ABSTRACT
BACKGROUND: The neurological effect of viral respiratory infections has been acknowledged in many studies. However, patients who recovered from this infection show neurological manifestations and are not being routinely transferred for electrodiagnostic evaluation. AIM: This study aimed to examine the neurological effect of viral respiratory infections on the nerve function using electrophysiology in patients fully recovered from viral respiratory infections. METHODS: To limit bias in the results, the authors decided to choose patients who recovered from one virus in all participants (coronavirus). Medical records were screened for patients who performed nerve conduction studies (NCSs) before the coronavirus pandemic. Thirty patients met our inclusion criteria, and only 10 showed up to perform NCS. Data of the NCS was compared before and after the coronavirus infection for motor and sensory NCS parameters. RESULTS: An increase in both the median and ulnar sensory nerve latencies and a decrease in the sensory nerve amplitude was observed. Also, there was a decrease in the motor conduction velocity (MCV) of the ulnar nerves and motor amplitude in the median nerve. In the lower limbs, there was a decrease in the sural nerve latency, increased MCV in the tibial nerves, and decreased MCV in the peroneal nerves. The proximal amplitudes of the tibial and peroneal nerves were increased, but the distal amplitude was increased only in the peroneal nerves and decreased in the tibial nerves. CONCLUSION: There is a significant impact of viral infections on the peripheral nerves. Large-scale prospective studies are required to investigate the pathogenesis of the neuropathy and myopathy after viral infections.
ABSTRACT
The effect of bisphenol-A (BPA) on Klotho protein (aging-suppressing protein) expression in different body organs has not been sufficiently addressed by literature studies. The study investigated the impact of BPA on Klotho expression in multiple organs including the liver, kidney, and pancreas and suggested the involved molecular pathways. Twenty-seven male Wistar albino rats were divided into 3 equal groups: control, low-dose BPA (4.5 µg/L), and high-dose BPA (8 µg/L) groups in drinking water for 45 consecutive days. Liver, kidney, and pancreatic specimens were prepared for a gene study of Klotho, HSP60, mTOR, and ULK1 mRNA expressions. Also, the tissue specimens were measured for malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels. Paraffin-embedded sections were also prepared and subjected to Hematoxylin and Eosin (H&E) staining and immunohistochemical detection of Klotho and HSP60. The results revealed an alteration in the MDA, SOD, NO tissue levels, disturbed gene expression profile, and apoptotic changes in the histological findings of the examined organs which were obvious (p < 0.05) in the high-dose group. The anti-aging Klotho gene/protein expression was reduced (p < 0.05) more in the high-dose BPA group than in the low dose. In contrast, HSP60 gene/protein expression was significantly increased (p < 0.05) more in the high dose. It was concluded that BPA exposure contributed to cell stress and markedly reduced Klotho protein expression in liver, kidney, and pancreatic tissues, possibly by modulation of the HSP60-activated mTOR/autophagy signaling.
Subject(s)
Kidney , Liver , Male , Rats , Animals , Pancreas , TOR Serine-Threonine Kinases/genetics , Autophagy , Nitric OxideABSTRACT
Unfortunately, humanity is exposed to mixed plasticizers such as bisphenol-A (BPA) and dibutyl phthalate (DBP) that are leached from the daily used plastic products. Previous studies have demonstrated their potential in pancreatic beta cell injury and diabetes induction. The study hypothesized that both compounds would affect the pancreatic alpha cells in albino rats when administered at environmentally relevant doses. Heat shock protein 60 (HSP60) and caspase-3 protein expression was also investigated as potential mechanisms. Thirty-six male Wistar albino rats were separated into four equal groups: control, BPA alone, DBP alone, and BPA + DBP combined groups. BPA and DBP were given in drinking water for 45 days in a dose of 4.5 and 0.8 µg/L, respectively. Fasting blood glucose, serum insulin, pancreatic tissue levels of malondialdehyde, and superoxide dismutase were measured. Pancreatic sections were subjected to hematoxylin & eosin (H & E) staining, glucagon, HSP60, and caspase-3 immunohistochemistry. Although all three experimental groups showed diffuse islet cell HSP60 immunoreactivity, rats exposed to BPA alone showed α-cell-only apoptosis, indicated by H & E changes and caspase-3 immunoreactivity, associated with reduced glucagon immunoreaction. However, rats exposed to DBP alone showed no changes in either α or ß-cells. Both combined-exposed animals displayed α and ß apoptotic changes associated with islet atrophy and reduced glucagon expression. In conclusion, the study suggested HSP60/caspase-3 interaction, caspase-3 activation, and initiation of apoptosis in α-cell only for BPA-alone exposure group, meanwhile DBP alone did not progress to apoptosis. Interestingly, both α/ß cell effect was observed in the mixed group implying synergetic/additive action of both chemicals when combined.
