Non-bacterial Inflammation Research Articles

Non-invasive diagnosis of bacterial and non-bacterial inflammations using a dual-enzyme-responsive fluorescent indicator.

Bacterial infections, as the second leading cause of global death, are commonly treated with antibiotics. However, the improper use of antibiotics contributes to the development of bacterial resistance. Therefore, the accurate differentiation between bacterial and non-bacterial inflammations is of utmost importance in the judicious administration of clinical antibiotics and the prevention of bacterial resistance. However, as of now, no fluorescent probes have yet been designed for the relevant assessments. To this end, the present study reports the development of a novel fluorescence probe (CyQ) that exhibits dual-enzyme responsiveness. The designed probe demonstrated excellent sensitivity in detecting NTR and NAD(P)H, which served as critical indicators for bacterial and non-bacterial inflammations. The utilization of CyQ enabled the efficient detection of NTR and NAD(P)H in distinct channels, exhibiting impressive detection limits of 0.26 μg mL-1 for NTR and 5.54 μM for NAD(P)H, respectively. Experimental trials conducted on living cells demonstrated CyQ's ability to differentiate the variations in NTR and NAD(P)H levels between A. baumannii, S. aureus, E. faecium, and P. aeruginosa-infected as well as LPS-stimulated HUVEC cells. Furthermore, in vivo zebrafish experiments demonstrated the efficacy of CyQ in accurately discerning variations in NTR and NAD(P)H levels resulting from bacterial infection or LPS stimulation, thereby facilitating non-invasive detection of both bacterial and non-bacterial inflammations. The outstanding discriminatory ability of CyQ between bacterial and non-bacterial inflammation positions it as a promising clinical diagnostic tool for acute inflammations.

ОБОСНОВАНИЕ ИСПОЛЬЗОВАНИЯ ОБЩЕЙ МАГНИТО- И ОКСИГЕНОТЕРАПИИ В ЛЕЧЕНИИ ИНТЕРСТИЦИАЛЬНОГО ЦИСТИТА/СИНДРОМА ХРОНИЧЕСКОЙ ТАЗОВОЙ БОЛИ

Introduction. Chronic interstitial cystitis is considered a non-bacterial inflammation in the submucosal layer that is difficult to treat with traditional means due to the development of tissue hypoxia and activation of the peripheral nervous system involving a large number of pain receptors. Objective. To evaluate the effectiveness of general magnetic and oxygen therapy in the treatment of chronic interstitial cystitis with severe pain. Materials and methods. The clinical study involved 17 women with chronic interstitial cystitis/chronic pelvic pain syndrome who received a course of general magnetic and oxygen therapy. Quantitative criteria for clinical signs were evaluated using the questionnaire for assessing symptoms of diseases of the genitourinary system ‘OSZ - IPPS-MS’ before and after treatment. Results. A decrease in the absolute value of the "Irritativ symptom" scale of 65.2% was recorded. The score on the "Painful symptom" scale decreased by 9 times from its initial level, a significant decrease in the "score" of the "Psychosomatic symptom" scale by 63.75%. Reduction of the total score "Total score" at the end of the combined course of physiotherapeutic rehabilitation by 68.62%. The "Motivational scale" indicator at the end of treatment decreased by 62.50%, which corresponds to "awareness of the fact of the disease with a moderate degree of readiness to undergo treatment". This dynamic is explained by the improvement in the clinical and psychosomatic symptoms of the disease, and its moderate value at the end of treatment is associated with their motivation for subsequent regular preventive rehabilitation measures. Conclusion. The impact of general magnetic therapy and hyperbaric oxygen therapy for interstitial cystitis is accompanied by a significant reduction in pain and irritative symptoms with an effective correction of psychoneurosomatic disorders.

