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M Chatterjee

Publications and source records attributed to M Chatterjee.

At least 19 recordsLinked to original sources

Distribution and possible source of trace elements in the sediment cores of a tropical macrotidal estuary and their ecotoxicological significance.

The paper presents the first document regarding concentration, distribution and possible sources of selected trace elements (Cu, Fe, Mn, Zn, Cr, Co, Ni, Pb, Al, B and Ba) in core sediments (<63 micro particle size) from the lower stretch of Hugli (Ganges) estuary, northeast coast of Bay of Bengal by ICP-AES and EDXRF to evaluate geochemical processes influencing their distribution and possible environmental consequences. The levels of elements showed a wide range of variations in different core depths, in upper and lower intertidal zones as well as among three sampling stations. The most interesting feature of the study is the downward increase of concentrations of majority of the elements reaching overall maximum values at a depth of 20-28 cm in upper littoral zone of the site located in the extreme downstream stretch of the estuary. Values of organic carbon showed very strong positive correlations with most of the elements as revealed by correlation matrix (r) values. The interelemental relationship revealed the identical behavior of element during its transport in the estuarine environment. The overall variation in concentration can be attributed to differential discharge of untreated effluents originating from industrial, agricultural, and aquacultural sources as well as from domestic sewage along with the fishing and boating activities. The resulting compositional dataset was tested by principal component analyses and cluster analyses. Pollution load index (PLI) and index of Geoaccumulation (Igeo) revealed overall low values but the enrichment factors (EFs) for Pb were typically high for all the stations. The mean concentrations of Zn and to some extent Cu exceeded the Effects Range-Low (ER-L) values in the majority of the cases indicating that there may be some ecotoxicological risk to organisms living in sediments. The concentration of the trace elements reported in this work is useful as baselines for comparison in future sediment quality studies.

Carbon↗

Metastatic breast carcinoma discovered in a dentigerous cyst - a case report.

This paper reports a patient with a history of breast cancer, who presented with altered sensation to the right lower lip and chin. An orthopantomogram showed a probable dentigerous cyst associated with an unerupted lower wisdom tooth, which was closely related to the inferior dental canal. The tooth and cyst were enucleated under general anaesthesia. The subsequent histopathology report concluded that the cyst contained metastatic adenocarcinoma from a primary breast tumour.

Adenocarcinoma↗

Vanadium inhibits DNA-protein cross-links and ameliorates surface level changes of aberrant crypt foci during 1,2-dimethylhydrazine induced rat colon carcinogenesis.

The trace mineral vanadium inhibits cancer development in a variety of experimental animal models. The present study was to gain insight into a putative anticancer effect of vanadium in a rat model of colon carcinogenesis. The in vivo study was intended to clarify the effect of vanadium on DNA-protein cross-links (DPC), surface level changes of aberrant crypt foci (ACF) and biotransformation status during 1,2-dimethylhydrazine (1,2-DMH) induced preneoplastic rat colon carcinogenesis. The comet assay showed statistically higher mean base values of DNA-protein mass (p<0.01) and mean frequencies of tailed cells (p<0.001) in the carcinogen-induced group after treatment with proteinase K. Treatment with vanadium in the form of ammonium monovanadate supplemented ad libitum in drinking water for the entire experimental period caused a significant (p<0.02) reduction (40%) in DNA-protein cross-links in colon cells. Further, the biotransformation status of vanadium was ascertained measuring the drug metabolising enzymes, glutathione S-transferase (GST) and cytochrome P-450 (Cyt P-450). Significantly, there was an increase in glutathione S-transferase and cytochrome P-450 levels (p<0.01 and p<0.02, respectively) in rats supplemented with vanadium as compared to their carcinogen controls. As an endpoint marker, we also evaluated the effect of vanadium on surface level changes of aberrant crypt foci induced by 1,2-DMH by scanning electron microscopy. Animals induced with 1,2-DMH and supplemented with vanadium showed a marked improvement in colonic architecture with less number of aberrant crypt foci in contrast to the animals induced with 1,2-DMH alone, thereby exhibiting its anti-carcinogenicity by modulating the markers studied herein.

1,2-Dimethylhydrazine↗

A novel recombinant bispecific single-chain antibody, bscWue-1 x CD3, induces T-cell-mediated cytotoxicity towards human multiple myeloma cells.

