Derangement Research Articles

Parathyroid and bone. Skeletal derangement in patients with primary hyperparathyroidism

One of the principle purposes in treatment of patients with primary hyperparathyroidism in Japan is to improve bone fragility by increasing bone mineral density. Persistent excess actions of parathyroid hormone could cause decrease in bone mineral density and bone fragility. Parathyroid surgery should be considered when bone mineral density in patients with the disease is in a range of osteoporosis. After surgery, bone mineral density is increased with time during several years. It is suggested relative risk of fracture decreases with parathyroid surgery. Recently, accumulating evidence indicates that treatment with oral bisphosphonates increases bone mineral density in patients with mild primary hyperparathyroidism, although it is yet uncertain whether it also prevents fracture.

Pathophysiology in rickets/osteomalacia

Rickets/osteomalacia is a disorder causing mineralization defect and bone and skeletal fragility, although production of bone matrix proteins and their architecture is not impaired. The disease is called rickets and osteomalacia in children during skeletal development and in adults, respectively. Pathophysiology in rickets/osteomalacia is defect in vitamin D actions and/or hypophosphatemia. Vitamin D deficiency, inability of activation of vitamin D in vivo or functional derangement in vitamin D receptor is involved in impaired actions of vitamin D. Common causes of hypophosphatemia are excessive actions of fibroblast growth factor (FGF) 23 and renal tubular dysfunction. Among them FGF23 could be a principal regulator for phosphate metabolism, and many investigators are engaged in exploration of physiological and pathophysiological roles of FGF23 in human.

Simple Oral Treatment Greatly Reduces Both Atherosclerosis and Diabetes in Mice

It is increasingly clear that metabolic derangements in adipocytes and inflammation are found in both atherosclerosis and diabetes. Adipocyte

Secondary osteoporosis. Glucocorticoid induced osteoporosis in childhood : prophylaxis and treatment

Bone turnover rate during growth is extremely rapid. Bone growth is under the control of various hormonal environments. Long term administration of glucocorticoid in childhood induced not only osteoporosis but also growth failure via direct action on bone and cartilage and indirectly via hormonal derangements. Sex steroid is one of the important hormones for the bone mineral accrual and for cartilage maturation. Thus glucocorticoid usage during puberty results in irreversible derangements in bone health including bone growth and peak bone mass accrual. Recently bisphosphonates have been widely used in prophylaxis and treatment of the steroid induced osteoporosis in adult with large amount of evidences, which is largely unknown for the pediatric patients.

Pharmakotherapie der akuten schweren Herzinsuffizienz

Die akute schwere Herzinsuffizienz basiert haufig auf einem myokardialen Pumpversagen und dominiert als „low output“ Syndrom (LOS). Katecholamine sind seit langem etablierte Therapeutika in dieser Situation. Unter Berucksichtigung der pathophysiologischen Mechanismen beim akuten myokardialen Pumpversagen muss ein differential-therapeutisches Konzept bezuglich der Indikation der einzelnen Substanzen erstellt werden. Die Fortschritte der pharmakologischen Intervention mussen sich dabei an den pathophysiologischen Erkenntnissen orientieren. Aufgrund der Veranderungen des normalen Adrenozeptor-Systems („down“–Regulation Phanomen) bzw. gleichzeitiger beta-Blockade muss die klassische katecholaminorientierte Therapie der akuten, schweren Herzinsuffizienz neu uberdacht werden. Phosphodiesterase (PDE) III Hemmer und Ca++-Sensitizer (Levosimendan) stellen neue Behandlungskonzepte in dieser Situation dar. Sie fuhren zu einer Verbesserung der Hamodynamik mit Steigerung der linksventrikularen Funktion und Senkung erhohter Gefaswiderstande verbunden zu einer Verbesserung der Organperfusion. Ca++-Sensitizer fuhren daruberhinaus zu einer Verbesserung der diastolischen Funktion und besitzen myokard-protektive Effekte. PDE III Hemmern bzw. Ca++-Sensitizer in Kombination mit Katecholaminen bieten sich aus pharmakologischer Sicht als aussichtsreiche Therapieform bei akuter Herzinsuffizienz mit LOS an und sollten die ausschliesliche Gabe von Katecholaminen erganzen.

Management of glucocorticoid-induced osteoporosis in childhood

Bone turnover rate during growth is extremely rapid. Bone growth is under the control of various hormonal environments. Long term administration of glucocorticoid in childhood induced not only osteoporosis but also growth failure via direct action on bone and cartilage and indirectly via hormonal derangements. Sex steroid is one of the important hormones for the bone mineral accrual and for cartilage maturation. Thus glucocorticoid usage during puberty resulted in irreversible effect on bone health including bone growth and peak bone mass accrual. Recently bisphosphonates have been widely used in the treatment of these steroid induced bone disorders in adult with large amount of evidences. But in pediatrics, we are far from the firm evidences. Large scale randomized controlled study (RCT) is necessary.

