Biomedical subjects
Publications and source records attributed to P Shah.
Fetus in fetu is a rare entity. The patient usually presents in childhood. A case in which the patient presented in adulthood, with a lump in the abdomen, is reported. Computed tomography findings were diagnostic of this condition and a prospective diagnosis could be made. Computed tomography also helped to differentiate it from mature teratoma.
PURPOSE: Penetrating keratoplasty for silicone oil keratopathy is associated with high risks and limited visual prognosis. This study examined the outcomes and factors influencing graft failure. METHODS: A retrospective, non-comparative, interventional case series of patients attending Moorfields Eye Hospital, London. RESULTS: A total of 24 penetrating keratoplasties were performed in 17 patients (13 men and four women) from 1991 to 2000. The mean age of patients undergoing surgery was 43.6 years (range 17-84 years, SD +/- 21.0). Silicone oil was removed before or during the time of initial penetrating keratoplasty in nine patients (52.9%) and left in situ in eight patients (47.1%). Ten out of 24 grafts survived (41.7%). The median duration of graft survival was 21 months (range 2 weeks-98 months) with median duration of follow up 33 months (range 2-100 months). At final follow up, the number of patients with a clear graft who had oil removed before or during the time of penetrating keratoplasty was seven out of 10 (70.0%). Risk factors for graft failure included hypotony, multiple keratoplasty, corneal neovascularization, rejection episode, silicone oil left in situ and postoperative glaucoma. CONCLUSIONS: Management of these complex patients requires a combined approach from anterior segment and vitreoretinal subspecialties. The long-term success of the graft can be improved if silicone oil is removed prior or during the time of penetrating keratoplasty.
BACKGROUND: The expression of endothelial constitutive nitric oxide synthase (NOS3) by squamous dysplasia and carcinomas of the head and neck has previously been described. We sought to compare NOS3 expression in squamous mucosa, glandular metaplasia, and adenocarcinoma of the esophagus. METHODS: Forty paraffin-embedded specimens from 20 patients with adenocarcinoma were stained with anti-NOS3 monoclonal antibody. The percentage of cells stained and the intensity of staining were determined for squamous epithelium, metaplasia, and adenocarcinoma. Staining characteristics were statistically analyzed according to clinical variables. RESULTS: NOS3 expression was significantly higher in adenocarcinoma and squamous epithelium compared with glandular metaplasia. Among the carcinomas, larger tumor size (T3/4), nodal positivity, and advanced TNM stage (III/IV) significantly correlated with increased NOS3 expression. CONCLUSIONS: NOS3 is expressed in reflux-induced lesions of the esophagus. Glandular metaplasia shows basal levels of NOS3 that significantly increase with malignant transformation and tumor progression. The role of free radicals in carcinogenesis is being actively studied.
In this paper, we describe the development and laboratory and field evaluation of a continuous coarse (2.5-10 microm) particle mass (PM) monitor that can provide reliable measurements of the coarse mass (CM) concentrations in time intervals as short as 5-10 min. The operating principle of the monitor is based on enriching CM concentrations by a factor of approximately 25 by means of a 2.5-microm cut point round nozzle virtual impactor while maintaining fine mass (FM)--that is, the mass of PM2.5 at ambient concentrations. The aerosol mixture is subsequently drawn through a standard tapered element oscillating microbalance (TEOM), the response of which is dominated by the contributions of the CM, due to concentration enrichment. Findings from the field study ascertain that a TEOM coupled with a PM10 inlet followed by a 2.5-microm cut point round nozzle virtual impactor can be used successfully for continuous CM concentration measurements. The average concentration-enriched CM concentrations measured by the TEOM were 26-27 times higher than those measured by the time-integrated PM10 samplers [the micro-orifice uniform deposit impactor (MOUDI) and the Partisol] and were highly correlated. CM concentrations measured by the concentration-enriched TEOM were independent of the ambient FM-to-CM concentration ratio, due to the decrease in ambient coarse particle mass median diameter with an increasing FM-to-CM concentration ratio. Finally, our results illustrate one of the main problems associated with the use of real impactors to sample particles at relative humidity (RH) values less than 40%. While PM10 concentrations obtained by means of the MOUDI and Partisol were in excellent agreement, CM concentrations measured by the MOUDI were low by 20%, and FM concentrations were high by a factor of 5, together suggesting particle bounce at low RH.
