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Authors are the souls of any journal, and deserve much respect. To publish a journal manuscripts are needed from authors. Authors have a great responsibility for producing facts of their work in terms of number and results truthfully and an individual honesty is expected from authors in this regards. Both ways its true "No authors-No manuscripts-No journals" and "No journals–No manuscripts–No authors". Reviewing a manuscript is also a very responsible and important task of any peer-reviewed journal and to be taken seriously. It needs knowledge on the subject, sincerity, honesty and determination. Although the process of reviewing a manuscript is a time consuming task butit is expected to give one's best remarks within the time frame of the journal.
Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
Timely publication of journal: Publication of manuscripts and bringing out the issue in time is one of the positive aspects of JCDR and is possible with strong support team in terms of peer reviewers, proof reading, language check, computer operators, etc. This is one of the great reasons for authors to submit their work with JCDR. Another best part of JCDR is "Online first Publications" facilities available for the authors. This facility not only provides the prompt publications of the manuscripts but at the same time also early availability of the manuscripts for the readers.
Indexation and online availability: Indexation transforms the journal in some sense from its local ownership to the worldwide professional community and to the public.JCDR is indexed with Embase & EMbiology, Google Scholar, Index Copernicus, Chemical Abstracts Service, Journal seek Database, Indian Science Abstracts, to name few of them. Manuscriptspublished in JCDR are available on major search engines ie; google, yahoo, msn.
In the era of fast growing newer technologies, and in computer and internet friendly environment the manuscripts preparation, submission, review, revision, etc and all can be done and checked with a click from all corer of the world, at any time. Of course there is always a scope for improvement in every field and none is perfect. To progress, one needs to identify the areas of one's weakness and to strengthen them.
It is well said that "happy beginning is half done" and it fits perfectly with JCDR. It has grown considerably and I feel it has already grown up from its infancy to adolescence, achieving the status of standard online e-journal form Indian continent since its inception in Feb 2007. This had been made possible due to the efforts and the hard work put in it. The way the JCDR is improving with every new volume, with good quality original manuscripts, makes it a quality journal for readers. I must thank and congratulate Dr Hemant Jain, Editor-in-Chief JCDR and his team for their sincere efforts, dedication, and determination for making JCDR a fast growing journal.
Every one of us: authors, reviewers, editors, and publisher are responsible for enhancing the stature of the journal. I wish for a great success for JCDR."
Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011
Dr. Shankar P.R.
"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
Areas for improvement: In certain cases, I felt that the peer review process of the manuscripts was not up to international standards and that it should be strengthened. Also, the number of manuscripts in an issue is high and it may be difficult for readers to go through all of them. The journal can consider tightening of the peer review process and increasing the quality standards for the acceptance of the manuscripts. I faced occasional problems with the online manuscript submission (Pre-publishing) system, which have to be addressed.
Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."
Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011 Anuradha
Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.
Dr. Anuradha
E-mail: anuradha2nittur@gmail.com
On Jan 2020
Original article / research
Full Version
Erythrocytic Pyruvate Kinase and Malondialdehyde Levels in Acute Leukaemia Patients
Correspondence Address :
Kiran Dahiya,
778/28, Bharat Colony,
Rohtak, Haryana, India - 124001
Phone: 09896111985
E-mail: kirandahiya_2002@yahoo.com
Introduction: Many acquired enzymopathies have been reported in patients with acute leukaemia. Oxidative stress is also found to be increased in acute leukaemia, which can be indicated by the increased malondialdehyde (MDA) levels. Malondialdehyde itself may lead to the alteration of the enzyme, pyruvate kinase. Therefore, this study was planned to estimate the levels of erythrocytic pyruvate kinase and malondialdehyde in patients of acute leukaemia before and after chemotherapy.
Methods: This study was conducted on 20 patients of acute myeloid leukaemia, 20 patients of acute lymphoblastic leukaemia and 20 healthy controls. The levels of pyruvate kinase and malondialdehyde were estimated in the haemolysate in the controls and in the patients at the time of diagnosis. These levels were also estimated in the patients after six weeks of chemotherapy or remission, whichever was earlier. The results were compared statistically.
