The Essence of Engineering consultancy contracts

The engineering consultancy contract is one of the most interesting contracts to study. It arranges the relationships between the consulting engineer, the specialized professional, and the employer. Because The Syrian Civil Law lacks clear texts classifying this contract, it was important to look into this contract's legal nature and discuss its parties’ obligations, in each of the contract’s phases, and know their legal nature and the legal grounds on which they’re based. The essence of an engineering consultancy contract is necessary to be studied under two section, the first deals with the definition of this contract, and the second deals with the obligations of the contract’s parties. مفهوم عقد الاستشارة الهندسيّة يعتبر عقد الاستشارة الهندسيّة من العقود الجديرة بالدراسة، نظراً للدّور الكبير الذي يلعبه في ضمان حسن سير المشاريع الإنشائيّة والصناعيّة الضخمة المنفذة في ظل النهضة العمرانيّة التي يشهدها عالمنا المعاصر، فالعقد ينظّم العلاقة بين المهندس الاستشاري، المهني المختص صاحب الخبرة الفنيّة والمهنيّة، وبين صاحب العمل. ونظراً لافتقاد القانون المدني السّوري لنصوص واضحة تتناول هذا العقد بالتنظيم، فكان لابدّ من البحث في ماهيّة هذا العقد لتحديد طبيعته القانونيّة، والوقوف على التزامات أطرافه، في كل مرحلة من مراحل العقد، لمعرفة تلك الالتزامات وبيان طبيعتها القانونيّة وتحديد الأساس القانوني الذي تقوم عليه. لهذا فإن البحث في مفهوم عقد الاستشارة الهندسيّة يقتضي أولاً التّعريف بعقد الاستشارة الهندسيّة في مبحثٍ أوّل، ثمّ تحديد التزامات أطرافه في مبحثٍ ثانٍ

Sheikh Daudal-Fatani as scholar in Malay Archipelago: overview on his writings

This paper explores the biography of Sheikh Daud al-Fatani, one of the most famous and prolific authors among Muslims in South East Asia. He produced writings in Madhhab Shafi’i in the Malay World during the nineteenth-century. This paper discusses his background as well as the lineage of his descendants. In addition, it discusses various opinions about the date of his birth, the place he was born and the date of his death. The paper also explores his education and his teachers, and emphasizes his contribution in producing kitab and other writings that have had a huge impact on the religious education of Muslims in this region of the Malay World. To achieve the article’s objectives, content analysis method was applied to the Sheikh Daud’s writing

Islamic Scholars in Malay Archipelago: Sheikh Daud al-Fatani (1769-1847M) Contribution‘s in Fiqh al-Shafie

Malay world had produced scholars who expert in fiqh, akidah, akhlak, Sufism, and another area. They actively disseminated Islam to local residents by producing plenty of publications as a valuable legacy to the Muslims, especially in the Malay archipelago. Among the scholars was Sheikh Daud bin Abdullah al-Fatani is known as a prolific scholar in various areas. However, his work in fiqh al-Shafie given less attention compared to other areas. This article examines the contribution of Sheikh Daud in writing descriptively and analyzes the works of fiqh al-Shafie. In order to achieve the objectives outlined, this article used the method of content analysis of these texts being entitled Bughyat al- Tullab, al-Saidu Wa al-Zabaih, al-Bahjat al-Saniyat, Mun al-Musalla, and Al-Hidayah Muta'allim. In addition, the method of semi-structured interviews was conducted to obtain additional data associated with the topic. The results showed Sheikh Daud gave a significant contribution to the development of Islam in the region of Malaya with the publication of scientific writing in the Fiqh Shafie area. He was able to do islah to the community around her by produced books and manuscripts. Those publications are still cited today

Analisis kitab tentang sifat dua puluh dalam Hidayah Al-Muta’allim Wa ‘Umdah Al-Mu’allim karangan Syeikh Daud Al-Fatani

