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Aquatic organisms are frequently exposed to various environmental stressors. Thus, the effects of high temperatures and herbicides on aquatic organisms are a major subject of interest. In this study, we studied the effects of short-term exposure (1 week) to Roundup®, a glyphosate-based herbicide (concentrations: 0.5 and 5 µg/L), on the morphology of gills, digestive glands, and connective tissues, and the expression of heat shock protein-70 (HSP70, a chaperone protein), cytochrome P450 (CYP450, a biomarker of environmental contaminants), dinitrophenyl protein (DNP, a biomarker of protein oxidation), nitrotyrosine protein (NTP, a biomarker of protein nitration), antioxidant enzymes such as superoxidase dismutase (SOD) and catalase (CAT) in tissues of American oyster, Crassostrea virginica (Gmelin, 1791) maintained at high temperature (30 °C). Histological analyses showed an increase in mucous production in the gills and digestive glands, and in hemocyte aggregation in the connective tissues as well as a structural change of lumen in the digestive glands of oysters exposed to Roundup. Immunohistochemical and quantitative RT-PCR analyses showed significant (P < 0.05) increases in HSP70, CYP450, DNP, NTP, CAT, and SOD mRNA and protein expressions in the tissues of oysters exposed to Roundup. Taken together, these results suggest that exposure to Roundup at high temperature induces overproduction of reactive oxygen species/reactive nitrogen species which in turn leads to altered prooxidant-antioxidant activity in oyster tissues. Moreover, our results provide new information on protein oxidation/nitration and antioxidant-dependent mechanisms for HSP70 and CYP450 regulations in oysters exposed to Roundup at high temperature. [ABSTRACT FROM AUTHOR]

Enhanced heat shock protein-70 (HSP-70) expression in the lungs is associated with attenuated acute lung injury (ALI) in a sepsis model. Chronic kidney disease (CKD) significantly contributes to the poor prognosis of patients with sepsis. This study examined the relationship between sepsis-induced ALI severity and altered lung HSP-70 expression in CKD. Experimental rats underwent a sham operation (control group) or 5/6 nephrectomy (CKD group). Sepsis was induced with cecal ligation and puncture (CLP). Laboratory tests and lung harvest were performed in the control group (without CLP and after 3, 12, 24, and 72 h of CLP) and in the CKD group (without CLP and after 72 h of CLP). ALI was the most severe after 12 h of sepsis. The mean lung injury score at 72 h after sepsis was significantly higher in the CKD group than in the control group (4.38 versus 3.30, p < 0.01). Nonetheless, enhanced lung HSP-70 expression was not observed in the CKD group. This study shows that altered lung HSP-70 expression is associated with the worsening of sepsis-induced ALI in patients with CKD. Enhancing lung HSP-70 is a novel treatment target for patients with CKD and sepsis-induced ALI. [ABSTRACT FROM AUTHOR]

Nimbolide is an active constituent of Azadirachta indica and is known for its anti‐inflammatory, anti‐oxidant, immune‐modulatory, and anti‐cancer effects. Few studies suggest that nimbolide treatment influences the responses to rheumatoid arthritis, but the underlying molecular mechanisms involved are not yet well established. Therefore, the present study was designed to determine the effect of nimbolide on expression regulation of toll‐like receptors to attenuate rheumatoid arthritis. The rheumatoid arthritis model was established by injecting complete Freund's adjuvant (CFA) intra‐dermally into the sub‐plantar region of the left hind paw of rats. Nimbolide (20 mg/kg) and piroxicam (10 mg/kg) were given to arthritic rats. Rats treated with nimbolide showed a significant reduction in inflammatory cells, rheumatoid factor, ESR, and improved the body weight. The results indicated that nimbolide possesses the capacity to attenuate rheumatoid arthritis by downregulating toll‐like receptors, IL‐17, IL‐23, HSP70, and IFN‐γ expression levels. Nimbolide treatment showed significant reduction in the severity of inflammation and destruction of joints and showed comparable effects to piroxicam, which is a standard non‐steroidal anti‐inflammatory drug used for the treatment of rheumatoid arthritis. It can be concluded that nimbolide can be considered as a potential candidate for therapeutic targeting of the toll‐like receptors pathway in rheumatoid arthritis. [ABSTRACT FROM AUTHOR]

