Severe Inflammatory Reaction Research Articles

Bone marrow-derived dendritic cells play a role in attenuating inflammation on Bothrops jararacussu venom muscle damage

The immune system is regulated by dendritic cells (DCs), which are highly specialized cells for presenting antigens. They are thought of as natural sentinels that start the immune response triggered by naive T cells against invasive infections. DCs participate in the initial stage of muscle damage in conjunction with monocytes, macrophages, and myogenic cells. The goal of this study was to determine whether DCs might mitigate tissue damage and aid in the regeneration of the gastrocnemius muscle following envenomation with Bothrops jararacussu venom (BjV). Mature bone marrow dendritic cells (BMDCs) were used to treat mice in an experimental envenomation model with BjV by activation with lipopolysaccharide (LPS). BMDCs were injected into the gastrocnemius muscle at the same site of the BjV injury, in a single dose, 3h after envenomation, and envenoming effects were observed at different periods for 7 days. In both untreated (NT) and treated (T) groups tissue necrosis, leukocyte influx, and hemorrhage at the injury site were observed. Results showed an increase in serum and tissue CK as well as IL-6, TNF-α, and IL-1β release in the first hours after envenoming. In contrast, after treatment with BMDCs results obtained demonstrated an attenuated local effect with a small leukocyte influx, decreased or non-existent necrosis and hemorrhage, as well as a reduction in both serum and tissue CK levels as well as cytokine release and, consequently, the onset of a moderate regenerative process. The present study's findings concluded that BjV causes a severe inflammatory reaction at the site of injury and that treating envenoming with BMDCs in the muscle was crucial for minimizing damage to the muscle and the inflammatory reaction and promoting the early onset of the tissue repair process.

Results of the study on the baseline status of flight-associated periodontal pathology in civil aviation flight personnel

Aim. To assess the baseline condition of periodontal structures in civil aviation flight personnel in order to improve the algorithm for treatment and preventive dental care.Materials and Methods. A periodontal examination of the oral cavity was conducted for 120 flight personnel at the physician-sanitary unit of Dushanbe International Airport. The participants were divided into five groups: flight personnel with mild chronic gingivitis, moderate chronic gingivitis, mild chronic periodontitis, moderate chronic periodontitis, and a control group of flight personnel with healthy periodontium. The clinical course of chronic gingivitis and periodontitis was evaluated using oral hygiene and periodontal indices.Results and Discussion. Inflammatory periodontal diseases, such as chronic gingivitis and periodontitis of moderate severity (Groups II and IV), presented with more pronounced symptoms, including severe inflammatory reactions of the periodontal tissues and poor oral hygiene, compared to those in Groups I and III.Conclusion. The study demonstrated that papillary-marginal-alveolar (PMA) index, bleeding index, and oral hygiene scores were significantly elevated in flight personnel with mild to moderate chronic periodontitis, highlighting the need for targeted treatment and preventive care.

Polysaccharide-Based Injectable Hydrogel Loaded with Quercetin Promotes Scarless Healing of Burn Wounds by Reducing Inflammation.

Moisture loss, infection, and severe inflammatory reactions are the primary factors affecting burn wound healing and leading to scar formation. Herein, we developed a quercetin-loaded polysaccharide-based injectable hydrogel (named PECE). The PECE consists of oxidized sodium alginate (OAlg) coupled with chitosan (CS) via Schiff bases and electrostatic interactions, while Que is incorporated via hydrogen bonding. Benefiting from the hydroxyl and carboxyl groups, PECE features distinguished moisturizing ability. Additionally, the sustained release of Que imparts remarkable antibacterial activity against Escherichia coli and Staphylococcus aureus. Likewise, PECE demonstrates favorable in vitro anti-inflammatory capacity as released Que significantly downregulates pro-inflammatory factors (IL-6 and TNF-α) secreted by RAW 264.7 macrophages. More importantly, in a rat model of deep second-degree burn wounds, PECE effectively inhibits wound infection, reduces inflammation, and promotes angiogenesis and collagen deposition, ultimately minimizing scar formation. Overall, this work presents a promising strategy for scarless healing of burn wounds.

