Self-esteem and optimism in patients with major depression disorder: a cross-sectional study.

Background: Depressive disorders are common mental illnesses characterized by persistent feelings of sadness, hopelessness, and loss of interest in activities. Self-esteem refers to the appraisal of one's worth and personality, whereas optimism reflects a positive attitude and the expectation of positive outcomes. Therefore, the present study aims to determine the average self-esteem and optimism of patients with depression in 2022. Methods: The present study is a single center and prospective descriptive-analytical study in which 121 patients out of 154 participants with major depression using convenience sampling were studied. Recruitment started on 10 June 2022 and ended on 12 July 2022. Data were collected using a demographic questionnaire, the Rosenberg Self-Esteem Scale (RSES), and the Revised Life Orientation Test (LOT -R). Data analysis was performed using statistical tests and the Pearson correlation coefficient with SPSS software version 21. Results: The mean and SD of patients' self-esteem scores were 14.68±1.30, and the mean and SD for optimism scores were 9.90±1.68. Pearson correlation analysis showed that educational level had a significant inverse relationship with patients' self-esteem scores (r=-0.009, P=0.03), and sex had a significant relationship with patients' optimism scores (r=0.175, P=0.008). Conclusion: Considering the importance of self-esteem and optimism in the recovery and return to society of patients with major depression, it is necessary to take measures to strengthen and increase self-esteem and optimism in these patients.

Frequency of Human Platelet Antigens -1 to -5 and -15 in Turkmen Blood Donors.

Background: Due to the presence of platelet antigen polymorphisms, human platelet membrane glycoproteins can be identified as an alloantigen or autoantigen. The aim of this study was to determine the frequencies of human platelet antigens (HPAs)-1 to-5 and-15 in Turkmen blood donors and establish a panel of accredited HPAs negative donors as well as an HPA-typed platelet donor registry. Materials and Methods: HPA-1 to-5 and-15 typing was performed by the polymerase chain reaction-sequence-specific primer techniques on 80 unrelated Turkmen donors who were referred to Aq-Qala Blood Transfusion Center in Golestan Province from September 2018 to October 2019. Results: The frequencies of HPA phenotypes were determined as follows: HPA-1aa: 92.5%, HPA-1ab: 7.5%, HPA-2aa: 77.5%, HPA-2ab: 20.0%, HPA-2bb: 2.5%, HPA-3aa: 75.3%, HPA-3ab: 50%, HPA-3bb: 11.2%, HPA-4aa: 100%, HPA-5aa: 78.5%, HPA-5ab: 21.5%, HPA-15aa: 41.2%, HPA-15ab: 56.2% and HPA-15bb: 17.5%. Conclusion: Determining the genotype of HPAs that play an important role in platelet refractory can improve the management of alloimmunization due to the incompatibility of HPAs between the recipients and donors. Therefore, the registration process for national platelet donors can help patients accelerate and improve the quality of transfused platelets.

Synergistic Effects of PI3K Inhibition on Arsenic Trioxide Cytotoxicity in Acute Promyelocytic Leukemia Cells: A New Portrait of Idelalisib as an Adjuvant Therapy.

The advent of small-molecule inhibitors targeting the components of oncogenic signaling pathways has revolutionized cancer treatment, where the pharmacological approaches have gone from an era of non-specific chemotherapeutic drugs to the golden age of targeted therapies. In the present study, we evaluated the therapeutic value of an isoform-specific inhibitor of PI3K (Idelalisib) in potentiating the anti-leukemic effects of arsenic trioxide (ATO), an eminent drug used in the treatment of acute promyelocytic leukemia (APL). We found that the abrogation of the PI3K axis profoundly reinforced the anti-leukemic effects of the lower concentrations of ATO, as revealed by the superior reduction in the viability, cell number, and metabolic activity of APL-derived NB4 cells as compared to either agent alone. The cytotoxic effect of Idelalisib in combination with ATO was probably mediated through suppression of c-Myc that was coupled with the elevation in the intracellular level of reactive oxygen species and induction of caspase-3-dependent apoptosis. Notably, our results showed that the suppression of autophagy reinforced the ability of the drugs in eradicating the leukemic cells, suggesting that the compensatory activation of this system may probably overshadow the success of Idelalisib-plus-ATO in APL cells. All in all and given the significant efficacy of Idelalisib against NB4 cells, we proposed the application of this PI3K inhibitor as a foreseeable approach with a safe profile in the treatment of APL.