Diagnosis of epigastric pain: a case report

Epigastric pain is the most significant symptom and a major clinical challenge in chronic pancreatitis. Pancreatic pain is characteristically described as a constant, severe, dull, epigastric pain that often radiates to the back and typically worsens after high-fat meals. However, many different pain patterns have been described, ranging from no pain to recurrent episodes of pain and pain free intervals, to constant pain with clusters of severe exacerbations. A 30-years old female inpatient with complaints of abdominal pain located on epigastric since 7 days ago. Patients also complain of nausea and vomiting, decreased appetite. The patient has a history of acute pancreatitis and was treated 6 months ago and is hyperthyroid. Physical examination within normal limits. On abdominal examination, there was tenderness in the epigastric part. Abdomen ultrasound examination revealed widening of the pancreatic duct. While hospitalized the patient was treated with meropenem 1 gram IV every 8 hours, pantoprazole 40 mg IV every 12 hours, ondansetron 8 mg IV every 12 hours, Kaltrofen supp if needed, Propranolol 5 mg PO every 12 hours and thyrozol 10 mg PO every 12 hours. Acute pancreatitis is an acute, non-bacterial inflammation of the pancreas organ. Radiographic examination must be done to establish diagnose beside anamnesis and laboratorium examination. To diagnose acute pancreatitis, at least 2 of 3 criteria must be met. Management of patients with acute pancreatitis includes non-operative and surgical. Antibiotics therapy in management of acute pancreatitis in the early stages is still controversial.

The Translational Role of Animal Models for Estrogen-Related Functional Bladder Outlet Obstruction and Prostatic Inflammation.

The prevalence of LUTS and prostatic diseases increases with age both in humans and companion animals, suggesting that a common underlying cause of these conditions may be age-associated alterations in the balance of sex hormones. The symptoms are present with different and variable micturition dysfunctions and can be assigned to different clinical conditions including bladder outlet obstruction (BOO). LUTS may also be linked to chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CP/CPPS), but the relationship between these conditions is unknown. This review summarizes the preclinical data that supports a role for excessive estrogen action in the development of obstructive voiding and nonbacterial prostatic inflammation. Preclinical studies that are emphasized in this review have unequivocally indicated that estrogens can induce functional and structural changes resembling those seen in human diseases. Recognizing excessive estrogen action as a possible hormonal basis for the effects observed at multiple sites in the LUT may inspire the development of innovative treatment options for human and animal patients with LUTS associated with functional BOO and CP/CPPS.

Role of NLRP3 Inflammasome in Myocardial Ischemia-Reperfusion Injury and Ventricular Remodeling

Reperfusion therapy is the optimal therapy for acute myocardial infarction (AMI), but acute inflammatory injury and chronic heart failure (HF) after myocardial ischemia and reperfusion (MI/R) remain the leading cause of death after AMI. Pyroptosis, a newly discovered form of cell death, has been proven to play a significant role in the acute reperfusion process and the subsequent chronic process of ventricular remodeling. Current research shows that multiple stimuli activate the pyroptotic signaling pathway and contribute to cell death and nonbacterial inflammation after MI/R. These stimuli promote the assembly of the nucleotide-binding and oligomerization-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome by activating NLRP3. The mature NLRP3 inflammasome cleaves procaspase-1 to active caspase-1, which leads to mature processing of interleukin (IL)-18, IL-1β, and gasdermin D (GSDMD) protein. That eventually results in cell lysis and generation of nonbacterial inflammation. The present review summarizes the mechanism of NLRP3 inflammasome activation after MI/R and discusses the role that NLRP3-mediated pyroptosis plays in the pathophysiology of MI/R injury and ventricular remodeling. We also discuss potential mechanisms and targeted therapy for which there is evidence supporting treatment of ischemic heart disease.

The Therapeutic Effects of Treadmill Exercise on Osteoarthritis in Rats by Inhibiting the HDAC3/NF-KappaB Pathway in vivo and in vitro.