Multifunctional conductive stem cell delivery hydrogel combined with low-frequency pulsed electromagnetic fields for spinal cord injury repair

Spinal cord injury (SCI) is a severe traumatic disease for which no satisfying treatment is available. The severe inflammatory reactions and poor endogenous regenerative capacity cause difficulty in functional recovery. Neural stem cells (NSCs) transplantation is currently a promising treatment for repairing SCI. However, there is a lack of effective ways to improve the survival rates of NSCs and promote the neuron differentiation rates of NSCs. Conductive hydrogel can mimic environment which is suitable for neurodevelopment. Low-frequency pulsed electromagnetic fields (LPEMFs) have the advantages of safety, non invasiveness, and tissue repair, making it a potential method of repairing SCI. In this study, an injectable, self-healing magnetic, and conductive hydrogel was synthesized to carry out NSCs with LPEMFs for repairing SCI. In vitro experiments, under the treatment of LPEMFs and conductive hydrogel, the microglia tend to polarize into M2 phenotype, rather than M1 phenotype. Meanwhile, NSCs tend to differentiate into neuronal direction. In SCI model, conductive hydrogel loaded with NSCs combined with LPEMFs can promote functional recovery, through reducing inflammation and promoting neuron differentiation of NSCs. This study provides a novel NSCs transplantation strategy combined with physical interventions for SCI treatment, which brings a new desire to repair SCI.

A rare case of hemophagocytic lymphohistiocytosis (HLH) secondary to Salmonella infection

HLH (Hemophagocytic lymphohistiocytosis) is a severe hyperinflammatory disease which could be caused by a range of pathogenic organisms, involving Salmonella. This unique case of bacterial-induced HLH tells the story of a 24y/o male who has been admitted to the hospital and is experiencing the severe symptoms of HLH that developed after an enteric fever caused by Salmonella. Despite earlier hospitalization and intravenous antibiotic treatment, he presented with a high temperature, excessive sweating, yellowish staining of urine and eyes, shortness of breath, and significant systemic inflammation. Laboratory studies revealed severe anemia, bicytopenia, and increased markers such as hyperferritinemia and hypertriglyceridemia, resulting in the diagnosis of HLH. The treatment method includes intensive care with intravenous immunoglobulins (IVIG), corticosteroids, and broad-spectrum antibiotics to address both the underlying infection and the inflammatory condition. Despite intense care, his condition was complex and created substantial complications. This instance emphasizes the significance of early detection as well as treatment of HLH, especially when accompanied by bacterial infections, which are not generally thought to produce this strong immunological response. The example emphasizes the requirement to include HLH in the individuals differential diagnosis with severe illness and systemic inflammatory reactions that do not respond to standard treatment. It also emphasizes the necessity of a comprehensive therapeutic approach, customized to the underlying cause and specific clinical presentations of the disease, in improving outcomes in critically sick patients.

The Mechanism of Bacterial Endotoxin Invasion Pathways in Porcine Reproductive and Respiratory Syndrome Virus-Positive Porcine Endometrial Epithelial Cells

Porcine reproductive and respiratory syndrome virus (PRRSV) causes abortions, stillbirths, and dummy pregnancies. Previous studies found that PRRSV can promote secondary bacterial infections and elevate bacterial endotoxin levels, further increasing the abortion rate in sows. However, the pathways by which bacterial endotoxins invade the bodies of PRRSV(+) sows and aggravate their clinical symptoms are unknown. In this study, we established a model of PRRSV and lipopolysaccharide (LPS) working together on porcine endometrial epithelial cells (PEECs). We speculate that PRRSV and LPS affect PEECs through viral protein interaction with cytokines and cytokine receptors, natural killer cell-mediated cytotoxicity, and regulation of actin cytoskeleton signaling pathways by analyzing seq-RNA. The PRRSV proteins act on inflammatory factors and their receptors to activate chemokines-5 (CCL5), chemokines-4 (CCL4), and chemokines-8 (CCL8) mRNA expression, causing severe inflammatory reactions. In addition, the elevation of MEK1/2 factors and the integrins acting on NK cells promote the upregulation of VAV1/Tiam1, RAC, and IRSp53, leading to increased expression of Arp2/3 and F-actin in PEECs in the PRRSV + LPS(+) groups. However, the highly expressed cell microfilaments and cytoskeleton disrupt the original network structure, causing changes in the original physiological function of the PEECs. In summary, the PRRSV protein interacts with cytokines and cytokine receptors of PEECs, thereby enhancing virus-mediated chemokine factors and their receptor activity, accelerating bacterial endotoxin entry into the body and the invasion of cells. They destroy the cytoskeletal structure of the cells and increase damage to uterine tissue.

