Raida W. Khalil

Multiple sclerosis in Arabs in Jordan.

In a 2-year hospital-based study (1992 and 1993), there were 131 multiple sclerosis patients attending 2 large referral hospitals in Jordan. Based on MS/ALS case ratios an overall rate of 32.1 (95% CI 19.7-55.2) was estimated. There were 126 Arabs of whom 84 were Palestinians and 36 indigenous Jordanians. Comparison of these subgroups, which had a similar age distribution revealed that the disease was twice as frequent in Palestinians (estimated 42.0/100,000 (CI 2.8-90.8)) among Jordanians (estimated 20.0/100,000 (CI 9.5-47.2)). Clinical presentation, pattern of disease, disability and HLA association were similar to that in the disease reported in Caucasians in the West. All investigations including neurophysiology and imaging were also very similar to Western reports.

Epidemiology of multiple sclerosis in Arabs in Jordan: a comparative study between Jordanians and Palestinians.

In a 2-year hospital-based study in Jordan 131 Arab multiple sclerosis patients were identified including 84 Palestinians and 36 Jordanians. Based on MS/ALS case ratio, multiple sclerosis was found to be twice as common among Palestinians than Jordanians. Other than the less marked female preponderance among Jordanian patients, the disease had the same clinical and paraclinical characteristics in both groups. It was more likely for Palestinian and Jordanian patients to originate from the northern parts of their countries, to be Rh negative and to be HLA-DR2 positive than their controls. Palestinians (patients and controls) did not show significant differences from Jordanians (patients and controls) in relation to their eye color, ABO and Rh blood groups distribution nor the HLA-DR or HLA-DQ (apart from HLA-DQ3) epitopes frequency, thus not offering any significant difference in the genetic-racial markers studies to explain the difference in the observed disease susceptibility. Previous studies demonstrated that 2 racially different populations sharing the same environment can have different risk of developing multiple sclerosis, but this study has shown that this can also be true for 2 racially similar populations sharing the same environment.

Enhancement of natural killer cell activity in vitro against human tumor cells by some plants from Jordan.

The effect of different concentrations (0, 0.01, 0.1, and 0.5 mg/ml) of plant aqueous extracts on the anti-tumor activity of natural killer (NK) cells isolated from human blood was examined. Plant extracts induced significant enhancement of (26.6–67.7%) of NK cell activity against K562 tumor cells. This increase in NK cell cytotoxicity was found to be due to the enhancement of NK cell production of interferon-γ (87–337%), and on tumor necrosis factor-α (60–200%). Furthermore, the release of both granzyme A and N-acetyl-β-D-glucosaminidase was increased significantly when compared with controls. Activation of granzyme A and N-acetyl-β-D-glucosaminidase was clearly observed ranging from 24.2–106.4% to 26.8–110.7%, respectively. Lastly, in the absence of IL–2, plant extracts caused a significant increase in NK-cell-induced cytotoxicity (256%) against K562 tumor cells, and in the presence of IL-2 stimulated cells plant extracts caused an increase in NK cell-cytotoxicity (112%).

Synthesis and cytotoxic activity of 4-O-β-D-galactopyranosyl derivatives of phenolic acids esters

Abstract The glycosylation of naturally occurring phenolic acids has a significant impact on their solubility, stability and physiochemical properties. D-Galactose residue was found to form a part of glycoconjugates in several tissues and involved in a variety of physiological process. To the best of our knowledge, we have noticed a little information about the glycosylation of the phenolic acids with galactose residue. In this work, we describe the glycosylation of methyl vanillate and methyl ferulate with peracetylated-β-D-galactopyranose in the presence of BF3·OEt2. The coupling reaction yielded efficiently and selectively only the acetylated β-D-galactopyranosides 3 and 6. Removal of the acetyl groups using sodium methoxide afforded the corresponding β-D-galactopyranosides 4 and 7 in good yields. Anticancer activity in vitro was evaluated against two human cancer cell lines (MCF-7 breast cancer cell lines and PC-3 prostate cancer cell lines). β-D-galactopyranosides 4 and 7 demonstrated improved cytotoxic activity compared to the parental esters.

