The Effects of Vitamin D Supplementation on C-Reactive Protein and Systolic and Diastolic Blood Pressure in Postmenopausal Women: A Meta-Analysis and Systematic Review of Randomized Controlled Trials.

BACKGROUND: An inverse relationship between vitamin D supplementation and C-reactive protein (CRP) and hypertension has been reported, mostly through observational data. This inverse relationship, however, has not been confirmed in randomized controlled trials (RCTs). A meta-analysis of RCTs is needed to provide more robust evidence. OBJECTIVE: This systematic review of RCTs was conducted to assess the effect of vitamin D supplementation on CRP, systolic blood pressure (SBP), and diastolic blood pressure (DBP) in postmenopausal women. METHODS: Four databases (PubMed, Web of Science, Embase, and Scopus) were systemically searched to identify relevant RCTs published in international scientific journals up to January 2023. Changes from baseline and SDs of CRP, SBP, and DBP were compared between postmenopausal women who received vitamin D supplementation and those who did not (controls). These parameters were applied to compute the overall effect sizes using the random-effects model. Data were summarized as mean difference (MD) with 95% CI. Heterogeneity among arms was scrutinized using the Cochrane's Q test and I2 statistic. Publication bias was judged by means of funnel plots and Egger's test. RESULTS: Seven studies with 6 arms on CRP, 6 arms on SBP, and 6 arms on DBP were included in the meta-analysis. Combined effect sizes suggested a significant effect of vitamin D supplementation on CRP (MD = -0.65 mg/L; 95% CI -0.93 to -0.37 mg/L; P < .001). In addition, CRP concentrations were significantly reduced after vitamin D supplementation in studies with a duration of more than 3 months (MD = -0.91 mg/L; 95% CI -1.37 to -0.45 mg/L; P < .001) and studies involving doses of ≤1,000 IU/d (MD = -2.10 mg/L; 95% CI -2.51 to -1.68 mg/L; P < .001). Vitamin D supplementation did not reduce SBP significantly (MD = -1.06 mm Hg; 95% CI -2.43 to 0.30 mm Hg; P = .127) and DBP (MD = 0.003 mm Hg; 95% CI -0.86 to 0.86 mm Hg; P = .994) levels compared with control groups. CONCLUSIONS: This meta-analysis concluded that vitamin D supplementation is associated with reduced CRP concentrations among postmenopausal women.

The effects of bupropion alone and combined with naltrexone on blood pressure and CRP concentration: A systematic review and meta-regression analysis of randomized controlled trials.

BACKGROUND: Considering the conflicting effects of bupropion on parameters related to cardiovascular system including blood pressure and inflammation, in this meta-analysis study, we investigated the effects of this drug alone or in combination with naltrexone on systolic (SBP) and diastolic blood pressure (DBP) and C-reactive protein (CRP). METHODS: Scopus, PubMed/Medline, Web of Science and Embase databases were searched using standard keywords to identify all controlled trials investigating effects of bupropion alone and combined with naltrexone on the BP and CRP. Pooled weighted mean difference and 95% confidence intervals (CIs) were achieved by random-effects model analysis for the best estimation of outcomes. RESULTS: The pooled findings showed that that bupropion alone or in combination with naltrexone would significantly increase SBP (weighted mean difference (WMD): 1.34 mmHg, 95% CI: 0.38-2.29) and DBP (WMD: 0.93 mmHg, 95% CI 0.88-0.99) as well as decrease CRP (WMD: -0.89 mg/L, 95% CI -1.09 to -0.70). The findings of the subgroup also show the greater effect of bupropion on blood pressure (SBP and DBP) increase in a dose greater than 360 mg and a duration of intervention less equal to 26 weeks. In addition, the subgroup analysis showed that changes in SBP after receiving bupropion together with naltrexone were more compared to bupropion alone. CONCLUSIONS: The addition of combination therapies such as bupropion and naltrexone can significantly improve CRP levels. However, its effect on blood pressure requires proper management of this drug.

Effect of Adopting Low Calories on Patients' Vital Signs in The Nutritional Support of Critically Ill Patients in the ICU: A Systematic Review and Network Meta-Analysis.

