scholarly journals Mercury Vapour Long-Lasting Exposure: Lymphocyte Muscarinic Receptors as Neurochemical Markers of Accidental Intoxication

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
E. Roda ◽  
A. Giampreti ◽  
S. Vecchio ◽  
P. Apostoli ◽  
T. Coccini
Keyword(s):  
Muscarinic Receptors ◽  
Therapy Monitoring ◽  
Clinical Manifestations ◽  
Fold Increase ◽  
Mercury Vapour ◽  
Home Setting ◽  
Indoor Exposure ◽  
Clinical Evaluations ◽  
Chronic Poisoning ◽  
Neurochemical Marker

Introduction. Chronic poisoning may result in home setting after mercury (Hg) vapours inhalation from damaged devices. We report a chronic, nonoccupational Hg poisoning due to 10-year indoor exposure to mercury spillage. Case Report. A 72-year-old man with polyneuropathy of suspected toxic origin. At hospitalization, toxicological clinical evaluations confirmed the altered neurological picture documented across the last decade. Periodic blood and urine Hg levels (BHg, UHg) monitoring were performed from admission (t0), until 1 year later (t2), paralleled by blood neurochemical markers assessment, that is, lymphocytes muscarinic receptors (l-MRs). At t0: BHg and UHg were 27 and 1.4 microg/L, respectively (normal values: BHg 1–4.5; UHg 0.1–4.5), associated with l-MRs increase, 185.82 femtomoL/million lymphocytes (normal range: 8.0–16.0). At t1 (two days after DMSA-mobilization test), BHg weak reduction, paralleled by UHg 3.7-fold increase, was measured together with further l-MRs enhancement (205.43 femtomoL/million lymphocytes). At t2 (eight months after two cycles of DMSA chelating therapy ending), gradual improving of clinical manifestations was accompanied by progressive decrease of BHg and UHg (4.0 and 2.8 microg/L, resp.) and peripheral l-MRs neurochemical marker (24.89 femtomoL/million lymphocytes). Conclusion. l-MRs modulatory effect supports their use as peripheral neurochemical marker in Hg poisoning diagnosis and chelation therapy monitoring.

P1279INSULIN RESISTANCE IN HEMODIALYSIS PATIENS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Pavel Filinyuk ◽  
Aleksander Rumyantsev
Keyword(s):  
Insulin Resistance ◽  
Systemic Inflammation ◽  
Clinical Manifestations ◽  
Biological Response ◽  
Fold Increase ◽  
Atherogenic Dyslipidemia ◽  
Model Assessment ◽  
Peripheral Tissues ◽  
Reactive Protein ◽  
Homeostatic Model Assessment

Abstract Background and Aims insulin resistance (IR) is a decrease in the biological response of sensitive tissues to insulin. IR is known as an adverse risk factor in cardiovascular disease, which largely determines the prognosis of patients receiving hemodialysis (HD). But this issue is not well understood. For the screening of IR, special indices have been developed that characterize the sensitivity of tissues to insulin. The aim of the study was to compare the methods of screening for IR in patients receiving HD in relation to the markers of systemic inflammation and atherogenic dyslipidemia (AtD). Method 124 patients receiving HD for 75.4 ± 44.5 months were examined including 66 men and 58 women aged 57.6 ± 13.6 years. For IR screening, the Homeostatic Model Assessment-1 and 2 indices (HOMA-1 and HOMA-2), the Quantitative Insulin Sensitivity Check Index (QUICKI) and triglycerides / glucose (Tri/G) were used. Patients were examined in accordance with the recommendations of KDIGO. Data analysis was carried out using “STATISTICA 10.0”. Results fasting insulin levels were elevated in 19% of patients. But, the calculated indices were consistent with the idea that IR is much more common. So, the IR index in the HOMA -1 model was increased in 47%, in the HOMA -2 model - in 33%, in the QUICKI model - in 36%, the TriH indicator - in 91%. The sensitivity of peripheral tissues in the HOMA-1 and HOMA-2 models was equally reduced by 35-40%. The results of the correlation analysis between indicators of IR and plasma concentration of C-reactive protein and lipid profile are presented in table 1. Informativeness of IR indicators depending on the presence of obesity is presented in table 2 We were also interested in whether insulin resistance affects the development of clinical manifestations of atherosclerosis, cardiac arrhythmias, and heart failure. An analysis of this relationship did not reveal. Only the IR index in the HOMA-1 model with a value of more than 2.7 units was associated with a 4.5-fold increase in the risk of developing clinical manifestations of atherosclerotic lesions (χ2 = 4.582 p = 0.032). Statistically significant it was only in men. Given our data, perhaps IR is one of the reasons for the higher morbidity and mortality of men at HD. Conclusion a comparison of IR models allows us to distinguish HOMA-2 as the most accurate index. The highest correlation with systemic inflammation and AtD was in the HOMA-1 and HOMA-2 indices.

