American Journal of the Medical Sciences最新文献

{"title":"The relationship between dietary niacin intake and the incidence of all-cause and cardiovascular mortality among chronic kidney disease patients","authors":"Hongxi Chen MM ,&nbsp;Xu He MM ,&nbsp;Junming Fan MD ,&nbsp;Yongjie Mi MM ,&nbsp;Feiyan Li MD","doi":"10.1016/j.amjms.2024.11.004","DOIUrl":"10.1016/j.amjms.2024.11.004","url":null,"abstract":"<div><h3>Background</h3><div>Chronic kidney disease (CKD) is a major cause of human mortality and cardiovascular disease (CVD)-related death. Niacin can treat dyslipidemia and can lower overall cardiovascular event incidence and mortality rates. The present study was designed to clarify the link between dietary consumption of niacin and cardiovascular mortality.</div></div><div><h3>Methods</h3><div>This study enrolled subjects ≥18 years of age from the National Health and Nutrition Examination Survey 2009-2014 and excluded any individuals for whom data regarding their CKD status, dietary niacin intake, or other covariate information was unavailable. Relationships between dietary niacin intake levels and overall or CVD-related mortality among these CKD patients were assessed using univariate and multivariate Cox regression analyses.</div></div><div><h3>Results</h3><div>The study included 1,798 subjects and recorded 514 and 186 instances of all-cause and cardiovascular death, respectively. Males comprised 51.8 % of the study cohort, and the mean age of these subjects was 65. Cox proportional hazard model analyses revealed no relationship between dietary niacin intake and all-cause or cardiovascular death risk among the overall CKD patient population (P &gt; 0.05). However, in age-stratified analyses, those subjects &lt;60 years of age exhibiting the highest levels of dietary niacin consumption (≥ 38 mg/day) were found to face a significantly higher risk of all-cause mortality, and this association remained intact in sensitivity analyses.</div></div><div><h3>Conclusion</h3><div>These results do not support any link between the dietary intake of niacin and all-cause or cardiovascular mortality risk among patients with CKD. Age and niacin intake exhibited a significant interaction related to all-cause mortality.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 460-466"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of leukemia inhibitory factor as a protective factor in ischemic acute kidney injury","authors":"Lemei Hu MM ,&nbsp;Chen Jiao MM ,&nbsp;Haiyu Gu BM ,&nbsp;Zhigang Zhu MD ,&nbsp;Ming Liang MD","doi":"10.1016/j.amjms.2024.09.010","DOIUrl":"10.1016/j.amjms.2024.09.010","url":null,"abstract":"<div><h3>Background</h3><div>Ischemia-reperfusion injury (IRI) is a common pathophysiological mechanism of acute kidney injury (AKI). There is an urgent need for a more comprehensive analysis of its underlying mechanisms.</div></div><div><h3>Materials and methods</h3><div>The RNA-sequencing dataset GSE153625 was used to examine differentially expressed genes (DEGs) of kidney tissues in IRI-AKI mice compared with sham mice. We used 10 algorithms provided by cytohubba plugin and four external datasets (GSE192532, GSE52004, GSE98622, and GSE185383) to screen for hub genes. The IRI-AKI mouse model with different reperfusion times was established to validate the expression of hub gene in the kidneys. HK-2 cells were cultured <em>in vitro</em> under hypoxia/reoxygenation (H/R) conditions, via transfection with si-LIF or supplementation with the LIF protein to explore the function of the <em>LIF</em> gene.</div></div><div><h3>Results</h3><div>We screened a total of 1,540 DEGs in the IRI group compared with the sham group and identified that the <em>LIF</em> hub gene may play potential roles in IRI-AKI. <em>LIF</em> was markedly upregulated in the kidney tissues of IRI-AKI mice, as well as in HK-2 cells grown under H/R conditions. The knockdown of <em>LIF</em> aggravated apoptosis and oxidative stress (OS) injury under H/R conditions. Administration of the LIF protein rescued the effects of si-LIF, alleviating cellular apoptosis and OS.</div></div><div><h3>Conclusion</h3><div>These findings indicate an important role of the <em>LIF</em> gene in term of regulating apoptosis and OS in the early phases of IRI-AKI. Targeting LIF may therefore represent a promising therapeutic strategy for IRI-AKI.