Activation Of Immune System Research Articles

The neutrophil–lymphocyte ratio as a risk factor for all-cause mortality among individuals with resolved HBV infection: evidence from the NHANES 1999–2018

BackgroundInflammation is a critical component in the process of resolved hepatitis B virus (HBV) infection. The neutrophil-to-lymphocyte ratio (NLR) serves as a sensitive indicator of systemic inflammation and immune activation. Our study aimed to investigate the correlation between elevated NLR levels and the risk of all-cause mortality in patients with resolved HBV infection. Additionally, we evaluated the potential mediating effect of diabetes mellitus (DM) on this correlation.MethodsOur study enrolled 1,146 adult patients with resolved HBV infection from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2018. We utilized the Restricted Cubic Splines (RCS) and Maximum Selection Rank Statistical Method (MSRSM) to analyze the relationship between the NLR and the risk of all-cause mortality. The impact of NLR was evaluated using a weighted multivariate Cox regression model, and the model’s predictive accuracy was assessed using time-dependent Receiver Operating Characteristic (ROC) curves. An intermediary analysis was conducted to explore the potential influence of DM on the observed relationship.ResultsDuring follow-up period of 103.54 ± 4.90 months, we recorded 207 deaths among the study participants. The analysis using the RCS method revealed a significant positive correlation between the NLR and the risk of all-cause mortality. Those with elevated NLR levels faced a substantially higher mortality risk compared to those with lower levels, as indicated by a Hazard Ratio (HR) of 1.84, with a 95% Confidence Interval (CI) of 1.17 to 2.89 (p < 0.05). The predictive accuracy of the model was substantial, as evidenced by the Area Under the Curve (AUC) for ROC curves at 3, 5, and 10 years, which were 0.873, 0.870, and 0.862, respectively. Furthermore, mediation analysis indicated that DM significantly influenced the relationship between the NLR and mortality, with a mediation effect of 6.57% (95% Confidence Interval [CI]: 0.64 to 15%; p = 0.02).ConclusionElevated NLR is significantly associated with an increased risk of all-cause mortality in patients with resolved HBV infection. Concurrently, DM acts as a partial mediator of this association.

Effects of Microbes on Insect Host Physiology and Behavior Mediated by the Host Immune System

Innate immunity is critical for insects to adjust to complicated environments. Studying the insect immune system can aid in identifying novel insecticide targets and provide insights for developing novel pest control strategies. Insects recognize environmental pathogens through pattern recognition receptors, thus activating the innate immune system to eliminate pathogens. The innate immune system of insects primarily comprises cellular immunity and humoral immunity. Toll, immune deficiency, and Janus kinase/signal transducers and activators of transcription are the main signaling pathways regulating insect humoral immunity. Nevertheless, increasing research has revealed that immune signaling activated by microbes also performs non-immune roles while exerting immune roles, and insulin signaling performs a key role in mediating the connection between the immune system and non-immune physiological activities. Therefore, this paper first briefly reviews the main innate immune signaling and insulin signaling of insects, then summarizes the relationship between immune signaling activated by microbes and insect growth and development, reproduction, pesticide resistance, chemical communication, cell turnover, lifespan, sleep, energy generation pathways and their possible underlying mechanisms. Future research directions and methodologies are also proposed, aiming to provide insights into further study on the physiological mechanism linking microbes and insect hosts.

The putative role of immune-inflammatory mechanisms in nociplastic pain pathways: a narrative review

Nociplastic pain is the fourth category of pain defined in recent years. It is a pain arising from altered nociception, despite the lack of clear evidence of actual or threatened tissue damage that causes activation of peripheral nociceptors nor evidence for disease or lesion of the somatosensory system causing the pain. This type of pain is usually multifocal, more diffuse or intense than expected and it is usually associated with other central nervous system-derived symptoms, such as fatigue, sleep, memory, and mood problems. It can occur in isolation or as part of a mixed-pain state in combination with ongoing nociceptive or neuropathic pain. It is associated with increased social and sanitary costs due to the difficulty of adequately treating it. Its pathogenesis is still poorly understood, even if a mounting body of evidence suggests a pivotal role in inflammation and immunity, which may be triggered by an infection and/or a trauma. This narrative review aims to summarise the current knowledge about the interplay of the immune system and nociplastic pathways activation and amplification. The challenge for the future will be to identify the exact role of inflammation and immunity, the cause of this activation, and its link to other pathogenetic factors of nociplastic pain, such as diet or microbiota alteration, social and phycological factors, together with a genetic and epigenetic predisposition.

