73 research outputs found

    Multiple cysticerci as an unusual cause of mesenteric lymph node enlargement: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>Cysticercosis is a disease caused by infestation with the larval stage of the intestinal cestode <it>Taenia solium</it>. The parasite usually localizes to subcutaneous tissues and muscles causing palpable or visible nodules, to the brain leading to epileptic attacks, and to the eyes with visible nodules leading to blindness and atrophy.</p> <p>Case presentation</p> <p>Here we present the case of a 15-year-old girl who was incidentally detected as having mesenteric lymph node enlargement caused by multiple cysticerci. This is the second case report of lymph node enlargement due to cysticercus infestation.</p> <p>Conclusion</p> <p>This rare mode of presentation of cysticercus infestation highlights the importance of parasites as a cause of treatable lymph node enlargement.</p

    Imaging using Tc99m-tetrofosmin for the detection of the recurrence of brain tumour: A comparative study with Tc99m-glucoheptonate

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    BACKGROUND: In the past "blood-brain barrier" agents such as Tc99m-glucoheptonate were routinely used for the diagnosis of brain tumours. Of late, agents used for studying myocardial perfusion namely, Tc99m-tetrofosmin, Thallium-201, and Tc99m-sestamibi have replaced the "blood-brain barrier agents" when imaging is undertaken for the detection of the recurrence of brain tumours. However, the incremental diagnostic information provided by Tc99m-tetrofosmin when compared with a blood brain barrier agent in the diagnosis of recurrent brain tumour has not been evaluated till date. AIMS: The study was carried out to substantiate whether Tc99m-tetrofosmin provides any incremental diagnostic information not provided by the blood brain barrier agent Tc99m-glucoheptonate. MATERIAL AND METHODS: Brain SPECT scans were performed using Tc99m-tetrofosmin and Tc99m-glucoheptonate in 126 patients of recurrent brain tumour. Bio-distribution and uptake properties of both the tracers were analysed by measuring relative uptake of both the tracers in tumour compared to background (T/B ratio), nasopharynx (T/N ratio) and scalp (T/S ratio). STATISTICAL ANALYSIS: Descriptive statistics were calculated for each variable. Pearson's correlation coefficient was applied to see agreement of the continuous variables. Paired t test was used to evaluate the difference between two means. RESULTS: Uptake properties of both the tracers were analysed in 105 patients in whom both Tc99m-tetrofosmin and Tc99m-glucoheptonate showed concentration. The remaining 21 patients in whom the tumour mass did not show Tc99m-tetrofosmin concentration were excluded from the study. Mean T/B ratio, T/N ratio and T/S ratio was 5.83 \ub1 2.09 and 5.99 \ub1 2.26, 0.53 \ub1 0.21 and 0.55 \ub1 0.22 and 1.11 \ub1 0.60 and 1.26 \ub1 0.52 for Tc99m-tetrofosmin and Tc99m-glucoheptonate respectively. No statistically significant difference between T/B ratio and T/N ratio of Tc99m-tetrofosmin and Tc99m-glucoheptonate was found; p values were 0.25 and 0.83 respectively. However there was significant difference (P=0.006) between the T/S ratio of Tc99m-tetrofosmin and that of Tc99m-glucoheptonate. CONCLUSION: Tc99m-tetrofosmin does not provide any incremental diagnostic information not provided by the blood brain barrier agent Tc99m-glucoheptonate

    Samarium-153 ethylenediamine tetramethylene phosphonate therapy for bone pain palliation in skeletal metastases

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    BACKGROUND: Systemic therapy with radionuclides may be used for the treatment of patients with painful skeletal metastases owing to its efficacy, low cost and low toxicity. Imported radionuclides for pain palliation, like Strontium-89 are expensive; particularly for developing countries. In the Indian scenario, Samarium-153 (Sm-153) is produced in our own reactors and as a result, it is readily available and economical. AIM: We undertook this study to determine the efficacy and toxicity of single-dose Sm-153 ethylenediamine tetramethylene phosphonate as a palliative treatment for painful skeletal metastases. MATERIALS AND METHODS: Eightysix patients with painful skeletal metastases from various primaries, were treated with Sm-153 EDTMP at a dose of 37 MBq/kg. The effects were evaluated according to change in visual analogue pain score, analgesic consumption, Karnofsky performance score, mobility score and blood count tests, conducted regularly for 16 weeks. STATISTICS: Repeated measures analysis. RESULTS: The overall response rates were 73%, while complete response was seen in 12.4%. Reduction in analgesic consumption with improvement in Karnofsky performance score and mobility score, was seen in all responders. Response rates were 80.3 and 80.5% in breast and prostate cancer, respectively. One case, each of Wilms tumor, ovarian cancer, germ cell tumor testis, multiple myeloma, primitive neuroectodermal tumor and oesophageal cancer, did not respond to therapy. No serious side-effects were noted, except for fall in white blood cell, platelet and haemoglobin counts, which gradually returned to normal levels by six-eight weeks. CONCLUSION: Sm-153 EDTMP provided effective palliation in 73% patients with painful bone metastases: the major toxicity was temporary myelosuppression

