The quality of mental health status in pregnancy and it's contributing factors on women visiting the health care centers of Shahrekord,(2001-2002)

Abstract There are many psychological and physiological changes during pregnancy and postpartum periods that are sometimes they become pathologic. Thus, it is necessary for a medical team to identify those patients and their families who have a predisposition to mental disorders and to guide them through this period. Aimed at assessing the prevalence and predisposing factors of mental disorders during pregnancy, an analytical-descriptive and cross-sectional study was performed on 267 pregnant women. The data were

Development of Hartmann screen test for measurement of stress during thin film deposition

The Hartmann screen test (HST) is a well-known technique that has been used for many years in optical metrology. This thesis describes how the technique has been adapted to create a system for continuous in situ monitoring of the internal stress in thin films during plasma deposition. Stress is almost always present in thin films. Stress can affect the physical properties of film, and also influence phenomena which are important in the technology of thin film manufacture such as adhesion and crystallographic defects. For these reasons, it is very important to control and manage the film stress during manufacture of devices based on thin films. The commonest way to infer stress is to measure the change in substrate curvature that it produces. This is often done by comparison of substrate curvatures before and after deposition with surface profilometry, or interferometry. However, these methods are unsuitable for implementing during film deposition in the vacuum chamber. A novel method for measuring changes in curvature of the thin film substrate in situ has been developed, making use of the HST. An expanded laser beam is passed through a screen containing a number of small apertures, which breaks it up into several rays. After reflecting from the surface of the thin film wafer, the rays are received on an array detector as a spot pattern. Image processing is performed on the recorded spot images to determine the positions of spots accurately. Spot centre positions are recorded at start of deposition as a reference, then their displacement is tracked with time during deposition. The spot deflections are fitted to a theoretical model, in which the change in sample profile is described by a second-order surface. The principal axes of curvature of this surface and their orientation are obtained by a least-squares fitting procedure. From this, the thin film stress can be inferred and monitored in real time. Equipment using this technique has been designed and developed in prototype form for eventual use in the RMIT cathodic arc deposition facility. First experiments with a classic Hartmann screen configuration proved that the technique gave good results, but precision was limited by diffraction and interference effects in the recorded image which made determination of spot centres more difficult. A modified configuration was developed, in which a camera is focused on the Hartmann screen, giving much sharper spot patterns and improved resolution. Tests on the prototype system and comparison with other techniques have shown that it is possible to determine changes in sample curvature with a precision of approximately 0.01 m-1. This corresponds to stress changes of around 0.5 GPa for typical wafer and film thicknesses used in practice. The Hartmann screen test is straightforward to use and to interpret. Image processing and analysis of the recorded spot patterns can be automated and performed continuously in real time during thin film deposition. The system promises to be very useful for monitoring stress and thus controlling the deposition process for improved quality of thin film manufacture

Molecular detection of Neospora caninum from naturally infected dogs in Lorestan province, West of Iran Dalimi 1

ABSTRACT Neospora caninum is a coccidian protozoan that causes abortion in dairy and beef cattle and neurological disorders in dogs and horses. To identify N. caninum oocysts in the dog feces the molecular approaches are known as sensitive methods that specifically detect the oocysts. In present study, a polymerase chain reaction (PCR) targeting N. caninum specific Nc5 genomic fragment was performed to identify the N. caninum DNA in the feces of naturally infected dogs of Lorestan province, West Iran. Fecal samples of dogs living in small dairy farms were collected. The samples were homogenized in 2.5% Potassium dichromate (K2Cr2O7) and stored at 4 °C. Genomic DNA was extracted from the feces using CTAB protocol. PCR assay and DNA sequencing were performed with specific primers. DNA amplification of the Nc5 formed a 340bp fragment for the N. caninum specimens; however, the fragment was 99% identical to the homologous sequences from Neospora caninum isolates. Totally, 9 positive samples of N. caninum were detected by PCR from 428 fecal specimens

Designer Exosomes: A New Platform for Biotechnology Therapeutics

Abstract: Desirable features of exosomes have made them a suitable manipulative platform for biomedical applications, including targeted drug delivery, gene therapy, cancer diagnosis and therapy, development of vaccines, and tissue regeneration. Although natural exosomes have various potentials, their clinical application is associated with some inherent limitations. Recently, these limitations inspired various attempts to engineer exosomes and develop designer exosomes. Mostly, designer exosomes are being developed to overcome the natural limitations of exosomes for targeted delivery of drugs and functional molecules to wounds, neurons, and the cardiovascular system for healing of damage. In this review, we summarize the possible improvements of natural exosomes by means of two main approaches: parental cell-based or pre-isolation exosome engineering and direct or post-isolation exosome engineering. Parental cell-based engineering methods use genetic engineering for loading of therapeutic molecules into the lumen or displaying them on the surface of exosomes. On the other hand, the post-isolation exosome engineering approach uses several chemical and mechanical methods including click chemistry, cloaking, bio-conjugation, sonication, extrusion, and electroporation. This review focuses on the latest research, mostly aimed at the development of designer exosomes using parental cell-based engineering and their application in cancer treatment and regenerative medicine. Graphic Abstract: Figure not available: see fulltext. © 2020, Springer Nature Switzerland AG

Mechanism Underlying Defective Interferon Gamma-Induced IDO Expression in Non-obese Diabetic Mouse Fibroblasts

