Associations of novel complete blood count-derived inflammatory markers with psoriasis: a systematic review and meta-analysis.

Psoriasis is an immune-mediated disorder which primarily affects skin and has systemic inflammatory involvement. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), and monocyte-to-lymphocyte ratio (MLR) are novel complete blood count (CBC)-derived markers which can reflect systemic inflammation. This study aimed to systematically investigate the associations of NLR, PLR, SII, and MLR with psoriasis. This study was performed in compliance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses statement. A comprehensive search of Pubmed, Embase, Scopus, and Google Scholar was conducted for relevant studies. Observational studies evaluating the correlations of NLR, PLR, SII, or MLR with psoriasis were included. The primary outcomes were the associations of these inflammatory markers with the presence and severity of psoriasis. The random-effect model was applied for meta-analysis. 36 studies comprising 4794 psoriasis patients and 55,121 individuals in total were included in the meta-analysis. All inflammatory markers were significantly increased in psoriasis groups compared to healthy controls (NLR: MD = 0.59, 95% CI: 0.47-0.7; PLR: MD = 15.53, 95% CI: 8.48-22.58; SII: MD = 111.58, 95% CI: 61.49-161.68; MLR: MD = 0.034, 95% CI: 0.021-0.048; all p < 0.001). Between-group mean differences in NLR and PLR were positively correlated with the mean scores of Psoriasis Area Severity Index (NLR: p = 0.041; PLR: p = 0.021). NLR, PLR, SII, and MLR are associated with the presence of psoriasis. NLR and PLR serve as significant indicators of psoriasis severity. These novel CBC-derived markers constitute potential targets in the screening and monitoring of psoriasis.

Risk Factors for Bladder Neck Contracture Following Transurethral Resection of the Prostate in Patients with Benign Prostatic Enlargement.

Introduction To investigate the risk factors associated with developing BNC after bipolar TURP. Methods This retrospective cohort study included patients with symptomatic BPE who underwent TURP at our institution between 2010 and 2021. Univariate and multivariate Cox regression analyses were used to evaluate the association of patient- and surgery-related factors to BNC. The preoperative urinary catheterization and resection speed with BNC were evaluated by dividing the patients into four groups as follows: (1) with or (2) without preoperative urinary catheterization and (3) high or (4) low resection speed. The risk of BNC3Y between the four groups was compared using the Kaplan-Meier analysis and log-rank tests. Results 2041 patients underwent TURP between 2010 and 2021 were enrolled. Within 3 years of surgery, 306 (15%) patients were diagnosed with BNC. COPD, congestive heart failure, preoperative urinary catheterization, and low resection speed were associated with a higher risk of BNC3Y. The Kaplan-Meier analysis and log-rank tests demonstrated an increased risk of BNC due to preoperative urinary catheterization, regardless of the resection speed. Multivariate analysis revealed that COPD and preoperative urinary catheterization were independent predictive factors for BNC. Conclusions Our study findings indicate that preoperative urinary catheterization and COPD are associated with an increased risk of BNC in patients with BPE undergoing bipolar TURP.

Association Between Long­Term Exposure to Air Pollution and the Rate of Mortality After Hip Fracture Surgery in Patients Older Than 60 Years: Nationwide Cohort Study in Taiwan.

