Enriched Environment Contributes to the Recovery from Neurotoxin-Induced Parkinson's Disease Pathology.

Parkinson's disease (PD) is a neurological disorder that affects dopaminergic neurons. The lack of understanding of the underlying molecular mechanisms of PD pathology makes treating it a challenge. Several pieces of evidence support the protective role of enriched environment (EE) and exercise on dopaminergic neurons.

Synergistic effect of CaCO addition and in-process cold atmospheric plasma treatment on the surface evolution, mechanical properties, and in-vitro degradation behavior of FDM-printed PLA scaffolds.

The ease of processing and biocompatibility of polylactic acid (PLA) have made it a widely used material for fused deposition modeling (FDM)-based 3D printing. In spite of this, PLA suffers from some limitations for its extensive use in tissue engineering applications, including poor wettability, low degradation rate, and insufficient mechanical properties. To address the previously mentioned limitations, this study examined how combining in-process cold atmospheric plasma treatment with the inclusion of CaCO influences the properties of FDM-printed PLA scaffolds.

Material extrusion additive manufacturing of poly(lactic acid)/Ti6Al4V@calcium phosphate core-shell nanocomposite scaffolds for bone tissue applications.

The use of porous scaffolds with appropriate mechanical and biological features for the host tissue is one of the challenges in repairing critical-size bone defects. With today's three-dimensional (3D) printing technology, scaffolds can be customized and personalized, thereby eliminating the problems associated with conventional methods. In this work, after preparing Ti6Al4V/Calcium phosphate (Ti64@CaP) core-shell nanocomposite via a solution-based process, by taking advantage of fused deposition modeling (FDM), porous poly(lactic acid) (PLA)-Ti64@CaP nanocomposite scaffolds were fabricated.

Improving physio-mechanical and biological properties of 3D-printed PLA scaffolds via in-situ argon cold plasma treatment.

As a bone tissue engineering material, polylactic acid (PLA) has received significant attention and interest due to its ease of processing and biocompatibility. However, its insufficient mechanical properties and poor wettability are two major drawbacks that limit its extensive use. For this purpose, the present study uses in-situ cold argon plasma treatment coupled with a fused deposition modeling printer to enhance the physio-mechanical and biological behavior of 3D-printed PLA scaffolds.

Enhanced bone tissue regeneration using a 3D-printed poly(lactic acid)/Ti6Al4V composite scaffold with plasma treatment modification.

The mechanical and biological properties of polylactic acid (PLA) need to be further improved in order to be used for bone tissue engineering (BTE). Utilizing a material extrusion technique, three-dimensional (3D) PLA-Ti6Al4V (Ti64) scaffolds with open pores and interconnected channels were successfully fabricated. In spite of the fact that the glass transition temperature of PLA increased with the addition of Ti64, the melting and crystallization temperatures as well as the thermal stability of filaments decreased slightly.

DNA sequencing validation by PCR-RFLP for evaluating butyrophilin-like 2 rs2076530 polymorphism in Iranian patients with sarcoidosis.

Background: Sarcoidosis is a multifactorial immune disorder with an uncertain origin. A single nucleotide polymorphism (G→A, rs2076530) in the butyrophilin-like 2 (BTNL2) gene results in the formation of truncating protein. This study aimed to genotype the predisposition of the BTNL2 rs2076530 polymorphism in Iranian patients with sarcoidosis using the RFLP technique.

Investigation of the affective factors on the survival rate of patients with laryngeal cancer using Cox proportional hazards and Lin -Ying's additive hazards models.

Determining the factors affecting survival and appropriate treatment methods leads to improving the survival rate and quality of life in cancer patients; therefore this study was aimed to determine the effective factors on the survival rate of patients with Laryngeal cancer in Kerman city, Iran. This retrospective cohort study included 370 patients with Laryngeal cancer who referred to the hospitals of Kerman city, Iran during 2008 to 2018. Data were analyzed using Cox Proportional Hazards and Lin-Ying's Additive Hazards models.

Insertion/Deletion Polymorphisms and Serum Angiotensin-converting Enzyme Levels in Iranian Patients with Sarcoidosis.