Kidney Injury Following Cardiac Surgery: A Review of Our Current Understanding.

Around one-quarter of all patients undergoing cardiac procedures, particularly those on cardiopulmonary bypass, develop cardiac surgery-associated acute kidney injury (CSA-AKI). This complication increases the risk of several serious morbidities and of mortality, representing a significant burden for both patients and the healthcare system. Patients with diminished kidney function before surgery, such as those with chronic kidney disease, are at heightened risk of developing CSA-AKI and have poorer outcomes than patients without preexisting kidney injury who develop CSA-AKI. Several mechanisms are involved in the development of CSA-AKI; injury is primarily thought to result from an amplification loop of inflammation and cell death, with complement and immune system activation, cardiopulmonary bypass, and ischemia-reperfusion injury all contributing to pathogenesis. At present there are no effective, targeted pharmacological therapies for the prevention or treatment of CSA-AKI, although several preclinical trials have shown promise, and clinical trials are under way. Progress in the understanding of the complex pathophysiology of CSA-AKI is needed to improve the development of successful strategies for its prevention, management, and treatment. In this review, we outline our current understanding of CSA-AKI development and management strategies and discuss potential future therapeutic targets under investigation.

Multi-omics integration and immune profiling identify possible causal networks leading to uterine microbiome dysbiosis in dairy cows that develop metritis

BackgroundCows that develop metritis experience dysbiosis of their uterine microbiome, where opportunistic pathogens overtake uterine commensals. An effective immune response is critical for maintaining uterine health. Nonetheless, periparturient cows experience immune dysregulation, which seems to be intensified by prepartum over-condition. Herein, Bayesian networks were applied to investigate the directional correlations between prepartum body weight (BW), BW loss, pre- and postpartum systemic immune profiling and plasma metabolome, and postpartum uterine metabolome and microbiome.ResultsThe Bayesian network analysis showed a positive directional correlation between prepartum BW, prepartum BW loss, and plasma fatty acids at parturition, suggesting that heavier cows were in lower energy balance than lighter cows. There was a positive directional correlation between prepartum BW, prepartum systemic leukocyte death, immune activation, systemic inflammation, and metabolomic changes associated with oxidative stress prepartum and at parturition. Immune activation and systemic inflammation were characterized by increased proportion of circulating polymorphonuclear cells (PMN) prepartum, B-cell activation at parturition, interleukin-8 prepartum and at parturition, and interleukin-1β at parturition. These immune changes together with plasma fatty acids at parturition had a positive directional correlation with PMN extravasation postpartum, which had a positive directional correlation with uterine metabolites associated with tissue damage. These results suggest that excessive PMN migration to the uterus leads to excessive endometrial damage. The aforementioned changes had a positive directional correlation with Fusobacterium, Porphyromonas, and Bacteroides in cows that developed metritis, suggesting that excessive tissue damage may disrupt physical barriers or increase substrate availability for bacterial growth.ConclusionsThis work provides robust mechanistic hypotheses for how prepartum BW may impact peripartum immune and metabolic profiles, which may lead to uterine opportunistic pathogens overgrowth and metritis development.

Investigating the impact of mitochondrial DNA: Insights into blood transfusion reactions and mitigation strategies.

