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PubMed2006

Sulfur the archetypal catalyst poison? The sulfur-induced promotion of the bonding of unsaturated hydrocarbons on Cu(111).

We have shown using a combination of temperature-programmed desorption and UV photoelectron spectroscopy that the presence of preadsorbed atomic sulfur promotes the bonding of cyclic unsaturated hydrocarbons (benzene and cyclohexene) to Cu(111). This promoting behavior of sulfur can be rationalized in terms of the ability of adsorbed sulfur to influence the balance between charge donation from the adsorbate to metal, and back-donation from the metal to adsorbate. The effects of sulfur on Cu(111) are dramatically different from those observed in previous studies on Pt(111), which found that it caused a downward shift in the desorption temperature of adsorbed benzene, through purely steric effects.

Journal Article↗

PubMed2001

Mesoscale vertical motion and the size structure of phytoplankton in the ocean.

Phytoplankton size structure is acknowledged as a fundamental property determining energy flow through 'microbial' or 'herbivore' pathways. The balance between these two pathways determines the ability of the ecosystem to recycle carbon within the upper layer or to export it to the ocean interior. Small cells are usually characteristic of oligotrophic, stratified ocean waters, in which regenerated ammonium is the only available form of inorganic nitrogen and recycling dominates. Large cells seem to characterize phytoplankton in which inputs of nitrate enter the euphotic layer and exported production is higher. But the size structure of phytoplankton may depend more directly on hydrodynamical forces than on the source of available nitrogen. Here we present an empirical model that relates the magnitude of mesoscale vertical motion to the slope of the size-abundance spectrum of phytoplankton in a frontal ecosystem. Our model indicates that the relative proportion of large cells increases with the magnitude of the upward velocity. This suggests that mesoscale vertical motion-a ubiquitous feature of eddies and unstable fronts-controls directly the size structure of phytoplankton in the ocean.

Chlorophyll↗

PubMed2005

Netrin-1 inhibits leukocyte migration in vitro and in vivo.

Cell migration plays important roles in embryonic development and inflammation, and this process is highly regulated to ensure tissue homeostasis. A number of barriers exist to prevent the inappropriate migration of leukocytes into healthy peripheral tissues, including retention of these cells in the inactive state and maintenance of the integrity and charge of the vascular endothelium. However, active signals also are likely to exist that can repulse cells or abolish existing cell migration. One such paradigm exists in the developing nervous system, where neuronal migration is mediated by a balance between chemoattractive and chemorepulsive signals. The ability of the guidance molecule netrin-1 to repulse or abolish attraction of neuronal cells expressing the UNC5b receptor makes it an attractive candidate for the regulation of inflammatory cell migration. Here, we show that netrin-1 is expressed on vascular endothelium, where it is regulated by infection and inflammatory cytokines. The netrin-1 receptor UNC5b is strongly expressed by leukocytes, upon which netrin-1 acts as a potent inhibitor of migration to different chemotactic stimuli both in vivo and in vitro. These data suggest that endothelial expression of netrin-1 may inhibit basal cell migration into tissues and that its down-regulation with the onset of sepsis/inflammation may facilitate leukocyte recruitment.

Animals↗

PubMed1997

The role of the thioredoxin and glutaredoxin pathways in reducing protein disulfide bonds in the Escherichia coli cytoplasm.

