قسم الطب الوقائي

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أ‌. علم سلوكيات ورعاية الحيوان:يهدف هذا المقرر إلى التعريف بأسس تربية ومعاملة الحيوانات ورعايتها مع تغطية كاملة لقواعد الرعاية الصحية والسلوكية المتعلقة بالفرد والقطيع.ب‌.علم الوراثة والأنسال:يهدف علم الوراثة والأنسال إلى التعريف بالقواعد الأساسية لعلم الوراثة وقوانينها للإستفادة منها في الرفع من الإنتاجية.ج‌. علم صحة وإدارة القطعان:يهدف هذا المقرر إلى التعريف بالبرامج المختلفة المتعلقة بصحة وإدارة القطعان الحيوانية.د‌. علم الوبائيات:يدرس الطالب في هذا المقرر العوامل المؤثرة على صحة القطعان الحيوانية ومسببات الأمراض وطرق انتشارها  وتركيب القطعان الحيوانية وأشكال حدوث الأمراض في القطعان الحيوانية وطرق التشخيص الوبائي إضافة إلى طرق قياس حدوث المرض في القطعان الحيوانية بهدف الوصول إلى فرضية تحديد مسببات المرض لكي يتم اختبار هذه الفرضية من خلال علم الوبائيات التحليلي والذي يتم من خلاله استخدام الدراسات التجريبية أو دراسات الملاحظة لتحديد العلاقة بين التعرض للمسبب المرضي وحدوث المرض، وفى هذا العلم يدرس الطالب المسوحات الوبائية والترصد الوبائي وعلم الوبائيات المصلي وهي المعلومات التي تستخدم من أجل التحكم في الوباء في حال حدوثه.هـ. علم الأمراض المشتركة:يدرس الطالب في هذا المقرر تصنيف الأمراض المشتركة وأهم أنواعها مع التركيز على وبائيتها وطرق مقاومتها على المستوى الوطني والعالمي مع التعريف بالمنظمات الدولية المختصة والأمراض الواجب التبليغ عنها حال اكتشافها محليا ودوليا.

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Blood profile in normal one humped dromedary (Camelus dromedarius) camel breeds in Libya. Part 2: Effect of breed variation on biochemical and haematological blood profile

Abstract As little is known about the blood profile of camels in libya, this article is the second of a 4-part series describing the biochemical and haematological blood profile in Libyan camels. In Part 1 of these manuscripts, the overall blood biochemical and haematological mean values of camels in Libya were determined, parts 2-4 evaluates the effects of breed, gender and age respectively on these values. Blood samples were collected from three camel breeds, namely, Fakhreya, Sirtaweya and Mahari, and the levels of enzymes, metabolites, electrolytes and haematological indices were measured. The blood of the Sirtaweya breed showed (i) higher levels of aspartate aminotransferase (AST), albumin and Phosphorus (Ph), than the other two breeds, (ii) higher levels of lactate dehydrogenase (LDH), amylase (AMS) and total proteins than the Fakhreya breed and (iii) higher levels of glucose, triglycerides, total cholesterol, Very Low Density Lipoprotein (VLDL), Low Density Lipoprotein (LDL), Calcium (Ca), Packed Cell volume (PCV), Mean Corpuscular Volume (MCV) and Albumin/Globulin (A/G) ratio than the Mahari breed. The Fakhreya breed had (i) higher levels of urea, Iron (Fe), Haemoglobin (Hb), Mean Corpuscular Haemoglobin (MCH) and neutrophils number than the other two breeds, (ii) higher levels of glucose, A/G, LDL, Ca, PCV, MCV and monocytes number than the Mahari breed and (iii) higher levels of erythrocyte osmotic fragility, MCH and Mean Corpuscular Hemoglobin Concentration (MCHC) than the Sirtaweya breed. The Mahari breed had (i) higher levels of globulin than the other two breeds, (ii) higher levels of AMS than the Fakhreya breed and (iii) higher levels of erythrocyte osmotic fragility, Erythrocyte Sedimentation Rate (ESR), MCHC than the Sirtaweya breed. The tested blood parameters in the three Libyan breeds in this study were affected by breed variations. arabic 28 English 143
Anwar Mustafa Abdalhadi Abdalmula, F. A. Alnagar, Amal Omar Elarif Buker, Fathia mahmoud Mohammad Ashour, I. M. Abograra , Mansur Ennuri Moftah Shmela(10-2018)
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Beckwith–Wiedemann syndrome caused by maternally inherited mutation of an OCT-binding motif in the IGF2/H19-imprinting control region, ICR1.

The imprinted expression of the IGF2 and H19 genes is controlled by the imprinting control region 1 (ICR1) located at chromosome 11p15.5. DNA methylation defects involving ICR1 result in two growth disorders with opposite phenotypes: an overgrowth disorder, the Beckwith-Wiedemann syndrome (maternal ICR1 hypermethylation in 10% of BWS cases) and a growth retardation disorder, the Silver-Russell syndrome (paternal ICR1 loss of methylation in 60% of SRS cases). In familial BWS, hypermethylation of ICR1 has been found in association with microdeletion of repetitive DNA motifs within ICR1 that bind the zinc finger protein CTCF; but more recently, ICR1 point mutations were described in BWS pedigrees. We present a case report of two brothers with BWS and prolonged post-pubertal growth resulting in very large stature. A maternally inherited point mutation was identified in ICR1 in both brothers, which altered binding of OCT transcription factors. The same mutation was present on the paternally inherited allele of their unaffected mother. This is a second report of a point mutation causing ICR1 hypermethylation by altering an OCT-binding motif. The atypical growth phenotype of the brothers may be connected to the unusual underlying cause of their BWS. arabic 24 English 118
Rebecca L Poole, Donald J Leith, Louise E Docherty, Mansur Ennuri Moftah Shmela, Christine Gicquel,, Miranda Splitt, I Karen Temple, Deborah J G Mackay(2-2012)
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Genetic variants within the second intron of the KCNQ1 gene affect CTCF binding and confer a risk of Beckwith–Wiedemann syndrome upon maternal transmission.

Background Disruption of 11p15 imprinting results in two fetal growth disorders with opposite phenotypes: the Beckwith–Wiedemann (BWS; MIM 130650) and the Silver–Russell (SRS; MIM 180860) syndromes. DNA methylation defects account for 60% of BWS and SRS cases and, in most cases, occur without any identified mutation in a cis-acting regulatory sequence or a trans-acting factor. Methods We investigated whether 11p15 cis-acting sequence variants account for primary DNA methylation defects in patients with SRS and BWS with loss of DNA methylation at ICR1 and ICR2, respectively. Results We identified a 4.5 kb haplotype that, upon maternal transmission, is associated with a risk of ICR2 loss of DNA methylation in patients with BWS. This novel region is located within the second intron of the KCNQ1 gene, 170 kb upstream of the ICR2 imprinting centre and encompasses two CTCF binding sites. We showed that, within the 4.5 kb region, two SNPs (rs11823023 and rs179436) affect CTCF occupancy at DNA motifs flanking the CTCF 20 bp core motif. Conclusions This study shows that genetic variants confer a risk of DNA methylation defect with a parent-of-origin effect and highlights the crucial role of CTCF for the regulation of genomic imprinting of the CDKN1C/KCNQ1 domain. arabic 26 English 132
Julie Demars, Mansur Ennuri Moftah Shmela, Abdul Waheed Khan , Kai Syin Lee, Salah Azzi, Patrice Dehais, Irène Netchine, Sylvie Rossignol, Yves Le Bouc, Assam El-Osta, Christine Gicquel(7-2014)
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