Fertility and unilateral undescended testis in the rat model III: ultrastructural changes in the contralateral descended testis

Sound conditioning (SC) is defined as “toughening” to lower levels of sound over time, which reduces a subsequent noise-induced threshold shift. Although the protective effect of SC in mammals is generally understood, the exact mechanisms involved have not yet been elucidated. To confirm the protective effect of SC against noise exposure (NE) and the stress-related signaling pathway of its rescue, we observed target molecule changes caused by SC of low frequency prior to NE as well as histology analysis in vivo and verified the suggested mechanisms in SGNs in vitro. Further, we investigated the potential role of Hsp70 and Bmi1 in SC by targeting SOD1 and SOD2 which are regulated by the FoxO1 signaling pathway based on mitochondrial function and reactive oxygen species (ROS) levels. Finally, we sought to identify the possible molecular mechanisms associated with the beneficial effects of SC against noise-induced trauma. Data from the rat model were evaluated by western blot, immunofluorescence, and RT-PCR. The results revealed that SC upregulated Hsp70, Bmi1, FoxO1, SOD1, and SOD2 expression in spiral ganglion neurons (SGNs). Moreover, the auditory brainstem responses (ABRs) and electron microscopy revealed that SC could protect against acute acoustic trauma (AAT) based on a significant reduction of hearing impairment and visible reduction in outer hair cell loss as well as ultrastructural changes in OHCs and SGNs. Collectively, these results suggested that the contribution of Bmi1 toward decreased sensitivity to noise-induced trauma following SC was triggered by Hsp70 induction and associated with enhancement of the antioxidant system and decreased mitochondrial superoxide accumulation. This contribution of Bmi1 was achieved by direct targeting of SOD1 and SOD2, which was regulated by FoxO1. Therefore, the Hsp70/Bmi1-FoxO1-SOD signaling pathway might contribute to the protective effect of SC against AAT in a rat model.

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Endocrinological parameters in experimental unilateral undescended testis

The Indian Journal of Pediatrics ◽

10.1007/bf02761205 ◽

1999 ◽

Vol 66 (2) ◽

pp. 193-196 ◽

Cited By ~ 1

Author(s):

M. Srinivas ◽

S. Agarwala ◽

P. Jha ◽

M. M. Misro ◽

D. K. Mitra

Keyword(s):

Undescended Testis ◽

Unilateral Undescended Testis

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Observations on the ultrastructure of inguinal cryptorchid testis in children

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100169018 ◽

1994 ◽

Vol 52 ◽

pp. 256-257

Author(s):

I. Bane Hani ◽

A. Abalkhail ◽

F. Al-Bagdadi ◽

Y. Abu-Ghalyun

Keyword(s):

Early Detection ◽

Teaching Hospital ◽

Early Detection Of Cancer ◽

Undescended Testis ◽

Surgical Correction ◽

Ultrastructural Changes ◽

Testicular Tumors ◽

Cryptorchid Testis ◽

The Difference ◽

Morphological Differences

Cryptorchidism is most frequently reported in horses, swine, and man. Neoplasia has been documented in the descended testes of unilateral cryptorchid testes in children. It has been reported that 10% of the testicular tumors in humans were associated with cryptorchidism. Most of the reported information did not specify the difference between inguinal and abdominal cryptorchid testes. Recently histological and ultrastructural morphological differences have been reported. The spermatoginia of many cryptorchid males bear a congenital lesion. It has been recommended that screening children for early detection of cancer, with undescended testis will reduce cancer. The purpose of this investigation is to characterize the ultrastructural changes of inguinal cryptorchid testes of children at different ages, treated at Princess Basmah teaching Hospital at Irbid, Jordan. It is anticipated that this study will provide information for timing decision for surgical correction. Children with cryptorchid testis between one and thirteen years old were presented to Princess Basmah teaching hospital.

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URB597 protects against NLRP3 inflammasome activation by inhibiting autophagy dysfunction in a rat model of chronic cerebral hypoperfusion

Journal of Neuroinflammation ◽

10.1186/s12974-019-1668-0 ◽

2019 ◽

Vol 16 (1) ◽

Cited By ~ 8

Author(s):

Shao-Hua Su ◽

Yi-Fang Wu ◽

Qi Lin ◽

Da-Peng Wang ◽

Jian Hai

Keyword(s):

Proinflammatory Cytokines ◽

Rat Model ◽

Nlrp3 Inflammasome ◽

Therapeutic Potential ◽

Artery Occlusion ◽

Chronic Cerebral Hypoperfusion ◽

Cerebral Hypoperfusion ◽

Ultrastructural Changes ◽

Inflammasome Activation ◽

Related Proteins

Abstract Background Previous studies reported that URB597 (URB) had therapeutic potential for treating chronic cerebral hypoperfusion (CCH)-induced neuroinflammation and autophagy dysfunction. However, the interaction mechanisms underlying the CCH-induced abnormal excessive autophagy and neuroinflammation remain unknown. In this study, we investigated the roles of impaired autophagy in nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing (NLRP) 3 inflammasome activation in the rat hippocampus and the underlying mechanisms under the condition of induced CCH as well as the effect of URB treatment. Methods The CCH rat model was established by bilateral common carotid artery occlusion (BCCAo), and rats were randomly divided into 11 groups as follows: (1) sham-operated, (2) BCCAo; (3) BCCAo+autophagy inhibitor 3-methyladenine (3-MA), (4) BCCAo+lysosome inhibitor chloroquine (CQ), (5) BCCAo+microglial activation inhibitor minocycline, (6) BCCAo+ROS scavenger N-acetylcysteine (NAC), (7) BCCAo+URB, (8) BCCAo+URB+3-MA, (9) BCCAo+URB+CQ, (10) BCCAo+URB+minocycline, (11) BCCAo+URB+NAC. The cell localizations of LC3, p62, LAMP1, TOM20 and NLRP3 were assessed by immunofluorescence staining. The levels of autophagy-related proteins (LC3, p62, LAMP1, BNIP3 and parkin), NLRP3 inflammasome-related proteins (NLRP3, CASP1 and IL-1β), microglial marker (OX-42) and proinflammatory cytokines (iNOS and COX-2) were evaluated by western blotting, and proinflammatory cytokines (IL-1β and TNF-a) were determined by ELISA. Reactive oxygen species (ROS) were assessed by dihydroethidium staining. The mitochondrial ultrastructural changes were examined by electron microscopy. Results CCH induced microglial overactivation and ROS accumulation, promoting the activation of the NLRP3 inflammasome and the release of IL-1β. Blocked autophagy and mitophagy flux enhanced the activation of the NLRP3-CASP1 inflammasome pathway. However, URB alleviated impaired autophagy and mitophagy by decreasing mitochondrial ROS and microglial overactivation as well as restoring lysosomal function, which would further inhibit the activation of the NLRP3-CASP1 inflammasome pathway. Conclusion These findings extended previous studies indicating the function of URB in the mitigation of chronic ischemic injury of the brain.

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