BACKGROUND: To enhance postoperative patient survival, particularly in older adults, understanding the predictors of mortality following hip fracture becomes paramount. Air pollution, a prominent global environmental issue, has been linked to heightened morbidity and mortality across a spectrum of diseases. Nevertheless, the precise impact of air pollution on hip fracture outcomes remains elusive. OBJECTIVE: This retrospective study aims to comprehensively investigate the profound influence of a decade-long exposure to 12 diverse air pollutants on the risk of post-hip fracture mortality among older Taiwanese patients (older than 60 years). We hypothesized that enduring long-term exposure to air pollution would significantly elevate the 1-year mortality rate following hip fracture surgery. METHODS: From Taiwan's National Health Insurance Research Database, we obtained the data of patients who underwent hip fracture surgery between July 1, 2003, and December 31, 2013. Using patients' insurance registration data, we estimated their cumulative exposure levels to sulfur dioxide (SO2), carbon dioxide (CO2), carbon monoxide (CO), ozone (O3), particulate matter having a size of <10 µm (PM10), particulate matter having a size of <2.5 µm (PM2.5), nitrogen oxides (NOX), nitrogen monoxide (NO), nitrogen dioxide (NO2), total hydrocarbons (THC), nonmethane hydrocarbons (NMHC), and methane (CH4). We quantified the dose-response relationship between these air pollutants and the risk of mortality by calculating hazard ratios associated with a 1 SD increase in exposure levels over a decade. RESULTS: Long-term exposure to SO2, CO, PM10, PM2.5, NOX, NO, NO2, THC, NMHC, and CH4 demonstrated significant associations with heightened all-cause mortality risk within 1 year post hip fracture surgery among older adults. For older adults, each 1 SD increment in the average exposure levels of SO2, CO, PM10, PM2.5, NOX, NO, NO2, THC, NMHC, and CH4 corresponded to a substantial escalation in mortality risk, with increments of 14%, 49%, 18%, 12%, 41%, 33%, 38%, 20%, 9%, and 26%, respectively. We further noted a 35% reduction in the hazard ratio for O3 exposure suggesting a potential protective effect, along with a trend of potentially protective effects of CO2. CONCLUSIONS: This comprehensive nationwide retrospective study, grounded in a population-based approach, demonstrated that long-term exposure to specific air pollutants significantly increased the risk of all-cause mortality within 1 year after hip fracture surgery in older Taiwanese adults. A reduction in the levels of SO2, CO, PM10, PM2.5, NOX, NO, NO2, THC, NMHC, and CH4 may reduce the risk of mortality after hip fracture surgery. This study provides robust evidence and highlights the substantial impact of air pollution on the outcomes of hip fractures.

Platelet-to-lymphocyte ratio and lymphocyte-to-monocyte ratio in glaucoma: a meta-analysis.

Aim: To explore the association between two systemic inflammation markers, platelet-to-lymphocyte ratio (PLR) and lymphocyte-to-monocyte ratio (LMR), and glaucoma. Materials & methods: The authors searched PubMed, Embase and the Cochrane Library for eligible studies comparing PLR and LMR levels in glaucoma patients and healthy controls. Results: Analysis revealed that glaucoma patients exhibited significantly elevated PLR levels and reduced LMR compared with nonglaucoma controls. These findings were consistent across various glaucoma types, with the exception of secondary glaucoma, where the association with PLR was less significant. Conclusion: The authors found PLR and LMR to be potential valuable biomarkers for glaucoma identification and progression monitoring. These findings highlight the role of systemic inflammation in glaucoma pathogenesis.

Association between adhesive capsulitis and thyroid disease: a meta-analysis.

HYPOTHESIS: Adhesive capsulitis (AC) is a common clinical condition of the shoulders without a clear pathophysiology or etiology. Although thyroid disease has been linked to AC, an appropriate understanding of the disease and its epidemiological evidence are lacking. This metaanalysis investigated the association of AC with thyroid disease and identified which manifestations of thyroid disease contribute to the risk of AC. MATERIALS AND METHODS: The databases of PubMed, Embase, and Scopus were searched for literature retrieval up to September 20, 2022. Articles evaluating the association between AC and any type of thyroid disease were enrolled. Data from studies reporting the prevalence and its 95% confidence interval (CI) were pooled. Subgroup analysis was performed on the different manifestations of thyroid disease. We explored heterogeneity with sensitivity analyses and publication bias with funnel plots and Egger's tests. A trim and fill analysis was conducted if publication bias was found. RESULTS: Results: In total, 10 case-control studies comprising a total of 127,967 patients were included. The prevalence of thyroid disease was significantly higher in patients with AC (odds ratio [OR] = 1.87, 95% CI: 1.37-2.57, P < .0001) than in patients without AC. The results of subgroup analysis indicated significantly higher rates of hypothyroidism (OR = 1.92, 95% CI: 1.09-3.39, P = .02) and subclinical hypothyroidism (OR = 2.56, 95% CI: 1.81-3.63, P < .00001), but not hyperthyroidism (OR = 1.42, 95% CI: 0.63-3.22, P = .40), among patients with AC than among those without AC. CONCLUSIONS: Our meta-analysis demonstrated that thyroid disease, especially when presenting as hypothyroidism or subclinical hypothyroidism, is associated with an increased risk of AC. Evidence for an association between hyperthyroidism and AC was not found, although this may be due to the lack of related studies. Further research on the pathogeneses of and relationship between these two diseases is warranted.

