Prevalence of depression and anxiety among adults with vitiligo in a Malaysian tertiary hospital.

INTRODUCTION: Vitiligo is a chronic disorder resulting in skin depigmentation with reported global prevalence of 1-2%. This disease is often accompanied by psychosocial distress owing to the cosmetic disfigurement associated with it. The primary objective of this study was to determine the prevalence of depression and anxiety among adults with vitiligo in a local tertiary hospital. In addition, this study also evaluated the association of depression and anxiety with patients' characteristics. MATERIALS AND METHODS: This cross-sectional study was conducted among vitiligo patients aged 18 years and older in Hospital Klang, Selangor between October 2021 and June 2022. Assessment instruments used were Vitiligo Area Scoring Index (VASI) and Hospital Anxiety and Depression Scale (HADS). Demographic data and clinical characteristics of vitiligo patients were recorded. RESULTS: Of the 100 participants, 12 (12%) and 21 (21%) had depression and anxiety, respectively. The mean depression score (HADS-depression component) was 3.4 (SD 3.4) and mean anxiety score (HADS-anxiety component) was 4.7 (SD 3.9). There were significantly higher number of patients with abnormal HADS-D score in the age group of 35-51 years (p=0.029), single status (p=0.001), with employment (p=0.014) and disease duration <2 years (p=0.004). Patients in the divorced/widowed group had a significant association with anxiety (p=0.011). CONCLUSION: The prevalence of depression was 12% while anxiety was 21% in our cohort. Vitiligo has a significant psychosocial impact, thus clinicians should actively evaluate the mental health of these patients with the use of screening tools such as HADS and provide appropriate referrals and management.

Variations in energy and phospholipid metabolism in normal and cancer human mammary epithelial cells.

By comparing the metabolism of human mammary epithelial cells and human breast cancer cells (MCF7 and T47D), proliferating at approximately the same rate, it was possible to isolate the effect of malignancy alone on the energetics and phospholipid metabolism of cancer cells. 31p NMR of perfused mammary cells and of water soluble extracts of these cells showed that the levels of phosphocholine, phosphoethanolamine, and glycerol derivatives of these metabolites were very low and significantly less than that in the cancer cells, suggesting an association of malignancy with induction of phospholipid biosynthesis and breakdown. The level of the high energy phosphates and the rates of glucose consumption and aerobic glycolysis did not reveal distinct differences between normal and cancer cells. The comparable energetic appear to be related to the similarity of proliferating capacity in culture of the normal and cancer cells.

In vivo metabolic studies of glucose, ATP and 2,3-DPG in beta-thalassaemia intermedia, heterozygous beta-thalassaemic and normal erythrocytes: 13C and 31P MRS studies.

13C and 31P magnetic resonance spectroscopy was used to characterize the in vivo kinetics of glucose metabolism and intracellular ATP and 2,3-DPG concentrations in erythrocytes obtained from beta-thalassaemia intermedia, heterozygous beta-thalassaemic and normal individuals and maintained in suspension. Except for an upfield chemical shift in the 2P and 3P resonance of 2,3-DPG in the thalassaemia intermedia erythrocytes, the 31P spectra were comparable between all three blood types, showing similar concentrations of ATP (from 4.5 to 5.2 mumol/g Hb) and 2,3-DPG (from 17.2 to 19.7 mumol/g Hb). However, the profile of glucose metabolism was quite different in beta-thalassaemia intermedia erythrocytes, whereas glucose was consumed at a rate of 0.089 +/- 0.035 fmol/cell/h, significantly higher than that of normal (0.032 +/- 0.018 fmol/cell/h; P = 0.01) and heterozygous (0.025 +/- 0.004 fmol/cell/h; P = 0.01) erythrocytes. This near 3-fold faster rate of glucose metabolism in the thalassaemia intermedia erythrocytes could not be accounted for by any increase in glucose flux via the Embden-Meyerhof pathway, since no significant difference in 3-13C-lactate synthesis was observed among the three blood types (in units of fmol/cell/h, normal, 0.021 +/- 0.013; heterozygous, 0.021 +/- 0.006; beta-thalassaemia intermedia 0.045 +/- 0.025). These results reflect an accelerated rate of glucose metabolism in thalassaemia intermedia erythrocytes because the contribution of reticulocytes to this altered pattern of metabolism could be excluded. As the only other route of glucose metabolism in erythrocytes is the pentose phosphate pathway (PPP), these results indicate that the PPP is more active in beta-thalassaemia intermedia erythrocytes, perhaps as a consequence of their elevated intracellular oxidative state.

