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Biomedical subjects

J Yip

Publications and source records attributed to J Yip.

At least 19 recordsLinked to original sources
PubMed2006

The action of TNFalpha and TGFbeta include specific alterations of the glycosylation of bovine and human chondrocytes.

Joint destruction in arthritis is often associated with high levels of inflammatory cytokines. Previous work has shown that inflammatory conditions can alter the activities of glycosyltransferases that synthesize the glycan chains of glycoproteins, and that these changes in turn can influence the functions of glycoproteins. We therefore examined glycosyltransferases involved in glycoprotein biosynthesis in primary cultures of bovine articular chondrocytes and human chondrocytes isolated from knee cartilage of osteoarthritis patients. Bovine chondrocytes exhibited enzyme activities involved in the synthesis of bi-antennary complex Asn-linked N-glycans, as well as the enzymes involved in the synthesis of GalNAc-Ser/Thr-linked O-glycans with the core 1 structure. Human chondrocytes, in addition, were able to synthesize more complex O-glycans with core 2 structures. TNFalpha was found to induce apoptosis in chondrocytes, and this process was associated with significant changes in lectin binding to chondrocyte cell surface glycans. TGFbeta increased cell proliferation, and had significant effects on cell surface glycosylation in bovine but not in human cells. These cytokine-specific effects were partially correlated with changes in glycosyltransferase activities. Thus, chondrocytes have many of the enzymes necessary for the synthesis of N- and O-glycan chains of glycoproteins. The O-glycosylation pathways and the effects of TNFalpha and TGFbeta on glycosylation differed between bovine and human chondrocytes. These alterations are of potential importance for the regulation of the functions of cell surface receptors on chondrocytes, and for an understanding of the pathophysiology of arthritis.

Aged↗
PubMed2006

Transcatheter device closure of atrial septal defects in the elderly: technical considerations and short-term outcomes.

BACKGROUND: Device closure of an atrial septal defect (ASD) results in symptom-reduction, right heart remodelling and lower pulmonary artery pressures. However it is unclear if there is a chronological limit to these benefits and whether device closure is safe in elderly subjects. The aim of this study was, therefore, to assess the safety and efficacy of device closure in patients >60 years. METHODS: Retrospective study of Amplatzer Septal Occluder device closures from a single institution (May 1999-August 2002). RESULTS: Fifty subjects aged >60 years (range 60-85 years) had ASD device closure (27% of the total cohort). Defect size and shunt size were similar for both younger and older groups (2.2:1 in both groups, p=0.9) as were procedural duration, fluoroscopy time and device size deployed. Baseline right ventricular (RV) systolic pressure ((younger vs. older) 39 vs. 49 mmHg, p<0.001) and right ventricular size (45 vs. 51 mm, p<0.001) were greater in the older group. Following closure RV systolic pressure (49 vs. 45 mmHg, p<0.01) and RV size (51 vs. 44 mm, p=0.01) decreased in the older group. CONCLUSION: Device closure of an ASD can be performed safely in older patients. The right heart shows signs of remodelling even in elderly subjects.

Aged↗
PubMed2004

Outcomes and alternative techniques for device closure of the large secundum atrial septal defect.

Outcomes of device closure of large and small secundum atrial septal defects (ASDs) as related to rim anatomy with the Amplatzer atrial septal occluder were compared. Rim adequacy (> or = 5mm) of the anterior, inferior, posterior, and superior rims was determined using transesophageal echocardiography. Balloon-stretched defect size defined patients into two groups: group 1, < or = 25 mm (n = 138); group 2, > 25 mm (n = 34). Rim deficiency (n = 62) was more frequent in group 2 compared to group 1 (50% vs. 33%; P = 0.07), especially inferior rim deficiency (35% vs. 2%; P = 0.005). Device deployment was successful in group 1 and group 2 (100% vs. 91%; P = 0.007). Unsuccessful deployment was associated with an ASD of > 25 mm (P = 0.007) and inferior rim deficiency (P = 0.001). At first follow-up (54 +/- 16 days), right ventricular systolic pressure had improved in both groups (P < 0.001). Closure of a large ASD associated with a lack of support in the inferior rim may warrant alternative strategies to position the device successfully.