Results: The levels of erythrocytic pyruvate kinase were found to be decreased significantly in the acute leukaemia patients as compared to controls and to be increased after chemotherapy, while the levels of erythrocytic malondialdehyde were found to be increased significantly in these patients as compared to the controls and to be decreased after chemotherapy. The levels were not statistically significantly different in acute myeloid and acute lymphoblastic leukaemia.
Conclusion: The erythrocytic pyruvate kinase and the malondialdehyde levels may help in the diagnosis, for asessing the severity and for the monitoring of the acute leukaemia patients.
Erythrocyte, Pyruvate kinase, Malondialdehyde, Acute leukaemia, Chemotherapy
Introduction
Leukaemias are caused by the clonal neoplastic proliferation of immature cells of the haematopoietic system, which are characterized by aberrant or arrested differentiation. These are divided into acute or chronic, depending upon the clinical course of the disease and into myeloid and lymphoid, depending upon the cell of origin (1). Abnormalities have been reported in the activity of a number of enzymes in haematological malignancies, which include glutathione reductase (2), glucose-6-phosphate dehydrogenase (3), phosphofructokinase (4), leucocytic alkaline phosphatase (5), adenosine deaminase (6) and 5' nucleotidase (7). Pyruvate kinase (PK) deficiency has also been reported in patients of acute leukaemia by some authors (8),(9).
Pyruvate kinase (PK) catalyzes the third irreversible step in glycolysis i.e. conversion of phosphoenolpyruvate to pyruvate, with the synthesis of one molecule of adenosine triphosphate (ATP). It requires K+ and Mg2+/ Mn2+ for its activity (8). PK has four different isoenzymic forms which are L, R, M1 and M2. The L-type PK is present in the liver cells, the R-type is present in the mature red blood cells and M1 and M2 are the muscular forms. Immature erythrocytes have both M2 PK and R-PK (10). R-PK has a typical four domain subunit structure. Several mechanisms including genetic and post-translational ones have been considered to be responsible for the enzyme defects in the erythrocytes of various blood disorders (11).
Malondialdehyde (MDA) is the by product of free radical mediated reactions which lead to the formation of lipid peroxides, alcohol andSectionaldehydes. Normally, MDA is quickly oxidized to acetate or malonate and then to carbondioxide by the Kreb’s cycle. If it is accumulated in excess, MDA can combine with different serum proteins and cell membrane components to form altered determinants (12). It can interact with deoxyribonucleic acid (DNA) and inhibit the biosynthesis of the DNA, ribonucleic acid (RNA) and proteins. The chemical structure of MDA closely resembles that of carcinogenic compounds like glycidaldehyde and beta propiolactone and it thus may itself, have carcinogenic properties (13). Erythrocytic lipids are more susceptible to auto-oxidation under coditions of oxidative stress, more so, in the acute leukaemia patients. Erythrocytic MDA (eMDA) has been found to be increased in leukaemia (14). As MDA has the propensity to attack the sulfhydryl group, it may be involved in the alteration of the erythrocytic PK (ePK) levels in acute leukaemia patients (15). Therefore, the present study was planned to estimate the levels of ePK and eMDA in patients of acute leukaemia before and after chemotherapy.
This study was conducted on 40 patients diagnosed with acute leukaemia, who were admitted in wards or were attending the Clinical Haematology Department of our institute, after obtaining informed consent and approval from the institutional board of studies. The diagnosis was made by doing a clinical examination and a complete haemogram, bone marrow examination and cytochemistry. All the patients were divided into two groups: group I (20 patients of acute myeloid leukaemia, AML) and group II (20 patients of acute lymphoblastic leukaemia, ALL). The patientswere monitored both clinically and haematologically. Heparinised blood samples were collected at the time of diagnosis i.e. before starting chemotherapy and after 6 weeks of chemotherapy or remission, whichever was earlier. The patients were considered to be in remission if the tumour cell mass was decreased below 109-1010 cells, if there were <5% blasts in the bone marrow, or there was absence of leukaemic cells in the blood, or there was restoration of the normal peripheral blood count, or there was absence of the physical findings which were attributable to the extramedullary involvement of leukaemia and or if there was the absence of Auer rods in acute myeloid leukaemia (16). Twenty age and sex matched healthy subjects were taken as the controls (group III).
