Issue Ebook
cover story
Latest Issue
Volume 9 ， Issue 3 ， 2022
-
Abstract：Background:The clinical efficiency of routine oxygen therapy is uncertain in patients with acute heart failure (AHF) who do not have hypoxemia. The aim of this study was to investigate the association between oxygen therapy and clinical outcomes in normoxemic patients hospitalized with AHF using real-world data.Methods:Normoxemic patients diagnosed with AHF on intensive care unit (ICU) admission from the electronic ICU (eICU) Collaborative Research Database were included in the current study, in which the study population was divided into the oxygen therapy group and the ambient air group. Propensity score matching (PSM) was applied to create a balanced covariate distribution between patients receiving supplemental oxygen and those exposed to ambient air. Linear regression and logistic regression models were performed to assess the associations between oxygen therapy and length of stay (LOS), and all-cause in-hospital as well as ICU mortality rates, respectively. A series of sensitivity and subgroup analyses were conducted to further validate the robustness of our findings.Results:A total of 2922 normoxemic patients with AHF were finally included in the analysis. Overall, 42.1% (1230/2922) patients were exposed to oxygen therapy, and 57.9% (1692/2922) patients did not receive oxygen therapy (defined as the ambient air group). After PSM analysis, 1122 pairs of patients were matched: each patient receiving oxygen therapy was matched with a patient without receiving supplemental oxygen. The multivariable logistic model showed that there was no significant interaction between the ambient air and oxygen therapy for all-cause in-hospital mortality [odds ratio (OR)=1.30; 95% confidence interval (CI) 0.92–1.82; P=0.138] or ICU mortality (OR=1.39; 95%CI 0.83–2.32; P=0.206) in the post-PSM cohorts. In addition, linear regression analysis revealed that oxygen therapy was associated with prolonged ICU LOS (OR=1.11; 95%CI 1.06–1.15; P<0.001) and hospital LOS (OR=1.06; 95%CI 1.01–1.10; P=0.009) after PSM. Furthermore, the absence of an effect of supplemental oxygen on mortality was consistent in all subgroups.Conclusions:Routine use of supplemental oxygen in AHF patients without hypoxemia was not found to reduce all cause in-hospital mortality or ICU mortality.Keywords：Acute heart failure;Death;Hyperoxia;Mortality;Oxygen therapy9|0|0Updated：2023-02-28 -
Abstract：Background:Pituicytoma is an extremely rare low-grade glial tumor that is closely related to the neurohypophysis axis. Most studies of pituicytomas include only several cases. To better understand this disease, we reviewed a series of cases of pituicytomas. The diagnosis and treatment of pituicytoma must be further elucidated.Methods:Eleven patients with pituicytoma admitted to Beijing Tiantan Hospital from 2012 to 2019 were selected. The clinical features, including radiological and histological examination, surgical records and prognosis were reviewed. Sixty-eight other previously published cases of pituicytoma also were used to analyze the predictive factors for the results. The Cox regression model was used for univariate and multivariate analyses.Results:Our patients included 5 males (45.5%) and 6 females (54.5%), with a mean age of 49.3 years. The tumor was located in the suprasellar region in 5 patients (45.5%), intrasellar region in 4 patients (36.4%), and intrasellar-suprasellar region in 2 patients (18.2%). All patients were misdiagnosed with other common tumors in the sellar region before the operation. During the operation, gross total resection (GTR) of the tumor was achieved in 6 patients (54.5%), and subtotal resection (STR) was achieved in 5 patients (45.5%). The mean progression-free survival (PFS) time was 29.82 months. Tumor progression after surgical resection occurred in 4 patients (36.4%). Among them, 60.0% of the patients (cases 4, 5, 7) with STR experienced progression, while 16.7% of the patients (case 2) with GTR experienced progression. Combined with the 68 cases in the literature, GTR was an independent risk factor for PFS time (P<0.05).Conclusions:Pituicytomas are more common in middle-aged people and the sellar region. The clinical manifestations of pituicytomas are different, but no diagnostic clinical features have been identified other than an abnormally abundant blood supply. Currently, GTR is the best approach for the treatment of pituicytomas. More patients and longer follow-up periods were needed to further elucidate the biological features of pituicytomas.Keywords：Pituicytoma;Endoscopic transsphenoidal surgery;Craniotomy;Posterior pituitary lobe tumor7|0|0Updated：2023-02-28 -
