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1.
J Mol Neurosci ; 2020 May 30.
Artigo em Inglês | MEDLINE | ID: mdl-32474900

RESUMO

Cerebral ischemia represents a major cause of disability, yet its precise mechanism remains unknown. In addition, ischemia-reperfusion injury which occurs during the blood recovery process increases the risk of mortality, and is not adequately addressed with current treatment. To improve therapeutic options, it is important to explore the vital substances that play a pivotal role in ischemia-reperfusion injury. This study is the first to investigate the role of IL-32, a vital pro-inflammatory factor, in models of cerebral ischemia-reperfusion injury. The results showed that IL-32 was highly expressed in both in vivo and in vitro models. The proteins of the NOD/MAPK/NF-κB pathway were also up-regulated, indicating a potential signaling pathway mechanism. Inhibition of IL-32 and blocking of the NOD/MAPK/NF-κB pathway increased cell survival, decreased the level of inflammatory factors and inflammasomes, and attenuated nitrosative stress. Taken together, the results show that inhibition of IL-32 expression ameliorates cerebral ischemia-reperfusion injury via the NOD/MAPK/NF-κB signaling pathway. The findings in this study reveal that IL-32 is a vital target of ischemia-reperfusion injury, providing a new avenue for treatment development.

2.
Artigo em Inglês | MEDLINE | ID: mdl-32572558

RESUMO

PURPOSE: NSCLC is the most common type of lung cancers. The purpose of this study is to screen cancer-related mutations in early LUAD in China through NGS technology, determine their correlation with clinical characteristics and provide basis for treatment decisions. METHODS: In this study, we performed a 583 gene panel to detect the mutational spectrum of the tumors which were collected from 98 LUAD patients. The sequencing data and clinical characteristics were analyzed. RESULTS: Mutations were identified in 94.9% of patients. EGFR had the highest mutation frequency which was detected in 66% of the patients and was significantly associated with female gender and non-smoking history. Other genes with high mutation frequency were TP53 (37%), ERBB2 (24%), BCOR (22%), ZFHX3 (19%), BTG1 (17%), ATR (16%), WWTR1 (15%), etc. TP53 mutations were significantly associated with medium and low differentiation of tumors; BCOR and BLM mutations with gender; WWTR1 mutations with age; and ATR mutations with visceral pleura invasion were observed. 61% of the patients harbored at less one actionable alteration associated with FDA-recognized or investigational drugs. CONCLUSION: Multiple mutations in LUAD patients in this study have not previously been reported in NSCLC. Moreover, mutations in driver genes including EGFR, TP53, BCOR, BLM, WWTR1, and ATR were significantly related to clinical features. The panel used in this study is an effective approach for molecular analysis and can be applied in personalized treatment decision-making and drug development.

3.
Aging (Albany NY) ; 12(9): 7774-7785, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-32357143

RESUMO

To identify potential therapeutic targets in non-small cell lung cancer NSCLC, we conducted a bioinformatics analysis of circRNAs differentially expressed between NSCLC tissues and adjacent normal tissues. Cell proliferation and apoptosis was assessed using CCK-8 and flow cytometry, respectively. A connection between hsa_circ_0018818 and miR-767-3p was confirmed in dual luciferase reporter assays. Gene and protein expression in NSCLC cells were measured using quantitative PCR and Western-blotting, respectively. And a xenograft tumor model was established to assess the function of hsa_circ_0018818 in NSCLC in vivo. Hsa_circ_0018818 was greatly upregulated in NSCLC tumor tissues. Knocking down hsa_circ_0018818 using a targeted shRNA inhibited the proliferation and invasiveness of NSCLC cells and induced their apoptosis via the miR-767-3p/Nidogen 1 (NID1) signaling axis. Hsa_circ_0018818 knockdown also inactivated Epithelial-mesenchymal transition (EMT) process and PI3K/Akt signaling. In summary, hsa_circ_0018818 knockdown inhibited NSCLC tumorigenesis in vitro and in vivo, which suggests it could potentially serve as a target for the treatment of NSCLC.

