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michael d hughson
  • 722 Solar Rd
    ALBQ, NM 87107

    Peshmerga General Hospital
    Quirga RD
    Sulaimania, Iraq
  • Retired professor and former chair of pathology. I have been working with the regional cancer hospital and the Peshm... more
    (Retired professor and former chair of pathology. I have been working  with the regional cancer hospital and the Peshmerga Military Hospital in  Sulaimaniyah of Iraqi Kurdistan since 2005. Our programs have contributed graduates to the Iraqi Board and the Arab Board of Medical Specialist. We conduct research in breast cancer and renal disease, emphasizing disease rates and outcome in low resource settings.)
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Acute leukemias that express antigens associated with more than one lineage have been classified as acute lymphocytic leukemia with myeloid markers, acute myeloid leukemia with lymphoid markers, or biphenotypic acute leukemia (BAL).... more
Acute leukemias that express antigens associated with more than one lineage have been classified as acute lymphocytic leukemia with myeloid markers, acute myeloid leukemia with lymphoid markers, or biphenotypic acute leukemia (BAL). Antibody to cytoplasmic CD79a has been recently introduced to flow cytometry. CD79a functions in and has a high degree of specificity for B-cell differentiation. It has only recently begun to be reported in biphenotypic acute leukemias. Cases of acute leukemia submitted to the flow cytometry laboratory were retrospectively reviewed beginning from the time analysis for cytoplasmic CD79a was added to leukemia and lymphoma panels. Among 89 cases of AML, 2 showed strong coexpression of CD79a. Both cases were differentiated FAB AML-M2 and demonstrated the t(8;21) with cytogenetics and the AML1/ETO rearrangement with fluorescence in situ hybridization (FISH). These are recurring abnormalities in FAB AML-M2. The immunophenotyping met proposed scoring criteria for a diagnosis of BAL. Nevertheless, the cytogenetic and FISH findings indicate that CD79a, despite its specificity for B-cell differentiation, represented the aberrant presence of a B-cell antigen in leukemias of distinct myeloid linage. It is doubtful that, in this setting, CD79a expression should be considered a manifestation of lineage ambiguity.
beta-Thalassemia (thal) is an important health problem in the Dohuk region of northern Iraq because of its high carrier rate and the frequency of consanguineous marriages. Thus, the need to establish an effective preventative program is... more
beta-Thalassemia (thal) is an important health problem in the Dohuk region of northern Iraq because of its high carrier rate and the frequency of consanguineous marriages. Thus, the need to establish an effective preventative program is paramount. As part of this effort, we initiated this study to determine the molecular basis of this disorder in the region. For the latter purpose, either parent of 104 registered beta-thal major/intermedia patients had their full blood counts, hemoglobin (Hb) electrophoresis, Hb A2 and Hb F quantitation performed. Their DNA was extracted, amplified and reverse hybridized to specific oligonucleotide probes to detect 20 beta-thal mutations. The testing detected 12 beta-thalassemic mutations. The eight most frequent were: IVS-II-1 (G-->A), codon 44 (-C), codon 5 (-CT), IVS-I-1 (G-->A), codon 39 (C-->T), IVS-I-6 (T-->C), codons 8/9 (+G) and IVS-I-5 (G-->C). These mutations accounted for 81.7% of the thalassemic defects in the studied individuals. The less frequent mutations were: codon 8 (-AA), IVS-I-110 (G-->A), codon 30 (G-->C) and codon 22 (-7 bp), and the beta-thalassemic defects remained uncharacterized in 11.5% of cases. This is the first study of beta-thal mutations from Iraq, and shows a frequency of thalassemic defects different from those reported in surrounding countries. It provides a foundation for prenatal genetic testing that will be part of a thalassemia prevention program in the Dohuk region.
A thrombotic microangiopathy that is identified in patients with the antiphospholipid syndrome (APS) represents only a part of the vascular pathology that can be associated with antiphospholipid antibodies (aPL). Tissues from two... more
A thrombotic microangiopathy that is identified in patients with the antiphospholipid syndrome (APS) represents only a part of the vascular pathology that can be associated with antiphospholipid antibodies (aPL). Tissues from two autopsies, four renal biopsies, two skin biopsies, and one amputated leg were obtained from six patients who met criteria for the diagnosis of APS. Three patients had systemic lupus erythematosus (SLE), one had lupus-like disease, and two had a primary APS. Five of the patients were hypertensive. Arteries of three patients disclosed fibrin thrombi along with widespread obstruction by recanalized intimal connective tissue. Small renal, leptomeningeal, and pulmonary arteries showed concentric cellular and fibrous intimal hyperplasia indistinguishable from hypertensive vascular disease. Glomerular capillary and afferent arteriolar thrombi were found in renal biopsies from two SLE patients. One of these SLE patients required a leg amputation in which the popliteal artery demonstrated thrombosis, intimal hyperplasia, and acute inflammation. The findings support clinical and experimental data that indicate aPLs cause thrombosis but suggest diversity in the pathogenetic mechanisms aPLs are capable of promoting. Inflammation seems to be rare and to accompany thrombosis. Intimal hyperplasia is particularly common. Its involvement of renal arteries may contribute to hypertension that develops in some APS patients.
