An unusual presentation of metastatic prostate cancer.
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Biomedical subjects
Publications and source records attributed to D A Cottrell.
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Tomographic radiographs of 44 healthy temporomandibular joints in 22 patients undergoing large upward and forward rotations of the maxillomandibular complex were evaluated. Immediate postsurgery results showed decreases in all areas of the joint space. Long-term results showed a decrease in the superior and posterior regions, 14.8% and 19.7%, with no significant change anteriorly. Simple and multiple regression analysis did not show any relationship with age, gender, or degree of change in the decrease of the occlusal plane angle, to the temporomandibular joint changes described. Some condylar remodeling was noted.
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Macroglossia can create dentomusculoskeletal deformities, instability of orthodontic and orthognathic surgical procedures, and masticatory, speech, and airway problems. The cause of macroglossia must be clearly defined, and true macroglossia separated from pseudomacroglossia (displacement of the tongue created by anatomic factors other than tongue size alone). This article discusses the signs and symptoms of macroglossia, including the clinical and radiographic features, treatment techniques, as well as previously reported results. Cases are shown to illustrate the applicability of this technique.
Despite the establishment of heterotopic, whole cadaveric, pancreas-kidney transplantation as an effective form of therapy for type I diabetes with chronic renal insufficiency, uncertainty remains regarding the potentially deleterious effects of severe peripheral hyperinsulinemia and long-term immunosuppressive therapy on insulin sensitivity (SI) and, subsequently, on beta-cell function and maintenance of euglycemia over years. To examine the alterations in SI that may occur over time and their impact on glucose homeostasis, beta-cell function, SI, and glucose effectiveness (SG) were measured using the frequently sampled iv glucose tolerance test (FSIGTT) and minimal model method in 39 glucose-tolerant type I diabetic pancreas-kidney transplant recipients in a cross-sectional manner at 3, 6, 12, 24, 36, and 48 months post transplantation. Mean basal and poststimulation (oral glucose tolerance test and FSIGTT) serum glucose responses were similar among the groups from 3-48 months. Plasma insulin response during the FSIGTT was higher (P < 0.001, repeated measures ANOVA) at 6 months vs. 12-48 months. Incremental integrated areas under the curve for 1st phase, glucose-stimulated, tolbutamide-stimulated, and total insulin responses tended to be higher (P = NS) at 6 months. Glucose disappearance rate constant, kG, did not differ significantly from 3-48 months. Mean +/- SE S1 in the pancreas-kidney recipients was 4.25 +/- 1.6 x 10(-4) min-1/microU.mL-1 at 3 months (group 1, n = 7) (vs. 7.9 +/- 0.9 x 10(-4) normal reference), decreased to 2.95 +/- 0.6 at 6 months (group 2, n = 11), improved to baseline values of 4.6 +/- 1.0 at 12 months (group 3, n = 10), and normalized at 24 months (group 4, n = 6) to 7.5 +/- 1.7 (P = 0.008). The normalisation in SI was sustained at 36 months (group 5, n = 3, 8.0 +/- 3.7, P = 0.03), and up to 48 months (group 6, n = 5, 6.1 +/- 1.6, P = 0.04) in the type I diabetic pancrease allograft recipients. Corresponding SG tended to increase but did not differ significantly from 3 (1.69 +/- 0.2 x 10(-2)/min), 6 (2.33 +/- 0.39), 12 (1.9 +/- 0.2), 24 (1.9 +/- 0.4), 36 (1.98 +/- 0.15), and 48 months (2.27 +/- 0.3). Hepatic insulin extraction did not differ among the groups. SI correlated significantly with prednisone dose (r = -0.45, P = 0.002). In summary, after successful whole cadaveric, heterotopic, pancreas-kidney transplantation in type I diabetic recipients: 1) euglycemia remains relatively stable over 48 months; 2) SI is diminished early after transplantation (3-6 months), possibly caused by the effects of initially high doses of prednisone and hyperinsulinemia. However, this is compensated by a normal SG and by hyperinsulinemia to maintain euglycemia; 3) SI improves by 12 months and normalizes from 24-48 months, after transplantation, despite hyperinsulinemia and long-term immunosuppressive therapy. The time-dependent decrease in poststimulation insulin response after successful pancreas-kidney transplantation in type I diabetic recipients, therefore, is not caused by gradual beta-cell decline but rather is a response to normalization of SI. However, longitudinal studies pre-and post pancreas transplantation over an extended period of time will be necessary to confirm the present findings.