Adult↗
PubMed2001

Localization of NK1 and NK3 receptors in guinea-pig brain.

In this study the localizations of tachykinin neurokinin-1 (NK1) and neurokinin-3 (NK3) receptors in the guinea-pig brain are described. In agreement with studies in rat and human brain, the neurons that exhibited the most marked NK1 receptor immunoreactivity were found in the dorsomedial caudate putamen. NK1 receptors were also widely distributed in diencephalic structures and in the mid and hind brain. NK3 receptors were distributed in both superficial and deep layers of the cortex and many appeared to be located on cells with astrocyte-like morphology in the glia limitans. In several regions including the thalamus, hypothalamus, amygdala, periaqueductal gray, substantia nigra and area postrema, both NK1 and NK3 immunoreactivity were found. The present study revealed that tachykinin receptors are widely distributed in the guinea-pig central nervous system.

Amino Acid Sequence↗
PubMed2001

Prevalence and risk indicators for destructive periodontal diseases in 3 urban American minority populations.

BACKGROUND, AIMS: Destructive periodontal diseases have been reported disproportionately more prevalent and severe in African-Americans relative to other American populations. Differences in subgingival microbiota and host immune response have also been reported for African-Americans, implying that risk factors for disease progression may also differ for these populations. Since it is not clear whether these differences are truly genetic or due to confounding variables such as social economic status, we examined a series of clinical, environmental, demographic, and microbiologic features associated with periodontal disease status in a group of 185 urban minority subjects resident within the greater New York metropolitan area. METHODS: The study population consisted of 56 Asian-American, 71 African-American and 58 Hispanic subjects. Clinical data recorded included pocket depth, attachment level, gingival erythema, bleeding upon probing, suppuration, and the presence of supragingival plaque. Environmental and demographic data recorded included smoking history, years resident in the United States, whether the subject reported a private dentist and occupational status. Subgingival plaque was sampled from the mesial aspect of all teeth exclusive of third molars and the levels of 40 subgingival species enumerated using checkerboard DNA-DNA hybridization. RESULTS: The African-American group had more missing teeth, deeper periodontal pocket depth and more attachment loss than the Asian-American or Hispanic groups. However, the African-American group were less likely to report having a private dentist, had a greater proportion of smokers and a greater proportion of unskilled individuals. The profile of subgingival species differed among the three ethnic/racial groups with A. actinomycetemcomitans, N. mucosa, S. noxia and T. socranskii significantly elevated in the Asian-American group and P. micros significantly elevated in the African-American group. When subset by occupational status, numbers of missing teeth, pocket depth, attachment level and prior disease activity were all found increased in the unskilled relative to the professional group. Local factors including the mean % of sites with plaque, marginal gingival erythema, bleeding upon probing and suppuration were also elevated in the unskilled group. The microbial profile differed among the 3 occupational groups with the unskilled group having elevated numbers of species associated with destructive periodontal diseases. CONCLUSIONS: Although greater destructive periodontal disease prevalence and severity were found in the African-American group, these results suggest that environmental and demographic variables, such as occupational status, may have a greater influence on risk indicators associated with disease prevalence and progression in these populations.

Adult↗
PubMed2000

Localization of tachykinin receptors and Fos-like immunoreactivity induced by substance P in guinea-pig brain.

