Serum Levels Of Markers Research Articles

Distinct peripheral pro‐inflammatory profile associated with tuberous sclerosis complex and epilepsy

AbstractObjectiveTuberous sclerosis complex (TSC) is a monogenetic disorder associated with sustained mechanistic target of rapamycin (mTOR) activation, leading to heterogeneous clinical manifestations. Epilepsy and renal angiomyolipoma are the most important causes of morbidity in adult people with TSC (pwTSC). mTOR is a key player in inflammation, which in turn could influence TSC‐related clinical manifestations. Reliable biomarkers are lacking to monitor and predict evolution and response to treatment for epilepsy in pwTSC. Inflammation has been implicated in epileptogenesis in non–TSC‐related epilepsy. We aimed to characterize the relation between markers of neuroglial activation/injury, markers of peripheral inflammation, and active epilepsy in pwTSC to identify accessible biomarkers and potential new therapeutic targets.MethodsWe performed a cross‐sectional study to investigate markers of central nervous system (CNS) (neurofilament light [NfL] and glial fibrillary acidic protein [GFAP]) and peripheral (45 cytokines) inflammation in the peripheral blood of pwTSC (n = 46) vs age‐ and sex‐matched healthy controls (HCs) (n = 26). In pwTSC, markers associated with active epilepsy (n = 23/46) were compared to non‐TSC epilepsy controls (n = 18). Observations on markers of neuroglial activation/injury (GFAP, NfL) were confirmed in an independent TSC cohort (n = 45; 69% with active epilepsy).ResultsWe report that TSC is characterized by elevated serum levels of marker of astrogliosis (GFAP), pro‐inflammatory molecules (interleukin 1β [IL‐1β], CXCL8) and trophic factor (epidermal growth factor [EGF]) compared to HCs and to non–TSC‐related epilepsy controls. Among pwTSC, renal angiomyolipoma presence and size was associated with IL‐15. It is notable that active epilepsy in pwTSC was associated with higher levels of GFAP compared to pwTSC without epilepsy, which was confirmed in an external validation cohort, and with elevated levels of pro‐inflammatory cytokines (IL‐17A, IL‐17C, tumor necrosis factor α [TNF‐α]), not significantly related to seizure activity or treatment with mTOR inhibitor. These associations remained significant after adjusting for age and sex.SignificanceThese results suggest that key inflammatory mediators could contribute to epileptogenesis and represent novel biomarkers and therapeutic targets in TSC.

Associations of nutritional intake and inflammatory factors with sarcopenia in community-dwelling older adults: a cross-sectional study.

Sarcopenia is an age-related disease that is related to nutritional intake and chronic low-grade inflammation. The aim of this study was to investigate the association of dietary intake, inflammatory markers and sarcopenia among the community-dwelling older adults. A total of 1001 older adults aged 60 and above were recruited. According to the criteria established by the Asian Working Group for Sarcopenia 2019, this paper assessed the presence of sarcopenia and using a Food Frequency Questionnaire to evaluate daily dietary intake. Serum levels of inflammatory markers were measured using the ELISA method. A total of 1001 participants took part in the study (mean 70.6years), comprising 396 males and 605 females, the prevalence of sarcopenia was 19.6%. Multivariate analysis revealed that high levels of leucine, methionine, threonine, histidine, aspartic acid, calcium, zinc, and vitamin C were associated with a lower risk of sarcopenia. Higher dietary inflammatory index scores were associated with a higher risk of sarcopenia (OR 1.67, 95% CI 1.12-2.47). Higher tumor necrosis factor-like weak inducer of apoptosis (TWEAK) (OR 1.04, 95% CI 1.02-1.07) was associated with a higher risk of sarcopenia, and a lower skeletal muscle mass, strength, and physical function. Conversely, higher insulin-like growth factor-1 (IGF-1) (OR 0.83, 95% CI 0.74-0.94) and glutathione S-transferase (GST) (OR 0.75, 95% CI 0.61-0.91) were associated with a lower risk of sarcopenia. This cross-sectional study revealed alterations in amino acid and micronutrient intake among older adults with sarcopenia. The levels of TWEAK were associated with an increased risk of sarcopenia, whereas IGF-1 and GST were associated with a reduced risk of sarcopenia.

