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Biomedical subjects

S Haque

Publications and source records attributed to S Haque.

At least 37 records · Page 2Linked to original sources
PubMed2000

Distribution of the interleukin-8 receptors, CXCR1 and CXCR2, in inflamed gut tissue.

There is increasing evidence to suggest that the potent neutrophil chemoattractant interleukin-8 (IL-8) has an important role in the pathogenesis of inflammatory bowel disease. IL-8 mediates its actions via two cell surface receptors, CXCR1 and CXCR2. This paper describes the distribution of these IL-8 receptors in the normal gastrointestinal tract and how this is modified in ulcerative colitis (UC). Paraffin-embedded colonic resection specimens were stained with monoclonal antibodies directed against CXCR1 and CXCR2 in ten cases of total UC, 16 cases of appendicitis, and 11 histologically normal sections. A semiquantitative scale of 0-4 was used to assess the proportion and intensity of positively stained cells within certain defined areas of tissue. A comparative assessment was made of the distribution of various cell populations. Dual immunostaining was used to confirm the phenotype of positively staining cells. In the histologically normal colon, the antibody against CXCR1 stained a subpopulation of macrophages deep to the epithelium and germinal centre lymphocytes. A similar pattern of staining was seen in acute appendicitis, with in addition some positively stained neutrophil polymorphs. In UC, there was up-regulation of CXCR1, with a striking increase in positively stained macrophages throughout the mucosa and of B and T lymphocytes outside the germinal centre areas. There was also intense up-regulation of CXCR1 expression by the luminal epithelium, reflected in the epithelial staining score (mean+/-SE=1.8+/-0.44 for UC cases, vs. 0.23+/-0.16 for controls and 0.25+/-0.14 for acute appendicitis). CXCR2 was only expressed on a small population of lamina propria mononuclear cells and crypt epithelial cells, with no significant differences observed between the groups. These results suggest that IL-8 may, through CXCR1, have a role beyond neutrophil recruitment in mediating the immune response in UC and that this is not merely a consequence of the acute inflammation seen in UC.

Acute Disease↗
PubMed1999

Immunization with heat-killed Toxoplasma gondii stimulates an early IFN-gamma response and induces protection against virulent murine malaria.

In this study, we describe protection of BALB/c mice by immunization with heat-killed T. gondii tachyzoites against infection with Plasmodium yoelii 17XL which causes cerebral malaria and death in mice by day 7-8 post infection. Immunization resulted significant reduction in parasitemia at the peak period of infection. Protection induced by heat-killed T. gondii was associated with marked increase in NK cell number and IFN-gamma mRNA expression early in the infection. The level of IFN-gamma or TNF-alpha was found to diminish in T. gondii-treated mice as the infection progressed to the late stage. This declined response of IFN-gamma or TNF-alpha was associated with marked increase in the expression of IL-10, a counterregulatory cytokine. Pretreatment of mice with live T. gondii induced poor level of protection as compared with that of heat-killed parasites. Mice that received P. yoelii infection alone, had an elevated IFN-gamma response in the late stage of infection. Development of cerebral malaria in untreated mice was accompanied by an augmented production of TNF-alpha and nitric oxide (NO), the proinflammatory mediators. These findings suggest that nonspecific immunization with T. gondii leads to restoration of an early IFN-gamma response in P. yoelii-infected mice and in the establishment of an immunoregulatory mechanism that effectively antagonizes the disease-promoting effects of proinflammatory cytokines in the late phase of infection.

Animals↗
PubMed1999

Protection against lethal toxoplasmosis in mice by an avirulent strain of Toxoplasma gondii: stimulation of IFN-gamma and TNF-alpha response.