Experiments were performed to determine the effect of ergothioneine on rectal temperature and the serum concentrations of heat shock protein-70 (HSP-70) and tumor necrosis factor-a (TNF-a) in stallions following a race of 2000 m in a hot-dry environment. Eighteen stallions weighing approximately 400 kg each were used for the experiment. They were divided into three groups of six stallions each. Group I (EEX) was the experimental group that was administered ergothioneine (0.5 mg/kg per os), while group II (EEC) did not receive ergothioneine before exercise. The third group (EEN) was neither administered ergothioneine nor exercised. The dry-bulb temperature and the relative humidity of the experiment were determined for six days and on the day of the experiment. The temperature-humidity index was also calculated. Rectal temperature, serum HSP-70, and TNF-a concentrations of all horses were measured before commencement, immediately after, and 2 h after the exercise. The dry-bulb temperature and relative humidity which showed diurnal fluctuations increased significantly (p < 0.05) between 06.00 h and 12.00 h (22.6 ± 1.23 and 38.6 ± 6.5, respectively). Serum TNF-a and HSP-70 levels of the stallions in the EEX group were higher than the values obtained in the EEC and EEN groups (p < 0.05). The values of rectal temperature obtained were lower (p < 0.05) in the EEX group than in the other groups. Therefore, it could be concluded that ergothioneine modulated rectal temperature, as well as TNF-a and HSP-70 concentrations in the stallions, and might be beneficial to horses during exercise. [ABSTRACT FROM AUTHOR]

Exposure to high ambient temperature is a stressor that influences both biological and behavioral functions and has been previously shown to have an extensive impact on brain structure and function. Physiological, cellular and behavioral responses to heat-stress (HS) (40–41 °C, 2 h) were evaluated in adult male Sprague-Dawley rats. The effect of HS exposure before predator-scent stress (PSS) exposure (i.e., HS preconditioning) was examined. Finally, a possible mechanism of HS-preconditioning to PSS was investigated. Immunohistochemical analyses of chosen cellular markers were performed in the hippocampus and in the hypothalamic paraventricular nucleus (PVN). Plasma corticosterone levels were evaluated, and the behavioral assessment included the elevated plus-maze (EPM) and the acoustic startle response (ASR) paradigms. Endogenous levels of heat shock protein (HSP)-70 were manipulated using an amino acid (L-glutamine) and a pharmacological agent (Doxazosin). A single exposure to an acute HS resulted in decreased body mass (BM), increased body temperature and increased corticosterone levels. Additionally, extensive cellular, but not behavioral changes were noted. HS-preconditioning provided behavioral resiliency to anxiety-like behavior associated with PSS, possibly through the induction of HSP-70. Targeting of HSP-70 is an attractive strategy for stress-related psychopathology treatment. [ABSTRACT FROM AUTHOR]

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(1) Background: Identifying early pancreas parenchymal changes remains a challenging radiologic diagnostic task. In this study, we hypothesized that applying artificial intelligence (AI) to contrast-enhanced ultrasound (CEUS) along with measurement of Heat Shock Protein (HSP)-70 levels could improve detection of early pancreatic necrosis in acute pancreatitis. (2) Methods: Acute pancreatitis (n = 146) and age- and sex matched healthy controls (n = 50) were enrolled in the study. The severity of acute pancreatitis was determined according to the revised Atlanta classification. The selected severe acute pancreatitis (AP) patient and an age/sex-matched healthy control were analysed for the algorithm initiation. Peripheral blood samples from the pancreatitis patient were collected on admission and HSP-70 levels were measured using ELISA. A CEUS device acquired multiple mechanical index contrast-specific mode images. Manual contour selection of the two-dimensional (2D) spatial region of interest (ROI) followed by calculations of the set of quantitative parameters. Image processing calculations and extraction of quantitative parameters from the CEUS diagnostic images were performed using algorithms implemented in the MATLAB software. (3) Results: Serum HSP-70 levels were 100.246 ng/ml (mean 76.4 ng/ml) at the time of the acute pancreatitis diagnosis. The CEUS Peek value was higher (155.5) and the mean transit time was longer (40.1 s) for healthy pancreas than in parenchyma affected by necrosis (46.5 and 34.6 s, respectively). (4) Conclusions: The extracted quantitative parameters and HSP-70 biochemical changes are suitable to be used further for AI-based classification of pancreas pathology cases and automatic estimation of pancreatic necrosis in AP. [ABSTRACT FROM AUTHOR]

