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Najmul Islam

Publications and source records attributed to Najmul Islam.

11 recordsLinked to original sources
PubMed2006

Suppression of Mycobacterium tuberculosis induced reactive oxygen species (ROS) and TNF-alpha mRNA expression in human monocytes by allicin.

Chronic inflammation associated with tumor necrosis factor (TNF)-alpha and reactive oxygen species (ROS) is the hallmark of tuberculosis. Mycobacterium tuberculosis (MTB) directly stimulates human monocytes to secrete TNF-alpha. We show the augmented expression of TNF-alpha mRNA in MTB-infected monocytes by cellular activation and ROS was suppressed by allicin in a dose-dependent manner. Also, allicin enhanced the glutathione peroxidase activity, which correlated inversely with the downregulation of ROS and TNF-alpha in MTB-infected monocytes. Hence, allicin may prove to be a valuable natural antioxidant in combating tuberculosis.

Base Sequence↗
PubMed2006

Minimally symptomatic severe hypercalcaemia in a patient with parathyroid carcinoma.

The case of a 38 years old man with generalized pains fatigue, anorexia, constipation, polyuria serum calcium level of 20.6mg/dl in paired renal function parathyroid hormone is presented. Sestamibi scan showed a functioning left inferior parathyroid tumor, which was successfully removed. Before surgery he was managed with rehydration, diuretics and pamidronate infusion. Five months post surgery the serum calcium levels are normal and renal function has improved.

Adult↗
PubMed2004

Role of cellular activation and tumor necrosis factor-alpha in the early expression of Mycobacterium tuberculosis 85B mRNA in human alveolar macrophages.

BACKGROUND: Infection of alveolar macrophages (AMs), which constitute the first line of defense against Mycobacterium tuberculosis, initiates an intense interaction between the host's innate immune response and mycobacteria that may assist in the successful intracellular parasitism of M. tuberculosis. METHODS: Expression of tumor necrosis factor (TNF)- alpha and M. tuberculosis 85B mRNA was studied in M. tuberculosis-infected AMs, to better delineate the role of macrophages in the early events in initiation of infection. RESULTS: Both TNF- alpha mRNA and M. tuberculosis 85B were induced in AMs; at 24 h, the time point of maximum TNF- alpha induction, the mRNA levels for TNF- alpha and M. tuberculosis 85B correlated with one another, and induction of either gene correlated strongly with their protein levels. Inhibition of endogenous TNF- alpha by soluble (s) TNF receptor (R) I and sTNFRII reduced expression of both TNF- alpha and M. tuberculosis 85B. The activation of nuclear factor- kappa B was found to underlie expression of both TNF- alpha and M. tuberculosis 85B. Exogenous TNF- alpha was slightly more potent than interleukin (IL)-6 and granulocyte-macrophage colony-stimulating factor and was significantly stronger than IL-1 in inducing expression of M. tuberculosis 85B. Interestingly, inhibition of bactericidal mediators, reactive oxygen intermediates (ROIs) and reactive nitrogen intermediates (RNIs), reduced expression of TNF- alpha and M. tuberculosis 85B genes in M. tuberculosis-infected AMs. CONCLUSION: Activation of AMs by M. tuberculosis initiates a cascade of events whereby TNF- alpha, ROI, and RNI enhance the expression of the M. tuberculosis 85B gene.

Acyltransferases↗
PubMed2004

Cervical spine tuberculosis.

We present a case that showed extensive tuberculous cervical, first thoracic and fifth lumbar vertebrae involvement. The involvement was non-contiguous with relative sparing of the inter-vertebral discs and involvement of posterior element. Diagnosis was made on histology. Patient received anti-tuberculosis treatment and showed remarkable response.

Adolescent↗
PubMed2004

Transactivation of human immunodeficiency virus-1 in T-cells by Mycobacterium tuberculosis-infected mononuclear phagocytes.

