Frequency of hearing loss among textile industry workers of weaving unit in Karachi, Pakistan.

OBJECTIVE: To determine the frequency of hearing loss among textile industry workers of weaving department. To record the noise level in the weaving sections and to compare it with the international standards. To determine the awareness about the effects of noise on hearing amongst the workers and the protective measures adopted by them. METHODS: A cross-sectional study was carried out at weaving department of five renowned textile industries of Karachi. The study included 248 workers exposed to noise, through non-probability convenient sampling technique. Equivalent sound pressure level Leq was measured with the help of a Class-1 type digital sound level meter. Hearing status of the workers was assessed through questionnaire and clinical tests (WHISPER, RINNE'S and WEBER). RESULT: Results showed that noise level was in range of 88.4-104 dB(A). The questionnaire results showed that: (i) 92.7% of the workers were aware that high noise level cause speech interference. (ii) 57.2% were unaware about the effect of noise on health. (iii) 54.8% used ear protection devices. (iv) 22.5% did not respond well to whisper test while 16.9% were found to have defective hearing on the basis of Rinne's test and 17.4% through Weber's test. It was observed that hearing loss was significantly associated with working experience of more than 10 years (25%) and overtime (28.8%). CONCLUSION: The results of study establish the fact that noise level is more than acceptable limit of 85 dB(A) for 8 hours exposure stipulated by OSHA.There is an immediate need to develop and implement noise regulations in Pakistan.

Role of acellular collagen matrix surgisis in the endoscopic management of ureteropelvic junction obstruction.

PURPOSE: To investigate the role of acellular collagen matrix (Surgisis during endopyelotomy. MATERIALS AND METHODS: Nine female pigs (25-35 kg) were enrolled in our protocol. The pigs were categorized as follows. Group I (N = 3) had endopyelotomy + insertion of SIS, Group II (N = 3) creation of UPJ stricture + endopyelotomy + insertion of SIS, and Group III (N = 3) Davis intubated ureterotomy using SIS. The contralateral side served as a control for each group (one pig in each group). In three pigs (two in Group III and one in Group II), Surgisis was treated with India ink prior to insertion at the endopyelotomy site. An endopyelotomy stent (14/8 F x 24 cm) was used to stent the ureteropelvic junction (UPJ) for 4 weeks. Four weeks after the stent was removed, laparoscopic nephroureterectomy was performed, and the animals were euthanized. Histopathologic analysis of the Surgisis-regenerated segment of the UPJ was performed using hematoxylin and eosin, reticular (collagen), smooth muscle actin, and S-100 (nerve) stains. RESULTS: All animals tolerated the procedure. The mean operative time was 162 minutes. One pig (Group II) developed pyonephrosis; one pig (Group III) developed significant ascites and was sacrificed 2 week before the end of the experiment. Histopathologic analysis showed complete epithelializaton at 8 weeks. Reticular stain demonstrated abundant collagen matrix in the submucosa. Smooth muscle staining revealed myofibroblastic proliferation within the SIS-regenerated tissue adjacent to disorganized smooth muscle cells. India ink-stained SIS-regenerated tissue did not show smooth muscle cells. The S-100 stain did not demonstrate neurons at 8 weeks; however, in three pigs, peristaltic activity was noted across the UPJ. CONCLUSION: The use of acellular collagen matrix in the endoscopic management of UPJ obstruction is a promising technique. The abundance of myofibroblasts and absence of abundant smooth muscle regeneration indicates a need to investigate the role of growth factors in SIS regeneration of host tissue.

Tubular cell-Escherichia coli interaction products modulate migration of monocytes through generation of transforming growth factor-beta and macrophage-monocyte chemoattractant protein-1.

BACKGROUND: Urinary tract infection is a common occurrence often associated with renal interstitial inflammation in the form of accumulation of mononuclear cells. We hypothesized that bacteria activate tubular cells to secrete cytokines, which may promote migration of mononuclear cells at the site of interaction. MATERIALS AND METHODS: We evaluated the migration of monocytes in response to tubular cell products (TC-S) and interaction products of E. coli with proximal tubular cells (TC-EC-S; concentrations of 5%, 10%, and 25%) using a modified Boyden chamber. To determine the molecular mechanism, we evaluated the effect of antibodies against macrophage-monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor-beta (TGF-beta) on E. coli-tubular cell interaction product-induced migration of monocytes. In addition, we studied the effect of free-radical scavengers on activation of tubular cells. RESULTS: The TC-EC-S enhanced (p < 0.0001) migration of monocytes compared with TC-S. Both anti-TGF-beta and anti-MCP-1 antibodies partly inhibited (p < 0.0001) TC-EC-S-induced monocyte migration. The modified TC-EC-S (produced in the presence of superoxide dismutase [SOD], dimethyl thiourea [DMTU], or catalase, all scavengers of free radicals) induced lesser monocyte migration than did TC-EC-S alone. CONCLUSIONS: These results suggest that E. coli activates tubular cells to generate cytokines such as MCP-1 and TGF-beta that promote migration of monocytes. Free radicals such as superoxide and hydrogen peroxide may be acting as second messengers in E. coli-induced tubular cell activation.

Morphine-induced macrophage apoptosis modulates migration of macrophages: use of in vitro model of urinary tract infection.

BACKGROUND: Morphine has been reported to alter immune function. Morphine-induced macrophage apoptosis has been shown to contribute to altered immune status in an opiate milieu. We studied the effect of morphine-induced macrophage apoptosis on the migration of macrophages. Because urinary tract infection (UTI) is one of the commonest infections to evoke an inflammatory response; i.e., migration of neutrophils and monocytes to the site of infection, we used an in vitro model of UTI to test our hypothesis. MATERIALS AND METHODS: We carried out both in vivo and in vitro studies. Mice of the FVB/N strain were treated with morphine for short (three doses, 24 hours) and long (11 doses, 96 hours) durations, and their bone marrow cells were isolated. In addition, apoptotic macrophages were prepared by heat treatment. To simulate the in vitro model of UTI, E. coli-activated tubular cell (TC)-conditioned medium containing transforming growth factor-beta (TGF-beta) and macrophage-monocyte chemoattractant protein-1 (MCP-1) was used to test migration of macrophages across a filter in a modified Boyden chamber. In addition, migration of macrophages into the peritoneal cavity was evaluated in both control and morphine-treated states. The effect of morphine on apoptosis as well as migration was studied in murine macrophages and bone marrow cells. RESULTS: Morphine not only promoted apoptosis of bone marrow cells (20% apoptotic cells) but also inhibited their migration across the filter. Control cells showed minimal apoptosis but displayed greater migration. Similarly, heat-treated (apoptotic) cells showed minimal migration. In peritoneal macrophage studies, morphine treatment retarded migration. CONCLUSION: Morphine inhibits macrophage migration both in vivo and in vitro. This attenuated transmigration of macrophages seems to be secondary to the apoptotic effect of morphine.