The effect of amitriptyline, mianserin, and viloxazine at pre- and post-junctional muscarinic receptors in guinea-pig ileal longitudinal muscle

1982 ◽  
Vol 60 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Y. H. Kwok ◽  
F. Mitchelson
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Muscarinic Receptors ◽  
Longitudinal Muscle ◽  
Fold Increase ◽  
Selective Inhibition

The antimuscarinic activity of amitriptyline, mianserin, and viloxazine was compared with atropine in guinea-pig ileal longitudinal muscle. The pA2 values obtained using carbachol (CCh) as agonist were as follows: atropine, 9.55; amitriptyline, 7.50; mianserin, 6.40; and viloxazine, 4.91. Responses to transmural electrical stimulation (1–50 Hz) were more resistant than those produced by CCh to inhibition by atropine and the antidepressants. This did not appear to be due to a selective inhibition of prejunctional inhibitory muscarinic receptors, as a pA2 of 8.73 was obtained with atropine for the depression of oxotremorine-induced inhibition of acetylcholine (ACh) output. Amitriptyline (10 μM) caused a 2.4-fold increase in ACh output and was 200-fold weaker than atropine at doubling ACh output in the longitudinal muscle stimulated at 0.3 Hz. Mianserin (10 μM) and viloxazine (1–10 μM) did not significantly affect ACh output. It is suggested that the antidepressants exhibit a greater affinity for the postjunctional muscarinic receptors in the guinea-pig ileal longitudinal muscle.

scholarly journals Canine Babesiosis: Where Do We Stand?

2018 ◽  
Vol 68 (2) ◽  
pp. 127-160 ◽  
Author(s):  
Bilić Petra ◽  
Kuleš Josipa ◽  
Barić Rafaj Renata ◽  
Mrljak Vladimir
Keyword(s):  
Species Recognition ◽  
Therapy Monitoring ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Canine Babesiosis ◽  
Treatment And Prevention ◽  
Clinicopathological Findings ◽  
Tick Borne Disease ◽  
Appropriate Therapy ◽  
Selection Of

Abstract Canine babesiosis is a tick-borne disease caused by protozoal haemoparasites of different Babesia species. Babesiosis is one of the most important globally extended and quickly spreading tick-borne infections of dogs. This comprehensive review gives an in-depth overview of Babesia species currently identified in dogs together with relevant vector tick species and their geographical distribution, life cycle and transmission of parasite. The main mechanisms in the pathogenesis of babesiosis are described and elucidated by recent literature overview. As Babesia infection causes a disease with very variable clinical manifestations, special attention is given to clinical signs, laboratory features and clinicopathological findings. The diagnosis of canine babesiosis by microscopy, serological and molecular methods is reviewed, together with recent advances in mass spectrometry based assays. Accurate detection and species recognition are important for the selection of the appropriate therapy, monitoring and prediction of the outcome of the disease. Finally, guidelines for the treatment and prevention of canine babesiosis are given.

The role of thyrotropin receptor antibodies in Grave’s Ophthalmopathy treatment

2016 ◽  
Vol 62 (5) ◽  
pp. 54-55
Author(s):  
Narine S. Martirosian ◽  
Nina A. Petunina ◽  
Liubov V. Trukhina
Keyword(s):  
Disease Management ◽  
Therapy Monitoring ◽  
Clinical Manifestations ◽  
Pulse Therapy ◽  
Clinical Activity ◽  
Inflammatory Disorder ◽  
Intravenous Methylprednisolone ◽  
Thyrotropin Receptor Antibodies ◽  
Receptor Antibodies