Syeikh Daud al-Fatani merupakan antara pengarang dan prolifik yang terkenal di Nusantara. Beliau adalah ulama Patani yang paling masyhur dan produktif di rantau ini kerana telah menghasilkan banyak karya. Karyanya dalam bidang akidah yang ditulis dalam bahasa Melayu Jawi telah menyumbang kepada kepercayaan yang kukuh dan asas beragama yang betul kepada umat Islam di rantau ini. Kertas kerja ini merupakan kajian takhkik teks kitab Hidayah al-Muta'allim Wa ‘Umdah al-Mu’allim yang memberi fokus kepada analisis perbincangan sifat dua puluh Allah S.W.T. Metode yang digunakan adalah metode analisis kandungan. Hasil kajian menunjukkan Syeikh Daud telah membahagikan sifat ini kepada sifat nafsiyyah dan sifat salbiyyah serta sifat ma’ani dan sifat ma’nawiyyah. Memandangkan bahasa yang digunakan adalah bahasa klasik, cadangan dikemukakan kitab ini ditahqiq dengan terperinci terutama istilah-istilah akidah

Differentiation of Trophoblast Giant Cells and Their Metabolic Functions Are Dependent on Peroxisome Proliferator-Activated Receptor β/δ

Mutation of the nuclear receptor peroxisome proliferator-activated receptor β/δ (PPARβ/δ) severely affects placenta development, leading to embryonic death at embryonic day 9.5 (E9.5) to E10.5 of most, but not all, PPARβ/δ-null mutant embryos. While very little is known at present about the pathway governed by PPARβ/δ in the developing placenta, this paper demonstrates that the main alteration of the placenta of PPARβ/δ-null embryos is found in the giant cell layer. PPARβ/δ activity is in fact essential for the differentiation of the Rcho-1 cells in giant cells, as shown by the severe inhibition of differentiation once PPARβ/δ is silenced. Conversely, exposure of Rcho-1 cells to a PPARβ/δ agonist triggers a massive differentiation via increased expression of 3-phosphoinositide-dependent kinase 1 and integrin-linked kinase and subsequent phosphorylation of Akt. The links between PPARβ/δ activity in giant cells and its role on Akt activity are further strengthened by the remarkable pattern of phospho-Akt expression in vivo at E9.5, specifically in the nucleus of the giant cells. In addition to this phosphatidylinositol 3-kinase/Akt main pathway, PPARβ/δ also induced giant cell differentiation via increased expression of I-mfa, an inhibitor of Mash-2 activity. Finally, giant cell differentiation at E9.5 is accompanied by a PPARβ/δ-dependent accumulation of lipid droplets and an increased expression of the adipose differentiation-related protein (also called adipophilin), which may participate to lipid metabolism and/or steroidogenesis. Altogether, this important role of PPARβ/δ in placenta development and giant cell differentiation should be considered when contemplating the potency of PPARβ/δ agonist as therapeutic agents of broad application

PPARgamma in placental angiogenesis.

Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor involved in diverse biological processes including adipocyte differentiation, glucose homeostasis, and inflammatory responses. Analyses of PPARγ knockout animals have been so far preempted by the early embryonic death of PPARγ-/- embryos as a consequence of the severe alteration of their placental vasculature. Using Sox2Cre/PPARγL2/L2 mice, we obtained fully viable PPARγ-null mice through specific and total epiblastic gene deletion, thereby demonstrating that the placental defect is the unique cause of PPARγ-/- embryonic lethality. The vasculature defects observed in PPARγ-/- placentas at embryonic d 9.5 correlated with an unsettled balance of pro- and antiangiogenic factors as demonstrated by increased levels of proliferin (Prl2c2, PLF) and decreased levels of proliferin-related protein (Prl7d1, PRP), respectively. To analyze the role of PPARγ in the later stage of placental development, when its expression peaks, we treated pregnant wild-type mice with the PPARγ agonist rosiglitazone. This treatment resulted in a disorganization of the placental layers and an altered placental microvasculature, accompanied by the decreased expression of proangiogenic genes such as Prl2c2, vascular endothelial growth factor, and Pecam1. Together our data demonstrate that PPARγ plays a pivotal role in controlling placental vascular proliferation and contributes to its termination in late pregnancy