To determine whether type 2 diabetes mellitus alters systemic and regional free fatty acid ([3H]palmitate) metabolism, 14 nondiabetic (ND) and 14 type 2 diabetic (D) subjects underwent hyperinsulinemic-hyperglycemic (approximately 9.3 mM) clamps. The subjects were matched for age, body mass index, percent body fat, and fat-free mass. D subjects had more (P < 0.05) visceral fat than ND. During somatostatin, replacement growth hormone, and glucagon infusions, insulin was infused to achieve moderate (approximately 75 pmol/l) and high (approximately 150 pmol/l) physiological insulin levels. D subjects had greater (P < 0.02) systemic and regional (splanchnic and leg) palmitate release than ND subjects during both insulin infusion intervals. The relative contributions of splanchnic, leg, and nonsplanchnic upper body regions to systemic palmitate release did not differ between groups, although the last contributed the most (approximately 75%) to systemic palmitate release. Visceral fat area correlated with systemic palmitate flux (r = 0.45, P < 0.03) during both insulin infusions. We conclude that type 2 diabetes is associated with a generalized impairment in insulin suppression of lipolysis compared with equally obese ND individuals.
Cryptococcal infection is common in immunocompromised patients, often presenting with meningitis or meningoencephalitis. We report an unusual presentation of cryptococcal infection in an immunocompetent patient presenting with headache and hemiplegia. CT demonstrated a large ring-enhancing lesion in the parietal region with intralesional calcification.
In vitro studies indicate that glucagon-like peptide-1(7-36)-amide (GLP-1) can enhance hepatic glucose uptake. To determine whether GLP-1 increases splanchnic glucose uptake in humans, we studied seven subjects with type 1 diabetes on two occasions. On both occasions, glucose was maintained at approximately 5.5 mmo/l during the night using a variable insulin infusion. On the morning of the study, a somatostatin, glucagon, and growth hormone infusion was started to maintain basal hormone levels. Glucose (containing [3H]glucose) was infused via an intraduodenal tube at a rate of 20 micromol.kg(-1).min(-1). Insulin concentrations were increased to approximately 500 pmol/l while glucose was clamped at approximately 8.8 mmol/l for the next 4 h by means of a variable intravenous glucose infusion labeled with [6,6-2H2]glucose. Surprisingly, the systemic appearance of intraduodenally infused glucose was higher (P = 0.01) during GLP-1 infusion than saline infusion, indicating a lower (P < 0.05) rate of initial splanchnic glucose uptake (1.4 +/- 1.5 vs. 4.8 +/- 0.8 micromol.kg(-1).min(-1)). On the other hand, flux through the hepatic uridine-diphosphate- glucose pool did not differ between study days (14.2 +/- 5.5 vs. 13.0 +/- 4.2 micromol.kg(-1).min(-1)), implying equivalent rates of glycogen synthesis. GLP-1 also impaired (P < 0.05) insulin-induced suppression of endogenous glucose production (6.9 +/- 2.9 vs. 1.3 +/- 1.4 micromol.kg(-1).min(-1)), but caused a time-dependent increase (P < 0.01) in glucose disappearance (93.7 +/- 10.0 vs. 69.3 +/- 6.3 micromol.kg(-1).min(-1); P < 0.01) that was evident only during the final hour of study. We conclude that in the presence of hyperglycemia, hyperinsulinemia, and enterally delivered glucose, GLP-1 increases total body but not splanchnic glucose uptake in humans with type 1 diabetes.
