bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Type 2 Diabetes on Insulin Secretion, Insulin Action, Glucose Effectiveness, and Postprandial Glucose Metabolism
Authors: Basu Ananda , Dalla Man Chiara , Basu Rita , Toffolo Gianna , Cobelli Claudio , Rizza Robert A. 
Published: February 2009

OBJECTIVE
In this study, we sought to determine whether postprandial insulin secretion, insulin action, glucose effectiveness, and glucose turnover were abnormal in type 2 diabetes.

RESEARCH DESIGN AND METHODS
Fourteen subjects with type 2 diabetes and 11 nondiabetic subjects matched for age, weight, and BMI underwent a mixed-meal test using the triple-tracer technique. Indexes of insulin secretion, insulin action, and glucose effectiveness were assessed using the oral “minimal” and C-peptide models.

RESULTS
Fasting and postprandial glucose concentrations were higher in the diabetic than nondiabetic subjects. Although peak insulin secretion was delayed (P &lt; 0.001) and lower (P &lt; 0.05) in type 2 diabetes, the integrated total postprandial insulin response did not differ between groups. Insulin action, insulin secretion, disposition indexes, and glucose effectiveness all were lower (P &lt; 0.05) in diabetic than in nondiabetic subjects. Whereas the rate of meal glucose appearance did not differ between groups, the percent suppression of endogenous glucose production (EGP) was slightly delayed and the increment in glucose disappearance was substantially lower (P &lt; 0.01) in diabetic subjects during the first 3 h after meal ingestion. Together, these defects resulted in an excessive rise in postprandial glucose concentrations in the diabetic subjects.

CONCLUSIONS
When measured using methods that avoid non–steady-state error, the rate of appearance of ingested glucose was normal and suppression of EGP was only minimally impaired. However, when considered in light of the prevailing glucose concentration, both were abnormal. In contrast, rates of postprandial glucose disappearance were substantially decreased due to defects in insulin secretion, insulin action, and glucose effectiveness.
Impaired Distal Thermoregulation in Diabetes and Diabetic Polyneuropathy
Authors: Rutkove Seward B. , Veves Aristidis , Mitsa Theophano , Nie Rui , Fogerson Patricia M. , Garmirian Lindsay P. , Nardin Rachel A. 
Published: February 2009

OBJECTIVE
To determine how thermoregulation of the feet is affected by diabetes and diabetic polyneuropathy in both wakefulness and sleep.

RESEARCH DESIGN AND METHODS
Normal subjects, diabetic subjects without neuropathy, diabetic subjects with small-fiber diabetic polyneuropathy, and those with advanced diabetic polyneuropathy were categorized based on neurological examination, nerve conduction studies, and quantitative sensory testing. Subjects underwent foot temperature monitoring using an iButton device attached to the foot and a second iButton for recording of ambient temperature. Socks and footwear were standardized, and subjects maintained an activity diary. Data were collected over a 32-h period and analyzed.

RESULTS
A total of 39 normal subjects, 28 patients with diabetes but without diabetic polyneuropathy, 14 patients with isolated small-fiber diabetic polyneuropathy, and 27 patients with more advanced diabetic polyneuropathy participated. No consistent differences in foot temperature regulation between the four groups were identified during wakefulness. During sleep, however, multiple metrics revealed significant abnormalities in the diabetic patients. These included reduced mean foot temperature (P &lt; 0.001), reduced maximal temperature (P &lt; 0.001), increased rate of cooling (P &lt; 0.001), as well as increased frequency of variation (P = 0.005), supporting that patients with diabetic polyneuropathy and even those with only diabetes but no diabetic polyneuropathy have impaired nocturnal thermoregulation.