The development of antibody-based strategies for the treatment of multiple myeloma (MM) has been hampered so far by the fact that suitable plasma cell-specific surface antigens have been missing. However, recently a novel monoclonal antibody, designated Wue-1, has been generated that specifically recognizes normal and malignant human plasma cells. Therefore, Wue-1 is an interesting and promising candidate to develop novel immunotherapeutic strategies for the treatment of MM. One variant for an antibody-based strategy is the bispecific antibody approach. Recombinant bispecific single-chain (bsc) antibodies are especially interesting candidates because they show exceptional biological properties. We have generated a novel MM-directed recombinant bsc antibody, bscWue-1 x CD3, and analyzed the biological properties of this antibody using the MM cell line NCI-H929 and primary cells from the bone marrow of patients with MM. We were able to show that bscWue-1 x CD3 induces efficient and selective T-cell-mediated cell death of NCI-H929 cells and primary myeloma cells in nine out of 11 cases. The bscWue-1 x CD3 Ab is efficacious even at low E:T ratios, and with or without additional T-cell pre- or costimulation. Target cell lyses were specific for Wue-1 antigen-positive cells and could be blocked by the Wue-1 monoclonal antibody.

Antibodies, Bispecific↗

PI3-K/AKT/FKHR and MAPK signaling cascades are redundantly stimulated by a variety of cytokines and contribute independently to proliferation and survival of multiple myeloma cells.

IL-6 has been reported to play a central role in growth and survival of multiple myeloma (MM) cells. However, recently we have demonstrated that in the presence of bone marrow stromal cells, survival of MM cells becomes independent of the IL-6/gp130/STAT3 pathway questioning the singular role of IL-6 in MM. Therefore, it was the aim of this study to identify additional factors and signaling pathways that might contribute to the growth and survival of MM cells. We found that in addition to IL-6 a number of bone marrow derived cytokines such as LIF, VEGF, bFGF, MIP-1alpha, SDF-1alpha, IL-1beta, SCF and IL-3 activate the MAPK pathway and induce proliferation of MM.1S and RPMI-8226 MM cells. In addition, these cytokines independently phosphorylate the forkhead family member FKHR via PI3-K/AKT and support survival of primary human MM cells. Inhibition of these pathways induces apoptosis in MM cell lines and primary MM cells. Thus, we provide evidence that in addition to IL-6 a number of different factors trigger important growth-promoting pathways to support the proliferation and survival of MM cells. Therefore, blocking such pathways, rather than blocking a single factor, might be a promising approach for the development of novel treatment strategies in MM.

Aged↗

Reversal of cadmium induced oxidative stress by chelating agent, antioxidant or their combination in rat.

The influence of an antioxidant agent such as N-acetyl cysteine (NAC) or mannitol on the cadmium chelating ability of monoisoamyl 2,3-dimercaptosuccinate (MiADMS) was investigated in cadmium pre-exposed rats. This ester of 2,3-dimercaptosuccinic acid (DMSA), an accepted drug for lead poisoning, being lipophilic in nature was expected to be an efficient cadmium chelator. The treatment of cadmium intoxicated animals with MiADMS reversed cadmium induced increase in blood catalase, superoxide dismutase (SOD) and malondialdehyde (MDA), liver MDA and brain SOD and MDA levels but not the decrease in blood, liver brain reduced glutathione (GSH) and increase in oxidized glutathione (GSSG) levels, consistent with the lowering of tissue cadmium burden. The administration of NAC or mannitol reversed the cadmium induced alterations in blood and liver GSH, GSSG, blood catalase, SOD, MDA, liver SOD, MDA and brain MDA levels without lowering blood and tissue cadmium contents. However, treatments with the combination of MiADMS and NAC or MiADMS and mannitol reversed these alterations as well as reduced blood and tissue cadmium concentrations. The combined treatment with MiADMS and mannitol was better than that with MiADMS and NAC, and was significantly more effective in normalizing blood, liver GSH, GSSG, brain GSSG, and their GSH/GSSG ratios than that by either of them alone. The combined treatments also improved liver and brain endogenous zinc levels, which were decreased due to cadmium toxicity. The results suggest that the administration of an antioxidant during chelation of cadmium may provide beneficial effects by reducing oxidative stress without its cadmium removing ability.

Acetylcysteine↗

Vanadium inhibits placental glutathione S-transferase (GST-P) positive foci in 1,2-dimethyl hydrazine induced rat colon carcinogenesis.

