Interventions for cancer-related fatigue: a scoping review.

Cancer-related fatigue (CRF) is common and can be distressing for some survivors. There is increasing interest in measuring levels of CRF, highlighting its impact on quality of life. This review describes the nature and scope of evidence relating to interventions for CRF. Scoping review methodology was used to identify studies, extract data, collate and summarise results. Data were collated according to cancer tumour streams, stage of illness and the types of trial interventions. A total of 447 trials and 37 systematic reviews met the inclusion criteria. Nine papers reported longitudinal results. Populations studied were predominantly of mixed cancer diagnoses and breast cancer. The most frequent interventions were exercise, pharmacological, psycho-education and mind-body interventions. Fatigue was identified as a primary outcome measure (OM) in 58% of studies, with 58 different fatigue measures reported. Emerging evidence exists for the effectiveness of fatigue interventions for some cancer types. More research on interventions with participants with the same cancer type and illness phase is needed. Measurement of severity and impact of CRF using fewer, robust OMs will permit comparisons across studies.

Complementary physical therapies for movement disorders in Parkinson's disease: a systematic review.

BACKGROUND: The growth and popularity of complementary physical therapies for Parkinson's disease (PD) attempt to fill the gap left by conventional exercises, which does not always directly target wellbeing, enjoyment and social participation. AIM: To evaluate the effects of complementary physical therapies on motor performance, quality of life and falls in people living with PD. DESIGN: Systematic review with meta-analysis. POPULATION: Outpatients--adults diagnosed with idiopathic PD, male or female, modified Hoehn and Yahr scale I-IV, any duration of PD, any duration of physical treatment or exercise. METHODS: Randomized controlled trials, non-randomized controlled trials and case series studies were identified by systematic searching of health and rehabilitation electronic databases. A standardized form was used to extract key data from studies by two independent researchers. RESULTS: 1210 participants from 20 randomized controlled trials, two non-randomized controlled trials and 13 case series studies were included. Most studies had moderately strong methodological quality. Dancing, water exercises and robotic gait training were an effective adjunct to medical management for some people living with PD. Virtual reality training, mental practice, aerobic training, boxing and Nordic walking training had a small amount of evidence supporting their use in PD. CONCLUSION: On balance, alternative physical therapies are worthy of consideration when selecting treatment options for people with this common chronic disease. CLINICAL REHABILITATION IMPACT: Complementary physical therapies such as dancing, hydrotherapy and robotic gait training appear to afford therapeutic benefits, increasing mobility and quality of life, in some people living with PD.

A screen for genes induced in the suprachiasmatic nucleus by light.

The mechanism by which mammalian circadian clocks are entrained to light-dark cycles is unknown. The clock that drives behavioral rhythms is located in the suprachiasmatic nucleus (SCN) of the brain, and entrainment is thought to require induction of genes in the SCN by light. A complementary DNA subtraction method based on genomic representational difference analysis was developed to identify such genes without making assumptions about their nature. Four clones corresponded to genes induced specifically in the SCN by light, all of which showed gating of induction by the circadian clock. Among these genes are c-fos and nur77, two of the five early-response genes known to be induced in the SCN by light, and egr-3, a zinc finger transcription factor not previously identified in the SCN. In contrast to known examples, egr-3 induction by light is restricted to the ventral SCN, a structure implicated in entrainment.

Effects of acute caffeine ingestion and menopause on sulfate homeostasis in women.

Inorganic sulfate is a physiological anion which is utilized in the metabolism of both endogenous compounds and xenobiotics. Its homeostasis is maintained predominantly by facilitated reabsorptive processes in the kidneys. The objectives of the present investigation were to evaluate the effects of menopausal status and caffeine ingestion on the serum concentrations and clearance of inorganic sulfate. Thirty-nine women who were classified as premenopausal, postmenopausal with or without estrogen treatment, and postmenopausal with osteoporosis participated in the study. The women were studied on two separate occasions following the ingestion of a decaffeinated beverage to which 6 mg caffeine/kg lean body mass or no caffeine was added. All women were habitual caffeine users (mean ingestion of 588 mg caffeine per day) but abstained from all caffeine sources for 2 weeks prior to the control study day. Postmenopausal women with estrogen supplementation exhibited significantly lower sulfate serum concentrations (0.24 +/- 0.02 mM vs. 0.32 +/- 0.04 mM in premenopausal women, mean +/- SD, p < 0.05) and a decreased renal reabsorption of sulfate for the control (no caffeine) period. There was no difference in serum sulfate or sulfate reabsorption in estrogen supplemented postmenopausal women, compared with women not taking estrogen. Postmenopausal women with osteoporosis had significantly lower creatinine and sulfate clearances than postmenopausal women with estrogen supplementation which may be related to their older age, or factors related to the disease process. The 6 mg/kg dose of caffeine caused a diuresis, but no change in GFR, as indicated by urine volume and creatinine clearance values, respectively. Caffeine administration resulted in an increase in the sulfate excretion rate; there was no change in sulfate serum concentrations. The results of this investigation indicate that menopause results in decreased sulfate serum concentrations that may be the consequence of a decreased renal reabsorption of sulfate. Secondly, this investigation demonstrated that caffeine ingestion increases the urinary excretion of sulfate, an effect that may be related to the diuretic effect of caffeine or due to a caffeine-induced alteration in the renal reabsorption of sulfate.

Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms.

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.

Electrogoniometric feedback: its effect on genu recurvatum in stroke.

The purpose of this study was to determine the effect of combining electrogoniometric feedback with contemporary physical therapy procedures for treatment of genu recurvatum following stroke. Twenty-six patients suffering knee hyperextension resulting from cerebrovascular disorders were allocated to either a control group or an experimental group. Both groups received treatment for knee hyperextension during two consecutive phases. During phase I the control group received physical therapy and the experimental group received electrogoniometric feedback as an adjunct to physical therapy. In phase II both groups received physical therapy alone. Each phase lasted four weeks, during which time patients were treated 45 minutes daily, five days every week. Subjects in the experimental group showed greater reduction in knee hyperextension. This was particularly evident in phase II when the difference between groups for reduction in knee hyperextension reached statistical significance (U = 40, p = 0.011). These results suggest that the addition of electrogoniometric feedback to standard physical therapy enhanced the effectiveness of treatment for genu recurvatum in stroke.

Sulfate homeostasis. IV. Probenecid-induced alterations of inorganic sulfate in rats.

Homeostasis of inorganic sulfate is maintained by the capacity-limited renal reabsorption of sulfate in the proximal tubule. The purpose of the present investigation was to determine if probenecid, the classical inhibitor of renal organic anion secretion, may affect sulfate renal clearance. Two groups of rats were administered in a randomized crossover design, an i.v. bolus dose (20.6 or 92.4 mg/kg) and 4-hr infusion (0.28 or 0.59 mg/min/kg) of probenecid or vehicle, and blood and urine samples were collected. At a steady-state serum concentration of 0.45 mM, probenecid had no significant effect on the serum concentrations or renal clearance of inorganic sulfate, whereas at a serum concentration of 1.4 mM, probenecid treatment caused a significant decrease in serum sulfate concentrations (0.57 +/- 0.11 vs 0.96 +/- 0.19 mM in controls, mean +/- SD, n = 6, P less than 0.001) due to an increase in the renal clearance of sulfate (3.88 +/- 1.18 vs 2.13 +/- 0.84 ml/min/kg in controls, P less than 0.01). The fraction of the filtered sulfate that was reabsorbed was significantly decreased (0.38 +/- 0.23, vs 0.74 +/- 0.09 in controls, P less than 0.01). Therefore, probenecid treatment results in the inhibition of the renal reabsorption of inorganic sulfate in rats in vivo.

Sulfate homeostasis. III. Effect of chronic naproxen or sulindac treatment on inorganic sulfate disposition in arthritic patients with renal impairment.

The purpose of the present investigation was to examine the influence of chronic naproxen (500 mg twice daily) or sulindac (200 mg twice daily) therapy on the disposition of inorganic sulfate in arthritic subjects with impaired renal function. Subjects were studied during a control period (after a 7-day NSAID washout) and after 14 days of treatment with either naproxen or sulindac. During the control period subjects in this investigation exhibited higher serum sulfate concentrations and lower sulfate renal clearance values than reported for younger subjects with normal renal function. Treatment with either sulindac or naproxen significantly decreased creatinine clearance. Sulindac therapy also increased the serum sulfate concentration and decreased the clearance of sulfate; a similar trend was observed after naproxen therapy but the average change was smaller and not statistically significant. There were significant correlations between the creatinine and the sulfate clearances or serum concentrations. The glomerular filtration rate of inorganic sulfate was not altered by drug treatment and there was no impairment of reabsorption. The serum concentrations and renal clearance of other electrolytes (sodium, potassium, magnesium, calcium, phosphorus) were largely unaffected. Therefore, chronic treatment with naproxen or sulindac decreases the renal clearance of endogenous sulfate in humans: this appears to be a consequence of the decrement in renal function observed in subjects with preexisting mild renal impairment.

