Aspirin inhibited preadipocyte differentiation and fat storage in mature 3T3-L1 adipocytes.

<p><b>A.</b> Cell proliferation of 3T3-L1 cells treated with increasing doses of aspirin for 48 h, assessed by MTT assay. <b>B.</b> Cell morphology of oil accumulation in 3T3-L1 adipocytes treated with aspirin during preadipocyte differentiation; mature cells were stained with Oil Red O and observed microscopically at 200× magnification. <b>C.</b> The oil accumulated in 3T3-L1 cells was dissolved in 2-propanol and quantified by reading the absorbance at 500 nm using a microplate reader. Data are presented as mean ± SEM. Statistical analysis was done by one-way ANOVA and LSD post hoc test; significantly different at * p < 0.05 or # p < 0.001 vs. control group.</p

Aspirin treatment of 4T1 breast cancer cells cultured in 3T3-L1 adipocyte-conditioned medium (Ad-CM) affected the proliferative ability and cytokine production of breast cancer cells.

<p><b>A.</b> The morphology of 4T1 cells cultured in the presence of increasing concentrations of Ad-CM for 48 h was observed microscopically at 100× magnification. <b>B.</b> Effect of the concentration of Ad-CM on the proliferation of 4T1 cells. Cells were cultured in the presence of increasing concentrations of Ad-CM for 48 h, and were then trypsinized and counted by NC-3000. <b>C.</b> The 4T1 cells were cultured either in 25% or 50% Ad-CM with or without aspirin for 48 h, and a cell proliferation assay was performed. <b>D.</b> The production of characteristic tumor cytokines after 48-h culture was measured in the supernatant by ELISA. Data are presented as mean ± SEM. Statistical analysis was done by one-way ANOVA and LSD post hoc test; significantly different at * p < 0.05 or # p < 0.001 vs. control group.</p

The effect of aspirin on MCP-1 secretion by 3T3-L1 adipocytes.

<p><b>A.</b> The 3T3-L1 adipocytes were cultured in the presence or absence of aspirin and stimulated by 2.5 ng/mL TNF-α for 24 h. <b>B.</b> The 3T3-L1 adipocytes were cultured in the presence or absence of aspirin in RAW264.7 conditioned medium for 24 h. Data are presented as mean ± SEM. Statistical analysis was done by one-way ANOVA and LSD post hoc test; significantly different at * p < 0.05 or # p < 0.001 vs. control group.</p

Aspirin treatment in a coculture of 4T1 breast cancer cells and mature 3T3-L1 adipocytes affected the proliferative ability and cytokine production of breast cancer cells.

<p><b>A.</b> The 4T1 cells were cultured for 48 h in the presence or absence of mature adipocytes using a transwell system. Cells were trypsinized and cell numbers counted by NC-3000. <b>B.</b> The secretion of cytokines relevant to tumor characteristics in the supernatant obtained from 48 h coculture was measured by ELISA. Data are presented as mean ± SEM. Statistical analysis was done by one-way ANOVA and LSD post hoc test; significantly different at * p < 0.05 or # p < 0.001 vs. control group.</p

The proposed schema of the mechanisms by which aspirin breaks the crosstalk between breast cancer cells and adipocytes.

<p>In 3T3-L1 cells, aspirin treatment inhibited the differentiation of adipocytes and the secretion of the inflammatory adipokine MCP-1. In 4T1 cells, treatment with aspirin decreased MCP-1 and VEGF production, and inhibited cell viability and migration. Subsequently, to clarify the relationship between these two cell types by the co-culture systems, including Ad-CM model and transwell system. Aspirin treatment significantly inhibited the proliferation of 4T1 cells, possibly by inhibiting MCP-1 and PAI-1 secretion and further diminishing the proliferation and migration of 4T1 cells. The arrows denote changes that display due to aspirin treatment.</p

Cell growth and migration of 4T1 cells treated with aspirin.

