Nicotine improves DSS-induced colitis by inhibiting NLRP3 and altering gut microbiota.

Ulcerative colitis (UC) is a chronic recurrent inflammatory disease affecting the rectum and colon. Numerous epidemiological studies have identified smoking as a protective factor for UC. Dysbiosis of intestinal microbiota and release of inflammatory factors are well-established characteristics associated with UC. Therefore, we have observed that nicotine exhibits the potential to ameliorate colitis symptoms in UC mice. Additionally, it exerts a regulatory effect on colonic microbiota dysbiosis by promoting the growth of beneficial bacteria while suppressing harmful bacteria. Combined in vivo and in vitro investigations demonstrate that nicotine primarily impedes the assembly of NLRP3, subsequently inhibiting downstream IL-1ß secretion.

Effects of dietary berberine on growth performance, lipid metabolism, antioxidant capacity and lipometabolism-related genes expression of AMPK signaling pathway in juvenile black carp (Mylopharyngodon piceus) fed high-fat diets.

This study aimed to investigate the effects of high-fat diet (HFD) supplemented with berberine on growth, lipid metabolism, antioxidant capacity and lipometabolism-related genes expression of AMPK signaling pathway in juvenile black carp (Mylopharyngodon piceus). Five hundred and forty healthy fish (4.04 ± 0.01 g) were randomly distributed into six groups, and fed six experimental diets: normal-fat diet (NFD, 5% fat), HFD (15% fat), and four HFDs supplemented with graded levels of berberine, respectively. The results showed that, compared with fish fed NFD, HFD had no effects on the growth of fish except for reducing survival rate, whereas HFD caused extensive lipid accumulation, oxidative stress injury and hepatic abnormalities. However, compared with the HFD group, fish fed HFD containing an appropriate berberine (98.26 or 196.21 mg/kg) improved the growth performance, increased hepatic lipid metabolism and antioxidant enzymes activities, and up-regulated the mRNA expression levels of ampk subunits and lipolysis genes such as pparα, cpt-1, acox, atgl and hsl (P < 0.05). Meanwhile, HFD supplemented with an appropriate berberine reduced crude lipid contents in liver and whole-body, decreased serum lipid contents, and ALT and AST activities, and down-regulated the mRNA expression levels of lipogenesis genes such as srebp-1, acc1, gpat, fas and pparγ, and lipid transporter genes such as fatp, fabp and fat/cd36 (P < 0.05). Thus, HFD supplemented with an appropriate berberine could improve growth of black carp, promote lipid metabolism and enhance antioxidant capacity. The lipid-lowering mechanism of berberine might be mediated by activating AMPK pathway, up-regulating lipolysis genes expression, and down-regulating lipogenesis and transport genes expression.

A Comprehensive Survey of Vision-Based Human Action Recognition Methods.

Although widely used in many applications, accurate and efficient human action recognition remains a challenging area of research in the field of computer vision. Most recent surveys have focused on narrow problems such as human action recognition methods using depth data, 3D-skeleton data, still image data, spatiotemporal interest point-based methods, and human walking motion recognition. However, there has been no systematic survey of human action recognition. To this end, we present a thorough review of human action recognition methods and provide a comprehensive overview of recent approaches in human action recognition research, including progress in hand-designed action features in RGB and depth data, current deep learning-based action feature representation methods, advances in human⁻object interaction recognition methods, and the current prominent research topic of action detection methods. Finally, we present several analysis recommendations for researchers. This survey paper provides an essential reference for those interested in further research on human action recognition.

Knocking down glycoprotein nonmetastatic melanoma protein B suppresses the proliferation, migration, and invasion in bladder cancer cells.