In Escherichia coli, two pathways use NADPH to reduce disulfide bonds that form in some cytoplasmic enzymes during catalysis: the thioredoxin system, which consists of thioredoxin reductase and thioredoxin, and the glutaredoxin system, composed of glutathione reductase, glutathione, and three glutaredoxins. These systems may also reduce disulfide bonds which form spontaneously in cytoplasmic proteins when E. coli is grown aerobically. We have investigated the role of both systems in determining the thiol-disulfide balance in the cytoplasm by determining the ability of protein disulfide bonds to form in mutants missing components of these systems. We find that both the thioredoxin and glutaredoxin systems contribute to reducing disulfide bonds in cytoplasmic proteins. In addition, these systems can partially substitute for each other in vivo since double mutants missing parts of both systems generally allow substantially more disulfide bond formation than mutants missing components of just one system. Some of these double mutants were found to require the addition of a disulfide reductant to the medium to grow well aerobically. Thus, E. coli requires either a functional thioredoxin or glutaredoxin system to reduce disulfide bonds which appear after each catalytic cycle in the essential enzyme ribonucleotide reductase and perhaps to reduce non-native disulfide bonds in cytoplasmic proteins. Our results suggest the existence of a novel thioredoxin in E. coli.

Bacterial Proteins↗

PubMed2006

Defining a noncarcinogenic dose of recombinant human parathyroid hormone 1-84 in a 2-year study in Fischer 344 rats.

The carcinogenic potential of human parathyroid hormone 1-84 (PTH) was assessed by daily subcutaneous injection (0, 10, 50, 150 microg/kg/day) for 2 years in Fischer 344 rats. Histopathological analyses were conducted on the standard set of soft tissues, tissues with macroscopic abnormalities, selected bones, and bones with abnormalities identified radiographically. All PTH doses caused widespread osteosclerosis and significant, dose-dependent increases in femoral and vertebral bone mineral content and density. In the mid-and high-dose groups, proliferative changes in bone increased with dose. Osteosarcoma was the most common change, followed by focal osteoblast hyperplasia, osteoblastoma, osteoma and skeletal fibrosarcoma. The incidence of bone neoplasms was comparable in control and low-dose groups providing a noncarcinogenic dose for PTH of 10 microg/kg/day at a systemic exposure to PTH that is 4.6-fold higher than for a 100 microg dose in humans. The ability of PTH to interact with and balance the effects of both the PTH-1 receptor and the putative C-terminal PTH receptor, may lead to the lower carcinogenic potential observed with PTH than reported previously for teriparatide.

Animals↗

PubMed2006

Whole-body vibration training compared with resistance training: effect on spasticity, muscle strength and motor performance in adults with cerebral palsy.

OBJECTIVE: The aim of this study was to evaluate the effect on spasticity, muscle strength and motor performance after 8 weeks of whole-body vibration training compared with resistance training in adults with cerebral palsy. METHODS: Fourteen persons with spastic diplegia (21-41 years) were randomized to intervention with either whole-body vibration training (n=7) or resistance training (n=7). Pre- and post-training measures of spasticity using the modified Ashworth scale, muscle strength using isokinetic dynamometry, walking ability using Six-Minute Walk Test, balance using Timed Up and Go test and gross motor performance using Gross Motor Function Measure were performed. RESULTS: Spasticity decreased in knee extensors in the whole-body vibration group. Muscle strength increased in the resistance training group at the velocity 30 degrees /s and in both groups at 90 degrees /s. Six-Minute Walk Test and Timed Up and Go test did not change significantly. Gross Motor Function Measure increased in the whole-body vibration group. CONCLUSION: These data suggest that an 8-week intervention of whole-body vibration training or resistance training can increase muscle strength, without negative effect on spasticity, in adults with cerebral palsy.

Adult↗

PubMed2006

The intensive care unit as a research laboratory: developing strategies to prevent antimicrobial resistance.

OBJECTIVE: To assemble the available clinical data on the prevention of antimicrobial resistance in the intensive care unit (ICU) setting. DATA SOURCE: A MEDLINE database search and references from identified articles were employed to obtain the literature relating to the prevention of antimicrobial resistance in the ICU. CONCLUSIONS: The ICU presents a unique environment for the conduct of clinical research. The closed physical space with centralized patient management and efficient data recovery allows important clinical questions to be evaluated in a timely manner. Antimicrobial resistance has emerged as an important determinant of mortality for patients in the ICU. Additionally, there is currently a limited pipeline of new agents for the treatment of emerging bacteria with new resistance genes that pose an increasing threat to the ICU patient. Effective strategies for the prevention of antimicrobial resistance within ICUs are available and should be implemented aggressively. These strategies can be divided into non-pharmacologic infection- control strategies (e.g., routine hand hygiene, infection-specific prevention protocols) and antibiotic management strategies (e.g., shorter courses of appropriate antibiotics, narrowing of the antimicrobial spectrum on the basis of culture results). Additional studies conducted in ICUs are needed urgently to identify the optimal approaches for the management of antibiotics in order to balance the need for efficacy with the ability to minimize resistance.