4.
Environ Pollut ; 264: 114718, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32388309

RESUMO

Diesel exhaust (DE) had been associated with cardiopulmonary toxicity and developmental toxicity. However, neonatal very early-in-life exposure had not been extensively studied previously. To investigate the potential effects of neonatal very early-in-life exposure to DE, a brand-new chicken embryo in ovo exposure model had been established, with which the cardiopulmonary effects of DE exposure via air cell infusion at embryonic day 18/19 (ED18/19) were assessed in hatchling chicks post-hatch 0-, 1-, or 2-weeks. Heart rates were assessed with electrocardiography. Cardiac and pulmonary morphologies were investigated with histopathological methods. Cardiopulmonary effects were explored with immunohistochemistry for alpha smooth muscle actin (alpha-SMA). In further investigations, the expression levels of phosphorylated AhR, serum levels of TGF-ß1, phosphorylated SMAD2/3 and phosphorylated p38MAPK were assessed in the lung tissues. Significantly elevated heart rates, increased right ventricular wall thickness and cardiac collagen deposition were observed in the hearts of exposed hatchling chicks. Significantly increased collagen deposition as well as increased vascular alpha-SMA layer thickness/decreased cavity area were observed in exposed animal lungs. These effects persisted up to two weeks post-hatch. Mechanistic studies revealed elevated phosphorylated AhR expression levels in 0-week and 1-week chicken lungs, while phosphorylated SMAD2/3 levels significantly increased in 0-week chicken lungs but decreased in 2-week chicken lungs following DE exposure. Phosphorylation of p38MAPK did not remarkably increase until 2-week post-hatch. In summary, the novel chicken neonatal very early-in-life exposure model effectively exposed the chicken embryos during the neonatal initial breathing, resulting in cardiopulmonary toxicity, which is associated with AHR, TGF-ß1 and MAPK signaling.

5.
Artigo em Inglês | MEDLINE | ID: mdl-32471209

RESUMO

Although hospital length of stay (LOS) has been identified as a proxy measure of healthcare expenditures in the United States, there are limited studies investigating the potentially important association between outdoor air pollution and LOS for pediatric asthma. This study aims to examine the effect of ambient air pollution on LOS among children with asthma in South Texas. It included retrospective data on 711 children aged 5-18 years old admitted for asthma to a pediatric tertiary care hospital in South Texas between 2010 and 2014. Air pollution data including particulate matter (PM2.5) and ozone were collected from the U.S. Centers for Disease Control and Prevention. The multivariate binomial logistic regression analyses were performed to determine the association between each air pollutant and LOS, controlling for confounders. The regression models showed the increased ozone level was significantly associated with prolonged LOS in the single- and two-pollutant models (p < 0.05). Furthermore, in the age-stratified models, PM2.5 was positively associated with LOS among children aged 5-11 years old (p < 0.05). In conclusion, this study revealed a concerning association between ambient air pollution and LOS for pediatric asthma in South Texas.

6.
Mol Cell Probes ; : 101585, 2020 May 03.
Artigo em Inglês | MEDLINE | ID: mdl-32376213

RESUMO

OBJECTIVE: Apoptosis is a prominent form of neuron death in cerebral ischemia-reperfusion-induced injury. Accompanied with the pathogenesis, Circ_002664 is upregulated. However, its role in the neuron apoptosis and the underlying mechanisms are unknown. METHODS: In this study, HT22 cells were treated with oxygen glucose deprivation and reoxygenation (OGD/R). The cell viability, apoptosis, proliferation and mitochondrial potential were examined. The expressions of interested genes, Circ_002664, miR-182-5p and Herpud1, were measured. The roles of these genes in OGD/R-induced cell injury were investigated by knockdown, overexpression alone or in combination. Additionally, the interactions between Circ_002664, miR-182-5p and Herpud1 were validated by luciferase report assay. The levels of MAP2, CHOP, Cytochrome C (CYC) and cleaved caspase-3 were determined. RESULTS: OGD/R treatment significantly increased cell apoptosis, decreased cell proliferation and mitochondrial potential, as well as increased Circ_002664 and Herpud1 expressions, and decreased miR-182-5p level. Circ_002664 knockdown markedly inhibited the effects by OGD/R on cell survival and altered expression of miR-182-5p and Herpud1. MiR-182-5p was observed sponged by Circ_002664 and negatively mediated its effect above mentioned, and this was by directly targeting Herpud1. Additionally, it was observed that CHOP expressions were regulated by Circ_002664/miR-182-5p/Herpud1 pathway, and in turn mediated its regulation in CYC and cleaved caspase-3. CONCLUSIONS: In summary, our data showed that the Circ_002664 importantly contributed to neuronal cell apoptosis induced by OGD/R treatment, and this might be achieved by directly targeting miR-182-5p/Herpud1 pathway.