Abstract：Background:Administration of propofol, an intravenous anesthetic with antioxidant property, immediately at the onset of post-ischemic reperfusion (propofol postconditioning, P-PostC) has been shown to confer cardioprotection against ischemia–reperfusion (I/R) injury, while the underlying mechanism remains incompletely understood. The forkhead box O (FoxO) transcription factors are reported to play critical roles in activating cardiomyocyte survival signaling throughout the process of cellular injuries induced by oxidative stress and are also involved in hypoxic postconditioning mediated neuroprotection, however, the role of FoxO in postconditioning mediated protection in the heart and in particular in high glucose condition is unknown.Methods:Rat heart-derived H9c2 cells were exposed to high glucose (HG) for 48 h, then subjected to hypoxia/reoxygenation (H/R, composed of 8 h of hypoxia followed by 12 h of reoxygenation) in the absence or presence of postconditioning with various concentrations of propofol (P-PostC) at the onset of reoxygenation. After having identified the optical concentration of propofol, H9c2 cells were subjected to H/R and P-PostC in the absence or presence of FoxO1 or FoxO3a gene silencing to explore their roles in P-PostC mediated protection against apoptotic and autophagic cell deaths under hyperglycemia.Results:The results showed that HG with or without H/R decreased cell viability, increased lactate dehydrogenase (LDH) leakage and the production of reactive oxygen species (ROS) in H9c2 cells, all of which were significantly reversed by propofol (P-PostC), especially at the concentration of 25 μmol/L (P25) (P<0.05, NC vs. HG; HG vs. HG+HR; HG+HR+P12.5 or HG+HR+P25 or HG+HR+P50 vs. HG+HR). Moreover, we found that propofol (P25) decreased H9c2 cells apoptosis and autophagy that were concomitant with increased FoxO1 and FoxO3a expression (P<0.05, HG+HR+P25 vs. HG+HR). The protective effects of propofol (P25) against H/R injury were reversed by silencing FoxO1 or FoxO3a (P<0.05, HG+HR+P25 vs. HG+HR+P25+siRNA-1 or HG+HR+P25+siRNA-5).Conclusions:It is concluded that propofol postconditioning attenuated H9c2 cardiac cells apoptosis and autophagy induced by H/R injury through upregulating FoxO1 and FoxO3a under hyperglycemia.Keywords：Hypoxia/reoxygenation injury;Hyperglycemia;High glucose;Propofol postconditioning;apoptosis;Autophagy;Forkhead box O11|0|0Updated：2023-02-28 -
Abstract：Background:The burden of kidney, bladder, and prostate cancers has changed in recent decades. This study aims to investigate the global and regional burden of, and attributable risk factors for genitourinary cancers during the past 30 years.Methods:We extracted data of kidney, bladder, and prostate cancers from the Global Burden of Disease 2019 database, including incidence, mortality, disability-adjusted life-years (DALYs), and attributable risk factors from 1990 to 2019. Estimated annual percentage changes (EAPC) were calculated to assess the changes in age-standardized incidence rate, age-standardized mortality rate (ASMR), and age-standardized DALYs rate (ASDR). The associations between cancers burden and socio-demographic index (SDI) were also analyzed.Results:Compared with 1990, the global incident cases in 2019 were higher by 154.78%, 123.34%, and 169.11% for kidney, bladder, and prostate cancers, respectively. During the 30-year study period, there was a downward trend in ASMR and ASDR for bladder cancer (EAPC=–0.68 and –0.83, respectively) and prostate cancer (EAPC=–0.75 and –0.71, respectively), but an upward trend for kidney cancer (EAPC=0.35 and 0.12, respectively). Regions and countries with higher SDI had higher incidence, mortality, and DALYs for all three types of cancers. The burden of bladder and prostate cancers was mainly distributed among older men, whereas the burden of kidney cancer increased among middle-aged men. Smoking related mortality and DALYs decreased, but high body mass index (BMI) and high fasting plasma glucose (FPG) related mortality and DALYs increased among kidney, bladder, and prostate cancers during the study period.Conclusions:Kidney, bladder, and prostate cancers remain major global public health challenges, but with distinct trend for different disease entity across different regions and socioeconomic status. More proactive intervention strategies, at both the administrative and academic levels, based on the dynamic changes, are needed.Keywords：Genitourinary cancer;Kidney cancer;Bladder cancer;prostate cancer;Incidence;Mortality;Disability-adjusted life-years;Global Burden of Disease10|0|0Updated：2023-02-28 -
