Malaria resurgence in India: a critical study

In 1953, the Indian National Malaria Control Programme (NMCP) was started. Encouraged by the results, and the fact that insecticide resistance in vector species may evolve and become an obstacle, in 1958 a control programme was converted to the National Malaria Eradication Programme (NMEP). By 1964, malaria was eradicated from 88% of the area and it was in the advanced stage of spraying in the remaining parts. At that time, focal outbreaks that occurred in 1965 and increased in later years, could not be contained due to the shortages of DDT. As a result, large areas in consolidation and maintenance phases were reverted to the attack phase. Besides, the infrastructure in general health services was not adequate and mature enough to take up surveillance and vigilance. This produced a large number of secondary cases due to the re-introduction and relapse of malaria. Added to this was the problem of urban malaria, the control of which was the responsibility of local bodies. Malaria cases increased in towns, and started diffusing to the rural areas, due to inadequate staff and the shortages of malarial larvicidal oil (MLO). Later, it turned out, that while it was technically feasible to eradicate malaria from 91% of the population, the strategy of indoor spraying of DDT to interrupt transmission did not succeed in 9.0% of the population, despite more than 12-14 years of regular spraying. During the years of resurgence, there was no research support to the programme, so that technical problems were not properly appreciated, understood and tackled. The reservoir of parasites that were present throughout the country started multiplying and spreading to newer areas due to the presence of vectors in high densities. Thus malaria resurged and re-established itself even in areas that were at one time freed from the disease. The analysis of the pattern of malaria resurgence revealed that malaria outbreaks preceded the true problem of insecticide resistance. It is noteworthy to mention that malaria resurgence occurred in towns where the control measures were non-insecticidal and in regions which were not under the influence of insecticide-resistant vectors. The study also revealed that resurgence occurred before the introduction of high-yielding varieties programme in the country, and had no relationship to either the cotton or rice growing or intensive agriculture.     

CT19PTRICUSPID VALVE REPAIR IN ‘TORRENTIAL TRICUSPID REGURGITATION’ FOLLOWING PERMANENT PACEMAKER LEAD EXTRACTION – A CASE REPORT

Introduction Traumatic tricuspid regurgitation secondary to blunt chest trauma has been reported in literature. We report our experience with a case of ‘Torrential Tricuspid Regurgitation’ following permanent pacemaker lead extraction which was successfully treated with tricuspid valve repair and annuloplasty. Report A 67 year old woman was treated for Sick sinus syndrome with permanent pacemaker implant. She had three generator changes for end of life and repositioning.Erosion of generator, led cardiologist to plan lead and generator extraction with the surgical backup. During lead extraction a small piece of papillary muscle was avulsed. The patient remained hemodynamically stable in the theatre. However in ward she developed right sided cardiac failure not responding to conservative therapy. A transthoracic echo (TTE) revealed torrential tricuspid regurgitation with a freely mobile posterior leaflet with attached chordae and avulsed papillary muscle.During surgery the tricuspid valve was successfully repaired and transesophageal (TOE) images showed trivial to mild tricuspid regurgitation at the end of repair procedure. Additional procedure also included ligation of both atrial appendages and implantation of epicardial leads and pacemaker. Patient made good recovery from operation. Conclusion To the best of our knowledge this is first report of repair of tricuspid valve in ‘Torrential Tricuspid Regurgitation’ following pacemaker lead extraction. We share our experience with tricuspid valve repair technique and annuloplasty.     

Protection against 7,12-dimethylbenzanthracene-induced tumour initiation by protein A in mouse skin.

Protein A is an immunostimulating glycoprotein obtained from Staphylococcus aureus Cowan I. Its antitumour activity is proven in various tumour models. Its ability to provide protection against tumour initiation by the chemical carcinogen 7,12-dimethylbenzanthracene (DMBA) has been investigated in the present study using a mouse skin model of two-stage carcinogenesis. Protein A was administered intraperitoneally (1 microgram/animal 20 g body wt.) twice a week for 2 weeks, prior to initiation by DMBA. The promotion was performed by twice weekly applications of 12-O-tetradecanoyl phorbol-13-acetate (TPA) (3 or 5 micrograms/animal in 100 microliters acetone). Protein A provided significant protection to animals from DMBA-induced tumour initiation as was observed by the decrease in cumulative number of tumours, percent of animals developing tumours, number of tumours per animal and rate of tumour growth. Our data indicate that protein A has anticarcinogenic properties.     