Metformin Alleviates Doxorubicin-Induced Cardiotoxicity via Preserving Mitochondrial Dynamics Balance and Calcium Homeostasis.

Doxorubicin (DOX) is a commonly used chemotherapeutic medication for treating malignancies, although its cardiotoxicity limits its use. There is growing evidence that alteration of the mitochondrial fission/fusion dynamic processes accompanied by excessive reactive oxygen species (ROS) production and alteration of calcium Ca2+ homeostasis are potential underlying mechanisms of DOX-induced cardiotoxicity (DIC). Metformin (Met) is an AMP-activated protein kinase (AMPK) activator that has antioxidant properties and cardioprotective effects. The purpose of the study is to assess Met's possible cardioprotective benefits against DOX-induced cardiotoxicity. The study included 32 adult male rats. They were randomly divided into four groups: administered saline, DOX, Met, or DOX combined with Met respectively. Heart tissues were used for biochemical assays that measured oxidative stress markers, malondialdehyde (MDA), reduced glutathione (GSH), mitochondrial dynamics markers, optic atrophy-1(OPA-1) and dynamin-1-like protein (Drp1), calcineurin and caspase-3. Serum levels of myocardial injury markers, cardiac troponin I (cTn-I), and aspartate aminotransferase (AST), were also measured. The results revealed that DOX intoxication was associated with a significant increase in the levels of serum cTn-I and AST, increased cardiac MDA level, increased cardiac Drp1, calcineurin, and caspase-3 expressions, as well as reduced cardiac GSH level and cardiac OPA-1 expression. On the other hand, Met treatment significantly reduced DIC by decreasing oxidative stress, apoptosis, and improving mitochondrial and calcium balance. Finally, this study shows that Met may be able to protect the heart from damage caused by DOX by working as an antioxidant and anti-apoptotic agent and keeping the balance of calcium and mitochondria.

Distinct response patterns of endothelial markers to the BNT162b2 mRNA COVID-19 booster vaccine are associated with the spike-specific IgG antibody production

IntroductionDespite the efficacy and safety of SARS-CoV-2 vaccines, inflammatory and/or thrombotic episodes have been reported. Since the impact of COVID-19 vaccines on the endothelium remains uncertain, our objective was to assess endothelial activation status before and 90 days after the third dose of the BNT162b2 mRNA COVID-19 vaccine.MethodsA prospective longitudinal study was conducted at University General Hospital of Albacete, involving 38 healthy health-care workers. Serum levels of endothelial markers (endocan and sVCAM-1) and spike S1-specific IgG antibodies were determined before and at 7, 15, 24 and 90days following vaccination. To analyze each participant´s individual response, we calculated relative increases/decreases (delta values) in endothelial markers and antibodies concentrations compared to their pre-vaccination levels.ResultsWe identified two significantly distinct profiles of endothelial markers response, characterized by either increased or decreased serum levels of endocan and sVCAM. Incremental and decremental response groups did not differ in terms of age, sex, cardiovascular risk factors, previous SARS-CoV-2 infection and influenza vaccine co-administration. However, these responses were significantly associated with the relative spike-specific antibody production. Specifically, the greatest relative increase in antibodies was found in the decremental responders. Additionally, the higher delta antibody production was observed in non-previously infected individualsConclusionAdministration of the BNT162b2 booster vaccine triggered a non-homogenous response of endothelial function markers among the study participants. Our findings improve the understanding of individual responses to the mRNA COVID-19 booster vaccine, which could be useful in assessing the need for booster doses, particularly in population at risk of vascular complications.

The profile of oxidative stress markers (arachidonic and linoleic acid derivatives) in patients with benign prostatic hyperplasia in relation to metabolic syndrome.