CONCLUSIONS
Nocturnal foot thermoregulation is impaired in patients with diabetes and diabetic polyneuropathy. Because neurons are highly temperature sensitive and because foot warming is part of the normal biology of sleep onset and maintenance, these findings suggest new potentially treatable mechanisms of diabetes-associated nocturnal pain and sleep disturbance.
Exercise Capacity and All-Cause Mortality in African American and Caucasian Men With Type 2 Diabetes
Authors: Kokkinos Peter , Myers Jonathan , Nylen Eric , Panagiotakos Demosthenes B. , Manolis Athanasios , Pittaras Andreas , Blackman Marc R. , Jacob-Issac Roshney , Faselis Charles , Abella Joshua , Singh Steven 
Published: February 2009

OBJECTIVE
The purpose of this study was to assess the association between exercise capacity and mortality in African Americans and Caucasians with type 2 diabetes and to explore racial differences regarding this relationship.

RESEARCH DESIGN AND METHODS
African American (n = 1,703; aged 60 ± 10 years) and Caucasian (n = 1,445; aged 62 ± 10 years) men with type 2 diabetes completed a maximal exercise test between 1986 and 2007 at the Veterans Affairs Medical Centers in Washington, DC, and Palo Alto, California. Three fitness categories were established (low-, moderate-, and high-fit) based on peak METs achieved. Subjects were followed for all-cause mortality for 7.3 ± 4.7 years.

RESULTS
The adjusted mortality risk was 23% higher in African Americans than in Caucasians (hazard ratio 1.23 [95% CI 1.1–1.4]). A graded reduction in mortality risk was noted with increased exercise capacity for both races. There was a significant interaction between race and METs (P &lt; 0.001) and among race and fitness categories (P &lt; 0.001). The association was stronger for Caucasians. Each 1-MET increase in exercise capacity yielded a 19% lower risk for Caucasians and 14% for African Americans (P &lt; 0.001). Similarly, the risk was 43% lower (0.57 [0.44–0.73]) for moderate-fit and 67% lower (0.33 [0.22–0.48]) for high-fit Caucasians. The comparable reductions in African Americans were 34% (0.66 [0.55–0.80]) and 46% (0.54 [0.39–0.73]), respectively.

CONCLUSIONS
Exercise capacity is a strong predictor of all-cause mortality in African American and Caucasian men with type 2 diabetes. The exercise capacity-related reduction in mortality appears to be stronger and more graded for Caucasians than for African Americans.
Metabolic Syndrome as a Risk Factor for Cardiovascular Disease, Mortality, and Progression of Diabetic Nephropathy in Type 1 Diabetes
Authors: Thorn Lena M. , Forsblom Carol , Wadén Johan , Saraheimo Markku , Tolonen Nina , Hietala Kustaa , Groop Per-Henrik ,   for the Finnish Diabetic Nephropathy (FinnDiane) Study Group
Published: February 2009

OBJECTIVE
To assess the predictive value of the metabolic syndrome in patients with type 1 diabetes.

RESEARCH DESIGN AND METHODS
Patients were from the prospective Finnish Diabetic Nephropathy (FinnDiane) Study (n = 3,783): mean age 37 ± 12 years and diabetes duration 23 ± 12 years. Metabolic syndrome was defined according to World Health Organization (WHO), National Cholesterol Education Program (NCEP), and International Diabetes Federation (IDF) definitions. Follow-up time was median 5.5 years (interquartile range 3.7–6.7). Mortality data were complete, whereas morbidity data were available in 69% of the patients.

RESULTS
The WHO definition was associated with a 2.1-fold increased risk of cardiovascular events and a 2.5-fold increased risk of cardiovascular- and diabetes-related mortality, after adjustment for traditional risk factors and diabetic nephropathy. The NCEP definition did not predict outcomes when adjusted for nephropathy but markedly added to the risk associated with elevated albuminuria alone (P &lt; 0.001). The IDF definition did not predict outcomes.