Ginsenoside Rh2 Alleviates LPS-Induced Inflammatory Responses by Binding to TLR4/MD-2 and Blocking TLR4 Dimerization.

Lipopolysaccharide (LPS) triggers a severe systemic inflammatory reaction in mammals, with the dimerization of TLR4/MD-2 upon LPS stimulation serving as the pivotal mechanism in the transmission of inflammatory signals. Ginsenoside Rh2 (G-Rh2), one of the active constituents of red ginseng, exerts potent anti-inflammatory activity. However, whether G-Rh2 can block the TLR4 dimerization to exert anti-inflammatory effects remains unclear. Here, we first investigated the non-cytotoxic concentration of G-Rh2 on RAW 264.7 cells, and detected the releases of pro-inflammatory cytokines in LPS-treated RAW 264.7 cells, and then uncovered the mechanisms involved in the anti-inflammatory activity of G-Rh2 through flow cytometry, fluorescent membrane localization, Western blotting, co-immunoprecipitation (Co-IP), molecular docking and surface plasmon resonance (SPR) analysis in LPS-stimulated macrophages. Our results show that G-Rh2 stimulation markedly inhibited the secretion of LPS-induced interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and nitric oxide (NO). Additionally, G-Rh2 blocked the binding of LPS with the membrane of RAW 264.7 cells through direct interaction with TLR4 and MD-2 proteins, leading to the disruption of the dimerization of TLR4 and MD-2, followed by suppression of the TLR4/NF-κB signaling pathway. Our results suggest that G-Rh2 acts as a new inhibitor of TLR4 dimerization and may serve as a promising therapeutic agent against inflammation.

Clinical applications of a novel poly-L-lactic acid microsphere and hyaluronic acid suspension for facial depression filling and rejuvenation.

Poly L-lactic acid (PLLA) can stimulate fibrous tissue regeneration to exert a filling effect. However, severe inflammatory reactions and unsatisfactory effects remain a concern. Herein, we describe the mechanism of action, efficacy, and safety of PLLA microspheres in suspension (PLLA-b-PEG/HA) for facial contouring and soft tissue augmentation. PLLA-b-PEG/HA, ssynthesized by copolymerization with ethylene glycol, were suspended in hyaluronic acid (HA). Physiological verification was performed using scanning electron microscopy and X-ray computed tomography. PLLA-b-PEG/HA were subcutaneously injected into the dorsal region of 4-month-old rabbits. Ultrasound assessed volumetric capacity at 3 days and 1, 2, 4, and 12 weeks. The inflammatory response, collagen production, and HA degradation were evaluated. A retrospective case series of 10 patients who received PLLA-b-PEG/HA injections was conducted to assess long-term efficacy and safety. PLLA-b-PEG exhibited a spherical structure with a smooth surface (20-45 μm diameter). In rabbits, implant site volume increased within 4 weeks, gradually decreasing thereafter. Fibrous capsules, microvessel density, and new collagen fiber formation progressively increased at 4, 12, and 26 weeks after injection. Clinical data demonstrated significant improvements in face contouring at months 3 and 12 after injection. All patients showed improved internal contours based on the Global Aesthetic Improvement Scale. After 12 months, 90% of the patients retained good shaping and support effects with minimal adverse reactions. PLLA-b-PEG/HA demonstrated superior biocompatibility and facial regeneration potential, with outstanding dual collagen-stimulating properties. The clinical efficacy and safety of PLLA-b-PEG/HA have been validated and established as a promising therapeutic option.