Correlations of insulin resistance and neoplasms

Insulin resistance is a worldwide risk factor for the two most dangerous human disease groups; namely, for cardiovascular lesions and malignancies. The insulin resistance syndrome have five basic criteria: hyperglycemia, visceral obesity, elevated serum triglyceride level, low HDL-cholesterol level (dyslipidemia) and hypertension. Each of these criteria alone are risk factors for cancer, and they mean together a multiple risk. Insulin resistance of the liver, skeletal muscles, and fatty tissue leads to a reactive hyperinsulinemia by the increased secretory activity of the beta-cells. Insulin has diverse metabolic effects, and at the same time is a growth factor. It enhances the production and mitogenic activity of other, insulin-like growth factors, and leads to pathological cell proliferation. In the uncompensated phase of insulin resistance hyperglycemia appears, which promotes tumor genesis by several pathways. The elevated serum glucose level is advantageous for the increased DNA synthesis of the tumor cells. It provokes deliberation of free radicals, which will cause derangement of both the DNA and the enzymes having a role in the repair mechanisms. Hyperglycemia leads to a nonenzymatic glycation of protein structures, and the glycated products enhance the deliberation of free radicals, cytokines and growth factors. Insulin resistance means an enhanced risk for breast, pancreas, liver, colon, bladder, prostate and oral cavity cancers. The moderately increased fasting glucose level is also a risk factor for breast, stomach and colon cancers, even without manifestation of type 2 diabetes. Insulin resistance promotes tumor progression as well. In cancer patients with hyperglycemia or type 2 diabetes, the rate of tumor recurrence, metastatic spread and fatal outcome is higher as compared with the tumor patients without metabolic disease. The correlation between insulin resistance and tumor promotion reveals new possibilities in the prevention and treatment of cancer. The healthy diet, physical activity and weight loss increase insulin sensitivity, and decrease the risk for both cardiovascular diseases and malignancies.

Adenosine deaminase activities and fasting blood glucose in obesity

Background : A complex relationship seems to exist between adenosine deaminase (ADA) and insulin in obesity. Through its effect on adenosine, the enzyme can modulate the action of insulin and affect blood glucose while the administration of insulin is said to decrease the activities of the enzyme. Aim : To investigate the relationship between ADA and fasting blood glucose, (FBG) in obesity and determine whether assay of the enzyme activities could be used to monitor glycaemic control in obesity. Materials and Methods : Thirty-four obese, otherwise apparently healthy subjects (males=19, females=15) aged 17-70 years and 48 apparently healthy, non-obese individuals (male=34, females=14) aged 21-60 years served as control. Their FBG and serum ADA activity were determined using appropriate methods. Results : There were significant differences between the BMI, 20.0 ± 3.1kg/m2; FBG, 5.0 ± 0.77mmol/l; ADA, 7.26 ± 0.95U/l of control and corresponding values; 35.05± 4.24kg/ m2; 5.49 ± 1.32 mmol/l and 8.72 ± 1.14 U/l of the test subjects (p=0.0001, 0.001, ›0.05 respectively) The FBG and ADA of the control correlated positively with the BMI (range 21-28) showing metabolic derangement in excess weight. The correlation was completely lost in the obese subjects with BMI in excess of 30 .There was no correlation between ADA and FBG. Conclusion : The result shows that serum ADA may influence FBG yet it may not serve as an index of glycaemia in obesity. The rise in ADA activities in obesity may be due to insulin resistance or increased secretion of adenosine. Keywords : Obesity, adenosine deaminase, fasting blood glucose, BMI Journal of College of Medicine Vol. 11 (2) 2006: 115-119

Generating derangements by interchanging at most four elements

For the set S = 1,2,,n, a permutation :S S such that (i)i is called a complete permutation, and the string (1)(2)(n) is called a derangement. In this paper, the authors consider the generation of a...

Experimental cerebral ischemia and magnesium.

Cerebral ischemia engages multiple terminal pathways involving the loss of ionic homeostasis, and acute and delayed neuronal damage. Several studies have focused on the derangement of energy metabolism and calcium, but not on magnesium. Hypomagnesium or low dietary magnesium intake may increase the risk of stroke and other cardiovascular diseases. The neuroprotective effects of magnesium have been attributed to a variety of effects on pathophysiologic mechanisms during and after cerebral ischemia, such as antagonizing calcium-mediated metabolic processes, inhibition of the N-methyl-D-aspartate (NMDA) receptors and relaxing vascular smooth muscles. Systemically administered magnesium provides beneficial effects in both clinical patients and cerebral ischemic animal models. Magnesium, as one of the therapeutic agents in stroke treatment, has the advantages of being inexpensive, widely available, and causing few side effects. The optimal doses for the treatment of cerebral ischemia both in animal models and in humans have not been defined yet. Thus, we attempted to evaluate the effects of magnesium on experimental cerebral ischemia.