Background. Graves' ophthalmopathy (GO) is an autoimmune inflammatory disorder affecting the retroorbital tissues. Although the role of TRAb in GO is now accepted by many researchers and clinicians, their use in the disease management of GO is less well studied than the role of TRAb for the diagnosis and therapy monitoring of Graves’ disease.Aim: to evaluate the relation between TRAb level and the activity of GO, the course of GO and the effectiveness of the treatment.Materials and methods. We have studied 26 patients with GO and Grave’s Disease. Activity of GO was measured with the clinical activity score (CAS), we defined active GO as a CAS≥3. TSH, FT4 and TRAb were evaluated. All patients had received intravenous methylprednisolone (ivMP) pulse therapy in cumulative dose 6000 mg. We observed patients for 1 year after pulse therapy. TRAb level was evaluated before, 3, 6 and 12 months after pulse therapy.Results: At the time of initial treatment all patients had active GO, 60% with CAS 3-4 and 40% with CAS 5-7. On year after the pulse therapy of GO, all patients were classified into responders (69,2%) and non-responders (30,8%) according to their clinical manifestations. Pulse therapy considered as effective if GO activity decreased with CAS ≤ 2. Serum TRAb level was significantly higher in patients who non-responded to therapy – 34,8 U/L vs 17,5 U/L (p≤0,01). This level was significantly decreased in patients responded to treatment – 1,6 U/L vs 12,4 U/L (p≤0,01). TRAb level above 28,8 U/L before treatment (p≤0,01), 10,1 U/L after 3 months of treatment (p≤0,01), 5,1 U/L after 6 months of treatment (p≤0,01) and 8,2 U/L after 3 months of treatment (p≤0.01) was associated with higher risk of non-responding.Conclusion: We conclude, that TRAb level may serve not only as predictor of GO activity and severity, but changes in the level of antibodies could be of additional help for the disease management with ivMP.

scholarly journals Differential transcript profile of inhibitors with potential anti-venom role in the liver of juvenile and adultBothrops jararacasnake

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3203 ◽  
Author(s):  
Cícera Maria Gomes ◽  
Karen de Morais-Zani ◽  
Stephen Lu ◽  
Diego de Souza Buarque ◽  
Glória Regina Cardoso Braz ◽  
...  
Keyword(s):  
Expression Profiles ◽  
Clinical Manifestations ◽  
Fold Increase ◽  
Phospholipase A ◽  
Natural Resistance ◽  
Physiological Adaptation ◽  
Natural Immunity ◽  
Venomous Snake ◽  
Snake Bites ◽  
A Minor

BackgroundSnakes belonging to theBothropsgenus are vastly distributed in Central and South America and are responsible for most cases of reported snake bites in Latin America. The clinical manifestations of the envenomation caused by this genus are due to three major activities—proteolytic, hemorrhagic and coagulant—mediated by metalloproteinases, serine proteinases, phospholipases A2and other toxic compounds present in snake venom. Interestingly, it was observed that snakes are resistant to the toxic effects of its own and other snake’s venoms. This natural immunity may occur due the absence of toxin target or the presence of molecules in the snake plasma able to neutralize such toxins.MethodsIn order to identify anti-venom molecules, we construct a cDNA library from the liver ofB. jararacasnakes. Moreover, we analyzed the expression profile of four molecules—the already known anti-hemorrhagic factor Bj46a, one gamma-phospholipase A2inhibitor, one inter-alpha inhibitor and one C1 plasma protease inhibitor—in the liver of juvenile and adult snakes by qPCR.ResultsThe results revealed a 30-fold increase of gamma-phospholipase A2inhibitor and a minor increase of the inter-alpha inhibitor (5-fold) and of the C1 inhibitor (3-fold) in adults. However, the Bj46a factor seems to be equally transcribed in adults and juveniles.DiscussionThe results suggest the up-regulation of different inhibitors observed in the adult snakes might be a physiological adaptation to the recurrent contact with their own and even other snake’s venoms throughout its lifespan. This is the first comparative analysis of ontogenetic variation of expression profiles of plasmatic proteins with potential anti-venom activities of the venomous snakeB. jararaca. Furthermore, the present data contributes to the understanding of the natural resistance described in these snakes.

CHRONIC POISONING DUE TO EXCESS OF VITAMIN A

PEDIATRICS ◽  
1950 ◽  
Vol 5 (4) ◽  
pp. 672-688
Author(s):  
JOHN CAFFEY
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Clinical Manifestations ◽  
Infants And Children ◽  
Group Of Seven ◽  
Vitamin Intake ◽  
Healthy Infants ◽  
Chronic Poisoning ◽  
Cortical Hyperostosis ◽  
Vitamin Concentrate