In this study, we examined whether the PTN strain (isolated from an AIDS patient) of Toxoplasma gondii could induce cross-protection in mice against infection with a lethal dose of the PLK strain. Mice were first infected with tachyzoites (5 x 10(5)) of PTN and 5 days later challenged with PLK (1 x 10(5), LD(90)) parasites. None of these mice succumbed to infection until day 21 after infection, whereas 100% of the mice given the same dose of PLK infection alone died between 5 and 11 days after infection. The protection was accompanied by an increased expansion of NK cells and CD4 + T cells. This condition was associated by increased production of IFN-gamma and an augmented number of IFN-gamma-producing cells in the spleen. Further, PTN + PLK-infected mice showed higher production of TNF-alpha and nitrite compared to PLK-infected mice. Mice infected with the PTN strain had an enhanced capacity to activate the immune system early in infection since they produced higher levels of IFN-gamma, TNF-alpha, and NO than PLK-infected mice. Administration of anti-IFN-gamma mAb or anti-asialo GM1 antibody resulted in 100 and 20% mortality, respectively, in PTN-infected mice but no death in PTN + PLK-infected mice. Together, these results suggest that early production of IFN-gamma and NK-cell activity is important in protection against PTN infection, whereas in PTN + PLK infection components of adaptive immunity rapidly developed following elaboration of an effective early innate immune response.

Animals↗
PubMed1999

Cell cycle genes in chondrocyte proliferation and differentiation.

Coordinated proliferation and differentiation of growth plate chondrocytes controls longitudinal growth of endochondral bones. While many extracellular factors regulating these processes have been identified, much less is known about the intracellular mechanisms transducing and integrating these extracellular signals. Recent evidence suggests that cell cycle proteins play an important role in the coordination of chondrocyte proliferation and differentiation. Our current knowledge of the function and regulation of cell cycle proteins in endochondral ossification is summarized.

Animals↗
PubMed1999

Ondansetron versus placebo for the control of nausea and vomiting during Caesarean section under spinal anaesthesia.

This prospective, randomised, placebo-controlled, double-blind study was performed to evaluate the effects of ondansetron on nausea and vomiting during elective Caesarean section under spinal anaesthesia. Seventy-four full-term parturients were studied. After umbilical-cord clamping, ondansetron 4 mg or 0.9% saline was injected intravenously and the study period continued for 2 h. The severity of nausea was graded from 0 = none to 10 = maximum, while that of vomiting was graded from single = once per min to continuous = multiple per min. The incidence of vomiting was lower following ondansetron (36%) compared with the control group (58%, p < 0.028). Neither the severity of vomiting nor the incidence of nausea was influenced by ondansetron. However, for those who experienced nausea, ondansetron reduced its severity (p = 0.05). We conclude that the intra-operative administration of 4 mg ondansetron intravenously during Caesarean section under spinal anaesthesia significantly reduces the incidence of vomiting and the severity of nausea.

Adult↗
PubMed1999

Infection of mice by a Toxoplasma gondii isolate from an AIDS patient: virulence and activation of hosts' immune responses are independent of parasite genotype.

Virulence of a Toxoplasma gondii isolate from an AIDS patient (designated as PTN) was compared with that of PLK, a variant of P-strain. Virulence was assessed in term of host survival upon inoculation in different strains of mice. All C57BL/6 mice died of acute toxoplasmosis by 7-10 days following intraperitoneal infection with 1 x 105 tachyzoites of PTN and 40% of BALB/c died on day 23 of infection, whereas 100% CBA/J infected with the same dose of PTN survived, as did outbred Swiss Webster mice. All C57BL/6, BALB/c, CBA/J, or Swiss Webster died of acute toxoplasmosis by 3-9 days postinfection upon inoculation with same dose of tachyzoites of the PLK strain. Further studies in CBA/J mice demonstrated that mice infected with PTN elicited a significantly higher lymphoproliferative response to crosslinked anti-CD3 mAb or Con A than PLK infected mice, and augmented production of TNFalpha, lower levels of nitrite and a higher number of NK cells. Genetical analysis indicated that both PLK and PTN strains of T. gondii are from type ll. Interestingly, being of the same genotype, the later showed less virulence upon inoculation in mice and had greater capacity to activate host immune system than the PLK strain.

AIDS-Related Opportunistic Infections↗
PubMed1999

Nutritional rickets without vitamin D deficiency in Bangladesh.

To understand nutritional rickets in Bangladesh better, 14 rachitic and 13 'unaffected' children were evaluated. Seventy per cent of children with active rickets had no evidence of either vitamin D deficiency or familial rickets. Rickets in Bangladesh is probably related to calcium deficiency. Abnormalities in 'unaffected' children suggest that subclinical calcium insufficiency is common.

Bangladesh↗
PubMed1999

Strongyloidiasis colitis: a case report and review of the literature.