Anti-Bacterial Agents↗

PubMed2003

Ventilator weaning after staged anteroposterior spine fusion in a ventilator-dependent patient with congenital scoliosis: a case report.

STUDY DESIGN: Ventilator weaning after staged revision anteroposterior spine fusion in a ventilator-dependent child with congenital scoliosis is reported. OBJECTIVE: To describe the improvement of pulmonary performance after deformity correction in a patient with severe deformity and severe restrictive lung disease. SUMMARY OF BACKGROUND DATA: The effect of scoliotic deformity correction on postoperative pulmonary function is debatable. Recent prospective studies suggest that corrective surgery, especially that involving violation of the chest cage, adversely affect pulmonary function in patients with adolescent idiopathic scoliosis. For patients with severe deformity and severely compromised preoperative pulmonary function, the effect of deformity correction has not been well studied. METHODS: A 15-year-old ventilator-dependent girl with progressive congenital thoracic scoliosis of 130 degrees and a forced vital capacity of 18% underwent staged revision anteroposterior spine fusion. Anterior release, multiple vertebral osteotomies, apical vertebrectomy, and multiple internal thoracoplasties were performed. Five weeks later, when she was medically stable, she underwent posterior reconstruction with multiple vertebral osteotomies, apical vertebrectomy, and translation and cantilever corrective techniques using Isola instrumentation. RESULTS: The patient's pulmonary function was stable 6 months after surgery, and her forced vital capacity was 19%. Currently, 1 year after surgery, she has been weaned to night-only ventilation. Her walking ability has improved. Her spine is well balanced with a thoracic scoliosis of 40 degrees, and she is neurologically intact. CONCLUSIONS: Surgical correction of a severe thoracic spinal deformity in the setting of severe restrictive lung disease can be performed successfully with stabilization of pulmonary volumes and improvement in pulmonary performance.

Abnormalities, Multiple↗

PubMed1984

Geriatric rehabilitation on an acute-care medical unit.

This study examined a geriatric rehabilitation pilot project on an acute-care medical unit. Over a 6-week period, using a 35-item geriatric rating scale and a mental assessment tool, changes in behaviours of 23 patients admitted to the geriatric rehabilitation module were compared to changes in behaviours of 10 elderly patients on a regular medical unit. The patients' demographic characteristics, their nursing and medical diagnoses, and discharge patterns were reviewed. Significant changes in behaviours of patients on the rehabilitation model included: increased ability to care for themselves, to maintain balance, and to communicate with others; decreased restlessness at night; decreased confusion; decreased incidence of incontinence; and improved social skills. The paper describes the geriatric rehabilitation programme and discusses implications for nursing of elderly patients in acute-care hospitals.

Activities of Daily Living↗

PubMed1987

Upper limb loadings of gait with crutches.

Long-term crutch users and patients with arthritis are particularly susceptible to upper limb joint degeneration during aided gait. The function of the walking aid for stability, support, and restraint/propulsion must be optimized with the upper limb loadings caused by the aids. Post-operative total hip replacement (THR) patients, tibial fracture, and paraplegic subjects using sticks and elbow crutches were analyzed in this study. Elbow and shoulder joint centers and aid orientations were monitored simultaneously in three dimensions and combined with aid forces to determine upper limb moment loadings. Three loading effects were observed: tendency for the aids to cause 1) the elbow to flex and shoulder to extend, 2) the elbow and shoulder to extend, and 3) the shoulder to abduct. Moment values of up to 0.10 Nm per body weight (BW) causing the shoulder to extend were measured, i.e., of similar magnitude to the moments at the hip in unaided gait. A modification of the elbow crutch, designed to improve medial-lateral stability, was unsuccessful in use due to wrist instability. This reinforced the requirement that crutch designs integrate the aid's function in gait with the ability of the upper limb joints to balance the applied loads.

