UPDATE ON THE USE OF METHOTREXATE IN THE MANAGEMENT OF RHEUMATOID ARTHRITIS.

Rheumatoid arthritis (RA) is an auto-immune disorder described by permanent inflammation of the articular synovial membrane. Non-treated RA can cause gradual joint damage, ending in complaint, poor lifestyle, and an upright ratio of death. Approximately one percent of the people are involved, and the disorder begins, in general, appears during the third and fifth decades of age, with more occurrences in females. The treatment is complicated as well as involves various stages of medications with variable methods of application as well as non-pharmacologic methods. The extra prevalent are disease person's culture, then, sports and mechanical and behavioral therapy. Due to more chance of ischemic heart disease, trials should be increased to lessen the assisting behaviors such as cigarette smoking, high lipid profile, elevation of blood pressure, and high body mass index.

Higher beta-hydroxybutyrate ketone levels associated with a slower kidney function decline in ADPKD.

BACKGROUND AND HYPOTHESIS: Dysregulated energy metabolism is a recently discovered key feature of Autosomal Dominant Polycystic Kidney Disease (ADPKD). Cystic cells depend on glucose and are poorly able to use other energy sources such as ketone bodies. Raising ketone body concentration reduced disease progression in animal models of polycystic kidney diseases. Therefore, we hypothesized that higher endogenous plasma beta-hydroxybutyrate concentrations are associated with reduced disease progression in patients with ADPKD. METHODS: We analyzed data from 670 patients with ADPKD participating in the DIPAK cohort, a multi-center prospective observational cohort study. Beta-hydroxybutyrate was measured at baseline using nuclear magnetic resonance spectroscopy. Participants were excluded if they had type 2 diabetes, were using disease-modifying drugs (e.g. tolvaptan, somatostatin analogs), were not fasting, or had missing beta-hydroxybutyrate levels, leaving 521 participants for the analyses. Linear regression analyses were used to study cross-sectional associations and linear mixed-effect modeling for longitudinal associations. RESULTS: Of the participants, 61% were female, with an age of 47.3 ± 11.8 years, a height-adjusted total kidney volume (htTKV) of 834 (IQR 495-1327) ml/m, and an estimated glomerular filtration rate (eGFR) of 63.3 ± 28.9 mL/min/1.73m2. The median concentration of beta-hydroxybutyrate was 94 (IQR 68-147) µmol/L. Cross-sectionally, beta-hydroxybutyrate was neither associated with eGFR nor with htTKV. Longitudinally, beta-hydroxybutyrate was positively associated with eGFR slope (B = 0.35 ml/min/1.73m2 (95% CI 0.09 to 0.61), p = 0.007), but not with kidney growth. After adjustment for potential confounders, every doubling in beta-hydroxybutyrate concentration was associated with an improvement in the annual rate of eGFR by 0.33 ml/min/1.73m2 (95% CI 0.09 to 0.57, p = 0.008). CONCLUSION: These observational analyses support the hypothesis that interventions that raise beta-hydroxybutyrate concentration could reduce the rate of kidney function decline in patients with ADPKD.

Quality of Victim Statement in Child Sexual Abuse in Turkey.

Child sexual abuse is the most challenging type of abuse to detect. Moreover, there are difficulties in gathering evidence, apprehending, and prosecuting the perpetrator. The trial is often based on the contradiction of the suspect's and the child's statements. The aim of this study is to identify the difficulties encountered during the entire trial in cases of sexual assault against the child in Turkey starting from the investigation phase, to determine the auditability of taking a child's statement, which is the basis of the judicial decision, and to evaluate the effectiveness of the principles set by the Supreme Court, which oversees the local court decision. It was determined that the trial was continued on abstract allegations, the Supreme Court's approval of the decision of the local court was based on "the slander of a person who wants to harm another person over the sexuality of a minor is contrary to the usual flow of life." Furthermore, the reason wassuggestive of subjective interpretations rather than material truths. This study, which is a master's thesis, has been submitted to the Turkish Ministry of Justice.

Genetic and phenotypic characterization of NKX6-2-related spastic ataxia and hypomyelination.