    Erectile dysfunction, physical activity and metabolic syndrome: differences in markers of atherosclerosis

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    <p>Abstract</p> <p>Background</p> <p>Erectile dysfunction (ED), impaired arterial elasticity, elevated resting heart rate as well as increased levels of oxidized LDL and fibrinogen associate with future cardiovascular events. Physical activity is crucial in the prevention of cardiovascular diseases (CVD), while metabolic syndrome (MetS) comprises an increased risk for CVD events. The aim of this study was to assess whether markers of subclinical atherosclerosis are associated with the presence of ED and MetS, and whether physical activity is protective of ED.</p> <p>Methods</p> <p>57 MetS (51.3 ± 8.0 years) and 48 physically active (PhA) (51.1 ± 8.1 years) subjects participated in the study. ED was assessed by the International Index of Erectile Function (IIEF) questionnaire, arterial elasticity by a radial artery tonometer (HDI/PulseWave™ CR-2000) and circulating oxLDL by a capture ELISA immunoassay. Fibrinogen and lipids were assessed by validated methods. The calculation of mean daily energy expenditure of physical exercise was based on a structured questionnaire.</p> <p>Results</p> <p>ED was more often present among MetS compared to PhA subjects, 63.2% and 27.1%, respectively (p < 0.001). Regular physical exercise at the level of > 400 kcal/day was protective of ED (OR 0.12, 95% CI 0.017-0.778, p = 0.027), whereas increased fibrinogen (OR 4.67, 95% CI 1.171-18.627, p = 0.029) and elevated resting heart rate (OR 1.07, 95% CI 1.003-1.138, p = 0.04) were independently associated with the presence of ED. In addition, large arterial elasticity (ml/mmHgx10) was lower among MetS compared to PhA subjects (16.6 ± 4.0 <it>vs</it>. 19.6 ± 4.2, p < 0.001), as well as among ED compared to non-ED subjects (16.7 ± 4.6 <it>vs</it>. 19.0 ± 3.9, p = 0.008). Fibrinogen and resting heart rate were highest and large arterial elasticity lowest among subjects with both MetS and ED.</p> <p>Conclusions</p> <p>Markers of subclinical atherosclerosis associated with the presence of ED and were most evident among subjects with both MetS and ED. Thus, especially MetS patients presenting with ED should be considered at high risk for CVD events. Physical activity, on its part, seems to be protective of ED.</p> <p>Trial registration</p> <p>ClinicalTrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT01119404">NCT01119404</a></p

    Membrane vesicles, current state-of-the-art: emerging role of extracellular vesicles

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    Release of membrane vesicles, a process conserved in both prokaryotes and eukaryotes, represents an evolutionary link, and suggests essential functions of a dynamic extracellular vesicular compartment (including exosomes, microparticles or microvesicles and apoptotic bodies). Compelling evidence supports the significance of this compartment in a broad range of physiological and pathological processes. However, classification of membrane vesicles, protocols of their isolation and detection, molecular details of vesicular release, clearance and biological functions are still under intense investigation. Here, we give a comprehensive overview of extracellular vesicles. After discussing the technical pitfalls and potential artifacts of the rapidly emerging field, we compare results from meta-analyses of published proteomic studies on membrane vesicles. We also summarize clinical implications of membrane vesicles. Lessons from this compartment challenge current paradigms concerning the mechanisms of intercellular communication and immune regulation. Furthermore, its clinical implementation may open new perspectives in translational medicine both in diagnostics and therapy

    Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

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    Adenosine is a neuromodulator that operates via the most abundant inhibitory adenosine A1 receptors (A1Rs) and the less abundant, but widespread, facilitatory A2ARs. It is commonly assumed that A1Rs play a key role in neuroprotection since they decrease glutamate release and hyperpolarize neurons. In fact, A1R activation at the onset of neuronal injury attenuates brain damage, whereas its blockade exacerbates damage in adult animals. However, there is a down-regulation of central A1Rs in chronic noxious situations. In contrast, A2ARs are up-regulated in noxious brain conditions and their blockade confers robust brain neuroprotection in adult animals. The brain neuroprotective effect of A2AR antagonists is maintained in chronic noxious brain conditions without observable peripheral effects, thus justifying the interest of A2AR antagonists as novel protective agents in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease, ischemic brain damage and epilepsy. The greater interest of A2AR blockade compared to A1R activation does not mean that A1R activation is irrelevant for a neuroprotective strategy. In fact, it is proposed that coupling A2AR antagonists with strategies aimed at bursting the levels of extracellular adenosine (by inhibiting adenosine kinase) to activate A1Rs might constitute the more robust brain neuroprotective strategy based on the adenosine neuromodulatory system. This strategy should be useful in adult animals and especially in the elderly (where brain pathologies are prevalent) but is not valid for fetus or newborns where the impact of adenosine receptors on brain damage is different
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