CONCLUSIONS
The metabolic syndrome is a risk factor, beyond albuminuria, for cardiovascular morbidity and diabetes-related mortality in type 1 diabetes.
A strategy for new macrocycle magnetic materials synthesis
Authors: Mroziński Jerzy , Bieńko Alina 
Published: February 2009

AbstractA study of a series of new types of copper(II) and rhenium(IV) macrocyclic complexes, important macrocyclic molecular magnets, is reported. A detailed description of crystal structure and magnetic behavior of mononuclear copper(II) macrocyclic compounds: CuL1(ClO4)2 (L1 = N-d-2,4,4,9,11,11-hexamethyl-1,5,8,12-tetraazacyclotetradeca-2,9-diene), CuL2(ClO4)2 (L2 = N-d-7,14-diisopropyl-5,12-dimethyl-1,4,8,11-tetraazacyclotetradeca-4,11-diene) and of heteropolynuclear complexes: [CuL1][ReCl4(ox)] · DMF and [(CuL2)(ox)ReCl4] is presented. The results indicate that all compounds behave as weak interacting magnets.
Application of isotachophoretic and conductometric methods for neomycin trisulphate determination
Authors: Kurzawa Marzanna , Jastrzębska Aneta , Szłyk Edward 
Published: February 2009

AbstractDetermination of neomycin trisulphate (NMS) in a dosage form (Neox and Neosol) was carried out by capillary isotachophoresis (cITP) with conductometric detection. The following electrolytes: leading: 10 mmol dm−3 sodium acetate + 0.08 % hydroxyethylcelulose (HEC) and acetic acid to pH = 5.5, and terminating: 10 mmol dm−3 β-alanine were tested for isotachophoretic separation of NMS. The calibration curve was linear over the range of 10.00 mg dm−3 to 100.00 mg dm−3 with LOD = 5.69 mg dm−3 and LOQ = 18.96 mg dm−3. The results were compared to the conductometric determination of NMS with: ammonium molybdate (VI), silver nitrate (V) and Reinecke salt. Good accuracy was obtained from conductometric titration of NMS with Reinecke salt, the recoveries being as follows: 100 % (RSD = 1.99 %); 96.17 % (RSD = 2.10 %) and 95.22 % (RSD = 1.55 %) for NMS in pure form, Neosol and Neox, respectively.
N2O catalytic decomposition — effect of pelleting pressure on activity of Co-Mn-Al mixed oxide catalysts
Authors: Galejová Kateřina , Obalová Lucie , Jirátová Květuše , Pacultová Kateřina , Kovanda František 
Published: February 2009

AbstractThe effect of pelleting pressure (0–10 MPa) during the preparation of Co-Mn-Al mixed oxide catalyst on its texture and activity for N2O catalytic decomposition was examined for small grain sizes used in laboratory experiments, and for model industry catalyst particles. Adsorption/desorption measurements of nitrogen, mercury porosimetry and helium pycnometry were used for detail characterization of porous structure. A volume of micropores of about 20 mm3 g−1 was evaluated using modified BET equation. This value did practically not change with the increasing pelletization pressure except that of the sample formed at the pressure of 10 MPa. Although an increase of pelleting pressure caused an increase in bulk density and a decrease in pore size and pore volume of the prepared catalyst (resulting in lower values of N2O effective diffusion coefficient), no direct correlation between pelleting pressure used and catalyst activity has been found. In contrary, estimation of the internal diffusion limitation according to the Weisz-Prater criterion indicated that even laboratory experimental data obtained for catalyst grains with particle size lower than 0.315 mm pelletized at higher pressures could be influenced by internal diffusion. Estimation of the internal mass transfer limitation in industrial catalyst particles described by the effectiveness factor showed that effectiveness factor of about 0.07 and 0.2 can be obtained for spheres with the radius of 1.5 mm and 0.5 mm, respectively, if pelleting pressure of about 6 MPa was used for the catalyst preparation.
Anatomical feasibility of transferring supinator motor branches to the posterior interosseous nerve in C7–T1 brachial plexus palsies
Authors: Bertelli Jayme Augusto , Kechele Paulo Roberto , Santos Marcos Antonio , Besen Bruno Adler Maccagnan Pinheiro , Duarte Hamilton 
Published: February 2009