Although transfusion reactions occur in less than 2% of recipients, they are currently one of the most serious concerns in blood transfusion. Damage-associated molecular patterns (DAMPs) are released from injured, stressed or dead cells, leading to inflammation and immune system activation. One of the recognized DAMPs is mitochondrial DNA (mtDNA). It is found in various blood products, including fresh frozen plasma (FFP), red blood cell units (RBCUs) and platelet concentrates (PCs), and can induce adverse reactions in recipients by stimulating the innate immune system and inflammatory cellular pathways. The aim of this study was to investigate the factors influencing the release of mtDNA in various blood products and its subsequent impact on transfusion reactions. In this study, mtDNA, mitochondrial DNA, mtDNA DAMPs, extracellular mtDNA, blood products, blood components and transfusion reactions between 2009 and 2023 were searched in Google Scholar, PubMed and Scopus databases. This study has demonstrated the presence of mtDNA in the extracellular milieu of various blood products, including PCs, FFP and RBCUs. Understanding the determinants of mtDNA release and its implications for transfusion safety is critical. Strategies aimed at reducing mtDNA release, such as optimizing preparation techniques and donor selection criteria, hold promise for reducing transfusion-related complications. By addressing these factors, healthcare providers can enhance the safety and efficacy of blood transfusion practices, ultimately improving patient outcomes.

The Amphibian Major Histocompatibility Complex-A Review and Future Outlook.

The major histocompatibility complex (MHC) is a cluster of functionally related genes encoding proteins which, among other functions, mediate immune system activation. While the MHC of many vertebrates has been extensively studied, less is known about the amphibian MHC. This represents an important knowledge gap because amphibians mark the evolutionary transition from an aquatic to a terrestrial lifestyle and often maintain a biphasic lifestyle. Hence, they tend to be exposed to both aquatic and terrestrial pathogen communities, providing opportunities to gain fundamental insights into how the immune system responds to different environmental challenges. Moreover, amphibians are globally threatened by invasive pathogens and the MHC may play a role in combating population decline. In this review, we summarize the current state of knowledge regarding the amphibian MHC and identify the major differences with other vertebrates. We also review how the number of MHC gene copies varies across amphibian groups and how MHC-based variation relates to amphibian ontogeny, behaviour, disease, and phylogeography. We conclude by identifying knowledge gaps and proposing priorities for future research.

Unraveling the ROS-Inflammation-Immune Balance: A New Perspective on Aging and Disease.

Increased entropy is a common cause of disease and aging. Lifespan entropy is the overall increase in disorder caused by a person over their lifetime. Aging leads to the excessive production of reactive oxygen species (ROS), which damage the antioxidant system and disrupt redox balance. Organ aging causes chronic inflammation, disrupting the balance of proinflammatory and anti-inflammatory factors. Inflammaging, which is a chronic low-grade inflammatory state, is activated by oxidative stress and can lead to immune system senescence. During this process, entropy increases significantly as the body transitions from a state of low order to high disorder. However, the connection among inflammation, aging, and immune system activity is still not fully understood. This review introduces the idea of the ROS-inflammation-immune balance for the first time and suggests that this balance may be connected to aging and the development of age-related diseases. We also explored how the balance of these three factors controls and affects age-related diseases. Moreover, imbalance in the relationship described above disrupts the regular structures of cells and alters their functions, leading to cellular damage and the emergence of a disorganized state marked by increased entropy. Maintaining a low entropy state is crucial for preventing and reversing aging processes. Consequently, we examined the current preclinical evidence for antiaging medications that target this balance. Ultimately, comprehending the intricate relationships between these three factors and the risk of age-related diseases in organisms will aid in the development of clinical interventions that promote long-term health.

Protein profile of purified plasma- and aqueous humor-derived extracellular vesicles from patients with ocular toxoplasmosis.

To characterize the extracellular vesicle protein cargo in the aqueous humor and plasma of patients with ocular toxoplasmosis. Aqueous humor and plasma were collected from six patients with active ocular toxoplasmosis and six patients with cataract. Extracellular vesicles were isolated, and western blotting and mass spectrometry were performed for protein analysis. All plasma samples from patients with ocular toxoplasmosis and cataract were positive for the tetraspanins CD63 and TSG101. However, the aqueous humor from patients with ocular toxoplasmosis was positive only for CD63. Sixty-seven new unreported proteins were identified in the aqueous humor and plasma of patients with the ocular toxoplasmosis and cataract. Of the 67 proteins, 10 and 7 were found only in the cataract and ocular toxoplasmosis groups, respectively. In general, these proteins were involved in immune system activation and retina homeostasis and were related to infections and retina-associated diseases. The distinct protein signatures between ocular toxoplasmosis and cataract may be helpful in the differential diagnosis of ocular toxoplasmosis. However, more studies are needed to better understand the role of these proteins in the pathogenesis of ocular toxoplasmosis.