<p><b>A.</b> The proliferation of cells treated with or without aspirin for 24, 48, and 72 h was analyzed using an MTT test. <b>B.</b> Migration patterns into the scraped area were observed for each condition and 4T1 cells were treated with or without aspirin for 16 and 24 h. <b>C.</b> The production of cytokines characteristic of tumors in the supernatant after a 24-h culture was measured by ELISA. Data are presented as mean ± SEM. Statistical analysis was done by one-way ANOVA and LSD post hoc test; significantly different at * p < 0.05 or # p < 0.001 vs. control group.</p

Changes of HBsAg levels in HIV/HBV-coinfected patients with lamivudine-resistant HBV or lamivudine-susceptible HBV on tenofovir-containing combination antiretroviral therapy

<p>Changes of HBsAg levels in HIV/HBV-coinfected patients with lamivudine-resistant HBV or lamivudine-susceptible HBV on tenofovir-containing combination antiretroviral therapy</p

Cumulative percentage of HIV/HBV-coinfected patients with lamivudine-resistant HBV (n = 33) or lamivudine-susceptible HBV (n = 56) who had achieved undetectable HBV DNA (<128 copies/mL) during the follow-up period of tenofovir-containing combination antiretroviral therapy

<p>Cumulative percentage of HIV/HBV-coinfected patients with lamivudine-resistant HBV (n = 33) or lamivudine-susceptible HBV (n = 56) who had achieved undetectable HBV DNA (<128 copies/mL) during the follow-up period of tenofovir-containing combination antiretroviral therapy</p

Changes of plasma HBV DNA load in HIV/HBV-coinfected patients with lamivudine-resistant HBV (n = 33) or lamivudine-susceptible HBV (n = 56) who were on tenofovir-containing combination antiretroviral therapy

<p>Changes of plasma HBV DNA load in HIV/HBV-coinfected patients with lamivudine-resistant HBV (n = 33) or lamivudine-susceptible HBV (n = 56) who were on tenofovir-containing combination antiretroviral therapy</p

Image_2_Sexually transmitted coinfections among at-risk HIV-positive MSM: implications for optimal preemptive treatment.TIF

BackgroundConcurrent sexually transmitted infections (STIs) are common in sexually active populations. We aimed to estimate the prevalence and coinfection rates of bacterial STIs among sexually active, HIV-positive men who have sex with men (MSM), and to assess the potential benefits of different combination treatment regimens in managing concurrent bacterial STIs.MethodsFrom September 2021 to September 2023, HIV-positive MSM underwent STI testing when they had symptoms suggestive of STIs or recently acquired hepatitis C virus (HCV) infection or early syphilis. The oral rinse, rectal swab, and urethral swab specimens were tested for Chlamydia trachomatis, Neisseria gonorrhoeae, Mycoplasma spp., Ureaplasma spp., and Trichomonas vaginalis with the use of multiplex real-time polymerase-chain-reaction assays. The estimated coinfection rates were used to evaluate the benefits of different combination treatment regimens for managing coinfections.ResultsDuring the study period, 535 participants (median age, 37 years; and CD4 count, 615 cells/mm3) were enrolled. On their first visits, at least one bacterial pathogen was detected in 57.9% and concomitant bacterial infections were found in 32.9% of the participants. The most commonly identified pathogen was U. urealyticum (36.3%), followed by C. trachomatis (22.8%), and N. gonorrhoeae (19.8%). The factors associated with any bacterial STIs included older age (per 1-year increase, adjusted odds ratio [AOR], 0.97; 95% confidence interval [CI], 0.95–1.00), early syphilis (AOR, 1.87; 95% CI, 1.22–2.84), and having more than 5 sex partners in the preceding 3 months (AOR, 2.08, 95% CI, 1.07–4.06). A combination therapy of benzathine penicillin G with a 7-day course of doxycycline could simultaneously treat 27.1% of C. trachomatis coinfections in participants with early syphilis, while a combination therapy of ceftriaxone with doxycycline could simultaneously treat 40.6% of chlamydial coinfections in participants with gonorrhea.ConclusionBacterial STIs were prevalent and concomitant infections were not uncommon among sexually active, HIV-positive MSM, supporting regular screening for bacterial STIs. The effectiveness of preemptive use of doxycycline as combination therapy for concurrent STIs warrants more investigations.</p