We have previously reported that splanchnic glucose uptake, hepatic glycogen synthesis, and hepatic glucokinase activity are decreased in people with type 2 diabetes during intravenous glucose infusion. To determine whether these defects are also present during more physiological enteral glucose administration, we studied 11 diabetic and 14 nondiabetic volunteers using a combined organ catheterization-tracer infusion technique. Glucose was infused into the duodenum at a rate of 22 micromol. kg(-1). min(-1) while supplemental glucose was given intravenously to clamp glucose at approximately 10 mmol/l in both groups. Endogenous hormone secretion was inhibited with somatostatin, and insulin was infused to maintain plasma concentrations at approximately 300 pmol/l (i.e., twofold higher than our previous experiments). Total body glucose disappearance, splanchnic, and leg glucose extractions were markedly lower (P < 0.01) in the diabetic subjects than in the nondiabetic subjects. UDP-glucose flux, a measure of glycogen synthesis, was approximately 35% lower (P < 0.02) in the diabetic subjects than in the nondiabetic subjects. This was entirely accounted for by a decrease (P < 0.01) in the contribution of extracellular glucose because the contribution of the indirect pathway to hepatic glycogen synthesis was similar between groups. Neither endogenous and splanchnic glucose productions nor rates of appearance of the intraduodenally infused glucose in the portal vein differed between groups. In summary, both muscle and splanchnic glucose uptake are impaired in type 2 diabetes during enteral glucose administration. The defect in splanchnic glucose uptake appears to be due to decreased uptake of extracellular glucose, implying decreased glucokinase activity. Thus, abnormal hepatic and muscle (but not gut) glucose metabolism are likely to contribute to postprandial hyperglycemia in people with type 2 diabetes.
The development of an infected aortic (pseudo)aneurysm which occurred after placement of a coronary artery stent is reported. Complications of cardiac catheterization and coronary artery stent placement are infrequent and this complication has not yet been reported in the literature.
OBJECTIVE: To verify the association between APOE gene promoter polymorphisms and the development of AD and to determine whether the effect of promoter polymorphisms on AD is independent of the APOE epsilon4 allele. BACKGROUND: Three polymorphisms in the APOE promoter have been shown to modify APOE expression in vitro. Several studies have suggested that these polymorphisms may also modulate risk for AD, either independently or by modifying the effect of the APOE coding polymorphism. METHODS: The authors analyzed allele and genotype distributions for APOE and all three known APOE promoter polymorphisms (-491 A/T, -427 T/C, and -219 G/T) in a study group consisting of 237 subjects with AD and 274 age-matched controls. They then used log-linear and logistic regression analyses to test for possible interactions between APOE genotype and the promoter polymorphisms on risk of AD. CONCLUSION: A strong association between the APOE epsilon 4 allele and AD was detected regardless of promoter polymorphism status. In addition, the -491 AA genotype appears to be an independent genetic risk factor for AD. The -427 T/C polymorphism and the -219 T/G polymorphism were not directly associated with AD.
In the rat dentate gyrus, beta-adrenergic receptor (beta-AR) activation is thought to be important in mediating the effects of norepinephrine (NE). beta-AR-immunoreactivity (beta-AR-I) was localized in this study by light and electron microscopy in the rat dentate gyrus by using two previously characterized antibodies to the beta-AR. By light microscopy, dense beta-AR-I was observed in the somata of granule cells and a few hilar interneurons. Diffuse and slightly granular beta-AR-I was found in all laminae, although it was most noticeable in the molecular layer. Ultrastructurally, the cytoplasm of granule cell and interneuronal perikarya (some of which contained parvalbumin immunoreactivity) contained beta-AR-I. beta-AR-I was associated primarily with the endoplasmic reticula; however, a few patches were observed near the plasmalemma. Quantitative analysis revealed that the greatest proportion of beta-AR-labeled profiles was found in the molecular layer. The majority of beta-AR-labeled profiles were either dendritic or astrocytic. In dendritic profiles, beta-AR-I was prominent near postsynaptic densities in large dendrites, many of which originated from granule cell somata. Moreover, some beta-AR-I was found in dendritic spines, sometimes affiliated with the spine apparati. Astrocytic profiles with beta-AR-I were commonly found next to unlabeled terminals which formed asymmetric (excitatory-type) synapses with dendritic spines. Additionally, beta-AR-I was observed in a few unmyelinated axons and axon terminals, many of which formed synapses with dendritic spines. Dual-labeling studies revealed that axons and axon terminals containing tyrosine hydroxylase (TH), the catecholamine synthesizing enzyme, often were near both neuronal and glial profiles containing beta-AR-I. These studies demonstrate that hippocampal beta-AR-I is localized: 1) principally in postsynaptic sites on granule cells and a few interneurons (some of which were basket cells); and 2) in glial processes. These observations add further support to the contention that beta-AR-activation modulates synaptic function through disparate pathways: directly, at either postsynaptic densities or presynaptic processes, or indirectly, through adjacent glial processes.
