effects of anemia education using web-based she smart to improve knowledge, attitudes, and practice in adolescent girls

Anemia is a state of hemoglobin levels in the bloodless than normal numbers according to the sex and age group. The impact of anemia in adolescents is a decrease in achievement and learning spirit and can cause symptoms such as paleness, lethargy, decreased appetite, and growth disorders. Anemia has an impact not only on the health of adolescent girls but can have a long impact on the health of the mother and fetus. You can see the influence of anemia education on knowledge, attitudes, and practice. Uses the Pre-experimental method with the design of one group pretest and posttest. Sampling technique using purposive sampling with the number of 47 adolescent girls. The research was conducted at Senior High School 12 Makassar in September-October 2021. Data analysis using the McNemar test. From the results of statistical tests showed that there was an influence on the use of web-based she smart education model on the use of adolescent girls about anemia with p-value = 0.000 (p<0.05), attitude p-value = 0.016 (p<0.05) and action p-value = 0.001 (p<0.05). Anemia education using web-based she smart can improve knowledge, attitudes, and practice before and after an intervention.

Trypanin Disruption Affects the Motility and Infectivity of the Protozoan Trypanosoma cruzi

The flagellum of Trypanosomatids is an organelle that contributes to multiple functions, including motility, cell division, and host–pathogen interaction. Trypanin was first described in Trypanosoma brucei and is part of the dynein regulatory complex. TbTrypanin knockdown parasites showed motility defects in procyclic forms; however, silencing in bloodstream forms was lethal. Since TbTrypanin mutants show drastic phenotypic changes in mammalian stages, we decided to evaluate if the Trypanosoma cruzi ortholog plays a similar role by using the CRISPR-Cas9 system to generate null mutants. A ribonucleoprotein complex of SaCas9 and sgRNA plus donor oligonucleotide were used to edit both alleles of TcTrypanin without any selectable marker. TcTrypanin −/− epimastigotes showed a lower growth rate, partially detached flagella, normal numbers of nuclei and kinetoplasts, and motility defects such as reduced displacement and speed and increased tumbling propensity. The epimastigote mutant also showed decreased efficiency of in-vitro metacyclogenesis. Mutant parasites were able to complete the entire life cycle in vitro; however, they showed a reduction in their infection capacity compared with WT and addback cultures. Our data show that T. cruzi life cycle stages have differing sensitivities to TcTrypanin deletion. In conclusion, additional work is needed to dissect the motility components of T. cruzi and to identify essential molecules for mammalian stages.

Case Report: Persistent Hypogammaglobulinemia More Than 10 Years After Rituximab Given Post-HSCT

Rituximab (RTX) is an anti-CD20 monoclonal antibody that targets B cells—from the immature pre-B-cell stage in the bone marrow to mature circulating B cells—while preserving stem cells and plasma cells. It is used to treat autoimmune diseases, hematological malignancies, or complications after hematopoietic stem cell transplantation (HSCT). Its safety profile is acceptable; however, a subset of patients can develop persistent hypogammaglobulinemia and associated severe complications, especially in pediatric populations. We report the unrelated cases of two young men aged 17 and 22, presenting with persistent hypogammaglobulinemia more than 7 and 10 years after treatment with RTX, respectively, and administered after HSCT for hemolytic anemia and Epstein–Barr virus reactivation, respectively. Both patients’ immunological workups showed low levels of total immunoglobulin, vaccine antibodies, and class switched-memory B cells but an increase in naive B cells, which can also be observed in primary immunodeficiencies such as those making up common variable immunodeficiency. Whole exome sequencing for one of the patients failed to detect a pathogenic variant causing a Mendelian immunological disorder. Annual assessments involving interruption of immunoglobulin replacement therapy each summer failed to demonstrate the recovery of endogenous immunoglobulin production or normal numbers of class switched-memory B cells 7 and 10 years after the patients’ respective treatments with RTX. Although the factors that may lead to prolonged hypogammaglobulinemia after rituximab treatment (if necessary) remain unclear, a comprehensive immunological workup before treatment and long-term follow-up are mandatory to assess long-term complications, especially in children.

