtypes of ER play different roles in spermatogenesis. Moreover, ERalpha or ERbeta may also act as a substitute of another.

[Relationship between spermatogenic cell apoptosis and serum estradiol level in rats exposed to fluoride].

OBJECTIVE: To observe the relationship between spermatogenic cell apoptosis and serum estradiol level in rats exposed to fluoride. METHODS: A total of 30 male Wistar rats were allocated into six groups randomly. The six experimental groups were 28-day control group, 28-day low-dose fluoride treatment group, 28-day high-dose fluoride treatment group, 38-day control group, 38-day low-dose fluoride treatment group, and 38-day high-dose fluoride treatment group. The fluorosis model was acquired by subcutaneous injection of NaF solution. The content of NaF in testis was measured by using fluorine selective electrode. The serum estradiol level was radioimmunochemically detected. And the apoptotic spermatogenic cells were quantitatively measured by TUNEL. RESULTS: The content of NaF in testis and the ratio of apoptotic spermatogenic cell in fluoride treatment groups significantly increased with increased experimental dosage and prolonged experimental period (P < 0.05). Meanwhile, the serum estradiol level significantly decreased (P < 0.05), which was negatively correlated with the content of NaF in testis as well as the ratio of apoptotic spermatogenic cell (P < 0.05). CONCLUSION: Excessive fluoride could lead disturbance to serum estradiol level during some range of dose and time, which is an important factor to spermatogenic cell apoptosis.