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 524-536"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142309551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between fluid bolus administration and the prognostic role of serum albumin in patients with sepsis","authors":"Gianni Turcato MD ,&nbsp;Lucia Filippi MD ,&nbsp;Arian Zaboli MSN ,&nbsp;Paolo Ferretto MD ,&nbsp;Daniela Milazzo MD ,&nbsp;Michael Maggi MD ,&nbsp;Francesca Stefani MD ,&nbsp;Marta Parodi RN ,&nbsp;Massimo Marchetti MD ,&nbsp;Christian J. Wiedermann MD","doi":"10.1016/j.amjms.2024.12.002","DOIUrl":"10.1016/j.amjms.2024.12.002","url":null,"abstract":"<div><h3>Background</h3><div>Serum albumin plays a pivotal role in the exchange between interstitial and vascular compartments, and reduced levels of this biomarker appear to be associated with negative prognosis in septic patients. The correlation between the volume effect in sepsis therapy and the kinetics of serum albumin is unclear.</div></div><div><h3>Aim</h3><div>To investigate the relationship between serum albumin and fluid bolus in relation to its prognostic role in septic patients.</div></div><div><h3>Methods</h3><div>A single-center prospective observational study conducted from September 2022 to February 2024. All patients with sepsis admitted from the Emergency Department to the Intermediate Medical Care Unit (IMCU) were considered. Post-fluid bolus serum albumin was obtained after fluid bolus. The albumin value was correlated with the volume effect of the fluid bolus, and multivariate models were performed to evaluate its potential independent effect on 30-day mortality.</div></div><div><h3>Results</h3><div>179 patients were enrolled. Pre-fluid bolus serum albumin was 2.55 g/dL (SD 0.51) with a multivariate OR for 30-day mortality of 1.170 (95 % CI 1.055–1.297, <em>p</em> = 0.003). After the fluid bolus, which resulted in a fluid balance percentage of +23.1 % (SD 7.1) and a mean Fractional Plasma Dilution of -0.48 (SD 0.18), albumin showed a mean decrease of -0.28 g/dL (SD 0.28) with a multivariate OR for 30-day mortality of 1.198 (95 % CI 1.065–1.348, <em>p</em> = 0.003). Post-fluid bolus albumin was negatively correlated with cumulative fluid balance and hemodilution.</div></div><div><h3>Conclusions</h3><div>The volume effect of fluid bolus is correlated with a decrease in serum albumin, and low albumin levels are associated with a high risk of mortality.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 451-459"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142788291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk prediction model for adult intolerance to enteral nutrition feeding – A literature review","authors":"Hui Yang BSN ,&nbsp;Jinmei Liu MSN ,&nbsp;Hongyan Sun MSN","doi":"10.1016/j.amjms.2024.11.012","DOIUrl":"10.1016/j.amjms.2024.11.012","url":null,"abstract":"<div><div>Enteral nutrition is an important clinical nutritional supplementation method, especially for adult patients who are unable to eat normally or require additional nutritional support. However, many patients experience intolerance to enteral nutrition, such as delayed gastric emptying, bloating, and diarrhea, which not only affect the patient's nutritional status but also increase the risk of medical complications. In recent years, medical researchers have been dedicated to identifying and analyzing various factors that contribute to enteral nutrition intolerance, including the patient's disease status, nutritional formula, feeding method, and rate. In addition, research is also exploring the establishment of risk prediction models to more accurately predict which patients may develop enteral nutrition intolerance. These models typically combine clinical parameters, biomarkers, and patient individual characteristics, aiming to assist clinicians in better planning and adjusting nutritional treatment plans, thereby reducing the occurrence of intolerance events. This review summarizes the research progress on enteral nutrition intolerance in adult patients, with a focus on the latest developments in intolerance factors and risk prediction models, providing valuable guidance for clinical practice and helping improve patients' nutritional status and overall health.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 427-433"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142776086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miRNA-105–5p regulates the histone deacetylase HDAC2 through FOXG1 to affect the malignant biological behavior of triple-negative breast cancer cells","authors":"Li Wang MD ,&nbsp;Zaoxiu Hu MD ,&nbsp;Han Bai master ,&nbsp;Li Chang MD ,&nbsp;Ceshi Chen MD ,&nbsp;Wenhui Li MD","doi":"10.1016/j.amjms.2024.09.009","DOIUrl":"10.1016/j.amjms.2024.09.009","url":null,"abstract":"<div><h3>Background</h3><div>Triple-negative breast cancer (TNBC) is a specific subtype of breast cancer (BC). Some potential molecular targets have been identified, and miR-105–5p was found to be abnormally expressed in TNBC tissues.</div></div><div><h3>Objective</h3><div>The objective of this study was to probe the effect of miR-105–5p on TNBC via FOXG1/HDAC2-mediated acetylation.