Gross hematuria and IgA nephropathy flare-up following the first dose of Moderna vaccine: A case report.

BACKGROUND: Since the mass vaccination for COVID-19, several case reports indicated the risk of autoimmune disease flare-ups after the vaccination. Among them, COVID-19 vaccine-induced glomerular diseases have drawn attention worldwide. The cases demonstrating the association between the mRNA vaccine and IgA nephropathy (IgAN) exacerbation had been noticed. Mostly mentioned, the flare-ups usually occurred after the second dose. METHODS: We present a Taiwanese female with IgAN who developed gross hematuria within only six hours after the first dose of the Moderna vaccine. RESULTS: Six hours after the first dose of Moderna vaccine on 8 June 2021, the patient developed gross hematuria and significantly decreased urine output. All symptoms resolved spontaneously on the fifth day after the vaccination without any intervention. On the fourth day after the vaccination, the patient were able to back to her original condition. CONCLUSION: This was an intriguing case of IgAN flare-up following the first dose of mRNA-based COVID-19 vaccination.

Knockdown of toll-like receptor 4 signaling pathways ameliorate bone graft rejection in a mouse model of allograft transplantation.

Non-union occurring in structural bone grafting is a major problem in allograft transplantation because of impaired interaction between the host and graft tissue. Activated toll-like receptor (TLR) induces inflammatory cytokines and chemokines and triggers cell-mediated immune responses. The TLR-mediated signal pathway is important for mediating allograft rejection. We evaluated the effects of local knockdown of the TLR4 signaling pathway in a mouse segmental femoral graft model. Allografts were coated with freeze-dried lentiviral vectors that encoded TLR4 and myeloid differentiation primary response gene 88 (MyD88) short-hairpin RNA (shRNA), which were individually transplanted into the mice. They were assessed morphologically, radiographically, and histologically for tissue remodeling. Union occurred in autografted but not in allografted mice at the graft and host junctions after 4 weeks. TLR4 and MyD88 expression was up-regulated in allografted mice. TLR4 and MyD88 shRNAs inhibited TLR4 and MyD88 expression, which led to better union in the grafted sites. More regulatory T-cells in the draining lymph nodes suggested inflammation suppression. Local inhibition of TLR4 and MyD88 might reduce immune responses and ameliorate allograft rejection.

Bitter melon seed oil-attenuated body fat accumulation in diet-induced obese mice is associated with cAMP-dependent protein kinase activation and cell death in white adipose tissue.

The aim of this study was to investigate the antiadiposity effect of bitter melon seed oil (BMSO), which is rich in the cis-9, trans-11, trans-13 isomer of conjugated linolenic acid. In Expt. 1, C57BL/6J mice were fed a butter-based, high-fat diet [HB; 29% butter + 1% soybean oil (SBO)] for 10 wk to induce obesity. They then continued to receive that diet or were switched to an SBO-based, high-fat diet alone (HS; 30% SBO) or containing bitter melon seed oil (BMSO) (HBM; 15% SBO + 15% BMSO) for 5 wk. The body fat percentage was significantly lower in mice fed the HBM diet (21%), but not the HS diet, compared with mice fed the HB diet. In Expt. 2, mice were fed an SBO-based, high-fat diet containing 0 (HS), 5 (LBM), 10 (MBM), or 15% (HBM) BMSO for 10 wk. In the LBM, MBM, and HBM groups, the body fat percentage was significantly lower by 32, 35, and 65%, respectively, compared with the HS control. The reduction in the HBM group was significantly greater than that in the LBM or MBM group. BMSO administration increased phosphorylation of acetyl-CoA carboxylase, cAMP-activated protein kinase (PKA), and signal transducer and activator of transcription 3 in the white adipose tissue (WAT), suggesting that PKA and leptin signaling might be involved in the BMSO-mediated reduction in lipogenesis and increase in thermogenesis and lipolysis. However, compared with the HS control, the HBM group had a significantly higher TNFα concentration in the WAT accompanied by TUNEL-positive nuclei. We conclude that BMSO is effective in attenuating body fat accumulation through mechanisms associated with PKA activation and programmed cell death in the WAT, but safety concerns need to be carefully addressed.