Vanadium (V) has recently been found to possess potent anti-neoplastic activity in rat colon carcinogenesis. In the present study attempts have been made to investigate the expression of the number and area of aberrant crypt foci positive for placental glutathione S-transferase (GST-P) during 1,2-dimethyl hydrazine (DMH)-induced rat colon carcinogenesis. Male Sprague Dawley rats were randomly divided into four groups. Rats in group A were designed as normal controls. Group B animals received DMH once a week (20 mg/kg body wt.) intraperitoneally for 16 weeks. Group C rats received the same treatment of DMH as in group B, along with 0.5-ppm vanadium as ammonium monovanadate ad libitum in drinking water throughout the experiment. Vanadium alone was given to Group D rats without any DMH injection. The expression of the number and the area of aberrant crypt foci (ACF) positive for GST-P was maximum in DMH-treated group. Vanadium-treated rats significantly reduced (P < 0.001) the expression of GST-P positive ACF cells (by 71.13%) for the entire period of the study. Moreover the histopathological examination also showed that vanadium action could minimize the aberrant crypt foci (P < 0.001). Furthermore, vanadium supplementation also elevated SOD activities in both liver and colon (P < 0.01, P < 0.02 and P < 0.01, P < 0.02 respectively) when compared to their carcinogen counterparts. Our results confirm that vanadium is particularly effective in limiting the action of the carcinogen, thereby establishing its anticarcinogenicity in chemically induced rat colon carcinogenesis.

1,2-Dimethylhydrazine↗

Effect of vanadium on colonic aberrant crypt foci induced in rats by 1,2 dimethyl hydrazine.

AIM: To investigate the chemo preventive effects of vanadium on rat colorectal carcinogenesis induced by 1,2-dimethylhydrazine (DMH). METHODS: Male Sprague-Dawley Rats were randomly divided into four groups. Rats in Group A received saline vehicle alone for 16 weeks. Rats in Group B were given DMH injection once a week intraperitoneally for 16 weeks; rats in Group C, with the same DMH treatment as in the Group B, but received 0.5-ppm vanadium in the form ammonium monovanadate ad libitum in drinking water. Rats in the Group D received vanadium alone as in the Group C without DMH injection. RESULTS: Aberrant crypt foci (ACF) were formed in animals in DMH-treated groups at the end of week 16. Compared to DMH group, vanadium treated group had less ACF (P<0.001). At the end of week 32, all rats in DMH group developed large intestinal tumors. Rats treated with vanadium contained significantly few colonic adenomas and carcinomas (P<0.05) compared to rats administered DMH only. In addition, a significant reduction (P<0.05) in colon tumor burden (sum of tumor sizes per animal) was also evident in animals of Group C when compared to those in rats of carcinogen control Group B. The results also showed that vanadium significantly lowered PCNA index in ACF (P<0.005). Furthermore, vanadium supplementation also elevated liver GST and Cyt P-450 activities (P<0.001 and P<0.02, respectively). CONCLUSION: Vanadium in the form of ammonium monovanadate supplemented in drinking water ad libitum has been found to be highly effective in reducing tumor incidence and preneoplastic foci on DMH-induced colorectal carcinogenesis. These findings suggest that vanadium administration can suppress colon carcinogenesis in rats.

1,2-Dimethylhydrazine↗

Diagnostic evaluation of extrapulmonary tuberculosis by fine needle aspiraton (FNA) supplemented with AFB smear and culture.

One hundred forty-three patients, 72 males and 71 females, with extrapulmonary tuberculosis were aspirated and subjected to cytological (Ziehl-Neelsen stain) examination and culture in Lowenstein-Jensen media. Routine haematological examination and Mantoux test were done in all the cases, x-ray chest in 112, skeletal x-ray in 3 relevant cases and sputum was examined for AFB in 16 cases where pulmonary tuberculosis was associated/suspected with extrapulmonary tuberculosis. HIV status was evaluated in 51 cases and 9 (7.64%) were seropositive. FNA cytology in 102 cases (71.3%) had caseating epithelioid granulomas while smear for AFB was positive in 57 cases (39.8%). Both culture and smear were positive in 29 (20.2%) cases. Combining both smear and culture yielded positive results in 47.5% cases. It was observed that AFB positivity was higher in untreated patients and with HIV positive cases. Further more, the triad of FNAC, AFB smear and culture were cheaper, foolproof and confirmatory than costlier tests like TB IgG, IgM, RTPCR and BACTEC.