</div></div><div><h3>Methods</h3><div>An animal model of TNBC was established by injecting BC cells into the axillary area of nude mice. The levels of miR-105–5p, FOXG1, HDAC2, Bcl-2, Bax, and Ki67 were detected via RT‒qPCR, Western blotting and immunohistochemistry. Flow cytometry, CCK-8, Transwell and colony formation assays were used to measure apoptosis, proliferation and migration, respectively. Total histone acetylation levels were measured by ELISA. The binding of FOXG1 to HDAC2 was detected by co-immunoprecipitation. The binding relationship between miR-105–5p and FOXG1 was verified using a dual-luciferase reporter gene assay.</div></div><div><h3>Results</h3><div>In this study, miR-105–5p and HDAC2 were highly expressed in the MDA-MB-231 and BT-549 BC cell lines, whereas FOXG1 was expressed at low levels. The inhibition of miR-105–5p inhibited the proliferation and migration of MDA-MB-231 and BT-549 cells and promoted their apoptosis. Bioinformatics analysis revealed that miR-105–5p and FOXG1 had a negative targeting regulatory relationship. FOXG1 overexpression had a similar effect on cancer cells as the inhibition of miR-105–5p. Moreover, experiments revealed that FOXG1 and HDAC2 could bind to each other and that HDAC2 overexpression or treatment with the histone acetyltransferase inhibitor Garcinol weakened the effect of FOXG1 overexpression. In addition, FOXG1 knockdown inhibited the effect of the miR-105–5p inhibitor, while Garcinol treatment further enhanced the effect of FOXG1 knockdown, inhibited histone acetylation, promoted the proliferation and migration of cancer cells, and inhibited apoptosis. Moreover, the in vivo results confirmed the in vitro results.</div></div><div><h3>Conclusion</h3><div>miR-105–5p promotes HDAC2 expression by reducing FOXG1, inhibits histone acetylation, and aggravates the malignant biological behavior of TNBC cells.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 513-523"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142309552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"General and central obesity were significantly correlated with blood lead level in non-smoking, general population aged 30–50, without hypertension","authors":"In Cheol Hwang MD, PhD. ,&nbsp;Kyoung Kon Kim MD, PhD. ,&nbsp;Jeong Heon Kim MD. ,&nbsp;Kyu Rae Lee MD, PhD.","doi":"10.1016/j.amjms.2024.11.007","DOIUrl":"10.1016/j.amjms.2024.11.007","url":null,"abstract":"<div><h3>Introduction</h3><div>To investigate the association between obesity and blood lead level (BLL) in the general population after controlled for menopause, blood pressure, calcium, and smoking; we assessed the relationship between BMI, WC (Waist Circumference), and blood lead levels in the non-smoking middle-aged subjects without hypertension among 2018 KNHANES. All data were recategorized into S1 (BMI&lt;25 kg/m² &amp; WC&lt;90 cm), S2 (intermediate), and S3 (BMI&gt;25 kg/m² &amp; WC&gt;90 cm).</div></div><div><h3>Methods</h3><div>We made the log transformation of blood lead levels to bring them closer to a normal distribution. Logarithmic transformed BLL was closely related to BMI (<em>p</em>=.010) and WC (<em>p</em>=.020) after adjusting for sociodemographic, energy, working factors, and cardiometabolic variables. The prevalence of ratios of S3, S2, and S1 was comparable according to the quarterly group of BLL.</div></div><div><h3>Results and Conclusions</h3><div>Blood lead levels might increase oxidative stress on triglycerides and low high-density lipoprotein (HDL)-cholesterol; consequently, lead exposure might form peroxynitrite, a reactive oxygen substrate (ROS) susceptible to destroying lipids. Consequently, obesity was significantly correlated with logarithmic blood lead levels irrespective of sociodemographic, energy, working, and cardiometabolic factors in the non-smoking middle-aged population without hypertension. Further controlled clinical trials would be considered.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 467-471"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142717794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coronary embolism and acute limb ischemia without pre-existing atrial fibrillation: Hunt for the hidden thrombus","authors":"Misha Aftab Khan MD,&nbsp;Noor Alsammarraie MD,&nbsp;Alycia Christina Bellino DO,&nbsp;Yash Bharatkumar Patel MD,&nbsp;Karldon Iwuchukwu Nwaezeapu MD","doi":"10.1016/j.amjms.2024.10.006","DOIUrl":"10.1016/j.amjms.2024.10.006","url":null,"abstract":"<div><div>Coronary embolism (CE) is an infrequent etiology of myocardial infarction secondary to embolization of occlusive thrombi within the coronary arteries, typically arising in patients with pre-existing atrial fibrillation. Clinical presentation is similar to atherosclerotic myocardial infarction, however the condition is likely underrecognized. The simultaneous presence of other embolic manifestations may assist with diagnosis, although definitive therapy, medical or interventional, remains inconclusive. We aim to lower the threshold for clinical suspicion in the appropriate setting and promote assessment of predisposing embolic conditions once a tentative diagnosis of CE is established. In addition, we intend to highlight the need for focused refinement of the existing diagnostic criteria and further optimization of management guidelines for CE.