As comprehensive review of all falls risk factors is unlikely to occur in the ED setting, identifying easily administered and interpretable testing modalities is crucial. The first steps in assessing such modalities include assessing their ability to be completed in the ED. In our study, both balance plate and TUG tests were obtainable in the ED as all patients were able to complete the TUG test and all but three were able to complete balance plate testing. The second step is to understand the NLG919 nmr relationship between the modalities. If results differ between modalities, further study would be required of all of them. Conversely, if results do Inhibitors,research,lifescience,medical not vary, future

studies could concentrate on only one. In our ED population, there was minimal correlation between TUG and balance plate results. This may be due to the different components of balance measured by the two modalities as TUG measures dynamic

balance and the balance plate Inhibitors,research,lifescience,medical measures static balance. Other studies have noted only moderate association between dynamic and static balance in elders [26]. In fact, balance assessment modalities measuring different constructs may be complementary [17]. As a result, further study should clarify the advantages, if any, of complementary testing as compared to selecting a single modality in Inhibitors,research,lifescience,medical the ED. Balance plates using limits of stability measurements have been used to predict fall risk in both institution-dwelling and community-dwelling elders [18,19,27,28]. In addition Inhibitors,research,lifescience,medical to the lack of correlation between balance plate and TUG testing, there was no relationship between the balance plate testing and patient provided history of falls in univariate logistic regression analysis. The balance plate NSEO and NSEC measures did have an AUC of >0.60 Inhibitors,research,lifescience,medical in identifying falls in the week prior to ED visit. For these measures, cutoffs could be identified with a sensitivity >80% which were somewhat useful in ruling out a fall within the past week with a negative likelihood ratio of approximately 0.3. However, specificity was low and the confidence intervals for the ROC curves Tolmetin were

wide, limiting the conclusions that may be drawn from them and indicating that few patients would be judged to be at low risk of falls. An additional concern limiting conclusions to be drawn from our use of the balance plate was the decision to proceed with a single assessment of each balance plate test. Several authors have noted that multiple repeat sessions may be required to obtain the most reliable intra-session measurements and best correlation between measurements when performing balance plate testing [29,30]. We chose a single measurement for two reasons. First, it is the recommended regimen from the balance plate manufacturer. Second, the test is most useful in the ED if it is short and easily accomplished. Repeat measurements would tend to decrease the usability of the test in the ED.

The doses of DNA encapsulated in THLs and administered IV was 5 or 70μg per rat or primate, respectively, which are equivalent 20 and 12μg/kg body weight, respectively. When the transgene is driven by the widely read SV40 promoter, the levels of luciferase were ~10pg luciferase/mg protein in the monkey brain. High levels of expression were also seen in peripheral tissues that are rich in the target receptor, including liver, spleen, and lung [27, 34]. A 50-fold increase in the tissue levels of luciferase was reported in primates, as compared to Inhibitors,research,lifescience,medical rat and mouse tissues.

The high levels of expression in monkey tissues were associated with intrinsic properties of the HIRMAb that targets the nuclear compartment of the cell [4]. Time course studies in both rodents Inhibitors,research,lifescience,medical and primates demonstrated that the peak of luciferase expression

occurs 48hs following injection of a single IV dose of THLs. The levels of luciferase activity decline thereafter and as a function of time. There are 2 Selleck AC220 potential mechanisms for the decline in the expression of the transgene, that is, promoter inactivation and plasmid degradation. The levels of both luciferase enzyme activity and plasmid DNA decay in the primate brain and liver were measured, and both processes decayed with a t1/2 of approximately 2 days, which indicates that the transient Inhibitors,research,lifescience,medical duration of the luciferase gene expression is mainly due to plasmid degradation [33]. The organ distribution of the lacZ transgene was also investigated at the cellular level with Inhibitors,research,lifescience,medical histochemistry following THL delivery of a reporter gene driven by the SV40 promoter and designated SV40-lacZ [4, 20, 34]. The latter was used to engineer THLs with either the TfRMAb or the HIRMAb (Table 1). The histochemical detection of the β-galactosidase is shown in Figure 2 for the mouse and the Rhesus monkey. The expression of the transgene

was widely detected through the cortical and subcortical structures of mouse and monkey brain, with a greater gene expression in gray matter relative to white matter in both cerebrum and cerebellum (Figure 2). On the contrary, the β-galactosidase Inhibitors,research,lifescience,medical histochemistry of control uninjected primate brain shows no β-galactosidase activity (Figure 2(b)). Light micrographs of the primate brain shows gene expression these within the choroid plexus epithelium (Figure 2(d)) and the capillary endothelium within white matter (Figure 2(f)). The gene expression was also confirmed within the neurons of the occipital cortex showing the columnar organization of this region in primate brain (Figure 2(e)). The molecular and granular layers of the cerebellum and the Purkinje cells were also positive for the transgene (Figure 2(f)). Confocal microscopy studies with antibodies against either bacterial β-galactoside or the neuronal neuN marker colocalized transgene expression in the neuronal compartment of brain [27, 34].

