Biomedical subjects

S Azar

Publications and source records attributed to S Azar.

At least 19 recordsLinked to original sources

PubMed2006

Hypercalcemia in glioblastoma multiforme.

Hypercalcemia is commonly associated with cancer, occurring in around 10-20% of cancer patients. Hypercalcemia is usually related to solid and non-solid malignancies specifically breast cancer, lung cancer and multiple myeloma. Hypercalcemia has been reported to occur in association with astrocytomas, and uncommonly in gliomas. We report a case of a previously healthy man presenting with glioblastoma multiforme . He was found to have persistently elevated serum calcium and calcitriol with normal parathyroid function. This is the first reported case of hypercalcemia associated with glioblastoma multiforme.

Adult↗

PubMed2004

Diabetes mellitus and optic atrophy: a study of Wolfram syndrome in the Lebanese population.

Wolfram syndrome (WFS) is a rare hereditary neurodegenerative disorder also known as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness). WFS seems to be a heterogeneous disease that has not yet been fully characterized in terms of clinical features and pathophysiological mechanisms because the number of patients in most series was small. In this study we describe 31 Lebanese WFS patients belonging to 17 families; this, to our knowledge, is the largest number of patients reported in one series so far. Criteria for diagnosis of WFS were the presence of insulin-dependent diabetes mellitus and optic atrophy unexplained by any other disease. Central diabetes insipidus was found in 87% of the patients, and sensorineural deafness confirmed by audiograms was present in 64.5%. Other less frequent features included neurological and psychiatric abnormalities, urodynamic abnormalities, limited joint motility, cardiovascular and gastrointestinal autonomic neuropathy, hypergonadotropic hypogonadism in males, and diabetic microvascular disease. New features, not reported in previous descriptions, such as heart malformations and anterior pituitary dysfunction, were recognized in some of the patients and participated in the morbidity and mortality of the disease. Genetic analysis revealed WFS1 gene mutations in three families (23.5%), whereas no abnormalities were detected in mitochondrial DNA. In conclusion, WFS is a devastating disease for the patients and their families. More information about WFS will lead to a better understanding of this disease and hopefully to improvement in means of its prevention and treatment.

Adolescent↗

PubMed1999

Multinucleated giant cells in fine-needle aspiration of thyroid nodules: their diagnostic significance.

Multinucleated giant cells (MNGCs) are reported in many thyroid lesions. This study examines whether their quantity and quality can help in the differential diagnosis. All fine-needle aspirations (FNAs) of the thyroid with a "significant" number of MNGCs were reviewed from 1995 -1998. There were 23 cases (<1% of thyroid FNAs): 8 papillary carcinomas (PC), 4 subacute thyroiditis (ST), 3 granulomas, 7 adenomatous goiters (AG), and one Hurthle-cell adenoma (HA). MNGCs with dense cytoplasm were seen exclusively in PC, ST, and granulomas. They had angulated shapes. They were most numerous, largest, and with the highest number of nuclei in ST and granulomas. MNGCs with foamy cytoplasm were seen in AG and HA and 80% of the other cases (PC, ST, and granulomas). In PC, rare MNGCs had intranuclear inclusions and grooves. The accompanying cell population was characteristic of each disease. The quantity and quality of MNGCs in thyroid FNA may be helpful in narrowing the differential diagnosis. Diagn. Cytopathol. 1999;21:307-312.

Adenoma↗

PubMed1999

High protein vs high carbohydrate hypoenergetic diet for the treatment of obese hyperinsulinemic subjects.