ANALISIS HASIL PEMERIKSAAN FISIK DAN LABORATORIUM DEMAM BERDARAH DENGUE DERAJAT I DAN II DI RSUD H. SAHUDIN KUTACANE TAHUN 2021

Dengue fever is a severe fever that is often deadly, caused by a virus, characterized by capillary permeability, hemostasis abnormalities and in severe cases, shock syndrome loss of protein. The disease is divided into several degrees. To ensure patients suffer from DENGUE disease, it is necessary to perform physical and laboratory examinations such as hematology tests. This study aims to analyze the results of physical examinations and laboratories of DBD degrees I and II at H.Sahudin Kutacane Hospital. The study used descriptive methods with a Cross Sectional approach. Accidental sampling and the number of samples obtained is 20 respondents, among others, degrees I and II are 10 respondents. The data collection tool is carried out using observation sheets including demographic data, physical examination of DBD degrees I and II, and normal standard numbers and laboratory examination units of Amanah Kutacane Clinic. The results of research conducted from a physical examination of DBD degrees I and II show signs and symptoms of DENGUD disease that appear differently because in addition to the condition of a person's body response is different, It may also be because it has been given symptomatic and supportive treatment, while the laboratory results of DBD degrees I and II are only platelets whose value is low from normal numbers (150,000-450,000/μl) of 88,500/μl and 42,300/μl respectively and these laboratory results are affected by adequate fluid and oxygen intake and nutritious food intake so as to support proper administration of action/management

Acute and endothelial-specific Robo4 deletion affect hematopoietic stem cell trafficking independent of VCAM1

Hematopoietic stem cell (HSC) trafficking is regulated by a number of complex mechanisms. Among them are the transmembrane protein Robo4 and the vascular cell adhesion molecule, VCAM1. Endothelial VCAM1 is a well-known regulator of hematopoietic cell trafficking, and our previous studies revealed that germline deletion of Robo4 led to impaired HSC trafficking, with an increase in vascular endothelial cell (VEC) numbers and downregulation of VCAM1 protein on sinusoidal VECs. Here, we utilized two Robo4 conditional deletion models in parallel with Robo4 germline knockout mice (R4KO) to evaluate the effects of acute and endothelial cell-specific Robo4 deletion on HSC trafficking. Strikingly similar to the R4KO, the acute deletion of Robo4 resulted in altered HSC distribution between the bone marrow and blood compartments, despite normal numbers of VECs and wild-type levels of VCAM1 cell surface protein on sinusoidal VECs. Additionally, consistent with the R4KO mice, acute loss of Robo4 in the host perturbed long-term engraftment of donor wild-type HSCs and improved HSC mobilization to the peripheral blood. These data demonstrate the significant role that endothelial Robo4 plays in directional HSC trafficking, independent of alterations in VEC numbers and VCAM1 expression.

MyD88-dependent TLR signaling oppositely regulates hematopoietic progenitor and stem cell formation in the embryo

Hemogenic endothelial (HE) cells in the dorsal aorta undergo an endothelial to hematopoietic transition (EHT) to form lympho-myeloid biased progenitors (LMPs), pre-hematopoietic stem cells (pre-HSCs) and adult-repopulating HSCs. These briefly accumulate in intra-arterial hematopoietic clusters (IAHCs) before being released into the circulation. It is generally assumed that the number of IAHC cells correlates with the number of HSCs. Here we show that changes in the number of IAHC cells, LMPs, and HSCs can be uncoupled. Mutations impairing MyD88-dependent toll-like receptor (TLR) signaling decreased the number of IAHC cells and LMPs but increased the number of HSCs in the aorta-gonad-mesonephros region of mouse embryos. TLR4 deficient embryos specified normal numbers of HE cells but the proliferation of IAHC cells was decreased. Loss of MyD88-dependent TLR signaling in innate immune myeloid cells had no effect on IAHC cell numbers. However, TLR4 deletion in endothelial cells recapitulated the phenotype observed with germline deletion, demonstrating that MyD88-dependent TLR signaling in endothelial cells and/or in IAHCs regulates the balance between generating LMPs and HSCs.

Normal Numbers of Stem Cell Memory T Cells Despite Strongly Reduced Naive T Cells Support Intact Memory T Cell Compartment in Ataxia Telangiectasia

