Endocr Pract. 2024 Mar 22:S1530-891X(24)00090-9. doi: 10.1016/j.eprac.2024.03.007. Online ahead of print.
NO ABSTRACT
PMID:38522824 | DOI:10.1016/j.eprac.2024.03.007
Endocr Pract. 2024 Mar 22:S1530-891X(24)00090-9. doi: 10.1016/j.eprac.2024.03.007. Online ahead of print.
NO ABSTRACT
PMID:38522824 | DOI:10.1016/j.eprac.2024.03.007
J Infect Chemother. 2024 Mar 22:S1341-321X(24)00083-7. doi: 10.1016/j.jiac.2024.03.008. Online ahead of print.
ABSTRACT
BACKGROUND: Time-dependent changes in cell populations during acute bacterial infections remain unclear. We assessed time-dependent changes in fluorescent light intensity of the neutrophil area (NE-SFL) and fluorescent light distribution width index of the neutrophil area (NE-WY) and their association with sepsis and bacteremia.
METHODS: Patients with acute bacterial infections were enrolled in this prospective, observational cohort study. Blood samples were collected from all patients at the onset of bacterial infections (day 0) and on days 1 and 3. Microbiological evaluation included the examination of blood bacterial load using PCR. Cell population data were assessed using an automated hematology analyzer (Sysmex series XN-2000).
RESULTS: Forty-three participants with acute bacterial infections were enrolled in the study. Twenty-five participants developed definite sepsis. All the participants improved after the onset of infection. NE-WY levels showed significant time-dependent changes in participants with sepsis, peaking on day 0 and significantly decreasing until day 3, whereas these changes were not statistically significant for NE-SFL. A significant correlation with the Sequential Organ Failure Assessment score was observed with NE-WY and NE-SFL in the entire cohort on days 0 and 1. However, only NE-WY showed a significant correlation with blood bacterial load on days 0 and 1.
CONCLUSION: This study demonstrated that NE-WY elevation in sepsis peaked earlier than NE-SFL, which may partly reflect the early bacterial invasion into circulation. These findings advocate caution in interpreting cell population data values as sepsis biomarkers and propose the potential of NE-WY as a therapeutic indicator.
PMID:38522794 | DOI:10.1016/j.jiac.2024.03.008
World Neurosurg. 2024 Mar 22:S1878-8750(24)00461-3. doi: 10.1016/j.wneu.2024.03.092. Online ahead of print.
ABSTRACT
OBJECTIVE: The process surrounding application to the national residency matching program changed drastically because of COVID. Virtual interviews, pre-interview zoom socials, and limitations on sub-internships are major changes that applicants worldwide have had to overcome. The available literature does not reflect the impact of major changes to the interview process. Here, we examine the neurosurgery resident cohort from 2021-2023 to investigate differences between United States medical schools pre- and post-COVID.
METHODS: A database was constructed reporting the number of students matched to neurosurgery for U.S. medical schools (MD and DO) from 2021-2023. Percentage of total graduates matched to neurosurgery was calculated and institutions were ranked by this metric. This rank was compared to the rank reported by Antar et al in 2021. Variables were compared across the pre- and post-COVID cohorts.
RESULTS: Case Western, Johns Hopkins, Mayo Clinic, Vanderbilt, University of Illinois and University of California San Francisco produced the most neurosurgical residents as a percentage of total graduates. There was a statistically significant difference in the post-COVID cohort between medical schools with a home program vs those without. For the top 20 ranked U.S. News medical schools, there was a statistically insignificant increase in the number of graduates matched to neurosurgery CONCLUSIONS: With the data provided, there have not been many significant changes in which medical schools produce the most neurosurgery residents since COVID changes were implemented. The playing field has remained relatively the same in the setting of major changes that were made.
PMID:38522786 | DOI:10.1016/j.wneu.2024.03.092
J Nutr. 2024 Mar 22:S0022-3166(24)00164-0. doi: 10.1016/j.tjnut.2024.03.015. Online ahead of print.
