The nirSTBM region coding for cytochrome cd1-dependent nitrite respiration of Pseudomonas stutzeri consists of a cluster of mono-, di-, and tetraheme proteins

AbstractGenes for respiratory nitrite reduction (denitrification) of Pseudomonas stutzeri are clustered within 7 kbp. A 4.6-kbp Hind III-Kpn I fragment carrying nirS, the structural gene for cytochrome cd1, was sequenced. An open reading frame immediately downstream of nirScodes for a 22.8-kDa protein with four heme c-binding motifs. Mutagenesis of this gene causes an apparent defect in electron donation to cytochrome cd1. Following this ORF are the structural genes for cytochrome c552, cytochrome c551, and ORF5 that codes for a 11.9-kDa monoheme protein. All cytochromes have a signal sequence for protein export

キュウセイ ジンフゼン, コウCPKケッショウ オ トモナイ, キュウゲキ ニ ケトアシドーシス オ テイシタ ヒ ジコ メンエキセイ ゲキショウガタ 1ガタ トウニョウビョウ ノ 1レイ

We present a 40 year male patient who developed diabetic ketoacidosis with acute renal failure and high serum values of CPK and uric acid. Because of acute onset of ketoacidosis during several days with an elevation of serum amylase, negative findings of antibodies associated with autoimmune type 1 diabetes mellitus, he was diagnosed of a non-autoimmune, fuluminant, type 1 diabetes mellitus, which is a newly established subtype of type 1 diabetes mellitus. Since the patient\u27s post-prandial plasma glucose was extremely high (1123 mg/dl) when he developed ketoacidosis, the severe dehydration due to extreme hyperglycemia might have caused acute renal failtire and rhabdomyolysis

THE ESSENTIAL BIOLOGY OF THE ENDOPLASMIC RETICULUM STRESS RESPONSE FOR STRUCTURAL AND COMPUTATIONAL BIOLOGISTS

The endoplasmic reticulum (ER) stress response is a cytoprotective mechanism that maintains homeostasis of the ER by upregulating the capacity of the ER in accordance with cellular demands. If the ER stress response cannot function correctly, because of reasons such as aging, genetic mutation or environmental stress, unfolded proteins accumulate in the ER and cause ER stress-induced apoptosis, resulting in the onset of folding diseases, including Alzheimer's disease and diabetes mellitus. Although the mechanism of the ER stress response has been analyzed extensively by biochemists, cell biologists and molecular biologists, many aspects remain to be elucidated. For example, it is unclear how sensor molecules detect ER stress, or how cells choose the two opposite cell fates (survival or apoptosis) during the ER stress response. To resolve these critical issues, structural and computational approaches will be indispensable, although the mechanism of the ER stress response is complicated and difficult to understand holistically at a glance. Here, we provide a concise introduction to the mammalian ER stress response for structural and computational biologists

Purification and Characterization of Serine Racemase from a Hyperthermophilic Archaeon, Pyrobaculum islandicum▿ †

Pyrobaculum islandicum is an anaerobic hyperthermophilic archaeon that is most active at 100°C. A pyridoxal 5′-phosphate-dependent serine racemase called Srr was purified from the organism. The corresponding srr gene was cloned, and recombinant Srr was purified from Escherichia coli. It showed the highest racemase activity toward l-serine, followed by l-threonine, d-serine, and d-threonine. Like rodent and plant serine racemases, Srr is bifunctional, showing high l-serine/l-threonine dehydratase activity. The sequence of Srr is 87% similar to that of Pyrobaculum aerophilum IlvA (a putative threonine dehydratase) but less than 32% similar to any other serine racemases and threonine dehydratases. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and gel filtration analyses revealed that Srr is a homotrimer of a 44,000-molecular-weight subunit. Both racemase and dehydratase activities were highest at 95°C, while racemization and dehydration were maximum at pH 8.2 and 7.8, respectively. Unlike other, related Ilv enzymes, Srr showed no allosteric properties: neither of these enzymatic activities was affected by either l-amino acids (isoleucine and valine) or most of the metal ions. Only Fe2+ and Cu2+ caused 20 to 30% inhibition and 30 to 40% stimulation of both enzyme activities, respectively. ATP inhibited racemase activity by 10 to 20%. The Km and Vmax values of the racemase activity of Srr for l-serine were 185 mM and 20.1 μmol/min/mg, respectively, while the corresponding values of the dehydratase activity of l-serine were 2.2 mM and 80.4 μmol/min/mg, respectively

Physical Activity Earlier in Life Is Inversely Associated With Insulin Resistance Among Adults in Japan

Background: It is known that physical activity affects glucose metabolism. However, there have been no reports on the influence of physical activity earlier in life on subsequent glucose metabolism. Therefore, we analyzed the influence of physical activity in earlier decades of life on insulin resistance in middle aged and older residents in Japan. Methods: The subjects were 6,883 residents of Okazaki City between the ages of 40 and 79 years who underwent physical examinations at the Okazaki City Medical Association Public Health Center from April 2007 through August 2011. They gave informed consent for participation in the study. Data on individual characteristics were collected via a questionnaire and from the health examination records. Fasting blood glucose and insulin levels were used to calculate the homeostatic model assessment of insulin resistance (HOMA-IR). HOMA-IR >1.6 was considered to indicate insulin resistance for the purpose of logistic regression models. Results: The study sample included 3,683 men and 3,200 women for whom complete information was available. For those who exercised regularly throughout their teens to their 30s–40s, the odds ratio for having insulin resistance was 0.75 (95% confidence interval [CI], 0.58–0.96) for men and 0.76 (95% CI, 0.58–0.99) for women after adjusting for other variables, including age, body mass index, and present physical activity. A linear trend was also observed in both men and women. Conclusions: Subjects who have exercised regularly in the early decades of life are less likely to have insulin resistance later in life