Adolescent↗

Lead poisoning in Indian silver refiners.

The refining of silver from old silver ornaments, articles and jeweller's waste by smelting these with lead scraps for the fabrication of new jewellery is an important small scale industry in India. The present survey and clinical investigations have shown that 31 out of 50 silver refiners with a mean blood lead level of 32.84+/-1.78 microg/dl (range 20.3-64.9), decrease in blood delta-aminolevulinic acid dehydratase (ALAD) activity and thiamine (as pyruvate) level and an enhanced urinary excretion of ALA as compared to control, were suffering from lead poisoning. Most of these workers have shown anaemia, abdominal colic, blue lining of gum and muscular wasting indicative of lead toxicity. Twenty-four workers with relatively high blood lead levels were equally divided into two groups and given either vitamin B1 (75 mg, once a day) or vitamin C (250 mg. twice a day) for 1 month. The treatment with both the vitamins significantly lowered the blood lead levels and reduced blood thiamine and copper deficiency. In addition, vitamin C was also effective in reversing the inhibition of blood ALAD activity while the effect of vitamin B1 on its activity was marginal. The daily intake of vitamin B1 and vitamin C may prevent the accumulation of lead and reduce its toxic effects particularly in those regularly exposed to lead.

Adolescent↗

The IL-6 receptor antagonist SANT-7 overcomes bone marrow stromal cell-mediated drug resistance of multiple myeloma cells.

The bone marrow micro-environment produces a number of different survival factors that are important for the malignant growth and drug resistance of multiple myeloma (MM) cells. One of the main factors reported to be essential for survival and growth of MM cells in some experimental systems is IL-6. Therefore, the development and testing of substances that interfere with IL-6 or IL-6 receptor (IL-6R) function might have therapeutic value for the treatment of MM. We analyzed the effect of the IL-6R antagonist SANT-7 on growth and survival of the IL-6--dependent MM cell lines INA-6 and XG-1 as well as primary MM cells from 7 patients co-cultured with bone marrow stromal cells (BMSCs). In particular, we were interested in whether SANT-7 enhances the growth-inhibitory effects of dexamethasone (Dex) and all-trans-retinoic acid (ATRA). None of the drugs when tested as a single substance, including SANT-7, induced major growth inhibition if MM cells were co-cultured with primary human BMSCs. However, when Dex and ATRA were given in combination with SANT-7, strong growth inhibition was achieved in cell lines and primary MM cells. This effect was due to cell-cycle arrest and induction of apoptosis.

Antineoplastic Agents↗

Vitamin D and genomic stability.

1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] has been shown to act on novel target tissues not related to calcium homeostasis. There have been reports characterizing 1,25(OH)(2)D(3) receptors and activities in diverse tissues such as brain, pancreas, pituitary, skin, muscle, placenta, immune cells and parathyroid. The receptor hormone complex becomes localized in the nucleus, and undergoes phosphorylation by reacting with a kinase. This form of the receptor then interacts with the Vitamin D responsive element of target gene and modifies the transcription of those genes to develop the action. The modulation of gene transcription results in either the induction or repression of specific messenger RNAs (m-RNAs), ultimately resulting in changes in protein expression needed to produce biological responses. Genes for carbonic anhydrase that are expressed at high levels in osteoclast are known to be involved in bone resorption and Id genes role in osteoblast-osteoclast differentiation reflects the genomic effect of Vitamin D on bones. Genomic action of Vitamin D also explains the biosynthesis of oncogenes, polyamines, lymphokines and calcium binding proteins. However, there is a possibility that some of the actions of 1,25(OH)(2)D(3) may be mediated by non-genomic mechanisms and may not require the binding to Vitamin D receptor (VDR). Vitamin D offers a protection from genotoxic effects of Vitamin D deficiency by increasing the insulin receptor gene expression and BSP (bone sialoprotein), bone-remodeling by decreasing the osteopontin (OPN) m-RNAs, maintaining the normal epidermal structure and enamel matrix. Gonadal insufficiency in Vitamin D deficiency was corrected by vitamin mediated direct regulation of the expression of aramotase gene. The supportive role of Vitamin D in placental function is also evident by its influence on human placental lactogen (hpl) gene transcription accompanied by increase hpl m-RNA levels. Further role of Vitamin D is envisaged in identifying cyclin C as an important target for Vitamin D in cell-cycle regulation. Vitamin D at physiological concentration has been found to protect cell proteins and membranes against oxidative stress by inhibiting the peroxidative attack on membrane lipids. Vitamin D, at a concentration range of 2x10(-8)-5x10(-8)M, induces apoptosis in most cancer cells, stabilizes chromosomal structure and prevents DNA double-strand breaks induced either by endogenous or exogenous factors. Vitamin D is also effective in stimulating DNA synthesis in adult alveolar II cells and provides a novel mechanism of modulation of epithelial cell proliferation in the context of lung development and repair against injury. The regulation of various proto-oncogenes (c-myc, c-fos, c-jun), differentiation inducing properties, antiproliferative effects on keratinocytes and inhibitory effects in several human malignancy ranks Vitamin D as a novel hormone that may have physiological and clinical implication in the carcinogenic process.