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A study of 56 patients (55 female, one male) with 100 reconstructed temporomandibular joints (TMJ) using the Techmedica custom-made total joint system (Techmedica Inc, Camarillo, CA) is presented. The patients ranged in age from 15 to 61 years (average, 39 years) and had 16 to 46 months' follow-up (average 30 months). Outcome groups were categorized as good, fair, or poor, based on clinical assessment. Results show that 35 patients (63%) with 58 joints (58%) had a good outcome, and 13 patients (23%) with 26 joints (26%) had a fair outcome, and 8 patients (14%) with 16 joints (16%) had a poor outcome. Patients with one or no previous temporomandibular joint surgeries had 86% in the good group, 14% in the fair group, and no patients in the poor group. In patients with two or more previous surgeries, the success rate decreased to 55% with good results, 26% with fair results and 19% with poor results. Long-term morbidity included five ramus prostheses that were removed or revised. Seventeen patients (30%) received further operations because of heterotopic bone formation, fibrosis, calcification, inflammation, and/or pain which occurred mostly in patients with previous Proplast/Teflon (Vitek, Inc, Houston, TX) implants. Continued pain has been associated with the poor group, which may be related to problems such as cervical neuropathy, sympathetic dystrophy, a residual inflammatory or immunologic reaction to Proplast/Teflon or silastic particles, fibrosis, calcification, heterotopic bone, or other unidentified factors.
Advances in orthognathic surgical treatment planning and in techniques for complex, simultaneous maxillary and mandibular repositioning have resulted in improved surgical accuracy. In traditional surgical sequencing, maxillary surgery is performed first; the maxilla is set, with or without an intermediate splint, using external reference points to verify and/or determine appropriate movement. However, errors in model surgery and intermediate splint fabrication can lead to surgical inaccuracy despite good surgical technique. In repositioning the maxilla first, when thin bony walls are present, and/or in conjunction with large mandibular advancements, maxillary shifting may occur when maxillomandibular fixation is applied. Soft tissue tension and surgical manipulation in this sequencing technique may result in a less desirable functional and esthetic outcome. This article presents an alternative to surgical sequencing and a modification of model surgery techniques to improve surgical accuracy, and thus predictability and stability of the results.
This study evaluated the long-term outcomes of 52 sternoclavicular grafts for temporomandibular joint (TMJ) reconstruction in 38 patients. Patients were divided into three groups according to preoperative diagnosis and evaluated an average of 45 months (range, 10 to 84 months) postsurgery. Group 1 consisted of 14 patients (24 joints) with previous Proplast/Teflon implants (P/T; Vitek, Inc, Houston, TX;); successful reconstruction was achieved in only four patients (29%) and seven joints (29%). Group 2 included 10 patients (14 joints) with inflammatory TMJ pathology (non-P/T); success occurred in five patients (50%) and eight joints (57%). Group 3 consisted of 14 patients (14 joints) with non-P/T and noninflammatory TMJ pathology. Success in this group occurred in 13 patients (93%) and 13 joints (93%), with only one failure. The results of this study support the use of the sternoclavicular graft for TMJ reconstruction in a select group of patients and demonstrate a high failure rate in patients with previous P/T implants.
We have examined the impact of race and positive family history of type 2 diabetes on glucose/insulin dynamics and the two components of glucose disposal in healthy, first-degree relatives of black and white American patients with type 2 diabetes mellitus who are at a greater risk from the disease and their healthy control subjects. Seventeen black and 15 white relatives were studied. Twenty-two black people and 24 white people, without family history of type 2 diabetes, served as healthy control subjects. Standard oral glucose tolerance test (OGTT) and tolbutamide-modified frequent sampling intravenous glucose tolerance (FSIGT) tests were performed in each subject. Insulin sensitivity index (SI) and glucose effectiveness (SG) were calculated using the MINIMOD method described by Bergman et al. Mean fasting and post-stimulation serum glucose levels were not significantly different in the black and white relatives. However, mean serum insulin responses to oral and/or intravenous stimulation were significantly greater in the blacks than whites, irrespective of positive family history of diabetes. The mean SI was significantly (P < 0.02) lower (52%) in the black (3.67 +/- 0.56) than the white [7.50 +/- 1.93 x 10(-4) min-1 (mU1)-1] relatives. Comparing the healthy controls, the mean SI was significantly (P < 0.02) lower (51%) in black than white controls (4.84 +/- 0.78 vs. 9.71 +/- 1.27 x 10 min-1(mU1)-1]. Mean SG and KG were greater (P < 0.05) in the blacks than whites, irrespective of family history of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
The pharmacological profile of FR115427 has been examined using ligand binding and electrophysiological techniques. Binding of [3H]dizocilpine in the presence of L-glutamate was inhibited by the (+) isomers of dizocilpine and FR115427. The corresponding (-) isomers were less active, and stereoselectivity was particularly marked in the case of FR115427. In contrast to dizocilpine, the affinity of FR115427 for [3H]dizocilpine binding sites was little affected by addition of either L-glutamate and/or glycine. In a cortical wedge preparation, FR115427 inhibited N-methyl-D-aspartate (NMDA)-induced responses in a non-competitive, use-dependent manner. Intracellularly recorded excitatory synaptic responses in hippocampal neurones were only partially inhibited by FR115427 thereby confirming a selective effect on the NMDA-mediated component of neuronal excitation induced by the endogenous neurotransmitter. The data suggest that FR115427 is a non-competitive, use-dependent NMDA receptor antagonist with more pronounced stereoselectivity and less marked use dependence than dizocilpine.