Indoleamine 2,3-dioxygenase (IDO) can locally suppress T cell-mediated immune responses. It has been shown that defective self-tolerance in early prediabetic female non-obese diabetic (NOD) mice can be attributed to the impaired interferon-gamma (IFN-γ)- induced IDO expression in dendritic cells of these animals. As IFN-γ can induce IDO in both dendritic cells and fibroblasts, we asked the question of whether there exists a similar defect in IFN-γ-induced IDO expression in NOD mice dermal fibroblasts. To this end, we examined the effect of IFN-γ on expression of IDO and its enzymatic activity in NOD dermal fibroblasts. The results showed that fibroblasts from either prediabetic (8 wks of age) female or male, and diabetic female or male (12 and 24 wks of age respectively) NOD mice failed to express IDO in response to IFN-γ treatment. To find underlying mechanisms, we scrutinized the IFN- γ signaling pathway and investigated expression of other IFN-γ-modulated factors including major histocompatibility complex class I (MHC-I) and type I collagen (COL-I). The findings revealed a defect of signal transducer and activator of transcription 1 (STAT1) phosphorylation in NOD cells relative to that of controls. Furthermore, we found an increase in MHC-I and suppression of COL-I expression in fibroblasts from both NOD and control mice following IFN-γ treatment; indicating that the impaired response to IFN-γ in NOD fibroblasts is specific to IDO gene. Finally, we showed that an IFN-γ-independent IDO expression pathway i.e. lipopolysaccharide (LPS)-mediated-c-Jun kinase is operative in NOD mice fibroblast. In conclusion, the findings of this study for the first time indicate that IFN-γ fails to induce IDO expression in NOD dermal fibroblasts; this may partially be due to defective STAT1 phosphorylation in IFN-γ-induced-IDO signaling pathway

An Observational Cohort Study of the Kynurenine to Tryptophan Ratio in Sepsis: Association with Impaired Immune and Microvascular Function

Both endothelial and immune dysfunction contribute to the high mortality rate in human sepsis, but the underlying mechanisms are unclear. In response to infection, interferon-γ activates indoleamine 2,3-dioxygenase (IDO) which metabolizes the essential amino acid tryptophan to the toxic metabolite kynurenine. IDO can be expressed in endothelial cells, hepatocytes and mononuclear leukocytes, all of which contribute to sepsis pathophysiology. Increased IDO activity (measured by the kynurenine to tryptophan [KT] ratio in plasma) causes T-cell apoptosis, vasodilation and nitric oxide synthase inhibition. We hypothesized that IDO activity in sepsis would be related to plasma interferon-γ, interleukin-10, T cell lymphopenia and impairment of microvascular reactivity, a measure of endothelial nitric oxide bioavailability. In an observational cohort study of 80 sepsis patients (50 severe and 30 non-severe) and 40 hospital controls, we determined the relationship between IDO activity (plasma KT ratio) and selected plasma cytokines, sepsis severity, nitric oxide-dependent microvascular reactivity and lymphocyte subsets in sepsis. Plasma amino acids were measured by high performance liquid chromatography and microvascular reactivity by peripheral arterial tonometry. The plasma KT ratio was increased in sepsis (median 141 [IQR 64–235]) compared to controls (36 [28–52]); p<0.0001), and correlated with plasma interferon-γ and interleukin-10, and inversely with total lymphocyte count, CD8+ and CD4+ T-lymphocytes, systolic blood pressure and microvascular reactivity. In response to treatment of severe sepsis, the median KT ratio decreased from 162 [IQR 100–286] on day 0 to 89 [65–139] by day 7; p = 0.0006) and this decrease in KT ratio correlated with a decrease in the Sequential Organ Failure Assessment score (p<0.0001). IDO-mediated tryptophan catabolism is associated with dysregulated immune responses and impaired microvascular reactivity in sepsis and may link these two fundamental processes in sepsis pathophysiology

Fibroblast cell-based therapy prevents induction of alopecia areata in an experimental model

YesAlopecia areata (AA) is an autoimmune hair loss disease with infiltration of proinflammatory cells into hair follicles. Current therapeutic regimens are unsatisfactory mainly because of the potential for side effects and/or limited efficacy. Here we report that cultured, transduced fibroblasts, which express the immunomodulatory molecule indoleamine 2,3-dioxygenase (IDO), can be applied to prevent hair loss in an experimental AA model. A single intraperitoneal (IP) injection of IDO-expressing primary dermal fibroblasts was given to C3H/HeJ mice at the time of AA induction. While 60–70% of mice that received either control fibroblasts or vehicle injections developed extensive AA, none of the IDO-expressing fibroblast-treated mice showed new hair loss up to 20 weeks post injection. IDO cell therapy significantly reduced infiltration of CD4+ and CD8+ T cells into hair follicles and resulted in decreased expression of TNF-α, IFN-γ and IL-17 in the skin. Skin draining lymph nodes of IDO fibroblast-treated mice were significantly smaller, with more CD4+ CD25+ FoxP3+ regulatory T cells and fewer Th17 cells than those of control fibroblast and vehicle-injected mice. These findings indicate that IP injected IDO-expressing dermal fibroblasts can control inflammation and thereby prevent AA hair loss.Canadian Institutes of Health Researches (Funding Reference Number: 134214 and 136945)