Object
In C7–T1 palsies of the brachial plexus, shoulder and elbow function is preserved, but finger motion is absent. Finger flexion has been reconstructed using tendon or nerve transfers. Finger extension has been restored ineffectively by attaching the extensor tendons to the distal side of the dorsal radius (that is, tenodesis). In these types of nerve palsy, supinator muscle function is preserved because innervation stems from the C-6 root. In the present study, the authors investigated the anatomy and the feasibility of transferring the supinator motor branches to the posterior interosseous nerve. Sacrifice of the supinator motor branches does not abolish supination because biceps muscle function is preserved in lower-type injuries of the brachial plexus.

Methods
The posterior interosseous nerve was dissected in 20 formalin-fixed forearms. Through posterior forearm access, the posterior interosseous nerve and its motor branches to the supinator muscle were dissected. Specimens were removed for histological study.

Results
In the vicinity of the supinator muscle's proximal margin (that is, the Frohse arcade), 2 nerve branches arose laterally and medially from the posterior interosseous nerve to innervate the superficial and deep heads of the supinator muscle, respectively. The supinator motor nerves, when divided, could be coapted directly to the posterior interosseous nerve. The number of myelinated fibers in the supinator motor branches corresponded to 70% that of the posterior interosseous nerve.

Conclusions
The supinator motor nerves can be transferred directly to the posterior interosseous nerve to restore thumb and finger extension in patients with C7–T1 brachial plexus lesions.
Clinical and angiographic long-term outcomes of vertebral artery–subclavian artery transposition to treat symptomatic stenosis of vertebral artery origin
Authors: Kakino Shunsuke , Ogasawara Kuniaki , Kubo Yoshitaka , Kashimura Hiroshi , Konno Hiromu , Sugawara Atsushi , Kobayashi Masakazu , Sasaki Makoto , Ogawa Akira 
Published: February 2009

Object
Although angioplasty and stent placement for vertebral artery (VA)–origin stenosis have been performed using endovascular techniques, a high likelihood of restenosis has been observed in the long term. Therefore, the authors assessed the long-term clinical and angiographic outcomes in patients after VA–subclavian artery (SA) transposition.

Methods
Thirty-six patients (31 men, 5 women; mean age 64.3 years, range 46–76 years) underwent clinical evaluation (modified Rankin Scale [mRS]) and cervical angiographic evaluation preoperatively and within 1 month of and 6 months after VA-SA transposition undertaken to treat symptomatic stenosis of VA origin.

Results
Postoperative neurological deficits due to intraoperative brain ischemia did not occur, and MR imaging demonstrated no new postoperative ischemic lesions in any of the patients. One patient died of acute myocardial infarction 2 months after surgery and another developed a left thalamic hemorrhage (mRS score of 5) at 42 months postsurgery. None of the remaining 34 patients experienced further ischemic events, and the mRS score in all of these patients remained unchanged during a mean follow-up period of 54 months. The degree of VA-origin stenosis (preoperative mean 84%) was reduced to ≤ 30% after surgery (mean 2%). Long-term follow-up angiography in 29 patients (81%) revealed the absence of restenosis, defined as > 50% luminal narrowing, in all of them.