BACKGROUND AND PURPOSE: Hypomyelinating leukodystrophies are a heterogeneous group of genetic disorders with a wide spectrum of phenotypes and a high rate of genetically unsolved cases. Bi-allelic mutations in NKX6-2 were recently linked to spastic ataxia 8 with hypomyelinating leukodystrophy. METHODS: Using a combination of homozygosity mapping, exome sequencing, and detailed clinical and neuroimaging assessment a series of new NKX6-2 mutations in a multicentre setting is described. Then, all reported NKX6-2 mutations and those identified in this study were combined and an in-depth analysis of NKX6-2-related disease spectrum was provided. RESULTS: Eleven new cases from eight families of different ethnic backgrounds carrying compound heterozygous and homozygous pathogenic variants in NKX6-2 were identified, evidencing a high NKX6-2 mutation burden in the hypomyelinating leukodystrophy disease spectrum. Our data reveal a phenotype spectrum with neonatal onset, global psychomotor delay and worse prognosis at the severe end and a childhood onset with mainly motor phenotype at the milder end. The phenotypic and neuroimaging expression in NKX6-2 is described and it is shown that phenotypes with epilepsy in the absence of overt hypomyelination and diffuse hypomyelination without seizures can occur. CONCLUSIONS: NKX6-2 mutations should be considered in patients with autosomal recessive, very early onset of nystagmus, cerebellar ataxia with hypotonia that rapidly progresses to spasticity, particularly when associated with neuroimaging signs of hypomyelination. Therefore, it is recommended that NXK6-2 should be included in hypomyelinating leukodystrophy and spastic ataxia diagnostic panels.

Genetic investigation of 93 families with microphthalmia or posterior microphthalmos.

Microphthalmia is a developmental eye defect that is highly variable in severity and in its potential for systemic association. Despite the discovery of many disease genes in microphthalmia, at least 50% of patients remain undiagnosed genetically. Here, we describe a cohort of 147 patients (93 families) from our highly consanguineous population with various forms of microphthalmia (including the distinct entity of posterior microphthalmos) that were investigated using a next-generation sequencing multi-gene panel (i-panel) as well as whole exome sequencing and molecular karyotyping. A potentially causal mutation was identified in the majority of the cohort with microphthalmia (61%) and posterior microphthalmos (82%). The identified mutations (55 point mutations, 15 of which are novel) spanned 24 known disease genes, some of which have not or only very rarely been linked to microphthalmia (PAX6, SLC18A2, DSC3 and CNKSR1). Our study has also identified interesting candidate variants in 2 genes that have not been linked to human diseases (MYO10 and ZNF219), which we present here as novel candidates for microphthalmia. In addition to revealing novel phenotypic aspects of microphthalmia, this study expands its allelic and locus heterogeneity and highlights the need for expanded testing of patients with this condition.

Clinical genomics expands the morbid genome of intellectual disability and offers a high diagnostic yield.

Intellectual disability (ID) is a measurable phenotypic consequence of genetic and environmental factors. In this study, we prospectively assessed the diagnostic yield of genomic tools (molecular karyotyping, multi-gene panel and exome sequencing) in a cohort of 337 ID subjects as a first-tier test and compared it with a standard clinical evaluation performed in parallel. Standard clinical evaluation suggested a diagnosis in 16% of cases (54/337) but only 70% of these (38/54) were subsequently confirmed. On the other hand, the genomic approach revealed a likely diagnosis in 58% (n=196). These included copy number variants in 14% (n=54, 15% are novel), and point mutations revealed by multi-gene panel and exome sequencing in the remaining 43% (1% were found to have Fragile-X). The identified point mutations were mostly recessive (n=117, 81%), consistent with the high consanguinity of the study cohort, but also X-linked (n=8, 6%) and de novo dominant (n=19, 13%). When applied directly on all cases with negative molecular karyotyping, the diagnostic yield of exome sequencing was 60% (77/129). Exome sequencing also identified likely pathogenic variants in three novel candidate genes (DENND5A, NEMF and DNHD1) each of which harbored independent homozygous mutations in patients with overlapping phenotypes. In addition, exome sequencing revealed de novo and recessive variants in 32 genes (MAMDC2, TUBAL3, CPNE6, KLHL24, USP2, PIP5K1A, UBE4A, TP53TG5, ATOH1, C16ORF90, SLC39A14, TRERF1, RGL1, CDH11, SYDE2, HIRA, FEZF2, PROCA1, PIANP, PLK2, QRFPR, AP3B2, NUDT2, UFC1, BTN3A2, TADA1, ARFGEF3, FAM160B1, ZMYM5, SLC45A1, ARHGAP33 and CAPS2), which we highlight as potential candidates on the basis of several lines of evidence, and one of these genes (SLC39A14) was biallelically inactivated in a potentially treatable form of hypermanganesemia and neurodegeneration. Finally, likely causal variants in previously published candidate genes were identified (ASTN1, HELZ, THOC6, WDR45B, ADRA2B and CLIP1), thus supporting their involvement in ID pathogenesis. Our results expand the morbid genome of ID and support the adoption of genomics as a first-tier test for individuals with ID.