Worldwide, tuberculosis (TB) is the most frequent coinfection with human immunodeficiency virus-1 (HIV-1), and active TB enhances the progression of HIV-1 disease in dually infected subjects. In the microenvironment of Mycobacterium tuberculosis (MTB)-infected foci, where HIV-1-infected CD4 T-cells come into contact with MTB-infected macrophages, the direct interaction of the two cell types in the activation of latent HIV-1 may be important. In this study we sought to determine whether MTB-infected human primary mononuclear phagocytes-namely, alveolar macrophages (AMs) and their less mature blood precursors, monocytes-activate HIV-1 in a T-cell line stably transfected with an HIV-1 long terminal repeat (LTR) reporter construct (1G5 cells) and induce HIV-1 expression in T-cells from HIV-1-infected subjects. MTB-infected monocytes and AMs, and not Mycobacterium avium-infected cells, activated HIV-1 LTR in 1G5 cells in the presence and absence of HIV-1 tat. Transactivation of HIV-1 LTR by MTB-infected mononuclear phagocytes was mediated mainly by tumor necrosis factor-alpha. In AMs, but not monocytes, membrane tumor necrosis factor-alpha contributed to transactivation of HIV-1 LTR. MTB-infected MNs from 60% of HIV-infected subjects induced HIV-1 LTR in 1G5 cells as well. Furthermore, HIV-1 transcription was induced in autologous T-cells from 30% of the HIV-1-infected subjects. We therefore conclude that MTB-infected mononuclear phagocytes can transactivate HIV-1 in CD4 cells. Transactivation of latent HIV-1 in CD4 T-cells by MTB-infected mononuclear phagocytes may in part be responsible for increased HIV activity at sites of MTB infection during dual infection in vivo.

AIDS-Related Opportunistic Infections↗
PubMed2003

Pulmonic valve endocarditis.

Pulmonic valve endocarditis is an extremely rare infection that shares epidemiologic, clinical, radiologic, microbiologic, and prognostic features with tricuspid valve endocarditis. We report a case of pulmonic valve infection on a structurally normal heart and review the English-language literature on this subject.

Echocardiography, Transesophageal↗
PubMed2003

Pathophysiological mechanisms in osteoarthritis lead to novel therapeutic strategies.

Osteoarthritis (OA) is a debilitating, progressive disease of diarthrodial joints associated with aging. At the molecular level, OA is characterized by an imbalance between anabolic (i.e. extracellular matrix biosynthesis) and catabolic (i.e. extracellular matrix degradation) pathways in which articular cartilage is the principal site of tissue injury responses. The pathophysiology of OA also involves the synovium in that 'nonclassical' inflammatory synovial processes contribute to OA progression. Chondrocytes are critical to the OA process in that the progression of OA can be judged by the vitality of chondrocytes and their ability to resist apoptosis. Growth factors exemplified by insulin-like growth factor-1, its binding proteins and transforming growth factor-beta contribute to anabolic pathways including compensatory biosynthesis of extracellular matrix proteins. Catabolic pathways are altered by cytokine genes such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) which are upregulated in OA. In addition, IL-1 and TNF-alpha downregulate extracellular matrix protein biosynthesis while concomitantly upregulating matrix metalloproteinase (MMP) gene expression. When MMPs are activated, cartilage extracellular matrix degradation ensues apparently because levels of endogenous cartilage MMP inhibitors cannot regulate MMP activity. Therapeutic strategies designed to modulate the imbalance between anabolic and catabolic pathways in OA may include neutralizing cytokine activity or MMP gene expression or inhibiting signaling pathways which result in apoptosis dependent on mature caspase activity or mitogen-activated protein kinase (MAPK) activity. MAPK activity appears critical for regulating chondrocyte and synoviocyte apoptosis and MMP genes.

Animals↗
PubMed2002

Epigallocatechin-3-gallate inhibits interleukin-1beta-induced expression of nitric oxide synthase and production of nitric oxide in human chondrocytes: suppression of nuclear factor kappaB activation by degradation of the inhibitor of nuclear factor kappaB.