We analysed blood insulin and glucose concentrations before and during frequently sampled intravenous glucose tolerance tests (FSIGT) in 2 groups of Nigerian subjects: (A) Control group (n = 18), without a positive family history of diabetes mellitus, and (B) Experimental group (n = 16), comprising age-, sex- and body mass-matched first-degree relatives of patients with non-insulin-dependent diabetes mellitus (NIDDM). In comparison with Group A subjects, those in Group B had: (i) higher fasting plasma glucose level (mean +/- S.E.M. 4.1 +/- 0.1 vs. 3.8 +/- 0.11 mmol/l, P < 0.05); (ii) similar fasting serum insulin levels (6.7 +/- 5.0 vs. 5.8 +/- 5.6 mU/l, P = NS); (iii) lower mean incremental area under the first-phase (t = 0-10 min) post-glucose challenge insulin curve (376.9 +/- 8.8 vs. 435.6 +/- 5.6 mU/min l-1, P < 0.05); (iv) increased incremental area under the second-phase (t = 10-182 min) post-glucose challenge insulin curve (432.9 +/- 11.5 vs. 161.3 +/- 8.7 mU/min l-1, P < 0.05); (v) reduced KG rate constant of glucose elimination (0.97 +/- 0.12 vs. 1.41 +/- 0.12%/min, P < 0.05). These results suggest that the subjects with a positive family history of NIDDM have a reduced beta-cell insulin secretory reserve (from reduced first-phase insulin response), tendency to rebound hyperinsulinemia during the latter phase of the insulin secretory response, a degree of tissue insulin insensitivity (as evident from high fasting plasma glucose despite similar insulin levels) and a diminished glucose disposal rate, in comparison with subjects without a family history of NIDDM. These features predict subsequent development of diabetes and suggest that as in Caucasians, first-degree relatives of Nigerian patients with NIDDM are at greater risk for future development of the disease.
Oral lipomas buried deep in soft tissues can be difficult to diagnose clinically. Computed tomography or magnetic resonance imaging can aid the diagnosis of this rare oral lipoma.
OBJECTIVE: To examine the phases of acute insulin release and glucose homeostasis in people of African descent with and without a positive family history of type II diabetes who reside in geographically diverse environments. The prevalence of type II diabetes in people of African descent varies considerably depending on the country of habitat. Family history is recognized as an important risk factor for the development of the disease. RESEARCH DESIGN AND METHODS: We studied serum glucose and insulin concentrations--before and after intravenous glucose challenge--in glucose-tolerant, first-degree relatives of African-American (n = 18) and Nigerian (n = 20) type II diabetic patients and their respective healthy control subjects (African American, n = 9; Nigerian, n = 18) living in their native countries. The acute first- (t = 0-5 min) and second-phase (t = 10-60 min) insulin releases were calculated as the sum of incremental insulin responses to the intravenous glucose stimulation. RESULTS: Mean serum glucose levels and glucose decay constant (KG) were not different in the African Americans and Nigerians. Fasting serum insulin in the African-American relatives was significantly greater than the Nigerian relatives (16.0 +/- 3.0 vs. 5.8 +/- 1.7 mU/L, P < 0.05). In contrast, FSI levels in the African-American control subjects were similar to Nigerian control subjects (6.3 +/- 1.4 vs. 4.5 +/- 1.8 mU/L). Acute first- and second-phase insulin levels were 2-3 times (P < 0.01) greater in African Americans than Nigerians, irrespective of family history of diabetes. Comparing the African-American relatives with healthy control subjects, we found significantly (P < 0.05) higher FSI in the relatives; whereas the acute first- (272 +/- 44 vs. 222 +/- 55 mU/L) and second-phase (388 +/- 61 vs. 235 +/- 53 mU/L) serum insulin release tended to be greater, but not significantly different in the relatives. In contrast, the acute first (101 +/- 15 vs. 120 +/- 20 mU/L) and second phase (88 +/- 14 vs. 111 +/- 17 mU/l) of insulin release were slightly lower, but not significantly different, in the Nigerian relatives versus the Nigerian healthy control subjects. In a subgroup of nonobese African-American (n = 11) and Nigerian (n = 11) relatives, and African-American (n = 8) and Nigerian (n = 7) healthy control subjects with a body mass index < 30 kg/m2, the mean fasting and post-stimulation serum glucose were not different. However, serum insulin concentrations in the African Americans were significantly different from those of the Nigerians. The pattern of insulin responses in the nonobese subjects was similar to those of the respective African-American and Nigerian groups. CONCLUSIONS: Our preliminary study demonstrates greater serum insulin responses and, perhaps, insulin resistance in glucose-tolerant African Americans than in their Nigerian counterparts, irrespective of family history of diabetes and obesity. We conclude that the antecedent lesions leading to the development of type II diabetes may be different in the first-degree relatives of African-American and Nigerian diabetic patients.