Arm↗

PubMed1989

Oxygen consumption after massive sympathetic nervous system discharge.

We evaluated the possibility that massive, sympathetic nervous system (SNS) activation [as may precede the development of neurogenic pulmonary edema (NPE)] increases O2 demand. O2 consumption (VO2) and plasma concentrations of the calorigenic agents, epinephrine (EPI) and norepinephrine (NE) were measured in alpha-chloralose-anesthetized dogs under control conditions and for 3 h after the administration of either 1) intracisternal (ic) veratrine to activate the SNS, 2) intravenous (iv) veratrine, 3) ic saline, or 4) ic veratrine, after clamping the adrenal blood vessels. VO2 increased 31.7 +/- 3.6% (SE), and EPI and NE increased to, respectively, 30,853 +/- 8,347 and 8,176 +/- 2,104 pg/ml in the ic veratrine group. No increases in VO2 and EPI and attenuated increases in NE were observed in the ic veratrine animals with clamped adrenals. No significant increases in VO2 or catecholamine concentrations were observed after ic saline or iv veratrine administration. These data suggest that the elevated VO2 may have been mediated by adrenal catecholamines and that an increased metabolic rate may complicate the ability of patients with severe NPE to balance O2 supply with demand.

Adrenal Glands↗

PubMed1997

Vasopressin V2 receptor mRNA expression and cAMP accumulation in aging rat kidney.

The ability of the kidney to regulate water balance is impaired with age, although the secretion of vasopressin is maintained in senescent animals. This suggests that the cellular response to antidiuretic hormone is reduced in aging kidney. To test this hypothesis, the relationship between the expression of the vasopressin. V2 receptor mRNA and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation was investigated in the medullary thick ascending limb of Henle's loop (MTAL) of adult and aging rats. Tubular suspensions of MTAL were prepared from 10- and 30-mo-old female WAG/Rij rats. The accumulation of cAMP for maximal concentration of vasopressin was 34% larger in adult than in old animals (9.5 +/- 0.5 pmol/4 min, n = 16, and 7.1 +/- 0.6 pmol/4 min, n = 12, respectively). The concentration of vasopressin corresponding to half-maximal stimulation was similar in the two groups (0.66 +/- 0.20 and 0.52 +/- 0.09 nmol, n = 5, in adult and old animals), indicating comparable sensitivity of the renal cells with age. The age-related impaired response to vasopressin of the V2 receptor was specific for females and was not observed in males. Direct stimulation of adenylyl cyclase by forskolin induced a comparable accumulation of cAMP in adult and senescent rats. The V2 receptor mRNA level in the MTAL was constant between 10 and 30 mo whether the animals were normally hydrated or dehydrated for 2 days. These data indicate that, in MTAL, the age-related impaired cAMP accumulation by vasopressin would be linked to a change either in the translation of V2 mRNA or in posttranslational processing mechanisms or in the coupling between the V2 receptor and adenylyl cyclase.

1-Methyl-3-isobutylxanthine↗

PubMed1999

Angiotensin II inhibits HCO-3 absorption via a cytochrome P-450-dependent pathway in MTAL.