So far, it has been proven that benign prostatic hyperplasia (BPH) is strongly associated with inflammation resulting from, i.a. the presence of infectious agent, autoimmune disease, aging process and lipid disorders associated with metabolic syndrome (MetS). We analyzed the association between serum eicosanoides (HETE, HODE, lipoxins, prostaglandin, and leucotrien) in aging man with benign prostatic hyperplasia (BPH) and healthy controls. The study involved 219 men (with BPH, n = 144; healthy controls, n = 75). We assessed the content arachidonic and linoleic acid derivatives in the serum samples of the study participants using liquid chromatography (HPLC). The levels of: RvE1 (p < 0.001); LXA4 5S,6R,15R (p = 0.001); 10S,17R-DiDHA (p < 0.001); MaR1 (p = 0.002); 9S-HODE (p < 0.05); 15S-HETE (p < 0.05); 12S-HETE (p < 0.001); 5-oxoETE (p < 0.05) and 5-HETE (p < 0.001) were significantly higher in patients with BPH than in the control group. PGE2 (p = 0.007), LTB4 (p < 0.001), and 18RS-HEPE (p < 0.001) were significantly higher in control group. We also analyzed the relationship between LXA4 5S,6R,15R serum levels of oxidative stress markers and concomitance of MetS. We noticed a relationship between levels and MetS (F1216 = 6.114965, p = 0.01). Our research results suggest that pro-inflammatory mediators and suppressors of inflammation are involved in the development of BPH, but their exact contribution has yet to be investigated.

Serum KL-6 levels reflect the severity of interstitial lung disease caused by immune checkpoint inhibitors.

Tumor immunotherapy, particularly immune checkpoint inhibitors (ICIs), has emerged as a powerful strategy in treating malignant tumors, exhibiting efficacy in both first-line and second-line treatments for advanced non-small cell lung cancer (NSCLC). Despite their success, ICIs can lead to adverse reactions, including interstitial lung disease (ILD), with an incidence ranging from 2.7% to 20.0%. The lack of clear correlations with dosage, duration, or drug efficacy, coupled with nonspecific clinical manifestations, poses challenges in timely diagnosis and effective management. This study examined the association between ICIs-related ILD and serum levels of KL-6 and inflammatory markers in NSCLC patients. A total of 382 NSCLC patients with squamous cell carcinoma (SQC, n=81), adenocarcinoma (ACA, n=132), and large cell carcinoma (LCC, n=169) were included, of whom 191 developed ILD following ICIs treatment. Serum KL-6, TNF-α, IL-8, and IL-6 were quantified using ELISA. Results showed significantly elevated serum KL-6 levels in ILD patients (759.35±214.14U/mL) compared to those without ILD (270.81±124.98U/mL). Cancer subtype analysis revealed increased KL-6 levels across SQC, ACA, and LCC ILD patients (SQC: 645.89±255.07, ACA: 797.39±192.30, LCC: 783.57±191.21; p<0.001). ROC analysis identified diagnostic thresholds for KL-6: 277.4U/mL for SQC (sensitivity 0.9756, specificity 0.8250), 346.9U/mL for ACA (sensitivity 0.9583, specificity 0.8333), and 281.3U/mL for LCC (sensitivity 0.9873, specificity 0.6111). Correlation analysis showed a significant relationship between KL-6 and TNF-α (r=0.4626, p=0.0023), IL-8 (r=0.5584, p=0.0001), and IL-6 (r=0.5336, p=0.0003) in SQC ILD patients. These findings suggest that elevated KL-6 levels and inflammatory markers are indicative of ILD in ICIs-treated NSCLC patients, with potential diagnostic implications across cancer subtypes.

Characterization of bioaerosol exposures in wastewater treatment plant workers and serum levels of lung and inflammatory markers

Characterization of bioaerosol exposures in wastewater treatment plant workers and serum levels of lung and inflammatory markers

Neurobiological mechanisms of antidepressant properties of psilocybin: A systematic review of blood biomarkers.