The clinical manifestations, the roentgenographic changes in the skeleton and the elevation of blood vitamin A are reported in a group of seven infants and younger children poisoned by ingestion of excessive quantities of vitamin concentrates A and D over periods of several months. The differential features of vitamin A poisoning and infantile cortical hyperostosis are discussed. Three types of vitamin concentrate A and D, commonly used in routine pediatric prophylaxis, were found to be toxic when ingested in sufficiently large quantities over sufficiently long periods. The minimal preclinical latent period of vitamin A poisoning was about six months and the minimal toxic daily dose was about 75,000 units. Excessive dosage was due to overenthusiasm for vitamins and ignorance of the dangers of high vitamin intake. The hazards of vitamin A poisoning from the routine prophylactic feeding of vitamin concentrates A and D to healthy infants and children on good diets are considerably greater than the hazards of vitamin A deficiency in healthy infants and children not fed vitamin concentrates.

Atherosclerotic disease and management challenges with nanomedicine: EU FP7 NMP funded “NanoAthero” and “CosmoPHOS-nano” large-scale projects

2014 ◽  
Vol 6 (2) ◽  
Author(s):  
Didier Letourneur ◽  
Panagiotis N. Trohopoulos
Keyword(s):  
Cardiovascular Diseases ◽  
Early Diagnosis ◽  
Targeted Therapies ◽  
Heart Attack ◽  
Large Scale ◽  
Arterial Wall ◽  
Therapy Monitoring ◽  
Clinical Manifestations ◽  
Arterial Stenosis ◽  
Medical Need

AbstractAtherosclerosis is the most important arterial wall disease that causes arterial stenosis and may lead to the clinical manifestations of angina, heart attack and stroke. There is a demanding unmet medical need for new approaches for early diagnosis and improved/novel targeted therapies and therapy monitoring of atherosclerosis. This is the focus of two European large scale projects, the NanoAthero and the CosmoPHOS-nano by using nanomedicine. The aim is to demonstrate that nanotechnology-enabled systems can be successfully developed and clinically proven to be safe and effective in tackling cardiovascular diseases.

scholarly journals Study on the expression level of NF-κB and clinical evaluations in spinal tuberculosis patients

2022 ◽  
Vol 67 (4) ◽  
pp. 135-142
Author(s):  
HengJie Bian ◽  
TongLin Li ◽  
Rui Wang ◽  
Wan Li ◽  
Yong Ma
Keyword(s):  
Spinal Cord ◽  
Clinical Symptoms ◽  
Spinal Tuberculosis ◽  
Clinical Manifestations ◽  
Response To Treatment ◽  
Control Group ◽  
Case Group ◽  
Clinical Evaluations ◽  
Parametric Data ◽  
Non Parametric

Spinal tuberculosis or tuberculous spondylitis is one of the most common types of skeletal tuberculosis. Complications of the spine and spinal cord tuberculosis include destruction of the vertebrae, deformity, and paraplegia. Since in some patients, the clinical manifestations of tuberculosis are unusual and timely diagnosis and treatment of this disease can prevent its serious consequences, so in the present study, some cases of rare manifestations of tuberculosis were investigated. The expression of the NF-κB gene in these patients was also evaluated. In this regard, 36 patients with spinal tuberculosis and 30 healthy individuals (as a control group) were assessed. Clinical symptoms, imaging, laboratory tests, pathology, and response to treatment related to patients with spinal tuberculosis and spinal cord tuberculosis were evaluated. NF-κB expression was also evaluated using the PCR technique in peripheral white blood cell samples. The obtained results were analyzed using SPSS ver. 16, χ2 and T-test statistical methods. Mann-Whitney U test and Kruskal–Wallis non-parametric tests were used to analyze non-parametric data. The results showed that out of 36 cases of spinal tuberculosis, 29 cases had spinal tuberculosis, five cases had tuberculous radiculomyelitis, one case had spinal intramedullary tuberculoma, and one case had syringomyelia. 52.78% of patients were male, and 70% of cases were observed between the ages of 35 and 55 years. Fever and back pain were seen in more than 80% of cases. The study of NF-κB expression in the control and case groups showed that the NF-κB expression in the case group increased compared to the control group. This increase was statistically significant (P = 0.0071). In general, in the present study, the methods of clinical diagnosis of spinal tuberculosis were evaluated. Also, the amount of NF-κB transcription factor was evaluated as an effective genetic factor in the diagnosis of this disease.

scholarly journals Enhancement of Shiga Toxin Production in Enterohemorrhagic Escherichia coli Serotype O157:H7 by DNase Colicins