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 498-502"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Co-administration of albumin and loop diuretic may be associated with reduced mortality in septic shock patients: A retrospective study with PSM analysis","authors":"Shui-qing Gui M.D.,&nbsp;Xi-si He M.D.,&nbsp;Zhi-ye Zou M.D.","doi":"10.1016/j.amjms.2024.11.010","DOIUrl":"10.1016/j.amjms.2024.11.010","url":null,"abstract":"<div><h3>Background</h3><div>This study aimed to investigate the potential impact of administering albumin and loop diuretics together on in-hospital mortality in septic shock patients.</div></div><div><h3>Methods</h3><div>Data from the MIMIC-IV database was used for a retrospective cohort study analyzing 3,298 adult septic shock patients. The Cox proportional hazards model and propensity score matching (PSM) were utilized to assess the relationship between loop diuretic administration and in-hospital mortality.</div></div><div><h3>Results</h3><div>The study found that septic shock patients who received albumin in combination with loop diuretic had a significantly lower in-hospital mortality rate compared to those who received albumin alone (19.4 % vs 33.1 %, <em>p</em> &lt; 0.001). Administering diuretics after albumin infusion was associated with lower mortality rates. Optimal furosemide dosages of 10 to 40 mg daily were linked to the lowest mortality rates.</div></div><div><h3>Conclusion</h3><div>Co-administering albumin and loop diuretics in septic shock patients receiving high-dose crystalloids may be associated with reduced in-hospital mortality. Further investigation through a prospective randomized controlled trial is recommended to validate these findings.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 443-450"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nodular scleroderma: Characterization of a distinct clinical phenotype","authors":"Anupam Somashekar MD ,&nbsp;Stephen Squires MD ,&nbsp;Anthony V Benedetto DO ,&nbsp;Thomas D. Griffin MD ,&nbsp;Sergio A Jimenez MD ,&nbsp;Fabian A Mendoza MD","doi":"10.1016/j.amjms.2024.09.011","DOIUrl":"10.1016/j.amjms.2024.09.011","url":null,"abstract":"<div><div>Nodular scleroderma is a rare variant of systemic sclerosis (SSc) characterized by fleshy, indurated nodules commonly distributed over the upper and lower extremities and in the trunk. Most scientific publications of the nodular and keloid variants of scleroderma use the terms interchangeably. However, nodular scleroderma has been recently differentiated from keloid forms. Although few cases of isolated local involvement have been reported, nodular scleroderma more commonly presents in conjunction with other manifestations of SSc. We performed a review of all cases of nodular scleroderma reported in the literature to characterize their clinical features.</div><div>This review indicated that Nodular Scleroderma is usually associated with a Diffuse SSc phenotype and develops during the early progressive skin involvement. Patients with the Nodular Scleroderma phenotype display antinuclear antibodies with speckled or nucleolar patterns, a low frequency of positive SSc-specific antibodies, and typical SSc multiorgan involvement. However, a very low frequency of pulmonary hypertension was found in these patients. Although immunosuppressive or antifibrotic treatment may improve skin thickening and organ involvement, the characteristic nodules are refractory to treatment with these agents. This is the first review, to our knowledge, characterizing the nodular phenotype in patients with SSc.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 4","pages":"Pages 423-426"},"PeriodicalIF":2.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142335556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uncontrolled anger: A fuel for cardiovascular disease?","authors":"Eeshal Fatima MBBS ,&nbsp;Um e Habibah MBBS ,&nbsp;Zain Ali Nadeem MBBS","doi":"10.1016/j.amjms.2024.09.005","DOIUrl":"10.1016/j.amjms.2024.09.005","url":null,"abstract":"","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"369 3","pages":"Pages 419-420"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142305283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}