Psilocybin represents a novel therapeutic approach for individuals with major depressive disorder (MDD) who do not respond to conventional antidepressant treatment. Investigating the influence of psilocybin on the pathophysiological processes involved in MDD could enhance our neurobiological understanding of the presumed antidepressant action mechanism. This systematic review aims to summarize the results of human studies investigating changes in blood-based biomarkers of MDD to guide future research on potentially relevant analytes that could be monitored in clinical trials. A systematic search was performed in MEDLINE, Embase, and Web of Science to retrieve studies investigating changes in serum and plasma levels of neurotrophic, immunologic, neuroendocrine, and metabolic markers. Nine studies were included, describing findings on 15 biomarkers, exclusively in healthy participants. Studies consistently reported a decrease in interleukin-6, C-reactive protein, and eosinophils, and an increase in cortisol, prolactin, oxytocin, thyroid-stimulating hormone, adrenocorticotropic hormone, brain-derived neurotrophic factor, and free fatty acids following psilocybin administration. Less consistent effects were observed on interleukin-1β, interleukin-8, tumour necrosis factor-alpha, soluble urokinase plasminogen activator receptor, and growth hormone. The results are in line with preclinical studies and provide initial support from human studies that psilocybin potentially leads to beneficial effects on biomarkers of MDD. However, given the limited number of studies, findings should be approached with caution prior to replication. Further research should include larger samples, clinical populations, longer-term assessment, rigorous experimental designs, and account for the potential confounding of psychological stress related to the psychedelic experience.

Zinc pretreatment for protection against intestinal ischemia-reperfusion injury.

Intestinal ischemia-reperfusion (I/R) injury (II/RI) is a critical condition that results in oxidative stress, inflammation, and damage to multiple organs. Zinc, an essential trace element, offers protective benefits in several tissues during I/R injury, but its effects on intestinal II/RI remain unclear. To investigate the effects of zinc pretreatment on II/RI and associated multiorgan damage. C57BL/6 mice were pretreated with zinc sulfate (ZnSO4, 10 mg/kg) daily for three days before I/R injury was induced via superior mesenteric artery occlusion (SMAO) and abdominal aortic occlusion (AAO) models. Tissue and serum samples were collected to evaluate intestinal, liver, and kidney damage using Chiu's score, Suzuki score, and histopathological analysis. Caco-2 cells and intestinal organoids were used for in vitro hypoxia-reoxygenation injury models to measure reactive oxygen species (ROS) and superoxide dismutase (SOD) levels. Zinc pretreatment significantly reduced intestinal damage in the SMAO and AAO models (P < 0.001). The serum levels of liver enzymes (alanine aminotransferase, aspartate aminotransferase) and kidney markers (creatinine and urea) were lower in the zinc-treated mice than in the control mice, indicating reduced hepatic and renal injury. In vitro, zinc decreased ROS levels and increased SOD activity in Caco-2 cells subject to hypoxia-reoxygenation injury. Intestinal organoids pretreated with zinc exhibited enhanced resilience to hypoxic injury compared to controls. Zinc pretreatment mitigates II/RI and reduces associated multiorgan damage. These findings suggest that zinc has potential clinical applications in protecting against I/R injuries.

WITHDRAWN: Serum Levels of Micronutrients, Magnesium, and Mark-ers of Immunity (CD4+) in Antiretroviral-naïve HIV-infected Individuals: Relationships and Predictors

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Impact of Thrombomodulin Polymorphism -33G>A on Acute Myocardial Infarction Risk and Circulating Inflammatory Markers.

There is increasing evidence that thrombomodulin (THBD) polymorphisms, along with inflammatory markers [i.e., C-reactive protein (CRP), fibrinogen, albumin], may increase the risk of acute myocardial infarction (AMI). The aim of the study was to investigate the role of the THBD -33G>A polymorphism (rs1042579) as a marker of AMI risk and to correlate it with serum levels of inflammatory markers. Case-control study of 277 AMI patients and 329 healthy controls. A binary logistic regression analysis was performed to evaluate the association between the parameters studied and AMI risk. The frequencies of genotypes AA, GA, and GG of the THBD -33G>A polymorphism were 31.4%, 45.5%, and 23.1% in patients and 21.6%, 44.1%, and 34.3% in controls. A significant association was found between the AA genotype of the THBD -33G>A polymorphism (AA: OR = 2.011, 95% CI 1.561-3.074, P < .001) or A allele (A: OR = 1.725, 95% CI 1.493-2.510, P < .001) and AMI risk. A backward stepwise logistic regression method combining AMI status as the dependent variable and conventional risk factors (age, smoking, arterial hypertension (HTA), diabetes, dyslipidemia, CRP, albumin, fibrinogen, serum angiotensin converting enzyme (ACE) activity, serum malondialdehyde, conjugated dienes, glutathione peroxidase, cardiac troponin-I (cTnI) and THBD AA genotype) as independent variables showed that the most predictive risk factors for AMI were smoking, HTA, albumin, fibrinogen, CRP, ACE activity, cTnI, and the THBD AA-genotype with odds ratios of 2.942, 2.203, 2.352, 1.323, 1.652, 1.014, 2.105, and 3.781 respectively. The AA genotype was associated with increased diastolic blood pressure, CRP, ACE activity, and albumin levels. The study shows that the THBD -33G>A polymorphism should be included in the stratification of AMI risk.