Osteoarthritis (OA) is a disease characterized by non-bacterial inflammation. Histone deacetylase 3 (HDAC3) is a crucial positive regulator in the inflammation that leads to the development of non-OA inflammatory disease. However, the precise involvement of HDAC3 in OA is still unknown, and the underlying mechanism of exercise therapy in OA requires more research. We investigated the involvement of HDAC3 in exercise therapy-treated OA. Expression levels of HDAC3, a disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS-5), matrix metalloproteinase-13 (MMP-13), HDAC3 and nuclear factor-kappaB (NF-kappaB) were measured by western blotting, reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. Cartilage damage and OA evaluation were measured by hematoxylin and eosin staining and Toluidine blue O staining according to the Mankin score and OARSI score, respectively. We found that moderate-intensity treadmill exercise could relieve OA. Meanwhile, the expression of HDAC3, MMP-13, ADAMTS-5 and NF-kappaB decreased, and collagen II increased in the OA + moderate-intensity treadmill exercise group (OAM) compared with the OA group (OAG) or OA + high- or low-intensity treadmill exercise groups (OAH or OAL). Furthermore, we found the selective HDAC3 inhibitor RGFP966 could also alleviate inflammation in OA rat model through inhibition of nuclear translocation of NF-kappaB. To further explore the relationship between HDAC3 and NF-kappaB, we investigated the change of NF-kappaB relocation in IL-1β-treated chondrocytes under the stimulation of RGFP966. We found that RGFP966 could inhibit the expression of inflammatory markers of OA via regulation of HDAC3/NF-kappaB pathway. These investigations revealed that RGFP966 is therefore a promising new drug for treating OA.

Chronic prostatitis/chronic pelvic pain syndrome increases susceptibility to seizures in rats and alters brain levels of IL-1β and IL-6

Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) is a result of interplay between psychological, immune, neurological and genetic factors, manifested by variety of urological, as well as brain-related symptoms. However, its relation with brain excitability has not been addressed. herefore, our aim was to assess susceptibility to seizures in rats with CP/CPPS.We induced CP/CPPS in adult rats by intraprostatic injection of 3% λ-carrageenan. Sham operated rats served as controls (0.9% NaCl, Sham). On day 7 upon injection, rats were treated with lindane (4 mg/kg) and observed for convulsive behavior (seizure incidence, latency and severity) and EEG manifestations (number and duration of ictal periods). Interleukin levels (IL-1β and IL-6) were measured in prostate, hippocampus, thalamus and cerebral cortex. Scrotal skin mechanical pain thresholds were determined and prostates were histologically evaluated. Animals with CP/CPPS showed significantly higher incidence, decreased latency time and augmented severity of lindane-induced seizures compared with Sham group. EEG revealed increased number of ictal periods in CP/CPPS rats. Higher levels of IL-1β and IL-6 were determined in the thalamus and cortex in CP/CPPS animals vs. Sham. IL-1β level was higher and IL-6 was lower in prostates from CP/CPPS animals comparing to Sham. CP/CPPS development was verified by histological findings of nonbacterial inflammation in the prostates, as well as by significantly decreased scrotal pain threshold in CP/CPPS animals. On the basis of this research, we concluded that CP/CPPS increases susceptibility to lindane-induced seizures in rats associated with increased level of IL-1β and IL-6 in the cortex and thalamus.

Bladder overactivity and afferent hyperexcitability induced by prostate-to-bladder cross-sensitization in rats with prostatic inflammation.