Abstract：Background:The healing of bone defects can be challenging for clinicians to manage, especially after exposure to ionizing radiation. In this regard, radiation therapy and accidental exposure to gamma (γ)-ray radiation have been shown to inhibit bone formation and increase the risk of fractures. Cortical bone-derived stem cells (CBSCs) are reportedly essential for osteogenic lineages, bone maintenance and repair. This study aimed to investigate the effects of melatonin on postradiation CBSCs and bone defect healing.Methods:CBSCs were extracted from C57BL/6 mice and were identified by flow cytometry. Then CBSCs were subjected to 6 Gy γ-ray radiation followed by treatment with various concentrations of melatonin. The effects of exogenous melatonin on the self-renewal and osteogenic capacity of postradiation CBSCs in vitro were analyzed. The underlying mechanisms involved in genomic stability, apoptosis and oxidative stress-related signaling were further analyzed by Western blotting, flow cytometry and immunofluorescence assays. Moreover, postradiation femoral defect models were established and treated with Matrigel and melatonin. The effects of melatonin on postradiation bone healing in vivo were evaluated by micro-CT and pathological analysis.Results:The decrease in radiation-induced self-renewal and osteogenic capacity were partially reversed in postradiation CBSCs treated with melatonin (P<0.05). Melatonin maintained genomic stability, reduced postradiation CBSC apoptosis and intracellular oxidative stress, and enhanced expression of antioxidant-related enzymes (P<0.05). Western blotting validated the anti-inflammatory effects of melatonin by downregulating interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) levels via the extracellular regulated kinase (ERK)/nuclear factor erythroid 2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) signaling pathway. Melatonin was also found to exhibit antioxidant effects via NRF2 signaling. In vivo experiments demonstrated that the newly formed bone in the melatonin plus Matrigel group had higher trabecular bone volume per tissue volume (BV/TV) and bone mineral density values with lower IL-6 and TNF-α levels than in the irradiation and the Matrigel groups (P<0.05).Conclusions:This study suggested that melatonin could protect CBSCs against γ-ray radiation and assist in the healing of postradiation bone defects.Keywords：melatonin;Stem cells;Ionizing radiation;Bone regeneration15|0|0Updated：2023-02-28 -
Abstract：Background:Ultrasound-triggered microbubble destruction (UTMD) is a widely used noninvasive technology in both military and civilian medicine, which could enhance radiosensitivity of various tumors. However, little information is available regarding the effects of UTMD on radiotherapy for glioblastoma or the underlying mechanism. This study aimed to delineate the effect of UTMD on the radiosensitivity of glioblastoma and the potential involvement of autophagy.Methods:GL261, U251 cells and orthotopic glioblastoma-bearing mice were treated with ionizing radiation (IR) or IR plus UTMD. Autophagy was observed by confocal microscopy and transmission electron microscopy. Western blotting and immunofluorescence analysis were used to detect progesterone receptor membrane component 1 (PGRMC1), light chain 3 beta 2 (LC3B2) and sequestosome 1 (SQSTM1/p62) levels. Lentiviral vectors or siRNAs transfection, and fluorescent probes staining were used to explore the underlying mechanism.Results:UTMD enhanced the radiosensitivity of glioblastoma in vitro and in vivo (P<0.01). UTMD inhibited autophagic flux by disrupting autophagosome-lysosome fusion without impairing lysosomal function or autophagosome synthesis in IR-treated glioblastoma cells. Suppression of autophagy by 3-methyladenine, bafilomycin A1 or ATG5 siRNA had no significant effect on UTMD-induced radiosensitization in glioblastoma cells (P<0.05). Similar results were found when autophagy was induced by rapamycin or ATG5 overexpression (P>0.05). Furthermore, UTMD inhibited PGRMC1 expression and binding with LC3B2 in IR-exposed glioblastoma cells (P<0.01). PGRMC1 inhibitor AG-205 or PGRMC1 siRNA pretreatment enhanced UTMD-induced LC3B2 and p62 accumulation in IR-exposed glioblastoma cells, thereby promoting UTMD-mediated radiosensitization (P<0.05). Moreover, PGRMC1 overexpression abolished UTMD-caused blockade of autophagic degradation, subsequently inhibiting UTMD-induced radiosensitization of glioblastoma cells. Finally, compared with IR plus UTMD group, PGRMC1 overexpression significantly increased tumor size [(3.8±1.1) mm2 vs. (8.0±1.9) mm2, P<0.05] and decreased survival time [(67.2±2.6) d vs. (40.0±1.2) d, P=0.0026] in glioblastoma-bearing mice.Conclusions:UTMD enhanced the radiosensitivity of glioblastoma partially by disrupting PGRMC1-mediated autophagy.Keywords：Ultrasound-triggered microbubble destruction;Radiosensitization;Progesterone receptor membrane component 1;Autophagy;Glioblastoma13|0|0Updated：2023-02-28
RESEARCH
-