OBJECTIVE: To test the hypothesis that hyperinsulinemic obese subjects would respond differently to changes in the composition of hypoenergetic diets. DESIGN: A 4-week randomized dietary intervention trial. SUBJECTS: Thirteen male obese hyperinsulinemic normoglycemic subjects were divided into two groups and fed hypoenergetic diets providing 80% of their resting energy expenditure (REE). One group received a high-protein diet (HP; 45% protein, 25% carbohydrates, and 30% fat as percent of dietary energy) and the other a high-carbohydrate diet (HC; 12% protein, 58% carbohydrates and 30% fat). MEASUREMENTS: Anthropometry, body composition, fasting serum insulin and lipids, and REE were performed before and after the feeding period. RESULTS: Weight loss was higher in the HP than HC group (8.3+/-0.7 vs 6.0+/-0.6 kg, P<0. 05). There was a decrease in body fat in both groups, whereas body water decreased significantly more in the HP group. REE decreased more in the HC than the HP group (-384.3+/-84.6 vs -132.3+/-51.0 kcal, P<0.05). Serum total cholesterol, triglycerides and LDL cholesterol decreased significantly to a similar extent in both diet groups, while HDL cholesterol was decreased significantly only in the HP group. Mean fasting insulin decreased significantly in both diet groups and reached the normal range only in the HP group. CONCLUSION: A low-carbohydrate (LC), HP hypoenergetic diet could be the diet composition of choice for a weight-reducing regimen in obese hyperinsulinemic subjects.

Basal Metabolism↗

PubMed1999

A low-calorie unrestricted protein diet attenuates kidney damage in uninephrectomized spontaneously hypertensive rats.

BACKGROUND/AIMS: Uninephrectomized, spontaneously hypertensive rats (UNX-SHR) develop glomerular hyperfiltration, hyperfusion, and interstitial infiltrate of the remnant kidney. Consequently, UNX-SHR is a useful animal model to investigate mechanisms involved in the progression of hypertensive renal disease. METHODS: Body weight; tail systolic blood pressure (SBP); urine excretion of protein, urea, and electrolytes; and serum biochemistry were determined in UNX-SHR at 2 months of age prior to uninephrectomy (week 0), prior to treatment (week 8) with a low-calorie (LC) or control diet, and one month after diet treatment (week 12). The LC diet was modified to allow equal intake of protein, sodium phosphorus, and other nutrients in both groups. RESULTS: UNX-SHR treated with the LC diet had significantly lower body weights and SBP at the end of the experiment than did the controls (p < 0.0001). Changes in serum biochemistry and 24-hour urinary excretion of protein, sodium, potassium, and urea nitrogen in both groups were not statistically significant. The final glomerular filtration rate and renal plasma flow were similar in both groups, but the LC diet significantly reduced the glomerular damage index (0.0007), mesangial expansion index (p < 0.002), volume of interstitium per cortex (p < 0.0003), tubular interstitium volume fraction (p < 0.0008), glomerular volume (p < 0.02), and remnant kidney weight (p < 0.01). CONCLUSION: We demonstrated that in UNX-SHR, the prevention of renal damage by LC diet may involve diminished glomerular growth and interstitial infiltrate without changes in renal hemodynamics. Consequently, LC diet, regardless of protein ingestion, may be an important tool in the prevention of renal damage in hypertension. Additional studies of obese-hypertensive rats may confirm the beneficial effect of a LC diet and weight reduction on the renal damage of obesity-hypertension.

Animals↗

PubMed1993

Clinicopathologic correlations of ABO and Rhesus blood type in colorectal cancer.

There is no specific association established between colorectal cancer and blood group type. In this study, the distribution of ABO and Rh blood groups was studied in 838 patients with colorectal cancer. There was no difference in distribution of ABO blood groups between patients who were Rh+ and Rh-. There was no difference in ABO blood group or Rh factor and tumor location. The highest A/O ratio was found in rectal cancer. Although there was no difference in stage distribution for each ABO blood group, there was a significant difference between the Rh+ and Rh- groups (P < 0.037). It is not clear, however, whether the prognosis is different between the two groups since there were more early tumors as well as incurable tumors in the Rh- group. All patients with synchronous cancer were Rh+. Further studies on blood group antigens are needed to elucidate the relationship between these antigens and colorectal cancer.

ABO Blood-Group System↗

PubMed1993

Low calorie unrestricted protein diet attenuates renal injury in hypertensive rats.