1. In the present study, a comparison was made between the distribution of tachykinin NK1 and NK3 receptor immunoreactivity and the distribution of Fos-like immunoreactivity induced by the tachykinin agonist substance P (SP) in the guinea-pig brain. 2. In agreement with results from previous studies in rat brain, NK1 receptor-immunoreactive neurons were found to be widely distributed throughout the brain in the striatum and in diencephalic and mesencephalic structures, while NK3 receptor-immunoreactive neurons were mainly in telencephalic structures. Considerable overlap was observed between NK1 and NK3 receptor distributions. 3. Substance P induced Fos-like immunoreactivity (Fos-LI) in extensive areas of the guinea-pig brain. The induction of Fos-LI was markedly inhibited in many areas by pretreatment with the NK1 receptor antagonist SR 140333. The NK3 receptor antagonist SR 142801 reduced Fos-LI staining in fewer areas, although a reduction was observed in the cortex, striatum and hypothalamus. 4. In general, tachykinin receptors were located at sites corresponding to areas of functional activation by SP, as shown by Fos-LI. These results extend previous studies by adding a functional dimension to tachykinin receptor localization studies.

Animals↗
PubMed1999

Distribution of Fos-like immunoreactivity in guinea-pig brain following administration of the neurokinin-1 receptor agonist, [SAR9,MET(O2)11]substance P.

The tachykinins are a family of peptides with putative neurotransmitter roles in the nervous system. They mediate their effects via neurokinin-1, neurokinin-2 and neurokinin-3 receptors. There has been increasing interest in the therapeutic application of the tachykinin neurokinin-1 receptor antagonists in the treatment of pain and emesis, and more recently in depression. However, the central role of neurokinin-1 receptors is not well understood. The aims of the present study were to determine the behavioural responses of guinea-pigs, and the distribution of Fos-like immunoreactivity in the guinea-pig brain, following intracerebroventricular administration of the neurokinin-1 receptor-selective agonist, [Sar9,Met(O2)11]substance P. The effects of pretreatment with the neurokinin-1 receptor antagonist, SR 140333, were also investigated. Administration of [Sar9,Met(O2)11]substance P induced increased locomotor activity, as well as face washing, grooming and wet-dog shake behaviours, all of which were inhibited by the neurokinin-1 receptor antagonist, SR 140333, indicating the involvement of neurokinin-1 receptors. In order to localize the brain regions activated by [Sar9,Met(O2)11]substance P, the distribution of neurons expressing Fos-like immunoreactivity was examined. [Sar9,Met(O2)11]substance P induced increased Fos-like immunoreactivity in widespread areas, including the frontal cortex, hippocampus, amygdala, thalamus, hypothalamus, periaqueductal gray, area postrema and nucleus of the solitary tract. SR 140333 reduced Fos-like immunoreactivity induced by [Sar9,Met(O2)11]substance P in most areas. Thus, brain regions associated with emotion, sensation, learning and memory, autonomic regulation and emesis were activated by stimulation of neurokinin-1 receptors. The present data have added a functional domain to previous neurokinin-1 receptor localization studies by describing the extensive regions of the CNS that may be activated by stimulation of these receptors, and the potential of neurokinin-1 receptor antagonists to inhibit activation of these regions.

Animals↗
PubMed1998

Resistance to insulin-mediated glucose disposal as a predictor of cardiovascular disease.

Resistance to insulin-mediated glucose disposal has been postulated to predispose individuals to a cluster of associated abnormalities (Syndrome X) known to increase risk of cardiovascular disease (CVD). Although several abnormalities subsumed under the rubric of Syndrome X have been shown to predict CVD, there has been no prospective study evaluating the power of insulin resistance, the putative fundamental defect in the syndrome, in this context. Therefore, this study was initiated to evaluate the hypothesis that resistance to insulin-mediated glucose disposal would predict the development of CVD in healthy volunteers. To accomplish this goal, 147 normal, healthy, nonobese, volunteers were evaluated [4.7 +/- 0.1 yr (mean +/- SEM)] after baseline measurements of steady state plasma glucose concentration (an estimate of insulin-mediated glucose disposal), as well as other CVD risk factors. Clinical end points developed in 13 subjects during the follow-up period; hypertension in 5, coronary artery disease in 4, cerebrovascular accident in 3, and peripheral vascular disease in 1. There was a significant univariate relationship between SSPG and CVD (P < 0.002), with the majority of the events taking place in the tertile of subjects with the highest SSPG concentration, i.e. the greatest degree of insulin resistance. In contrast, no CVD events were observed in the tertile with the lowest SSPG concentrations; the most insulin sensitive. SSPG was also related significantly to diastolic blood pressure, triglyceride, and low-density lipoprotein and high-density lipoprotein cholesterol concentrations, and the glucose and insulin responses to oral glucose. All of these relationships were independent of age, gender, body mass index, estimates of physical activity, and smoking history. When SSPG was paired with each of the other variables in a series of multiple regression models, only SSPG, or insulin response, were independent predictors of CVD events. In conclusion, approximately one of every five healthy, nonobese subjects in the most insulin-resistant tertile, followed for approximately 5 yr, had a serious clinical event. These data highlight the importance of insulin resistance as a predictor of CVD.