Lathyrus excitotoxin: mechanism of neuronal excitation by L-2-oxalylamino-3-amino- and L-3-oxalylamino-2-amino-propionic acid.

Intracellular recordings were made in cultured neurones from foetal mouse spinal cord. The effects of applications of the neurotoxin, L-3-oxalylamino-2-amino-propionic acid (a constituent of the chickling pea, Lathyrus sativus) and its 2-oxalylamino isomer on membrane potential and conductance were examined in the presence of TTX and TEA and compared to those of other excitatory amino acids. Although both compounds produced membrane depolarization and an increase in input conductance, the 3-oxalylamino isomer (beta-ODAP) was approximately equal to 10 times more potent than the 2-oxalylamino isomer (alpha-ODAP). beta-ODAP caused a voltage-independent change in conductance, as compared to an apparent voltage-dependent decrease produced in the same neurons by L-aspartic acid (L-ASP). Although reversal potentials determined for beta-ODAP resembled those for alpha-ODAP and kainic acid, they were consistently and significantly lower than the reversal level for L-ASP. Although the receptor antagonist 2-amino-5-phosphonovaleric acid (APV) and the divalent cation Cd2+ did not alter the conductance increase evoked by beta-ODAP, they markedly depressed responses to L-ASP. Such differences suggest a mechanism of excitatory action for the neurotoxin, beta-ODAP, which does not involve a Ca2+-dependent mechanism and is quite different from that for L-ASP and N-methyl-D-aspartic acid, but similar to that of kainic and quisqualic acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption of sulfate from orally administered magnesium sulfate in man.

The purpose of this investigation was to determine the suitability of orally administered magnesium sulfate as a source of inorganic sulfate for counteracting the systemic depletion of sulfate caused by large doses of acetaminophen and certain other drugs that are metabolized to sulfate conjugates. Oral administration of 13.9 g magnesium sulfate U.S.P., in 4 equal hourly increments, to seven healthy men resulted in the urinary excretion (corrected for baseline excretion rate) of an amount of inorganic sulfate equivalent to 30.2 +/- 17.2 percent (mean +/- SD) of the dose during the first 24 hours. Excretion during the subsequent 48 hours was negligible. Six of the subjects experienced loose stools or diarrhea. Compared to sodium sulfate, magnesium sulfate appears to be absorbed less completely and more erratically, and to produce more adverse effects.

The effect of mouthrinse containing calcium glycerophosphate on the chemical composition and development of plaque in humans.

Children rinsed twice daily with one of two concentrations of calcium glycerophosphate or a placebo. Plaque was collected at two-week intervals for eight weeks, and Löe and Silness Indices determined. Results indicate a lower index rating and a higher phosphorus content for experimental groups than for the control at the four-week examination.

Oral contraceptive-induced ischemic bowel disease.

PIP: A case report of subacute, reversible ischemic colitis associated with use of oral contraceptives (OCs) is reported. A 19-year-old woman was admitted to the hospital with chief complaints of abdominal cramps, nausea, vomiting, diarrhea, and rectal bleeding of 2 days' duration. Past medical history and family history were noncontributory. The patient was receiving no medication other than Norinyl 2 (2 mg of norethindrone and .1 mg of mestranol), which she had been taking for 6 months. 2 days before admission the patient had taken 100 mg of dimenhydrinate and 2 ExLax tablets (90 mg of phenolphthalein) for constipation. Colonic roentgenograms revealed impaired mesenteric circulation and bowel ischemia; OC-induced ischemic bowel disease was diagnosed. Patient symptoms subsided within 96 hours of discontinuing the OC and initiating supportive therapy (including intravenous fluid infusion, nasogastric suction, analgesics, and antiemetics). When a repeat barium enema was performed, it showed resolution of the ischemia. In a short review following the case report, these drugs were indicted in causation of colitis-like syndrome: amoxicillin, ampicillin, cephazolin, chloramphenicol, chlorpropamide, clindamycin, cloxacillin, cotrimoxasole, cyclophosphamide, digitalis, ergotamine tartrate, flucytosine, fluorouracil, gold salts, laxative and cathartic abuse, mercurous chloride, methyldopa, penicillin V, and tetracycline. Ischemic bowel disease secondary to OC use is a rare but important complication because of its significant morbidity and potential mortality, and because of the widespread use of the drugs. The case report emphasizes the need to consider the differential diagnosis of acute vascular insult with bowel ischemia when acute abdominal pain progressing to bloody diarrhea occurs in young women taking OCs.^ieng