Glycoprotein nonmetastatic melanoma protein B is a type 1 transmembrane protein that has been recently found to play a role in cancer cell proliferation, angiogenesis, and invasion. Due to its potential responsibility in cancer aggressiveness, the main objective of this work was to investigate its expression in bladder cancer and the biological functions in bladder cancer cells. Using immunohistochemistry, western blot, and reverse transcription polymerase chain reaction, we analyzed the expression of glycoprotein nonmetastatic melanoma protein B in bladder cancer tissues and bladder cancer cell lines. The effects of glycoprotein nonmetastatic melanoma protein B on proliferation, migration, and invasion were tested after knocking down the glycoprotein nonmetastatic melanoma protein B in bladder cancer cells with small interfering RNAs by CCK-8, Transwell, and Matrigel assays. Our results showed that glycoprotein nonmetastatic melanoma protein B protein was highly expressed in the bladder cancer tissues and cell lines. Downregulating glycoprotein nonmetastatic melanoma protein B could suppress the proliferation, migration, and invasion in bladder cancer cells. Glycoprotein nonmetastatic melanoma protein B expression was related to the poor differentiation and recurrence by immunohistochemistry analysis. The survival analysis also showed that glycoprotein nonmetastatic melanoma protein B was related to the patient prognosis. In conclusion, Glycoprotein nonmetastatic melanoma protein B protein was highly expressed in the bladder cancer, which was related to the poor prognosis in bladder cancer patients. Glycoprotein nonmetastatic melanoma protein B promoted the proliferation, migration, and invasion in bladder cancer cells.

Psychological burden, sexual satisfaction and erectile function in men whose partners experience recurrent pregnancy loss in China: a cross-sectional study.

BACKGROUND: The aim of this study was to elucidate recurrent pregnancy loss (RPL)-associated psychosocial effects and sexual functions of Chinese men whose partners experience a history of RPL. METHODS: Questionnaire data from a total of 236 men whose partners experience RPL(RPL group) and another 236 non-RPL male volunteers(control group) were analyzed. The self-administered questionnaires included anxiety and depression measures (SAS & SDS), the Index of Sexual Satisfaction (ISS) and the International Index of Erectile Function (IIEF-5) for evaluating psychological burden, sexual satisfaction and erectile function, respectively. RESULTS: The mean age of the RPL group and control group was 29.8 ± 8.6 and 28.2 ± 7.3, respectively. The incidence of erectile dysfunction was significantly higher in the RPL group than in the control group (19.07 % vs. 7.63 %, P < 0.001). Anxiety and depression were also more prevalent in RPL group than in the control group (anxiety: 36.90 % vs. 19.08 %, P < 0.001; depression: 26.30 % vs. 7.63 %, P < 0.001). Furthermore, after adjusting for age in the RPL group, negative relationships were observed between the IIEF-5 score and anxiety and depression (P < 0.001), and a positive correlation was found between the ISS and anxiety and depression (P < 0.001). In addition, history of RPL, anxiety and depressive symptoms were significantly associated with a higher risk of ED. CONCLUSIONS: Psychological functioning, sexual satisfaction and erectile function are impaired in infertile men with RPL partners. These men should be targeted for psychological consultation.

The effects of Ficus carica polysaccharide on immune response and expression of some immune-related genes in grass carp, Ctenopharyngodon idella.

The present study investigated the effect of Ficus carica polysaccharide (FCP), isolated from the fruit of F. carica L., at 0%, 0.1%, 0.5% and 1.0% doses supplementation with feed on genes Interleukin 1-ß (IL-1ß), Tumor Necrosis Factor α (TNF-α) and heat shock protein 70 (HSP70) gene expression in blood, humoral innate immune parameters and resistant to Flavobacterium columnare of grass carp at weeks 1, 2 and 3. The results revealed that administration of FCP significantly (P<0.05) up regulated IL-1ß and TNF-α gene expression. HSP70 gene expression was significantly (P<0.05) lower in FCP-fed fish at the end of trial. The serum total protein, albumin and globulin did not significantly increased in any diet on the first week whereas it was significantly enhanced in 0.5% and 1.0% supplementation diets on weeks 2 and 3 when compared to control. The serum complement C3 was significantly (P<0.05) increased on weeks 1 and 2 when compared to control, however, no significant difference was found in this activity after 3 weeks of treatment. All diets significantly enhanced the serum lysozyme activity, bactericidal activity from weeks 1-2 as compared to control. Grass carp fed with FCP showed remarkably higher resistance against F. columnare (60% survival) compared to the control group (30% survival). These results confirm that FCP can up regulate immune related genes expression, stimulates immune response that per se enhances disease resistance in grass carp.

