Sodium hypochlorite (NaOCl), the most commonly used irrigant, has many potential properties like its unique ability to dissolve pulp tissue, excellent antimicrobial activity, but has a cytotoxic ...effect when injected into periapical tissues. It is also known to produce allergic reactions, foul smell and taste, and potential for corrosion. Facultative organisms such as
and aerobes like
are considered to be the most resistant species and one of the possible causes of root canal treatment failure. So there is a need to find an alternative to sodium hypochlorite to act against these resistant microorganisms.
To evaluate and compare the antibacterial efficacy of morinda citrifolia and turmeric extract with 3% NaOCl as a root canal irrigant, against
and
.
The antimicrobial efficacy was assessed in vitro using agar well diffusion method. Agar plates were prepared using Brain-Heart Infusion (BHI) agar. Cultures of
and
were grown in nutrient broth at 37°C. Plates were incubated for 24 hours at 37°C and microbial zones of inhibition were recorded. Statistical analysis was performed using ANOVA.
NaOCl (3%) showed larger zones of inhibition than herbal irrigants against both the microorganisms. Among the herbal irrigants, morinda citrifolia showed larger zones of inhibition than turmeric hydro-alcoholic extract and turmeric water extract which was statistically significant (p<0.05).
NaOCl (3%) showed maximum antibacterial activity against
, followed by morinda citrifolia and turmeric extracts. Considering the potential for undesirable properties of NaOCl, use of herbal alternatives in endodontics might prove to be advantageous.
Management of large cystic lesion requires a multidisciplinary approach. In this case report a large radicular cyst is managed by conventional root canal treatment with triple antibiotic paste ...followed by surgical enucleation. In this case, patient presented with a 4 cm symptomatic swelling of the palate adjacent to teeth 21, 22 and 23. The swelling was soft on palpation and the overlying mucosa was of normal color. Radiographically, a well-defined unilocular radiolucency with corticated margins was seen. A full-thickness flap was reflected and revealed a large cyst-like lesion that had perforated the lingual cortical plate. The lesion was enucleated and submitted for microscopic examination. The biopsy report confirmed the diagnosis as radicular cyst.The patient was recalled after 6 months, and no symptoms or signs were noted. Radiograph showed the healing lesion.
Recent studies have identified the importance of proinflammatory mediators in regulating cardiac structure in health and disease. Recent studies suggest that cytokines that are expressed within the ...myocardium in response to a environmental injury, namely tumor necrosis factor-alpha (TNF), interleukin-1 (IL-1) and the interleukin-6 (IL-6) family of cytokines play an important role in initiating and integrating homeostatic responses within the heart. However, these "stress-activated" cytokines all have the potential to produce cardiac decompensation when expressed at sufficiently high concentrations. Indeed, there is now a growing appreciation that these molecules may play an important role in mediating disease progression in the failing heart. The growing appreciation of the pathophysiological consequences of sustained expression of proinflammatory mediators in pre-clinical and clinical heart failure models culminated in a series of multicenter clinical trials that utilized "targeted" approaches to neutralize tumor necrosis factor (TNF) in patients with moderate to advanced heart failure. However, these targeted approaches have resulted in worsening heart failure, thereby raising a number of important questions about what role, if any, proinflammatory cytokines play in the pathogenesis of heart failure. This review will summarize the tremendous growth of knowledge that has taken place in this field, with a focus on what we have learned from the negative clinical trials, as well as the potential direction of future research in this area.
Abstract only
Introduction:
Although extensively studied, the mechanisms responsible for the development of cardioprotection following preconditioning stimuli are not known. Our group showed that ...isoproterenol (ISO) mediated cardiac injury induces potent cardioprotection against a second ISO challenge for up to 5 weeks. The lack of an immune response after the second ISO dose and the durability of protection suggested that trained innate immunity might represent a novel mechanism for cardioprotection.
Hypothesis:
We hypothesized that ISO confers cardioprotection through trained immunity via Toll-like receptor 4 (TLR4) signaling that is activated by damage-associated molecular patterns released by ISO-induced cell necrosis.
