Subacute cutaneous lupus erythematosus leukoderma treated with melanocyte‐keratinocyte transplantation procedure

Depigmented lesions may occur as postinflammatory sequelae of subacute cutaneous lupus erythematosus (SCLE), leading to great psychosocial impact. A 53‐year‐old male patient presented with post‐SCLE depigmented facial lesions after five years of disease stability. We proposed surgical treatment with melanocyte‐keratinocyte transplantation procedure (MKTP), and after five months the patient achieved 90% repigmentation, without Koebner phenomenon (KP). In theory, KP is a possible complication of MKTP procedure since the preparation of the receptor area involves the use of dermabrasion. In an attempt to avoid it, we suggest to maintain the treatment of the underlying disease and wait for a minimum period of disease stability before the procedure.     

Costimulation and Autoimmune Diabetes in BB Rats

Costimulatory signals regulate T-cell activation. To investigate the role of costimulation in autoimmunity and transplantation, we studied the BB rat model of type 1 diabetes. Diabetes-prone BB (BBDP) rats spontaneously develop disease when 55–120 days of age. We observed that two anti-CD28 monoclonal antibodies (mAb) with different functional activities completely prevented diabetes in BBDP rats. Anti-CD154 mAb delayed diabetes, whereas treatment with CTLA4-Ig or anti-CD80 mAb accelerated disease. Anti-CD86 or anti-CD134L mAbs had no effect. Diabetes resistant BB (BBDR) rats are disease-free, but >95% of them develop diabetes after treatment with polyinosinic-polycytidylic acid and an mAb that depletes Treg cells. In the induced BBDR model, anti-CD154 mAb delayed onset of diabetes, whereas CTLA4-Ig, anti-CD134L or either of the anti-CD28 mAbs had little or no effect. In contrast, blockade of the CD134-CD134L pathway was highly effective for preventing autoimmune recurrence against syngeneic islet grafts in diabetic BBDR hosts. Blockade of the CD40-CD154 pathway was also effective, but less so. These data suggest that the effectiveness of costimulation blockade in the treatment of type 1 diabetes is dependent on both the costimulatory pathway targeted and the mechanism of induction, stage, intensity and duration of the pathogenic process.     

Spectral analysis of intercycle heart fluctuations in the diethyl-ether-anaesthetized or pithed rat treated with l-hyoscyamine

1 Within the context of neural regulation of the activity of sinus node pacemaker cells, the study of heart rate variability, as explored in the frequency domain by spectral analysis, was proposed about 15 years ago as a quantitative tool for the evaluation of short-term autonomic cardiovascular control. It has since been postulated that the two main oscillations observed, one at low and the other at high frequency, may respectively be markers of sympathetic vs. vagal efferent cardiac activity, and that the low- and high-frequency signals may reflect a reciprocal or ‘push–pull’ relationship between sympathetic and parasympathetic control. 2 In our power spectra assessment, ECG R–R intervals were submitted to fast Fourier transformation analysis in order to study the mechanisms underlying the control of heart beats in rats. Data were acquired in conditions of steady arterial blood pressure and cardiac and respiratory activity (spontaneous or artificially stimulated) in diethyl-ether-anaesthetized and pithed rats, as well as in a group of control rats, all in the presence and absence of l-hyoscyamine. 3 With increasing doses of the parasympathetic antagonist, the fractal dimension of the time-series structure remained stable in most cases. The low-frequency spectral component narrowed with increasing drug doses and the high-frequency band underwent either no, or only very slight, changes. 4 In these rodent assays, the low- and high-frequency signals cannot be interpreted as a push–pull relationship between sympathetic and parasympathetic control.     

Screening for sediment toxicity in the Rio Santiago basin: A baseline study

Toxicity testing of sediment samples from the Rio Santiago and its main tributaries was performed using a battery of tests that included the ECHA dipstick biocide monitor, the MetPad test, the lettuce seed germination and the root elongation test, the nematode test, spot plate test, and the SOS Chromotest. Assessment was carried out on organic extracts, pore water, and direct sediment. Results of bioassays showed toxicity sources from tributaries and canals flowing into the river and areas being degraded by insults from industrial spills. © by John Wiley & Sons, Inc.     

Sources of cortical rhythms change as a function of cognitive impairment in pathological aging: a multicenter study.