A giant pigmented nevus grew rapidly as several discrete tumors at different locations in the scalp of a 5-mo-old child. One tumor located beneath the skin in the occipital calvarium invaded bone and dura mater. Five years after the... more
A giant pigmented nevus grew rapidly as several discrete tumors at different locations in the scalp of a 5-mo-old child. One tumor located beneath the skin in the occipital calvarium invaded bone and dura mater. Five years after the excision of the larger tumors, the child was asymptomatic having no further evidence of recurrence or continued growth of the neoplasma. In view of the propensity for giant pigmented nevi to concomitantly involve the central nervous system (leptomeningeal melanocytosis) and to rarely give rise to melanomas, this case is reported as demonstrating the subsequent benign behavior of a tumor that at first presented alarming growth, suggesting malignancy.
Zuni is a Pueblo Indian village having more than a sixfold greater incidence of nondiabetic end-stage renal disease than the rest of the United States. Renal biopsy specimens from 44 patients with nondiabetic renal disease were subdivided... more
Zuni is a Pueblo Indian village having more than a sixfold greater incidence of nondiabetic end-stage renal disease than the rest of the United States. Renal biopsy specimens from 44 patients with nondiabetic renal disease were subdivided into two groups. In group 1, 21 patients with asymptomatic microscopic hematuria revealed a mild mesangiopathic glomerulonephritis in 18 cases. The predominantly staining immunoglobulin was IgM in ten specimens and IgA in eight specimens. In group 2, 23 patients with symptomatic renal disease presented with nephrotic range proteinuria (11), renal insufficiency (eight), and hypertension (four). A mesangiopathic glomerulonephritis was diagnosed in 16 cases, and in 11 was IgA predominant. Three cases of membranoproliferative glomerulonephritis occurred in group 2. Five cases revealed focal glomerulosclerosis without immune deposits (three in group 1 and two in group 2). More than half (57%) of the patients undergoing biopsy were related. Cases of symptomatic nondiabetic renal disease showed a significant tendency to cluster among the members of four families, suggesting a hereditary influence in the pathogenesis of immune-mediated glomerulonephritis in the Zuni.
ABSTRACT
... Correspondence: Bahar Rasul Khdhir University of Sulaimani, Iraq Email: arammerza@ymail. com ABSTRACT ... (25), found a positive association with aging, and Murray et al. ... 2. Rothenbacher, D., Bode, G., Berg, G., Gommel, R.,... more
... Correspondence: Bahar Rasul Khdhir University of Sulaimani, Iraq Email: arammerza@ymail. com ABSTRACT ... (25), found a positive association with aging, and Murray et al. ... 2. Rothenbacher, D., Bode, G., Berg, G., Gommel, R., Gonser, T., Adler ,G., et al. (1998). ...
Examination of kidneys of ten patients with uremia and severe hypertension treated by chronic intermittent hemodialysis revealed a deposition of glycogen within interstitial cells of the renal medulla. This is unlike any described renal... more
Examination of kidneys of ten patients with uremia and severe hypertension treated by chronic intermittent hemodialysis revealed a deposition of glycogen within interstitial cells of the renal medulla. This is unlike any described renal distribution of glycogen. Electron microscopic studies performed in one case demonstrated monoparticulate glycogen both diffuse in the interstitial cell cytoplasm and locally aggregated beside lipid droplets. The findings provide evidence for a metabolic abnormality of renal medullary interstitial cells in patients who have protracted uremia.
Aim: To establish the contribution of macrophage mineralocorticoid receptor (MR) signalling to kidney infl ammation and injury in progressive kidney disease. Background: Clinical and experimental studies have identifi ed that MR... more
Aim: To establish the contribution of macrophage mineralocorticoid receptor (MR) signalling to kidney infl ammation and injury in progressive kidney disease. Background: Clinical and experimental studies have identifi ed that MR antagonists substantially reduce kidney injury; however, the side effect of hyperkalaemia, particularly in the context of renal impairment, is a major barrier to the use of this therapy. Thus, it would be benefi cial to determine the specifi c cellular targets and mechanisms by which MR antagonists protect against kidney injury. Methods: A 15 day model of accelerated anti-GBM glomerulonephritis was examined in groups (n = 8) of: (i) wild type (WT) mice; (ii) MR ox/fl /LysM mice lacking MR signalling in macrophages; and (iii) WT mice receiving the MR antagonist eplerenone (100 mg/kg/bid). Results: WT mice with anti-GBM glomerulonephritis developed glomerular crescents (37 ± 5%), severe proteinuria and a 6-fold increase in serum cystatin-C. In comparison to these disease controls, MR ox/fl /LysM mice and eplerenonetreated WT mice with anti-GBM glomerulonephritis displayed similar proteinuria; however, both groups had a 35% reduction in serum cystatin-C levels (p < 0.05 vs WT) and had reduced crescent numbers (MR ox/fl /LysM = 26 ± 4%, eplerenone-treated = 11 ± 5%, both p < 0.001 vs WT). The protection seen in MR ox/fl /LysM mice was associated with a 50% reduction in macrophages and a marked reduction in gene expression of M1 proinfl ammatory markers (TNF-α, iNOS, MMP-12). In contrast, the gene expression of profi brotic molecules (TGFβ1, PAI-1, collagen IV) was not affected. Conclusions: MR signalling in macrophages contributes to the proinfl ammatory response, glomerular damage and loss of renal function in mouse anti-GBM nephritis. Our comparison with eplerenone treatment shows that MR signalling in macrophages accounts for a substantial degree of the protection achieved systemic MR blockade in this disease model.