Background: Vitiligo is a progressive depigmenting disorder characterized by the loss of functional melanocytes from the epidermis. The etiopathogenesis of vitiligo is still unclear. Heat shock proteins (HSPs) are prime candidates to connect stress to the skin. HSPs were found to be implicated in autoimmune diseases such as rheumatoid arthritis and other skin disorders as psoriasis. Aim and Objectives: The aim of this study was to map the level of HSP-70 in vitiligo lesions to declare its role in the pathogenesis and activity of vitiligo. Materials and Methods: The study included thirty patients with vitiligo and 30 age- and sex-matched healthy controls. Vitiligo patients were divided as regards to the disease activity into highly active, moderately active, and inactive vitiligo groups. Skin biopsies were taken from the lesional and nonlesional skin of patients and from the normal skin of the controls. HSP-70 messenger RNA (mRNA) expression was estimated using quantitative real-time polymerase chain reaction. Results: Our analysis revealed a significantly higher expression of HSP-70 mRNA in lesional skin biopsies from vitiligo patients compared to nonlesional skin biopsies from vitiligo patients (P < 0.001) and compared to skin biopsies from healthy controls (P < 0.001). The level of HSP-70 was not found to be correlated with age, sex, or disease duration. The expression of HSP-70 was correlated with the disease activity and patients with active vitiligo showed higher mean HSP-70 level compared to those with inactive disease. Conclusions: HSP-70 plays a role in the pathogenesis of vitiligo and may enhance the immune response in active disease. [ABSTRACT FROM AUTHOR]

Context: Aegle marmelos L. Corr (Rutaceae) is an important Indian Ayurvedic medicinal plant used for the treatment of various ailments. However, little information is available on the anti-fatigue properties of its fruit. Objective: Evaluation of the physical endurance and exercise-induced oxidative stress modulating properties of A. marmelos fruit in mice. Material and methods: Radical scavenging activity of the fruit hydroalcoholic extract was evaluated using in vitro systems. The extract was further evaluated for its endurance-enhancing properties at three oral doses (100, 200 and 400 mg/kg b.wt) in BALB/c mice for 21 d using a swimming test. Results and discussion: The extract exhibited significant scavenging activity against DPPH (IC50, 351 ± 37 µg/ml) and ABTS radicals (IC50, 228 ± 25 µg/ml), respectively, with the polyphenol content of 95 µg/mg extract. It also inhibited AAPH radical-induced oxidation of biomolecules such as BSA protein (63%), plasmid DNA (81%) and lipids (80.5%). Administration of extract resulted in an increase in the duration of swimming time to exhaustion by 23.4 and 47.5% for medium and higher doses, respectively. The extract significantly normalized the fatigue-related biochemical parameters and also down-regulated the swim stress-induced over-expression of heat shock protein-70 and up-regulated the skeletal muscle metabolic regulators (GLUT-4 and AMPK1-α) by 2- and 3-fold, respectively, at the higher dose in muscle tissues. Conclusion: Our study demonstrates the anti-fatigue properties of A. marmelos fruit, most probably manifested by delaying the accumulation of serum lactic acid, increasing the fat utilization and up-regulating the skeletal muscle metabolic regulators. [ABSTRACT FROM AUTHOR]

