Correlation of periodontal inflamed surface area with glycated hemoglobin,interleukin-6 and lipoprotein(a)in type 2 diabetes with retinopathy

BACKGROUND The two-way relationship between periodontitis and type 2 diabetes mellitus(T2DM)is well established.Prolonged hyperglycemia contributes to increased periodontal destruction and severe periodontitis,accentuating diabetic complications.An inflammatory link exists between diabetic retinopathy(DR)and periodontitis,but the studies regarding this association and the role of lipoprotein(a)[Lp(a)]and interleukin-6(IL-6)in these conditions are scarce in the literature.AIM To determine the correlation of periodontal inflamed surface area(PISA)with glycated Hb(HbA1c),serum IL-6 and Lp(a)in T2DM subjects with retinopathy.METHODS This cross-sectional study comprised 40 T2DM subjects with DR and 40 T2DM subjects without DR.All subjects were assessed for periodontal parameters[bleeding on probing(BOP),probing pocket depth,clinical attachment loss(CAL),oral hygiene index-simplified,plaque index(PI)and PISA],and systemic parameters[HbA1c,fasting plasma glucose and postprandial plasma glucose,fasting lipid profile,serum IL-6 and serum Lp(a)].RESULTS The proportion of periodontitis in T2DM with and without DR was 47.5%and 27.5%respectively.Severity of periodontitis,CAL,PISA,IL-6 and Lp(a)were higher in T2DM with DR group compared to T2DM without DR group.Significant difference was observed in the mean percentage of sites with BOP between T2DM with DR(69%)and T2DM without DR(41%),but there was no significant difference in PI(P>0.05).HbA1c was positively correlated with CAL(r=0.351,P=0.001),and PISA(r=0.393,P≤0.001)in study subjects.A positive correlation was found between PISA and IL-6(r=0.651,P<0.0001);PISA and Lp(a)(r=0.59,P<0.001);CAL and IL-6(r=0.527,P<0.0001)and CAL and Lp(a)(r=0.631,P<0.001)among study subjects.CONCLUSION Despite both groups having poor glycemic control and comparable plaque scores,the periodontal parameters were higher in DR as compared to T2DM without DR.Since a bidirectional link exists between periodontitis and DM,the presence of DR may have contributed to the severity of periodontal destruction and periodontitis may have influenced the progression of DR.

NLRP3 inflammasome plays a vital role in the pathogenesis of age-related diseases in the eye and brain

Key points:With aging,there is increased nucleotide-binding oligomerization domain-(NOD-)like receptor(NLR) protein-3(NLRP3) activation in neural and ocular tissues.Activation of the NLRP3 inflammasome appears to be a common denominator in the pathogenesis of age-related diseases of the eye and brain.Pharmacological inhibition of the NLRP3 inflammasome may be a potent therapy for preventing the development and progression of age-related eye and brain diseases.

Caspase-11 mediated inflammasome activation in macrophages by systemic infection of A.actinomycetemcomitans exacerbates arthritis

Clinical studies have shown that Aggregatibacter actinomycetemcomitans(A.actinomycetemcomitans)is associated with aggressive periodontitis and can potentially trigger or exacerbate rheumatoid arthritis(RA).However,the mechanism is poorly understood.Here,we show that systemic infection with A.actinomycetemcomitans triggers the progression of arthritis in mice anti-collagen antibody-induced arthritis(CAIA)model following IL-1βsecretion and cell infiltration in paws in a manner that is dependent on caspase-11-mediated inflammasome activation in macrophages.The administration of polymyxin B(PMB),chloroquine,and anti-CD11b antibody suppressed inflammasome activation in macrophages and arthritis in mice,suggesting that the recognition of lipopolysaccharide(LPS)in the cytosol after bacterial degradation by lysosomes and invasion via CD11b are needed to trigger arthritis following inflammasome activation in macrophages.These data reveal that the inhibition of caspase-11-mediated inflammasome activation potentiates aggravation of RA induced by infection with A.actinomycetemcomitans.This work highlights how RA can be progressed by inflammasome activation as a result of periodontitis-associated bacterial infection and discusses the mechanism of inflammasome activation in response to infection with A.actinomycetemcomitans.