Background: Feeding critically ill persons in Intensive Care Units (ICUs) is challenging as the nutritional substances pose severe health outcomes or can improve their well-being and length of stay (LOS) in the hospital. Our main objective is to investigate the effects of adopting low caloric intake among patients with vital signs in the nutritional support of critically ill patients in ICUs, focusing on reducing mortality rates and length of stay (LOS) in hospitals. Method: The initial literature search was performed in PubMed, the Cochrane Library of Trials, and MEDLINE. The network meta-analysis was performed per the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Two independent reviewers were assigned data selection and extraction roles. Our study mainly included randomised controlled trials (RCTs) whose titles and abstracts were screened, after which duplicates were excluded. The remaining eligible studies were subjected to full-text analysis to identify data related to the topic of the present study. Analyses were performed using the Cochrane Risk of Bias tool, R software and MS Excel. Results: Twenty-two studies (involving 9 539 participants) met the inclusion criteria and were subjected to the network meta-analysis. In mortality rates, the greatest rank observed corresponded to a reduction of 71%. The regression of the effects of low caloric intake explained a 5.29% variation in LOS. A weak positive correlation was found between LOS and low caloric intake among critically ill patients in ICUs. Thus, Low caloric intake decreased mortality rates and lowered LOS. Conclusions: Our study found that low caloric intake reduces mortality rate and hospital LOS among critically ill patients. Secondary outcomes include nosocomial infection, clinical outcomes, functions, digestive infections, improved quality of life, resulting survival rates, ventilator days, bacteremia, blood glucose levels, diarrhoea, and tube replacement. Our findings have clinical implications for clinicians in the ICU, who should consider developing individualised nutritional plans for critically ill patients. Moreover, regular monitoring of nutritional intake and response is crucial. Healthcare providers should closely monitor patients' nutritional status, vital signs, and clinical outcomes.

Effect of Early Low-Calorie Enteral Nutrition Support in Critically Ill Patients: A Systematic Review and Meta-analysis.

Objective: The purpose of this research was to rigorously assess the impact of early low-fever enteral feeding supplementation in critically sick patients. Methods: PubMed, Embase, Web of Science, Cochrane Central Register of Controlled Trials, Cumulative Index to Nursing and Allied Health Literature, and Physiotherapy Evidence Database were searched for randomized controlled trials related to enteral nutrition support of critically ill patients (retrieval time was limited to June 30, 2021); data were extracted after screening the literature, and the quality of meta-analysis was evaluated. Results: When compared to adequate caloric enteral nutrition support, early low caloric enteral nutrition support reduces the incidence of intolerance to nutrition support (MD = 0.60, 95 percent CI: -0.18 to 1.39, P = 0.13) and the insulin dose during enteral nutrition support (MD = -17.21, 95 percent CI: -19.91 to -14.51, P = 0.00001). However, it had no effect on intensive care unit (ICU) treatment duration (MD = 0.60, 95 percent CI: -0.18 to 1.39, P = 0.13), in-hospital mortality (MD = 0.60, 95 percent CI: -0.18 to 1.39, P = 0.13), or infection incidence (OR = 1.00, 95 percent CI: 0.85, 1.19, P = 0.98). Conclusion: When compared to sufficient caloric enteral nutrition support, early low-calorie enteral nutrition support lowers the risk of severe illness. The rate of intolerance to nutritional assistance and the decrease in insulin dosage supplied had no effect on the length of ICU therapy, patient death, or infection incidence.

Characterization and Prevalence of Campylobacter spp. From Broiler Chicken Rearing Period to the Slaughtering Process in Eastern China.

Campylobacter is one of the most important foodborne pathogens worldwide, and poultry is regarded as the main reservoir of Campylobacter. The contamination of Campylobacter in broiler chickens at the farm level is closely related to the transmission of Campylobacter in the poultry production chain. This study identified 464 Campylobacter isolates from 1,534 samples from broiler rearing period and slaughtering process including 233 Campylobacter jejuni isolates and 231 Campylobacter coli isolates. We have observed a dynamic distribution of Campylobacter during broiler chicken production, that 66.3% of Campylobacter isolates were C. jejuni during broiler rearing period, while C. coli occupied 60.4% of Campylobacter isolates during the broiler slaughtering process. A tag-label method allowed us to track the dynamic of Campylobacter in each broiler chicken from 31-day age at rearing to the partition step in the slaughterhouse. At the 31-day during rearing, 150 broiler chicken were labeled, and was tracked for Campylobacter positive from rearing period to slaughtering process. Among the labeled broiler, 11 of the tracking broiler samples were able to detect Campylobacter from rearing period to slaughtering. All Campylobacter isolates from the 11 tracking samples were sequenced and analyzed. C. jejuni isolates were divided into four STs and C. coli isolates were divided into six STs. Isolates with identical core genome were observed from the same tag-labeled samples at different stages indicating a vertical transmission of Campylobacter in the early broiler meat production. Meanwhile, the core genome analysis elucidated the cross-contamination of Campylobacter during the rearing period and the slaughtering process. The virulotyping analysis revealed that all C. jejuni isolates shared the same virulotypes, while C. coli isolates were divided into three different virulotypes. The antimicrobial resistance gene analysis demonstrated that all Campylobacter isolates contained at least two antibiotic resistance genes (ARGs), and the ARG profiles were well-corresponding to each ST type. Our study observed a high prevalence of Campylobacter during the early chicken meat production, and further studies will be needed to investigate the diversity and transmission of Campylobacter in the poultry production chain.