For analyzing the changes in immunoglobulins, HSP70, ghrelin levels in blood samples were collected from volunteers vaccinated against swine flu before the vaccinations and on days 3, and 15, and 1 and 2 months after the vaccination in the presence or absence of fever associated with the it. The study included 11 subjects having developed a fever, and 13 subjects not having a fever, and 20 control subjects. Immunoglobulins were measured by nephelometry, and HSP70 and ghrelins by appropriate ELISA tests. The level of ghrelin was reduced, while the level of HSP70 was significantly increased in subjects who developed fevers. When temperatures were normalized, both levels were found similar to the control group. These results indicate that the increase in serum immunoglobulins levels associated with vaccinations, along with, elevations in HSP70 and reduced ghrelin levels associated with fever, may be the important parameters in the clinical evaluation and follow-up of treatments with vaccines. [ABSTRACT FROM AUTHOR]

Photodynamic therapy (PDT)-generated cancer vaccines have shown promising results in preclinical studies and are being introduced in the clinics. Using an SCCVII mouse squamous cell carcinoma-based whole-cell autologous PDT vaccine model developed in our previous work, we have examined systemic effects in vaccinated mice that could be related to the induction of acute phase response. The upregulation of gene encoding serum amyloid P component (prototypic mouse acute phase reactant) was detected in the liver and to a lesser degree in the tumor of vaccinated mice at 24 h post-PDT vaccine treatment. A strong upregulation of gene for heat shock protein 70 was found in both the liver and tumor of mice at 4 h after their PDT vaccine treatment. Changes in the expression of genes for glucocorticoid-induced leucine zipper and serum- and glucocorticoid-regulated kinase 1 that are highly responsive to glucocorticoid modulation were uncovered in both the tumor and liver of vaccinated mice. A rise in the levels of serum corticosterone was detected in mice at 24 h after PDT vaccine treatment. The results indicate that a sudden appearance of a large number of PDT vaccine cells elicits host responses for securing their optimized clearance, which in addition to producing seminal acute phase reactants includes the engagement of glucocorticoid hormones. It is becoming increasingly clear that a consummate execution of this process of PDT vaccine cell removal is critical for tumor antigen recognition and the attainment of potent antitumor immune response. [ABSTRACT FROM AUTHOR]

Objectives: The neurobiological basis for autism remains poorly understood. However, research suggests that environmentalfactors and neuroinflammation, as well as genetic factors, are contributors. This study aims to test the role that might be played by heat shock protein (HSP)70, transforming growth factor (TGF)-β2, Caspase 7 and interferon-γ (IFN-γ)in the pathophysiology of autism. Materials and methods: HSP70, TGF-β2, Caspase 7 and INF-γ as biochemical parameters related to inflammation were determined in plasma of 20 Saudi autistic male patients and compared to 19 age- and gender-matched control samples. Results: The obtained data recorded that Saudi autistic patients have remarkably higher plasma HSP70, TGF-β2, Caspase 7 and INF-γ compared to age and gender-matched controls. INF-γ recorded the highest (67.8%) while TGF-β recorded the lowest increase (49.04%). Receiver Operating Characteristics (ROC) analysis together with predictiveness diagrams proved that the measured parameters recorded satisfactory levels of specificity and sensitivity and all could be used as predictive biomarkers. Conclusion: Alteration of the selected parameters confirm the role of neuroinflammation and apoptosis mechanisms in the etiology of autism together with the possibility of the use of HSP70, TGF-β2, Caspase 7 and INF-γ as predictive biomarkers that could be used to predict safety, efficacy of a specific suggested therapy or natural supplements, thereby providing guidance in selecting it for patients or tailoring its dose. [ABSTRACT FROM AUTHOR]

