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Background: This study aimed to investigate cell degeneration, apoptosis, and ultrastructural differences in refractive lenticules (RL) obtained using small incision lenticule extraction (SMILE) compared with spherical equivalence (SE) refraction values. Methods: This study included 84 eyes from 42 patients. Patients were divided into two groups according to the SE values: those with values below 4 diopters (D) (Group 1) and above 4 diopters (D) (Group 2). Patients who did not belong to the same SE group were excluded from the study. One RL obtained from each patient was separated for light microscopy and immunohistochemical examinations, and another for transmission electron microscopy (TEM) examinations. Caspase‐3 for apoptosis and alpha‐smooth muscle actin (α‐SMA) for cell degeneration were evaluated using immunohistochemical examinations. Results: Histological analyses showed that the density of collagen fibres was greater in Group 1 than in Group 2. Glycoaminoglycan and glycoprotein staining intensities were also higher in Group 1. TEM observations showed that Group 1 had intact cell and nuclear membranes, peripheral heterochromatin, and large nuclei, while Group 2 showed heterochromatin condensation and fragmentation, increased intracellular vacuoles, and loss of cytoplasm. Immunohistochemical analyses revealed that α‐SMA and caspase‐3 were significantly higher in Group 2 than in Group 1 (p < 0.001 and p < 0.001, respectively). Conclusions: Cell degeneration and apoptosis were significantly more common in the RLs with high SE values after SMILE surgery. The tissue response induced by surgery was more severe in the RLs with high SE values. This should be considered when reusing RLs. [ABSTRACT FROM AUTHOR]

Purpose: The G-protein coated receptor (GPCR) family, including the Insulin-Like Peptide 3 (INSL3) receptor, is involved in the Nuclear Factor kappa B (NF-κB)-mediated pathway in inflammation. In this regard, it can be thought that INSL3 plays a role in inflammation via the NF-κB pathway. In this study, we investigated the effect of INSL3 on inflammation and cell viability in the lipopolysaccharide (LPS)-induced N9 microglia cell line. Materials and Methods: N9 microglial cells were pretreated with INSL3 for 2 hours, and then treated with LPS for 6 hours. Cell viability was identified by WST-8 assay. Immunostaining was performed to evaluate the levels of Interleukin-1β (IL-1β), Tumor necrosis factor (TNF)-α, and NF-κB. Results: The cells in the LPS group showed degenerative changes in morphology and decreased cell viability. In the INSL3+LPS group (1.21±0.06), the general appearance and viability of the cells were more similar to the control group (1.92±0.04) compared to the LPS group (0.61±0.05). It was determined that INSL3 prevented the LPS-induced increase in IL-1β, TNF-α, and NF-κB levels and decreased cell death. Conclusion: INSL3 suppresses inflammation and thus promotes cellular healing and can be considered a therapeutic agent that reduces inflammation. [ABSTRACT FROM AUTHOR]

Neuronal networks in the nervous system play a central role in various behaviors essential for living organisms, such as movement, breathing, posture, and balance. Synaptic connections between different types of neurons during development form the basic architecture of neural networks that facilitate vital functions. The spinal cord contains a balanced number of excitatory (Glutamatergic) and inhibitory (GABAergic) neurons that connect to each other to create neural networks. Studies to date have investigated transcription factor (TF) networks that are expressed and function throughout central nervous system (CNS) development to identify and guide the development of diverse populations of neurons in the spinal cord. The balance between inhibitory and excitatory neurons in the dorsal spinal cord is established early in development in a process dominated by the interplay between basic helix-loop-helix (bHLH) transcriptional activators and a PRDM repressor PRDM13. The bHLH TFs, ASCL1 and PTF1A, initiate excitatory and inhibitory neuron gene expression programs, respectively, while PRDM13 is necessary to silence alternative cell fates. The central premise is that bHLH and PRDM factors sit poised at critical fate choice points in multiple lineages throughout the embryo, including those generating neuronal diversity. Although substantial progress has been made in identifying these factors and their functions in neuronal sub-type specification, the mechanisms how regulate specific gene programs are not yet clear. Uncovering these mechanisms will shed light on future research on the solution of disorder in the development of the nervous system and the treatment of clinical problems resulting from developmental anomalies. [ABSTRACT FROM AUTHOR]