7.
Bioanalysis ; 12(9): 615-624, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32441529

RESUMO

Glucuronides, especially acyl glucuronides, were often found to be unstable in vitro and in vivo. Acyl glucuronide metabolites can convert back to the parent drugs at physiological pH through hydrolysis. Glucuronides can also undergo in-source fragmentation during MS ionization to form the same ions as those of the parent compounds, which could cause interference to the analysis of the parent compounds. All of these may cause significant challenges in developing LC-MS/MS bioanalytical assays of labile glucuronides or parent compounds in the presence of glucuronide metabolites. In this manuscript, we will discuss these challenges and summarize recommended strategies and practices for fast and efficient method development. Critical considerations in assay development will also be discussed.

8.
Andrologia ; 52(6): e13602, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32352591

RESUMO

Sex chromosome abnormality (SCA) is one of the major causes of male spermatogenesis dysfunction. In our study, we sought to investigate the novel X chromosome inversion leading to severe oligozoospermia. Here, we report two brothers with severe oligozoospermia without any other abnormal clinical phenotype. The chromosome karyotypes in peripheral blood of both brothers were 46, Y, inv (X) (p22.3, q22), and no Y chromosome microdeletion was found. The karyotype of their mother was 46, X, inv (X) (p22.3, q22) and that of their father was 46, XY. This is the first report in China that X chromosomal inversion, 46, Y, inv (X) (p22.3, q22), is associated with severe oligozoospermia. This inversion may be a direct genetic risk factor for spermatogenesis.

10.
FASEB J ; 34(5): 7058-7074, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32275331

RESUMO

The role of central juxtaposed with another zinc finger gene 1 (JAZF1) in glucose regulation remains unclear. Here, we activated mediobasal hypothalamus (MBH) JAZF1 in high-fat diet (HFD)-fed rats by an adenovirus expressing JAZF1 (Ad-JAZF1). We evaluated the changes in the hypothalamic insulin receptor (InsR)-PI3K-Akt-AMPK pathway and hepatic glucose production (HGP). To investigate the impact of MBH Ad-JAZF1 on HGP, we activated MBH JAZF1 in the presence or absence of ATP-dependent potassium (KATP ) channel inhibition, hepatic branch vagotomy (HVG), or an AMPK activator (AICAR). In HFD-fed rats, MBH Ad-JAZF1 decreased body weight and food intake, and inhibited HGP by increasing hepatic insulin signaling. Under insulin stimulation, MBH Ad-JAZF1 increased InsR and Akt phosphorylation, and phosphatidylinositol 3, 4, 5-trisphosphate (PIP3) formation; however, AMPK phosphorylation was decreased in the hypothalamus. The positive effect of MBH JAZF1 on hepatic insulin signaling and HGP was prevented by treatment with a KATP channel inhibitor or HVG. The metabolic impact of hypothalamic JAZF1 was also blocked by MBH AICAR. Ad-JAZF1 treatment in SH-SY5Y cells resulted in an elevation of InsR and Akt phosphorylation following insulin stimulation. Our findings show that hypothalamic JAZF1 regulates HGP via the InsR-PI3K-Akt-AMPK pathway and KATP channels.

11.
Sci Rep ; 10(1): 7012, 2020 Apr 24.
Artigo em Inglês | MEDLINE | ID: mdl-32332879

RESUMO

Stroke and subsequent cerebral ischemia/reperfusion (I/R) injury is a frequently occurring disease that can have serious consequences in the absence of timely intervention. Circular RNAs (circRNAs) in association with microRNAs (miRNAs) and RNA-binding proteins (RBPs) can influence gene expression. However, whether circRNAs have a role in cerebral I/R injury pathogenesis, especially soon after onset, is unclear. In this study, we used the SD rat middle cerebral artery occlusion (MCAO) model of stroke to examine the role of circRNAs in cerebral I/R injury. We used high-throughput sequencing (HTS) to compare the expression levels of circRNAs in cerebral cortex tissue from MCAO rats during the occlusion-reperfusion latency period 3 hours after I/R injury with those in control cerebral cortices. Our sequencing results revealed that expression levels of 44 circRNAs were significantly altered after I/R, with 16 and 28 circRNAs showing significant up- and down-regulation, respectively, relative to levels in control cortex. We extended these results in vitro in primary cultured neuron cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R) using qRT-PCR to show that levels of circ-camk4 were increased in OGD/R neurons relative to control neurons. Bioinformatics analyses predicted that several miRNAs could be associated with circ-camk4 and this prediction was confirmed in a RNA pull-down assay. KEGG analysis to predict pathways that involve circ-camk4 included the glutamatergic synapse pathway, MAPK signaling pathway, and apoptosis signaling pathways, all of which are known to be involved in brain injury after I/R. Our results also demonstrate that levels of the human homolog to circ-camk4 (hsa-circ-camk4) are elevated in SH-SY5Y cells exposed to OGD/R treatment. Overexpression of hsa-circ-camk4 in SH-SY5Y cells significantly increased the rate of cell death after OGD/R, suggesting that circ-camk4 may play a key role in progression of cerebral I/R injury.