There is clinical evidence showing that prostatic inflammation contributes to overactive bladder symptoms in male patients; however, little is known about the underlying mechanisms In this study, we investigated the mechanism that prostatic inflammation causes detrusor overactivity by using a rat model of chemically induced prostatic inflammation. We observed a significant number of dorsal root ganglion neurons with dichotomized afferents innervating both prostate and bladder. We also found that prostatic inflammation induces bladder overactivity and urothelial NGF overexpression in the bladder, both dependent on activation of the pelvic nerve, as well as changes in ion channel expression and hyperexcitability of bladder afferent neurons. These results indicate that the prostate-to-bladder cross-sensitization through primary afferent pathways in the pelvic nerve, which contain dichotomized afferents, could be an important mechanism contributing to bladder overactivity and afferent hyperexcitability induced by prostatic inflammation. Prostatic inflammation is reportedly an important factor inducing lower urinary tract symptoms (LUTS) including urinary frequency, urgency and incontinence in patients with benign prostatic hyperplasia (BPH). However, the underlying mechanisms inducing bladder dysfunction after prostatic inflammation are not well clarified. We therefore investigated the effects of prostatic inflammation on bladder activity and afferent function using a rat model of non-bacterial prostatic inflammation. We demonstrated that bladder overactivity, evident as decreased voided volume and shorter intercontraction intervals in cystometry, was observed in rats with prostatic inflammation versus controls. Tissue inflammation, evident as increased myeloperoxidase activity, and IL-1α, IL-1β, and IL-6 levels inside the prostate, but not in the bladder, following intraprostatic formalin injection induced an increase in NGF expression in the bladder urothelium, which depended on activation of the pelvic nerve. A significant proportion (18-19%) of dorsal root ganglion neurons were double labelled by dye tracers injected into either bladder or prostate. In rats with prostatic inflammation, TRPV1, TRPA1 and P2X2 increased, and Kv1.4, a potassium channel α-subunit that can form A-type potassium (KA ) channels, decreased at mRNA levels in bladder afferent and double-labelled neurons vs. non-labelled neurons, and slow KA current density decreased in association with hyperexcitability of these neurons. Collectively, non-bacterial inflammation localized in the prostate induces bladder overactivity and enhances bladder afferent function. Thus, prostate-to-bladder afferent cross-sensitization through primary afferents in the pelvic nerve, which contain dichotomized afferents, could underlie storage LUTS in symptomatic BPH with prostatic inflammation.

Rapamycin Alleviates Hormone Imbalance-Induced Chronic Nonbacterial Inflammation in Rat Prostate Through Activating Autophagy via the mTOR/ULK1/ATG13 Signaling Pathway.

Chronic prostatitis (CP) is a clinically common disease with high morbidity. It affects the patients' quality of life (QoL) as well as physical and mental health seriously due to the recurring symptoms of lower urinary tract and genitalia. As the opinions about the etiology of CP are still not uniform, it is very difficult to be treated or even cured. Autophagy is a highly conserved physiological function which is widely found in eukaryotic cells. In general, cells maintain a certain level of autophagy under physiological conditions, and the basal level of autophagy can be regulated by a variety of autophagy-related genes under stress such as hunger, infection, trauma, and other circumstances. Therefore, the main purpose of this study is to investigate the role of autophagy in chronic nonbacterial prostatitis (CNP, also called CP). In this paper, we established the CNP model via hypodermic injection of 17β-estradiol and subsequently abdominal rapamycin (a common autophagy inducer) treatment based on castrated rats. Then, the expression of nuclear factor-κB (NF-κB), interleukin-1β (IL-1β), and autophagy-related markers as well as autophagosome formation in prostate tissues, peripheral blood mononuclear cells (PBMCs), and serum of rats were evaluated respectively. In addition to some histological changes in the prostate tissues, we found the levels of NF-κB and IL-1β were significantly increased in the model group, along with significantly suppressed autophagy, whereas rapamycin could reverse these effects which involved in the mTOR/ULK1/ATG13 signaling pathway. In conclusion, our results suggested that rapamycin could ameliorate hormone imbalance-induced CNP by activating autophagy.