Production and Characterization of a Recombinant Camel Full Heavy Chain Antibody against Human IgE

Camel heavy chain antibodies (HCAbs) have novel properties that render them useful in diagnosis and immunotherapy of various diseases. The purpose of this study was to produce recombinant camel HCAbs directed against a synthetic loop polypeptide that mimics the FceRІ binding site on human IgE. A recombinant camel HCAb was purified and characterized after being cloned using One Shot TOP10 Escherichia coli, expressed in BL21 Star (DE3) E. coli. Out of nineteen successful clones only one named IgG211 was found to contain the IgG2 HCAb coding sequence in the correct orientation with 85% homology to camel IgG2. A 62kDa fusion protein was expressed in an insoluble form under Isopropyl β-D-1Thiogalactopyranoside (IPTG) induction. Probond purified fusion protein was localized by immunoblot using mouse anti camel antibody. The reactivity of recombinant camel IgG211to its corresponding antigen using ELISA was 72.9% of the camel polyclonal IgG2. Thus, a successful production of a recombinant camel HCAb of the IgG2 isotype was achieved. Such achievement may contribute towards the application of the unique properties of camel HCAbs in the field of antibody-based therapy for the treatment of asthma and allergy.

Detection of novel LAMA3 mutation in Herlitz junctional epidermolysis bullosa in a Jordanian family

The Herlitz junctional epidermolysis bullosa (H‐JEB) subtype usually presents as a severe lethal inherited variant of epidermolysis bullosa (EB) caused by a homozygous mutation in the genes LAMA3, LMAB3, or LAMAC3. Each gene encodes one of the three chains of heterotrimer laminin‐332 proteins (including the alpha‐3 chain, beta‐3 chain and gamma‐2‐chain) responsible for the adherence of the epidermis to the underlying dermis. The aim of this report is to add to the existing knowledge about EB by describing a novel mutation in a gene responsible for genodermatosis. A case of a Jordanian male neonate, born to healthy, first cousin consanguineous parents, who developed nonhealing blistering skin and mucous membrane lesions, crusted erosions with significant granulation tissue and dystrophic nails immediately after birth is described. The patient was diagnosed as having a novel LAMA3 mutation causing (H‐JEB) by immunofluorescence mapping and molecular analysis. Both parents and this babys sibling were shown to be heterozygous carriers of the same mutation. Pre‐implantation diagnosis using molecular analysis for subsequent pregnancies in this family is crucial for managing any new pregnancy.

Characterization of glucokinase polymorphisms associated with Maturity-Onset Diabetes of the Young (MODY2) in Jordanian population

Maturity-Onset Diabetes of the Young (MODY) is a monogenic form of Diabetes Mellitus (DM) characterized by an autosomal dominant inheritance, onset usually before 25 years of age and a primary defect in glucose-stimulated insulin secretion, Glucokinase (GCK) acts as a glucose sensor in the pancreatic beta cell and regulates insulin secretion. The mutation in the gene encoding GCK results in enzyme inactivation cause MODY2. Functional studies of naturally occurring GCK mutations associated with hyperglycaemia provide further insight into the biochemical basis of glucose sensor regulation. In this study 100 diabetic Jordanian patients with MODY2 phenotype and 150 Normal control subjects were screened for the presence of GCK gene mutations including the missense mutations at position Thr228Ala in exon 7, Gly299Arg in exon 8 and nonsense mutation Ser383Ter in exon 9, utilizing polymerase chain reaction with restriction fragment length polymorphism (PCR-RFLP) analysis. The results shows no Thr228Ala, Gly299Arg and Ser383Ter mutations were detected in both groups, which was differ from the results obtained for Italian and Caucasian from the Oxford region in UK MODY2 patients. Our data indicated that the previously studied mutations in Italian and Caucasian patients in the GCK gene are not common in MODY Jordanian population, suggesting a racial difference can be found in the frequency of the GCK polymorphism.