BackgroundThe global burden from cancer is rising, especially as low-income countries like Bangladesh observe rapid aging. So far, there are no comprehensive descriptions reporting diagnosed cancer group that include hematological malignancies in Bangladesh.MethodsThis was a multi-center hospital-based retrospective descriptive study of over 5000 confirmed hematological cancer cases in between January 2008 to December 2012. Morphological typing was carried out using the “French American British” classification system.ResultsA total of 5013 patients aged between 2 to 90 years had been diagnosed with malignant hematological disorders. A 69.2% were males (n = 3468) and 30.8% females (n = 1545), with a male to female ratio of 2.2:1. The overall median age at diagnosis was 42 years. Acute myeloid leukemia was most frequent (28.3%) with a median age of 35 years, followed by chronic myeloid leukemia with 18.2% (median age 40 years), non-Hodgkin lymphoma (16.9%; median age 48 years), acute lymphoblastic leukemia (14.1%; median age 27 years), multiple myeloma (10.5%; median age 55 years), myelodysplastic syndromes (4.5%; median age 57 years) and Hodgkin’s lymphoma (3.9%; median age 36 years). The least common was chronic lymphocytic leukemia (3.7%; median age 60 years). Below the age of 20 years, acute lymphoblastic leukemia was predominant (37.3%), followed by acute myeloid leukemia (34%). Chronic lymphocytic leukemia and multiple myeloma had mostly occurred among older patients, aged 50-over.ConclusionsFor the first time, our study presents the pattern and distribution of diagnosed hematological cancers in Bangladesh. It shows differences in population distributions as compared to other settings with possibly a lower presence of non-Hodgkin lymphoma. There might be under-reporting of affected women. Further studies are necessary on the epidemiology, genetics and potential environmental risk factors within this rapidly aging country.
Tumor necrosis factor activates p38-MAPK in the intact heart and in isolated cardiac myocytes through MKK3. This activation likely contributes to the early cardiodepressant action of TNFalpha.
To examine whether cardioprotection initiated by reactive oxygen species (ROS) is dependent on protein kinase Cepsilon (PKCepsilon), isolated buffer-perfused mouse hearts were randomized to four groups: 1) antimycin A (AA) (0.1 microg/ml) for 3 min followed by 10 min washout and then 30 min global ischemia (I) and 2 h reperfusion (R); 2) controls of I/R alone; 3) AA bracketed with 13 min of N-2-mercaptopropionyl- glycine (MPG) followed by I/R; and 4) MPG (200 microM) alone, followed by I/R. Isolated adult rat ventricular myocytes (ARVM) were exposed to AA (0.1 microg/ml), and lucigenin was used to measure ROS production. Murine hearts and ARVM were exposed to AA (0.1 microg/ml) with or without MPG, and PKCepsilon translocation was measured by cell fractionation and subsequent Western blot analysis. Finally, the dependence of AA protection on PKCepsilon was determined by the use of knockout mice (-/-) lacking PKCepsilon. AA exposure caused ROS production, which was abolished by the mitochondrial uncoupler mesoxalonitrile 4-trifluoromethoxyphenylhydrazone. In addition, AA significantly reduced the percent infarction-left ventricular volume compared with control I/R (26 +/- 4 vs. 43 +/- 2%; P < 0.05). Bracketing AA with MPG caused a loss of protection (52 +/- 7 vs. 26 +/- 4%; P < 0.05). AA caused PKCepsilon translocation only in the absence of MPG, and protection was lost on the pkcepsilon(-/-) background (38 +/- 3 vs. 15 +/- 4%; P < 0.001). AA causes ROS production, on which protection and PKCepsilon translocation depend. In addition, protection is absent in PKCepsilon null hearts. Our results imply that, in common with ischemic preconditioning, PKCepsilon is crucial to ROS-mediated protection.
Blistering diseases are alarming skin conditions where blister formation occurs in various ways and cannot be differentiated clinically. For confirmation of diagnosis, along with routine histological examination, immunofluorescence study is essential. Tzanck smear may be used as a rapid diagnostic tool. We included here 34 cases of different blistering lesions. Other than routine Hematoxylin and Eosin stain, direct immunofluorescence test was done in 31 cases, indirect immunofluorescence in 28 cases and Tzanck smear in 33 cases. Direct immunofluorescence stain was also applied on Tzanck smears. The most frequent diagnoses were pemphigus (n=16), bullous pemphigoid (n=11) and linear IgA dermatosis (n=3). Clinical findings and histological examination were sufficient for the diagnosis of most cases. Direct immunofluorescence study is essential in many cases, and indirect immunofluorescence study is a useful method for diagnosis of some of the blistering diseases, especially in pemphigus. Direct immunofluorescence staining on Tzanck smear is a novel technique for the diagnosis of pemphigus.