Energetics and glucose metabolism in hippocampal slices during depolarization: 31P and 13C NMR studies.

Alterations in the energy state and glucose metabolism of hippocampal slices exposed to high extracellular K+ ([K+]o) were monitored using 31P and 13C NMR spectroscopy. Slices were perfused (37 degrees C) continuously within the NMR spectrometer and tissue viability and metabolic activity were maintained for at least 18 h. 31P spectra showed that upon exposure to 40 mM [K+]o, there was a rapid compromise in tissue energetics where, by 15 min of exposure, the ratio of phosphocreatine and of nucleoside triphosphates to inorganic phosphate (extra- and intracellular) decreased 30-50% relative to pre-exposure values. This was accompanied by a pH decrease of approximately 0.3 units in both the intra and extracellular environments. A lower but stable energy state was reached at approximately 15 min of exposure and full recovery was observed by 30 min following the removal of high [K+]o. Utilizing 13C NMR in the presence of [1-13C]glucose, an immediate and dramatic acceleration in tissue glycolysis was observed when slices were exposed to 40 mM [K+]o: the rates of both [1-13C]glucose consumption and [3-13C] acetate synthesis increased by approximately 20 fold. By 60 min following the removal of high-[K+]o, pre-exposure rates of tissue glycolysis were restored. The results indicated that the rapid and dramatic induction of energy production via glycolysis probably accounts for the ability of hippocampal slices to maintain viability and recuperate from brief but intense depolarizing conditions which are reminiscent of seizure states in vivo.

Thin-section MR imaging of rat brain at 4.7 T.

The brains of anesthetized 7-month-old male hooded rats were imaged in coronal, sagittal, and horizontal planes at 4.7 T. Images were obtained with a section thickness of 0.6 mm and in-plane pixel size of 0.18-0.20 mm, resulting in finer combined spatial and contrast resolution than in most previously published reports. This allowed detailed anatomic assignment of many brain structures on the basis of comparison with a histologic brain atlas. T1, apparent T2, and water proton density values of gray matter, white matter, and cerebrospinal fluid (CSF) were derived from saturation-recovery and multi-echo measurements. These values were used to calculate expected contrast-to-noise ratios as a function of TR and TE in spin-echo imaging sequences. The optimal simultaneous contrast between gray and white matter and between CSF and gray matter was obtained on images with moderate T2 weighing, with a TR of 3.6 seconds and a TE of 45 msec. The use of thin sections was found to be essential for resolving many fine structures, and the improved sensitivity provided by the high magnetic field strength was crucial for imaging such thin sections at adequate signal-to-noise ratios.

The in vitro hippocampal slice preparation as a screen for neurotoxicity.

One of the current goals of neurotoxicology research is to develop methods of assessing the neurotoxicity of chemical agents in the most sensitive, rapid and economical ways possible. Although no single method is likely to fulfil the role of a general screen for toxicity of all organ systems, in vitro brain-slice methods may hold the key to increased sensitivity in screening within the more restricted domain of central nervous system toxicity. The hippocampal brain-slice preparation is particularly well suited for screening purposes because the neurophysiology of the hippocampal slice is relatively well understood and generally matches what is known about the intact hippocampus. Potential practical advantages of a hippocampal slice screen include the fact that multiple tests of a variety of neuronal properties can be carried out using a single slice, many comparable slice 'samples' may be obtained from each animal donor, and testing should be easily automated. In addition, the hippocampal slice assay may have important practical and conceptual advantages over other assay methods because of the putative importance of the hippocampus to a variety of behaviours. Thus the in vitro hippocampal slice preparation as a screen for neurotoxicity offers the advantages of in vitro methods while allowing guarded, but relatively direct extrapolation to dysfunction of learning, memory and other behavioural processes.