Until recently, little has been written concerning the area of combined orthognathic and rhinoplastic surgery. This may be due to the paucity of surgeons trained in these disciplines and the technical difficulty of the simultaneous performance of surgical procedures. A general approach to combine orthognathic and rhinoplastic treatment planning is presented in this paper. The advantages and disadvantages of combined orthognathic and rhinoplastic surgery are discussed and guidelines for performing combined surgery are given.
Decreased insulin sensitivity and glucose-dependent glucose disposal (glucose effectiveness) have been demonstrated in poorly-controlled Type 1 (insulin-dependent) diabetic patients. We have therefore examined the effects of successful pancreas transplantation that results in long-term physiologic normoglycaemia as measured by insulin sensitivity index and glucose effectiveness in 14 Type 1 diabetic recipients (Group 1) using the Bergman minimal model method. Their results were compared with those of five non-diabetic patients with kidney transplant alone (Group 2) and 10 healthy control subjects (Group 3). Mean plasma glucose levels were indistinguishable in Group 1 when compared to Groups 2 and 3. However, mean basal plasma insulin levels were two- and eight-fold greater in Group 1 (36 +/- 6 microU/ml) than in Group 2 (17 +/- 7 microU/ml) and Group 3 (4.5 +/- 0.6 microU/ml), respectively. Following intravenous glucose (t = 0 min) and tolbutamide (t = 20), peak incremental insulin levels were significantly (p less than 0.001) greater in Group 1 vs Groups 2 and 3. Mean insulin sensitivity index was 65% and 50% lower in Group 1 (2.89 +/- 0.45) and Group 2 (4.11 +/- 1.30), respectively, when compared to Group 3 (8.40 +/- 1.24 x 10(-1) min-1 (microU/ml)-1. In contrast, glucose effectiveness was similar in the three groups (Group 1, 2.48 +/- 0.26; Group 2, 2.05 +/- 0.21; and Group 3, 2.10 +/- 0.17 x 10(-2).min-1). We conclude that, despite prednisone-induced insulin resistance, normal glucose tolerance is achieved by hyperinsulinaemia and normalisation of glucose-dependent glucose disposal following pancreas-kidney transplantation in Type 1 diabetic patients.
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We have previously shown that the loss of acute first phase insulin secretion precedes pancreas allograft rejection and development of glucose intolerance in Type 1 diabetic patients. In order to examine whether there is a progressive loss of phases of insulin secretion and beta-cell function in technically successful pancreas transplants during the first year, we measured glucose, insulin, and C-peptide responses to physiological (mixed meal) and pharmacological (IV glucose and IV glucagon) stimulation in 27 glucose-tolerant, insulin-independent allograft recipients at 3, 6, and 12 months. Mean +/- SE fasting serum glucose levels were normalized throughout the study period. Postprandial serum glucose profiles tended to increase by 12 months compared to 3 and 6 months, although peak glucose levels were not statistically different. Following pancreas transplantation, basal serum insulin levels were high at 3 months (163 +/- 17 pM), 6 months (165 +/- 22 pM), and 12 months (248 +/- 54 pM, p = NS) in the Type 1 diabetic pancreas allograft recipients when compared to normal (25 +/- 3 pM). We observed slight elevations in postprandial insulin and C-peptide profiles at 12 months compared to 3 and 6 months. Following IV glucose and glucagon stimulation, serum insulin and C-peptide levels as well as phases of insulin release did not differ over the 12-month study period. Similarly, the glucose decay constant (KG) was nearly identical at 3, 6, and 12 months. In summary, 1 year following successful whole cadaveric, heterotopic pancreas transplantation in Type 1 diabetic recipients, fasting serum glucose remains normalized, while postprandial glucose tends to rise.(ABSTRACT TRUNCATED AT 250 WORDS)