Blood Glucose↗
PubMed1997

Distribution and substrate properties of agrin, a heparan sulfate proteoglycan of developing axonal pathways.

The distribution and substrate properties of agrin, an extracellular matrix heparan sulfate proteoglycan (HSPG), was investigated in the developing chick nervous system by immunocytochemistry, Western blotting, and in neurite outgrowth assays. By comparing the distribution of agrin with that of laminin-1, merosin (laminin-2), neurofilament, and neural cell adhesion molecule (NCAM), it was found that throughout development, agrin is a constituent of all basal laminae. From embryonic day (E) 4 onwards, agrin is also abundant in axonal pathways of the central nervous system, such as the optic nerve, the tectobulbar pathway, the white matter of the spinal cord, and the marginal and the molecular layers of the forebrain and the cerebellum. The abundance of agrin in brain decreases from E13 onwards. In the peripheral nervous system, agrin is present throughout development as a constituent of the Schwann cell basal laminae. Western blots confirmed the immunocytochemical data, showing maximum expression of agrin occurs during the early to medium stages of brain development. Western blots also showed that in mouse and human brain, agrin exists as an HSPG. Purified agrin did not support neurite outgrowth, rather it inhibited retinal neurite extension on mixed agrin/merosin substrates. Despite the fact that agrin, when used as a substrate inhibited neurite outgrowth, its temporal and spatial overlap with growing axons suggests that agrin has a supportive role in the development of axonal pathways, possibly as a binding component for growth factors and cell adhesion proteins.

Agrin↗
PubMed1997

Localization of Fos-like immunoreactivity induced by the NK3 tachykinin receptor agonist, senktide, in the guinea-pig brain.

1. The effects of intracerebroventricular (i.c.v.) administration of the NK3 tachykinin receptor agonist, senktide (10 nmol each side), in guinea-pigs pretreated with the selective NK3 tachykinin receptor antagonist, SR142801 (3 mg kg(-1) subcutaneous, s.c., 30 min before senktide), or its less active enantiomer, SR142806 (3 mg kg(-1) s.c. 30 min before senktide), on behaviour and on the distribution of Fos-like immunoreactivity (Fos-LI) in central neurones were investigated. Guinea-pigs were chosen for the study since they possess NK3 tachykinin receptors with pharmacological characteristics similar to those in man. 2. Wet-dog shakes, but not locomotor activity, elicited by senktide i.c.v. were significantly reduced by SR142801 but not by SR142806, confirming the involvement of NK3 tachykinin receptors in wet-dog shake behaviour. 3. Senktide induced increased numbers of Fos-LI neurones in the following brain areas: frontal, parietal and piriform cortex, the lateral septum, the CA1, CA2, subiculum and dentate gyrus of the hippocampus, most areas in the amygdala, thalamus and hypothalamus, medial geniculate nucleus and the ventral cochlear nucleus. Pretreatment with SR142801, but not with SR142806, before administration of senktide inhibited Fos-LI expression in the cingulate cortex, dentate gyrus of the hippocampus, some regions of the thalamus, hypothalamus and amygdala and the ventral cochlear nucleus. 4. The present results are the first demonstration that senktide induces Fos-LI in widespread areas of the guinea-pig brain. It is proposed that NK3 tachykinin receptors may play a more extensive role in the control of diverse brain functions, including cortical processing, learning and memory, neuroendocrine and behavioural regulation, than is currently recognized.

