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The proposal to develop an Iraqi-British project to protect and promote cultural heritage in Southern Iraq was first mooted at a lunch in the British Museum on 24 September 2007, involving Major-General Barney White-Spunner, Charles Moore, former editor of the Daily Telegraph, Neil MacGregor, Director of the British Museum, and John Curtis, Keeper of the Department of the Middle East at the British Museum. The lunch had been arranged to provide Major-General White-Spunner with recent information about the state of the Iraqi cultural heritage, as he was due to be deployed to Iraq in February 2008 as Commander-in-Chief of British troops and General Officer Commanding the Multi-National Division South-East. At the lunch, it was suggested that the greatest need would be to arrange for the inspection of archaeological sites and, if necessary, to arrange for the protection of them, and also to consider facilitating the reopening of some provincial museums. It is known that archaeological sites particularly in Southern Iraq suffered grievously from looting, particularly after the Second Gulf War, and most provincial museums were sacked following the First Gulf War in 1991 and again in 2003. Major-General White-Spunner immediately recognised the importance of these proposals and appointed a project manager, Major Hugo Clarke, to work up a scheme with John Curtis. The project has been made possible by a generous grant from the Department of Culture, Media and Sport, that has covered all costs except those incurred in Iraq, which have been met by the British Army.

Studies to date have demonstrated epidermal growth factor (EGF) receptors primarily on the outer plasma membrane of the human placental syncytiotrophoblasts facing maternal blood and to a lesser extent on the cytotrophoblast stem cells. In the present studies, first- and third-trimester human placental tissues were immunostained with monoclonal antibodies (MAb) to the EGF binding domain of the human EGF receptor or to the activated (tyrosine-phosphorylated) human EGF receptor. Cytotrophoblasts, syncytiotrophoblasts, and fetal connective tissue cells in first-trimester tissues immunostained with both MAb, with the notable exception of the absence of staining of activated EGF receptor over cytotrophoblast plasma membranes. In contrast, staining of third-trimester placentas with either MAb yielded little to no staining of either trophoblast cell layer but intense staining of fetal connective tissue cells. Staining for EGF receptors over cytotrophoblasts in the first trimester is consistent with the hypothesis that maternal EGF or TGF-alpha derived from the endometrium or placenta may be the mitogen responsible for cytotrophoblast cell division and that the receptors localized to the syncytiotrophoblast are involved in EGF regulation of differentiated function. The absence of heavy staining of activated EGF receptor on trophoblast plasma membranes in third-trimester placentas is consistent with down-regulation of EGF receptor activity.

Atopy has been said to make C/F clinically both better and worse. Since many of the symptoms of C/F resemble respiratory allergy,It is difficult to determine the presence of atopy in C/F on clinical grounds alone.Thirty-two C/F patients(13 males, 19 females;7-23 yrs.)of varying severity(scores 47-94)were studied to determine the presence of Type I (IgE mediated)hypersensitivity. Scratch and intradermal tests with 40 allergens(epidermoids,dust, mite, pollens, molds), peripheral eosinophil and basophil counts, and serum IgE levels (PRIST) were done. Sputum was cultured for fungus.Eight(25%) patients were sensitive to grass and/or ragweed. Twenty-three(72%)were sensitive to mold spores. Thirteen(41%)were sensitive to Aspergillus fumigatus. Eight(8/26=3l%)had positive sputum cultures for Aspergillus fumigatus. Five(16%)had serum IgE levels greater than normal (>122 U/ml.).Patients were grouped according to severity(I)n=11, score < 80; (II)n=21,score > 81. There was no relationship between IgE levels, eosinophil or basophil counts and severity of disease. Group I was more atopic when one of the criteria used for determining atopy was 5 or more positive skin tests (p < .05). These were usually due to mold allergens.Atopy occurs frequently in C/F and more commonly in the more severe C/F patients. Whether atopy is the cause or result of C/F severity remains to be determined. If the result, then a damaged and colonized respiratory tract may facilitate the development of atopy in C/F.

Urinary glycoprotein of Tamm and Horsfall (T & H) is a renal substance found in the ascending limb of the loop of Henle and the distal convoluted tubule. Excretion can be measured by 0.58 M NaCl precipitation. Normal excretion = (1.7–2.1 mg/hr/1.73 sq. m. body surface area). Increased excretion occurs with dichromate-induced renal tubular damage in rats. This observation suggested that monitoring T & H excretion might provide an early index of kidney damage in human allograft rejection. Eight patients (4 males, 4 females. Age 9–49 years) were studied during the first 37–120 days post-transplantation. Seven rejection episodes in 5 patients were diagnosed clinically. In each instance T & H excretion exceeded 25 mg/24 hours (½ upper limit of normal adult excretion = normal excretion of one kidney) prior to the onset of clinical rejection. The interval between onset of increased excretion and clinical rejection was between 4 and 14 days (mean = 9 days). Peak excretion rates up to 110 mg/24 hours occurred. High excretion rates in chronic rejection (1 patient) and in glomerulonephritis of the transplanted kidney (1 patient) were also observed. In these instances T & H was primarily in the form of insoluble urinary casts. Since anti-rejection measures are likely to be more effective when the diagnosis of a rejection episode is early, T & H measurement has a practical clinical value.