GLI3-related polydactyly: a review.

GLI3 mutations are known to be associated with nine syndromes/conditions in which polydactyly is a feature. In this review, the embryology, pathogenesis, and animal models of GLI3-related polydactyly are discussed first. This is followed by a detailed review of the genotype-phenotype correlations. Based on our review of the literature and our clinical experiences, we recommend viewing GLI3-related syndromes/conditions as four separate entities; each characterized by a specific pattern of polydactyly. These four entities are: the preaxial polydactyly type IV-Greig-acrocallosal spectrum, postaxial polydactyly types A/B, Pallister-Hall syndrome (PHS), and oral-facial-digital overlap syndrome. We also provide illustrative clinical examples from our practice including a family with a novel GLI3 mutation causing PHS. The review also introduces the term 'Forme Fruste' preaxial polydactyly and gives several conclusions/recommendations including the recommendation to revise the current criteria for the clinical diagnosis of PHS.

Confirming the recessive inheritance of SCN1B mutations in developmental epileptic encephalopathy.

Dominant SCN1B mutations are known to cause several epilepsy syndromes in humans. Only 2 epilepsy patients to date have been reported to have recessive mutations in SCN1B as the likely cause of their phenotype. Here, we confirm the recessive inheritance of 2 novel SCN1B mutations in 5 children from 3 families with developmental epileptic encephalopathy. The recessive inheritance and early death in these patients is consistent with the Dravet-like phenotype observed in Scn1b-/- mice. The 'negative' clinical exome in one of these families highlights the need to consider recessive mutations in the interpretation of variants in typically dominant genes.

Expression profiling of Sudanese visceral leishmaniasis patients pre- and post-treatment with sodium stibogluconate.

Visceral leishmaniasis (VL) in Sudan caused by Leishmania donovani is fatal in susceptible individuals if untreated. Treatment with sodium stibogluconate (SSG) leads to post-kala-azar dermal leishmaniasis (PKDL) in 58% of patients. Here, Affymetrix microarrays were used to identify genes differentially expressed in lymph nodes (N=9 paired samples) pre- and post-treatment with SSG. Using the Bioconductor package limma, 438 genes from 28 869 post-quality-control probe sets were differentially expressed (Pnominal ≤.02) post- vs pretreatment. Canonical pathway analysis using Ingenuity Pathway Analysis™ identified "role of nuclear factor of activated T-cell in regulation of immune response" (Pnominal =1.35×10-5 ; PBH-adjusted =4.79×10-3 ), "B-cell development" (Pnominal =2.04×10-4 ; PBH-adjusted =.024), "Fcγ receptor-mediated phagocytosis in macrophages and monocytes" (Pnominal =2.04×10-4 ; PBH-adjusted =.024) and "OX40 signalling" (Pnominal =2.82×10-4 ; PBH-adjusted =.025) as pathways differentially regulated post- vs pretreatment. Major network hub genes included TP53, FN1, MYC, BCL2, JUN, SYK, RUNX2, MMP1 and ACTA2. Top endogenous upstream regulators included IL-7 (P=2.28×10-6 ), TNF (P=4.26×10-6 ), Amyloid Precursor Protein (P=4.23×10-5 ) and SPI1/PI.1 (P=1.17×10-7 ). Top predicted chemical drug regulators included the flavonoid genistein (P=4.56×10-7 ) and the quinoline alkaloid camptothecin (P=5.14×10-5 ). These results contribute to our understanding of immunopathology associated with VL and response to SSG treatment. Further replication could identify novel therapeutic strategies that improve on SSG treatment and reduce the likelihood of progression to PKDL.

Value of cardiac MRI for evaluation of chronic Chagas disease cardiomyopathy.