2007 ◽  
Vol 73 (23) ◽  
pp. 7582-7588 ◽  
Author(s):  
Hirono Toshima ◽  
Ayana Yoshimura ◽  
Kentaro Arikawa ◽  
Ayumi Hidaka ◽  
Jun Ogasawara ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Clinical Manifestations ◽  
Fold Increase ◽  
Toxin Production ◽  
Enterohemorrhagic Escherichia Coli ◽  
Mrna Levels ◽  
Rt Pcr ◽  
E Coli ◽  
Reverse Transcription Pcr

ABSTRACT Colicins are proteins produced by and active against several strains of Escherichia coli. Previously we reported that colicinogenic bacteria seemed beneficial in preventing the clinical manifestations of infectious disease caused by enterohemorrhagic E. coli O157 in humans. The inhibitory effects could be due to a decrease in O157 levels and/or pathogenicity. This study investigated the effects of colicinogenic E. coli on the production of Shiga toxin (Stx) by O157. Standard strains of colicinogenic bacteria carrying plasmids for each type of colicin (E3/5/8/9) were used for the study. The O157 strains were cultured in the presence of colicinogenic bacteria or extracted colicins. Compared with results for controls, DNase colicins (E8/9) facilitated an 8- to 64-fold increase in production of Stx2, while RNase colicins (E3/5) suppressed Stx production in only two strains. Stx prophages were induced in synchrony with Stx production. Semiquantitative real-time reverse transcription-PCR (RT-PCR) was then performed to examine SOS gene expression. The RT-PCR results clearly indicated a marked increase in mRNA levels of SOS reaction-associated genes after the addition of DNase colicins. We believe that Stx prophages are induced by the SOS response to DNA damage caused by DNase colicins, thus leading to higher Stx production. These findings suggest that while colicinogenic bacteria can be antagonistic to O157 infection, DNase colicins may enhance Stx production. Thus, colicinogenic flora is likely to be involved in the complex pathogenic pathways of O157 infection, and further investigation should be performed before the use of colicinogenic bacteria as an intervention method.

scholarly journals Agonist-induced desensitization of cholinergically stimulated phosphoinositide breakdown is independent of endogenously activated protein kinase C in HT-29 human colon carcinoma cells

1990 ◽  
Vol 269 (1) ◽  
pp. 73-78 ◽  
Author(s):  
R Kopp ◽  
P Mayer ◽  
A Pfeiffer
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
G Protein ◽  
Muscarinic Receptors ◽  
Phorbol Esters ◽  
Fold Increase ◽  
Human Colon ◽  
Kinase C ◽  
Ht 29

Activation of M3 muscarinic receptors in HT-29 cells by carbachol rapidly increases polyphosphoinositide breakdown. Pretreatment of these cells with carbachol (0.1 mM) for 5 h completely inhibits the subsequent ability of carbachol to increase [3H]inositol monophosphate ([3H]InsP) accumulation, paralleled by a total loss of muscarinic binding sites. In contrast, protein kinase C (PK-C)-mediated desensitization by incubation with phorbol esters [PMA (phorbol 12-myristate 13-acetate)], leading to a time- and dose-dependent inhibition of cholinergically stimulated InsP release (95% inhibition after 4 h with 0.1 microM-PMA), is accompanied by only a 40% decrease in muscarinic receptor binding, which suggests an additional mechanism of negative-feedback control. Neither carbachol nor PMA pretreatment had any effect on receptor affinity. Incubation with carbachol for 15 min caused a small increase of membrane-associated PK-C activity (15% increase, P less than 0.05) as compared with the potency of phorbol esters (PMA) (3-4-fold increase, P less than 0.01). Long-term incubation (4-24 h) with PMA resulted in a complete down-regulation of cytosolic and particulate PK-C activity. Stimulation of InsP release by NaF (20 mM) was not affected after a pretreatment with phorbol esters or carbachol, demonstrating an intact function of G-protein and phospholipase-C (PL-C) at the effector side. Determination of PL-C activity in a liposomal system with [3H]PtdInsP2 as substrate, showed no change in PL-C activity after carbachol (13 h) and short-term PMA (2.5 h) pretreatment, whereas long-term preincubation with phorbol esters (13 h) caused a small but significant decrease in PL-C activity (19%, P less than 0.05). Our results indicate that agonist-induced desensitization of phosphoinositide turnover occurs predominantly at the receptor level, with a rapid loss of muscarinic receptors. Exogenous activation of PK-C by phorbol esters seems to dissociate the interaction between receptor and G-protein/PL-C, without major effects on total cellular PL-C activity.

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