Melatonin alleviates intervertebral disc degeneration by disrupting the IL-1β/NF-κB-NLRP3 inflammasome positive feedback loop

The inflammatory response is induced by the overexpression of inflammatory cytokines, mainly interleukin(IL)-1β, and is one of the main causes of intervertebral disc degeneration(IVDD). NLR pyrin domain containing 3(NLRP3) inflammasome activation is an important source of IL-1β. As an anti-inflammatory neuroendocrine hormone, melatonin plays various roles in different pathophysiological conditions. However, its roles in IVDD are still not well understood and require more examination. First, we demonstrated that melatonin delayed the progression of IVDD and relieved IVDD-related low back pain in a rat needle puncture IVDD model;moreover, NLRP3 inflammasome activation(NLRP3, p20, and IL-1β levels) was significantly upregulated in severely degenerated human discs and a rat IVDD model. Subsequently, an IL-1β/NF-κB-NLRP3 inflammasome activation positive feedback loop was found in nucleus pulposus(NP) cells that were treated with IL-1β. In these cells, expression of NLRP3 and p20 was significantly increased, NF-κB signaling was involved in this regulation, and mitochondrial reactive oxygen species(mt ROS)production increased. Furthermore, we found that melatonin disrupted the IL-1β/NF-κB-NLRP3 inflammasome activation positive feedback loop in vitro and in vivo. Melatonin treatment decreased NLRP3, p20, and IL-1β levels by inhibiting NF-κB signaling and downregulating mt ROS production. Finally, we showed that melatonin mediated the disruption of the positive feedback loop of IL-1β in vivo. In this study, we showed for the first time that IL-1β promotes its own expression by upregulating NLRP3 inflammasome activation. Furthermore, melatonin disrupts the IL-1β positive feedback loop and may be a potential therapeutic agent for IVDD.

Correlation of periodontal inflamed surface area with glycemic status in controlled and uncontrolled type 2 diabetes mellitus

BACKGROUND The bidirectional link between periodontitis and diabetes mellitus(DM)has been established.Periodontitis causes systemic inflammatory burden through inflammatory mediators.The currently utilized tools[clinical attachment loss(CAL)and probing pocket depth(PPD)]are linear measurements,that do not exactly quantify the inflammatory burden of periodontitis.Periodontal inflamed surface area(PISA)quantifies the surface area of bleeding pocket epithelium and estimates the inflammatory burden.Studies relating to the periodontal status of diabetic patients with and without microvascular complications are scarce.This study assessed the proportion of periodontitis and correlation of PISA with glycemic status in controlled,uncontrolled type 2 DM(T2DM)with and without microvascular complications.AIM To assess the proportion of periodontitis and correlation of PISA with glycemic status in controlled,and uncontrolled T2DM with and without microvascular complications.METHODS This study comprised 180 T2DM patients.Based on glycated hemoglobin(HbA1c)levels,they were grouped into:(1)Controlled T2DMgroup:(HbA1c≤7%);(2)Uncontrolled T2DM group:(HbA1c>7%)without microvascular complications;and(3)Uncontrolled T2DM group:(HbA1c>7%)with microvascular complications.Each group comprised 60 patients.All patients were assessed for periodontal parameters(Bleeding on Probing,PPD,CAL,Oral hygiene index simplified and PISA),and systemic parameters(HbA1c,fasting plasma glucose and post prandial plasma glucose).RESULTS The proportion of periodontitis among controlled T2DM group,uncontrolled T2DM group without microvascular complications,uncontrolled T2DM group with micro-vascular complications was 75%,93.4%and 96.6%respectively.Extent and severity of periodontitis were high in the uncontrolled T2DM group.A significant positive correlation was found between PISA and HbA1c among all patients(r=0.393,P<0.001).The dose–response relationship between PISA and HbA1c was observed.An increase of PISA with 168 mm^(2) was associated with a 1.0%increase of HbA1c.CONCLUSION High proportion and severity of periodontitis,and increased inflamed surface area in uncontrolled T2DM may have contributed to the poor glycemic control and microvascular complications.