In the present investigation we researched the effects of low calorie diet without protein restriction on the renal function and glomerular injury of uninephrectomized spontaneously hypertensive rats. We compared the findings with those that occurred in two different groups of uninephrectomized spontaneously hypertensive rats: one treated with oral hydralazine (10 mg/kg per day) and a second fed regular food. The low calorie diet and hydralazine treatment significantly reduced intra-arterial blood pressure in each group (p < 0.05 and p < 0.001, respectively). The control group showed at the end of the experiment a slight but not significantly different increase in the intra-arterial blood pressure. Low calorie diet was more effective in protecting the kidney function. Creatinine clearance after treatment was significantly higher in uninephrectomized spontaneously hypertensive rats on a low calorie diet than in either the hydralazine-treated or control groups (p < 0.01). The 24-hour urinary protein excretion in the low calorie diet group was significantly lower than in the control group (p < 0.05) and lower but not statistically different from the hydralazine-treated group. The mean glomerular injury index of the remaining kidney in the low calorie diet group was lower than in either the hydralazine-treated or control groups (p < 0.05), and the mean mesangial expansion index in the low calorie diet group was significantly lower than in the control group (p < 0.05). The favorable effect of low calorie diet on renal function was independent of protein restriction or sodium and potassium content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Characterization of the adrenal 11 beta-hydroxylase in inbred salt-sensitive and resistant rats.

Rats have been bred for susceptibility and resistance to the hypertensive effect of dietary salt (S/JR & R/JR). S/JR have an abnormal adrenal steroid 11 beta,18-hydroxylase activity resulting in increased production of 18-OH-DOC. S/JR also produce increased quantities of 19-nor-DOC, which may be related, since the 11 beta,18-hydroxylase also catalyzes the 19-hydroxylation of DOC, a pivotal step in 19-nor-DOC biosynthesis. The purpose of the present studies was to further characterize the mutant S/JR adrenal steroid 11 beta,18-hydroxylase. Preliminary studies are also presented on assessing the renal 19-desmolase, the last step in 19-nor-DOC biosynthesis. Adrenal glands were harvested from R/JR and S/JR and prepared for incubation studies, protein immunoblotting, and RNA analysis. Kidneys from Sprague-Dawley rats were also used for isolated renal perfusion studies. Both S/JR and R/JR strains had a single immunostaining band for 11 beta,18-hydroxylase at 51,000 molecular weight which were equal in intensity. Both strains had a single RNA transcript at 4.3 kilobases which hybridized with equal intensity to the bovine cDNA (pB11-9). The Km for 11 beta- and 18-hydroxylation was identical within strains but was different between strains. The Km for 19-hydroxylation was different between S/JR and R/JR, and was much greater than 11 beta- and 18-hydroxylation in both strains. This suggests that the catalytic site for 19-hydroxylation is different than that for 11 beta- and 18-hydroxylation and that the S/JR enzyme binds the substrate with higher affinity than the R/JR enzyme. In the isolated perfusion studies the rat kidneys converted 80% of 19-oxo-DOC to either 19-oic-DOC or 19-nor-DOC. These data demonstrate that the difference in S/JR enzyme activity is probably due to a point mutation in the enzyme or to a change in a regulatory protein.

Adrenal Glands↗

PubMed1991

Environmental factor(s) during suckling exert long-term effects upon blood pressure and body weight in spontaneously hypertensive and normotensive rats.

To define the role of nurse and pup strain (spontaneously hypertensive rats: SHR nurses and shr pups; Wistar-Kyoto rats: WKY nurses and wky pups) and dietary salt in nurses and pups (low salt and high salt) upon pup body weight and blood pressure, we cross-suckled shr and wky from birth. Nurses after delivery and pups after weaning received either low- or high-salt diets. Pup body weight indicated that WKY dams were better nurses than SHR and that high salt in the nurse and pup diet decreased body weight. At 7 days, WKY on a low-salt diet normalized shr blood pressure and SHR on a high-salt diet reduced shr blood pressure. At 100 days, pup strain strongly affected blood pressure. Salt sensitivity to pup dietary salt depended upon a low-salt diet in nurses. Salt resistance depended on a high-salt diet in WKY nurses. At 300 days, pup strain accounted for most of the blood pressure variability. However, pup diet, pup strain and nurse diet also affected blood pressure (P = 0.05); the blood pressure of shr on a high-salt diet was higher if the nurse was an SHR on a high-salt diet. Thus, nurse environment modulated shr hypertension throughout life.

Animals↗

PubMed1991

Elevated 18-hydroxy-corticosterone in inbred salt-sensitive rats.