The role of ANG II in the regulation of ion reabsorption by the renal thick ascending limb is poorly understood. Here, we demonstrate that ANG II (10(-8) M in the bath) inhibits HCO-3 absorption by 40% in the isolated, perfused medullary thick ascending limb (MTAL) of the rat. The inhibition by ANG II was abolished by pretreatment with eicosatetraynoic acid (10 microM), a general inhibitor of arachidonic acid metabolism, or 17-octadecynoic acid (10 microM), a highly selective inhibitor of cytochrome P-450 pathways. Bath addition of 20-hydroxyeicosatetraenoic acid (20-HETE; 10(-8) M), the major P-450 metabolite in the MTAL, inhibited HCO-3 absorption, whereas pretreatment with 20-HETE prevented the inhibition by ANG II. The addition of 15-HETE (10(-8) M) to the bath had no effect on HCO-3 absorption. The inhibition of HCO-3 absorption by ANG II was reduced by >50% in the presence of the tyrosine kinase inhibitors genistein (7 microM) or herbimycin A (1 microM). We found no role for cAMP, protein kinase C, or NO in the inhibition by ANG II. However, addition of the exogenous NO donor S-nitroso-N-acetylpenicillamine (SNAP; 10 microM) or the NO synthase (NOS) substrate L-arginine (1 mM) to the bath stimulated HCO-3 absorption by 35%, suggesting that NO directly regulates MTAL HCO-3 absorption. Addition of 10(-11) to 10(-10) M ANG II to the bath did not affect HCO-3 absorption. We conclude that ANG II inhibits HCO-3 absorption in the MTAL via a cytochrome P-450-dependent signaling pathway, most likely involving the production of 20-HETE. Tyrosine kinase pathways also appear to play a role in the ANG II-induced transport inhibition. The inhibition of HCO-3 absorption by ANG II in the MTAL may play a key role in the ability of the kidney to regulate sodium balance and extracellular fluid volume independently of acid-base balance.

5,8,11,14-Eicosatetraynoic Acid↗

PubMed2005

Cardiac neurobiology of nitric oxide synthases.

Nitric oxide (NO) is a potent modulator of cardiac and vascular regulation. Its role in cardiac-autonomic neural signaling has received much attention over the last decade because of the ability of NO to alter cardiac sympathovagal balance to favor more anti-arrhythmic states. Complexity and controversy have arisen, however, because of the numerous sources of NO in the brain, peripheral nerves, and cardiomyocytes, all of which are potential regulators of cardiac excitability and calcium signaling. This review addresses the integrative role of NO as a relatively ubiquitous signaling molecule with respect to cardiac neurobiology. The present idea, that divergent NO-signaling pathways from multiple sources within the heart and nervous system converge to modulate cardiac excitability and impact on morbidity and mortality in health and disease, is discussed.

Animals↗

PubMed2003

American Society of Clinical Oncology policy statement: oversight of clinical research.