Detection of Adhesion Molecules on Inflamed Macrophages at Early-Stage Using SERS Probe Gold Nanorods

In recent years, it has been shown that inflammatory biomarkers can be used as an effective signal for disease diagnoses. The early detection of these signals provides useful information that could prevent the occurrence of severe diseases. Here, we employed surface-enhanced Raman scattering(SERS) probe gold nanorods(GNRs) as a tool for the early detection of inflammatory molecules in inflamed cells. A murine macrophage cell line(Raw264.7) stimulated with lipopolysaccharide(LPS) was used as a model in this study. The prepared SERS probe GNRs containing 4-mercaptobenzoic acid as a Raman reporter to generate SERS signals were used for detection of intracellular adhesion molecule-1(ICAM-1) in macrophages after treatment with LPS for varying lengths of time. Our results show that SERS probe GNRs could detect significant differences in the expression of ICAM-1 molecules in LPS-treated macrophages compared to those in untreated macrophages after only 1 h of LPS treatment. In contrast, when using fluorescent labeling or enzyme-linked immunosorbent assays(ELISA) to detect ICAM-1, significant differences between inflamed and un-inflamed macrophages were not seen until the cells had been treated with LPS for 5 h. These results indicate that our SERS probe GNRs provide a higher sensitivity for detecting biomarker molecules in inflamed macrophages than the conventional fluorescence and ELISA techniques, and could therefore be useful as a potential diagnostic tool for managing disease risk.

COMPARATIVE OBSERVATIONS ON THE TYPES OF ATROPHIC GASTRITIS AND BIOPSY PATHOLOGY OF GASTRIC MUCOSA

300 cases of chronic atrophic gastritis were classified into 3 types of qi-dificiency of spleen and stomach, yang-deficiency of spleen and stomach, and yin-deficiency of spleen and stomach according to syndrom differentiation of traditional Chinese medicine. The biopsy specimens of gastric mucosa were examined histopathologically and for the presence of pyloric spirobaeteria. The results showed that the type of yin-deficiency was the most seri-ous in the degree of pathologic changes, or the glandular atrophy and the interstitial inflam-matory cellular infiltration, while the rate of pyloric spirobacteria presence was comparable in all types.

Histological healing after infliximab induction therapy in children with ulcerative colitis

AIM: To verify the impact of induction therapy with infliximab(IFX) on mucosal healing in children with ulcerative colitis(UC).METHODS: The study included all UC pediatric patients treated with IFX at our center over the last10 years. The data were collected from patients' medical charts and analyzed retrospectively. A total of 16 patients with UC underwent colonoscopy with sample collection before and after three IFX injections.Pediatric Ulcerative Colitis Activity Index(PUCAI)was used to assess the clinical condition; endoscopic features were classified according to the Baron scale;and histological changes were evaluated according to the protocol of The British Society of Gastroenterology and Geboes Index. Clinical response was defined as a ≥ 20-point reduction in PUCAI index, and clinical remission as PUCAI index < 10 points. Endoscopic mucosal remission was defined as completely normal(score 0) on the Baron scale. Histological remission was defined as grade 0 in the Geboes Index. To assess correlation between variables, Spearman's rank correlation coefficient was used.RESULTS: Clinical remission(PUCAI < 10) at week 8 was achieved in 68.75% of investigated subjects. Endoscopic mucosal remission at week 8(Baron 0) was observed in 12.5% of patients. Histological remission(Geboes 0)after induction therapy with IFX was noticed in 18.75%cases. A general histological improvement, expressedby normal surface and crypt architecture, number of crypts, and lamina propria cellularity, was observed in six(37.5%) patients; there was no improvement in nine(56.25%) individuals, and worsening was observed in one(3.75%) case. Changes were not related to UC location. A reduction of inflammatory process was observed in 10(62.5%) patients; there were no changes in four(25%) individuals, and the inflammation became more severe in two(12.5 %) cases. Simultaneous clinical, endoscopic and histological improvement of parameters assessing disease activity at week 8 was noticed in six(37.5%) patients. 55.5% of investigated patients with normal mucosa seen on endoscopy showed no inflammation on histology. A Baron score of 2 and 3showed a good correlation with histology results(78.2%of patients with a Geboes Index ≥ 3).CONCLUSION: IFX has a positive histological effect in more than one-third of UC patients. IFX reduces intestinal inflammation and improves clinical condition.