The Role of Dapagliflozin in the Modulation of Hypothermia and Renal Injury Caused by Septic Shock in Euglycemic and Hyperglycemic Rat Models.

Recent research has validated the efficacy of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in reducing glucose levels and exerting a nephroprotective role. This study aimed to examine the impact of dapagliflozin in preventing sepsis-induced acute kidney injury (AKI) and related consequences. The study used both normal and diabetic rat models to investigate whether the effectiveness of dapagliflozin is influenced by glycemia levels. Normal and diabetic Wistar albino rats were treated with dapagliflozin for two weeks and then received a single dose of lipopolysaccharide (LPS). After sepsis induction, skin and deep body temperatures were recorded every two hours. Blood and kidneys were collected for analysis using histological examination and biochemical assays. Dapagliflozin attenuated the consequences of sepsis through mitigation of LPS-induced hypothermia and AKI in the normal and diabetic septic groups. Dapagliflozin regulated the serum levels of AKI markers, including creatinine and blood urea nitrogen, as well as ion levels. Dapagliflozin attenuated LPS-induced AKI through modulation of renal inflammation and oxidative stress, which showed well-abundant glomeruli. These results indicated the protective effect of dapagliflozin against LPS-induced hypothermia and AKI, which was likely unrelated to its glucose-lowering properties, as evidenced in the non-diabetic septic group. The outcomes suggest that dapagliflozin has a potential impact in preventing sepsis-induced hypothermia and AKI via modulation of inflammation and oxidative stress, irrespective of glycemic levels.

Effects of Nutritional Support with a Leucine-Enriched Essential Amino Acid Supplement on Body Composition, Muscle Strength, and Physical Function in Stroke Patients Undergoing Rehabilitation.

Dietary protein intake can potentially influence renal function. This study aimed to elucidate the association between dietary protein supplementation and a decrease in the estimated glomerular filtration rate (eGFR) in Japanese stroke patients undergoing rehabilitation. From July 2017 to June 2021, 60 patients undergoing post-stroke rehabilitation were randomly assigned to a rehabilitation alone or rehabilitation nutrition group, which received 120 g Reha-Time Jelly® after each session. Both groups were followed up for 3 months. Serum nutritional markers (prealbumin and retinol-binding protein), muscle strength, body composition, renal function markers (eGFR based on creatinine [eGFR-Cr] and cystatin C [eGFR-Cys]), urinary protein-to-creatinine ratio (UPCR), and motor function (walking speed, 2-min walk distance, and chair stand test) were assessed at baseline and post-intervention. Of the 60 participants (mean age: 70.2 ± 10.0 years), 39 were men (65.0%) and 19 (31.7%) had chronic kidney disease. Initial eGFR-Cr and eGFR-Cys values were 70.5 ± 17.2 and 66.6 ± 14.8 mL/min/1.73 m2, respectively. After the intervention, the rehabilitation nutrition group demonstrated a significantly greater increase in body mass index (BMI) and a smaller decrease in bone mineral content than the rehabilitation alone group. However, no significant between-group differences were noted in serum marker levels or motor function, including grip strength and knee extensor strength, on the paralyzed and non-paralyzed sides. The change in chair stand test performance indicated a trend toward improvement in the rehabilitation nutrition group. No significant differences were observed in the changes in renal function. A 3-month nutritional supplementation intervention may help increase BMI, preserve bone mineral content, and support physical activity levels in patients undergoing post-stroke rehabilitation without negatively affecting renal function.

Protective effects of Pelargonium graveolens (geranium) oil against cefotaxime-induced hepato-renal toxicity in rats.