OBJECTIVE: The proinflammatory cytokine interleukin-1beta (IL-1beta) induces the production of high levels of nitric oxide (NO) in human chondrocytes. Green tea (Camellia sinensis) polyphenols are potent antiinflammatory agents and have been shown to inhibit NO production in tumor cell lines. In the present study, we examined the effect of epigallocatechin-3-gallate (EGCG), a green tea polyphenol, on IL-1beta-induced production of NO in primary human osteoarthritis (OA) chondrocytes. METHODS: Human chondrocytes were derived from OA cartilage and were treated with EGCG (100 microM) and IL-1beta (2 ng/ml) for different periods, and inducible nitric oxide synthase (iNOS) messenger RNA and protein expression was determined by real-time quantitative reverse transcriptase-polymerase chain reaction and Western blotting, respectively. Production of NO was determined as nitrite in culture supernatant. Activation and translocation of nuclear factor kappaB (NF-kappaB), levels of inhibitor of nuclear factor kappaB (IkappaB), and NF-kappaB DNA binding activity were determined by Western blotting and a highly sensitive and specific enzyme-linked immunosorbent assay. Activity of IkappaB kinase was determined using in vitro kinase assay. RESULTS: Human chondrocytes cotreated with EGCG produced significantly less NO compared with chondrocytes stimulated with IL-1beta alone (P < 0.005). The inhibition of NO production correlated with the suppression of induction and expression of NF-kappaB-dependent gene iNOS. EGCG inhibited the activation and translocation of NF-kappaB to the nucleus by suppressing the degradation of its inhibitory protein IkappaBalpha in the cytoplasm. CONCLUSION: Our results indicate that EGCG inhibits the IL-1beta-induced production of NO in human chondrocytes by interfering with the activation of NF-kappaB through a novel mechanism. Our data further suggest that EGCG may be a therapeutically effective inhibitor of IL-1beta-induced inflammatory effects that are dependent on NF-kappaB activation in human OA chondrocytes.

Antioxidants↗
PubMed2002

Hydrostatic pressure induces apoptosis in human chondrocytes from osteoarthritic cartilage through up-regulation of tumor necrosis factor-alpha, inducible nitric oxide synthase, p53, c-myc, and bax-alpha, and suppression of bcl-2.

Hydrostatic pressure (HP) is thought to increase within cartilage extracellular matrix as a consequence of fluid flow inhibition. The biosynthetic response of human articular chondrocytes to HP in vitro varies with the load magnitude, load frequency, as well as duration of loading. We found that continuous cyclic HP (5 MegaPascals (MPa) for 4 h; 1 Hz frequency) induced apoptosis in human chondrocytes derived from osteoarthritic cartilage in vitro as evidenced by reduced chondrocyte viability which was independent of initial cell densities ranging from 8.1 x 10(4) to 1.3 x 10(6) cells ml(-1). HP resulted in internucleosomal DNA fragmentation, activation of caspase-3, and cleavage of poly-ADP-ribose polymerase (PARP). At the molecular level, induction of apoptosis by HP was characterized by up-regulation of p53, c-myc, and bax-alpha after 4 h with concomitant down-regulation of bcl-2 after 2 h at 5 MPa as measured by RT-PCR. In contrast, beta-actin expression was unchanged. Real-time quantitative RT-PCR confirmed a HP-induced (5 MPa) 1.3-2.6 log-fold decrease in bcl-2 mRNA copy number after 2 and 4 h, respectively, and a significant increase (1.9-2.5 log-fold) in tumor necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS) mRNA copy number after 2 and 4 h, respectively. The up-regulation of p53 and c-myc, and the down-regulation of bcl-2 caused by HP were confirmed at the protein level by Western blotting. These results indicated that HP is a strong inducer of apoptosis in osteoarthritic human chondrocytes in vitro.

Apoptosis↗
PubMedDate not supplied

Clinical presentation of hypothyroidism: a case control analysis.

BACKGROUND: Hypothyroidism is a common endocrinological disorder. Its clinical presentation is variable but well established. However, clinical features vary significantly among different populations owing to their climate, education status and awareness about the disease. This study is designed to evaluate the difference in clinical presentation of our population from already available literature. METHODS: In this study we have compared the symptoms and signs of hypothyroid and euthyroid patients coming to a diagnostic centre (PINUM, Faisalabad) from January to July 1999. Of the 1594 patients coming to the centre, 394 were included in the study and were examined. After the laboratory investigations, 109 were identified as the cases of hypothyroidism, the rest were declared as euthyroid and selected as controls. We compared the 21 common signs and symptoms of hypothyroidism in our patients. RESULTS: Lethargy was the commonest symptom and facial oedema was the most prevalent sign in our population. Old age is reported to be a risk factor for hypothyroidism but in this study we could not find a rising trend with increasing age (odds ratio 1.15, p-value 0.71). We also compared the clinical presentation of our patients with the available literature. It was also proved that the signs elicited by the physicians were more reliable and specific for the identification of hypothyroidism. CONCLUSION: Thus, the presentation of hypothyroidism is non-specific and high degree of suspicion is required for its early diagnosis.

Adult↗