Animals↗
PubMed1997

Enhanced collagen synthesis in cultured skin fibroblasts from insulin-dependent diabetic patients with nephropathy.

Excessive production and deposition of extracellular matrix proteins are characteristic features of diabetic nephropathy. This study tests the hypothesis that cells from diabetic patients who develop nephropathy have a disturbance in collagen metabolism compared with cells from diabetic patients without complications. Kinetics of overall collagen metabolism and total protein synthesis were examined in serially passaged, subconfluent, quiescent skin fibroblasts cultured in either normal (5 mM) or high (25 mM) glucose concentrations from 14 insulin-dependent diabetic (IDDM) patients with nephropathy; 14 IDDM patients without nephropathy matched for age, diabetes duration, and body mass index; and 14 healthy subjects. Fibroblasts were incubated in the presence of 2 microCi/ml [3H]proline, and after labeling the incorporation of [3H]proline into total protein, collagen (collagenase-sensitive material), and noncollagen proteins (collagenase-resistant material) was determined at different time points. Collagen degradation was determined in pulse-chase experiments by following the residual collagen-bound radioactivity after incubation for 8 h with 10 microCi/ml [3H]proline. In high glucose concentrations (25 mM), overall collagen synthesis (measured as [3H]proline incorporation into extracellular and intracellular collagenase-sensitive material) was significantly greater in the patients with nephropathy (mean +/- SEM after a 24-h labeling period: 7189 +/- 671 dpm/10(6) cells) than in the patients without (4341 +/- 267 dpm/10(6) cells; P < 0.01) or healthy control subjects (3836 +/- 234 dpm/10(6) cells; P < 0.01). No significant differences were observed in noncollagen protein production or in collagen degradation rates among the three groups of subjects. In the presence of normal glucose concentrations (5 mM), collagen synthesis was lower in all groups studied, but the differences between IDDM patients with nephropathy and those without remained unaltered. These results suggest that long-term cultured fibroblasts derived from diabetic patients with nephropathy exhibit an abnormality in collagen metabolism. Cells from long-standing diabetic patients without nephropathy have normal collagen metabolism. The increased collagen synthesis is likely to be intrinsic to those diabetic patients susceptible to nephropathy and may play an important role in the sclerotic processes that occur in the kidneys, arteries, and heart.

Adult↗
PubMed1996

The dorsal neural tube organizes the dermamyotome and induces axial myocytes in the avian embryo.