Rats susceptible to the hypertensive effect of dietary salt (SS/Jr) have excess 18-hydroxydeoxycorticosterone (18-OH-DOC) and 19-nor-DOC compared to control rats (SR/Jr). This may be caused by an abnormal adrenal 11 beta-hydroxylase, which catalyzes the 11 beta, 18, and 19-hydroxylations of DOC. A comparison of the urinary products of this enzyme including 18-OH-DOC, 19-nor-DOC, corticosterone (B), and 18-OH-B have not been described in the SS/Jr. Therefore, these steroid products were measured at 7 and 12 weeks of age in 36 weanling male and female, SS/Jr and SR/Jr (n = 9 in each group), on a low-salt diet. In both the male and female SS/Jr urinary free levels of 18-OH-DOC, 19-nor-DOC, and 18-OH-B were elevated, while B was not different at 6 and 10 weeks of age. The largest increases were in 18-OH-B levels, and these levels correlated with 18-OH-DOC and B but not 19-nor-DOC. The high degree of correlation between these steroids probably reflects their closely related dependence on adrenal 11 beta-hydroxylase biosynthesis.

18-Hydroxycorticosterone↗

PubMed1990

Studies of renal autoregulation in pancreatectomized and streptozotocin diabetic rats.

We studied renal autoregulation in pancreatectomized Munich-Wistar diabetic rats and in their sham-operated controls. In a second experiment we studied renal autoregulation in untreated and insulin treated streptozotocin diabetic Munich-Wistar rats and their nondiabetic controls. In the first experiment the diabetic rats had higher baseline renal blood flows (RBF). There was a fall in renal vascular resistance (RVR) and sustained RBF in both diabetic and control rats as renal perfusion pressures (RPP) was reduced from 130 and 110 mm Hg. As RPP was reduced from 110 and 80 mm Hg, there was no significant Change in RVR in control rats and RBF began to fall. Below RPP of 80 mm Hg RVR rose and RBF fell sharply in these rats. In contrast, there was a progressive fall in RVR as RPP was lowered to 60 mm Hg in the diabetic rats and, thus, RBF was much better sustained in these animals. In the second experiment the plasma glucose level was 502 +/- 52 mg/dl (X +/- SD) in the untreated diabetic rats and only modestly reduced to 411 +/- 49 mg/dl in the insulin treated animals. Untreated streptozotocin diabetic rats had moderately reduced and insulin-treated diabetic rats had mildly reduced baseline RVR and RBF. However, in these animals as in the pancreatectomized rats the increases in RVR noted in control rats at subautoregulatory RPPs were not seen. Thus, regardless of whether baseline RBFs were increased or decreased, diabetic rats sustained RBF at markedly reduced RPPs far more efficiently than did nondiabetic rats. The pathogenesis of these abnormalities in diabetic rats was not learned in these studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Na(+)-H+ antiporter and Na(+)-(HCO3-)n symporter regulate intracellular pH in mouse medullary thick limbs of Henle.

To determine mechanisms of intracellular pH (pHi) regulation in mouse medullary thick limbs (MTAL), pHi was measured in MTAL suspensions and in the isolated perfused MTAL by use of 2',7'-bis(carboxyethyl)-5(6)carboxyfluorescein (BCECF). A method to obtain MTAL suspensions from the mouse outer medulla is reported. Characterization of suspensions with microscopy, anti-Tamm-Horsfall antibody labeling, measurement of O2 consumption, and adenosine 3',5'-cyclic monophosphate responses to antidiuretic hormone indicated that these suspensions were highly purified for viable MTAL tubules. The resting pHi was 7.41 +/- 0.02 (means +/- SE) in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered media and 7.23 +/- 0.02 in CO2- HCO3(-)-buffered media, both at extracellular pH 7.4. MTAL tubules exhibited rapid pHi recovery from intracellular acidification. Recovery of pHi was dependent on luminal Na+ (apparent Km = 13.2 +/- 3.2 mM) and was inhibited by amiloride (apparent Ki = 10.6 microM), consistent with the activity of an apical Na(+)-H+ antiporter. Antiporter activity was enhanced by acidification and was diminished at the resting pHi. Recovery from intracellular alkalinization (rapid withdrawal of CO2- HCO3-) was sensitive to the stilbene anion transport inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, Cl(-)-insensitive, and Na(+)-sensitive, consistent with the activity of a Na(+)-(HCO3-)n symporter. Both transporters were significantly involved in steady-state pHi regulation in the presence of CO2- HCO3-. In contrast, the Na(+)-H+ antiporter played the dominant role in steady-state pHi regulation in the absence of CO2- HCO3-.