The innate immune system is vital in host defense against pathogens entering the body. The NLRP3 (NACHT-, LRRand Pyrin Domain Containing 3) inflammasome, a component of the innate immune system, is a multimeric protein complex. Inflammasome activation is a process that starts and improves differently from classical inflammatory responses. In order to induce inflammasome activation, there must be a danger signal such as DAMP (Damage- Associated Molecular Pattern) or PAMP (Pathogen-Associated Molecular Pattern) detected. In response to these stimuli, caspase-1 is activated. This in turn leads to cleavage and maturation of potent pro-inflammatory cytokines, IL-1β (interleukin-1β) and IL-18 (interleukin-18) by mature caspase-1. Thus, inflammatory responses mediated by IL-1β and IL-18 are activated. Although NLPR3 activation is an important immune response, its overactivation can cause inflammatory disorders and cell death. For this reason, regulation and inhibition of the NLRP3 inflammasome may be a promising treatment approach for these autoinflammatory diseases. In this review presents the current understanding of the mechanisms of NLRP3 inflammasome activation, as well as recent advances in the non-canonical and alternative inflammasome pathways. [ABSTRACT FROM AUTHOR]

We aimed to create a mechanical optic nerve damage model in rats and to investigate the neuroprotective effects of topical Coenzyme Q10 + Vitamin E TPGS (CoQ10+Vit E) molecule on retinal ganglion cells. In our study, 30 eyes of 20 male Wistar rats were used. Three groups, each consisting of 10 eyes, were formed as control, experimental, and treatment groups. The control group was used to test the formation of optic nerve damage. Topical CoQ10 + Vit E TPGS solution was applied to the rats in the treatment group, one drop twice a day for 3 weeks. On the other hand, physiological drops were applied to the experimental group 2 times a day for 3 weeks. After 3 weeks, the optic nerves of the rats were dissected and examined histopathologically. In electron microscopic examination of the treatment group, it was noted that the myelin sheath in the majority of myelinated nerve fibers and the normal structures of mitochondria, neurotubules, and neurofilaments in the axoplasm were preserved. It was observed that the oligodendrocytes surrounded the myelinated axons. In the experimental group, significant degenerative changes were observed in myelinated nerve fibers in many areas. The number of myelinated axons was significantly increased in the treatment group compared to the experimental group (p =.0028). In the light of the data obtained, the neuroprotective effect of the topically used CoQ10 + Vit E TPGS molecule was found to be histopathologically effective in our experimental study. Abbreviations: NAAION: Nonarteritic anterior ischemic optic neuropathy; CoQ10: Coenzyme q10; CG: Control group; EG: Experimental group; TG: Treatment group. [ABSTRACT FROM AUTHOR]

In this study, the expression of the androgen receptor (AR) and estrogen receptor alpha (ERα) in testicular tissue of male patients with obstructive azoospermia (OA) and non-obstructive azoospermia (NOA) were evaluated by immunohistochemistry. NOA (n = 23) and OA (n = 21) groups were created according to clinical and laboratory archival records. Testicular sperm extraction tissue sections were evaluated according to Johnsen's tubular biopsy scoring (JTBS) method. ERα and AR immunostaining results were evaluated semiquantitatively. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, and estradiol were analyzed. Serum FSH and LH concentrations were greater, and testosterone concentrations were lower than the normal values in the NOA group, whereas the OA group revealed normal hormonal values. Serum estradiol concentrations in groups were in the normal range. JTBSs were significantly lower in the NOA group. Decreased AR expression and increased ERα expression were observed in the NOA group compared to the OA group. This suggests that ERα and AR are expressed in Sertoli cells, Leydig cells, and myoid cells and are required for normal testicular function. Decreased expression of the AR and increased expression of ERα in the testis may negatively affect spermatogenesis. Abbreviations: AR: androgen receptor; ER: estrogen receptor; ERα: estrogen receptor alpha; FSH: follicle-stimulating hormone; JTBS: Johnsen's tubular biopsy scoring; LH: luteinizing hormone; NOA: non-obstructive azoospermia; OA: obstructive azoospermia; TESE: testicular sperm extraction [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) is a chemical agent known to have detrimental reproductive and developmental effects. The tissue-specific impacts of BPA exposures and target tissues sensitiveness to BPA are still unclear. The aim of this study was to determine the short- and long-term dose-dependent toxic effects of BPA on rat testes. Forty-eight Wistar albino male rats were divided into four groups each containing 12 rats. To induce toxicity, BPA was administered orally at three different dosages (50, 100, and 200 mg/kg) for 14 and 28 days, respectively. Testis tissues were examined using light and electron microscopy, immunohistochemistry, and biochemical methods. Serum testosterone (T) and luteinizing hormone (LH) levels were measured. Additionally, insulin-like factor 3 (INSL3) as a marker of Leydig cell function was evaluated immunohistochemically. Groups administered high doses of BPA showed severe degenerations such as testicular atrophy, spermatogenic arrest, and interstitial edema in testis. Also, a significant decrease in INSL3 immunoreactivity and serum LH and T levels was found. The results indicated that both increased exposure time and dosage of BPA caused more serious detrimental effects on testes in the rat. Decreased INSL3 and T levels was evidence of Leydig cell function impairment due to BPA. [ABSTRACT FROM AUTHOR]

