scholarly journals Effect of dithiothreitol on the differential cell count of equine tracheal wash aspirates

2019 ◽  
Vol 51 (S53) ◽  
pp. 26-26
Author(s):  
Sri Anita ◽  
Liong Boy Kurniawan ◽  
Darwati Muhadi

Myocardial infarction is a necrosis of myocardial cells due to lack of blood and oxygen supply caused by obstruction of coronary arteries, mostly due to atherosclerosis processes. Increased inflammatory marker level is associated with poor cardiovascular prognosis. This study was aimed to know whether leukocytes count, differential cell count and the Ratio of Neutrophils-Lymphocytes (RNL) could distinguish between types of Acute Myocardial Infarction (AMI) and to evaluate its correlation with mortality. This was a cross-sectional retrospective study using medical records patients which were diagnosed as AMI by clinicians in Cardiac Centre of the Dr. Wahidin Sudirohusodo Hospital during the period of April 1st, 2015 - May 31st, 2016. Statistical analysis used the Mann-Whitney and Chi-Square test, p<0.05 was considered as significant. The total subjects were 435 patients divided into 289 ST- Elevation Myocardial Infarction (STEMI) and 146 Non-ST-Elevation Myocardial Infarction (NSTEMI). There were significant differences in that mean of leukocytes, neutrophils, lymphocytes, monocytes, eosinophils counts and RNL between STEMI and NSTEMI (p <0.05). Significant differences were also found in leukocyte, neutrophils, lymphocytes, eosinophils, basophils and RNL mean between those who died and survived (p <0.05) and a significant correlation between increased leukocytes, neutrophils, basophils counts with mortality (p <0.05). In conclusion, the number of leukocytes and leukocyte count can be used as diagnostic markers of AMI between STEMI and NSTEMI, as well as prognostic markers among patients who died and survived. Routine blood sampling cohort studies in patients with AMI can avoid the bias of the results obtained. 


2007 ◽  
Vol 74 (2) ◽  
pp. 174-179 ◽  
Author(s):  
Roswitha Merle ◽  
Anke Schröder ◽  
Jörn Hamann

Udder defence mechanisms are not completely explained by current mastitis research. The anatomical construction of the udder implies that infection of one udder quarter does not influence the immune status of neighbouring quarters. To test this hypothesis, we compared the immune reactions of individual udder quarters in response to microbial attacks. In the course of immune reactions, polymorphonuclear leucocytes (PMN) release oxygen radicals, which can be determined by chemiluminescence (CL). Milk from 140 udder quarters of 36 cows was analysed for somatic cell count (SCC), differential cell count, viability and CL activity. Quarters with an SCC <100000 cells/ml and free of pathogens were defined as uninfected, all other quarters were categorized as infected. Three groups of cows were classified cytologically: group A (healthy, 11 animals, SCC limit <100000 cells/ml); group B (moderate mastitis, 8 cows, SCC [ges ]100000 and <400000 cells/ml in at least one quarter); and group C (severe mastitis, 17 cows, SCC [ges ]400000 cells/ml in at least one quarter). Infected and uninfected quarters in groups B and C were analysed separately. Viability of PMN leucocytes was significantly (P=0·0012) lower in group A (72·6%) than in healthy quarters of group C (84·0%). Lowering the SCC limit of healthy quarters to <50000 cells/ml (group A: all quarters within the udder) revealed striking differences between samples of groups B and C: in addition to varying differential cell counts and viabilities, CL activity of group B<50 (2929 CL units/million PMN) was markedly lower than that of the other groups (5616 in group A<50 and 6445 CL units/million PMN in group C<50). These results allow the conclusion that the infection of one udder quarter influences the cell activity of neighbouring quarters. When the SCC threshold for healthy quarters was reduced to 50000 cells/ml, greater differences in cell activities were detected between healthy udders and healthy quarters of infected udders.


2018 ◽  
Vol 5 (1) ◽  
pp. 131
Author(s):  
Abhishek Agarwal ◽  
Ahbab Hussain ◽  
Rajendra Prasad ◽  
Anand Verma ◽  
Amitabh Banka ◽  
...  