Peculiarities of laboratory parameters dynamics during helicobacter pylori eradication in patients with rheumatoid arthritis

Helicobacter pylori (H. pylori) is able to participate in the pathogenesis of a number of autoimmune diseases, actively maintains chronic inflammation and stimulates the systemic immune response. The virulence factor of H. pylori is cytotoxin-associated gene A (CagA) is associated with more severe inflammatory reactions, increased risk of poor clinical outcomes and is able to influence the efficacy of infection eradication in patients with rheumatoid arthritis (RA).Purpose of the study. To evaluate laboratory parameters of H. pylori eradication efficacy in RA patients with chronic infection with the strain encoding cytotoxin-associated gene A.Materials and methods. Forty women with RA and confirmed chronic H. pylori infection were included in the study (mean age 55.5±8.7 years; mean disease duration 13.9±9.1 years; DAS-28–3.96±0.56). CagA-IgG associated H. pylori infection was diagnosed in 22 (group I, CagA+) and not diagnosed in 18 (group II, CagA-) patients. All RA patients underwent a course of H. pylori eradication therapy.Results. The process of H. pylori eradication had the most significant effect on laboratory parameters of CagA-negative RA patients (group II). In this group the levels of rheumatoid factor (p=0,028), C-reactive protein (CRP, p=0.001), interleukin-6 (IL-6, p=0.002), tumor necrosis factor alpha (p=0,023), angiopoietinlike protein type 3 (p=0.026) and antibodies to cyclic citrullinated peptide (ACCP, p=0,016) decreased significantly. In patients from group I (CagA+) most parameters remained practically unchanged (p>0.05), except for CRP (p=0.01) and IL-6 (p=0.011). In the short term, the success of eradication in CagA+ patients was significantly lower than in CagA- patients (p=0.033). Moreover, confirmation of successful eradication of H. pylori within the established period of time was extremely rare (p=0.009) in the combination of CagA+ and high titers of ACCP and antibodies to modified citrullinated vimentin.Conclusions. The effectiveness of H. pylori eradication in RA patients depends on the presence of chronic infection with the strain encoding the cytotoxin-associated gene A and the level of antibodies to citrullinated proteins, which should be taken into account when choosing the therapeutic effect on H. pylori in this group.

Study of the Effect of Tumor Necrosis Factor Alpha (TNF-α) Antagonist (Adalimumab) on Giardiasis in Mice

Abstract Giardia lamblia (G. lamblia) is the most common worldwide intestinal protozoal. Serum TNF-α contributes to the recovery from Giardia lamblia infection especially in the first and second week of infection. TNF-α antagonists are biologics used to treat many inflammatory diseases as rheumatoid arthritis. The present study aimed to study the effect of TNF-α antagonist (Adalimumab) on experimental giardiasis in mice by parasitological and histopathological examination. A total of 45 parasite-free laboratory-bred Swiss albino mice included into 2 main groups: test group and control group were used. Test group included mice infected with G. lamblia and receiving three intraperitoneal Adalimumab injections from days 9 till 15 post infection (pi). This group was further subdivided into 3 subgroups (Ia, Ib, Ic) according to Adalimumab doses which were 1.5, 3 and 6 mg/kg BW, received, respectively. Control group (non-Adalimumab-treated group) included a non-infected healthy group and Giardia -infected group. Monitoring the serum TNF-α level in all mice was done on two occasions (day 16 and 28 pi) by ELISA to follow variation in its level with and without administration of the drug. Infection outcome was assessed by following cyst shedding in stools of infected mice on intermittent days, counting trophozoites in intestinal wash, registering weight of animals, and recording pathological changes occurring in histopathological sections from small intestine. Highly significant increase in serum TNF-α was recorded in infected control mice on day 16 post-infection than in normal control group. Similarly, a significant increase in TNF-α level in the 3 test subgroups but attaining significant lower levels. On day 28 post infection, serum TNF- α level decreased in all infected mice with no significant differences being higher in infected control group than in non-infected control group. On assessing the effect of decreased serum TNF-α by the drug on infection outcome, highly significant increases in cyst shedding were recorded in the test group specifically group receiving 3 mg/kg BW than in control infected group on day 16 pi, and in trophozoite counts on day 28 pi. Mice weight gain was highly significant being more in control non-infected group than in control infected group. It was significantly lower in test group than normal infection control. The intestinal sections of test subgroups showed moderate to severe inflammatory reaction with more inflammatory cellular infiltration in the lamina propria causing villous shortening and blunting more than that observed in infection control group. Furthermore, lymphoid follicles and sloughing of the epithelium were only observed in test subgroups on day 16 p.i. It was concluded that TNF-α antagonist (Adalimumab) led to increased parasitic load as evidenced by cyst shedding, trophozoite count, less weight gains with moderate to severe histopathological damage in test subgroups.