Methods:
Wild-type C57BL/6J mice were intraperitoneally injected with TLR agonists or diluent (saline), and then 300 mg/kg ISO a week later. Mice were assessed before and after receiving ISO via serum cardiac troponin analysis, flow cytometry, and 2-D echocardiography.
Results:
The TLR4 agonist lipopolysaccharide (LPS), but not TLR1/2 or TLR3 agonists, induced cardioprotection as shown by decreased troponin I release (p<0.01), reduced cardiac neutrophil influx (p<0.05), and decreased left ventricle wall motion abnormalities (p<0.05) following ISO injury compared to saline treated controls . RNA sequencing identified interferon signaling as commonly upregulated (p<0.05) in mouse hearts a week after LPS or ISO pre-treatment. Blocking type I/II interferon receptors partially abolished LPS-induced cardioprotection, while pre-treatment with recombinant interferon β+γ conferred cardioprotection as shown by decreased troponin I release post-ISO (p<0.01). Given that β-glucan reverses the epigenetic tolerizing effects of LPS in immune cells, we treated mice with β-glucan following LPS pre-treatment and observed that the cardioprotection to ISO was abolished.
Conclusions:
Viewed together this study shows for the first time that TLR4/interferon signaling confers cardioprotection against ISO-induced injury. Our findings further suggest that this cardioprotective response may be secondary to TLR4 mediated epigenetic changes that dampen immune responses following tissue injury, consistent with trained innate immunity.
Mechanisms that control aging are important yet poorly defined. To discover longevity control genes, we performed a forward genetic screen for delayed reproductive aging in C. elegans. Here, we show ...that am117 is a nonsense mutation in the phm-2 gene, which encodes a protein homologous to human scaffold attachment factor B. phm-2(lf) mutant worms have an abnormal pharynx grinder, which allows live bacteria to accumulate in the intestine. This defect shortens lifespan on highly pathogenic bacteria but extends lifespan and health span on the standard E. coli diet by activating innate immunity pathways that lead to bacterial avoidance behavior and dietary restriction. eat-2(lf) mutants displayed a similar phenotype, indicating accumulation of live bacteria also triggers extended longevity in this mutant. The analysis of phm-2 elucidates connections between pathogen response and aging by defining a mechanism of longevity extension in C. elegans—bacterial colonization, innate immune activation, and bacterial avoidance behavior.
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•phm-2 encodes a SAFB protein conserved in mammals•phm-2 and eat-2 mutants have a defective pharynx and accumulate bacteria in the gut•Bacterial accumulation activates innate immunity and bacterial avoidance behavior•Bacterial avoidance leads to dietary restriction and delays aging
Kumar et al. link immunity and aging in C. elegans. The authors characterize phm-2 and eat-2, mutants that allow live bacteria to accumulate in the intestine, causing delayed reproductive and somatic aging. The mechanism combines molecular immune activation and behavioral food avoidance, leading to dietary restriction and extended lifespan.
Metabolic control of mitophagy Zimmermann, Andreas; Madeo, Frank; Diwan, Abhinav ...
European journal of clinical investigation,
April 2024, 2024-Apr, 2024-04-00, 20240401, Letnik:
54, Številka:
4
Journal Article
Recenzirano
Odprti dostop
Mitochondrial dysfunction is a major hallmark of ageing and related chronic disorders. Controlled removal of damaged mitochondria by the autophagic machinery, a process known as mitophagy, is vital ...for mitochondrial homeostasis and cell survival. The central role of mitochondria in cellular metabolism places mitochondrial removal at the interface of key metabolic pathways affecting the biosynthesis or catabolism of acetyl‐coenzyme A, nicotinamide adenine dinucleotide, polyamines, as well as fatty acids and amino acids. Molecular switches that integrate the metabolic status of the cell, like AMP‐dependent protein kinase, protein kinase A, mechanistic target of rapamycin and sirtuins, have also emerged as important regulators of mitophagy. In this review, we discuss how metabolic regulation intersects with mitophagy. We place special emphasis on the metabolic regulatory circuits that may be therapeutically targeted to delay ageing and mitochondria‐associated chronic diseases. Moreover, we identify outstanding knowledge gaps, such as the ill‐defined distinction between basal and damage‐induced mitophagy, which must be resolved to boost progress in this area.
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