Insights into the impact of flhF inactivation on Campylobacter jejuni colonization of chick and mice gut.

BACKGROUND: Campylobacter jejuni (C. jejuni) is a leading cause of foodborne gastroenteritis worldwide. This bacterium lacks many of the classical virulence factors, and flagellum-associated persistent colonization has been shown to be crucial for its pathogenesis. The flagellum plays a multifunctional role in C. jejuni pathogenesis, and different flagellar elements make diverse contributions. The flhF gene encodes the flagellar biosynthesis regulator, which is important for flagellar biosynthesis. In this study, the influence of flhF on C. jejuni colonization was systematically studied, and the possible mechanisms were also analyzed. RESULTS: The flhF gene has a significant influence on C. jejuni colonization, and its inactivation resulted in severe defects in the commensal colonization of chicks, with approximately 104- to 107-fold reductions (for NCTC 11168 and a C. jejuni isolate respectively) observed in the bacterial caecal loads. Similar effects were observed in mice where the flhF mutant strain completely lost the ability to continuously colonize mice, which cleared the isolate at 7 days post inoculation. Characterization of the phenotypic properties of C. jejuni that influence colonization showed that the adhesion and invasion abilities of the C. jejuni flhF mutant were reduced to approximately 52 and 27% of that of the wild-type strain, respectively. The autoagglutination and biofilm-formation abilities of the flhF mutant strain were also significantly decreased. Further genetic investigation revealed that flhF is continuously upregulated during the infection process, which indicates a close association of this gene with C. jejuni pathogenesis. The transcription of some other infection-related genes that are not directly involved in flagellar assembly were also influenced by its inactivation, with the flagellar coexpressed determinants (Feds) being apparently affected. CONCLUSIONS: Inactivation of flhF has a significant influence on C. jejuni colonization in both birds and mammals. This defect may be caused by the decreased adhesion, invasion, autoagglutination and biofilm-formation abilities of the flhF mutant strain, as well as the influence on the transcription of other infection related genes, which provides insights into this virulence factor and the flagellum mediated co-regulation of C. jejuni pathogenesis.

[microRNA-34a participates in lipopolysaccharide mediated sepsis related renal function impairment via Kruppel-like factor 4].

OBJECTIVE: To investigate whether microRNA-34a (miR-34a) participates in lipopolysaccharide (LPS) mediated sepsis related renal function impairment via Kruppel-like factor 4 (KLF4). METHODS: Thirty healthy male Sprague-Dawley (SD) rats, weighing 180-200 g, were randomly divided into two groups: control group and model group, with 15 rats in each group. The SD rats from model group were injected with LPS 7.5 mg/kg to induce sepsis related renal function impairment model, the SD rats from control group were injected with normal saline. The serum creatinine concentration (SCr) and blood urine nitrogen (BUN) content was detected by multifunction biochemical analyzer; the morphological changes of renal tissue were observed by hematoxylin and eosin stain (HE) staining; the expression of miR-34a and KLF4 gene in plasma and renal tissue were detected by real-time quantitative reverse transcriptase polymerase chain reaction (qRT-PCR); the protein expression of KLF4 in renal tissue was detected by Western Blot; the target gene of miR-34a was verified by double luciferase reporter gene analysis. RESULTS: Compared with control group, inflammatory cell infiltration in renal tissue was increased in model group, the SCr and BUN were significantly increased [SCr (µmol/L): 142.5±10.6 vs. 46.4±5.6, BUN (mmol/L): 31.6±6.2 vs. 8.5±1.2, both P < 0.01], the gene expression of miR-34 in plasma and renal tissue were significantly increased (2-ΔΔCt: 2.26±0.11 vs. 1.14±0.05 in plasma, 4.23±0.12 vs. 1.12±0.04 in renal tissue, both P < 0.01), the gene and protein expressions of KLF4 were significantly decreased [KLF4 gene (2-ΔΔCt): 0.52±0.03 vs. 1.21±0.06, KLF4 protein (A value): 0.72±0.03 vs. 1.05±0.04, both P < 0.01], which indicated that kidney injury occurred in rats. Pearson correlation analysis showed that plasma miR-34a was positively correlated with SCr and BUN (r value were 0.678, 0.721, respectively, both P < 0.05). Double luciferase reporter assay confirmed that KLF4 was the target gene of miR-34a. CONCLUSIONS: The miR-34a participates in LPS mediated sepsis related renal function impairment via KLF4.