Moreover, amphetamines and MDMA have been shown to be neurotoxic in animal studies, particularly when given at high and repeated doses. This neurotoxic potential of the drugs may be relevant for humans. In the following sections we review the evidence for neurotoxicity in animal studies and in human

populations. Animal studies Brain morphology and neurochemistry Several studies in different laboratories and with different species demonstrate long-term alterations in brain 5-HT systems following high and repeated doses of MDMA. In studies with primates, even single doses of MDMA were found to elicit some degree of serotonergic depletion lasting over a few weeks;4 Inhibitors,research,lifescience,medical However, the lowest MDMA dose which was shown to produce longterm neurotoxic effects that persisted over months Inhibitors,research,lifescience,medical and years has been 5 mg/kg given parenterally twice dailyover 4 days, ie, 40 mg/kg overall in 4 days.9-11 The alterations include depletion of 5-HT and its major metabolite 5-hydroxyindoleacetic acid (5-HIAA), reduced [3H]paroxetine binding, reflecting reduced GABA Receptor inhibitor density of SERT, and reduced serotonergic axonal density in several brain regions.6-12 All but one species tested so far, including nonhuman primates, have confirmed the

pattern Inhibitors,research,lifescience,medical of selective neurotoxicity for serotonergic axons, with the sole exception of mice, which exhibit neurotoxic alterations of serotonergic and dopaminergic Inhibitors,research,lifescience,medical axons.4 The rate of recovery was shown to be region-dependent. This probably corresponds to the very different distances that must be covered in the process of reinnervation. Axons need to be regrown from their origin in the serotonergic cell bodies in the raphe nuclei of the brain stem to the different terminal areas of the brain. In rats, full

recovery was shown in most studies and most brain regions after 1 year, but some individual studies reported only Inhibitors,research,lifescience,medical partial recovery in the hippocampus and some cortical areas and hyperinnervation in the hypothalamus. In nonhuman primates, sensitivity to the neurotoxic effects of MDMA was shown to be more pronounced than in rodents, Urease resulting in higher rates of 5-HT depletion with smaller doses of MDMA and persisting hypoinnervation patterns in most neocortical regions and the hippocampus in the range of 20% to 40% lower SERT binding depending on the brain region examined) for as long as 7 years post-treatment.9-11 Similarly to MDMA, stimulant amphetamines, particularly METH, have also been shown to be neurotoxic in rodent and nonhuman primate studies.6,13 Typical neurotoxic METH regimens are 5 to 10 mg/kg given parenterally 4 to 10 times within 1 to 4 days. Stimulant-related neurotoxicity is not restricted to the serotonergic system.

2002). Subjects with other axis I diagnosis, active suicidality, unstable medical conditions, current

or past history of thyroid disease or abnormal thyroid function tests, or a positive urine toxicology screen were excluded. Assessments Depressive symptoms were rated over eight visits (Screening, day 3, weeks 1, 2, 3, 4, 5, and 6) using the following rating SKI-606 chemical structure scales: Montgomery and Asberg Depression Rating Scale (MADRS) (Montgomery and Asberg 1979), Beck Depression Inventory (BDI) (Beck et al. 1961), Clinical Global Impression – Severity of illness (CGI-S) (Guy 1976), Scale for Suicidal Ideation (SSI) (Beck et al. 1979). Medications All subjects received open label citalopram (20 mg) for 6 weeks Inhibitors,research,lifescience,medical and were randomized in a blinded fashion to receive additionally triiodothyronine (T3) 25 μg BID (n = 7), pindolol 5 mg BID (n = 8), or placebo (n = 8) at the start of citalopram treatment. Thyroid function tests Serum TFTs were checked at baseline and at the end visit. TSH and total triiodothyronine Inhibitors,research,lifescience,medical (TT3) were assessed by immunoassay (ROCHE Elecsys 170 Analyzers, Roche Diagnostics, Indianapolis, IN), free triiodothyronine (FT3), and free thyroxine (FT4) by Enzyme Immunoassay Assay Diagnostic System Laboratory (EIA-DSL). Statistical analysis Primary outcome measure was the time to 50% reduction in baseline MADRS scores. Collected data were screened for distributional properties

Inhibitors,research,lifescience,medical and determined to be appropriate for parametric analysis. Simple correlation analysis and proportional hazard regression (Cox Model) and accelerated failure time survival regression analysis were used

to predict time to response (i.e. 50% improvement in MADRS scores) and remission (MADRS score ≤ 7) with baseline Inhibitors,research,lifescience,medical and delta TSH, FT4, FT3, and TT3 as independent variables. Analysis was done using SPSS software (SPSS IBM, Armonk, New York). Results Demographics and baseline depression scores Of the randomized 23 subjects, 19 completed the study. Two subjects Inhibitors,research,lifescience,medical in the placebo group dropped out (one due to worsening of depression, and the other one due to excessive use of lorazepam) and two subjects missed follow-up. The mean age of the cohort was 38.34 (±12.6) years and the mean length of the index episode was 8.9 (±5.9) months with an age of onset of 32.9 (±13.5) years. All patients were required to not be receiving antidepressants for at least one month prior to starting. All, but five, patients were antidepressant naive at the time of the through study. The mean baseline MADRS score was 29.7 (±5.85), BDI score was 23.4 (±7.3), and a mean CGI severity score was 4.1 (±0.3). Six patients met DSM-IV criteria of life comorbid generalized anxiety disorder, four with posttraumatic stress disorder, and one patient with social phobia. All comorbid conditions were clinically stable and none of the patients receives treatment or therapy for comorbid conditions during the study.