Animals↗

1 alpha,25-Dihydroxyvitamin D(3) inhibits rat liver ultrastructural changes in diethylnitrosamine-initiated and phenobarbital promoted rat hepatocarcinogenesis.

The active metabolite of vitamin D, 1 alpha,25-dihydroxyvitamin D(3)[1,25(OH)(2)D(3)] has been receiving increasing attention and has come to the forefront of cancer chemoprevention research as being a regulator of cellular growth, differentiation and death. In the present study, attempts have been made to investigate the in vivo chemopreventive effect of 1,25(OH)(2)D(3) in two-stage rat liver carcinogenesis. Hepatocarcinogenesis was initiated with a single intraperitoneal injection of diethylnitrosamine [DEN] (200 mg/kg b. wt.) at week 4. After a brief recovery period of 2 weeks, all the DEN-treated rats were given phenobarbital (0.05%) in the basal diet and continued thereafter till the completion of the experiment. The results of our experiment showed that the rats which received 1,25(OH)(2)D(3) for 14 weeks (0.3 microg/100 microL propylene glycol, per os, twice a week), starting the treatment 4 weeks prior to DEN injection, exhibited maximum protective effect in maintaining the normal cellular architecture of the hepatocytes than the group of rats which received this micronutrient for only 9 weeks. Moreover, continuous supplementation of 1,25(OH)(2)D(3) maintains the concentration of hepatic microsomal cytochrome P-450 like that of normal vehicle control. Thus, long-term supplementation of 1,25(OH)(2)D(3) significantly (P < 0.001) inhibits hepatic cytosolic lipid peroxidation, thereby protecting the cell membranes from free-radical mediated damage. These results suggest that 1,25(OH)(2)D(3) is useful in the inhibition of rat liver carcinogenesis.

Animals↗

Involvement of Fas receptor and not tumor necrosis factor-alpha receptor in ultraviolet-induced activation of acid sphingomyelinase.

Fas receptor and tumor necrosis factor receptor-1 (TNFR1) mediate the activation of acid sphingomyelinase (ASMase), which catalyzes the hydrolysis of sphingomyelin to ceramide. Ceramide acts as a second messenger in mediating cell growth, differentiation, stress response, and apoptosis. Ultraviolet (UV) irradiation induces Fas receptor and TNFR1 aggregation. However, the roles of Fas receptor and TNFR1 in mediating UV-induced ASMase activation have not been explored. In this report, we demonstrate that Fas receptor, not TNFR1, mediated UV-induced activation of ASMase. Our data indicate that ASMase activity was not induced with UV irradiation but by TNFalpha in MCF-7 cells that expressed low levels of Fas receptor. In contrast, ASMase was activated by UV irradiation or TNFalpha treatment in Fas stably transfected MCF-7 cells. Immunofluorescence staining of TNFR1 on MCF-7 cells showed that TNFR1 was aggregated after treatment with UV irradiation or TNFalpha. However, UV-induced aggregation of TNFR1 did not lead to induction of ASMase activity. These results suggest that Fas receptor aggregation is solely responsible for UV-induced activation of ASMase. Further, with the use of BJAB and dominant-negative Fas-associated death domain-containing protein (FADD) stably transfected BJAB cells, we demonstrated that dominant-negative FADD partly inhibited UV-induced ASMase activation. Our results suggest that FADD is involved in UV-induced and Fas-mediated signaling pathways for activation of ASMase. Mol. Carcinog. 30:47-55, 2001.