MP45-06 BLADDER UROTHELIAL AND AFFERENT DYSFUNCTIONS UNDERLYING BLADDER OVERACTIVITY IN RATS WITH CHEMICALLY INDUCED PROSTATIC INFLAMMATION

You have accessJournal of UrologyBenign Prostatic Hyperplasia: Basic Research & Pathophysiology1 Apr 2018MP45-06 BLADDER UROTHELIAL AND AFFERENT DYSFUNCTIONS UNDERLYING BLADDER OVERACTIVITY IN RATS WITH CHEMICALLY INDUCED PROSTATIC INFLAMMATION Shinsuke Mizoguchi, Amanda S. Wolf-Johnson, Takahisa Suzuki, Eiichiro Takaoka, Donald B. DeFranco, Zhou Wang, Lori A. Birder, and Naoki Yoshimura Shinsuke MizoguchiShinsuke Mizoguchi More articles by this author , Amanda S. Wolf-JohnsonAmanda S. Wolf-Johnson More articles by this author , Takahisa SuzukiTakahisa Suzuki More articles by this author , Eiichiro TakaokaEiichiro Takaoka More articles by this author , Donald B. DeFrancoDonald B. DeFranco More articles by this author , Zhou WangZhou Wang More articles by this author , Lori A. BirderLori A. Birder More articles by this author , and Naoki YoshimuraNaoki Yoshimura More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2018.02.1445AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES There is increasing evidence showing the positive correlation between prostatic inflammation and lower urinary tract symptoms (LUTS) in males with benign prostatic hyperplasia (BPH). Therefore, this study used a rat model of non-bacterial prostatic inflammation to investigate the changes in bladder activity and molecular characteristics of bladder afferent pathways and urothelium after prostatic inflammation. METHODS Male SD rats were used, and prostatic inflammation was induced by formalin (5%; 50 µl per lobe) injection into bilateral ventral lobes of the prostate. Bladder function was evaluated 1 and 4 weeks after formalin injection using awake cystometry. Also, after 10 days of prostatic inflammation, prostaglandin E2 (PGE2) concentrations in bladder tissues were measured by ELISA. In bladder mucosa, protein levels of TRPV1 and PGE2 receptors (EP1 to 4) as well as mRNA levels of ASICs (1-3), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were evaluated by Western blot and RT-PCR, respectively. NGF immunoreactivity in bladder sections was also examined. In addition, mRNA levels of TRPV1 and TRPA1 receptors were measured in bladder afferent neurons labeled by Fast Blue (FB) injected into the bladder wall using laser-capture microdissection and RT-PCR methods. RESULTS Compared to vehicle-injected rats, formalin-treated rats exhibited a significant (p<0.05) decrease in intercontraction intervals in cystometry at 1 and 4 weeks after formalin injection. Tissue inflammation evident as inflammatory cell infiltration was found in the prostate, but not in the bladder from formalin-injected rats. In rats with prostatic inflammation (10 days), bladder PGE2 concentrations were significantly increased, and protein levels of TRPV1 and EP4 receptors as well as mRNA levels of all ASICs, BDNF and NGF were significantly elevated in bladder mucosa of formalin-injected rats. NGF immunoreactivity was also increased in bladder urothelium after prostatic inflammation. In FB-labeled bladder afferent neurons, mRNA levels of TRPV1 and TRPA1 were increased compared to non-labelled neurons in prostatic inflammation rats. CONCLUSIONS These results indicate that non-bacterial inflammation confined in the prostate induces bladder overactivity, enhanced PGE2 production in the bladder and upregulations of receptors and growth factors in bladder urothelium and/or afferent pathways, which could contribute to storage LUTS in BPH patients with prostatic inflammation. © 2018FiguresReferencesRelatedDetails Volume 199Issue 4SApril 2018Page: e599 Advertisement Copyright & Permissions© 2018MetricsAuthor Information Shinsuke Mizoguchi More articles by this author Amanda S. Wolf-Johnson More articles by this author Takahisa Suzuki More articles by this author Eiichiro Takaoka More articles by this author Donald B. DeFranco More articles by this author Zhou Wang More articles by this author Lori A. Birder More articles by this author Naoki Yoshimura More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Experimental Analysis of the Efficacy of Dihydroquercetin on the Model of Chronic Nonbacterial Inflammation of the Prostatic Gland.