Background: The aim was to determine whether Bcl-2-associated athanogene-1 (Bag-1) and/or its binding protein heat shock protein-70 (Hsp70) exhibit deregulated expression in epidermal squamous cell carcinoma (SCC) and whether Bag-1 confers apoptosis resistance.Method: Immunohistochemistry for Bag-1 and Hsp70 was performed on 60 epidermal SCC and 10 normal skin samples. The epidermal SCC cell line SCC-13 was treated with 5-fluorouracil (5-FU) after Bag-1 knockdown to determine whether high Bag-1 levels contribute to growth and/or apoptosis resistance.Results: Normal epithelium expressed primarily nuclear Bag-1. Most tumours showed reduced nuclear Bag-1 staining, but a subset exhibited strong Bag-1 staining, with cytoplasmic Bag-1 staining intensity correlating with cytoplasmic Hsp70 staining intensity (r(s)=0.462; P<0.001) and less differentiation (P<0.001). Bag-1 knockdown resulted in markedly reduced SCC-13 cell yield, increased spontaneous apoptosis and enhanced sensitivity to 5-FU-induced apoptosis. Apoptosis induced by 5-FU in the Bag-1-knockdown cells was significantly greater than the additive apoptotic effect of 5-FU or Bag-1 knockdown alone.Conclusions: Overexpression of Bag-1 and Hsp70 in poorly differentiated SCC may confer both enhanced tumour cell growth and apoptosis resistance. Bag-1 may contribute to the resistance of more advanced epidermal SCC to chemotherapy. [ABSTRACT FROM AUTHOR]

The PO2 within the kidney changes dramatically from cortex to medulla. The present experiments examined the effect of changing PO2 on epithelial Na channel (ENaC)-mediated Na transport in the collecting duct using the mpkCCD-c14 cell line. Decreasing ambient O2 concentration from 20 to 8% decreased ENaC activity by 40%; increasing O2 content to 40% increased ENaC activity by 50%. The O2 effect required several hours to develop and was not mimicked by the acid pH that developed in monolayers incubated in low-O2 medium. Corticosteroids increased ENaC activity at each O2 concentration; there was no interaction. The pathways for O2 and steroid regulation of ENaC are different since O2 did not substantially affect Sgk1, α-ENaC, Gilz, or Usp2-45 mRNA levels, genes involved in steroid-mediated ENaC regulation. The regulation of ENaC activity by these levels of O2 appears not to be mediated by changes in hypoxia-inducible factor-1α or -2α activity or a change in AMP kinase activity. Changes in O2 concentration had minimal effect on α- or γ-ENaC mRNA and protein levels; there were moderate effects on β-ENaC levels. However, 40% O2 induced substantially greater total β- and γ-ENaC on the apical surface compared with 8% O2; both subunits demonstrated a greater increase in the mature forms. The α-ENaC subunit was difficult to detect on the apical surface, perhaps because our antibodies do not recognize the major mature form. These results identify a mechanism of ENaC regulation that may be important in different regions of the kidney and in responses to changes in dietary NaCl. [ABSTRACT FROM AUTHOR]