ABSTRACT
There is an increasing body of evidence supporting a link between low intakes of omega-3 long chain polyunsaturated fatty acids (LCPUFA) and numerous diseases and health conditions. However, few people are achieving the levels of fish/seafood or eicosapentaenoic acid and docosahexaenoic acid intake recommended in national and international guidelines. Knowledge of a person’s omega-3 LCPUFA status will benefit the interpretation of research results and could be expected to lead to an increased effort to increase intake. Dietary intake survey methods are often used as a surrogate for measuring omega-3 PUFA tissue status and its impact on health and functional outcomes. However, since individuals vary widely in their ability to digest and absorb omega-3 PUFA, analytical testing of biological samples is desirable to accurately evaluate omega-3 PUFA status. Adipose tissue is the reference biospecimen for measuring tissue fatty acids, but less invasive methods, such as measurements in whole blood or its components (e.g., plasma, serum, red blood cell membranes) or breast milk are often used. Numerous commercial laboratories provide fatty acid testing of blood and breast milk samples by different methods and present their results in a variety of reports such as a full fatty acid profile, omega-3 and omega-6 fatty acid profiles, fatty acid ratios, as well as the Omega-3 Index, the Holman Omega-3 Test, OmegaScore™, and OmegaCheck®, among others. This narrative review provides information about the different ways to measure omega-3 LCPUFA status (including both dietary assessments and selected commercially available analytical tests of blood and breast milk samples) and discusses evidence linking increased omega-3 LCPUFA intake or status to improved health, focusing on cardiovascular, neurological, pregnancy, and eye health, in support of recommendations to increase omega-3 LCPUFA intake and testing.
PMID:38522783 | DOI:10.1016/j.tjnut.2024.03.015
Parasitol Int. 2024 Mar 22:102889. doi: 10.1016/j.parint.2024.102889. Online ahead of print.
ABSTRACT
There are various diagnostic techniques available for chronic fasciolosis in ruminants. However, many of them exhibit low specificity and sensitivity, making them impractical for field use and in low-resource laboratories. The present study evaluates the usefulness of the Natural Sedimentation technique in diagnosing chronic fasciolosis in three domestic species conducted at the Laboratorio de Parasitología y Enfermedades Parasitarias, Facultad de Ciencias Veterinas, Universidad Nacional de Cajamarca. Fecal samples were collected from n = 323 cattle, n = 362 sheep, and n = 231 swine for Fasciola hepatica fecal egg counts. The visualization of adult parasites in animal livers post-mortem was considered the gold standard. Additionally, the sensitivity of the technique was evaluated using five different amounts of feces. In cattle, a sensitivity of 0.93 ± 0.03, specificity of 0.91 ± 0.06, positive predictive value of 0.96 ± 0.03, and negative predictive value of 0.86 ± 0.07 were obtained. In sheep, a sensitivity of 0.79 ± 0.05, specificity of 0.83 ± 0.07, positive predictive value of 0.90 ± 0.04, and negative predictive value of 0.66 ± 0.08 were observed. In swine, a sensitivity of 0.92 ± 0.06, specificity of 1.00 ± 0.00, positive predictive value of 1.00 ± 0.00, and negative predictive value of 0.96 ± 0.03 were found. There was no statistical difference in egg counts when using 1, 2, 3, 4, and 5 g of feces (p = 0.907). Furthermore, 1 to 688 fecal eggs of F. hepatica were counted in 1 g of feces. The Natural Sedimentation technique has both qualitative and quantitative applications with satisfactory results when using 1 g of feces in the diagnosis of chronic fasciolosis in domestic animals. Due to its simplicity, it can be implemented in field conditions and low-resource laboratories.
PMID:38522780 | DOI:10.1016/j.parint.2024.102889
J Shoulder Elbow Surg. 2024 Mar 22:S1058-2746(24)00215-5. doi: 10.1016/j.jse.2024.01.054. Online ahead of print.
ABSTRACT
BACKGROUND: The purpose of this study is to systematically review the evidence in the literature to ascertain the functional outcomes, recurrence rates, and subsequent revision rates following type V superior labrum anterior-posterior (SLAP) repair.
METHODS: Two independent reviewers performed a literature search based on PRISMA guidelines, utilizing the EMBASE, MEDLINE, and The Cochrane Library Databases. Studies were included if they had clinical outcomes on the patients undergoing type V SLAP repair. Statistical analysis was performed using SPSS (IBM, Armonk, NY, USA). A P value of < 0.05 was considered to be statistically significant.
RESULTS: Our review found 13 studies, including 451 shoulders meeting our inclusion criteria. The majority of patients were male (89.3%), with an average age of 25.9 years (range 15-58) and a mean follow-up of 53.8 months. The Rowe score was the most utilized functional outcome score, with a weighted mean of 88.5. Additionally, the mean Constant score was 91.0, the mean ASES score was 88.3, the mean SSV score was 85.5%, and the mean VAS pain score was 1.2. The overall rate of return to play was 84.8%, with 80.2% returning to the same level of play. The overall reoperation rate was 6.1%, with a recurrent dislocation rate of 8.2%. In the studies comparing type V SLAP and isolated Bankart repair, there were statistically insignificant differences in VAS pain scores (MD; 0.15, 95% CI, -0.13 to 0.44, I2 = 0%, p = 0.29) and recurrence rates (RR; 1.38, 95% CI, 0.88 to 2.15, I2 = 0%, p = 0.16).