We studied the efficiency of dihydroquercetin on the model of chronic nonbacterial inflammation of the prostatic gland in rats. It was found that administration of dihydroquercetin was followed by a significant decrease in the area of the connective tissue in the prostatic gland to initial levels, which attested to antifibrotic properties of this oxidant. Additionally, the substance prevented the development of atrophy of acinus epithelium. After administration of reference drug Prostamol Uno, only moderate antifibrotic effects were observed.

Diagnostic Value of Procalcitonin in Predicting Bacteremia in Intensive Care Unit.

Background and Aims:Several biomarkers are used in the diagnosis of bacteremia. Procalcitonin (PCT) is more specific than other biomarkers in differentiating bacterial and nonbacterial inflammation. It was aimed to evaluate the diagnostic and prognostic value of PCT in bacteremic patients in Intensive Care Unit (ICU).Materials and Methods:A total of 156 patients diagnosed with noninfectious systemic inflammatory response syndrome, sepsis, and severe sepsis/septic shock in ICU between December 2014 and July 2015 were evaluated in this prospective cohort study.Results:The study group consisted of 64 (41%) bacteremic patients and the control group consisted of 92 (59%) nonbacteremic patients. The overall mortality rate was 60.3%. Although PCT levels in the bacteremic group (11.9 ± 21.5 ng/dL) were higher than nonbacteremic group (5.9 ± 11.5 ng/dL), this difference was not significant (P = 0.168). The mean levels of PCT in bacteremic patients with Gram-negative bacteria were 16.3 ± 27.6 ng/dL, whereas Gram-positive bacteria were 7.3 ± 10.7 ng/dL (P = 0.145). The mean PCT levels were significantly higher in nonsurvivors compared to survivors (10.1 ± 18.0 vs. 5.7 ± 13.7 ng/dL; P < 0.001).Conclusions:PCT may be an effective biomarker for diagnosing sepsis and predicting disease severity and mortality. There is a need for further well-designed studies to confirm the diagnostic and prognostic value of PCT in septic patients in critical care.

Facile and Versatile Strategy for Construction of Anti-Inflammatory and Antibacterial Surfaces with Polydopamine-Mediated Liposomes Releasing Dexamethasone and Minocycline for Potential Implant Applications.

Reducing early nonbacterial inflammation induced by implanted materials and infection resulting from bacterial contamination around the implant-abutment interface could greatly decrease implant failure rates, which would be of clinical significance. In this work, we presented a facile and versatile strategy for the construction of anti-inflammatory and antibacterial surfaces. Briefly, the surfaces of polystyrene culture plates were first coated with polydopamine and then decorated with dexamethasone plus minocycline-loaded liposomes (Dex/Mino liposomes), which was validated by contact angle goniometry, quartz crystal microbalance, and fluorescence microscopy. Dex/Mino liposomes were dispersed on functional surfaces and the drug release kinetics exhibited the sustained release of dexamethasone and minocycline. Our results demonstrated that the Dex/Mino liposome-modified surfaces had good biocompatibility. Additionally, liposomal dexamethasone reduced proinflammatory mediator expression (particularly IL-6 and TNF-α) in lipopolysaccharide-stimulated human gingival fibroblasts and human mesenchymal stem cells. Moreover, liposomal minocycline prevented the adhesion and proliferation of Porphyromonas gingivalis (Gram-negative bacteria) and Streptococcus mutans (Gram-positive bacteria). These findings demonstrate that an anti-inflammatory and antibacterial surface was developed, using dopamine as a medium and combining a liposomal delivery device, which has potential for use to reduce implant failure rates. Accordingly, the surface modification strategy presented could be useful in biofunctionalization of implant materials.

The anti-inflammatory effect of montelukast, a cysteinyl leukotriene receptor-1 antagonist, against estradiol-induced nonbacterial inflammation in the rat prostate.