Abstract：The military population face a unique set of risk factors that may increase the risk of being diagnosed with dementia. Traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) have a higher prevalence in this group in comparison to the civilian population. By delving into the individual relationships between TBI and dementia, and PTSD and dementia, we are able to better explore dementia in the military and veteran populations. While there are some inconsistencies in results, the TBI-dementia association has become more widely accepted. Moderate-to-severe TBI has been found to increase the risk of being diagnosed with Alzheimer’s disease. A correlation between PTSD and dementia has been established, however, whether or not it is a causal relationship remains unclear. Factors such as blast, combat and chemical exposure may occur during a deployment, along with TBI and/or PTSD diagnosis, and can impact the risk of dementia. However, there is a lack of literature exploring the direct effects of deployment on dementia risk. Sleep problems have been observed to occur in those following TBI, PTSD and deployment. Poor sleep has been associated with possible dementia risk. Although limited studies have focused on the link between sleep and dementia in military and veteran populations, sleep is a valuable factor to study due to its association and interconnection with other military/veteran factors. This review aims to inform of various risk factors to the cognitive health of military members and veterans: TBI, PTSD, deployment, and sleep.Keywords：Dementia;Alzheimer’s disease;Traumatic brain injury;Post-traumatic stress disorder;Military;Veteran;Deployment;Sleep13|1|0Updated：2023-02-28 -
Abstract：Targeting immune checkpoints has achieved great therapeutic effects in the treatment of early-stage tumors. However, most patients develop adaptive resistance to this therapy. The latest evidence demonstrates that tumor-derived exosomes may play a key role in systemic immune suppression and tumor progression. In this article, we highlight the role of exosomal immune checkpoint proteins in tumor immunity, with an emphasis on programmed death ligand 1 (PD-L1) and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), as well as emerging evidence on roles of T cell immunoglobulin-3 (TIM-3), arginase 1 (ARG1), and estrogen receptor binding fragment-associated antigen 9 (EBAG9) expressed by exosomes.Keywords：Exosomes;Tumor;Immune checkpoints12|0|0Updated：2023-02-28
REVIEW
- Abstract：To determine the prevalence and clinical features of olfactory and taste disorders among coronavirus disease 2019 (COVID-19) patients in China. A cross-sectional study was performed in Wuhan from April 3, 2020 to April 15, 2020. A total of 187 patients with confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) completed face-to-face interviews or telephone follow-ups. We found that the prevalence of olfactory and taste disorders was significantly lower in the Chinese cohort than in foreign COVID-19 cohorts. Females were more prone to olfactory and taste disorders. In some patients, olfactory and taste disorders precede other symptoms and can be used as early screening and warning signs.Keywords：Coronavirus disease 2019;Severe acute respiratory syndrome coronavirus 2;Olfactory;Taste11|0|0Updated：2023-02-28
-
Abstract：Despite the widespread use of malaria rapid diagnostic test (RDT) in clinical practice, there are a lot of challenges. We conducted a secondary analysis of 129 malaria RDT data from rounds 5–8 of the World Health Organization (WHO) product testing summary and discuss the causes of false-negative (FN) results with a focus on low parasite density, improper RDT storage, operation and interpretation, and Plasmodium falciparum with a pfhrp2/3 gene deletion. The results demonstrated that the malaria RDTs currently commercially available might cause FN results in practice.Keywords：Malaria;Rapid diagnostic tests;False-negative results;WHO product testing7|0|0Updated：2023-02-28 - Abstract：The present study demonstrates that the down-regulation of peroxisome proliferator-activated receptor-α (PPARα) results in chronic low ambient temperature (LT) exposure-induced cardiac dysfunction and remodeling, emphasizing the therapeutic potential of PPARα activation strategies (e.g., fenofibrate treatment) in LT-associated cardiac injury.Keywords：Low ambient temperature;Cardiac dysfunction;Remodeling;Peroxisome proliferator-activated receptor-α;Fatty acid metabolism8|0|0Updated：2023-02-28
LETTER TO THE EDITOR
LETTER TO THE EDITO
- Technical support is provided by Beijing Founder electronics co., LTD 京ICP备09064830号-19
京公网安备11010802024621 - It is recommended to read the content of this site in Chrome&IE9+. Please switch to extreme mode in browser 360.
- Cookies We use cookies to help provide and enhance our service and tailor content. By continuing, you agree to the use of cookies.
0