AIM: To determine whether cardiac magnetic resonance imaging (cMRI) is more sensitive than electrocardiogram (ECG) and echocardiogram (ECHO) for detecting myocardial involvement in a Latin American migrant population with untreated Chagas disease (CD) in the United States. MATERIALS AND METHODS: All untreated CD patients with ECG and ECHO examinations who underwent cMRI at Olive View-UCLA Medical Center from September 2010 to December 2013 (n=81) were analysed in three groups: Group 1, normal ECG and ECHO examinations (n=50); Group 2, abnormal ECG and normal ECHO examinations (n=10); and Group 3, abnormal ECHO examination (n=21). Frequencies of ECG, ECHO, and cMRI findings were compared across groups. RESULTS: Seventy percent (57/81) of the study population was female, with a mean age of 47 years (range, 17-77 years). Twenty-six percent (21/81) had delayed myocardial enhancement (DME), which was most commonly inferolateral in location (27%, 32/117 segments) and transmural in pattern (56%, 65/117 segments). Eight percent (4/50), 30% (3/10), and 67% (14/21) of Groups 1-3, respectively, had DME. Of these individuals with DME, 50% (2/4), 67% (2/3), and 100% (14/14) of Groups 1-3, respectively, also had wall motion abnormality (WMA) on cMRI. In addition to the highest percentages of DME and WMA, Group 3 also had significantly higher mean myocardial mass (p<0.01), mean left ventricular end-diastolic (p<0.01) and end-systolic volumes (p<0.0005), and significantly lower mean left ventricular ejection fraction (p<0.001). CONCLUSION: cMRI may detect myocardial involvement in untreated CD that is otherwise unrecognised on ECG and ECHO.

Pellagra-like condition is xeroderma pigmentosum/Cockayne syndrome complex and niacin confers clinical benefit.

An extremely rare pellagra-like condition has been described, which was partially responsive to niacin and associated with a multisystem involvement. The condition was proposed to represent a novel autosomal recessive entity but the underlying mutation remained unknown for almost three decades. The objective of this study was to identify the causal mutation in the pellagra-like condition and investigate the mechanism by which niacin confers clinical benefit. Autozygosity mapping and exome sequencing were used to identify the causal mutation, and comet assay on patient fibroblasts before and after niacin treatment to assess its effect on DNA damage. We identified a single disease locus that harbors a novel mutation in ERCC5, thus confirming that the condition is in fact xeroderma pigmentosum/Cockayne syndrome (XP/CS) complex. Importantly, we also show that the previously described dermatological response to niacin is consistent with a dramatic protective effect against ultraviolet-induced DNA damage in patient fibroblasts conferred by niacin treatment. Our findings show the power of exome sequencing in reassigning previously described novel clinical entities, and suggest a mechanism for the dermatological response to niacin in patients with XP/CS complex. This raises interesting possibilities about the potential therapeutic use of niacin in XP.

NPHP4 mutation is linked to cerebello-oculo-renal syndrome and male infertility.

Nephronophthisis is the most common genetic cause of renal failure in children and young adults. It is genetically heterogeneous and can be seen in isolation or in combination with other ciliopathy phenotypes. Here we report an index case where nephronophthisis is associated with oculomotor apraxia and cerebellar abnormalities, consistent with the clinical diagnosis of cerebello-oculo-renal syndrome. Prompted by a family history of an uncle with early onset end stage renal failure and infertility, we performed semen analysis on the index. This revealed marked reduction in the count of motile sperms as well as multiple abnormalities in the head and tail. Autozygome-guided mutation analysis followed by exome sequencing and segregation analysis revealed a homozygous truncating mutation in NPHP4, indicating that mutations of this gene can on rare occasions cause cerebello-oculo-renal syndrome. Our finding of severe male infertility in a family with NPHP4 truncation is strongly supported by the mouse model and, to our knowledge, is the first reported male infertility phenotype in association with NPHP4 or any other nephrocystin in humans.

The nature of persistent conformational chirality, racemization mechanisms, and predictions in diarylether heptanoid cyclophane natural products.

Restricted rotations of chemical bonds can lead to the presence of persistent conformational chirality in molecules lacking stereocenters. We report the development of first-of-a-kind predictive rules that enable identification of conformational chirality and prediction of racemization barriers in the diarylether heptanoid (DAEH) natural products that do not possess stereocenters. These empirical rules-of-thumb are based on quantum mechanical computations (SCS-MP2/∞//B3LYP/6-31G*/PCM) of racemization barriers of four representative DAEHs. Specifically, the local symmetry of ring B and the E/Z configuration of the vinylogous acid/ester are critical in determining conformational chirality in the DAEH natural product family.