The mysterious relation between inflammation and prostate cancer

Recent studies showed that inflammation is a critical cause for initiation and/or development of many cancers. In prostate cancer(PC), the inflammatory cells usually populate an immune-competent organ. This inflammatory organ can be involved in the initiation and progression of PC. Here, we mainly focus on the role of inflammation in the PC and progression of castration-resistant PC(CRPC). Moreover, we summarize the roles of inflammation factors(such as chemokines and cytokines) in PC and CRPC. Taken together, this review gives an insight into therapy for PC and CRPC through anti-inflammation.

TREATMENT OF PERIARTHRITIS HUMEROSCAPULARIS WITH ACUPUNCTURE AND ACUPOINT BLOCKING

Periarthritis humeroscapularis is alsoknown as adhesive capsulitis of theshoulder,or commonly called frozen shoul-der;evidently it is related to seniledegenerative changes.It is usually due torupture of the rotator cuff,chronic inflam-mation of the periarticular muscles,the ten-dons,the synovial bursa or articular

A REPORT OF 22 CASES OF TEMPOROMANDIBULAR JOINT DYSFUNCTION SYNDROME TREATED WITH ACUPUNCTURE AND LASER RADIATION

Temporomandibular joint dysfunctionsyndrome(TJDS)is non-bacterial inflam-mation of the tissues around the joint due toinjury of neuromuscular structures causedby lengthy dysfunctioning of mastication,such as unilateral mastication,or to trauma.The author has treated 22 cases of this kindwith acupuncture combined

ON THE THERAPEUTIC EFFICACY OF ELECTRIC ACUPUNCTURE WITH MOXIBUSTION IN 95 CASES OF CHRONIC PELVIC INFECTIOUS DISEASE (PID)

This article presents the joint use of electricacupuncture and moxibustion in the treatment of95 cases of chronic PID.Clinical cure in 42 cases,marked improvement in 22 cases,some improve-ment in 17 cases,and no effect in 12 cases.Theoverall effective rate was 88.4%,which was superiorto that of the control group (P【0.05) using an-tibiotics.

Imperatorin alleviates Aβ-induced spatial learning memory impairment and neuroinflam⁃mation in model mice of Alzheimer disease

OBJECTIVE To investigate the effects of imperatorin on the spatial learning memory impairment and neuroinflammation in model mice of Alzheimer disease(AD)induced by intracerebroventricular injection of Aβ1-42.METHODS Mouse model of AD was established by injection of Aβ1-42 into the lateral ventricles.Im⁃peratorin(2.5 and 5.0 mg·kg-1,daily)was inject⁃ed by intraperitoneally 1 h after intracerebroven⁃tricular injection for 13 d.The effect of imperato⁃rin on the spatial learning and memory impair⁃ment was assessed by eight arm maze tests.The levels of cytokines TNF-α,IL-1β,IL-6,IL-18 and chemokines MCP-1 in mouse cortex and hip⁃pocampus were detected by ELISA.The protein expression of NF-κB P65,TLR4,MyD88,p-P38,p-ERK,and p-JNK were detected by Western blotting.RESULTS As compared with the AD model group,imperatorin treatment significantly attenuated Aβ1-42-induced spatial learning and memory impairment assessed by eight arm maze tests.In addition,imperatorin significantly reduced the levels of cytokines TNF-α,IL-1β,IL-6,IL-18 and chemokines MCP-1 in the cerebral cortex and hippocampus.Meanwhile,Western blotting results showed that imperatorin treat⁃ment significantly down-regulated the protein expression of NF-κB P65,TLR4,MyD88,p-P38,p-ERK,and p-JNK.CONCLUSION Imperatorin has neuroprotective effects in the Aβ1-42 induced AD model mice and its mechanism may be partially associated with the inhibition of inflam⁃matory response in the cortex and hippocampus.