The Relationship of Th1/Th2 Cytokine Polarization at Parturition in Cows and SOCS3 Level With Some Postpartum Diseases.

Th1/Th2 polarisation and suppressor of cytokine signalling-3 (SOCS3) are important indicators of the humoral and cellular immune system activity in cows. The aim of this study was to determine the correlation of postpartum diseases with the levels of Th1/Th2 polarisation and SOCS3 at the time of parturition. The study examined 180 cows (90 with normal parturition [NP] and 90 with dystocia [D]). Blood samples were taken from the cows once at the time of calving. Two subgroups were created among cows with NP: those without the postpartum disease (NP [-], n = 45) and those with postpartum disease (NP [+], n = 45). Likewise, two subgroups were created among D cows: those without postpartum disease (D [-], n = 45) and those with postpartum disease (D [+], n = 45). Cytokine analyses were performed using species-specific commercial ELISA kits. In the NP (-) group, it was found that Th1/Th2 cytokine polarisation was in the Th1 direction due to the increase in the concentration of IFN-γ, TNF-α and IL-2 in four subgroups grouping with different types of parturition and diseases. It was concluded that it would be appropriate to strengthen cellular immunity. In cases of postpartum diseases, Th1/Th2 polarisation shifted towards Th2 due to the increase in IL-4 and IL-5 concentrations in cows that performed NP and developed mastitis in the postpartum period. These results suggest that it would be beneficial to support the Th2 aspect (i.e. humoral immunity) in cows that have undergone NP and develop mastitis in the postpartum period.

Concurrent Amplification of Ferroptosis and Immune System Activation Via Nanomedicine-Mediated Radiosensitization for Triple-Negative Breast Cancer Therapy.

Radiation therapy (RT) is one of the core therapies for current cancer management. However, the emergence of radioresistance has become a major cause of radiotherapy failure and disease progression. Therefore, overcoming radioresistance to achieve highly effective treatment for refractory tumors is significant yet challenging. Here, pH-responsive DSPE-PEoz modified hollow Bi2Se3-RSL3/diABZi (DP-HBN/RA) nanomedicine is designed as a radiation sensitizer for efficient treatment of triple-negative breast cancer by simultaneously amplifying ferroptosis and immune system activation. DP-HBN/RA can efficiently concentrate X-ray radiation energy inside the tumor, thereby promoting precise ionizing radiation exposure in tumor cells to produce large amounts of reactive oxygen species (ROS), leading to lipid peroxidation-induced ferroptosis. Meanwhile, ferroptotic cell death is intensified through the inactivation of GPX4 by RSL3 released from DP-HBN/RA to acidic conditions in the tumor microenvironment. Additionally, DP-HBN/RA enhances RT efficacy to exacerbate unrepairable DNA damage and release DNA fragments that activate the cGAS-STING signal pathway, evoking a systematic immune response. Ingeniously, the released diABZi reinforces cGAS-STING activation to boost the immunology antitumor effect. This work links the induction of ferroptosis and the initiation of systematic immune response to achieve highly effective tumor suppression, which opens up new avenues for future treatments of refractory tumors.

The role of kynurenine and kynurenine metabolites in psoriasis

Abstract Objectives Psoriasis is a widespread immunological disease characterised by inflammation and primarily associated with skin and joint symptoms. The kynurenine pathway significantly influences inflammation and immune system activity. The aim of this study is to determine serum concentrations of kynurenine metabolites in patients with psoriasis and investigate their correlation with disease severity. Methods This study included 30 participants with psoriasis and 30 individuals without the disease as healthy controls. Serum levels of tryptophan, kynurenine, 3-OH anthranilic acid, quinolinic acid, 3-OH kynurenine, and kynurenic acid were determined by liquid chromatography-mass spectrometry (LC-MS/MS). Results Serum levels of kynurenic acid (p<0.001), tryptophan (p<0.001) and the tryptophan/kynurenine ratio (TKR) (p<0.001) were statistically significantly lower in psoriasis patients than in healthy controls, while levels of quinolinic acid (p=0.007) and kynurenine (p=0.001) were significantly higher. The Psoriasis Area Severity Index (PASI) correlated positively with 3-hydroxykynurenine and kynurenic acid. Conclusions Kynurenine metabolites are associated with the pathophysiology of psoriasis and could serve as valuable candidate markers for monitoring inflammation.