Cefotaxime is a broad-spectrum antibiotic targeting Gram-negative bacteria used for diverse infections, but it can be toxic to the stomach, liver, and kidneys. This study explored the protective effects of geranium oil against cefotaxime-induced hepatotoxicity and nephrotoxicity in rats, employing biochemical, histopathological, and immunohistochemical evaluations. Thirty rats were divided into five groups of six animals each one. Group 1 received orally normal saline for 14days, Group 2 was given orally 2.5% DMSO for 14days, Group 3 received cefotaxime (200mg/kg/day IM) for 14days, Group 4 received with cefotaxime (200mg/kg/day IM) and geranium oil (67mg/kg b. w./day orally in DMSO) for 14days, and Group 5 received geranium oil alone (67mg/kg b. w./day orally in DMSO) for 14days. Geranium oil significantly reduced cefotaxime-induced damage, evidenced by lower serum levels of liver enzymes (AST, ALT), renal markers (urea, creatinine), and other indicators (alkaline phosphatase, TNF-alpha, IL-1Beta, MAPK, nitric oxide, MDA). It also increased levels of protective tissue biomarkers such as NrF2, albumin, catalase, Beclin 1, and reduced glutathione (GSH). Histopathological and immunohistochemical analyses revealed significant protective effects in liver and renal tissues in rats treated with Geranium oil. These results suggest that Geranium oil is effective in mitigating cefotaxime-induced hepatotoxicity and renal toxicity.

Determining the Relationship Between Zinc Status and Blood Manganese Levels on Enzymatic Markers of Tissue Damage: An Epidemiological Study Using NHANES 2013-2016 Data

Manganese is an essential trace element required for various physiological processes. However, excessive exposure to this metal can lead to health issues. This study aims to evaluate whether adequate zinc intake can influence the relationship between blood manganese levels and markers indicating damage to the liver and other organs in populations using epidemiological data. We conducted a comprehensive analysis utilizing 2013–2016 data from the National Health and Nutrition Examination Survey (NHANES). The findings indicated that blood manganese exhibits a significant positive association with the serum levels of enzymatic markers of liver damage alkaline phosphatase and aspartate aminotransferase. However, when investigating the interaction of blood manganese and zinc intake at the second quartile, a significant negative association was found with alkaline phosphatase in three different linear regression models. A similar association was found between the fourth quartile of zinc intake and lactate dehydrogenase activity in all three models of the study. The findings suggest that unhealthy high levels of manganese in population could be widespread and may lead to tissue injury and disease. Nevertheless, having an adequate zinc intake could help mitigate manganese toxicity.

Clinical study of different interventional treatments for primary hepatocellular carcinoma based on propensity-score matching

BACKGROUND Transcatheter arterial chemoembolization (TACE) is the main treatment for patients with primary hepatocellular carcinoma (PHC) who miss the opportunity to undergo surgery. Conventional TACE (c-TACE) uses iodized oil as an embolic agent, which is easily washed by blood and affects its efficacy. Drug-eluting bead TACE (DEB-TACE) can sustainably release chemotherapeutic drugs and has a long embolization time. However, the clinical characteristics of patients before the two types of interventional therapies may differ, possibly affecting the conclusion. Only a few studies have compared these two interventions using propensity-score matching (PSM). AIM To analyze the clinical effects of DEB-TACE and c-TACE on patients with PHC based on PSM. METHODS Patients with PHC admitted to Dangyang People’s Hospital (March 2020 to March 2024) were retrospectively enrolled and categorized into groups A (DEB-TACE, n = 125) and B (c-TACE, n = 106). Sex, age, Child-Pugh grade, tumor-node-metastasis stage, and Eastern Cooperative Oncology Group score were selected for 1:1 PSM. Eighty-six patients each were included post-matching. Clinical efficacy, liver function indices (aspartate aminotransferase, alanine aminotransferase, total bilirubin, and albumin), tumor serum markers, and adverse reactions were compared between the groups. RESULTS The objective response and disease control rates were significantly higher in group A (80.23% and 97.67%, respectively) than in group B (60.47% and 87.21%, respectively) (P &lt; 0.05). Post-treatment levels of aspartate aminotransferase, alanine aminotransferase, and total bilirubin were lower in group A than in group B (P &lt; 0.05), whereas post-treatment levels of albumin in group A were comparable to those in group B (P &gt; 0.05). Post-treatment levels of tumor serum markers were significantly lower in group A than in group B (P &lt; 0.05). Patients in groups A and B had mild-to-moderate fever and vomiting symptoms, which improved with conservative treatment. The total incidence of adverse reactions was significantly higher in group B (22.09%) than in group A (6.97%) (P &lt; 0.05). CONCLUSION DEB-TACE has obvious therapeutic effects on patients with PHC. It can improve liver function indices and tumor markers of patients without increasing the rate of liver toxicity or adverse reactions.