[Expression and significance of CMTM5 and epidermal growth factor receptor in prostate cancer].

OBJECTIVE: To investigate the expression patterns of CKLF-like MARVEL transmembrane domain containing 5 (CMTM5), a novel tumor suppressor, and epidermal growth factor receptor (EGFR) in prostate cancer (PCa) tissues and cells and to analyze the relationship between CMTM5 and EGFR in PCa. METHODS: The expression patterns of CMTM5 and EGFR in PCa tissues and cells were detected by immunohistochemistry and Western blot, respectively. RESULTS: CMTM5 was highly expressed in 75% (27/36) of benigh prostatic hyperplasia (BPH) tissues but 35.9% (23/64) of PCa tissues (P<0.001). There was a significant difference of CMTM5 expression between the two groups of PCa tissues with different Gleason scores (P=0.003), though its expression was not related to the age, clinical stage, and metastatic situation (P>0.05). EGFR was highly expressed in 57.8% (37/64) of PCa tissues, it had statistical significance between EGFR and CMTM5 expressions in PCa tissues. Furthermore, 23 cases (35.9%) had low CMTM5 expression and high EGFR expression. Western blot showed that CMTM5 was undetectable in PCa cells, in which the EGFR expression was upregulated. CONCLUSION: The loss of CMTM5 may participate in the progression of PCa resulting from deregulated EGFR.

Aberrant AKT activation drives well-differentiated liposarcoma.

Well-differentiated liposarcoma (WDLPS), one of the most common human sarcomas, is poorly responsive to radiation and chemotherapy, and the lack of animal models suitable for experimental analysis has seriously impeded functional investigation of its pathobiology and development of effective targeted therapies. Here, we show that zebrafish expressing constitutively active Akt2 in mesenchymal progenitors develop WDLPS that closely resembles the human disease. Tumor incidence rates were 8% in p53 wild-type zebrafish, 6% in p53 heterozygotes, and 29% in p53-homozygous mutant zebrafish (P = 0.013), indicating that aberrant Akt activation collaborates with p53 mutation in WDLPS pathogenesis. Analysis of primary clinical specimens of WDLPS, and of the closely related dedifferentiated liposarcoma (DDLPS) subtype, revealed immunohistochemical evidence of AKT activation in 27% of cases. Western blot analysis of a panel of cell lines derived from patients with WDLPS or DDLPS revealed robust AKT phosphorylation in all cell lines examined, even when these cells were cultured in serum-free media. Moreover, BEZ235, a small molecule inhibitor of PI3K and mammalian target of rapamycin that effectively inhibits AKT activation in these cells, impaired viability at nanomolar concentrations. Our findings are unique in providing an animal model to decipher the molecular pathogenesis of WDLPS, and implicate AKT as a previously unexplored therapeutic target in this chemoresistant sarcoma.

Therapeutic targeting of white adipose tissue metabolic dysfunction in obesity: mechanisms and opportunities.

