Alteration in cellular and biochemical markers of pulmonary toxicity in rat lung exposed to carpet dusts

Epidemiological studies of workers in weaving units in carpet industries have shown relationships between the airborne dust concentrations and pulmonary ill health. Therefore, to predict the health risk of carpet weavers, this preliminary experiment was conducted to evaluate the effect of carpet dust (knotted, tufted) on cellular and biochemical mediators considered as potential biological markers of lung injury. Lung cytoplasmic (lactate dehydrogenase, LDH), lysosomal (acid phosphatase, ACP), type II (alkaline phoshatase, ALP) and Clara-cell marker enzymes (gamma-glutamyl transferase, GGT) were monitored in rat cell-free lung lavage (BAL) during postexposure days 1, 4, 8, and 16. Furthermore, lung microsomal cytochrome P-450 (CYP450) and Clara-cell secretory protein (CC16) content in BAL was also evaluated. These pulmonary marker enzymes were significantly elevated during the postexposure period over the respective untreated control; however, tufted carpet dust shows more responses than knotted carpet dust. Lung CYP450 content was reduced significantly at early days; the pattern shows the reoccurrence of CYP450 content in the later stage of postexposure to carpet dust. Clara-cell secretory protein in BAL shows decline in the carpet-treated group; however, tufted carpet shows more decline than knotted carpet. Thus, reduction in CC16 level may have important implication in the development of chronic lung inflammation and diseases. Present investigation found that modulation of these cellular marker enzymes is clear evidence of pulmonary damage caused by exposure to carpet dust.     

Role of antimicrobials in third molar surgery: prospective, double blind,randomized, placebo-controlled clinical study

AIM: To test the efficacy of two dosing regimens of antimicrobial prophylaxis during the removal of impacted lower third molars. DESIGN: Double blind, prospective, placebo-controlled trial. SETTING: Teaching hospital, India. SUBJECTS: 151 patients aged 19-36 having impacted lower third molars removed. METHODS: Random allocation into three groups: placebo (n= 34), metronidazole 1g orally, 1 hour preoperatively (n= 44), or metronidazole 400mg orally eight hourly for 5 days postoperatively (n= 47). Patients were recalled on the sixth postoperative day for assessment of pain scores on the second and sixth days, swelling, differences in mouth opening between preoperative and the sixth postoperative day, and the state of the wound. RESULTS: There were no significant differences in the outcome between the three groups (P= 0.09). CONCLUSION: Antimicrobial prophylaxis does not seem to reduce morbidity after removal of lower third molars.     

Rapid diagnosis of Mycobacterium tuberculosis by multiplex polymerase chain reaction from clinical specimens

An essential element in the control of tuberculosis is the rapid, sensitive and specific identification of the causative agent. Until now, screening and diagnosis are largely based on clinical signs, radiological examination, tuberculin tests, sputum examination under the microscope, or culture for mycobacteria. Tuberculin tests lack specificity and only give an indication of previous exposure to mycobacteria. Direct microscopic examination of sputum is neither specific nor sensitive enough, and mycobacterial isolation is time-consuming. As an alternative to these classical methods, new nucleic acid-based technologies show promise as a more rapid, sensitive, and specific means of identification of mycobacteria. Two commercial standardized nucleic acid-based amplification techniques have been reported to yield reliable results within 5 to 7 hrs. Roche Amplicor MTB (Roche Diagnostic System, Somerville, N.J.) and Gen-Probe AMTB (Gen-Probe Inc., San Diego, Calif.). The amplified target is part of the 16S rRNA gene which is common to all the mycobacteria. An attempt has been made to describe the use of the target DNA, SenX3-RegX3, in a multiplex PCR to detect and differentiate M. tuberculosis from other mycobacteria directly from clinical specimens.     

What is health? Where GPs' and patients' worlds collide.

Qualitative studies have highlighted the complexity of patient models of health. The present quantitative study aimed to compare general practitioners' (GPs) and patients' models of health. A questionnaire consisting of 27 'markers of health' was completed by 472 patients (response rate 78.8%) and 64 GPs (response rate 71%). The results showed that GPs and patients were comparable in their ratings of those markers relating to arousal, such as sleep, sex drive and energy and infections, such as neck glands and having lots of colds. However, in the main GPs and patients were consistently different. In particular, the patients showed a higher rating for those markers relating to digestion (e.g. appetite, bloatedness), bodily fluids (e.g. the colour and smell of urine, regularity of bowels), the condition of the tongue, hair and complexion and for more traditional medical markers (e.g. heart beat, body weight). In contrast, GPs reported higher ratings for mood and emotions. To conclude, patients appeared to hold much more diverse models of health than GPs and reported greater endorsement for markers consistent with both a humoral and medical approach to health. These results suggest that GPs and patients do not have a shared understanding of health, which has implications for the effectiveness of primary care consultations.     