Major histocompatibility complex (MHC) antigens polymorphism and alloimmunization study in thalassemia patients with febrile non-hemolytic transfusion reaction (FNHTR).

OBJECTIVES: HLA alloimmunization is one of the most troublesome consequence of regular transfusion which is itself a mainstay measure to provide longevity to the thalassemia patients. Febrile non-hemolytic transfusion reaction (FNHTR) is one of the most common complication which might be related to the HLA alloimmunization. Here, we studied the HLA antigenic system and alloimmunization rate in the Iranian ß-thalassemia patients who suffered from FNHTR compare to the ß-thalassemia patients without FNHTR. MATERIALS & METHODS: Total of 60 ß-thalassemia patients with FNHTR (case group) and 20 ß-thalassemia patients without FNHTR (control group) randomly have been selected and enrolled in the study. All were tested for HLA-A and -B loci by PCR-SSP method and also for the presence of anti-lymphocyte antibodies by LIFT method. Comparisons between two groups were performed by Pearson's χ2 test. RESULTS: Totally, a significant predominance was noted for two HLA alleles, HLA-A*24 (P = 0.029) and B*55 (P = 0.034) which have higher prevalence in control group. Although no significant association was found between the presence of anti-leukocyte antibodies and the development of FNHTR, the HLA-A*32 (P = 0.047) allele was considered as possible genetic markers in the susceptibility to the development of anti-leukocyte antibodies. CONCLUSION: Here some evidences about the possible role of HLA polymorphism in susceptibility to FNHTR are provided. Those results indicated that HLA-A*24 and HLA-B*55 might play protective role on inducing FNHTR in ß-thalassemia patients. Further studies which investigate the allele level of HLA-I alongside with specific reactivity of HLA-I antibodies might reveal more deep data about these phenomena.

Putative RNA Ligase RtcB Affects the Switch between T6SS and T3SS in Pseudomonas aeruginosa.

The opportunistic pathogen Pseudomonas aeruginosa is a significant cause of infection in immunocompromised individuals, cystic fibrosis patients, and burn victims. To benefit its survival, the bacterium adapt to either a motile or sessile lifestyle when infecting the host. The motile bacterium has an often activated type III secretion system (T3SS), which is virulent to the host, whereas the sessile bacterium harbors an active T6SS and lives in biofilms. Regulatory pathways involving Gac-Rsm or secondary messengers such as c-di-GMP determine which lifestyle is favorable for P. aeruginosa. Here, we introduce the RNA binding protein RtcB as a modulator of the switch between motile and sessile bacterial lifestyles. Using the wild-type P. aeruginosa PAO1, and a retS mutant PAO1(∆retS) in which T3SS is repressed and T6SS active, we show that deleting rtcB led to simultaneous expression of T3SS and T6SS in both PAO1(∆rtcB) and PAO1(∆rtcB∆retS). The deletion of rtcB also increased biofilm formation in PAO1(∆rtcB) and restored the motility of PAO1(∆rtcB∆retS). RNA-sequencing data suggested RtcB as a global modulator affecting multiple virulence factors, including bacterial secretion systems. Competitive killing and infection assays showed that the three T6SS systems (H1, H2, and H3) in PAO1(∆rtcB) were activated into a functional syringe, and could compete with Escherichia coli and effectively infect lettuce. Western blotting and RT-PCR results showed that RtcB probably exerted its function through RsmA in PAO1(∆rtcB∆retS). Quantification of c-di-GMP showed an elevated intracellular levels in PAO1(∆rtcB), which likely drove the switch between T6SS and T3SS, and contributed to the altered phenotypes and characteristics observed. Our data demonstrate a pivotal role of RtcB in the virulence of P. aeruginosa by controlling multiple virulence determinants, such as biofilm formation, motility, pyocyanin production, T3SS, and T6SS secretion systems towards eukaryotic and prokaryotic cells. These findings suggest RtcB as a potential target for controlling P. aeruginosa colonization, establishment, and pathogenicity.

Anti-tumor activity of PI3K-δ inhibitor in hematologic malignant cells: Shedding new light on resistance to Idelalisib.