Galectin-3 does not reliably distinguish benign from malignant thyroid neoplasms

AIMS: To determine whether galectin-3 is a sensitive indicator of thyroid malignancy. It has been suggested as a potential marker for differentiating thyroid carcinoma from benign or non-neoplastic lesions in preoperative fine-needle aspirates (FNAs). METHODS: Galectin-3 protein expression was assessed by immunohistochemistry in formalin-fixed thyroid tissues from 124 patients with histological diagnoses of papillary carcinoma (n = 38), follicular carcinoma (n = 19), follicular adenoma (n = 32) and dominant nodules of multinodular goitre (n = 35). Expression of galectin-3 was also assessed by Western blotting in 24 fresh thyroid tissues. RESULTS: Galectin-3 expression was observed in the majority of carcinomas (papillary 92%; follicular 74%). However, a large proportion of follicular adenomas (72%) and multinodular goitres (57%) also expressed galectin-3. In addition, galectin-3 expression was observed in epithelial cells of normal thyroid tissue and Hashimoto's thyroiditis. Galectin-3 immunopositivity was significantly greater in papillary carcinomas than in dominant nodules or follicular adenomas (P < 0.0001, P = 0.0005, respectively). However, galectin-3 expression was no greater in follicular carcinomas than in follicular adenomas (P = 0.8735). Western blotting analysis confirmed both the specificity of the antiserum and expression of galectin-3 in multinodular goitres, follicular adenomas/carcinomas and papillary carcinomas. CONCLUSION: The data demonstrate that galectin-3 is not a reliable immunohistochemical marker to distinguish benign from malignant thyroid follicular lesions.     

Immunomodulation by biphalin,dimeric synthetic opioid peptide,and its analog

The opioid pentapeptides called enkephalins were originally described as the endogenous ligands for the opioid receptors. Although their precise physiological significance still remains elusive, the enkephalins have been reported to exhibit analgesic, antidepressant, antianxiety and anticonvulsant activities. In addition, enkephalins have also been shown to act as immunomodulator. The first generation of dimeric peptides was derived from enkephalins. Biphalin [(Tyr-D-Ala-Gly-Phe-NH)2] is a bivalent opioid analog containing two tyrosine residues. We have evaluated the immunomodulatory properties of biphalin and its analogs in various in vitro tests. We report that biphalin and one of its analogs [Tyr-D-Ala-Gly-Phe-NH.NH-Phe(p-Cl)-H] stimulate human T cell proliferation, natural killer (NK) cell cytotoxicity in vitro and interleukin-2 (IL-2) production. Biphalin and its analog also released chemokine like factor in the culture supernatant that was responsible for increased chemotaxis of monocytes. Furthermore, these peptides inhibited tumor necrosis factor (TNF-alpha) production in lipopolysaccharide (LPS) stimulated peripheral blood mononuclear cells (PBMC) and nitric oxide (NO) production in mouse macrophage cells, RAW 264.7. Our observations suggest immunomodulatory property of biphalin and its analog.     

Antilymphoproliferative activity of ethanolic extract of Boerhaavia diffusa roots

Extracts of plants have been widely evaluated for possible antiproliferative and anticarcinogenic properties. The antiproliferative activity of ethanolic extract of Boerhaavia diffusa, a plant used in traditional medicine, was evaluated in several cells. It inhibited T cell mitogen phytohemagglutinin and concanavalin A-stimulated proliferation of human peripheral blood mononuclear cells (PBMC). It also inhibited purified protein derivative antigen-stimulated PBMC proliferation and human mixed lymphocyte culture. In addition, B. diffusa extract inhibited the growth of several cell lines of mouse and human origin, such as mouse macrophage cells (RAW 264.7), human macrophage cells (U937), human monocytic cells (THP-1), mouse fibroblast cells (L929), human embryonic kidney cells (HEK293), mouse liver cells (BNLCL.2), African green monkey kidney cells (COS-1), mouse lymphoma cells (EL-4), human erythroleukemic cells (K562), and human T cells (Jurkat). The present study has demonstrated the antiproliferative potential of ethanolic extract of B. diffusa in vitro.     

Radiation-related cytological changes in oral malignant cells

Carcinoma of the oral cavity constitutes approximately 40% of overall malignant tumours in India, with an incidence of about 56,000 cases per year. Radiation responses in oral cancer cells by cytology have not been extensively studied. 102 patients with squamous cell carcinoma of the oral cavity treated by fractionated radiotherapy were studied. Serial scrape smears were taken from each tumour before and after irradiation. The abnormal nuclear counts per 1000 malignant cells were 1.6 and 14.1(p<0.001) for micronucleation, 0.9 and 5.5 (p<0.001) for nuclear budding, 7.6 and 28.1(p<0.001) for binucleation and 2.4 and 11.7(p<0.001) for multinucleation respectively. The study showed a significant rise in radiation induced cytological responses. In addition, radiation changes observed included abnormal and incomplete divisions of a nucleus, fibroblast like appearance cells, and enlargement of nuclear size as well as cytoplasmic granulation. These changes may have an important role to play in understanding the mechanism of cell killing after radiotherapy.