BACKGROUND: Recent data indicate that colorectal cancer incidence and mortality in white Americans have been declining since 1985 at a rate of 2% to 3% per year. In African Americans, however, mortality from colorectal cancer appears to be increasing. We sought to evaluate the prevalence of colonic neoplasia in asymptomatic African Americans. METHODS: We performed a cross-sectional colonoscopy screening study to determine the prevalence of colonic neoplasia in asymptomatic African Americans older than 50 years of age. RESULTS: One hundred sixty-six subjects were evaluated for the study of whom 121 (69 women) were deemed to be asymptomatic average-risk persons and completed colonoscopy. Forty-two individuals (35%) had a total of 72 adenomas (67 tubular and 5 tubulovillous); 47 (65.3%) of these were proximal to the splenic flexure. Three subjects had an adenoma 1 cm or greater in diameter and none had severe dysplasia. CONCLUSIONS: The overall prevalence of adenomas in asymptomatic average-risk African Americans was comparable to that of previously described populations. The predominance of right-sided adenomas in this study confirms previous findings and is an area requiring further study. Until this issue is resolved, we suggest the use of colonoscopy rather than sigmoidoscopy for screening for colorectal neoplasia in asymptomatic, average-risk African Americans.
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A performa-guided survey was conducted among 47 young patients of diabetes mellitus (onset of diabetes <30 years). Questions included were regarding the type of treatment, health status information about diabetes, and the assumptions and experiences of the patients on certain psychosocial behavior. A total of 59.6% subjects said that they could disclose everything about their disease to their friends and acquaintances. Twenty-seven percent felt that they could divulge only partial information and 12.8% did not want to discuss their disease with their friends and acquaintances. Subjects who said that they could disclose about their disease felt that they could do so because they were putting a lot of effort into achieving better control of their blood glucose. One of the fears expressed about not discussing their disease was that in doing so people would treat them differently or perceive them as sick. However only 38% experienced such a change in the behaviour of their acquaintances. Seventy-three percent of them had received unsolicited advice from others about food and dietary restrictions. Forty-three percent of the subjects had received instructions from acquaintances to stop all treatment and shift to household remedies. Hypoglycemia could be a motivating factor to help patients to discuss their illness with the acquaintances.
Burns of the face often affect the ear causing deformation of the pinna or ear lobe due to perichondritis or loss of cartilage and excess scarring. The reconstruction of the ear lobe may be limited due to scarring of the surrounding tissues. We describe a preauricular flap for reconstruction of the anterior and posterior surface of the ear lobe following burn injury. This two stage technique of ear lobe reconstruction by a preauricular flap is not described in the available literature. An inferiorly based preauricular flap was harvested in a young lady who had post burn loss of the right ear lobe. This was folded on itself and sutured to reconstruct both surfaces of the ear lobe. After 6 months, it was released from its attachment at the retromandibular area to define the cheek lobe angle and to shape it. The preauricular flap for ear lobe contouring is a simple and easy technique. An adequate length may be harvested without significant donor site morbidity.
OBJECTIVE: To compare radial artery (RA) patency with internal mammary artery (IMA) patency for coronary artery bypass surgery in our early experience. METHODS: Symptomatic as well as asymptomatic patients with > or =1 RA coronary graft underwent postoperative angiography. Each anastomosis was considered separately. A string sign referred to a diffusely narrowed conduit, which did not fill the grafted coronary artery, as well as all occluded conduits. The raw value of P was adjusted for the testing of multiple hypotheses (P'). The patency data for each conduit was divided into two parts. 'Cut-off' stenosis for a conduit was the lowest dividing coronary stenosis at which a difference in patency rate with P< or =0.05 occurred. RESULTS: One-hundred-and-twenty-nine patients had 137 radial arteries and 157 angiograms. Only the most recent angiogram was analyzed for each patient at 13+/-0.7 months (n=129). Overall patency for arterial conduit 91% (n=404) was not different from venous conduit 91% (n=42) and patency for RA 90% (n=226) was not different from IMA 92% (n=178), (P'=0.999). Cut-off stenosis for RA was 70% and IMA was 40%. Patent arterial conduit had a mean coronary stenosis of 85% and non-patent conduit 64%, (P'<0.001). Right coronary territory patency was 82 vs. 94% for other territories (P'=0.022). No overall differences in patency were noted for patients with sequential anastomoses, symptoms or coronary disease at the anastomosis at the time of surgery. Reversible ischaemia was detected in the distribution of only two of 14 string signs in patients undergoing sestamibi exercise protocol following angiogram. CONCLUSION: There were no differences in patency between radial artery and internal mammary artery at 13 months post-operative. Lower coronary stenosis and right coronary territory predicted lower patency. The clinical importance of a string sign remains to be determined.