Quantitative and Qualitative Analysis of Serum Exosomes at Different Stages after Ischemic Stroke

Ischemic stroke (IS) is one of the leading causes of long-term disability worldwide. At the same time, there is still no unequivocal understanding of the reasons for the varying degrees and speed of recovery of patients after IS. Recovery from IS is due to the highly organized interaction of brain structures and cells with other organs and tissues and involves a number of pathophysiological processes occurring both inside and outside the brain. Exosomes are involved in modulating pathophysiological processes after IS by mediating cell-tissue communication, primarily by delivering cargo such as proteins and microRNAs. A comparative quantitative analysis of the protein profiles of serum exosomes of patients examined at different stages after IS was carried out. Protein levels are associated with immune system functioning and coagulation in the serum exosomes of patients examined 1.5–2 years after IS was significantly higher compared to the parameters of patients examined in the earlier post-stroke period. The results indicate an increased level of immune system activation in the long post-stroke period compared to the early post-stroke period and the involvement of exosomes in this process. Further study of the molecular and biochemical parameters of exosomes in the long-term post-stroke period will allow us to assess the risks of functional outcomes of more fully IS and find potential targets for their reduction.

Silver nanoparticle toxicity in rainbow trout: insights into physiological and molecular responses

Metallic nanoparticles, with their large surface area to volume ratio, are increasingly important in various life fields, but they can cause varying toxic effects on fish. This study investigates the toxicological effects of silver nanoparticles (AgNPs) on rainbow trout (Oncorhynchus mykiss), focusing on hematological, biochemical, antioxidant, and histopathological changes. Fish were exposed to varying concentrations of AgNPs (0.2, 0.8, and 1.4 mg/L) for 21 days. Hematological analysis revealed significant reductions in red blood cell (RBC) counts, hemoglobin (Hb), and hematocrit (HCT) at higher AgNPs concentrations, while white blood cell (WBC) counts increased, indicating immune system activation. Biochemical assays demonstrated dose-dependent decreases in total protein and albumin, alongside increased cholesterol and triglyceride levels, suggesting impaired liver function and disrupted lipid metabolism. Antioxidant enzyme activity (SOD, CAT, GST) initially increased at lower AgNPs concentrations but declined at higher exposures, indicating oxidative stress. Molecular analysis further supported these findings, with upregulation of oxidative stress-related genes (SOD1, CAT) and inflammatory markers (HSP70, IL-1β). Histopathological examinations revealed necrosis, hyperplasia, and lamellar fusion in the gills, along with significant liver damage, including vacuolation and Kupffer cell proliferation, particularly at the highest exposure. Behavioral assays showed erratic swimming and reduced feeding in fish exposed to higher AgNPs concentrations. This study highlights the dose-dependent toxic effects of AgNPs on rainbow trout and underscores the potential for long-term, possibly irreversible damage at higher exposure levels. These findings emphasize the need for stricter environmental regulations on nanoparticle use to mitigate their ecological impact.

Strategies Used by SARS-CoV-2 to Evade the Innate Immune System in an Evolutionary Perspective.

By the end of 2019, the COVID-19 pandemic, resulting from the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), had diffused widely across the globe, with 770 million infected individuals and over 7 million deaths reported. In addition to its high infectivity and pathogenicity and its rapid mutation rate, the unique capacity of SARS-CoV-2 to circumvent the immune system has also contributed to the widespread nature of this pandemic. SARS-CoV-2 elicits the onset of innate immune system activation and initiates antiviral responses once it has infected the host. While battling the host's immune responses, SARS-CoV-2 has established many countermeasures to evade attack and clearance. As the exploration of SARS-CoV-2 continues, substantial evidence has revealed that the 29 proteins synthesized by the SARS-CoV-2 genome are integral to the viral infection process. They not only facilitate viral replication and transmission, but also assist SARS-CoV-2 in escaping the host's immune defenses, positioning them as promising therapeutic targets that have attracted considerable attention in recent studies. This review summarizes the manner in which SARS-CoV-2 interfaces with the innate immune system, with a particular focus on the continuous evolution of SARS-CoV-2 and the implications of mutations.