SCAP is required for timely and proper myelin membrane synthesis

Myelination requires a massive increase in glial cell membrane synthesis. Here, we demonstrate that the acute phase of myelin lipid synthesis is regulated by sterol regulatory element-binding protein (SREBP) cleavage activation protein (SCAP), an activator of SREBPs. Deletion of SCAP in Schwann cells led to a loss of SREBP-mediated gene expression involving cholesterol and fatty acid synthesis. Schwann cell SCAP mutant mice show congenital hypomyelination and abnormal gait. Interestingly, aging SCAP mutant mice showed partial regain of function; they exhibited improved gait and produced small amounts of myelin indicating a slow SCAP-independent uptake of external lipids. Accordingly, extracellular lipoproteins partially rescued myelination by SCAP mutant Schwann cells. However, SCAP mutant myelin never reached normal thickness and had biophysical abnormalities concordant with abnormal lipid composition. These data demonstrate that SCAP-mediated regulation of glial lipogenesis is key to the proper synthesis of myelin membrane, and provide insight into abnormal Schwann cell function under conditions affecting lipid metabolism

The glucocorticoid-induced leucine zipper (gilz/tsc22d3-2) gene locus plays a crucial role in male fertility.

The glucocorticoid-induced leucine zipper (Tsc22d3-2) is a widely expressed dexamethasone-induced transcript that has been proposed to be important in immunity, adipogenesis, and renal sodium handling based on in vitro studies. To address its function in vivo, we have used Cre/loxP technology to generate mice deficient for Tsc22d3-2. Male knockout mice were viable but surprisingly did not show any major deficiencies in immunological processes or inflammatory responses. Tsc22d3-2 knockout mice adapted to a sodium-deprived diet and to water deprivation conditions but developed a subtle deficiency in renal sodium and water handling. Moreover, the affected animals developed a mild metabolic phenotype evident by a reduction in weight from 6 months of age, mild hyperinsulinemia, and resistance to a high-fat diet. Tsc22d3-2-deficient males were infertile and exhibited severe testis dysplasia from postnatal d 10 onward with increases in apoptotic cells within seminiferous tubules, an increased number of Leydig cells, and significantly elevated FSH and testosterone levels. Thus, our analysis of the Tsc22d3-2-deficient mice demonstrated a previously uncharacterized function of glucocorticoid-induced leucine zipper protein in testis development

A hypomorphic mutation in lpin1 induces progressively improving neuropathy and lipodystrophy in the rat.

The Lpin1 gene encodes the phosphatidate phosphatase (PAP1) enzyme Lipin 1, which plays a critical role in lipid metabolism. In this study we describe the identification and characterization of a rat model with a mutated Lpin1 gene (Lpin1(1Hubr)), generated by N-ethyl-N-nitrosourea mutagenesis. Lpin1(1Hubr) rats are characterized by hindlimb paralysis and mild lipodystrophy that are detectable from the second postnatal week. Sequencing of Lpin1 identified a point mutation in the 5'-end splice site of intron 18 resulting in mis-splicing, a reading frameshift, and a premature stop codon. As this mutation does not induce nonsense-mediated decay, it allows the production of a truncated Lipin 1 protein lacking PAP1 activity. Lpin1(1Hubr) rats developed hypomyelination and mild lipodystrophy rather than the pronounced demyelination and adipocyte defects characteristic of Lpin1(fld/fld) mice, which carry a null allele for Lpin1. Furthermore, biochemical, histological, and molecular analyses revealed that these lesions improve in older Lpin1(1Hubr) rats as compared with young Lpin1(1Hubr) rats and Lpin1(fld/fld) mice. We observed activation of compensatory biochemical pathways substituting for missing PAP1 activity that, in combination with a possible non-enzymatic Lipin 1 function residing outside of its PAP1 domain, may contribute to the less severe phenotypes observed in Lpin1(1Hubr) rats as compared with Lpin1(fld/fld) mice. Although we are cautious in making a direct parallel between the presented rodent model and human disease, our data may provide new insight into the pathogenicity of recently identified human LPIN1 mutations