We tested the hypothesis that a lack of suppression of glucagon causes postprandial hyperglycemia in subjects with type 2 diabetes. Nine diabetic subjects ingested 50 g glucose on two occasions. On both occasions, somatostatin was infused at a rate of 4.3 nmol/kg x min, and insulin was infused in a diabetic insulin profile. On one occasion, glucagon was also infused at a rate of 1.25 ng/kg x min to maintain portal glucagon concentrations constant (nonsuppressed study day). On the other occasion, glucagon infusion was delayed by 2 h to create a transient decrease in glucagon (suppressed study day). Glucagon concentrations on the suppressed study day fell to about 70 ng/L during the first 2 h, rising thereafter to approximately 120 ng/L. In contrast, glucagon concentrations on the nonsuppressed study day remained constant at about 120 ng/L throughout. The decrease in glucagon resulted in substantially lower (P < 0.001) glucose concentrations on the suppressed compared with the nonsuppressed study days (9.2+/-0.7 vs. 10.9+/-0.8 mmol/L) and a lower (P < 0.001) rate of release of [14C]glucose from glycogen (labeled by infusing [1-14C]galactose). On the other hand, flux through the hepatic UDP-glucose pool (and, by implication, glycogen synthesis), measured using the acetaminophen glucuronide method, did not differ on the two occasions. We conclude that lack of suppression of glucagon contributes to postprandial hyperglycemia in subjects with type 2 diabetes at least in part by accelerating glycogenolysis. These data suggest that agents that antagonize glucagon action or secretion are likely to be of value in the treatment of patients with type 2 diabetes.
Insulin-induced stimulation of muscle glucose uptake (MGU) is impaired in people with type 2 diabetes. To determine whether insulin-induced stimulation of splanchnic glucose uptake (SGU) is also impaired, we simultaneously measured leg glucose uptake (LGU) and SGU in 14 nondiabetic subjects and 16 subjects with type 2 diabetes using a combined organ catheterization-tracer infusion technique. Glucose was clamped at approximately 9.3 mmol/l, while insulin concentrations were maintained at approximately 72 pmol/l (low) and approximately 150 pmol/l (high) for 3 h each. Endogenous hormone secretion was inhibited with somatostatin. Total body glucose disappearance was lower (P < 0.01) and glucose production higher (P < 0.01) during both insulin infusions in the diabetic compared with the nondiabetic subjects, indicating insulin resistance. Splanchnic glucose production was higher (P < 0.05) in the diabetic subjects during the low but not the high insulin infusion. SGU was slightly lower in the diabetic than in the nondiabetic subjects during the low insulin infusion and 50-60% lower (P < 0.05) during the high insulin infusion. LGU (P < 0.001), but not SGU, was inversely correlated with the degree of visceral adiposity. The contribution of the indirect pathway to hepatic glycogen synthesis did not differ in the diabetic and nondiabetic subjects. In contrast, both flux through the UDP-glucose pool (P < 0.05) and the contribution of the direct pathway to glycogen synthesis (P < 0.01) were lower in the diabetic than in the nondiabetic subjects, indicating decreased uptake and/or phosphorylation of extracellular glucose. On the other hand, glycogenolysis was equally suppressed in both groups. In summary, type 2 diabetes impairs the ability of insulin to stimulate both MGU and SGU. The defect appears to reside at a proximal (e.g., glucokinase) metabolic step and is not related to the degree of visceral adiposity. These data suggest that impaired hepatic glucose uptake as well as MGU contribute to hyperglycemia in people with type 2 diabetes.