Infiltration of leukocytes into post-ischemic cerebrum is a well-described phenomenon in stroke injury. Because CD-8 T-lymphocytes secrete cytotoxic proteases, including granzyme-b (Gra-b) that exacerbates post-ischemic brain damage, we investigated roles of Gra-b in human stroke. To study the role of Gra-b in stroke, ischemic and non-ischemic tissues (from post-mortem stroke patients) were analyzed using immunoblotting, co-immunoprecipitation, terminal deoxy uridine nick end labeling (TUNEL) and Annexin-V immunostaining, and in vitro neuron survival assays. Activated CG-SH cells and supernatants were used to model leukocyte-dependent injury. Non-ischemic brain tissues were used as non-pathological controls. Non-activated CG-SH cells and supernatants were used as controls for in vitro experiments. Human stroke (ischemic) samples contained significantly higher levels of Gra-b and interferon-gamma inducible protein-10 (IP-10/CXCL10) than non-ischemic controls. In stroke, poly (ADP-ribose) polymerase-1 and heat shock protein-70 were cleaved to canonical proteolytic 'signature' fragments by Gra-b. Gra-b was also found to bind to Bid and caspase-3. Gra-b also co-localized with Annexin-V/TUNEL in degenerating neurons. Importantly, Gra-b inhibition protected both normal and ischemia-reperfused neurons against in vitro neurotoxicity mediated by activated CG-SH cells and supernatants. These results suggest that increased leukocyte infiltration and elevated Gra-b levels in the post-stroke brain can induce contact-dependent and independent post-ischemic neuronal death to aggravate stroke injury. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a common, potentially serious metabolic disorder. Over the long term, diabetes leads to serious consequences in a number of tissues, especially those that are insulin insensitive (retina, neurons, kidneys). It also causes a variety of functional and structural disorders in the central and peripheral nervous systems. We investigated whether neurodegenerative changes were observable in the hippocampus, cortex, and cerebellum after 4 weeks of streptozotocin (STZ)-induced diabetes in rats and the effect(s) of melatonin. Male Wistar rats (n = 32) were divided into four groups (n = 8 each): untreated controls, melatonin-treated controls, untreated diabetics, and melatonin-treated diabetics. Experimental diabetes was induced by a single dose of STZ (60 mg/kg, intraperitoneal (ip)). For 3 days before the administration of STZ, melatonin (200 μg/kg/day, ip) was injected and continued for 4 weeks. Sections of hippocampus, cortex, and cerebellum were stained with hematoxylin and eosin and examined using light microscopy. In addition, brain tissues were examined immunohistochemically for the expression of glial and neuronal markers, including glial fibrillary acidic protein (GFAP), neuron-specific enolase (NSE), and heat shock protein-70 (HSP-70). No neurodegenerative changes were observed in the hippocampus, cortex, or cerebellum of the untreated diabetic group after 4 weeks compared with the other groups. We did not observe any change in GFAP, NSE, or HSP-70 immunostaining in the brain tissues of STZ-induced diabetic rats. In summary, after 4 weeks of STZ-induced diabetes in rats, no degenerative or immunohistochemical changes were detected in the hippocampus, cortex, or cerebellum. [ABSTRACT FROM AUTHOR]

Serological immunoscreening was used to identify a gene encoding heat shock protein-70 from Babesia gibsoni (BgHSP-70) that showed high homology with HSP-70s from other apicomplexan parasites. This gene corresponded to a full-length cDNA containing an open reading frame of 1968 bp predicted to result in a 70-kDa mature protein consisting of 656 amino acids. Analysis of the expression levels of BgHSP-70 indicated elevated transcription from cultured parasites incubated at 40°C for 1 h, but not at 30°C. Interestingly, antiserum raised against recombinant BgHSP-70 protein reacted specifically not only with a 70-kDa protein of B. gibsoni but also with a corresponding native protein of B. microti (BmHSP-70), indicating the high degree of conservation of this protein. The BmHSP-70 gene was then isolated and characterized and the immunoprotective properties of recombinant BgHSP-70 (rBgHSP-70) and rBmHSP-70 were compared in vitro and in vivo. Both proteins had potent mitogenic effects on murine and canine mononuclear cells as evidenced by high proliferative responses and IFN-γ production after stimulation. Immunization regimes in BALB/c and C57BL/6 mice using rBgHSP-70 and rBmHSP-70 elicited high antibody levels, with concurrent significant reductions in peripheral parasitaemias. Taken together, these results emphasize the potential of HSP-70s as a molecular adjuvant vaccine. [ABSTRACT FROM AUTHOR]