Histological Improvement of Hepatic Fibrosis of Decompensated Liver Cirrhosis after Prednisolone and Azathioprine Treatment in a Patient with Autoimmune Hepatitis.

The treatment of the underlying cause of liver disease may potentially reverse hepatic fibrosis. However, it remains uncertain whether improvement in fibrosis can be observed in decompensated liver cirrhosis (LC). Here, we present a case of autoimmune hepatitis (AIH)-related LC in which histological improvement of fibrosis was achieved despite the presence of decompensated LC. A Japanese female in her 20s was initially identified as having liver function impairments during her employment medical checkup. Following a laparoscopic liver biopsy, she was diagnosed with AIH-related decompensated LC (F4 and A3) with a Child-Pugh score of 10. The patient initially received treatment with prednisolone at a daily dose of 40 mg, followed by 20 mg/day of prednisolone plus 25 mg/day of azathioprine (subsequent increase of azathioprine to 100 mg/day). With this treatment, the abnormal serum marker levels returned to normal, thereby enabling the patient to avoid liver transplantation eight months after the initiation of treatment. Moreover, marked improvement was observed in non-invasive tests for hepatic fibrosis, including the FIB-4 index and FibroIndex, as well as liver stiffness evaluated by FibroScan®. Eleven months after diagnosis, the patient developed a cholestatic liver injury and was diagnosed with drug-induced cholestatic liver disease (azathioprine overcapacity as the causative agent). By percutaneous liver biopsy at this point, hepatic fibrosis (F2-3) was markedly improved compared with that at the diagnosis. Along with the improvement of hepatic fibrosis, notable improvements were also observed in patient-reported outcomes such as the SF-36® score and chronic liver disease questionnaire. In this report, we first described a case of AIH that showed a histological improvement of hepatic fibrosis even in decompensated LC by treatment with prednisolone and azathioprine.

Therapeutic Effects of Liposomal Resveratrol in the Mitigation of Diabetic Nephropathy via Modulating Inflammatory Response, Oxidative Stress, and Apoptosis.

An important factor in the development of diabetes and its associated consequences is prolonged chronic hyperglycemia, which weakens the antioxidant defense system and produces reactive oxygen species. Phytochemicals have been found to scavenge free radicals and exhibit antioxidant effects necessary to increase insulin sensitivity and reduce the development of diabetes-related complications. Current treatments for managing diabetes and diabetic nephropathy are often not very effective and come with several limitations and side effects. Resveratrol, for example, has shown therapeutic potential in mitigating kidney damage induced by high glucose levels, but its short bioavailability is a significant limitation. This accentuates the need for alternatives that not only improve the disease but also reduce the side effects associated with treatment. To enhance the therapeutic efficacy of resveratrol, we investigated the protective effects of liposomal resveratrol (LR) in a streptozotocin-induced diabetic rat model at doses of 20 and 40mg/kg. We compared the impact of LR to that of resveratrol alone (at a dose of 40mg/kg) on various parameters, including serum levels of biochemical markers, tissue levels of pro-inflammatory cytokines, nuclear transcription factor, oxidative stress indices, and apoptotic markers. LR, as a highly absorbable and metabolized form of resveratrol, has demonstrated beneficial effects in diabetic rats. Administered at both 20mg/kg and 40mg/kg dosages over a 5-week period, it demonstrated notable efficacy in alleviating inflammation. This was accomplished by diminishing the levels of pro-inflammatory mediators, TNF-α and IL-6, through the inhibition of NF-κB translocation. Additionally, LR influenced apoptotic markers, specifically caspase, BCL-2, and BAX. Furthermore, it enhanced the expression of key antioxidant enzymes such as catalase and glutathione peroxidase while significantly lowering malondialdehyde levels. These significant biochemical and immunological protective effects correlated with improved histological integrity and overall kidney architecture. Notably, resveratrol alone was not as effective as LR in restoring kidney function, highlighting its potential as a therapeutic candidate for the treatment of diabetic nephropathy. However, more in-depth studies are needed to explore its mechanism of action and improved bioavailability.

