17 beta-estradiol oxidative stress attenuation and autophagy-induced dopaminergic neuroprotection

Objective: Degeneration of dopaminergic neurons in the substantia nigra of the brain stem is the main pathological aspect of Parkinson's disease [PD]. 17 beta-estradiol [E2] has neuroprotective effects on substantia nigra, however, the underlined mechanism is not well-known. In this study, we evaluated the neuroprotective effects of E2 in the ovariectomized 6-hydroxydopamine- [6-OHDA] rat model of PD

Materials and Methods: In this experimental study, all animals were ovariectomized to avoid any further bias in E2 levels and then these ovariectomized rats were randomly assigned into three experimental groups [10 rats in each group]: ovariectomized control group [OCG], ovariectomized degeneration group receiving 25 µg of 6-OHDA into the left corpus striatum [ODG], and ovariectomized E2 pretreatment group pretreated with 0.1 mgkg-1of 17 beta-estradiol for three days prior to the destruction of corpus striatum with 6-OHDA [OE2PTG]. The apomorphine behavioral test and Nissl staining were performed in all experimental groups. The expressions of Sequestosome-1 [P62], Unc- 51 like autophagy activating kinase [Ulk1], and microtubule-associated proteins 1A/1B light chain 3B [Lc3] genes were evaluated using reverse transcription- polymerase chain reaction [RT-PCR]

Results: E2 administration reduced the damages to the dopaminergic neurons of the substantia nigra. The motor behavior, the number of rotations, and histological tests in the treatment group showed the cell survival improvement in comparison with the control groups indicating that E2 can inhibit the neurodegeneration. P62 and Lc3 were expressed in all experimental groups while Ulk1 was not expressed in ODG group. Moreover, Ulk1 was expressed after the treatment with E2 in OE2PTG group

Conclusion: E2 prevents neurodegeneration in dopaminergic neurons of the midbrain by over-expression of Ulk1 gene and augmenting the induction of autophagy

Di-[2-ethylhexyl] phthalate-induced hippocampus-derived neural stem cells proliferation

The brain and spinal cord have a limited capacity for self-repair under damaged conditions. One of the best options to overcome these limitations involves the use of phytochemicals as potential therapeutic agents. In this study, we have aimed to investigate the effects of di-[2-ethylhexyl] phthalate [DEHP] on hippocampus-derived neural stem cells [NSCs] proliferation to search phytochemical candidates for possible treatment of neurological diseases using endogenous capacity. In this experimental study, neonatal rat hippocampus-derived NSCs were cultured and treated with various concentrations of DEHP [0, 100, 200, 400 and 600 micro M] and Cirsium vulgare [C. vulgare] hydroethanolic extract [0, 200, 400, 600, 800 and 1000 micro g/ml] for 48 hours under in vitro conditions. Cell proliferation rates and quantitative Sox2 gene expression were evaluated using MTT assay and real-time reverse transcription polymerase chain reaction [RT-PCR]. We observed the highest average growth rate in the 400 micro M DEHP and 800 micro g/ml C. vulgare extract treated groups. Sox2 expression in the DEHP-treated NSCs significantly increased compared to the control group. Gas chromatography/mass spectrometry [GC/ MS] results demonstrated that the active ingredients that naturally occurred in the C. vulgare hydroethanolic extract were 2-ethyl-1-hexanamine, n-heptacosane, 1-cyclopentanecarboxylic acid, 1-heptadecanamine, 2,6-octadien-1-ol,2,6,10,14,18,22-tetracosahexaene, and DEHP. DEHP profoundly stimulated NSCs proliferation through Sox2 gene overexpression. These results provide and opportunity for further use of the C. vulgure phytochemicals for prevention and/or treatment of neurological diseases via phytochemical mediated-proliferation of endogenous adult NSCs

Molecular and parasitological study of cryptosporidium isolates from cattle in Ilam, west of Iran

Cryptosporidiosis is one of the most important parasitic infections in human and animals. This study was designed for survey on the prevalence of Cryptosporidium infection in farms of Ilam, west of Iran, using parasitology method and genotyping by Nested PCR-RFLP. Fecal samples of 217 cattle were collected fresh and directly from the rectum of cattle. All of the samples were examined by microscopic observation after staining with modified Ziehl-Neelsen [MZN]. Genomic DNA extracted by using EURx DNA kit. A Nested PCR-RFLP protocol amplifying 825 bp fragment of 18s rRNA gene conducted to differentiate species and genotyping of the isolates using SspI and VspI as restriction enzymes. The prevalence of Cryptosporidium infection in cattle using both methods is 3.68%. Most of the positive cattle were calves under six months. Species diagnosis carried out by digesting the secondary PCR product with SspI that C. parvum generated 3 visible bands of 448, 247 and 106 bp and digested by VspI restriction enzyme generated 2 visible bands of 628 and 104bp. In this investigation all of the positive samples were Cryptosporidium parvum. C. parvum [bovine genotype] detected in all positive cattle samples in Ilam, west of Iran. The results of the present study can help for public health care systems to prevention and management of cryptosporidiosis in cattle and the assessment of cattle cryptosporidiosis as a reservoir for the human infection

Hypopituitarism in a neonate with hyperbilirubinemia and decreased level of consciousness: a case report study

Decreased level of consciousness in neonates may result from different etiologies, including rare metabolic and hormonal disorder due to anterior pituitary insufficiency. In this case report, a five-day-old newborn boy was referred to the neonatal intensive care unit of Mustafa Khomeini hospital of Ilam, Iran. He had an open anterior fontanel with no history of prenatal and familial diseases. Clinical examination showed decreased level of consciousness so that this patient responded only to painful stimuli. Furthermore, unconsciousness, hyperbilirubinemia, and hypotonia were fully evident. Given the clinical findings and decreased level of consciousness, hormonal diagnostic tests and brain CT scan were performed for any evidence of hypopituitarism. Clinical and experimental findings were consistent with the generalized edema and pituitary insufficiency secondary to central hypothyroidism and cortisol deficiency. Based on the findings, the neonate was put on the hormonal replacement therapy and, as the result, all of the abnormal clinical symptoms disappeared. In conclusion, fatal neonatal diseases may be mistaken with unimportant clinical findings at the first examination. Therefore, comprehensive attention to all potential causes of such symptoms in the neonates should be given for early diagnosis and treatment, and to prevent any fatal and irreversible complications