Sudden sensorineural hearing loss (SSNHL) is frequently classified as ‘idiopathic’ since the causative factor responsible for its onset is not identified in most cases. In the present study, we determined whether SSNHL is clinically associated with serum anti-heat shock protein-70 (anti-HSP70) and antiphospholipids (anti-PLs) autoantibodies and whether these autoantibodies have an impact on the prognosis of SSNHL. Sera from 63 patients with SSNHL were screened prospectively for the presence of anti-HSP70 and anti-PLs autoantibodies by an enzyme-linked immunosorbent assay test. Anti-PLs antibodies in this study consisted of anticardiolipin, and anti-β2-glycoprotein-1 antibodies. Serum was assayed for anti-HSP70 IgG antibodies using recombinant human HSP70. Demographic, clinical, and audiometric variables were analyzed to find the possible role of serum autoantibodies in SSNHL patients. Sixteen patients (25.4%) had demonstrable anti-HSP70 antibodies in serum. Twenty-one patients (33.3%) showed a positive result for at least one isotype (IgM or IgG) of anti-PLs. In 19% of the patients, anti-HSP70 and anti-PLs antibodies were positive in two combinations. A statistically significant association was found between anti-HSP70 antibodies and the Siegel recovery grade subgroup. SSNHL patients who were positive for anti-HSP70 antibodies showed a significantly higher rate of complete recovery and incomplete but partial recovery than SSNHL patients without anti-HSP70 antibodies (p = 0.0496). Statistically significant association was found between total anticardiolipin, total anti-β2-glycoprotein-1, total anti-PLs, and anti-PLs in combination with anti-HSP70 antibodies and age (p = 0.0229). The detection of autoantibodies to HSP70 and PLs offers a pliable explanation for the immune-mediated mechanism of SSNHL. The present study confirms and supports previous studies regarding the association between anti-HSP70 and anti-PLs antibodies with SSNHL, and is the first to identify a positive association between anti-HSP70 antibodies and a positive outcome of SSNHL. Further studies are necessary in order to identify and further clarify the immunologic role of the presence of autoantibodies and their impact on the prognosis of SSNHL. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective To assess the validity of the Western blot immunoassay for heat shock protein-70 (hsp-70) for diagnosis of autoimmune inner ear disease. Study Design Retrospective study of 53 patients affected by sudden deafness (n = 19), idiopathic progressive sensorineural hearing loss (n = 24), and Meniere's disease (n = 10) who were treated from 1995 to 1999. The clinical course and response to corticosteroid were evaluated. Methods A purified hsp-70 antigen from bovine kidney cell line was used for the Western blot immunoassay. Results Only five patients (9.4%) showed anti-hsp-70 antibodies: Two presented a sudden sensorineural hearing loss (sudden deafness group), two showed an idiopathic progressive sensorineural hearing loss (idiopathic progressive sensorineural hearing loss group), and one was affected by fluctuating hearing loss (Meniere's disease group). A systemic autoimmune condition was observed in 29.1% of patients with idiopathic progressive sensorineural hearing loss. Conclusions The low sensitivity of Western blot immunoassay for patients affected by idiopathic progressive sensorineural hearing loss and Meniere's disease may result from either the long time elapsed from the hearing loss and vertigo to the initial examination or from the increased percentage of cases of systemic autoimmune disease present in patients with idiopathic progressive sensorineural hearing loss. More studies to detect the immune-mediated inner ear disease in Western blot immunoassay-negative patients are required. [ABSTRACT FROM AUTHOR]

Growing evidences demonstrated that zinc oxide nanoparticles (ZnONPs) could reach the brain after oral ingestion; however, the “neurotoxicity of” ZnONPs after oral exposure has not been fully investigated. This study aimed to explore the “neurotoxicity of” ZnONPs (<100 nm) after oral exposure to two doses; 40 and 100 mg/kg for 24 h and 7 days. The exposure to 40 and 100 mg/kg of ZnONPs for 24 h did not elicit “neurotoxicity” compared to normal control. However, the daily exposure to both doses for 7 days caused oxidative stress in brain tissue as detected by the elevation of the levels of malondialdehyde, the main product of lipid peroxidation and nitrite as an index of nitric oxide with concomitant decline in the concentrations of antioxidants. In addition, both doses resulted in DNA fragmentation which was confirmed by increased percentage of tailed DNA, DNA tail intensity and length and tail moment particularly with the dose 100 mg/kg. Moreover, both doses led to the elevation of the inflammatory cytokines along with increased apoptotic markers including caspase-3 and Fas. Heat shock protein-70 levels were also elevated possibly as a compensatory mechanism to counteract the ZnONPs-induced oxidative stress and apoptosis. The present results indicate the “neurotoxicity of” ZnONPs after recurrent oral exposure via oxidative stress, genotoxicity, inflammatory response and apoptosis. [ABSTRACT FROM AUTHOR]