The efficacy and active compounds of Chaihuang Qingyi Huoxue granule to Ameliorate intestinal mucosal barrier injury in rats with severe acute pancreatitis by suppressing the HMGB1/TLR4/NF-κB signaling pathway

Intestinal mucosal barrier injury represents a critical complication of severe acute pancreatitis (SAP) without effective treatment. This study investigated the efficacy, underlying mechanism, and responsible active compounds of the traditional Chinese medicinal prescription Chaihuang Qingyi Huoxue granule (CHQY) in treating SAP-induced intestinal mucosal barrier injury. SAP was established in Sprague-Dawley rats via intra-pancreaticobiliary duct infusion of sodium taurocholate, followed by oral CHQY administration (3.15 g/kg every 6 h for 12 and 24 h). Blood and tissues were harvested to assess the severity of pancreatitis, intestinal mucosal barrier integrity, and extent of inflammatory injury. Intestine-absorbing compounds were identified using ultra-high-performance liquid chromatography coupled with high-resolution mass spectrometry (UHPLC-HRMS). Our results showed that CHQY treatment effectively mitigated SAP-induced intestinal mucosal injury, as evidenced by improved intestinal epithelial structure, decreased serum levels of intestinal injury markers (d-lactic acid, diamine oxidase, I-FABP, and Zonulin), restored expression of the tight junction protein ZO-1, and reduced serum endotoxin levels. Furthermore, CHQY administration suppressed the expression of proinflammatory mediator HMGB1, its receptor TLR4, and downstream NF-κB signaling in the intestine, leading to downregulated intestinal IL-1β expression and reduced circulating TNF-α and IL-6. UHPLC-HRMS analysis identified 15 intestine-absorbing compounds in CHQY, of which paeoniflorin sulfite and chrysin-7-O-glucuronide independently inhibited TNF-α-induced tight junction loss in IEC-6 cells and mitigated intestinal mucosal barrier injury in SAP rats through suppressing NF-κB signaling. In summary, CHQY ameliorates SAP-induced intestinal mucosal barrier injury by downregulating the proinflammatory HMGB1/TLR4/NF-κB signaling, with efficacy partially attributed to its active compounds paeoniflorin sulfite and chrysin-7-O-glucuronide.

The feasibility of using a multivariate regression model incorporating ultrasound findings and serum markers to predict thyroid cancer metastasis.

This study aimed to assess the viability of a multivariate regression model utilizing ultrasound findings and serum markers for predicting thyroid cancer metastasis. A retrospective analysis of 98 thyroid patients admitted from January 2022 to October 2022 was conducted to categorize them into a metastasis group (n=20) and a non-metastasis group (n=78) based on postoperative pathological results. Both groups underwent ultrasound examination and serum marker testing. Correlative analysis was performed to explore the association between various indicators and thyroid cancer metastasis. A multivariate regression model was developed, and receiver operating characteristic (ROC) curves were used to assess the predictive value of ultrasound findings, serum markers, and their combination for thyroid cancer metastasis. Statistically significant differences were found in the levels of ultrasound findings and serum markers between the two groups. Nodule boundaries, presence or absence of halos, margins, lobulation, capsular invasion, surface smoothness, nodule aspect ratio, uric acid, total cholesterol, triglyceride, and LDL cholesterol levels were predictors of metastasis in thyroid cancer. The AUC value of 0.950 for the prediction of thyroid cancer metastasis by ultrasound signs combined with serologic indicators was significantly higher than 0.728 and 0.711 predicted by ultrasound signs or serologic indicators alone. The multivariate regression model incorporating ultrasound findings and serum markers enhances the predictive accuracy for thyroid cancer metastasis, offering essential guidance for early prediction and intervention in a clinical setting.