Ataxia Telangiectasia (AT) is a rare inherited disorder characterized by progressive cerebellar ataxia, chromosomal instability, cancer susceptibility and immunodeficiency. AT is caused by mutations in the ATM gene, which is involved in multiple processes linked to DNA double strand break repair. Immunologically, ATM mutations lead to hampered V(D)J recombination and consequently reduced numbers of naive B and T cells. In addition, class switch recombination is disturbed resulting in antibody deficiency causing common, mostly sinopulmonary, bacterial infections. Yet, AT patients in general have no clinical T cell associated infections and numbers of memory T cells are usually normal. In this study we investigated the naive and memory T cell compartment in five patients with classical AT and compared them with five healthy controls using a 24-color antibody panel and spectral flow cytometry. Multidimensional analysis of CD4 and CD8 TCRαβ+ cells revealed that early naive T cell populations, i.e. CD4+CD31+ recent thymic emigrants and CD8+CCR7++CD45RA++ T cells, were strongly reduced in AT patients. However, we identified normal numbers of stem cell memory T cells expressing CD95, which are antigen-experienced T cells that can persist for decades because of their self-renewal capacity. We hypothesize that the presence of stem cell memory T cells explains why AT patients have an intact memory T cell compartment. In line with this novel finding, memory T cells of AT patients were normal in number and expressed chemokine receptors, activating and inhibitory receptors in comparable percentages as controls. Comparing memory T cell phenotypes by Boolean gating revealed similar diversity indices in AT compared to controls. We conclude that AT patients have a fully developed memory T cell compartment despite strongly reduced naive T cells. This could be explained by the presence of normal numbers of stem cell memory T cells in the naive T cell compartment, which support the maintenance of the memory T cells. The identification of stem cell memory T cells via our spectral flow cytometric approach is highly relevant for better understanding of T cell immunity in AT. Moreover, it provides possibilities for further research on this recently identified T cell population in other inborn errors of immunity.

Vaccination in PADs

Primary antibody deficiencies (PADs) are the most common primary immunodeficiencies (PIDs). They can be divided into the following groups, depending on their immunological features: agammaglobulinemia; common variable immunodeficiency (CVID) isotype; hyper IgM isotype; light chain or functional deficiencies with normal B cell count; specific antibody deficiency with normal Ig concentrations and normal numbers of B cells and transient hypogammaglobulinemia of infancy. The role of vaccination in PADs is recognized as therapeutic, diagnostic and prognostic and may be used in patients with residual B-cell function to provide humoral immunity to specific infective agents. According to their content and mechanisms, vaccines are grouped as live attenuated, inactivated (conjugated, polysaccharide), mRNA or replication-deficient vector vaccines. Vaccination may be unsafe or less effective when using certain vaccines and in specific types of immunodeficiency. Inactivated vaccines can be administered in PAD patients even if they could not generate a protective response; live attenuated vaccines are not recommended in major antibody deficiencies. From December 2020, European Medicines Agency (EMA) approved vaccines against COVID-19 infection: according to ESID advises, those vaccinations are recommended in patients with PADs. No specific data are available on safety and efficacy in PAD patients.

Platelet Count in Dengue Fever Patients

Dengue hemorrhagic fever (DHF) is an acute infectious disease caused by the dengue virus. This virus is transmitted by mosquitoes from the genus Aedes, for example Aedes aegypti and Aedes albopictus. Patients who are infected will have symptoms in the form of a mild to high fever, accompanied by headaches, pain in the eyes, muscles and joints, and spontaneous bleeding. DHF in Indonesia, has become a public health problem for the last 45 years since 1968. These cases are spread across 33 provinces and in 436 districts / cities out of 497 districts / cities (88%) in Indonesia. The number of people with Dengue Hemorrhagic Fever (DHF) tends to increase. The laboratory chooses to use a blood cell counter or a hematology analyzer to count the patient's blood cell count. The results of laboratory examinations with platelet counts in dengue fever patients were obtained 19 (14.84%) samples of patients with platelets d below 100,000 per micrometer (mcL) from 128 patients from January to March 2019. With 2 days of fever patients were 44 people. , 37 patients had fever for 4 days, and 5 fever patients were 47, in normal numbers and brought to a normal range of 150,000-400,000/ mmᶾ.

Long-term persistent mixed chimerism in a patient with Wiskott–Aldrich syndrome after allogeneic hematopoietic stem cell transplantation

The article describes a clinical case of a patient with Wiskott–Aldrich syndrome, in whom long- term persistence of mixed chimerism was determined after hematopoietic stem cell transplantation (HSCT) from a haploidentical donor. Based on the analysis of the patient's clinical picture after HSCT, it was shown that the presence of> 50% of donor cells in the myeloid lineage is necessary for the correction of thrombocytopenia. In addition, the presence of mixed chimerism in B-lymphocytes possibly contributed to the development of autoimmune complications in the patient, as well as to the persistent hypogammaglobulinemia, despite the restoration of the normal numbers of lymphocytes in all main sub-populations. The role of mixed chimerism in the pathogenesis of immune post-transplant complications requires study in large groups of patients with primary immunodeficiencies. The patient's parents agreed to use the information, including the child's photo, in scientific research and publications.