Background: Tuberculosis continues to be an important health problem globally. The bacteriological confirmation of diagnosis in extrapulmonary tuberculosis patients is more difficult because most of the cases of extrapulmonary tuberculosis are paucibacillary in nature. In this study we have compared the pleural fluid ADA levels with PCR for MTB in pleural fluid to confirm the diagnosis of tuberculosis in the pleural fluid.Methods: The study was done over two years and a total of 106 patients with a clinico-radiological diagnosis of pleural effusion were enrolled for the study. The pleural fluid was aspirated and examined for total cell count, differential cell count, protein, sugar, ADA and PCR for MTB.A CT Thorax was done in all the 106 patients of pleural effusion and underlying consolidation along with pleural effusion was found in 60 patients.Results: The pleural fluid was exudative in nature in all the patients. 90 patients (84.9%) had lymphocyte predominant pleural effusion while 16 patients (15.1%) had neutrophil predominant pleural effusion. The overall sensitivity of ADA in all the cases of pleural effusion was 85.2% while the overall sensitivity of PCR for MTB in all the cases of pleural effusion was 51.1%. However, in the 60 patients of pleural effusion with underlying lung consolidation, the overall sensitivity of ADA was 69.1% while the overall sensitivity of PCR for MTB was 92.8% for diagnosing tubercular pleural effusion.Conclusions: PCR for MTB is a useful test along with ADA for diagnosing tubercular pleural effusion. PCR for MTB is especially useful in the diagnosis of tubercular pleural effusion in patients with underlying lung consolidation.  


2018 ◽  
Vol 18 (1) ◽  
pp. 460-465 ◽  
Author(s):  
Alfonso Zecconi ◽  
Diego Vairani ◽  
Micaela Cipolla ◽  
Nicoletta Rizzi ◽  
Lucio Zanini

Author(s):  
Daniel Soriano ◽  
Sebastian Fähndrich ◽  
Thomas Köhler ◽  
Wolfram Meschede ◽  
Joachim Müller-Quernheim ◽  
...  

2011 ◽  
Vol 97 (1-3) ◽  
pp. 117-123 ◽  
Author(s):  
Annika Boulaaba ◽  
Nils Grabowski ◽  
Günter Klein

1996 ◽  
Vol 21 (3) ◽  
pp. 265-271 ◽  
Author(s):  
M. Morgante ◽  
S. Ranucci ◽  
M. Pauselli ◽  
C. Casoli ◽  
E. Duranti

2016 ◽  
Vol 94 (2) ◽  
pp. 140-146 ◽  
Author(s):  
Marwa E. Abdelmageed ◽  
Mohammed S. El-Awady ◽  
Mona Abdelrahim ◽  
Ghada M. Suddek

In this study, we studied the effect of lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), an inhibitor of Toll-like receptor 4 (TLR4), in LPS-induced acute lung injury (ALI). Male Sprague–Dawley rats were treated with LPS-RS (0.1 mg/kg body mass, by intraperitoneal (i.p.) injection) 1 h before LPS injection (10 mg/kg, i.p.). Bronchoalveolar lavage fluid (BALF) and lung tissues were collected 24 h later to determine total and differential cell count, total protein content, levels of lactate dehydrogenase (LDH), histopathological changes, markers of oxidative stress, and mRNA expression of the inhibitory protein nuclear factor kappaB-α (NFκBIA) and TLR4. Additionally, rings of pulmonary artery were isolated for measuring vascular reactivity. LPS-induced ALI was indicated by increases in total and differential cell count, total protein, and LDH in BALF, and increased lung levels of malondialdehyde (MDA), as well as decreased activity of reduced glutathione (GSH) and superoxide dismutase (SOD). Moreover, LPS increased pulmonary artery contraction in response to phenylephrine (PE). Additionally, LPS downregulated mRNA expression of NFκBIA and upregulated mRNA expression of TLR4. LPS caused a marked inflammation in the lung tissue, with tubercular granuloma and numerous neutrophils. Pretreatment with LPS-RS protected against LPS-induced ALI by decreasing total and differential cell count, total protein, and LDH in BALF, and increased pulmonary GSH content and SOD activity without affecting MDA content. Additionally, it decreased the elevated PE-induced pulmonary artery contraction. LPS-RS upregulated mRNA expression of NFκBIA and downregulated mRNA expression of TLR4. Moreover, LPS-RS prevented inflammation in lung tissues. In conclusion, pretreatment with LPS-RS protects against LPS-induced ALI in rats through its anti-inflammatory effects, possibly by decreasing the mRNA expression of TLR4 and increasing that of NFκBIA.


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