Animals↗

PubMed1989

Effects of dietary protein content in streptozotocin-diabetic rats.

We evaluated the influence of increased dietary protein intake on glomerular structure and function in Lewis rats made diabetic with streptozotocin. We found that diabetic animals on a 20% or 50% protein diet ate approximately 50% more protein and excreted about 50% more urinary urea nitrogen than did their respective similarly-fed nondiabetic controls. The 50% protein diet was associated with higher glomerular filtration rates (GFR) and renal blood flows (RBF) at two months in both diabetic and control animals compared to their respective controls on the lower protein diet. However, GFR and RBF were not significantly higher in the diabetic animals on the 50% protein diet in the controls on the 20% diet and were slightly, albeit not significantly lower than controls on the 50% diet. Glomerular capillary pressure (PGC) tended to be lower in the diabetic compared to their respective controls, while the high protein diet was associated with higher PGC in diabetic and nondiabetic animals. The PGC in the 50% diabetic rats was not different from the PGC in the nondiabetic rats. Urinary albumin excretion (UAE) rate was greater in the diabetic than in the nondiabetic animals. UAE was greatest in the high protein diabetic animals at six months. Glomerular basement membrane thickness after six months of diabetes was increased essentially equally in both normal and high-protein fed diabetic groups and was largely uninfluenced by diet in the controls. Fractional mesangial volume was increased and relative filtration surface was decreased only in the 50%-protein diet diabetic rats at six months. Thus, high protein diet was associated with increased fractional mesangial volume in diabetic rats, but this could not be explained by increased glomerular capillary flows or pressures. The mechanism of acceleration of mesangial expansion by high protein diet in diabetic animals was not elucidated by these studies.

Animals↗

PubMed1989

Effects of sorbinil on glomerular structure and function in long-term-diabetic rats.

We investigated the role of the aldose reductase pathway in the pathogenesis of the nephropathy of rats with sever (non-insulin-treated) streptozocin-induced diabetes of 6 mo duration. The initial experiment included four groups of rats: diabetic and control animals on a 20% protein diet, which were untreated or treated with sorbinil (an aldose reductase inhibitor). Food intake was increased by diabetes but was uninfluenced by sorbinil, whereas urinary urea nitrogen excretion was increased and body weight was decreased by both variables. Glomerular basement membrane (GBM) width was increased by diabetes and decreased by sorbinil. No other structural changes were noted. We speculated that sorbinil could have slowed the abnormal rate of GBM thickening in diabetic rats and the normal increase in GBM width in control rats by inducing a mild catabolic state. The second experiment also involved four groups of rats: diabetic and control animals on a 50% protein diet, which were untreated or treated with sorbinil. In these studies, diabetes was again associated with reduced body weight, but sorbinil had no influence on urinary urea nitrogen. Urinary albumin excretion, which was increased by diabetes, was not affected by sorbinil. GBM width was increased by diabetes, but in contrast to animals on 20% protein diets, the animals on 50% protein diets and treated with sorbinil did not have reduced GBM widths. Mesangial volume fraction was greater in diabetic animals than in controls, and sorbinil largely prevented mesangial expansion in them. Surprisingly, the control animals on the 50% protein diet and given sorbinil had increased mesangial volume fraction compared with control rats on the same diet not given the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehyde Reductase↗

PubMed1986

Umbilical blood pressures and utero-placental blood flow in spontaneously hypertensive rats.