OBJECTIVE: The present study tested the hypothesis that cortical electroencephalographic (EEG) rhythms. change across normal elderly (Nold), mild cognitive impairment (MCI), and Alzheimer's disease (AD) subjects as a function of the global cognitive level. METHODS: Resting eyes-closed EEG data were recorded in 155 MCI, 193 mild AD, and 126 age-matched Nold subjects. EEG rhythms of interest were delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), and beta 2 (20-30 Hz). EEG cortical sources were estimated by LORETA. RESULTS: Occipital delta and alpha 1 sources in parietal, occipital, temporal, and 'limbic' areas had an intermediate magnitude in MCI subjects compared to mild AD and Nold subjects. These five EEG sources presented both linear and nonlinear (linear, exponential, logarithmic, and power) correlations with the global cognitive level (as revealed by mini mental state examination score) across all subjects. CONCLUSIONS: Cortical EEG rhythms change in pathological aging as a function of the global cognitive level. SIGNIFICANCE: The present functional data on large populations support the 'transitional hypothesis' of a shadow zone across normality, pre-clinical stage of dementia (MCI), and AD.     

Intermittent etidronate partially prevents bone loss in hirsute hyperandrogenic women treated with GnRH agonist

Treatment with gonadotropin-releasing hormone (GnRH) agonist leads to enhanced bone turnover and accelerated bone loss in premenopausal women with endometriosis, uterine leiomyomatomas and hirsutism. Sodium etidronate is a powerful inhibitor of bone resorption which has been proven efficacious in the prevention and treatment of postmenopausal osteoporosis. The objective of this study was to evaluate the skeletal effects of 6 months of therapy with the depot preparation of the GnRH agonist triptorelin (decapeptil 3.75 mg intramuscularly every 4 weeks) in 24 hirsute patients, aged 24–33 years, with hyperandrogenic chronic anovulation. Ten patients also received cyclical etidronate in an oral dose of 400 mg/day for 2 weeks, followed by an 11-week period of 500 mg/day elemental oral calcium (one cycle). The remaining 14 patients received 500 mg/day of elemental calcium continuously. After 6 months all treatments were discontinued for at least a further 6 months. Bone mineral density (BMD) at lumbar spine and hip (dual-energy X-ray absorptiometry, Sophos LXRA, France) and biochemical markers (serum alkaline phosphatase, osteocalcin, urinary N-telopeptide and hydroxyproline/creatinine ratio) were evaluated at baseline, 6 months and 12 months. In the group given GnRH agonist alone BMD fell significantly at all measured skeletal sites during the first 6 months. In the patients treated with etidronate a significant decrease in BMD was observed at lumbar spine but not in the femoral neck and trochanter, and the changes at lumbar spine and trochanter were significantly smaller than those in the control group. At 6 months bone turnover was also increased in patients treated with GnRH and calcium. Cyclical etidronate prevented the increase in biochemical markers of bone formation and resorption, with the exception of calcium/creatinine excretion, which was significantly increased in both groups. Six months after treatment withdrawal BMD did not recover in either group. Biochemical markers (N-telopeptide, serum alkaline phosphatase) remained increased in those patients previously treated with calcium alone while they remained close to baseline values in the patients treated with cyclical etidronate.Our study indicates that: (1) GnRH agonist therapy causes remarkable bone loss in young individuals with androgen excess who are expected to have increased bone mass; (2) this bone loss can be partially prevented by intermittent cyclical etidronate therapy.     

Short-term brain ‘plasticity’ in humans: transient finger representation changes in sensory cortex somatotopy following ischemic anesthesia

Transient rearrangements of finger representation in primary somatosensory cortex induced by an anesthetic block of the sensory information from adjacent fingers have been shown invasively in animals. Such a phenomenon has been now replicated in seven healthy human volunteers. Somatosensory Evoked Fields (SEFs) have been recorded during separate electrical stimulation of the 1st, 3rd, or 5th finger. Recordings were obtained in control conditions (stage A), following complete ischemic anesthesia of the 4 non-stimulated fingers (stage B), and after regaining sensation (stage C). SEFs were recorded using a 28-channel DC-SQUID magnetometer; a single position of the sensor was enough to identify the source of N20m, P30m and following components using the Equivalent Current Dipole (ECD) model. The amount of afferent input during stages A through C was monitored with surface electrodes placed on the nerve at wrist and elbow. No variation of the nerve compound potential was observed during stages A through C. In stage A, the localizing algorithm was able to discriminate the individual finger representation in accordance with the somatotopic organisation of the sensory homunculus. It was observed that the ECDs responsible for the cortical responses from the unanesthetized finger were significantly changing following a relatively brief period of sensory deprivation from the adjacent fingers. Such changes of the ECDs with respect to the control conditions were characterized by an increase in strength and deepening for the middle finger, and by a shift on the coronal plane for the thumb and the little finger (medial for the former, lateral for the latter). Such changes became progressively evident in stage B, but were persisting in stage C.