Conclusions
The clinical and angiographic long-term outcomes demonstrated here suggest that VA-SA transposition will be useful in patients with symptomatic stenosis of VA origin.
Knee Joint Tuberculosis Presenting as Immune Thrombocytopenia
Authors: Khan Mohammad Abdullah Az Zubayer , Mohammed Fazle Rabbi , Shams Md Ziaus , Sarker Shaymal , Alam Md Billal 
Published: February 2009

Tuberculosis (TB) is a major public health problem of increasing proportions in Bangladesh for last several decades. A total of 350,641 cases were reported in Bangladesh in 2006 representing an incidence of 225 per 100,000 population for that year. Many hematological derangements such as anaemia, leukocytosis or pancytopenia can occur in association with TB. However isolated thrombocytopenia is rare and most commonly occur via a non immune mechanism in the setting of pancytopenia that develop secondary to granulomatous infiltration of the bone marrow. Â However immune thrombocytopenic purpura (ITP) in a patient with TB is exceedingly a rare event. Here we report a case of ITP associated with TB of knee joint in whom thrombocytopenia and TB were successfully treated. A casual association between joint TB and ITP is extraordinarily rare and to our knowledge this is the first such case documentation in Bangladesh, although a few case reports citing association of TB and ITP are found in literature. Â doi:10.3329/jom.v10i1.2001 J Medicine 2009; 10: 28-30
Hypothyroidism and Nephrotic Syndrome- A Rare Association
Authors: Uddin Md Julhash , Alam Kazi Monjurul , Mohammed Fazle Rabbi , Alam Md Billal 
Published: February 2009

Hypothyroidism may coexist with different renal pathologies. Several cases of glomerular diseases have been associated with thyroid diseases of which the most frequent lesion described is membranous glomerulopathy, presented as a nephrotic syndrome. Although pseudohypothyroidism is well-known in nephrotic pathophysiology, actual hypothyroidism are uncommon. We report here an unusual association of hypothyroidism due to Hashimoto's disease with nephrotic syndrome due to membranoproliferative glumerulonephritis which were revealed by hormone & antibody assay and renal biopsy respectively. Â doi:10.3329/jom.v10i1.2003 J Medicine 2009; 10: 34-35
Dengue Haemorrhagic Fever with Bradycardia
Authors: Arif SM , Ahmed H , Khokon KZ , Azad AK , Faiz MA 
Published: February 2009

Dengue fever (DF) and dengue hemorrhagic fever (DHF) is a viral disease, caused by dengue (DEN) virus and transmitted by bites of Aedes aegypti mosquito. There are four serotypes of dengue viruses- DEN-1, DEN-2, DEN-3 and DEN-4.In Bangladesh dengue has started as epidemic & has created panic among the people since the year 2000 and as per the sero-survey findings, 3 sero-types of the virus circulating.2 Here we describe a case of DHF with subsequent cardiac complication, treated in Dhaka Medial College Hospital (DMCH). Â doi:10.3329/jom.v10i1.2004 J Medicine 2009; 10: 36-37
Doctor in the Dock
Authors: Mathew Biju C , Daniel Reji Susan , Bordom Jamal Al Baylool , Campbell Ian W 
Published: February 2009

Tobacco smoking is one of the greatest threats to human health. The global epidemic of tobacco killed 100 million in the 20th century, and if not dealt with on a war- footing shall entice and kill another one billion in this century. In the society , physicians play a leading role as ambassadors of promoting issues related to health. They play a vital role in helping patients to stop smoking as they occupy an important position as tobacco control exemplars. Unfortunately, the rate of smoking in the medical profession in some developed countries and newly-developing countries is still high. Considering the staggering cost of smoking in terms of human lives, physicians should not rest until they have successfully kicked the habit. Tobacco-related issues are to be included in the medical school curricula, as medical students can play decisive roles in tobacco-prevention programs. Â doi:10.3329/jom.v10i3.2013 J Medicine 2009; 10 (Supplement 1): 27-31
Upper Body Hypertension with Gross Atherosclerotic Narrowing and Diffuse Calcification of the Descending and Abdominal Aorta
Authors: Hilaly Shah Mahboob Rashid , Sarma Apurba Kumar , Hussain M Zakir 
Published: February 2009