X-ray triggered bimetallic nanoassemblies as radiosensitizers and STING agonists for a CDT/radio-immunotherapy strategy.

Radiotherapy (RT) is a cornerstone of cancer therapy, but its effectiveness is constrained by dose-limiting toxicity and inadequate systemic immune activation. To overcome these limitations, we have engineered an X-ray-responsive nanoassembly (sMnAu NAs) by cross-linking monodisperse MnAu nanoparticles (NPs) with radiation-responsive diselenide-containing linkers. MnAu alloy NPs not only provide Au NPs for radiosensitization, but also control Mn (0) release, which stimulates Fenton-like reaction for chemodynamic therapy and is transferred into Mn2+ to activate the STING pathway for immunotherapy. The responsive design not only improves tumor accumulation via EPR effect during circulation, but also achieves deep penetration of MnAu NPs following X-ray induced disassembly. The synergistic combination of chemodynamic therapy, radiotherapy and immunotherapy exhibits remarkable inhibition of tumor growth and metastasis. Overall, our sMnAu NAs represent a promising radiosensitizer for chemodynamic therapy and radiotherapy to enhance immunotherapy. STATEMENT OF SIGNIFICANCE: As a principal treatment modality in cancer management, RT is limited due to the co-irradiation of organs at risk and subsequent normal tissue toxicities. This study reported an X-ray responsive radiosensitizer prepared by cross-linking monodisperse MnAu NPs with diselenide-containing linkers. Upon X-ray irradiation, sMnAu NAs accumulate in tumors and disassemble into MnAu NPs, enabling deeper penetration. The increased surface area of MnAu NPs enhances the exposure of Mn(0), which reacts into Mn2+ and enhances ROS generation. The released Mn2+ activates the STING pathway, potentiating the X-ray-induced immune response. The synergistic integration of CDT, RT, and immunotherapy results in a potent suppression of tumor growth and metastasis. Collectively, this X-ray activatable CDT/radio-immunotherapy strategy holds great potential for effective cancer treatment.

Peripheral Circulating Blood Cells Deviation Based on Tumor Inflammatory Microenvironment Activity in Resected Upstaged Lung Adenocarcinomas.

Background: The tumour inflammatory microenvironment (TIME) reflects a selective activation of the central immune system (IS), particularly T-cells expansion, which leads to immune cells migrating to the target, such as lung cancer, via the bloodstream and lymphatic vessels. In this study, the aim is to investigate whether the distribution of peripheral blood cells varies based on the immune status of patients with lung adenocarcinoma. Methods: This is a single-center retrospective study conducted in the Thoracic Surgery Unit of the University of Padua (Italy) between 1 January 2016 and 1 April 2024. It included patients (>18 years old) with lung adenocarcinoma deemed resectable (cT2bN0M0 or lower) who experienced pathological upstaging (IIB or higher). Patients were classified as TIME-active (with tumour-infiltrating lymphocytes-TILs and/or PD-L1 expression) or TIME-silent (without TILs or PD-L1). According to the TIME status, peripheral blood cell counts with clinical and pathological data were compared between groups using the Fisher's, Pearson's or Wilcoxon's test when appropriate. A Kaplan-Meier estimator investigated overall survival (OS) and recurrence-free survival (RFS) adopting the log-rank test. Results: Preoperatively, the TIME-a group demonstrated a significantly higher lymphocyte count (p = 0.02) and a lower absolute neutrophil rate (p = 0.01) than TIME-s. These differences persisted after resection (p = 0.06 and p = 0.02) while they became similar one month after surgery (p = 1 and p = 0.32). The neutrophil-to-lymphocyte ratio-NLR showed similar trends (p = 0.01 and p = 1). Better OS and RFS were shown in the TIME-a group (p = 0.02 and 0.03, respectively). Conclusions: Resected upstaged lung adenocarcinomas show distinct peripheral blood cell profiles based on immune status. TIME-active patients had a significantly lower NLR, which normalized post-surgery. Surgical resection may help restore native immune surveillance.

Radionuclide treatments of cancer: molecular mechanisms, biological responses, histopathological changes, and role of PET imaging.