Background: Sarcoidosis is a multisystem inflammatory disease of unknown origin with characterization of small granulomas. Angiotensin-converting enzyme (ACE) is a pathophysiologic marker of sarcoidosis. We present the ACE insertion/deletion (I/D) polymorphism in correlation with serum ACE level in Iranian patients with sarcoidosis.

Upregulation of STREX splice variant of the large conductance Ca2+-activated potassium (BK) channel in a rat model of mesial temporal lobe epilepsy.

Functional properties of large conductance Ca(2+) activated potassium (BK) channels are determined by complex alternative splicing of the Kcnma1 gene encoding the alpha pore-forming subunit. Inclusion of the STREX exon in a C-terminal splice site is dynamically regulated and confers enhanced Ca(2+) sensitivity and channel inhibition via cAMP-dependent phosphorylation. Here, we describe a real time quantitative PCR (qPCR) approach to investigate relative changes in the expression of STREX and ZERO splice variants using a newly designed set of probes and primers for TaqMan-based qPCR analysis of cDNA from the rat dentate gyrus at different time points following pilocarpine-induced status epilepticus.

Deficit of Kcnma1 mRNA expression in the dentate gyrus of epileptic rats.

Epileptogenesis in mesial temporal lobe epilepsy is determined by several factors including abnormalities in the expression and function of ion channels. Here, we report a long-lasting deficit in gene expression of Kcnma1 coding for the large-conductance calcium-activated potassium (BK, MaxiK) channel alpha-subunits after pilocarpine-induced status epilepticus. By using comparative real-time PCR, Taqman gene expression assays, and the delta-delta comparative threshold method we detected a significant reduction in Kcnma1 expression in microdissected dentate gyrus at different intervals after status epilepticus (24 h, 10 days, 1 month, and more than 2 months).

Differential changes in mGlu2 and mGlu3 gene expression following pilocarpine-induced status epilepticus: a comparative real-time PCR analysis.

Group II metabotropic glutamate (mGlu II) receptors subtype 2 and 3 (mGlu2 and mGlu3) are subtle regulators of neuronal excitability and synaptic plasticity in the hippocampus. In recent years, researchers have investigated the potential neuroprotective and anticonvulsant effects of compounds acting on mGlu II receptors. However, abnormal expression and function of mGlu2 and mGlu3 have been reported in temporal lobe epilepsy, a phenomena that may limit the therapeutic effectiveness of these potentially new antiepileptic drugs.

Down-regulation of BK channel expression in the pilocarpine model of temporal lobe epilepsy.

In the hippocampus, BK channels are preferentially localized in presynaptic glutamatergic terminals including mossy fibers where they are thought to play an important role regulating excessive glutamate release during hyperactive states. Large conductance calcium-activated potassium channels (BK, MaxiK, Slo) have recently been implicated in the pathogenesis of genetic epilepsy. However, the role of BK channels in acquired mesial temporal lobe epilepsy (MTLE) remains unknown.

Abnormal mGluR2/3 expression in the perforant path termination zones and mossy fibers of chronically epileptic rats.

Epilepsy is characterized by hyperexcitability of hippocampal networks, excessive release of glutamate, and progressive neurodegeneration. Presynaptic group II metabotropic receptors (mGluR2 and mGluR3) are among different mechanisms that modulate presynaptic release of glutamate, especially at the mossy fibers in the hippocampus. Here, we explore whether mGluR2/3 expression is affected in a rat model of temporal lobe epilepsy obtained via pilocarpine-induced status epilepticus (SE).

Coupling of c-Src to large conductance voltage- and Ca2+-activated K+ channels as a new mechanism of agonist-induced vasoconstriction.

The voltage-dependent and Ca(2+)-activated K(+) channel (MaxiK, BK) and the cellular proto-oncogene pp60(c-Src) (c-Src) are abundant proteins in vascular smooth muscle. The role of MaxiK channels as a vasorelaxing force is well established, but their role in vasoconstriction is unclear. Because Src participates in regulating vasoconstriction, we investigated whether c-Src inhibits MaxiK as a mechanism for agonist-induced vasoconstriction.