Of the hypertensive patients presenting to the primary care providers, 95-99% have essential hypertension. Remaining 1-5% have an underlying diagnosis.1 Narrowing of the aorta distal to the origin of the arteries to the head, neck & upper limbs causes upper body hypertension. Coarctation of the aorta, a congenital narrowing of the aorta just distal to the insertion of ductus arteriosus, is the major cause of upper body hypertension. Gross atherosclerotic narrowing & diffuse calcification of the descending & abdominal aorta rarely emulates the features of coarctation of the aorta. We report a case of upper body hypertension due to gross atherosclerotic narrowing & diffuse calcification of the descending & abdominal aorta after extensive medline search we have not come across of such reports yet. Â doi:10.3329/jom.v10i3.2014 Â J Medicine 2009; 10 (Supplement 1): 32-35
Duchenne Muscular Dystrophy - Family in a Crisis
Authors: Amin M Robed , Borua Chowdhury Chironjib , Alam Kaji Shafiqul , Chowdhury Fazle Rabbi , Sarkar Rabiul Jahan , Khandaker Md Abul Kashem , Faiz MA 
Published: February 2009

Progressive muscular weakness with deformity leading to crippled states develop due to musculoskeletal and neurological disorders. Sometimes it is difficult to differentiate between primary muscle disease and neurological disease. But there is some classical presentation of muscle diseases which have its own entity and thus can be clinically differentiated from neurological disorder especially spinal cord and motor neuron diseases. Muscular dystrophy is one of those disorder with distinct clinical features. Muscular dystrophy refers to a group of genetic, hereditary muscle diseases that cause progressive muscle weakness. Most types of MD are multi-system disorders with manifestations in body systems including skeletal system, the heart, gastrointestinal and nervous systems, endocrine glands, skin, eyes and other organs. Duchenne muscular dystrophy (DMD), is inherited in an X-linked recessive pattern, meaning that the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes, and is thus considered sex-linked. Males are therefore affected by X-linked recessive disorders much more often than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons. Duchenne muscular dystrophy and Backers muscular dystrophy are caused by mutations of the gene for the dystrophin protein and lead to an overabundance of the enzyme creatine kinase. The dystrophin gene is the largest gene in humans. In this case series a family with three brothers suffering from Duchenne muscular dystrophy is described and review with literature was done. Â doi:10.3329/jom.v10i3.2015 J Medicine 2009; 10 (Supplement 1): 36-39
Local Type I IFN Receptor Signaling Protects against Virus Spread within the Central Nervous System
Authors: Detje Claudia N. , Meyer Thomas , Schmidt Hauke , Kreuz Dorothea , Rose John K. , Bechmann Ingo , Prinz Marco , Kalinke Ulrich 
Published: February 2009

Abstract
Several neurotropic viruses such as vesicular stomatitis virus (VSV) induce peripheral neutralizing Ab responses and still can infect cells within the CNS. To address whether local type I IFN receptor (IFNAR) triggering plays a role in controlling virus replication within the brain, we generated mice with a cell type-specific IFNAR deletion in neuroectodermal cells of the CNS (NesCre+/−IFNARflox/flox). Intranasal VSV infection with 103 PFU was well tolerated by wild-type mice, whereas conventional IFNAR−/− mice died within 2–3 days. In contrast, brain-specific NesCre+/−IFNARflox/flox mice survived until day 5–6 and then became hemiplegic and died. Terminally ill NesCre+/−IFNARflox/flox mice showed 10- to 100-fold higher virus loads in the brain than IFNAR−/− mice, whereas little or no virus was found in other organs. In wild-type animals, virus could be reisolated only from the olfactory bulb until day 6 where also STAT1 activation as a measure of IFNAR triggering was detected. Virus infection was found exclusively in glomerular structures of the olfactory bulb, whereas surrounding cells that showed STAT1 phosphorylation as a measure of IFNAR trigging were free of virus. Our data indicate that upon intranasal VSV instillation, early and localized IFNAR triggering in the glomerular layer of the olfactory bulb is critically required to prevent viral spread over the entire CNS and thus confers survival.