Slit2–Robo4 signal pathway and tight junction in intestine mediate LPS-induced inflammation in mice

BackgroundSepsis is one of the most common clinical diseases, which is characterized by a serious and uncontrollable inflammatory response. LPS-induced inflammation is a critical pathological event in sepsis, but the underlying mechanism has not yet been fully elucidated.MethodsThe animal model was established for two batches. In the first batch of experiments, Adult C57BL/6J mice were randomly divided into control group and LPS (5 mg/kg, i.p.)group . In the second batch of experiments, mice were randomly divided into control group, LPS group, and LPS+VX765(10 mg/kg, i.p., an inhibitor of NLRP3 inflammasome) group. After 24 hours, mice were anesthetized with isoflurane, blood and intestinal tissue were collected for tissue immunohistochemistry, Western blot analysis and ELISA assays.ResultsThe C57BL/6J mice injected with LPS for twenty-four hours could exhibit severe inflammatory reaction including an increased IL-1β, IL-18 in serum and activation of NLRP3 inflammasome in intestine. The injection of VX765 could reverse these effects induced by LPS. These results indicated that the increased level of IL-1β and IL-18 in serum induced by LPS is related to the increased intestinal permeability and activation of NLRP3 inflammasome. In the second batch of experiments, results of western blot and immunohistochemistry showed that Slit2 and Robo4 were significant decreased in intestine of LPS group, while the expression of VEGF was significant increased. Meanwhile, the protein level of tight junction protein ZO-1, occludin, and claudin-5 were significantly lower than in control group, which could also be reversed by VX765 injection.ConclusionsIn this study, we revealed that Slit2-Robo4 signaling pathway and tight junction in intestine may be involved in LPS-induced inflammation in mice, which may account for the molecular mechanism of sepsis.

Clinical, radiological, and laboratory features of HIV-negative pulmonary cryptococcosis with regard to serum lateral flow assay.

Cryptococcosis is the second most common invasive yeast infection in China. Pulmonary cryptococcosis (PC) is difficult to diagnose due to the lack of specific clinical features and the limitation of diagnostic techniques. Although lateral flow assay was very useful in diagnosing cryptococcal infection, quite a few patients with PC presented negative serum lateral flow assay (sLFA). We conducted a retrospective study of HIV-negative patients who were diagnosed with PC in our hospital over the past decade to explore the potential relationship between the clinical profiles and sLFA in PC. In total, 112 patients with sLFA tested were enrolled in this study, of which 58.93% were male. The positivity rate of sLFA for PC was 91.07%. The extent of pulmonary lesions was positively correlated with sLFA grade (Spearman r = 0.268, p < 0.01). Solitary nodule (SN) and pneumonia were the most common imaging findings in PC with negative and positive sLFA respectively. Among 65 symptomatic PC patients, 14 presented with fever and had higher hypersensitive C-reactive protein (hsCRP) level and more extensive pulmonary involvement (Mann-Whitney U test, p < 0.05) than those without fever. Symptomatic PC patients were more likely to have positive results of sLFA (Mann-Whitney U test, p = 0.05) compared against asymptomatic ones. In conclusion, negative sLFA cannot exclude PC in patients with a solitary nodule in lung. Positive sLFA is more reliable in diagnosing PC in symptomatic patients with diffused lesions in lung who generally experience a more severe systemic inflammatory reaction.