12.
Artigo em Inglês | MEDLINE | ID: mdl-32276490

RESUMO

BACKGROUND: In this paper, we aimed to investigate the potential impacts of a fire accident in a fertilizer warehouse on chromosomal anomalies, including Trisomy 21 (T21) and Trisomy (T18) among pregnancies in Brazos County, Texas. We conducted an observational study in Brazos County, TX, with all patients of T18 and T21 cases in the live births in Brazos County between 2005-2014. The prevalence of T18 and T21 before, during, and after the accident in Brazos County were calculated and compared. The Standardized Morbidity Ratio (SMR) was applied to compare the prevalence of T18 and T21 in Brazos County to the statewide prevalence in Texas after adjusting for maternal race and age. Compared with statewide risk, the risk of T18 during the impacted years in Brazos county was found to be significantly higher (SMR = 5.0, 95% Confidence Interval(CI): 2.19-9.89), while there was no significant difference before (SMR = 0.77, 0.13-2.54) and after the accident (SMR = 0.71, 0.12-2.36). However, the prevalence of T21 during the impacted years was not significantly different from those before or after the accident. This study conclusively suggests that this fertilizer fire may be related to the increased prevalence of T18 in Brazos County, though the findings warrant further investigation.

13.
Aging (Albany NY) ; 12(6): 4711-4726, 2020 03 25.
Artigo em Inglês | MEDLINE | ID: mdl-32209729

RESUMO

Long noncoding RNAs (lncRNAs) play critical roles in tumour progression and metastasis. Emerging evidence indicates that the lncRNA X inactive-specific transcript (XIST) is dysregulated in several tumor types, including non-small cell lung cancer (NSCLC). However, in NSCLC and other cancers the oncogenic mechanism of XIST remains incompletely understood. Here, we confirmed that XIST is upregulated in human NSCLC specimens, and is especially overexpressed in tumors previously treated with cisplatin (cis-diamminedichloroplatinum(II); DDP). In vitro, XIST knockdown inhibited NSCLC cell growth and promoted DDP chemosensitivity by stimulating apoptosis and pyroptosis. Moreover, XIST's oncogenic effects and ability to promote DDP chemoresistance were largely related to its binding to the TGF-ß effector SMAD2, which inhibited its translocation to the nucleus and prevented the transcription of p53 and NLRP3, crucial regulators of apoptosis and pyroptosis, respectively. Using DDP-resistant NSCLC cells, mouse xenograft studies verified the oncogenic function of XIST and its ability to inhibit programmed cell death, thereby mediating DDP chemoresistance. These findings suggest that XIST expression may serve as a novel biomarker to predict DDP treatment efficacy, and may help in the design of new therapies to circumvent DDP chemoresistance in NSCLC and other tumor types.