UNLABELLED: Well-publicized lapses in the review or implementation of clinical research studies have raised public questions about the integrity of the clinical research process. Public trust in the integrity of research is critical not only for funding and participation in clinical trials but also for confidence in the treatments that result from the trials. The questions raised by these unfortunate cases pose an important opportunity to reassess the clinical trials oversight system to ensure the integrity of clinical research and the safety of those who enroll in clinical trials. Since its inception, the American Society of Clinical Oncology (ASCO) has worked for the advancement of cancer treatments through clinical research and to help patients gain prompt access to scientifically excellent and ethically unimpeachable clinical trials. As an extension of its mission, ASCO is affirming with this policy statement the critical importance of a robust review and oversight system to ensure that clinical trials participants give fully informed consent and that their safety is a top priority. Ensuring the integrity of research cannot be stressed enough because of its seminal connection to the advancement of clinical cancer treatment. The overall goal of this policy is to enhance public trust in the cancer clinical trials process. To achieve this, the following elements are essential: 1. Ensure safety precautions for clinical trial participants and their fully informed consent. 2. Ensure the validity and integrity of scientific research. 3. Enhance the educational training of clinical scientists and research staff to ensure the highest standards of research conduct. 4. Promote accountability and responsibility among all those involved in clinical research (not just those serving on institutional review boards [IRBs], but also institutional officials, researchers, sponsors, and participants) and ensure support for an effective oversight process. 5. Enhance the professional and public understanding of clinical research oversight. 6. Enhance the efficiency and cost-effectiveness of the clinical research oversight system. This policy statement makes recommendations in several areas that serve as principles to support an improved system of oversight for clinical research. ASCO will work with all parties involved in the clinical research system to develop the steps necessary to implement these recommendations. Centralized Trial Review: A large percentage of oncology clinical trials are coordinated through the National Cancer Institute's (NCI) system of cooperative groups, which already incorporates centralized scientific review. As such, there is a tremendous opportunity to employ a centralized mechanism to provide ethical review by highly trained IRB members, allowing local IRBs to take advantage of the financial and time efficiencies that central review provides. Centralized review boards (CRBs) would also contribute consistency and efficiency to the process. Once successfully completed, the review would represent an approval to open the protocol at all of the institutions that have subscribed to the centralized review system. Local IRBs would be able to devote time usually spent on initial review to ongoing monitoring of the trial taking place at their institution. Considering the enormous size and complexity of the clinical research enterprise, ASCO envisions multiple CRBs, which could be distributed as regional review boards. Central review will use a single protocol and consent form, and monitor and evaluate adverse events (AEs) on a global basis, eliminating many of the time-consuming steps for the local IRB. Global monitoring and assessment of AEs has real potential to enhance trial participants' safety by giving local institutions more information on the overall trial and enabling them to devote more time to ongoing review of the trial onsite. Use of a CRB also has real potential to reduce the costs of clinical trial oversight by allowing local IRBs to eliminate the costs of initial review. These efficiencies will likely lead to institutions redirecting funds toward monitoring ongoing trials. Although a CRB has potential to improve the efficiency of the process, a CRB could also have tremendous ability to delay valuable trials. Checks and balances must be included in the newly devised system to ensure timely review and appeals of CRB actions. ASCO proposes the advent of a new pilot program for centralizing review of clinical trials. It requires clear engagement of all stakeholders in planning the experiment, clear articulation of the goals, and assurance of federal regulatory protection for institutions choosing to participate. If successful, this CRB pilot project could be expanded to include multi-institutional industry-sponsored research. Education and Training:Education and training are critical to the ultimate success of an improved oversight system. All members of the research team should receive comprehensive education on conducting scientifically and ethically valid clinical research. The curriculum should also include information on the prevailing local and federal regulations that pertain to the clinical trials process. IRB members should also receive ongoing education and training in the review of clinical research protocols. IRB training should pay particular attention to nonscientific members to give them the tools necessary to speak on behalf of research participants. ASCO should develop a curriculum that focuses on the proper conduct of human research and emphasize ethically sound clinical research in the context of its Annual Meeting. Informed Consent: Investigators and review boards have specific roles to play in ensuring the education of trial participants through the informed consent process, both when they are considering trial enrollment and as they participate in the trial. Review boards and investigators should focus primarily on the informed consent process, rather than the informed consent documents. Federal Oversight: The federal government has an important role to play in the oversight of clinical research. This role should be expanded to cover all research, not just that which is funded by the federal government or conducted with the oversight of the Food and Drug Administration (FDA). The Department of Health and Human Services (HHS) Office for Human Research Protections (OHRP) and the FDA should provide clear regulatory support and guidance for local institutions that choose to employ a CRB. In the case of the pilot CRB discussed in this policy statement, it should serve as the preferred option for the cancer cooperative group clinical trials. Ideally, the federal government should unify and streamline its regulations for the oversight of clinical research. Resources Supporting Clinical Research Infrastructure:An effective oversight process demands the highest quality scientific and ethical review and onsite monitoring of the safety of trial participants. This can only be accomplished by the involvement of an experienced IRB that receives funding, resources, and institutional support enabling it to fulfill its mandate. CONFLICT OF INTEREST: Critical to the integrity of research is the absence of bias in the process. ASCO strongly recommends the adoption of standards for the identification, management, and, where appropriate, elimination of conflicts of interests, whether they are actual, potential, or apparent.