There is no standard treatment of chronic nonbacterial prostatitis in humans. The current study was aimed to investigate the effect of montelukast, an antagonist of cysteinyl leukotriene receptor-1, against estrogen-induced, nonbacterial lateral lobe-specific prostate inflammation in rats. Male Wistar rats were randomized into five groups of six rats, including sham controls (group 1) and castrated rats (group 2), whereas nonbacterial prostatitis (NBP) was induced in groups 3-5 by castration followed by a daily subcutaneous injection of estradiol (0.25mg/kg body weight) for 30days. The rats were left otherwise untreated (group 3) or received a daily oral administration of montelukast (1 and 10mg/kg body weight for groups 4 and 5, respectively) from the 17th day after castration for two consecutive weeks. Compared with sham controls, induction of NBP led to a significant increase in serum leukotriene B4 (LTB4), tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) levels, along with a significant upregulation in the transcript level of proinflammatory molecules (nuclear factor kappa beta [NF-κβ] and inducible nitric oxide synthase [iNOS]), chemokines (monocyte chemoattractant protein-1 [MCP-1] and eotaxin), and E-selectin in the lateral prostate. Histological examination revealed intense inflammation in the prostate with leukocyte infiltration and acinar degeneration following estradiol treatment of castrated rats. Montelukast significantly suppressed the increase in serum and prostate proinflammatory mediators/chemokines expression and abolished the histologically inflammatory changes in the lateral prostate. These findings indicate that montelukast inhibits estradiol-induced NBP in a rat model through anti-inflammatory mechanisms, suggesting its future beneficial effect for the treatment of clinical chronic NBP.

Aetiological factors of Acute Pancreatitis

Acute pancreatitis is a non-bacterial inflammation of pancrease. It is caused by a variety of aetiological factors. The two most common being gall stones and alcoholism. Tegether they account for 80%0 cases of acute pancreatitis. The other causes are abdominal trauma, hyperlipidaemia, hypercalcaemia and viral infections. This descriptive, non-interventional case report study was conducted at Mayo Hospital, Lahore from March 1998 to February 2000, to study the aetiological factors in our circumstances. It included 45 patients with mean age of 45 years and male to female ratio of 1:1. Gall stones were the commonest factor in 53.33% (n=24), followed by abdominal trauma is 28.88% (n=13). Alcohol in take, ERCP, hyperlipidaemia and idiopathic pancreatitis were 6.66%, 4.44%, 4.44% and 2.22% respectively. The overall mortality was 22.22% (n=10).

Lack Of PRSS1 And SPINK1 Polymorphisms In Serbian Acute Pancreatitis Patients

Abstract Acute pancreatitis represents an acute nonbacterial inflammation of the pancreas caused by a premature and ectopic activation of pancreatic digestive enzymes. Two of the most important genes in pancreatic autodigestion, PRSS1 and SPINK1, were implicated in the earliest discoveries of the genetic background of pancreatitis. However, the distribution of their variations displays interethnic variability, which could significantly affect the magnitude of their proposed effects on this disease worldwide. The aim of the present study was to investigate the distribution of the most important functional variations of PRSS1 (86A&gt;T and 365G&gt;A) and SPINK1 (101A&gt;G), and their influence on the clinical course of acute pancreatitis in Serbian patients. The study enrolled 81 subjects, the severity of disease course was determined using the Atlanta Classification system, and the genotyping was conducted using a PCR-RFLP method. PRSS1 86A&gt;T and 365G&gt;A SNPs were not observed in the study population, while SPINK1 101A&gt;G was present with the frequency of 0.62% (95% CI: 0.00, 3.83%). Due to extremely low frequencies or absences of examined variations, the proposed effect of these SNPs on the severity of acute pancreatitis could not be confirmed. The results do not support routine genotyping of either PRSS1 or SPINK1 in Serbs.

Substrate-anchored and degradation-sensitive anti-inflammatory coatings for implant materials.