14.
J Affect Disord ; 268: 95-101, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-32158012

RESUMO

BACKGROUND: Depression in China has risen from the 15th leading cause of all-cause disability-adjusted life years (DALYs) in 1990 to the 10th in 2017. However, the burden of depression and the epidemiological trend in Chinese provinces remain unclear. This study aimed to estimate the prevalence and burden of depression among different sexes, ages, disease types and provincial administrative units in China. METHODS: Based on a general analysis of the Global Burden of Disease study (GBD) in 2017, we analyzed the age- sex- and province-specific prevalence and DALYs of depression in China from 1990 to 2017. RESULTS: From 1990 to 2017, the all-age prevalence rate of depression per 100,000 rose from 3224.6 (95% UI:2976.6-3509.1) to 3990.5 (95% UI: 3667.8-4353.0), and the DALY rate per 100,000 rose from 525.1 (95% UI: 373.5-719.0) to 607.4 (95% UI: 427.7-820.2). The prevalence rate decreased in the population aged 5-54 years, and increased in the population aged over 55 years. In 2017, the prevalence rate of females (5039.6, 95% UI: 4630.0-5502.8) was significantly higher than that of males (2984.9, 95% UI: 2736.0-3265.3). The prevalence and DALY rate increased in all provinces. However, the age-standardized prevalence and DALYs rate decreased in 31 provinces. CONCLUSIONS: Depression has gradually become a major public health issue in China. The government should take measures to prevent the development of depression immediately. Women and the elderly are at high risk for depression.

15.
Bioresour Technol ; 302: 122829, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32028147

RESUMO

The existence of CO2 in biogas will affect its practicality, so the methanation of CO2 is of great significance. Carrier materials play a key role in bioconversion of CO2 to methane during biogas upgrading. Herein, different materials were used to evaluate the bioconversion process of CO2 to methane, which consisted of black ceramsite (BC) and biochars prepared from corn straw and digestate. The results showed that after adding the carrier materials, the methane production rate increased by more than 20%, and the corn straw biochar (CSB) group even increased by more than 70%. This may be attributed to the large specific surface area and more functional groups in corn straw biochar which was suitable for the immobilization of hydrogenotrophic methanogens (HMs). Therefore, corn straw biochar is a good carrier material for the accelerated bioconversion of CO2 to methane.


Assuntos
Reatores Biológicos , Euryarchaeota , Biocombustíveis , Carvão Vegetal , Metano
16.
J Neurointerv Surg ; 2020 Feb 17.
Artigo em Inglês | MEDLINE | ID: mdl-32066569

RESUMO

BACKGROUND: Intracranial vertebrobasilar artery stenosis is an important cause of ischemic stroke. With its high resolution, intravascular optical coherence tomography (OCT) provides detailed assessment of vessel wall features. It is widely applied to identify high-risk plaque in the cardiovascular system, but its use in the intracranial artery has been limited. OBJECTIVE: To explore, in this pilot study, the usefulness of OCT in imaging of the intracranial artery wall. METHODS: Between November 2017 and July 2018, four patients with severe intracranial vertebrobasilar artery stenosis were enrolled for preintervention OCT evaluation of the lesion artery. Stenosis was present in the basilar artery in one case and in the intracranial vertebral artery in three cases. RESULTS: OCT images of the lesions showed various features of plaque vulnerability, such as intraluminal thrombus, lipid-rich plaque with plaque rupture, thin fibrous cap, macrophage accumulations, and a mixed lesion with dissecting aneurysm. In view of the OCT findings, all patients received balloon angioplasty and stent implantation. CONCLUSIONS: These cases describe the successful implementation of OCT in intracranial vertebrobasilar artery stenosis. No side effects were seen during the OCT imaging. This technology may help in the diagnosis and treatment of cerebrovascular disease.

17.
Biomed Res Int ; 2020: 6458204, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32090104

RESUMO

Background: Studies have elucidated that the variable expression levels of miRNAs influence the inflammatory process in ischemic stroke. Nevertheless, the impact and potential mechanism of miR-155 in cerebral ischemia-reperfusion injury (CIRI) keep to be incompletely known. Methods: The levels of miR-155 and MafB were determined via qRT-PCR, western blot, or immunohistochemistry assays in plasma of patients with CIRI, oxygen glucose deprivation/reoxygenation (OGD/R) induced SH-SY5Y cells, and mouse models with middle cerebral artery occlusion (MCAO). The association between miR-155 and MafB was validated via dual-luciferase reporter and western blot assays. Cell viability, apoptosis, invasion, and migration were evaluated through MTT, flow cytometry, Transwell and wound healing assays. Infarction volume was measured in MCAO mouse brain tissues by TTC assay. The expression of inflammatory mediators was measured by ELISA in cells and brain tissues. Results: miR-155 level was upregulated whereas MafB was downregulated in the plasma of patients with CIRI, OGD/R-induced SH-SY5Y cells, also as mouse models with MCAO injury. Mechanistically, miR-155 directly targeted 3'UTR of MafB and restrained MafB expression in OGD/R injury SH-SY5Y cells. Downregulation of miR-155 attenuated OGD/R-induced injury through increasing proliferation, inhibiting apoptosis, enhancing invasion and migration abilities, and constraining the expression of inflammatory mediators (IL-1ß, IL-6, and TNF-α) and inflammatory enzymes (iNOS and COX-2) in SH-SY5Y cells following OGD/R, while MafB inhibition reversed the protective effects. In vivo, downregulating miR-155 reduced the infarction volume in the MACO mouse brain. Furthermore, miR-155 knockdown inhibited the IL-1ß, IL-6, and TNF-α) and inflammatory enzymes (iNOS and COX-2) in SH-SY5Y cells following OGD/R, while MafB inhibition reversed the protective effects. Conclusion: Our results suggest that miR-155 knockdown alleviated ischemia-reperfusion injury by targeting MafB to improve the neurological function and inhibit inflammation response, highlighting a novel therapeutic strategist for CIRI.