Environmental pollutants PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) impair human cognitive functions.

OBJECTIVE: Environmental pollution is an emerging global public health problem across the world and causes serious threats to ecosystems, human health, and the planet. This study is designed to explore the impact of environmental pollution particulate matter PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) on cognitive functions in students from schools located in or away from air-polluted areas. SUBJECTS AND METHODS: In this study, two schools were selected: one was located near a traffic-polluted area (school #1), and the second was in an area away from the traffic-polluted area (school #2). In this study, a total of 300 students were recruited: 150 (75 male and 75 female) students from school #1 located in a traffic-polluted area, and 150 students (75 male and 75 female) from school #2 located away from a traffic polluted area. The overall average age of students was 13.53±1.20 years. The students were selected based on age, gender, health status, height, weight, BMI, ethnicity, and homogenous socio-economic and educational status. The pollutants PM2.5, PM10, CO, NO2, O3, and SO2 were recorded in the surrounding environment. The overall mean concentration of environmental pollutants in school #1 was 35.00±0.65 and in school #2 was 29.95±0.32. The levels of airborne particles were measured, and the cognitive functions were recorded using the Cambridge Neuropsychological Test Automated Battery (CANTAB). The students performed the cognitive functions tasks, including the attention switching task (AST), choice reaction time (CRT), and motor screening task (MOT). RESULTS: The results revealed that the AST-Mean 928.34±182.23 vs. 483.79±146.73 (p=0.001), AST-mean congruent 889.12±197.12 vs. 473.30±120.11 (p=0.001), AST-mean in-congruent 988.98±201.27  vs. 483.87±144.57 (p=0.001), CRT-Mean 721.36±251.72  vs. 418.17±89.71 (p=0.001), and MOT-Mean 995.07±394.37 vs. 526.03±57.83 (p=0.001) were significantly delayed among the students who studied in school located in the traffic polluted area compared to students who studied in school which was located away from the traffic-polluted area. CONCLUSIONS: Environmental pollution was significantly higher in motor vehicle-congested areas. Cognitive functions were impaired among the students who were studying in a school located in a polluted area. The results further revealed that the students studying in schools located in environmentally polluted areas have attention, thinking, and decision-making abilities related to cognitive function impairment.

Comparison of Optic Nerve Sheath Diameter (ONSD) Measurements Obtained from USG Before and After Placement of Ventriculoperitoneal Shunt in Obstructive Hydrocephalus as a Surrogate Marker for Adequacy of Shunt Function: A Prospective Observational Study.

Introduction Optic nerve sheath diameter (ONSD) measured using ultrasonography has been widely used as a surrogate marker of elevated intracranial pressure. However, literature is sparse on the correlation between ONSD and ventriculoperitoneal (VP) shunt function, especially in adults with hydrocephalus. Our study was designed to assess the correlation between ONSD measured using ultrasonography before and 12 hours after VP shunt placement and the success of VP shunt placement assessed using computed tomography (CT) of the brain. Materials and Methods Fifty-one patients between 16 and 60 years of age, with obstructive hydrocephalus scheduled for VP shunt surgery were included in this prospective, observational study. ONSD measurements were obtained from both eyes prior to induction of anesthesia, immediately after the surgery, and at 6, 12, and 24 hours after the surgery. An average of three readings was obtained from each eye. Cerebrospinal fluid (CSF) opening pressure was noted after entry into the lateral ventricle. Noncontrast CT (NCCT) brain was obtained 12 hours after the surgery and was interpreted by the same neurosurgeon for signs of successful VP shunt placement. Results There was a significant reduction in ONSD in the postoperative period compared to ONSD measured preoperatively. The average ONSD (mean ± standard deviation) measured prior to induction of anesthesia, immediately after the surgery, and at 6, 12, and 24 hours after the surgery was 5.71 ± 0.95, 5.20 ± 0.84, 5.06 ± 0.79, 4.90 ± 0.79, and 4.76 ± 0.75 mm, respectively. The mean CSF opening pressure was 19.6 ± 6.9 mm Hg. Postoperative NCCT brain revealed misplacement of the shunt tip in only one patient. Conclusion ONSD measured using ultrasonography may be used as a reliable indicator of VP shunt function in adults with obstructive hydrocephalus.

The impact of ketogenic diet on some metabolic and non-metabolic diseases: Evidence from human and animal model experiments.