说文解字话英语

十五说“黑”(bhleg—) 初学英语的人都知道black(黑色的),派生词有blacken(变黑、中伤)、blackening(变黑、黑色涂料)、blacking(黑色涂料、黑鞋油)、blackish(稍黑的)、bla ckly(黑、阴郁地、残忍地)、blackness(黑色、阴险)等。由 black 形成的复合词更是不计其数,一目了然的 blackboard(黑板)、black book(黑名单)、black—hearted(黑心肠的)、black market(黑市)跟汉语的说法相类似;

The Simulation on Dynamic of Rotary Inertia and Engine’s Inflamer in Light Vehicle

According to formula we can simulate their driven force and acceleration.The mechanical formula is used to obtain dynamics is used to simulate.The driven force increases when torque increases and tire diameter decreases.We need torque to increase so this is our plan.Acceleration raises when torque raises and it reduces when its weight raises.With the decreasing of radius of road the centripetal acceleration is increasing in the condition of light vehicle.It is that it decreases sluggishly before 0.35m/s2 then it maintains a steep decline to 0.62m/s2 and at last becomes sluggish again.It is valued that the economical efficiency about consumed fuel under different power.In the time of 0.2hr the fuel inflamer inclines sharply first then turns stable.It is the smallest value.Beyond it the fuel maintains a high value all the time.The discharged pollution gas decreases with the decreasing initial temperature.The low initial temperature is good to fuel gas.Meantime the smallest incline range is 300~350K which explains that it is the most save one.

Egypt Inflamed

Egypt is a river of tension in the wake of the anti-President Morsi demonstrators demanding his removal for abuse of power,leading to the army ousting the country＇s first democratically elected president in a July 3 military coup.The preceding violent days in early August saw Islamist President Morsi＇s supporters clashing with the country＇s police force in ongoing clashes that have already seen more than 1.000 lives lost,most of them Islamists and their supporters.The court decision to release former President Hosni Mubarak from prison may also inflame public anger.

The role of inflammasomes in human diseases and their potential as therapeutic targets

Inflammasomes are large protein complexes that play a major role in sensing inflammatory signals and triggering the innate immune response.Each inflammasome complex has three major components:an upstream sensor molecule that is connected to a downstream effector protein such as caspase-1 through the adapter protein ASC.Inflammasome formation typically occurs in response to infectious agents or cellular damage.The active inflammasome then triggers caspase-1 activation,followed by the secretion of pro-inflammatory cytokines and pyroptotic cell death.Aberrant inflammasome activation and activity contribute to the development of diabetes,cancer,and several cardiovascular and neurodegenerative disorders.As a result,recent research has increasingly focused on investigating the mechanisms that regulate inflammasome assembly and activation,as well as the potential of targeting inflammasomes to treat various diseases.Multiple clinical trials are currently underway to evaluate the therapeutic potential of several distinct inflammasome-targeting therapies.Therefore,understanding how different inflammasomes contribute to disease pathology may have significant implications for developing novel therapeutic strategies.In this article,we provide a summary of the biological and pathological roles of inflammasomes in health and disease.We also highlight key evidence that suggests targeting inflammasomes could be a novel strategy for developing new disease-modifying therapies that may be effective in several conditions.

You had me at PELO:a"Ribosome Rescuer"induces NLR inflammasome assembly

Pyroptosis,an inflammatory form of programmed cell death,eliminates a niche where pathogens replicate,providing overall benefits to a host.When left uncontrolled,pyroptosis can lead to severe pathology.Overactive pyroptotic activation has been implicated in neuroinflammation,cardiovascular disease,acute respiratory distress syndrome(ARDS),and many other diseases[1,2,3].Because of its multiple and permanent consequences,pyroptosis is a highly regulated signaling pathway.Major regulators of pyroptosis are NLR inflammasomes,which are activated by various“danger”signals such as ATP.

Breaking barriers:noncanonical inflammasome executes blood–brain barrier disruption

In a landmark study recently published in Nature,1 Wei and colleagues demonstrate that the activation of GSDMD by the cytosolic lipopolysaccharide(LPS)sensor caspase-11 triggers blood–brain barrier(BBB)breakdown upon LPS challenge independent of TLR4-induced cytokine release.Their work identifies the noncanonical inflammasome and GSDMD pore formation as a potential target for treating central nervous system(CNS)disorders associated with inflammatory BBB dysfunction.