Antimyelin basic protein and antimyelin antibody-producing cells in multiple sclerosis.

The B-cell response to myelin and myelin basic protein was studied in patients with multiple sclerosis and in patients with acute aseptic meningoencephalitis by using a nitrocellulose immunospot assay. This method allows detection of single cells producing antibodies. Twenty-seven (79%) of 34 patients with multiple sclerosis had cells producing IgG antibodies against myelin, and 11 (57%) of 19 had cells producing IgG antibodies against myelin basic protein in cerebrospinal fluid (CSF), with mean values of 30 and 14 per 10(4) mononuclear cells, respectively. Total numbers of IgG-producing cells occurred at a mean number of 75 per 10(4) CSF cells. Cells producing antimyelin or anti-myelin basic protein antibodies of IgA or IgM isotypes were rarely found in CSF. Patients with acute aseptic meningoencephalitis less frequently showed CSF cells producing IgG antibodies against myelin and myelin basic protein. No cells producing antibodies against myelin or myelin basic protein were detected in peripheral blood of patients with multiple sclerosis or meningoencephalitis. Thus, a majority of patients with multiple sclerosis had CSF cells that produced IgG antibodies against myelin and myelin basic protein. These cells comprised a large proportion of the total IgG-producing cells. A pronounced B-cell response against autoantigens produced at the target for immune attack might be important in the pathogenesis of multiple sclerosis.     

Immunoglobulin producing cells in bone marrow and blood of patients with multiple sclerosis and controls.

Multiple sclerosis (MS) is characterised by intrathecal synthesis of IgG, less frequently of IgA and IgM. Local production of antibodies to myelin basic protein (MBP) and other myelin components has also been reported, and autoimmune pathogenesis has been postulated. Whether MS is accompanied by a systemic B cell response is less clear. To elucidate this question, we examined bone marrow and peripheral blood from patients with MS and controls for cells secreting IgG, IgA and IgM, as well as anti-MBP antibodies of these three isotypes. Patients with MS without any signs of concurrent infections had higher numbers of IgG + IgA + IgM secreting cells both in bone marrow and peripheral blood compared with healthy controls. The same abnormalities were observed in patients with other inflammatory neurological diseases (OIND). When analysing individual isotypes, patients with MS and OIND had higher numbers of IgA secreting cells both in bone marrow and blood compared with healthy controls. Only one of 13 MS patients examined had anti-MBP antibody secreting cells in bone marrow and blood. The systemic B cell response registered in MS is also present in other inflammatory neurological diseases and its specificity and possible role in the pathogenesis of MS remains unknown.     

Hypercalcaemia: a clue to Mycobacterium avium intracellulare infection in a patient with AIDS

Hypercalcaemia is uncommon in HIV-infected patients and should suggest a different priority for differential diagnosis than would be considered in other settings. Although hypercalcaemia has long been associated with granulomatous diseases including tuberculosis, it has only recently been recognised that patients with illness due to Mycobacterium avium intracellulare (MAI) may develop it. We report a patient with AIDS in whom unexplained hypercalcaemia was the harbinger of clinically significant MAI infection. Patients with AIDS who develop hypercalcaemia should be closely evaluated for underlying MAI infection.     

Antiviral treatment normalizes neurophysiological but not movement abnormalities in simian immunodeficiency virus-infected monkeys

Simian immunodeficiency virus (SIV) infection of rhesus monkeys provides an excellent model of the central nervous system (CNS) consequences of HIV infection. To discern the relationship between viral load and abnormalities induced in the CNS by the virus, we infected animals with SIV and later instituted antiviral treatment to lower peripheral viral load. Measurement of sensory-evoked potentials, assessing CNS neuronal circuitry, revealed delayed latencies after infection that could be reversed by lowering viral load. Cessation of treatment led to the reappearance of these abnormalities. In contrast, the decline in general motor activity induced by SIV infection was unaffected by antiviral treatment. An acute increase in the level of the chemokine monocyte chemoattractant protein-1 (MCP-1) was found in the cerebrospinal fluid (CSF) relative to plasma in the infected animals at the peak of acute viremia, likely contributing to an early influx of immune cells into the CNS. Examination of the brains of the infected animals after return of the electrophysiological abnormalities revealed diverse viral and inflammatory findings. Although some of the physiological abnormalities resulting from SIV infection can be at least temporarily reversed by lowering viral load, the viral-host interactions initiated by infection may result in long-lasting changes in CNS-mediated functions.