The ketogenic diet (KD) is recognized as minimum carbohydrate and maximum fat intakes, which leads to ketosis stimulation, a state that is thought to metabolize fat more than carbohydrates for energy supply. KD has gained more interest in recent years and is for many purposes, including weight loss and managing serious diseases like type 2 diabetes. On the other hand, many believe that KD has safety issues and are uncertain about the health drawbacks. Thus, the outcomes of the effect of KD on metabolic and non-metabolic disease remain disputable. The current narrative review aims to evaluate the effect of KD on several diseases concerning the human health. To our best knowledge, the first report aims to investigate the efficacy of KD on multiple human health issues including type 2 diabetes and weight loss, cardiovascular disease, kidney failure and hypertension, non-alcoholic fatty liver, mental problem, oral health, libido, and osteoporosis. The literature searches were performed in Databases, PubMed, Scopus, and web of Science looking for both animal and human model designs. The results heterogeneity seems to be explained by differences in diet composition and duration. Also, the available findings may show that proper control of carbohydrates, a significant reduction in glycemic control and glycated hemoglobin, and weight loss by KD can be an approach to improve diabetes and obesity, hypertension, non-alcoholic fatty liver, PCOS, libido, oral health, and mental problem if isocaloric is considered. However, for some other diseases like cardiovascular disease and osteoporosis, more robust data are needed. Therefore, there is robust data to support the notion that KD can be effective for some metabolic and non-metabolic diseases but not for all of them. So they have to be followed cautiously and under the supervision of health professionals.

The Salih ataxia mutation impairs Rubicon endosomal localization.

We previously described a new form of recessive ataxia, Salih ataxia, in a large consanguineous Saudi Arabian family with three affected children carrying a new identified mutation in the KIAA0226 gene (c.2624delC; p.Ala875ValfsX146) coding for Rubicon. The pathogenicity of such mutation remains to be identified. Hence, we address the cellular impact of Rubicon p.Ala875ValfsX146 on endosomal/lysosomal machinery on cultured cells. We confirm that Rubicon colocalizes with the late endosome marker Rab7 and demonstrate that it also colocalizes with LampI at lysosomes. The Salih ataxia mutation leads to a diffuse cytosolic distribution and mislocalized protein from the late endosomes, indicating that deletion of the diacylglycerol binding-like motif in the mutant protein interferes with normal Rubicon subcellular localization and confirming the pathogenicity of the mutation.

The garuganin and garugamblin diarylether heptanoids: total synthesis and determination of chiral properties using dynamic NMR.

The synthesis of the garuganin and garugamblin diarylether heptanoids using an intramolecular Ullmann coupling is reported. Alkene stereoisomers, vinylogous ester regioisomers, and ß-diketone congeners are also synthesized. The chiral properties and free energies of activation for racemization of the garuganin and garugamblin diarylether heptanoids and congeners are determined using dynamic NMR methods. A combination of techniques including coalescence measurements, line shape analysis, and selective inversion experiments are used to measure racemization barriers. None of the garuganin or garugamblin diarylether heptanoids are chiral, despite their reported specific rotation values.

Charcot-Marie-Tooth type 4B is caused by mutations in the gene encoding myotubularin-related protein-2.

A gene mutated in Charcot-Marie-Tooth disease type 4B (CMT4B), an autosomal recessive demyelinating neuropathy with myelin outfoldings, has been mapped on chromosome 11q22. Using a positional-cloning strategy, we identified in unrelated CMT4B patients mutations occurring in the gene MTMR2, encoding myotubularin-related protein-2, a dual specificity phosphatase (DSP).

Iraqi parents' views of barriers to childhood immunization.

Deficiencies in knowledge about immunization among parents often leads to poor utake or errors in immunization dosage and timing. The aims of this study were to determine Iraqi parents' views of barriers to immunization and beliefs about ways to promote immunization. A questionnaire survey was carried out among 528 Iraqi parents with children who had incomplete immunization status. The main barriers to immunization agreed by the parents were lack of vaccine availability (51.5% of parents) and parents' lack of education (42.4%), while 88.4% of parents thought that lack of funding was not an important barrier. More than 60% of the parents suggested promoting childhood immunization via the media, and 77.5% thought that an increase in funding would not remove barriers to childhood immunization. Better vaccine availability in public health clinics and improving parents' literacy might enhance immunization uptake in Iraq.