White adipose tissue is not only a highly heterogeneous organ containing various cells, such as adipocytes, adipose stem and progenitor cells, and immune cells, but also an endocrine organ that is highly important for regulating metabolic and immune homeostasis. In individuals with obesity, dynamic cellular changes in adipose tissue result in phenotypic switching and adipose tissue dysfunction, including pathological expansion, WAT fibrosis, immune cell infiltration, endoplasmic reticulum stress, and ectopic lipid accumulation, ultimately leading to chronic low-grade inflammation and insulin resistance. Recently, many distinct subpopulations of adipose tissue have been identified, providing new insights into the potential mechanisms of adipose dysfunction in individuals with obesity. Therefore, targeting white adipose tissue as a therapeutic agent for treating obesity and obesity-related metabolic diseases is of great scientific interest. Here, we provide an overview of white adipose tissue remodeling in individuals with obesity including cellular changes and discuss the underlying regulatory mechanisms of white adipose tissue metabolic dysfunction. Currently, various studies have uncovered promising targets and strategies for obesity treatment. We also outline the potential therapeutic signaling pathways of targeting adipose tissue and summarize existing therapeutic strategies for antiobesity treatment including pharmacological approaches, lifestyle interventions, and novel therapies.

The genomic history and global migration of a windborne pest.

Many insect pests, including the brown planthopper (BPH), undergo windborne migration that is challenging to observe and track. It remains controversial about their migration patterns and largely unknown regarding the underlying genetic basis. By analyzing 360 whole genomes from around the globe, we clarify the genetic sources of worldwide BPHs and illuminate a landscape of BPH migration showing that East Asian populations perform closed-circuit journeys between Indochina and the Far East, while populations of Malay Archipelago and South Asia undergo one-way migration to Indochina. We further find round-trip migration accelerates population differentiation, with highly diverged regions enriching in a gene desert chromosome that is simultaneously the speciation hotspot between BPH and related species. This study not only shows the power of applying genomic approaches to demystify the migration in windborne migrants but also enhances our understanding of how seasonal movements affect speciation and evolution in insects.

Loss of expression of SDHA predicts SDHA mutations in gastrointestinal stromal tumors.

Gastrointestinal stromal tumors (GISTs) are usually driven by mutations in KIT or PDGFRA, although 15% of GISTs in adults and >90% in children lack such mutations. The majority of gastric KIT/PDGFRA wild-type GISTs show distinctive morphological and clinical features and loss of expression of succinate dehydrogenase (SDH) B. Only a small subset of SDHB-deficient GISTs carries loss-of-function mutations in SDHB, SDHC, or SDHD. Because of the complexity of its locus (15 exons) and the presence of three pseudogenes, SDHA is rarely analyzed. Recently, mutations in SDHA were shown to lead to loss of expression of SDHA in a small group of paragangliomas. We sought to determine whether immunohistochemistry for SDHA could identify GISTs with SDHA mutations. Tumors (n=33) with pathological features of SDH-deficient GIST were analyzed for expression of SDHA and SDHB by immunohistochemistry, and SDHA exons were sequenced from tumors lacking SDHA expression. Exons harboring somatic mutations were examined in DNA from corresponding normal tissue. All 33 tumors showed loss of SDHB expression. A total of 9 out of 33 (27%) tumors also lacked expression of SDHA. SDHA-deficient GISTs affected five men and four women (median age 38 years). SDHA expression was intact in the 24 remaining tumors, including those with known SDHB (n=3) or SDHC (n=2) mutations. Nonsense (n=8) or missense (n=1) mutations in SDHA were identified in all SDHA-deficient tumors. Heterozygous mutations were also found in DNA from normal tissues from six patients with available material. Somatic loss of the second allele has been found in seven tumors, five by loss of heterozygosity, one by a 13-bp deletion, and one by a missense mutation. Loss of SDHA expression in GIST reliably predicts the presence of SDHA mutations, which represent a relatively common cause of SDH-deficient GIST in adults. Immunohistochemistry for SDHA can be used to select patients for SDHA-specific genetic testing.

Effect of Telmisartan on local cardiovascular oxidative stress in mouse under chronic intermittent hypoxia condition.