Unraveling the Molecular Regulation of Ferroptosis in Respiratory Diseases.

Ferroptosis, a type of programmed cell death that relies on iron, is distinct in terms of its morphological, biochemical and genetic features. Unlike other forms of cell death, such as autophagy, apoptosis, necrosis, and pyroptosis, ferroptosis is primarily caused by lipid peroxidation. Cells that die due to iron can potentially trigger an immune response which intensifies inflammation and causes severe inflammatory reactions that eventually lead to multiple organ failure. In recent years, ferroptosis has been identified in an increasing number of medical fields, including neurological pathologies, chronic liver diseases and sepsis. Ferroptosis has the potential to cause an inflammatory tempest, with many of the catalysts and pathological indications of respiratory ailments being linked to inflammatory reactions. The growing investigation into ferroptosis in respiratory disorders has also garnered significant interest to better understand the mechanism of ferroptosis in these diseases. In this review, the recent progress in understanding the molecular control of ferroptosis and its mechanism in different respiratory disorders is examined. In addition, this review discusses current challenges and prospects for understanding the link between respiratory diseases and ferroptosis.

Injectable nanoparticle-crosslinked xyloglucan/ε-poly-l-lysine composite hydrogel with hemostatic, antimicrobial, and angiogenic properties for infected wound healing

Skin wounds are susceptible to infection, leading to severe inflammatory reactions that can progress to chronic wounds, ultimately causing significant physical and mental distress to the patient. In this study, we propose an injectable composite hydrogel achieved through one-pot gelation of oxidized xyloglucan (OXG), cationic polyamide ε-poly-l-lysine (EPL), and surface amino-rich silicon nanoparticles (SiNPs). OXG exhibits commendable anti-inflammatory properties and provides crosslinking sites. SiNPs serve as mechanically reinforced crosslinkers, facilitating the construction of a dynamic Schiff base network. SiNPs significantly reduced the gelation time to 3 s and tripled the storage modulus of the hydrogels. Additionally, the combination of EPL and SiNPs demonstrated synergistic antimicrobial activity against both S. aureus and E. coli. Notably, the hydrogel effectively halted liver bleeding within 30 s. The hydrogel demonstrated outstanding shear-thinning and self-healing properties, crucial considerations for the design of injectable hydrogels. Furthermore, its efficacy was evaluated as a wound dressing in a mouse model with S. aureus infection. The results indicated that, compared to commercial products, the hydrogel exhibited a shorter wound healing time, decreased inflammation, thinner epithelium, increased hair follicles, enhanced neovascularization, and more substantial collagen deposition. These findings strongly suggest the promising potential of the proposed hydrogel as an effective wound dressing for the treatment of infected wounds.

Combined Plasma Olink Proteomics and Transcriptomics Identifies CXCL1 and TNFRSF12A as Potential Predictive and Diagnostic Inflammatory Markers for Acute Kidney Injury.

Acute kidney injury (AKI) poses a significant global public health challenge. Current methods for detecting AKI rely on monitoring changes in serum creatinine (Scr), blood urea nitrogen (BUN), urinary output and some commonly employed biomarkers. However, these indicators are usually neither specific nor sensitive to AKI, especially in cases of mild kidney injury. AKI is accompanied by severe inflammatory reactions, resulting in the upregulation of numerous inflammation-associated proteins in the plasma. Plasma biomarkers are a noninvasive method for detecting kidney injury, and to date, plasma inflammation-associated cytokines have not been adequately studied in AKI patients. The objective of our research was to identify novel inflammatory biomarkers for AKI. We utilized Olink proteomics to analyze the alterations in plasma inflammation-related proteins in the serum of healthy mice (n = 2) or mice treated with cisplatin (n = 6). Additionally, transcriptome datasets for the lipopolysaccharide (LPS), cisplatin, and ischemia‒reperfusion injury (IRI) groups were obtained from the National Center of Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database. We calculated the intersection of differentially expressed proteins (DEPs) and genes (DEGs) from both datasets. In the Olink proteomics analysis, the AKI group had significantly greater levels of 11 DEPs than did the control group. In addition, 56 common upregulated DEGs were obtained from the transcriptome dataset. The expression of CXCL1 and TNFRSF12A overlapped across all the datasets. The transcription and protein expression levels of CXCL1 and TNFRSF12A were detected in vivo. The gene and protein levels of CXCL1 and TNFRSF12A were significantly increased in different AKI mouse models and clinical patients, suggesting that these genes and proteins could be potential specific biomarkers for the identification of AKI.