Outcomes of 152 temporomandibular joints following arthroscopic anterolateral capsular release by holmium: YAG laser or electrocautery.

The aim of this study was to investigate the clinical results and efficacy of arthroscopic anterolateral capsular release achieved through the use of a holmium:YAG laser or electrocautery for the management of patients with internal derangements of the temporomandibular joint (TMJ). We studied internal derangement (106 joints) and osteoarthritis (46 joints) of the TMJ in 129 patients. Preoperatively, the mean mouth-opening degree was 31 mm and 129 TMJs exhibited moderate to severe arthralgia. All patients underwent arthroscopic anterolateral capsular release achieved with a holmium:YAG laser (84 TMJs) or through electrocautery (68 TMJs). At the end of each patient's respective follow-up period, which ranged from 2 to 72 months (mean, 19 months), the mean mouth-opening degree was 43 mm (P<.0001). Also during that time, 105 joints were discovered to exhibit no arthralgia and 36 had mild arthralgia. The total success rates with 2 sets of criteria were 92.8% and 95.6%. Arthroscopic anterolateral capsular release is a minimally invasive and effective surgical method for the treatment of patients with TMJ intracapsular disorders.

88.18 Cycles in graphs and derangements

88.18 Cycles in graphs and derangements

Fallacies and Useful Truths: An Overview of History and Science for the Anesthesiologist… or Lust, Torture and Depravity: The Anatomy of Derangement

Fallacies and Useful Truths: An Overview of History and Science for the Anesthesiologist… or Lust, Torture and Depravity: The Anatomy of Derangement

A study on relationship between the contour of articular eminence and traces of the condylar kinematic center and its application in TMD patients

To investigate the relationship between the contour of articular eminence and traces of the condylar kinematic center during jaw opening movement in healthy subjects, and compare trace characteristics of condylar kinematic center and MRI findings in TMD patients. In 10 healthy subjects, jaw-opening motion was recorded. The kinematic center and terminal hinge axis point of the condyle were used as trace reference points. The contour of articular eminence was examined by MRI. Seven patients with TMD signs and/or symptoms (disk displacement) were selected for this study. The condylar trace was recorded during jaw protrusion and opening-closing. The internal derangement in temporomandibular joints was detected by MRI and defined as: (1). normal disk position, (2). disk displacement with reduction, (3). disk displacement without reduction. In healthy subjects, most of the opening traces of the kinematic center coincided with the contour of articular eminence (8/10 joints in left, 9/10 joints in right). For terminal hinge axis point, no trace coincided with the contour of articular eminence (0/20 joints in left and right). In TMD patients, according to MRI findings, the condylar traces of kinematic center in 3 normal disk position joints showed normal shape. However, in 6 disk displacements with reduction joints and 5 disk displacement without reduction joints, the condylar traces of kinematic center showed irregular patterns except 1 disk displacement with reduction joint. In comparison with the terminal hinge axis point, the opening traces of the kinematic center can be interpreted as the translatory movement of the condyle/disc along the articular eminence. The study suggests the use of kinematic center in condylar movement studies.

87.44 The Premiership and a measure of derangement

87.44 The Premiership and a measure of derangement

The 2002 Moyer Award. Metabolic effects of vitamin D on serum calcium, magnesium, and phosphorus in pediatric burn patients.