ABSTRACT
An epidemic of renal disease is occurring among the Zuni Indians in western New Mexico. In 1985, 1.6% of Zunis had clinically recognized renal disease and 1% had renal insufficiency. The incidence of end-stage renal disease (ESRD) in 1984... more
An epidemic of renal disease is occurring among the Zuni Indians in western New Mexico. In 1985, 1.6% of Zunis had clinically recognized renal disease and 1% had renal insufficiency. The incidence of end-stage renal disease (ESRD) in 1984 and 1985 was 14 times the rate for US whites, and three times the rates of other Indians in ESRD network 6. One third of the cases of renal disease and ESRD is due to type 2 diabetes, but the etiology of disease in most of the remainder is unknown. Affected subjects range from early childhood to old age. Early signs are hematuria, mild to moderate proteinuria, normal BP, and low total hemolytic complement, normal or low C3 and C4 levels, in about 40% of the cases. The clinical course varies from benign to rapidly progressive renal failure. Biopsies usually reflect an immune-complex mediated mesangiopathic glomerulonephritis, with IgA, IgG, IgM, and C3 variably present in the mesangium. In some cases, there is a very strong familial pattern suggesting autosomal dominant inheritance or a marked communal exposure effect. This may be a genetic disease educed by the consanguinity in the ethnically homogeneous Zuni population. Mesangiopathic renal disease is common in some Oriental populations, and this phenomenon may reflect the American Indians' Oriental ancestry. This disease may also be due to toxic exposures related to jewelry-making, potting, Zuni water, Zuni salt, or herbal or other products used for medicinal or religious purposes. This epidemic is much morbidity and generating huge costs for ESRD treatment. Further study is needed to better understand its etiology.
The number of nephrons in a single human kidney without overt disease ranges over a wide range, from approximately 200,000 to more than 2.7 million. Human birth weight is directly associated with higher nephron endowment, and accordingly... more
The number of nephrons in a single human kidney without overt disease ranges over a wide range, from approximately 200,000 to more than 2.7 million. Human birth weight is directly associated with higher nephron endowment, and accordingly much of the variation in adult human nephron number is present at birth. Whereas many animal studies have investigated the associations between low nephron number, adult blood pressure, and kidney disease, relatively few studies have been conducted in humans. However, available data suggest that lower nephron number in humans, at least in some populations, is associated with higher blood pressure and increased renal pathology. Until now, estimation of nephron number has required access to whole kidneys at autopsy. Recent reports of using magnetic resonance imaging to image, count, and size glomeruli in whole kidneys suggest that the noninvasive estimation of nephron number is close at hand.
Context: African Americans have a 4-fold greater risk than whites for developing end-stage renal disease. Glomerulomegaly, possibly related to obesity, has been identified in high-risk populations and is suggested to be a marker for... more
Context: African Americans have a 4-fold greater risk than whites for developing end-stage renal disease. Glomerulomegaly, possibly related to obesity, has been identified in high-risk populations and is suggested to be a marker for end-stage renal disease risk. Objective: To investigate differences in glomerular size and patient clinical characteristics at the time of renal biopsy for the major diseases contributing to end-stage renal disease. Design: Mean glomerular tuft volumes were estimated by the Weibel-Gomez method (1964) in native renal biopsies of 203 African American and 100 white patients 18 years of age and older by point counting on a stereologic grid. Glomerulosclerosis was graded on individual glomeruli from 0 to 4, and a glomerular sclerosis index was calculated for each biopsy. Relationships between the mean volume of nonsclerotic glomeruli, age, sex, race, sclerosis index, cortical fibrosis, estimated glomerular filtration rate, body mass index, and disease diagnosis were analyzed. Results: Racial differences in mean volume of nonsclerotic glomeruli and body mass index were not significant in any disease category, and African Americans had more severe disease as determined by sclerosis index, cortical fibrosis, and estimated glomerular filtration rate only in focal segmental glomerulosclerosis. For all patients, increased sclerosis index and cortical fibrosis and lower estimated glomerular filtration rate were best predicted by increased age (P < .001). Conclusions: For approximately the same severity of disease, African Americans were 10 years or more younger than whites with the difference being seen in all disease categories except membranous glomerulonephritis and diabetes. Glomerulomegaly relative to whites was not a distinguishing feature of African American renal biopsies.

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