Surgical therapy and pathogen detection in endogenous endophthalmitis : Analysis of data from five German eye hospitals

Endogenous endophthalmitis results from hematogenous spread of bacterial or fungal infection in severely diseased patients. Specific systemic and intraocular therapy is required. The basis for this treatment is causal pathogen detection in blood culture or vitreous sample. However, functional results are limited. The current article provides practical hints for surgical therapy and pathogen detection in patients with endogenous endophthalmitis. Aretrospective analysis of anonymous data of 68male and female patients from 2018-2023 from five ophthalmology clinics in Germany was performed. Mean age of affected patients was 71.4years (31-96years). Surgical therapy included pars plana vitrectomy (ppV) and intravitreal injection (IVOM). In 44of 68patients (65%), 1-3 surgeries were performed, 4-6surgeries were required in 14/68 (21%) of patients, and 10or more surgeries were required in 4/68patients (6%). Pathogen detection was possible in 34% of vitreous specimens and in 11% of anterior chamber samples. Mean initial visual acuity was logMAR1.5. After treatment and amean follow-up of 2.5months, mean visual acuity was logMAR1.3. Preanalytical methods for specimen collection like the Freiburg endophthalmitis set to optimize pathogen detection are presented. Severe inflammatory intraocular reactions in endogenous endophthalmitis necessitate acombination of ppV and repeated IVOM. In addition to providing avitreous sample, ppV also serves to remove inflammatory fibrin membranes. Early pars plana vitrectomy with specific antibiotic or antifungal therapy should be sought in addition to the focus search and systemic therapy.

THERAPEUTIC EVALUATION OF CENTELLA ASIATICA MACERATE ON SURGICAL COMPLICATIONS OF OVARIOHYSTERECTOMY IN THE BITCH

Background and objectives: The management of post-operative complications such as severe inflammatory reactions, suture dehiscence and abdominal hernia in farm animals calls for a variety of practices, including the use of plant resources. The aim of this study is to explore practices for managing surgical complications in bitches and the healing properties of Centella asiatica. Methods: Discussions were organised with bitch owners about the practice of ovariohysterectomy and its importance for the well-being of the animals. The harvested plant was then prepared and the resulting crushed material was macerated, followed by the addition of drinking water. The subjects were divided into two batches of 6 animals: the control batch (batch 1) and the extract batch (batch 2). Before applying the macerate, the wounds were cleaned with distilled water and then an absorbent paper towel was used to dry them. Results : Application of C. asiatica macerate to post-operative wounds in female dogs showed good clinical applicability, with anti-inflammatory and wound-healing accelerating activity. The therapeutic potential of the plant is thought to be attributable to its most important bioactive components. Conclusion : The study argues that C. asiatica could be a better alternative for surgical wound closure, helping breeders to minimize intervention costs. Peer Review History: Received: 19 October 2023; Revised: 10 November; Accepted: 25 December, Available online: 15 January 2024 Academic Editor: Dr. Emmanuel O. Olorunsola, Department of Pharmaceutics &amp; Pharmaceutical Technology, University of Uyo, Nigeria, olorunsolaeo@yahoo.com Received file: Reviewer's Comments: Average Peer review marks at initial stage: 5.5/10 Average Peer review marks at publication stage: 7.0/10 Reviewers: Dr. Adebayo Gege Grace Iyabo, University of Ibadan, Nigeria, funbimbola@gmail.com Dr. Alfonso Alexander Aguileral, University of Veracruz, Mexico, aalexander_2000@yahoo.com

Microparticle-associated tissue factor activity correlates with the inflammatory response in septic disseminated intravascular coagulation patients.