CONCLUSION: Arthroscopic repair of type V SLAP tears results in excellent functional outcomes, with high return to play rates in athletes. There are low rates of reoperations and recurrent dislocations. Additionally, in comparison to an isolated Bankart repair, SLAP repair does not increase recurrence rates or postoperative pain.
PMID:38522776 | DOI:10.1016/j.jse.2024.01.054
J Heart Lung Transplant. 2024 Mar 22:S1053-2498(24)01536-5. doi: 10.1016/j.healun.2024.03.016. Online ahead of print.
ABSTRACT
BACKGROUND: Identification of differences in mortality risk between female and male heart transplant recipients may prompt sex-specific management strategies. Because worldwide, males of all ages have higher absolute mortality rates than females, we aimed to compare the excess risk of mortality (risk above the general population) in female versus male heart transplant recipients.
METHODS: We used relative survival models conducted separately in SRTR and CTS cohorts from 1988-2019, and subsequently combined using two-stage individual patient data meta-analysis, to compare the excess risk of mortality in female versus male first heart transplant recipients, accounting for the modifying effects of donor sex and recipient current age.
RESULTS: We analyzed 108,918 patients. When the donor was male, female recipients 0-12 years (Relative excess risk (RER) 1.13, 95% CI 1.00-1.26), 13-44 years (RER 1.17, 95% CI 1.10-1.25), and ≥45 years (RER 1.14, 95% CI 1.02-1.27) showed higher excess mortality risks than male recipients of the same age. When the donor was female, only female recipients 13-44 years showed higher excess risks of mortality than males (RER 1.09, 95% CI 1.00-1.20), though not significantly (p= 0.05).
CONCLUSIONS: In the setting of a male donor, female recipients of all ages had significantly higher excess mortality than males. When the donor was female, female recipients of reproductive age had higher excess risks of mortality than male recipients of the same age, though this was not statistically significant. Further investigation is required to determine the reasons underlying these differences.
PMID:38522764 | DOI:10.1016/j.healun.2024.03.016
Pharmacol Res. 2024 Mar 22:107142. doi: 10.1016/j.phrs.2024.107142. Online ahead of print.
ABSTRACT
ZLDI-8 is an A disintegrin and metalloproteinase domain 17 (ADAM17) inhibitor that suppresses the shedding of Notch1 to the Notch1 intracellular domain (NICD). In previous studies, we found that ZLDI-8 was able to sensitize HCC to sorafenib, but the mechanism of action remains unclear. The sensitizing effects of ZLDI-8 were tested both in vitro and in vivo. EMT-related factors, sorafenib sensitivity-related proteins and ECM-related gene expression were assessed using immunohistochemistry, RTPCR and Western blotting. Knockdown assays were conducted to determine the relationship between the Notch and Integrin pathways. CoIP assays, nuclear and cytoplasmic fractionation and immunofluorescence colocalization were applied to explore the interaction between the Notch and Integrin pathways. Appropriate statistical analysis methods were used to assess the significance of the experimental results and to ensure the scientific validity and reliability of the experimental design. We found that ECM- and EMT-related proteins were downregulated after ZLDI-8 treatment (P<0.05). ZLDI-8 significantly downregulated Integrinβ1 and Integrinβ3 in HCC in vitro and in vivo (P<0.05), possibly through Foxc2-dependent regulation. Mechanistically, interfering with the expression of both Integrin-linked kinase (ILK) and the NICD may downregulate the expression of proteins targeted by sorafenib, thereby sensitizing cells to sorafenib. The retroregulation of Integrinβ by ILK may occur through the interaction between the NICD and ILK and may be the result of the translocation of the complexus. Our study indicates that blocking the Notch pathway may affect Integrinβ through crosstalk between the Notch1 and Integrinβ/ILK signaling pathways, thus providing a potential therapeutic strategy for HCC.
PMID:38522759 | DOI:10.1016/j.phrs.2024.107142
J Stroke Cerebrovasc Dis. 2024 Mar 22:107686. doi: 10.1016/j.jstrokecerebrovasdis.2024.107686. Online ahead of print.