Biomedical Research↗

PubMed1980

Effect of indomethacin in a patient with Bartter's syndrome: evidence against a primary role of prostaglandin in this disorder.

It has been claimed that in patients with Bartter's syndrome, enhanced prostaglandin synthesis causes the blunted vasopressor response to angiotensin II. The present study was undertaken to test this hypothesis by administering indomethacin to a patient with Bartter's syndrome. In domethacin corrected the subnormal pressor response to angiotensin II and lowered plasma renin activity from 115 to 15 ng/ml/hr. This effect was associated with renal sodium retention and a 7% increase in body weight. In contrast, when indomethacin was given but the sodium retention prevented by concomitant administration of furosemide, the blunted vasopressor response to angiotensin II and the hyperreninemia were not corrected. It is concluded that the effectiveness of indomethacin to correct the hyperreninemia and the blunted vasopressor to angiotensin II in the preset patient was due in large part to the ability of the drug to correct sodium balance rather than by inhibition of prostaglandin synthesis.

Adolescent↗

PubMed2001

Maximum cold-induced food consumption in mice selected for high locomotor activity: implications for the evolution of endotherm energy budgets.

We studied house mice (Mus domesticus) that had been artificially selected for high activity to test the hypothesis that a high capacity for energy assimilation in cold-exposed endotherms could evolve as a correlated response to selection for increased locomotor activity. After 10 generations of selection for increased voluntary wheel-running, mice from four selected lines ran 75 % more wheel revolutions per day than did mice from four random-bred, control lines. The maximum cold-induced rates of food consumption (C(max); mean 10.6 g day(-1)) and energy assimilation (A(max); mean 141 kJ day(-1)) were not significantly higher in the selected than in the control mice. However, in cold-exposure trials, mice from the selected lines maintained body mass better than did mice from the control lines. C(max) and A(max) were positively correlated with the amount of wheel-running activity measured before cold-exposure and also with the rates of food consumption measured when the mice had access to running wheels. In females at least, the correlation was significant not only among individuals but also among adjusted means of the replicate lines, which suggests the presence of a positive genetic correlation between the traits. Thus, despite the lack of a significant difference between the selected and control lines in maximum rate of food consumption, the remaining results conform to the hypothesis that a selection for increased locomotor activity could be a factor behind the evolution of the ability to sustain activity and maintain energy balance during prolonged cold-exposure, as occurred during the evolution of mammalian and avian endothermy.

Animals↗

PubMed2006

A polyphosphate-lon protease complex in the adaptation of Escherichia coli to amino acid starvation.

Cells must balance energy-efficient growth with the ability to adapt rapidly to sudden changes in their environment. For example, in an environment rich in amino acids, cells do not expend energy for making amino acid biosynthetic enzymes. However, if the environment becomes depleted of amino acids (nutritional downshift), cells will be exposed to a lack of both the amino acid biosynthetic enzymes and the amino acids required to make these enzymes. To solve this dilemma, cells must use their own proteins as sources of amino acids in response to the nutritional downshift. Once amino acid biosynthetic enzymes start to accumulate, the cell is able to produce its own amino acids, and a new growth phase begins. In Escherichia coli, amino acid starvation leads to the accumulation of an unusual molecule, polyphosphate (polyP), a linear polymer of many hundreds of orthophosphate residues. Protein degradation in this bacterium appears to be triggered by the accumulation of polyP. PolyP forms a complex with the ATP-dependent Lon protease. The formation of a complex then enables Lon to degrade free ribosomal proteins. Certain very abundant ribosomal proteins can be the sacrificial substrates targeted for degradation at the onset of the downshift. Here I propose to call the polyP-Lon complex the "stringent protease," and I discuss new insights of protein degradation control in bacteria.

Adaptation, Biological↗