Sepsis is often accompanied by the formation of disseminated intravascular coagulation (DIC). Microparticles can exert their procoagulant and proinflammatory properties in a variety of ways. The purpose of this study was to investigate the relationship between microparticle-associated tissue factor activity (TF+-MP activity) and the inflammatory response. Data from a total of 31 DIC patients with sepsis and 31 non-DIC patients with sepsis admitted to the ICU of the First Affiliated Hospital of Harbin Medical University from December 2017 to March 2019 were collected. Blood samples were collected and DIC scores were calculated on the day of enrollment. The hospital's clinical laboratory completed routine blood, procalcitonin, and C-reactive protein tests. TF+-MP activity was measured using a tissue factor-dependent FXa generation assay. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) levels were determined using ELISA kits. Compared with the non-DIC group, the DIC group had higher levels of leukocytes, neutrophils, procalcitonin, C-reactive protein, IL-1β, and TNF-α, and more severe inflammatory reactions. TF+-MP activity in the DIC group was higher than that in the non-DIC group. In sepsis patients, TF+-MP activity was strongly correlated with inflammatory response indices and DIC scores. TF+-MP activity may play a major role in promoting inflammatory response in septic DIC.

Isoflurane preconditioning protects against renal ischemia/reperfusion injury in diabetes via activation of the Brg1/Nrf2/HO-1 signaling pathway.

To examine whether isoflurane preconditioning (IsoP) has a protective effect against renal ischemia/reperfusion injury (I/RI) in diabetic conditions and to further clarify the underlying mechanisms. Control and streptozotocin-induced diabetic rats were randomly assigned to five groups, as follows: normal sham, normal I/R, diabetic sham, diabetic I/R, and diabetic I/R + isoflurane. Renal I/RI was induced by clamping renal pedicle for 45 min followed by reperfusion for 24 h. IsoP was achieved by exposing the rats to 2% isoflurane for 30 min before vascular occlusion. Kidneys and blood were collected after reperfusion for further analysis. Renal histology, blood urea nitrogen, serum creatinine, oxidative stress, inflammatory cytokines, and renal cell apoptosis were assessed. Furthermore, the expression of brahma related gene 1 (Brg1), nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and nuclear factor-κB (NF-κB) were determined. Compared with control, diabetic rats undergoing I/R presented more severe renal injury, oxidative stress, inflammatory reaction, and apoptosis with the impairment of Brg1/Nrf2/HO-1 signaling. All these alterations were significantly attenuated by pretreatment with isoflurane. These findings suggest that isoflurane could alleviate renal I/RI in diabetes, possibly through improving Brg1/Nrf2/HO-1 signaling.

Immunohistochemical Alterations of Syndecan-1 in Sheep Liver with Cystic Echinococcosis

Cystic echinococcosis is formed by the larval forms of Echinococcus granulosus, causes health problems in humans and different species of animals worldwide. There is still limited information about the pathophysiological response to cystic echinococcosis in the liver. Syndecan-1 (Sdc1) is a cell surface proteoglycan of the liver. It has a crucial role in the pathophysiology of various liver diseases. This study aimed to investigate the immunohistochemical expression of Sdc1 in the liver with cystic echinococcosis in sheep. A total number of 51 liver tissue samples with cystic echinococcosis and ten healthy livers were examined. The tissue samples were stained with hematoxylin-eosin (HE) for histopathological examinations. Sdc1 was determined in the same liver tissues by immunohistochemistry. Infected liver tissues mainly showed severe inflammatory reactions, congestion, diffuse degeneration, and necrosis of hepatocytes around the cysts. The results indicated severe Sdc1-positive staining in hepatocytes around the cysts. Liver tissues of the control group showed relatively mild immunopositive reactions. This study determined that the Sdc1 significantly increased in the sheep livers with cystic echinococcosis infection.