OBJECTIVE: The objective of this study is to explore the protective effect of an angiotensin receptor blocker (ARB) on local cardiovascular angiotensin II (AngII) and oxidative stress markers such as malondialdehyde (MDA), NADPH oxydase p47(phox), and 8-hydroxy-2'-deoxyguanosine/8-hydroxyguanosine (8-OHdG/8-OHG) of mice that had chronic intermittent hypoxia (CIH). METHODS: Thirty-two healthy male C57B6J mice were randomly divided into four groups: CIH (12 weeks of CIH), ARB (CIH+Telmisartan), air control (room air delivery), and blank control (no treatment). AngII, p47(phox), and 8-OHdG/8-OHG were detected in mouse cardiocytes by immunohistochemistry. MDA was measured with the thiobarbituric acid method. MEASUREMENTS AND RESULTS: The highest AngII levels occur in the ARB treatment group (P < 0.05), followed by the CIH group (which was higher than the two control groups; P = 0.000). The levels of p47(phox) were statistically higher in the CIH group than in the other groups (P = 0.000) and lower in the ARB group (but still higher than in the two control groups, P = 0.000). The levels of 8-OHdG/8-OHG were the highest in the CIH group (P < 0.05), followed by the ARB group (which was higher than the two control groups, P = 0.000). The levels of MDA in the myocardial homogenate of mice were the highest in the CIH group (P = 0.000). CONCLUSIONS: Based on the above results, it can be concluded that Telmisartan may protect mouse cardiocytes from oxidative stress damage due to CIH.

Lanthanum carbonate for the treatment of hyperphosphatemia in CKD 5D: multicenter, double blind, randomized, controlled trial in mainland China.

BACKGROUND: Serum phosphorus control is critical for chronic kidney disease (CKD) 5D patients. Currently, clinical profile for an oral phosphorus binder in the mainland Chinese population is not available. OBJECTIVE: To establish the efficacy, safety, and tolerability of lanthanum carbonate in CKD 5D patients. DESIGN: Multicenter, randomized, double blind, placebo-controlled study. A central randomization center used computer generated tables to allocate treatments. SETTING: Twelve tertiary teaching hospitals and medical university affiliated hospitals in mainland China. PARTICIPANTS: Overall, 258 hemodialysis or continuous ambulatory peritoneal dialysis (CAPD) adult patients were enrolled. INTERVENTION: After a 0-3-week washout period and a 4-week lanthanum carbonate dose-titration period, 230 patients were randomized 1:1 to receive lanthanum carbonate (1500 mg-3000 mg) or placebo for a further 4-week maintenance phase. MAIN OUTCOME MEASURES: Efficacy and safety of lanthanum carbonate to achieve and maintain target serum phosphorus concentrations were assessed. RESULTS: In the titration phase, serum phosphorus concentrations of all patients decreased significantly. About three-fifths achieved target levels without significantly disturbing serum calcium levels. At the end of the maintenance period, the mean difference in serum phosphorus was significantly different between the lanthanum carbonate and placebo-treated groups (0.63±0.62 mmol/L vs. 0.15±0.52 mmol/L, P < 0.001). The drug-related adverse effects were mild and mostly gastrointestinal in nature. CONCLUSION: Lanthanum carbonate is an efficacious and well-tolerated oral phosphate binder with a mild AE profile in hemodialysis and CAPD patients. This agent may provide an alternative for the treatment of hyperphosphatemia in CKD 5D patients in mainland China. TRIAL REGISTRATION: No. ChiCTR-TRC-10000817.

Adipose tissue aging is regulated by an altered immune system.