Some substrains of spontaneously hypertensive rats (SHR) are hypertensive at birth, suggesting the possibility of pre-natal hypertension. Fetal haemodynamics are sensitive to utero-placental blood flow changes. Thus, we used micropuncture to measure umbilical vein blood pressure (BP) in SHR and Wistar-Kyoto rats (WKY) at 18 and 20 days post-conception. We determined utero-placental blood flow (UPBF) at 17 and 20 days post-conception by the microsphere method. Results showed that SHR fetuses were hypertensive only at 20 days. Fetal heart:body weight ratio was higher in SHR, decreased with age and was not associated with BP or heart rate. Utero-placental weight was not affected by either age or strain. However, utero-placental blood flow was low in SHR at 20 days. Thus, in SHR pre-natal hypertension occurs between 18 and 20 days post-conception; pre-natal hypertension is associated with low utero-placental blood flow.

Animals↗

PubMed1986

Parent and social-skills training for mentally retarded mothers identified as child maltreaters.

The effectiveness and generality of a parent- and social-skills training program for three mildly retarded mothers identified as child maltreaters were investigated. The program was conducted by one trainer in a community-based facility and included the following components: individualized performance standards, response-specific feedback, self-monitoring, and group rewards. A multiple-baseline design across parenting- and social-skill areas was used to evaluate the training. The findings revealed that the game contingencies effectively increased the mothers' ability to identify the most effective action to take in common problematic parenting and social situations. Generalization and recidivism data supported the efficacy of treatment gains.

Adult↗

PubMed1985

The role of the anteromedial hypothalamus in Dahl hypertension.

Radiofrequency lesions were placed in the anteromedial hypothalamus in Dahl rats to investigate the role of this area in salt-induced hypertension. Lesions of the paraventricular and suprachiasmatic nuclei and intervening tissue (PVN-SCN lesions) prevented the rise in blood pressure (mmHg) in salt-sensitive (DS) rats fed a high-salt (8% NaCl) diet for 15 weeks (controls: 195 +/- 9, lesioned: 128 +/- 11, p less than 0.01). Similar lesions in salt-resistant (DR) rats did not alter long-term blood pressure (controls: 121 +/- 6 mmHg, lesioned: 131 +/- 5). Lesions sparing the PVN had no effect on blood pressure in DS rats, while lesions primarily confined to the PVN delayed the rise of blood pressure in DS fed a high salt diet. Round-the-clock determinations demonstrated that the blood pressure of DS rats with PVN-SCN lesions was reduced relative to controls at all times of the day throughout the study. No differences were observed between the angiotensin-induced drinking and plasma sodium concentrations of rats with PVN-SCN lesions and those of controls. Twenty-four hour mean heart rate was decreased by 10% in DS rats with PVN-SCN lesions. The anteromedial hypothalamus may participate in the initiation of Dahl hypertension.

Animals↗

PubMed1984

Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats.

Hypertension frequently accompanies chronic glomerulonephritis. Mesangial injury and glomerulosclerosis are common in glomerulonephritis and are often harbingers of progressive glomerular destruction. Thus, in a model of mesangial immune injury we studied the relationship between hypertension, mesangial injury, and glomerulosclerosis. We induced mesangial ferritin-antiferritin immune complex disease (FIC) in Dahl salt-sensitive (S) and salt-resistant (R) rats. S and R rats with FIC were fed chow containing 0.3% NaCl until 14 weeks of age and then switched to 8.0% NaCl chow until 28 weeks of age. Groups of control S and R rats (no FIC) were either fed 0.3% NaCl for 28 weeks or switched to 8.0% NaCl chow at 14 weeks of age. Blood pressure, serum creatinine, urinary protein, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined at 14 and 28 weeks of age. R rats with or without FIC did not develop hypertension; mesangial injury was minimal. At 14 weeks of age, only S FIC rats developed hypertension, proteinuria, significant mesangial expansion and early glomerulosclerosis. At 28 weeks of age, proteinuria, mesangial expansion, and glomerulosclerosis were significantly more severe in hypertensive S rats with FIC than in those without FIC. These studies show that despite a normal salt intake, mesangial injury hastened the onset of hypertension, but only in rats genetically predisposed to hypertension (S FIC at 14 weeks). High dietary salt further aggravated hypertension, which, in turn, magnified both mesangial injury and glomerulosclerosis. Clinically, the different rates of progression of human glomerulonephritis associated with hypertension may be in part dependent on similar mechanisms.

Animals↗