Genetic and laboratory experiments have brought remarkable advances in management of human malignancies, which not only revolutionized the understanding of the disease, but also led to development of novel and effective targeted therapies against specific deregulated pathways. This study aimed to investigate anti-cancer effects of Idelalisib, a potent PI3K-δ inhibitor, in a panel of hematological cell lines. The resulting data showed that Idelalisib decreased cell survival in all the tested cell lines; however, as compared to NB4, viability of other cell lines, irrespective of their molecular characteristics or even the compensatory activation of MEK/ERK pathway, was inhibited at higher concentrations. This study suggests for the first time that there is a significant correlation between relative response to Idelalisib and basal expression levels of anti-apoptotic genes, in particular survivin and MCL-1. Intriguingly, we found that Idelalisib-induced apoptosis in NB4, as the most sensitive cell line with the lowest expression level of the aforementioned genes, is executed probably via alteration in the transcriptional level of apoptosis-related genes coupled with p21-mediated caspase-3 activation. Moreover, the lower concentrations of Idelalisib combined with arsenic trioxide (ATO) produced synergistic anti-cancer effect in APL-derived NB4 cells. Overall, due to the pharmacologic safety of Idelalisib and its broad clinical effectiveness in chronic lymphoproliferative disorders, our study suggests that this inhibitor is a promising agent for the treatment of acute promyelocytic leukemia, either as single agent or in a combined-modality strategy.

Cystic fibrosis lung environment and Pseudomonas aeruginosa infection.

BACKGROUND: The airways of patients with cystic fibrosis (CF) are highly complex, subject to various environmental conditions as well as a distinct microbiota. Pseudomonas aeruginosa is recognized as one of the most important pulmonary pathogens and the predominant cause of morbidity and mortality in CF. A multifarious interplay between the host, pathogens, microbiota, and the environment shapes the course of the disease. There have been several excellent reviews detailing CF pathology, Pseudomonas and the role of environment in CF but only a few reviews connect these entities with regards to influence on the overall course of the disease. A holistic understanding of contributing factors is pertinent to inform new research and therapeutics. DISCUSSION: In this article, we discuss the deterministic alterations in lung physiology as a result of CF. We also revisit the impact of those changes on the microbiota, with special emphasis on P. aeruginosa and the influence of other non-genetic factors on CF. Substantial past and current research on various genetic and non-genetic aspects of cystic fibrosis has been reviewed to assess the effect of different factors on CF pulmonary infection. A thorough review of contributing factors in CF and the alterations in lung physiology indicate that CF lung infection is multi-factorial with no isolated cause that should be solely targeted to control disease progression. A combinatorial approach may be required to ensure better disease outcomes. CONCLUSION: CF lung infection is a complex disease and requires a broad multidisciplinary approach to improve CF disease outcomes. A holistic understanding of the underlying mechanisms and non-genetic contributing factors in CF is central to development of new and targeted therapeutic strategies.

Effect of Argon Laser on Enamel Demineralization around Orthodontic Brackets: An In Vitro Study.

OBJECTIVE: This study was designed to evaluate the effect of argon laser irradiation on development and progress of enamel demineralization around orthodontic brackets. MATERIALS AND METHODS: Fifty caries-free, intact human premolars were randomly assigned to one of the following five equal groups: Groups 1 (control) and 2: The brackets were bonded using conventional halogen light for 40s and argon laser for 10s, respectively. Teeth in group 3 were lased with argon laser for 10s before bracket bonding with halogen light. Group 4 was the same as group 3 except that brackets were also bonded with argon laser. In group 5 samples were bonded conventionally, immersed in an artificial caries solution for two days and then irradiated for 10s with argon laser. All samples were subjected to demineralization by artificial caries solution for 10 days. After bracket removal, samples were buccolingually sectioned and evaluated by polarized light microscopy. Decalcified lesion depth in each section was measured by a trained examiner in a blind fashion. Data were analyzed in SPSS 14 using one-way ANOVA and Tukey's HSD post hoc test. RESULTS: The control group showed the greatest mean lesion depth while group 5 revealed the lowest. The laser-treated groups had significantly lower mean lesion depth compared with the control group (P<0.05) except for group 4 (P=0.192). CONCLUSION: Argon laser irradiation for 10s before or during bracket bonding can increase caries resistance of intact and demineralized enamel.