A systematic review of commercial weight loss programmes' effect on glycemic outcomes among overweight and obese adults with and without type 2 diabetes mellitus.

OBJECTIVE: We examined the glycemic benefits of commercial weight loss programmes as compared with control/education or counselling among overweight and obese adults with and without type 2 diabetes mellitus (T2DM). METHODS: We searched MEDLINE, Cochrane Database of Systematic Reviews, and references cited by individual programmes. We included randomized controlled trials of ≥12 weeks duration. Two reviewers extracted information on study design, population characteristics, interventions, and mean changes in haemoglobin A1c and glucose. RESULTS: We included 18 randomized controlled trials. Few trials occurred among individuals with T2DM. In this population, Jenny Craig reduced A1c at least 0.4% more than counselling at 12 months, Nutrisystem significantly reduced A1c 0.3% more than counselling at 6 months, and OPTIFAST reduced A1c 0.3% more than counselling at 6 months. Among individuals without T2DM, few studies evaluated glycemic outcomes, and when reported, most did not show substantial reductions. DISCUSSION: Few trials have examined whether commercial weight loss programmes result in glycemic benefits for their participants, particularly among overweight and obese individuals without T2DM. Jenny Craig, Nutrisystem and OPTIFAST show promising glycemic lowering benefits for patients with T2DM, although additional studies are needed to confirm these conclusions. © 2016 World Obesity.

The difference in shape of spontaneous and uniquantal evoked synaptic potentials in frog muscle.

1. Spontaneous and stimulation-induced uniquantal synaptic activity at the frog cutaneous pectoris muscle, treated with neostigmine, was recorded by focal extracellular microelectrodes. A monoexponential curve was fitted to the decay of each synaptic response. 2. A highly significant positive relationship was found between the amplitude and the decay time constant of spontaneous extracellular miniature endplate potentials (MEPPs(o)), whereas the relationship displayed by evoked uniquantal extracellular endplate potentials (EPPs(o)) was only slightly greater than zero. 3. The difference did not stem from changes in the muscle membrane conductance or from inclusion of outstanding MEPPs(o) formed as a result of the block of acetylcholinesterase. 4. The dependence of the rise time on the amplitude was also stronger in MEPPs(o) than in EPPs(o). 5. In the absence of neostigmine, MEPPs(o) exhibited a positive correlation between decay time constant and amplitude, while EPPs(o) did not show such a correlation. 6. In view of previously published models of transmitter release, it is suggested that spontaneous secretion of quanta occurs both within and outside the active zones facing postsynaptic areas of variable receptor density.

Postsynaptic effects of DMSO at the frog neuromuscular junction.

Postsynaptic effects of dimethylsulfoxide (DMSO) were studied at the frog cutaneous pectoris neuromuscular junction using electrophysiological techniques and computer assisted analysis. It was found that the average amplitude of extracellularly recorded miniature end-plate potentials (meppse) as well as the time constant of their monoexponential decay (tau) were both elevated in the presence of DMSO. In spite of increased scatter of individual values, amplitude and tau of meppse highly correlated with each other. These results imply that DMSO partially blocked the activity of acetylcholine esterase in addition to its already known presynaptic action of acetylcholine release enhancement. Inhibitory action of DMSO on activity of isolated acetylcholine esterase was previously demonstrated by biochemical methods.

Acetylcholine release at identified nerve terminals in the organ-cultured frog neuromuscular preparation.

1. The frog cutaneous pectoris neuromuscular preparation was maintained in organ culture for a few days, at either 24 or 14 degrees C. The synaptic activity of identified nerve terminals was repeatedly examined in order to describe the sequence and time course of changes from normal synaptic activity to a complete synaptic silence. 2. We found that the 'transient stage' (stage II, according to Ko, 1981) consists of at least three distinct periods each characterized by a unique trend of change in synaptic activity. The initial change involved a simultaneous decay of both spontaneous and nerve stimulation-evoked release of acetylcholine (sub-stage II1). Subsequently, the frequency of spontaneous miniature endplate potentials (MEPPs) increased gradually, while the evoked release continued its monotonous decay (sub-stage II2). During the third sub-stage spontaneous MEPPs, but no evoked endplate potentials (EPPs), were observed (sub-stage II3). 3. Statistical properties of acetylcholine release in still-transmitting junctions at sub-stage II2 and in non-transmitting junctions at sub-stage II3 were investigated. MEPPs with skewed amplitude histograms and bursting behaviour were evident at both sub-stages. However, the incidence and the extent of these distortions were higher in the non-transmitting junctions. 4. An inverse relation between the quantal content of evoked release and the rate of spontaneous secretion was found in the transmitting junctions. 5. These results suggest that some of the deterioration of synaptic activity in organ culture is caused by an impairment of the release process itself. Possible cellular mechanisms are discussed.

Delayed appearance of vancomycin-induced neutropenia in a patient with chronic renal failure.

A patient receiving hemodialysis for chronic renal failure had neutropenia six weeks after administration of his last dose of intravenous vancomycin and in the absence of other drug therapy. This case provides confirmation that neutropenia can be seen with vancomycin therapy; suggests an immunologic basis for the reaction, since the patient exhibited a concomitant hypersensitivity rash; and points out that delayed clearance of vancomycin in patients with chronic renal failure can produce late onset of side effects in such patients.