18.
Diabetes ; 69(4): 760-770, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31974145

RESUMO

Long-term hyperglycemia in patients with diabetes leads to human serum albumin (HSA) glycation, which may impair HSA function as a transport protein and affect the therapeutic efficacy of anticoagulants in patients with diabetes. In this study, a novel mass spectrometry approach was developed to reveal the differences in the profiles of HSA glycation sites between patients with diabetes and healthy subjects. K199 was the glycation site most significantly changed in patients with diabetes, contributing to different interactions of glycated HSA and normal HSA with two types of anticoagulant drugs, heparin and warfarin. An in vitro experiment showed that the binding affinity to warfarin became stronger when HSA was glycated, while HSA binding to heparin was not significantly influenced by glycation. A pharmacokinetic study showed a decreased level of free warfarin in the plasma of diabetic rats. A preliminary retrospective clinical study also revealed that there was a statistically significant difference in the anticoagulant efficacy between patients with diabetes and patients without diabetes who had been treated with warfarin. Our work suggests that larger studies are needed to provide additional specific guidance for patients with diabetes when they are administered anticoagulant drugs or drugs for treating other chronic diseases.

19.
Angew Chem Int Ed Engl ; 59(13): 5326-5331, 2020 Mar 23.
Artigo em Inglês | MEDLINE | ID: mdl-31967403

RESUMO

Discoveries of the accurate spatial arrangement of active sites in biological systems and cooperation between them for high catalytic efficiency are two major events in biology. However, precise tuning of these aspects is largely missing in the design of artificial catalysts. Here, a series of metal-organic frameworks (MOFs) were used, not only to overcome the limit of distance between active sites in bio-systems, but also to unveil the critical role of this distance for efficient catalysis. A linear correlation was established between photocatalytic activity and the reciprocal of inter active-site distance; a smaller distance led to higher activity. Vacancies created at selected crystallographic positions of MOFs promoted their photocatalytic efficiency. MOF-525-J33 with 15.6 Šinter active-site distance and 33 % vacancies exhibited unprecedented high turnover frequency of 29.5 h-1 in visible-light-driven acceptorless dehydrogenation of tetrahydroquinoline at room temperature.

20.
Aging Male ; 23(2): 112-118, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30857458

RESUMO

Objectives: To investigate whether testosterone replacement therapy (TRT) reduces prostate cancer (PCa) risk via stabilizing serum testosterone (T) levels beyond simply elevating serum T levels and whether TRT reduces PCa risk due to low serum T levels at a young age.Methods: We analyzed data of 776 hypogonadal men from a urology center in Bremerhaven, Germany through 2004-2016 to investigate whether the TRT group has more stable T levels and whether TRT can reduce the risk of PCa due to low serum T levels at an early age. We derived an index, Maximum Decline of T Relative to Baseline (MDRB), to describe the magnitude of T declines and variations over time.Results: We found the TRT group has more stable serum T levels (e.g. smaller drop-offs) during the follow-up period as compared to the non-TRT group, and the mean of MDRB is significantly higher in the untreated group (1.553 nmol/L VS 0.013 nmol/L; p-value < .001). TRT significantly reduces the risk of PCa associated with T deficiency at a young age (p-value = .00087).Conclusions: TRT may reduce PCa risk via maintaining serum T levels within individual's normal range; T surveillance may be needed for males who have low serum T levels at a young age to monitor abnormal variations of T levels and ensure timely treatment when necessary to reduce PCa risk.

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