Adipose tissue is a widely distributed organ that plays a critical role in age-related physiological dysfunctions as an important source of chronic sterile low-grade inflammation. Adipose tissue undergoes diverse changes during aging, including fat depot redistribution, brown and beige fat decrease, functional decline of adipose progenitor and stem cells, senescent cell accumulation, and immune cell dysregulation. Specifically, inflammaging is common in aged adipose tissue. Adipose tissue inflammaging reduces adipose plasticity and pathologically contributes to adipocyte hypertrophy, fibrosis, and ultimately, adipose tissue dysfunction. Adipose tissue inflammaging also contributes to age-related diseases, such as diabetes, cardiovascular disease and cancer. There is an increased infiltration of immune cells into adipose tissue, and these infiltrating immune cells secrete proinflammatory cytokines and chemokines. Several important molecular and signaling pathways mediate the process, including JAK/STAT, NFκB and JNK, etc. The roles of immune cells in aging adipose tissue are complex, and the underlying mechanisms remain largely unclear. In this review, we summarize the consequences and causes of inflammaging in adipose tissue. We further outline the cellular/molecular mechanisms of adipose tissue inflammaging and propose potential therapeutic targets to alleviate age-related problems.

Loss of Wdr5 attenuates MLL-rearranged leukemogenesis by suppressing Myc targets.

WD repeat domain 5 (WDR5) is a prominent target for pharmacological inhibition in cancer through its scaffolding role with various oncogenic partners such as MLL and MYC. WDR5-related drug discovery efforts center on blocking these binding interfaces or degradation have been devoted to developing small-molecule inhibitors or degraders of WDR5 for cancer treatment. Nevertheless, the precise role of WDR5 in these cancer cells has not been well elucidated genetically. Here, by using an MLL-AF9 murine leukemia model, we found that genetically deletion of Wdr5 impairs cell growth and colony forming ability of MLL-AF9 leukemia cells in vitro or ex vivo and attenuates the leukemogenesis in vivo as well, which acts through direct regulation of ribosomal genes. Pharmacological inhibition of Wdr5 recapitulates genetic study results in the same model. In conclusion, our current study demonstrated the first genetic evidence for the indispensable role of Wdr5 in MLL-r leukemogenesis in vivo, which supports therapeutically targeting WDR5 in MLL-rearranged leukemia by strengthening its disease linkage genetically and deepening insights into its mechanism of action.

Microbial Response to Fungal Infection in a Fungus-Growing Termite, Odontotermes formosanus (Shiraki).

The crosstalk between gut microbiota and host immunity has emerged as one of the research foci of microbiome studies in recent years. The purpose of this study was to determine how gut microbes respond to fungal infection in termites, given their reliance on gut symbionts for food intake as well as maintaining host health. Here, we used Metarhizium robertsii, an entomopathogenic fungus, to infect Odontotermes formosanus, a fungus-growing termite in the family Termitidae, and documented changes in host gut microbiota via a combination of bacterial 16S rDNA sequencing, metagenomic shotgun sequencing, and transmission electron microscopy. Our analyses found that when challenged with Metarhizium, the termite gut showed reduced microbial diversity within the first 12 h of fungal infection and then recovered and even surpassed pre-infection flora levels. These combined results shed light on the role of gut flora in maintaining homeostasis and immune homeostasis in the host, and the impact of gut flora dysbiosis on host susceptibility to infection.

[Characteristics and Source Apportionment of Ambient VOCs in Spring in Zhengzhou].

Ambient volatile organic compounds (VOCs) samples were collected at five sites in Zhengzhou during the spring of 2018. VOCs concentrations, the ozone formation potential (OFP), the aerosol formation potential (AFP), and source apportionment using a positive matrix factorization (PMF) model were studied based on chemical composition analysis. The results showed that the averaged concentration of VOCs in Zhengzhou during spring was (30.66±13.60)×10-9, of which the proportion of alkanes was the highest (35.3%) followed by oxygenated VOCs (OVOCs, 25.3%), halocarbons (24.1%), aromatics (10.0%), and alkenes (5.2%). The total OFP was 195.53 µg·m-3 and the contributions of alkanes, alkenes, aromatics, halocarbons, and OVOCs were 25.6%, 17.8%, 38.9%, 5.8%, and 11.9%, respectively. The total AFP was 0.95 µg·m-3 with an 87.6% contribution from aromatics and 12.4% from alkanes. The correlation between major species showed that pentane, isopentane, benzene, and toluene in Qinlinglu (QLL) site and Jingkaiqu (JKQ) site were greatly influenced by motor vehicles, but these were mainly influenced by combustion sources in Zhengzhou University (ZZU) site. The five factors that were identified by the PMF model were vehicle and liquefied petroleum gas (LPG) volatilization source (30.5%), solvent coating source (27.3%), industrial process source (22.1%), aging air mass (14.4%), and biogenic source (5.7%).