Severe burn injury results in profound metabolic derangements. Recently, we have shown that vitamin D metabolism is disturbed after burn injury. Vitamin D is essential for calcium and phosphorus homeostasis and skeletal bone integrity. The role of vitamin D on magnesium homeostasis is not well understood. The purpose of this study was to assess the effects of vitamin D deficiency on serum electrolytes. Forty-one pediatric burn patients with a mean (+/- SEM) total body surface area burn of 53.1 +/- 2.9% and full-thickness injury of 44.2 +/- 4.1% were studied from July 1996 to December 2000. The mean age of the patients was 6.5 +/- 0.8 years. Patients were studied for 6 weeks after admission to the hospital. Blood samples were obtained weekly for serum 25-hydroxycholecalciferol (25D), 1,25-dihydroxycholecalciferol (1,25D), and daily for calcium, magnesium, and phosphorus. Total intravenous (IV) replacement of calcium, magnesium, and phosphorus was also quantitated retrospectively. Bivariate and multivariate correlational analysis was used for statistical comparison. For the study duration, multivariate analysis demonstrated a positive correlation between 25D and serum calcium (r =.47, P <.05) and 1,25D and calcium (r =.27, P <.05). Overall, calcium had a positive correlation with phosphorus and a negative correlation with IV calcium replacement (ie, patients with lower calcium received more IV replacement). During the initial week of hospitalization (week 0), decreased 25D (mean 11.6 ng/ml; normal range 15-57 ng/ml) and 1,25D (mean 13.9 pg/ml; normal range 15-75 pg/ml) did not correlate with any other measured variable. In week 1, 1,25D (mean 15.2 ng/ml) had a positive correlation (r =.410, P <.05) with calcium (mean 7.70 mg/dl). Hypovitaminosis D observed in burn injury correlates with serum calcium and phosphorus abnormalities. Early after injury (<1 week) there was no observed correlation between vitamin D and other variables possibly because of the effects of burn shock. After 1 week, vitamin D appears to significantly effect phosphorus homeostasis. The relationship between vitamin D and magnesium is not well established. These results may indicate a role for vitamin D replacement therapy during the initial phase of burn resuscitation.

Limiting Distributions for Derangements

(2001). Limiting Distributions for Derangements. The American Mathematical Monthly: Vol. 108, No. 8, pp. 755-755.

Self-Deception and Superiority Complex: Derangement of Hierarchy in Jane Austen's Emma

Self-Deception and Superiority Complex: Derangement of Hierarchy in Jane Austen's Emma

Prevalence of TMJ disc displacement in a pre-orthodontic adolescent sample.

This study evaluated the prevalence of temporomandibular joint (TMJ) disc displacement in preorthodontic adolescents (75 boys, 119 girls) by means of magnetic resonance imaging (MRI). One hundred thirty-eight consecutive subjects were recruited regardless of TMJ signs or symptoms, whereas 56 other subjects were referred with associated signs or symptoms. Quantitative measurements of disc displacement and disc length were used to classify the degree of internal derangement into 6 categories on the basis of sagittal MRI slices of the joints. In addition, sideways disc displacement was determined from coronal MRI images of the joint. Unilateral and bilateral normal disc position was more prevalent in boys compared to girls. All forms of anterior and rotational disc displacement were more prevalent in the female sample than in the male. Sideways displacement was more prevalent in girls than boys and occurred more frequently in a lateral rather than a medial direction. This study supports previous studies in suggesting that disc displacements occur frequently in preorthodontic adolescents.

Dual Action of Leptin on Renal Sodium Handling

66 BACKGROUND: Leptin exerts a natriuretic effect when infused directly into renal artery. However, in the conditions like obesity where circulating level of leptin is increased, this local effect may be opposed by centrally mediated stimulation of renal sympathetic nerve activity (RSNA). To investigate the interrelationship of the two factors, we made renal clearance study during intravenous leptin infusion in male Sprague-Dawley rats pretreated with unilateral renal denervation. METHODS: Rats were anesthetized with 50 mg/kg body weight (BW) intraperitoneal pentobarbital and supplementation with intravenous α-chloralose. Left renal vessels were isolated from surrounding tissue and applied with 10% phenol solution. Catheters were inserted into bladder and the proximal cut end of left ureter. Recombinant murine leptin was infused intravenously at 1 mg/kg BW over 3 hours. Renal function was assessed by timed collection of urine from each kidney and arterial blood under constant infusion of inulin. In another series of experiment, RSNA was recorded from left renal nerve and expressed as percent change from baseline. RESULTS: Mean blood pressure and heart rate were not affected by leptin. RSNA increased gradually by 45% at 105 min after leptin infusion and remained elevated. Glomerular filtration rates were 0.49±0.04 and 0.44±0.03 ml/min/100 gBW in intact and denervated kidney and both did not change significantly after leptin infusion. Urinary sodium excretion (UNaV) from the intact kidney was 527±42 nEq/min at baseline, increased to 1098±173 at 45 min, and returned to 606±82 nEq/min at 135 min after leptin infusion. Concomitant values from the denervated kidney were 898±105, 1822±272, and 1305±159 nEq/min, respectively. Thus, the ratio of UNaV from denervated to intact kidney increased significantly from 1.71±0.14 and 1.68±0.16 at baseline and 45 min to 2.27±0.30 at 135 min after leptin infusion. CONCLUSIONS: These results suggest that sodium balance after exogenous leptin infusion is determined by tubular effect and renal sympathetic nerve activity. Derangement of these factors may facilitate hypertension in obese subjects.