Upregulation of lipogenesis and protein tyrosine phosphatase-1B expression in the liver of Wistar rats with metabolic syndrome chronically induced by drinking sucrose water.

BACKGROUND: Establishing animal models with metabolic disorders similar to human metabolic syndrome (MS) is important. In terms of eliciting a full array of MS, we have previously shown that Wistar rats are more responsive to sucrose water drinking than are C57BL/6J mice. This study was aimed at investigating the underlying molecular mechanism of sucrose water-induced MS in Wistar rats. METHODS: Male Wistar rats were divided into 2 groups (n = 8 for each group) which were given plain water (C group) or 30% sucrose water (SW group) to drink ad libitum. After 20 weeks, the transcriptional levels and protein translocation of hepatic sterol regulatory element-binding protein-1c (SREBP-1c) and carbohydrate response element-binding protein (ChREBP) as well as the protein levels of protein tyrosine phosphatase-1B (PTP-1B) in insulin-responsive tissues (liver, muscle, and adipose tissue) were measured. RESULTS: The sucrose water regimen successfully elicited visceral obesity, hypertriglyceridemia, insulin resistance, and high blood pressure. The upregulation of de novo lipogenesis in the liver of the sucrose water-treated rats was demonstrated by an increased activity of enzymes, mRNA levels of lipogenic proteins, and nuclear levels of SREBP-1c and ChREBP. Moreover, in the sucrose water-treated rats, protein levels of PTP-1B were significantly increased in liver and skeletal muscle but decreased in adipose tissue. CONCLUSION: The susceptibility of Wistar rats to sucrose water-induced MS is associated with the transactivation of SREBP-1c and ChREBP in the liver, and PTP-1B is involved in the upregulation of de novo lipogenesis in the liver and the pathology of systemic insulin resistance in rats with MS chronically induced by drinking sucrose water.

Fangchinoline inhibits glutamate release from rat cerebral cortex nerve terminals (synaptosomes).

Fangchinoline, an active component of radix stephaniae tetrandrinea, has been shown to possess neuroprotective properties. It has been reported that excessive glutamate release has been proposed to be involved in the pathogenesis of several neurological diseases. The primary purpose of the present study was to investigate the effect of fangchinoline on glutamate release in rat cerebral cortex nerve terminals and to explore the possible mechanism. Fangchinoline inhibited the release of glutamate evoked by 4-aminopyridine (4-AP) in a concentration-dependent manner, and this phenomenon resulted from a reduction of vesicular exocytosis but not from an inhibition of Ca(2+)-independent efflux via glutamate transporter. Fangchinoline did not alter the resting synaptosomal membrane potential or 4-AP-mediated depolarization, but significantly reduced depolarization-induced increase in [Ca(2+)](C). Fangchinoline-mediated inhibition of glutamate release was significantly prevented by the N- and P/Q-type Ca(2+) channel blocker omega-conotoxin MVIIC, and by the PKC inhibitors, GF109203X and Ro318220. In addition, the glutamate release mediated by direct Ca(2+) entry with Ca(2+) ionophore (ionomycin) was unaffected by fangchinoline, which suggests that the inhibitory effect of fangchinoline is not due to directly interfering with the release process at some point subsequent to Ca(2+) influx. These results suggest that fangchinoline inhibits glutamate release from the rat cortical synaptosomes through the suppression of voltage-dependent Ca(2+) channel activity and subsequent reduces Ca(2+) entry into nerve terminals, rather than any upstream effect on nerve terminal excitability. This inhibition appears to involve the suppression of PKC signal transduction pathway. This finding may explain the neuroprotective effects of fangchinoline against neurotoxicity.