Effects of 17beta-estradiol on distribution of primordial germ cell migration in male chicks.

AIM: To assess whether exogenous estradiol has any effect on migration of primordial germ cells (PGCs) in the chick. METHODS: Fertilized eggs were treated with 17beta-estradiol (E(2)) (80 microg/egg) at stage X (day 0 of incubation), stages 8-10 (incubation 30 h) and 13-15 (incubation 55 h). Controls received vehicle (emulsion) only. Changes in PGC number were measured on different days according to developmental stages. RESULTS: In male right gonads, but not in female left gonads, at stages 28-30 (incubation 132 h) significant decreases in the mean number of PGCs aggregating were observed compared with the controls (P < 0.05) while the total PGC number in the right and left gonads at each stage did not change (P > 0.05). CONCLUSION: The present study provides evidence that E(2) has significant effects on the localization of PGCs in male right, but not female left, gonads of chicken embryos at stages 28-30, compared with controls.

Decreased expression of hepatic cytochrome P450 1A2 (CYP1A2) in a chronic intermittent hypoxia mouse model.

BACKGROUND: Hepatic cytochrome P450 (CYP) isoforms, CYP1A2, is one of important enzymes for many drugs metabolism. Studies have confirmed that sustained hypoxia can influence the expression of hepatic CYP, including CYP1A2. The impact of chronic intermittent hypoxia (CIH), a marked characteristic of sleep apnea, on CYP1A2 remains unclear. The aim of the present study was to evaluate the effect of CIH on the expression of hepatic CYP1A2 in a mouse model with sleep apnea. METHODS: Twenty four old male (6-8 weeks) C57BL/6J mice (n=12 in each group) were randomly assigned to either normoxia group or CIH group. Mice in CIH group underwent 12 weeks intermittent hypoxia exposure. The different gene expression of hepatic CYP1A2 between two groups was analyzed by quantity real-time polymerase chain reaction. The protein levels of hepatic CYP1A2 in each group were observed by using western blotting and immunohistochemistry. RESULTS: After 12 weeks of exposure to intermittent hypoxia, the expression of hepatic CYP1A2, at the mRNA and protein levels was decreased more significantly in the CIH group than the normoxia group (P<0.01). CONCLUSIONS: CIH contributes to inhibiting the expression of hepatic CYP1A2. This implies that the dosage of drugs metabolized by CYP1A2, should be adjusted in patients with sleep apnea.

MicroRNA-1469, a p53-responsive microRNA promotes Genistein induced apoptosis by targeting Mcl1 in human laryngeal cancer cells.

Genistein, a plant isoflavone, is reported to have therapeutic potentials in multiple cancers, However, the molecular mechanism underlying promoting cell apoptosis in laryngeal cancer remains unclear. In this study, we report that miR-1469 was induced by genistein in laryngeal cancer. Elevated miR-1469 promoted cell apoptosis and inhibited Mcl1 expression. In addition, we also observed that tumor suppressor p53 was increased under genistein treatment. Elevation of p53 promoted miR-1469 expression, leading to miR-1469 increase and Mcl1 decrease. Therefore, our findings suggest that genistein can suppress laryngeal cancer cell survival through p53 -miR-1469-Mcl1pathway.