A case is described of a nonimmunocompromised man who presented with diarrhea, weight loss, and microcytic anemia. Colonoscopy revealed a pancolitis characterized by aphthoid ulceration on endoscopy and intense tissue eosinophilic infiltrates on biopsy. Both colonic biopsies and stool aspirates revealed the larvae of Strongyloides stercoralis, thus confirming this parasite as the causative agent for the colitis.

Aged↗
PubMed1999

Does acid suppression by antacids and H2 receptor antagonists increase the incidence of atrophic gastritis in patients with or without H. pylori gastritis?

Currently there is controversial evidence that suggests that the accepted incidence of atrophic gastritis of 1.2 to 3.3% in patients with Helicobacter pylori gastritis may be increased by the long-term suppression of acid by a proton pump inhibitor (omeprazole). The purpose of this study is to show whether lesser forms of acid suppression by antacids or H2 receptor antagonists may have an influence on the development of atrophic gastritis. The authors recently reported a study in which a cohort of 36 patients with symptoms of dyspepsia were followed clinically for a period of 7 to 19 years. In that report all subjects underwent upper endoscopy with two biopsy specimens each from the antrum and fundus, on at least two occasions, 7 to 19 years apart. A diagnosis of atrophic gastritis was based on the interpretation of these biopsies by two gastrointestinal pathologists. The presence of H. pylori colonization was determined by tissue sampling and by a campylobacter-like organisms test of the antrum. Of the 36 patients in the authors' previous report, 33 had adequate baseline and follow-up data on medications consumed throughout the period of the study. In their current report they now present the findings of a retrospective review in which they correlate the presence of atrophic gastritis with the sole use of antacids and H2 receptor antagonists throughout the period of the study. In the cohort of 33 patients evaluated from the previous report, the authors found that atrophic gastritis had developed in all 28 patients positive for H. pylori, and in none of the 5 patients negative for H. pylori (p < 0.0001). A retrospective analysis of this previously studied cohort of 33 patients revealed that the use of antacids and H2 receptor antagonists did not predict the development of atrophic gastritis in either H. pylori-negative or -positive subjects. In a retrospective analysis of a cohort of 33 patients followed for an average of 11.7 years, atrophic gastritis developed in H. pylori-positive but not in H. pylori-negative subjects, irrespective of the use and duration of antacids or H2 receptor antagonists.

Aged↗
PubMed1998

Alteration of intracellular calcium flux and impairment of nuclear factor-AT translocation in T cells during acute Toxoplasma gondii infection in mice.

Down-regulation of host immune response to Toxoplasma gondii is associated with the expression of specific cytokines, in particular IL-10, and the induction of CD4+ T cell anergy. In the present study we report that the expression of both CD4 and CD2 antigen is down-regulated during the acute phase of infection. A decrease in the expression of CD2 was apparent during the acute phase of T. gondii infection in three genetically distinct strains of mice, CBA/J, C57BL/6, and BALB/c. The lymphoproliferative response induced by cross-linked anti-CD3 mAb or by Con A was markedly depressed. This suppressed response was associated with a reduction in the influx of Ca2+. We have examined whether lymphocytes from T. gondii mice maintain NF-AT transcription factors in the nucleus where they participate in the Ca2+-dependent induction of genes required for lymphocyte activation and proliferation. Immunofluorescence with confocal microscopy using an Ab to NF-ATc demonstrates a decrease in translocation of NF-ATc in T lymphocytes from acutely infected mice. Together, these results suggest that the defect in T cell expansion that occurs during acute murine toxoplasmosis is related to reduced activity of NF-AT, a calcium-dependent transcription factor required for T cell proliferation.

Acute Disease↗
PubMed1998

Does rheumatic fever occur usually between the ages of 5 and 15 years?

