TEMPORARY THRESHOLD SHIFT AND NOISE-INDUCED HEARING HANDICAP IN A GROUP OF TEXTILE WORKERS

Exposing the ear to an intense noise will probably cause to hearing loss. This loss may be temporary threshold shift (TTS), permanent threshold shift (PTS), or a combination of the two. The average audiograms for the 157 textile workers, exposed to an average 100 dB (A) overall noise level, in 5 age groups indicated that the losses were most prominent for frequencies of 3 to 6 KC/S showing a peak at 4 KC/S. with continued exposure and aging significant permanent losses appeared at other neighboring frequencies as well as still further increases in the 3-6 KC/S range. The mean hearing loss of the three frequencies 0.5, 1 and 2 KC/S was chosen as an index of hearing impairment, and for this, beginning handicap was placed at 26 dB hearing level, where difficulty may encounter with low levels of everyday speech. Therefore, it was shown that the men older than 45 years were handicap even before starting their daily work. But at the end of working shift, the average of TTS combined with PTS was quantitatively about the same for the population studied independent of their ages. So, it was demonstrated that in the noise-exposed subjects TTS was inversely related to hearing level, and it was concluded that PTS might biologically protect the ear from further damage

HEARING LOSS RESULTING FROM NOISE EXPOSURE IN TEXTILE WORKERS

Measurement and analysis of noise level in various frequency bands was carried out in a textile factory. It was shown that the noise level in various working places, particularly in the weaving workshop, was quite excessive comparing to the standards and so, it may very likely result in producing hearing loss in the workers. To determine the hearing loss of the workers due to excessive noise, 136 weavers were randomly selected and examined. However, the number of samples was not large enough to give reliable results. It was concluded that the intensive noise level in the weaving workshops may have produced considerable hearing loss in the workers. Large the expo­sure to noise, more the hearing loss was observed

Superparamagnetic iron oxide nanoparticles alter expression of obesity and T2D-associated risk genes in human adipocytes

<p>Adipocytes hypertrophy is the main cause of obesity and its affliction such as type 2 diabetes (T2D). Since superparamagnetic iron oxide nanoparticles (SPIONs) are used for a wide range of biomedical/medical applications, we aimed to study the effect of SPIONs on 22 and 29 risk genes (Based on gene wide association studies) for obesity and T2D in human adipocytes. The mRNA expression of lipid and glucose metabolism genes was changed upon the treatment of human primary adipocytes with SPIONs. mRNA of GULP1, SLC30A8, NEGR1, SEC16B, MTCH2, MAF, MC4R, and TMEM195 were severely induced, whereas INSIG2, NAMPT, MTMR9, PFKP, KCTD15, LPL and GNPDA2 were down-regulated upon SPIONs stimulation. Since SEC16B gene assist the phagocytosis of apoptotic cells and this gene were highly expressed upon SPIONs treatment in adipocytes, it is logic to assume that SPIONs may play a crucial role in this direction, which requires more consideration in the future.</p>

Age-related obesity and type 2 diabetes dysregulate neuronal associated genes and proteins in humans.

Contains fulltext : 153710.pdf (Publisher’s version ) (Open Access)Despite numerous developed drugs based on glucose metabolism interventions for treatment of age-related diseases such as diabetes neuropathies (DNs), DNs are still increasing in patients with type 1 or type 2 diabetes (T1D, T2D). We aimed to identify novel candidates in adipose tissue (AT) and pancreas with T2D for targeting to develop new drugs for DNs therapy.AT-T2D displayed 15 (e.g. SYT4 up-regulated and VGF down-regulated) and pancreas-T2D showed 10 (e.g. BAG3 up-regulated, VAV3 and APOA1 down-regulated) highly differentially expressed genes with neuronal functions as compared to control tissues. ELISA was blindly performed to measure proteins of 5 most differentially expressed genes in 41 human subjects. SYT4 protein was upregulated, VAV3 and APOA1 were down-regulated, and BAG3 remained unchanged in 1- Obese and 2- Obese-T2D without insulin, VGF protein was higher in these two groups as well as in group 3- Obese-T2D receiving insulin than 4-lean subjects. Interaction networks analysis of these 5 genes showed several metabolic pathways (e.g. lipid metabolism and insulin signaling).Pancreas is a novel site for APOA1 synthesis. VGF is synthesized in AT and could be considered as good diagnostic, and even prognostic, marker for age-induced diseases obesity and T2D. This study provides new targets for rational drugs development for the therapy of age-related DNs

Age-related obesity and type 2 diabetes dysregulate neuronal associated genes and proteins in humans

Despite numerous developed drugs based on glucose metabolism interventions for treatment of age-related diseases such as diabetes neuropathies (DNs), DNs are still increasing in patients with type 1 or type 2 diabetes (T1D, T2D). We aimed to identify novel candidates in adipose tissue (AT) and pancreas with T2D for targeting to develop new drugs for DNs therapy. AT-T2D displayed 15 (e.g. SYT4 up-regulated and VGF down-regulated) and pancreas-T2D showed 10 (e.g. BAG3 up-regulated, VAV3 and APOA1 down-regulated) highly differentially expressed genes with neuronal functions as compared to control tissues. ELISA was blindly performed to measure proteins of 5 most differentially expressed genes in 41 human subjects. SYT4 protein was upregulated, VAV3 and APOA1 were down-regulated, and BAG3 remained unchanged in 1- Obese and 2- Obese-T2D without insulin, VGF protein was higher in these two groups as well as in group 3- Obese-T2D receiving insulin than 4-lean subjects. Interaction networks analysis of these 5 genes showed several metabolic pathways (e.g. lipid metabolism and insulin signaling). Pancreas is a novel site for APOA1 synthesis. VGF is synthesized in AT and could be considered as good diagnostic, and even prognostic, marker for age-induced diseases obesity and T2D. This study provides new targets for rational drugs development for the therapy of age-related DNs