Blotting, Western↗

1alpha, 25-Dihydroxyvitamin D3 suppresses the effect of streptozotocin-induced diabetes during chemical rat liver carcinogenesis.

The effect of streptozotocin-induced diabetes in male Sprague-Dawley rats was investigated to ascertain whether it has had any modulating role in hepatocarcinogenesis. Hepatocarcinogenesis was initiated with a single sub-necrogenic dose of diethylnitrosamine (DEN) (125 mg/kg body weight, i.p.) whilst acute diabetes was produced with a single i.p. injection of streptozotocin (STZ) (65 mg/kg body weight). STZ was administered either before or after initiation with DEN at 3-week intervals. With this basic experimental regimen, the effect of an antioxidant vitamin, 1alpha, 25-dihydroxyvitamin D3 (VD) (0.3 microg/ 0.1 ml propylene glycol per os twice a week), was investigated with effect from 4 weeks prior to the exposure of DEN or STZ. Primary routine histopathology, hepatic nodular morphometric analysis and major preneoplastic antioxidant and drug metabolising enzymes were tested either with or without VD treatment in different experimental and control groups. Observation of the hepatic nodulogenesis, pathology and level of the antioxidant and drug metabolising enzyme pattern of the tissue showed a marked protection in different experimental groups of rats treated with VD. It may be that VD could elicit an anticarcinogenic potential in the aforesaid regimen by resetting the effects of these biomarkers induced by DEN and/or STZ. We further propose that STZ, when administered 3 weeks after DEN, caused massive damage where its action in vivo could be comparable with any known promoter that could propel the process of carcinogenesis more efficiently than when it was applied before the carcinogen.

Alkylating Agents↗

1Alpha,25-dihydroxyvitamin D3 inhibits hepatic chromosomal aberrations, DNA strand breaks and specific DNA adducts during rat hepatocarcinogenesis.

The possible promoting effect of streptozotocin (STZ; 65 mg/kg body weight, intraperitoneal)-induced diabetes during 2-acetylaminofluorene (2-AAF; 0.04% in basal diet)-initiated hepatocarcinogenesis and modulatory effect of 1alpha,25-dihydroxyvitamin D3 (VD3; 0.3 microg/0.1 ml in propylene glycol, per os) were investigated by monitoring chromosomal aberrations (CAs), DNA strand breaks and specific DNA adducts in rat liver. VD3 treatment (twice a week) was started 4 weeks before the 2-AAF regimen and continued throughout the study. Aberrant metaphase chromosomes were counted from the regenerating hepatocytes 15, 30 or 45 weeks after STZ injection, while DNA strand break and adduct assays were performed 45 days post-STZ treatment. Dietary exposure to 2-AAF elicited a substantial increase in CAs and elevated the extent of DNA strand breaks and formation of N-(deoxyguanosin-8-yl)-2-aminofluorene. A promoting effect of STZ was evident from CAs coupled with DNA strand break analysis. VD3 treatment substantially reducted 2-AAF+STZ-induced CAs as well as DNA strand breaks and adducts. Thus, VD3 appears to be effective in suppressing liver-specific early chromosomal as well as DNA damage during the process of rat hepatocarcinogenesis initiated with 2-AAF and promoted by STZ contributing to its promise as a cancer chemotherapeutic agent.

2-Acetylaminofluorene↗

Noise enhances modulation sensitivity in cochlear implant listeners: stochastic resonance in a prosthetic sensory system?

Cochlear implants restore auditory sensitivity to the profoundly hearing-impaired by means of electrical stimulation of residual auditory nerve fibers. Sensorineural hearing loss results in a loss of spontaneous activity among the remaining auditory neurons and is accompanied by a reduction in the normal stochastic nature of neural firing in response to electric stimulation. It has been hypothesized that the natural stochasticity of the neural response is important for auditory signal processing and that introducing some optimal amount of noise into the stimulus may improve auditory perception through the implant. In this article we show that, for soft but audible stimuli, an optimal amount of "prosthetic" noise significantly improves sensitivity to envelope modulation in cochlear implant listeners. A nonmonotonic function relates modulation sensitivity and noise level, suggesting the presence of stochastic resonance.

Adult↗