It has long been considered that rheumatic fever usually occurs in children between the ages of 5 and 15 years. However, supporting data from the developing countries are insufficient. It is important to know the age of occurrence of rheumatic fever for clinical and public health purposes. To describe the age distribution of Bangladeshi subjects, we have reviewed the records of all patients who attended with acute rheumatic fever in the outpatient department of the National Center for Control of Rheumatic Fever and Heart Diseases, Dhaka, during June 1990 through November 1995. During this period 630 subjects were diagnosed to have acute rheumatic fever defined by the revised Jones criteria. Of them, 535 (84.9%) presented with first attack. Their age ranged from 3 to 30 years, and a skewness to the right of the age distribution was observed. Thus, we used percentile distribution to determine reference range of age. The 2.5 and 97.5 percentiles were 5 and 22 years, respectively. Their mean (standard deviation) and median age were 12.7 (4.4) and 12 years, respectively. Slightly more than 22% of subjects were older than 15 while less than 1% were younger than 5 years. This finding was supported by multiethnic data from other developing countries. The current analysis warrants reevaluation of the prevailing conviction for age of occurrence of rheumatic fever. In conclusion, the age reference range for occurrence of rheumatic fever in Bangladesh should be considered to be 5 to 22 years but not 5 to 15 years.

Adolescent↗
PubMed1998

Distinct, autosomal recessive form of spondyloepimetaphyseal dysplasia segregating in an inbred Pakistani kindred.

We describe a large inbred kindred from a remote area of Pakistan, comprising eight generations, with a distinct form of spondyloepimetaphyseal dysplasia (SEMD). We evaluated 16 affected individuals: 11 males and 5 females. Analysis of the pedigree strongly suggests autosomal recessive inheritance, and consanguineous loops could account for all the affected individuals being homozygous for the abnormal allele. The clinical findings included short stature evident at birth, short bowed lower limbs, mild brachydactyly, kyphoscoliosis, an abnormal gait, enlarged knee joints, precocious osteoarthropathy, and normal intelligence. Radiographs demonstrated delayed epiphyseal ossification at the hips and knees, platyspondyly with irregular end plates and narrowed joint spaces, diffuse, early osteoarthritic changes, primarily in the spine and hands, and mild brachydactyly. Mild metaphyseal abnormalities were seen predominantly at hips and knees. This distinctive phenotype is distinct from other autosomal recessive forms of SEMD because of the mild degree of metaphyseal involvement, the type of brachydactyly, and the absence of loose joints or other clinical findings.

Abnormalities, Multiple↗
PubMed1998

Mutations in orthologous genes in human spondyloepimetaphyseal dysplasia and the brachymorphic mouse.

The osteochondrodysplasias are a genetically heterogeneous group of disorders affecting skeletal development, linear growth and the maintenance of cartilage and bone. We have studied a large inbred Pakistani family with a distinct form of recessively inherited spondyloepimetaphyseal dysplasia (SEMD) and mapped a gene associated with this dwarfing condition to chromosome 10q23-24, a region syntenic with the locus for the brachymorphic mutation on mouse chromosome 19. We identified two orthologous genes, ATPSK2 and Atpsk2, encoding novel ATP sulfurylase/APS kinase orthologues in the respective regions of the human and mouse genomes. We characterized a nonsense mutation in ATPSK2 in the SEMD family and a missense mutation in the region of Atpsk2 encoding the APS kinase activity in the brachymorphic mouse. ATP sulfurylase/APS kinase catalyses the metabolic activation of inorganic sulfate to PAPS, the universal donor for post-translational protein sulfation in all cell types. The cartilage-specificity of the human and mouse phenotypes provides further evidence of the critical role of sulfate activation in the maturation of cartilage extracellular matrix molecules and the effect of defects in this process on the architecture of cartilage and skeletogenesis.

Amino Acid Sequence↗
PubMed1998

A gene for universal congenital alopecia maps to chromosome 8p21-22.

Complete or partial congenital absence of hair (congenital alopecia) may occur either in isolation or with associated defects. The majority of families with isolated congenital alopecia has been reported to follow an autosomal-recessive mode of inheritance (MIM 203655). As yet, no gene has been linked to isolated congenital alopecia, nor has linkage been established to a specific region of the genome. In an attempt to map the gene for the autosomal recessive form of the disorder, we have performed genetic linkage analysis on a large inbred Pakistani family in which affected persons show complete absence of hair development (universal congenital alopecia). We have analyzed individuals of this family, using >175 microsatellite polymorphic markers of the human genome. A maximum LOD score of 7.90 at a recombination fraction of 0 has been obtained with locus D8S258. Haplotype analysis of recombination events localized the disease to a 15-cM region between marker loci D8S261 and D8S1771. We have thus mapped the gene for this hereditary form of isolated congenital alopecia to a locus on chromosome 8p21-22 (ALUNC [alopecia universalis congenitalis]). This will aid future identification of the responsible gene, which will be extremely useful for the understanding of the biochemistry of hair development.