Peripheral nerve injury (PNI) is a major health problem that results in loss of motor and sensory functions. In treatment of PNI, various methods such as anastomosis, nerve grafts, nonneural tissue grafts, and nerve conduits are applied. In the present study, it was aimed to investigate the effects of Theranekron and Alpha-lipoic acid (ALA) combined treatment on nerve healing in experimental PNI by using histomorphometric, electron microscopic, immunohistochemical and molecular biological methods. Sixty-two Wistar rats were divided into six groups; the normal control group, sham operation group, experimental control group having a crush type injury with no treatment, Theranekron treatment group, ALA treatment group and Theranekron+ALA combined treatment group. Sciatic nerve tissue samples were obtained on days 1, 7 and 14 following injury in all groups. GAP-43 expression was upregulated in all PNI received groups compared to the control group. Krox-20 expression was downregulated in all groups that received PNI compared to the control group. While intensely positive TNF-α and IL-6 expressions were observed up to the 1st to the 14th day for the experimental control group, these expressions were seen as "weakly positive" in the treatment groups from the 1st day to the 14th day. The number of myelinated fibers was higher in the control and sham operation groups. Additionally, the number of myelinated nerve fibers increased in the combined treatment group. In conclusion, these findings suggest that combined therapy of Theranekron and ALA promotes structural recovery and it should be considered as an effective treatment protocol following PNI. [ABSTRACT FROM AUTHOR]

Peripheral nerve injuries (PNI) are an important health problem in the world. In this study, the effects of nerve growth factor (NGF) and betamethasone on nerve regeneration after sciatic nerve crush injury were examined by footprint analysis, electron microscopic, histomorphometric, and biochemical methods. Fifty Wistar rats were divided into five groups as intact control, experimental control, NGF, betamethasone, and NGF+betamethasone combined treatment groups. After the injury, betamethasone was subcutaneously injected into the lesion area of the treatment groups three times during the first day. NGF was subcutaneously injected into the lesion area of treatment groups for 14 days. Footprint analysis was made on 7, 14, 21, 28, and 35 days and after 6 weeks, tissue samples were obtained from all groups. In the experimental control group, there were severe degenerative changes in most of the axons and myelin sheaths of the nerve fibers. Moreover, an increase of MDA levels and a decrease in SOD activities were found in this group. On the other hand, malondialdehyde (MDA) levels decreased, superoxide dismutase (SOD) activities increased and significant motor functional recovery were found in the combined treatment group. The number of axons, axon diameters, and myelin thickness were significantly greater in the combined treatment group when compared with experimental control and other treatment groups. It was thought that nerve regenerative effects of NGF and anti-inflammatory and/or anti-edematous effects of betamethasone could induce functional recovery in the combined treatment group. In conclusion, combined therapy of NGF and betamethasone may be an effective approach for the treatment of PNI. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study was to investigate miR-20a expression in glioblastoma cell line (U87) after applying cyclopamine and temozolomide (TMZ) treatment separately and in combination and to evaluate the efficiency of miR-20a in glioblastoma treatment. Materials and Methods: U87 MG was placed on a 35 mm culture dish before treatment. Within the scope of the study, 7 groups were formed: Group 1: Control group, Group 2: Sham group (Dimethyl sulfoxide), Group 3: 2 Days TMZ, Group 4: 5 Days TMZ, Group 5: 3 Hours Cyclopamine, Group 6: 2 Days TMZ + 3 Hours Cyclopamine, Group 7: 5 Days TMZ + 3 Hours Cyclopamine Total miRNA isolation and qRT-PCR was performed after treatment. Results: MiR-20a expression in the glioblastoma cell line was found to be significantly decreased in group 3, group 4, group 5, group 6 and group 7. However, it was determined that this decrease was highest in group 7. In addition, it was observed that the number of cells decreased in group 7. Conclusion: MiR-20a is highly expressed in glioblastoma cells; however, it was determined that the expressions decreased after Cyclopamine and TMZ treatments. miR- 20a can be used as a new therapeutic target and biomarker for glioblastoma, Cyclopamine and TMZ can be used for treatment in glioblastoma, but further studies are needed on this subject. [ABSTRACT FROM AUTHOR]