Somites, like all axial structures, display dorsoventral polarity. The dorsal portion of the somite forms the dermamyotome, which gives rise to the dermis and axial musculature, whereas the ventromedial somite disperses to generate the sclerotome, which later comprises the vertebrae and intervertebral discs. Although the neural tube and notochord are known to regulate some aspects of this dorsoventral pattern, the precise tissues that initially specify the dermamyotome, and later the myotome from it, have been controversial. Indeed, dorsal and ventral neural tube, notochord, ectoderm and neural crest cells have all been proposed to influence dermamyotome formation or to regulate myocyte differentiation. In this report we describe a series of experimental manipulations in the chick embryo to show that dermamyotome formation is regulated by interactions with the dorsal neural tube. First, we demonstrate that when a neural tube is rotated 180 degrees around its dorsoventral axis, a secondary dermamyotome is induced from what would normally have developed as sclerotome. Second, if we ablate the dorsal neural tube, dermamyotomes are absent in the majority of embryos. Third, if we graft pieces of dorsal neural tube into a ventral position between the notochord and ventral somite, a dermamyotome develops from the sclerotome that is proximate to the graft, and myocytes differentiate. In addition, we also show that myogenesis can be regulated by the dorsal neural tube because when pieces of dorsal neural tube and unsegmented paraxial mesoderm are combined in tissue culture, myocytes differentiate, whereas mesoderm cultures alone do not produce myocytes autonomously. In all of the experimental perturbations in vivo, the dorsal neural tube induced dorsal structures from the mesoderm in the presence of notochord and floorplate, which have been reported previously to induce sclerotome. Thus, we have demonstrated that in the context of the embryonic environment, a dorsalizing signal from the dorsal neural tube can compete with the diffusible ventralizing signal from the notochord. In contrast to dorsal neural tube, pieces of ventral neural tube, dorsal ectoderm or neural crest cells, all of which have been postulated to control dermamyotome formation or to induce myogenesis, either fail to do so or provoke only minimal inductive responses in any of our assays. However, complicating the issue, we find consistent with previous studies that following ablation of the entire neural tube, dermamyotome formation still proceeds adjacent to the dorsal ectoderm. Together these results suggest that, although dorsal ectoderm may be less potent than the dorsal neural tube in inducing dermamyotome, it does nonetheless possess some dermamyotomal-inducing activity. Based on our data and that of others, we propose a model for somite dorsoventral patterning in which competing diffusible signals from the dorsal neural tube and from the notochord/floorplate specify dermamyotome and sclerotome, respectively. In our model, the positioning of the dermamyotome dorsally is due to the absence or reduced levels of the notochord-derived ventralizing signals, as well as to the presence of dominant dorsalizing signals. These dorsal signals are possibly localized and amplified by binding to the basal lamina of the ectoderm, where they can signal the underlying somite, and may also be produced by the ectoderm as well.

Animals↗
PubMed1995

Effect of aqueous solutions of sucralose on plaque pH.

PURPOSE: To compare the effect on in vivo plaque pH of rinsing with an aqueous solution of sucralose (alone or in combination with maltodextrin or maltodextrin and dextrose) to the effect of rinsing with an aqueous solution of sucrose. MATERIALS AND METHODS: Each solution (four in total) had a sweetness equivalent to two teaspoons of sucrose in 6 oz. of water. The four test solutions were administered randomly over four test visits (one solution per visit) to 10 subjects presenting 2-day resting plaque. Before, and at specified time intervals over 60 minutes following the rinse, in vivo plaque pH was monitored at six designated sites using a Beckman 3500 digital pH meter. Data were analyzed by ANOVA. RESULTS: The mean pH minimum for the sucralose rinse (6.56) was significantly higher than the sucralose/maltodextrin (SM), sucralose/maltodextrin/dextrose (SMD), and sucrose rinses (6.15, 5.84, and 5.29, respectively). The mean delta pH (difference between resting and minimum pH) for the sucralose rinse (0.45) was significantly lower when compared to the SM (0.79), SMD (1.14), and sucrose (1.69) rinses. The differences seen in mean pH minimum and mean delta pH for the SM and SMD groups vs. the sucrose group were also statistically significant. Mean areas under the pH vs. time curve for the sucralose, SM and SMD rinses were all significantly less compared to the sucrose rinse. Rinsing with aqueous solutions of sucralose, or of sucralose in combination with maltodextrin and/or dextrose (commercially available formulations, of sucralose) was less acidogenic than rinsing with a sucrose solution of equivalent sweetness.

Adult↗
PubMed1994

A comparison of intralesional triamcinolone and cryosurgery in the treatment of acne keloids.

Keloid scarring presents a difficult therapeutic problem. It is a recognized sequel to acne vulgaris, and may be extensive and disfiguring. The data from this double-blind study, in which intralesional triamcinolone or cryosurgery were used as treatment for keloids, demonstrate that by treating early, and in particular vascular, keloids with the latter, 85% will show a moderate to good response in terms of flattening. Treatment with intralesional triamcinolone was also beneficial, but the response to cryosurgery was significantly better in early, vascular lesions.