Radiation treatments [radiotherapy and radionuclide treatments (RNTs)] are one of the main and effective treatment modalities of cancer. Globally, the number of cancer patients treated with radionuclides are much less as compared to number of radiotherapy cases but with the development of new radiotracers, most notably 177Lu and 225Ac-labeled prostate-specific membrane antigen ligands, and 223Ra-dichloride for prostate cancer and 177Lu-somatostatin analogs for neuroendocrine tumors, there is a significant rise in RNTs in the last decade. As therapeutic applications of nuclear medicine is on the rise, the aim of this review is to summarize biological responses to radiation treatments and molecular mechanisms of radiation-induced cell death (e.g. ionization, DNA damages such as double-strand breaks, DNA repair mechanisms, types of cell deaths such as apoptosis, necrosis, and immunogenic cell death), histopathological changes with radiation treatments, and role of PET imaging in RNTs as part of radionuclide theranostics for selecting and planning patients for RNTs, dosimetry, predicting and assessing response to RNTs, predicting toxicities, and other possible PET findings which may be seen after RNTs such as activation of immune system.

Association of Chronic Periodontitis with Hemorrhagic Stroke: A Systematic Review and Meta-Analysis.

Periodontitis is a chronic, multifactorial inflammatory condition linked to dysbiotic plaque biofilms and characterized by the gradual destruction of the structures supporting the teeth owing to compromised immune system function. Hemorrhagic stroke, which primarily occurs within the brain tissue or in the subarachnoid space as a blood leak of ruptured vessels, is a sudden neurological impairment caused by vascular damage in the central nervous system, resulting in focal neurological deficits. Chronic periodontitis (CP) and hemorrhagic stroke may share common pathogenic features involving inflammation and immune system activation, prompting researchers to investigate their potential connection. The aim of the study is to systematically review the literature on the epidemiological association between CP and hemorrhagic stroke in adults. The study protocol adhered to the PRISMA 2020 guidelines, and the design followed the Cochrane methodology. A thorough literature search encompassing PubMed, Scopus, and Web of Science databases and a manual search and evaluation of gray literature was conducted. Meta-analysis was performed using Review Manager (RevMan) 5.4, with the effect size represented by the odds ratio (OR) and a 95% confidence interval (CI). Heterogeneity was assessed using the chi-squared and I 2 statistics. The selected articles, written in English without time constraints, focused on observational studies involving patients and controls and included disease diagnostic criteria. Duplicate entries were eliminated. The reliability of each study's results was evaluated using the Newcastle-Ottawa Scale and GRADE tools. Two reviewers conducted the assessments, and a third reviewer resolved any disagreements. The meta-analysis comprised four observational studies involving 1,882 individuals. It revealed that individuals diagnosed with hemorrhagic stroke were notably more likely to have concurrent CP (OR: 6.32; 95% CI: 1.35-29.49; p = 0.02) or severe CP (OR: 3.08; 95% CI: 1.56-6.06; p = 0.001) compared with healthy controls. A notable occurrence of CP was detected in patients with hemorrhagic stroke compared with controls. Health care professionals need to acknowledge the connection between the two conditions, as it allows them to provide optimal holistic care through a thorough approach to diagnosis and treatment.

Secondary haemophagocytic lymphohistiocytosis associated with scrub typhus: A case report with a brief review of literature.

Scrub typhus is a very important cause of acute undifferentiated febrile illness in the Asia-Pacific region. Haemophagocytic lymphohistiocytosis (HLH) is a rare and life-threatening condition characterised by widespread immune system activation, resulting in tissue damage throughout multiple organ systems. HLH is categorised into primary HLH, arising from intrinsic defects in lymphocytes and macrophages, and secondary HLH, primarily triggered by infections or connective tissue disorders. HLH is one of the rarest complications of scrub typhus. We present the case of a previously healthy young man who presented to our facility with a history of acute febrile illness. Clinical examination revealed an eschar and subsequent laboratory investigations confirmed the diagnosis of scrub typhus. The patient's haematological parameters showed pancytopenia, raising suspicion of this rare association. Confirmatory tests established the diagnosis of HLH, and the patient achieved an uneventful recovery following treatment for the underlying illness and supportive care.