The heparinised blood was centrifuged for 10 minutes at 3000 rpm. After removing the supernatent plasma and the buffy coat, the red blood cells (RBCs) were washed thrice with normal saline. The washed RBCs were lysed by adding distilled water and by keeping the cell pellet in a refrigerator for 15 minutes (17). After estimating the haemoglobin (Hb) concentration of this haemolysate (17), the levels of ePK (18) and eMDA (19) were estimated in both the controls and the patients by using standard colorimetric methods and a semi-autoanalyser (Techno 168). The results were expressed as per gram of Hb and they were compared statistically.
The mean age of presentation was 37.6 years (range 21-88 years) in group I, 39.40 years (range 21-82 years) in group II and 38.5 years (range 20-85 years) in group III. The male to female ratio was 2:3 in all the three groups. The presenting complaints of the patients included generalised weakness, swelling, bleeding tendencies, pallor and fever. All the patients had anaemia (mean Hb 5.99 g/dL) and hepatosplenomegaly. Lymphadenoapthy was observed in362approximately 30% of the patients of both the groups. The levels of ePK and eMDA, before and after chemotherapy, in the patients of AML and ALL and the controls, is shown in (Table/Fig 1). After chemotherapy, most of the patients i.e 17 out of 20 in AML and 18 out of 20 in ALL were found to be in complete remission. The levels of ePK and eMDA were compared between the AML and ALL patients who achieved remission and who were not in remission n (Table/Fig 2) and (Table/Fig 3) respectively.
In the present study, the ePK levels were found to be decreased significantly in the patients of acute leukaemia (both AML and ALL) as compared to the healthy controls and they were observed to increase after chemotherapy (p<0.001). These results were in accordance with those of earlier studies (8),(9). The mechanism which has been put forward has been explained at two levels. It was considered that the defect was true molecular and that the decreased concentration of the ePK-related antigen was irreversible. In the other mechanism, the defect in the ePK was considered to be primarily functional and the enzyme activity was hoped to be be restored with treatment. Various posttranslational modifications may be responsible for this kind of defect (11). The intra-cellular stress of the leukaemic blasts on the RBCs may also lead to the temporary inhibition of the erythrocytic glycolytic enzymes (20). But in another study, no correlation could be established between the number of blast cells and the ePK levels (21). Another author has suggested a selective abnormality in the erythroid precursor stem cells (2). The ePK levels were found to be higher in ALL as compared to those in the AML patients, but the difference was not statistically significant. So, these levels could not be used for the differentiation between the AML and the ALL patients.
The eMDA levels were found to be increased in the patients of AML and ALL as compared to the controls and a statistically significantdecrease was observed after chemotherapy. The difference in the eMDA levels between the AML and the ALL patients was not statistically significant. This increase in the eMDA levels in the acute leukaemia patients may be due to the increased oxidative stress in leukaemia (22). There is an increased cellular turnover in leukaemia which leads to the increased breakdown of purine to uric acid. This reaction produces hydrogen peroxide as a byproduct. Increased oxidative stress may lead to cytotoxicity, mutagenecity and alteration in the gene expression, which may culminate in the initiation and propagation of carcinogenesis (22).
In has been reported that certain lipid peroxidation products like MDA can attack the sulfhydryl groups and the amino group in proteins (15). The sulfhydryl group of PK is prone to this action by MDA (15). Thus, increased eMDA may also be a causative factor for the decrease of the ePK activity in acute leukaemia patients. No significant difference was observed in the ePK and the eMDA levels in patients who attained remission and in patients who were not in remission. The difference in these levels after chemotherapy was statistically significant in patients in remission, but it was not significant in patients who were not in remission. But the number of patients who did not achieve remission was too small in both the AML and ALL groups and so it is difficult to comment on the findings. A larger study group with a greater number of such patients is required to confirm this observation. Therefore, it was concluded that the estimation of the ePK and the eMDA levels in patients of acute leukaemia may be helpful in assessing the disease activity and in predicting the response to chemotherapy. It could serve as a prognostic indicator in these patients. The results need to be substantiated by further research which comprises of larger study groups.
DOI: JCDR/3552:2063
DECLARATI ON ON COMPETING INTERESTS:
No competing Interests.
Date of Submission: Nov 04, 2011
Date of Peer Review: Dec 06, 2011
Date of Acceptance: Dec 28, 2011
Date of Publishing: May 01, 2012
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