ABSTRACT
OBJECTIVE: Cross-sectional and cohort studies have found insufficient evidence of a causal relationship between sex hormone-binding globulin and ischemic stroke, only associations. Here, we performed a sex-stratified, bidirectional, two-sample Mendelian randomization analysis to evaluate whether a causal relationship exists between sex hormone-binding globulin and ischemic stroke.
METHODS: Single-nucleotide polymorphisms associated with sex hormone-binding globulin and ischemic stroke were screened from genome-wide association studies summary data as instrumental variables to enable a bidirectional, two-sample Mendelian randomization study design. Inverse-variance weighted analysis was used as the main method to evaluate potential causality, and additional methods, including the weighted median and MR-Egger tests, were used to validate the Mendelian randomization results. Cochran’s Q statistic, MR-Egger intercept test, and Mendelian Randomization-Pleiotropy Residual Sum and Outlier global test were used as sensitivity analysis techniques to assure the reliability of the results. Multivariable analysis was used to show the robustness of the results with key theorized confounders.
RESULTS: Inverse-variance weighted analysis showed that genetically predicted higher serum sex hormone-binding globulin levels were associated with significantly decreased risk of ischemic stroke in males (odds radio = 0.934, 95% confidence interval = 0.885-0.985, P = 0.012) and females (odds radio = 0.924, 95% confidence interval = 0.868-0.983, P = 0.013). In an analysis of ischemic stroke subtypes, genetically predicted higher serum sex hormone-binding globulin levels were also associated with significantly decreased risk of small-vessel occlusion in both males (odds radio = 0.849, 95% confidence interval = 0.759-0.949, P = 0.004) and females (odds radio = 0.829, 95% confidence interval = 0.724-0.949, P = 0.006). The association remained in sensitivity analyses and multivariable analyses. The reverse analysis suggested an association between genetically predicted risk of cardioembolism and increased serum sex hormone-binding globulin in females (Beta = 0.029 nmol/L, Standard Error = 0.010, P = 0.003).
CONCLUSION: Our findings provide new insight into the etiology of ischemic stroke and suggest that modulating serum sex hormone-binding globulin may be a therapeutic strategy to protect against ischemic stroke.
PMID:38522757 | DOI:10.1016/j.jstrokecerebrovasdis.2024.107686
J Stroke Cerebrovasc Dis. 2024 Mar 22:107685. doi: 10.1016/j.jstrokecerebrovasdis.2024.107685. Online ahead of print.
ABSTRACT
OBJECTIVES: Increased plasma gamma-glutamyl transferase (GGT1) has been identified as a robust and independent risk factor for ischemic stroke (IS), but the molecular mechanisms of the enzyme-disease association are unclear. The present study investigated whether polymorphisms in the GGT1 gene contribute to IS susceptibility.
MATERIALS AND METHODS: DNA samples obtained from 1288 unrelated individuals (600 IS patients and 688 controls) were genotyped for common single nucleotide polymorphisms of GGT1 using the MassArray-4 platform.
RESULTS: The rs5751909 polymorphism was significantly associated with decreased risk of ischemic stroke regardless sex and age (Pperm≤0.01, dominant genetic model). The haplotype rs4820599A-rs5760489A-rs5751909A showed strong protection against ischemic stroke (OR 0.53, 95%CI 0.36 – 0.77, Pperm≤0.0001). The protective effect of SNP rs5751909 in the stroke phenotype was successfully replicated in the UK Biobank, SiGN, and ISGC cohorts (P≤0.01). GGT1 polymorphisms showed joint (epistatic) effects on the risk of ischemic stroke, with some known IS-associated GWAS loci (e.g., rs4322086 and rs12646447) investigated in our population. In addition, SNP rs5751909 was found to be strongly associated with a decreased risk of ischemic stroke in non-smokers (OR 0.54 95%CI 0.39-0.75, Pperm=0.0002) and non-alcohol abusers (OR 0.43 95%CI 0.30-0.61, Pperm=2.0 × 10-6), whereas no protective effects of this SNP against disease risk were observed in smokers and alcohol abusers (Pperm<0.05).
CONCLUSIONS: We propose mechanisms underlying the observed associations between GGT1 polymorphisms and ischemic stroke risk. This pilot study is the first to demonstrate that GGT1 is a novel susceptibility gene for ischemic stroke and provides additional evidence of the genetic contribution to impaired redox homeostasis underlying disease pathogenesis.
PMID:38522756 | DOI:10.1016/j.jstrokecerebrovasdis.2024.107685