Implant materials need to be highly biocompatible to avoid inflammation in clinical practice. Although biodegradable polymeric implants can eliminate the need for a second surgical intervention to remove the implant materials, they may produce acidic degradation products in vivo and cause non-bacterial inflammation. Here we show the strategy of “substrate-anchored and degradation-sensitive coatings” for biodegradable implants. Using poly(lactic acid)/hydroxyapatite as an implant material model, we constructed a layer-by-layer coating using pH-sensitive star polymers and dendrimers loaded with an anti-inflammatory drug, which was immobilised through a hydroxyapatite-anchored layer. The multifunctional coating can effectively suppress the local inflammation caused by the degradation of implant materials for at least 8 weeks in vivo. Moreover, the substrate-anchored coating is able to modulate the degradation of the substrate in a more homogeneous manner. The “substrate-anchored and degradation-sensitive coating” strategy therefore exhibits potential for the design of various self-anti-inflammatory biodegradable implant materials.

Value of Procalcitonin Arise Markedly after Use of ATG in Conditioning of HSCT without Value in Differentiating Bacterial and Non-Bacteria Inflammation

Background It is difficult how to differentiate bacterial infections from viral infections and to differentiate bacterial infections from other non-infective systemic inflammation. Especially in the patients with lack of neutrophil bacteria infection is usually life-threaten. The prognosis for those patients is high dependent on early diagnosis and treatment. We still feel confusing in spite of monitoring serum procalcitonin (PCT) and C-reactive protein (CRP) levels with temperature.Aim To find out whether PCT and CRP are helpful to differentiate bacterial infection and non-bacterial inflammation after use of anti-human T-lymphocyte globulin (ATG) in conditioning of hematopoietic stem cell transplantation (HSCT).Method Total 60 patients were involved in current study, who underwent HSCT and received conditioning included Cyclophosphamide, Fludarabine, ivBusufan, Thiotepa and ATG (at total dose of 5mg/kg for thymoglobulin, and 15-30mg/kg for ATG-Fresenius, respectively, on day-3 to -1). Blood samples were obtained in the morning from day-3 to 0 for testing PCT and CRP associated by daily recording temperature. Patients were grouped into Group 1 (G1, with antibiotics, n=30), Group 2 (G2, without antibiotics, n=30), Group 3 (G3, bacteria culture positive, n=7) and Group 4 (G4, bacteria culture negative, n=47)Results The value of PCT was not significant difference when G1 vs. G2 (p=0.061), and G3 vs. G4 (p=0.891), but CRP value and temperature were of significant difference between G1 and G2 (p=0.001 and 0.000, respectively). When comparing G3 with G4, CRP was significant (p=0.021) but temperature was no (0.377). However, the deference of daily CRP value was proved not to be enough to do a differential diagnosis by ROC (AUROC=0.685, 0.665, 0.643 and 0.643 on day-3 to 0, respectively).Conclusion The current study shows the value of PCT is insignificant to differentiate bacterial infection and non-bacterial inflammation after use of ATG in conditioning of HSCT. DisclosuresNo relevant conflicts of interest to declare.

Extreme Procalcitonin Elevation without Proven Bacterial Infection Related to Amphetamine Abuse.

Systemic inflammatory response with rhabdomyolysis and consequent multiorgan failure is a known sequela of psychotropic drug abuse. However, in cases with uncertain past medical history the initial diagnosis can be challenging. Here we report the case of a 21-year-old male who was admitted to the intensive care unit with severe neurological impairment caused by amphetamine intoxication. First laboratory investigations revealed extremely high serum procalcitonin (PCT) levels reaching a maximum concentration of 1640 ng/mL on the second day of observation. Although PCT has high sensitivity and specificity in differentiating bacterial sepsis from nonbacterial inflammation, our case report shows for the first time that it can be extremely elevated following serious amphetamine intoxication without bacterial infection.

S98 The beneficial effect of dexpanthenol on 17β-estradiol-induced nonbacterial inflammation in the rat prostate

S98 The beneficial effect of dexpanthenol on 17β-estradiol-induced nonbacterial inflammation in the rat prostate