Extracellular Ca(2+) modulation of triethyltin neurotoxicity in area CA1 of the rat hippocampal slice.

The present study examined the possible role of extracellular Ca(2+) in triethyltin (TET) neurotoxicity in area CA1 of the rat hippocampal slice. Slices were exposed to 20 mum-TET-Br for 30 min in an environment of normal or no extracellular Ca(2+), and were then monitored for 4 hr post-exposure. In a normal Ca(2+) environment, TET exposure suppressed population excitatory post-synaptic potentials (EPSPs) by 95 min post-exposure, and no recovery was observed following washout of TET. This direct effect of TET on neurotransmission occurred without changes in the conductive properties of the presynaptic Schaffer collaterals; the amplitude of population afferent fibre volley potentials remained stable. In a Ca(2+)-free environment, however, the same TET exposure led to rapid tissue death following the onset of TET exposure. Thus, extracellular Ca(2+) decreased the apparent neurotoxicity of TET observed in a Ca(2+)-free environment. The results suggest that extracellular Ca(2+) modulates TET neurotoxicity, manifested as suppression of synaptic potentials, in area CA1 of the hippocampal slice. However, the mechanisms underlying TET-induced suppression of evoked synaptic potentials in a normal Ca(2+) environment and tissue death in a Ca(2+)-free environment remain to be elucidated.

Threshold procedures for assessing the impact of agents on brain reward systems.

Chemical effects on the reinforcing quality of electrical stimulation of the rat brain can be assessed using a variety of methods, most commonly by observing changes in response rates maintained under specific schedules of reinforcement. We present results demonstrating the utility of procedures for assessing the minimum amount of electrical stimulation required to support rat leverpress responding, that is, the brain-stimulation reward (BSR) threshold. In these threshold procedures, each leverpress produced by the rat decreases the duration of the electrical stimulus delivered to the posterior lateral hypothalamus until the rat fails to respond. The stimulus duration is then reset to its initial value and the procedure begins again. The last stimulus duration in a series supporting a response is defined as the stimulus duration (SD) threshold, and the mean SD threshold is determined daily. Stable SD thresholds are achieved within 2 weeks, and this measure is sensitive to agent-induced changes in rats' response to BSR. To illustrate the utility of this approach, data are presented showing that rats' BSR thresholds changed significantly following exposure to triethyltin or carbon monoxide. The results support the view that threshold methods can be used to dissociate agent-induced effects on brain reward systems and BSR quality from changes in performance or effects on other behavioral processes.

Triethyltin exposure suppresses synaptic transmission in area CA1 of the rat hippocampal slice.

To examine the effects of TET on the electrophysiology of area CA1 of hippocampus, hippocampal slices were obtained from adult hooded rats and were maintained in vitro using standard techniques. Stimulating and recording electrodes were placed in the Schaffer collaterals and CA1 pyramidal cell body layer, respectively. Following baseline measurements, slices were exposed to either 0, 1, 3, 6, or 10 microM TET in the incubating medium. Both pyramidal cell excitability and recurrent/feedforward inhibition were suppressed in a dose-dependent manner within 3 hr postexposure. The evoked population spike and population excitatory postsynaptic potential (EPSP) were suppressed significantly by 2 hr postexposure for 1 and 3 microM TET exposures, and by 45 min postexposure for 6 and 10 microM exposures. A similar dose-dependency was observed for the suppression of recurrent/feedforward inhibition in hippocampal CA1. A second procedure tested the specificity of TET effects to axonal conduction of Schaffer collaterals. Both the stimulating and recording electrode were placed in the Schaffer collaterals so that both the Schaffer collateral population fiber volley and the CA1 pyramidal cell population EPSP could be recorded. TET exposure suppressed pyramidal cell EPSPs without significantly affecting the amplitude of Schaffer collateral fiber volleys. The results support the view that acute TET exposure suppresses synaptic transmission in area CA1 of hippocampus.