Introduction: COVID-19 is a major threat to human beings. Clinical characterization, rapid identification of cases and isolation are vital for containments of rapidly spreading disease. The objectives of the study were to evaluate the clinico pathologic profile of Covid 19 positive Bangladeshi patients and also to see their clinical outcome within defined period. Methods: This cohort study on 201 Bangladeshi cases was done in Combined Military Hospital, a tertiary level hospital in Dhaka, Bangladesh from April 2020 to May 2020. Total 201 COVID-19 cases were enrolled after getting the result positive for RT-PCR. After collection, data were analysed to show the characteristics of Covid 19 and their outcome after treatment.
Results: Among 201 cases, 180 (90%) were male and 21 (10%) were female. The most prevalent affected age groups were 71 (35.5%) patients in 26-35 years age, 54 (27%) in 16- 25 years, 49 (24.5%) in 35-45 years. Mean age is 32.2±2. Among the total cases, 146 (73%) have positive history of contact, 37 (18.5%) have no history of any contact, 8 (4%) denied any contact with COVID-19 patients. Regarding clinical presentations, 67 (33.5%) patients presented with only one symptoms, 125 (62.5%) had multiple symptoms and 9 (4.5%) cases were asymptomatic. 154 (77%) patients presented with fever. Other presentations were cough 71 (35.5%), headache 27 (13.5%), myalgia 25 (12.5%), sore throat 25 (12.5%), malaise 15 (7.5%), respiratory distress 11 (5.5%). Respiratory system was the dominant domain of clinical presentation. Leukopenia was presented by 12 patients and 12 had lymphopenia. 18 patients had mild thrombocytopenia. Pulse oxymetry showed oxygen saturation below 88% in 12 cases. After oxygen therapy 7 cases were improved and 5 cases were shifted to Corona ICU as their saturation fell below 70. These 5 patients are categorised as severe disease, rest 196 patients were mild in nature.
Conclusion: COVID 19 affects male more than female. Common symptoms are fever, cough, headache, myalgia, sore throat, malaise, respiratory distress. Respiratory system is the dominant domain of clinical presentation. ICU support was needed in 2.5 % cases and death rate was 1% which was associated with comorbidity of CKD.
J Bangladesh Coll Phys Surg 2020; 38(0): 37-42
MAPKAPK-2 (MK2) is a protein kinase activated downstream of p38-MAPK which phosphorylates the small heat shock proteins HSP27 and αB crystallin and modulates p38-MAPK cellular distribution. p38-MAPK activation is thought to contribute to myocardial ischemic injury; therefore, we investigated MK2 effects on ischemic injury and p38 cellular localization using MK2-deficient mice (KO). Immunoblotting of extracts from Langendorffperfused hearts subjected to aerobic perfusion or global ischemia or reperfusion showed that the total and phosphorylated p38 levels were significantly lower in MK2 −/− compared to MK2 +/+ hearts at baseline, but the ratio of phosphorylated/total p38 was similar. These results were confirmed by cellular fractionation and immunoblotting for both cytosolic and nuclear compartments. Furthermore, HSP27 and αB crsytallin phosphorylation were reduced to baseline in MK2 −/− hearts. On semiquantitative immunofluorescence laser confocal microscopy of hearts during aerobic perfusion, the mean total p38 fluorescence was significantly higher in the nuclear compared to extranuclear (cytoplasmic, sarcomeric, and sarcolemmal compartments) in MK2 +/+ hearts. However, although the increase in phosphorylated p38 fluorescence intensity in all compartments following ischemia in MK2 +/+ hearts was lost in MK2 −/− hearts, it was basally elevated in nuclei of MK2 −/− hearts and was similar to that seen during ischemia in MK2 +/+ hearts. Despite these differences, similar infarct volumes were recorded in wild-type MK2 +/+ and MK2 −/− hearts, which were decreased by the p38 inhibitor SB203580 (1 μM) in both genotypes. In conclusion, p38 MAPKinduced myocardial ischemic injury is not modulated by MK2. However, the absence of MK2 perturbs the cellular distribution of p38. The preserved nuclear distribution of active p38 MAPK in MK2 −/− hearts and the conserved
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