Alopecia↗
PubMed1998

Cloning, genomic organization, alternative transcripts and mutational analysis of the gene responsible for autosomal recessive universal congenital alopecia.

Complete or partial congenital absence of hair (congenital alopecia) may occur isolated or with associated defects. The majority of families with isolated congenital alopecia has been reported to follow an autosomal recessive mode of inheritance (MIM 203655). We have previously mapped the gene for autosomal recessive congenital alopecia in a large inbred Pakistani family in which affected persons show complete absence of hair development (universal congenital alopecia) to a 15 cM region on chromosome 8p21-22. Here we report the cloning and characterization of the human homologue of the mouse hairless gene and show that it is located in the critical region on chromosome 8p21-22. Determining the exon-intron structure allowed detailed mutational analysis of DNA samples of patients with universal congenital alopecia. We detected a homozygous missense mutation in the Pakistani family and a homozygous splice donor mutation in a family from Oman. In addition, we show that the human hairless gene undergoes alternative splicing and that at least two isoforms generated by alternative usage of exon 17 are found in human tissues. Interestingly, the isoform containing exon 17 is the predominantly expressed isoform in all tissues but skin, where exclusive expression of the shorter isoform was observed. We speculate that this tissue-specific difference in the proportion of hairless transcripts lacking exon 17 sequences could contribute to the tissue-specific disease phenotype observed in individuals with isolated congenital alopecia.

Adult↗
PubMed1998

Nutritional factors associated with rheumatic fever.

The determinants for a child with group A beta-haemolytic streptococcal throat infection (BHS infection) to develop rheumatic fever (RF) remain unclear. In this case-control study, we deal with BHS infected children to examine whether nutritional factors are related to RF. In a RF hospital in Dhaka (Bangladesh) we examined 218 consecutive out-patients who had antecedent BHS infection. Sixty of them met the updated Jones criteria for RF (cases) while 104 did not (controls). Fifty-four possible RF patients were excluded. We used anthropometric measurements and a food frequency questionnaire to assess nutritional factors. Higher risk of RF was observed for low height for age (odds ratio 3.82, 95% confidence interval 1.73-8.42); low weight for age (2.41, 1.12-5.57); low upper arm circumference for age (3.76, 1.87-7.89); and low consumption of eggs (3.81, 1.95-7.63), milk (2.60, 1.36-5.08), chicken (2.62, 1.35-5.21), pulses (1.98, 1.03-3.84), fruits 2.29, 1.20-4.45), and ruti (home-made bread) (3.15, 1.61-6.34). Reduced risk was observed for soybean oil consumption (0.28, 0.12-0.62). The significant association of upper arm circumference and eggs persisted after adjustment for multiple sociodemographic confounders. The association of ruti and soybean oil appeared to be suggestive (0.05 < p < 0.1). Protein-energy malnutrition is likely to be associated with RF. The protective effect of moderate consumption of eggs and soybean oil may support other published work which suggests that the anti-inflammatory substance present in these food items may prevent maturation of the rheumatic process.

Acute Disease↗
PubMed1998

Loss of resistance to a highly immunogenic tumor with age corresponds to the decline of CD8 T cell activity.

A number of ultraviolet light-induced tumors that do not grow progressively in 3- or 9-month-old animals grow progressively in animals starting at approximately 15 months of age. We investigated the immune response to one such tumor, 6130, in young and old mice to determine in nature of this breakdown in immune protection with age. The 6130 tumor cells that grow progressively in 22-month-old animals still retain sensitivity of cytotoxic T lymphocytes (CTLs) generated against the highly immunogenic "6130-A" antigen and consequently are still immunologically rejected when transplanted into 3- and 9-month-old animals, but not in mice older than 15 months. Investigation of the CD8+ CTL response found that in animals 3-12 months old, primary and secondary tumor-specific CTL responses to 6130 can be generated in vivo and in vitro. On the other hand, the CD8+ CTL responses to 6130 seen in animals 15 months of age or older were significantly depressed or absent. These results indicate that a decline in antigen-specific CD8+ CTL is the major cause of increased susceptibility to 6130 tumor growth in older animals.

Aging↗