Acne Keloid↗
PubMed1994

Serum sialic acid, a risk factor for cardiovascular disease, is increased in IDDM patients with microalbuminuria and clinical proteinuria.

OBJECTIVE: An elevated serum sialic acid concentration has recently been shown to be a potent cardiovascular risk factor in the general population. Because clinical proteinuria is associated with a high frequency of cardiovascular disease, and because microalbuminuria predicts the development of renal and cardiovascular disease in diabetes, we investigated whether serum sialic acid levels are increased in insulin-dependent diabetes mellitus (IDDM) patients with microalbuminuria or clinical proteinuria. RESEARCH DESIGN AND METHODS: We studied 23 patients with IDDM who had a normal urinary albumin excretion rate, 23 patients who had microalbuminuria, and 23 patients with clinical proteinuria. The patients were matched for age, sex, duration of diabetes, GHb levels, and body mass index (BMI). Fasting blood samples were taken for measurement of sialic acid, cholesterol, triglyceride, creatinine, and GHb. RESULTS: Serum sialic acid was significantly higher in the microalbuminuric patients compared with the normoalbuminuric group (mean +/- SD: 1.93 +/- 0.26 vs. 1.76 +/- 0.27 mM, P < 0.01). Moreover, serum sialic acid was also significantly higher in the group with clinical proteinuria compared with the microalbuminuric patients (2.34 +/- 0.24 vs. 1.93 +/- 0.26 mM, P < 0.001). Serum sialic acid was not related independently to age, BMI, diabetes duration, GHb, blood pressure, serum cholesterol, triglyceride, or creatinine concentration in any of the diabetic groups. CONCLUSIONS: These observations suggest that the serum sialic acid concentration is raised in IDDM patients with both microalbuminuria and clinical proteinuria and may play a role as a cardiovascular risk factor or disease marker in these conditions.

Adult↗
PubMed1993

Insulin resistance in insulin-dependent diabetic patients with microalbuminuria.

In insulin-dependent diabetes, microalbuminuria increases the risk of cardiovascular and renal disease. By means of a euglycaemic hyperinsulinaemic clamp method, we measured total-body glucose utilisation rate and studied the interaction of this measure of insulin sensitivity with known risk factors for cardiovascular disease in 14 diabetic patients with microalbuminuria and 14 with normal albumin excretion (median albumin excretion rate [AER] 56.2 [range 39.2-80.6] vs 8.8 [7.4-10.7] micrograms per min). The two groups were of similar age, duration of diabetes, and body-mass index. Total-body glucose disposal rate was significantly lower in the patients with microalbuminuria than in those without (mean 7.86 [SD 1.40] vs 9.04 [0.90] mg/kg per min; p < 0.05). There were also significant differences between the groups in the daily insulin dose needed for equivalent glucose control (0.76 [0.20] vs 0.65 [0.10] U/kg, p < 0.05), mean systolic blood pressure over 24 h ambulatory monitoring (134 [7] vs 127 [7] mm Hg; p < 0.05), and various plasma lipid concentrations, contributing to a more atherogenic profile in the microalbuminuric group. Total-body glucose disposal rate was inversely correlated with body-mass index and log10 AER. The insulin sensitivity of the microalbuminuric group remained impaired after adjustment for blood pressure and body-mass index. Impaired insulin sensitivity is a feature of insulin-dependent diabetic patients with microalbuminuria, which adds, with other factors, to the increased risks of renal and cardiovascular disease in these patients.

Adult↗
PubMed1993

Light cautery and EMLA in the treatment of chloracne lesions.

We report six patients with chloracne, unresponsive to conventional therapy, whose lesions were cleared by treatment with EMLA (eutectic mixture of lignocaine [lidocaine] 25 mg/g and prilocaine 25 mg/g) topical anaesthesia and light cautery. To the best of our knowledge, this form of treatment for chloracne has not previously been reported.

Adult↗