TABLE III. Brief

Grief Questionaire for screening for Complicated Grief. This copyrighted instrument is reprinted with permission from Katherine Shear, MD. In later life, PD184352 ic50 losses commonly include spouses, siblings, and peers, and less commonly adult children and grand children, the latter of which are generally perceived as unnatural and unfair. Spousal loss may have followed a lengthy illness in which the care-giving burden may have been exhausting Inhibitors,research,lifescience,medical and the death a welcomed relief from terrible suffering but also might be a possible nidus for guilty rumination over admitting to having thoughts that they sometimes hoped for the death to occur in order to relieve their burden of care, thoughts they now consider be overly Inhibitors,research,lifescience,medical selfish in retrospect. Couples who have aged successfully as a unit of shared responsibility for each other sometimes find that being alone without their partner’s contribution can feel overwhelming, with either the perception they can no longer cope in the same way and are

therefore Inhibitors,research,lifescience,medical forced to accept help from other sources or possibly a move to an alternative living arrangement; or alternatively, the perception that their life is now empty without the caregiving role that organized their whole daily routine. A marital relationship that is mutually satisfying over a long period is viewed by some grievers with gratitude for lasting as long as it did. Finding new sources of support, however, can run the gamut from greater reliance on children, friends, religious institutions, or supportive environs such as life-care communities as well as hired help and potential Inhibitors,research,lifescience,medical new romantic relationships. Remarriage

is protective against depression for widowers, but not necessarily widows, and older survivors of losses through death sometimes conclude that too many complications would arise from remarriage as the multiple allegiances Inhibitors,research,lifescience,medical to each respective extended family are too cumbersome. A sustained romantic friendship is often chosen over remarriage or cohabitation in these cases. Increasing medical burden, disability, and cognitive impairment can occur within a large age range but all are more likely to accumulate with advancing age and thus the necessity of greater dependence on others can complicate the grieving process and further lead to demoralization or depression. Case vignette: recognizing and treating complicated grief in late life CG and its treatment are Calpain best illustrated with the case vignette of Sophia, age 72, whose husband of 52 years had died 9 months earlier after an acute illness. He had been well up to 2 days prior to death, and they had imminent travel plans until the point his illness turned grave with complications. Sophia was shocked that her husband, a prominent local businessman, had died so suddenly. She said she felt like “someone had cut her in two with a saw.

31 One study on clomipramine in a group of MDD patients using spectral analysis has shown a significant increase in the delta bands, corresponding to SWS. Desipramine was associated with sleep-onset difficulty in a group of MDD patients.32 Tetracyclics Mianserin has been shown to reduce REMS in rats.33 It does not change REMS duration in HCs34 and MDD patients.35 Maprotiline

reduces REMS and increases stage 2 sleep in HCs.36 These compounds tend to increase SWS.33 Selective serotonin reuptake inhibitors The selective serotonin reuptake inhibitor (SSRI) fluvoxamine was found to suppress REMS and Inhibitors,research,lifescience,medical Selleckchem ARRY 162 prolong the RL in a group of MDD patients, but had no significant action on SWS or delta band in spectral analysis.32 Paroxetine was shown to reduce total sleep time and sleep efficiency in MDD patients,37,38 while REMS decreased and RL increased. In MDD patients, fluoxetine was associated with more Inhibitors,research,lifescience,medical awakenings, decreased sleep efficiency, decreased SWS, and decreased sleep efficiency. RL is prolonged and REMS is reduced.39-41 Treatment of MDD patients showed sertraline to prolong sleep latency and decrease REMS time.42 Citalopram was shown to suppress REMS in a sustained

manner and to be accompanied by REMS rebound at withdrawal43 No change was observed in the delta band upon spectral analysis. Trazodone (100 to 150 mg/day) was found to reduce REMS and increase SWS, as well as subjective Inhibitors,research,lifescience,medical estimations of sleep quality in a group of middle-aged patients with insomnia.44 Mouret et al45 found total sleep time and Inhibitors,research,lifescience,medical SWS to be increased with 400 to 600 mg/day of trazodone in a group of MDD patients, whereas REMS and RL were not significantly modified. In another study using lower doses, Van Bemmel et al46 found

no changes in SWS. Nefazodone was shown to reduce the number of awakenings Inhibitors,research,lifescience,medical and improve sleep efficiency, and also stabilize,40 or even increase,47 REMS time in HCs and MDD patients. SWS was reduced. SSRIs have been shown to exacerbate periodic limb movement syndrome.48 Serotonin and norepinephrine reuptake inhibitors The serotonin and norepinephrine reuptake inhibitor (SNRI) venlafaxine was found to increase wake time and sleep stages 1, 2, and 3 in HCs. REMS was strongly suppressed and RL was prolonged.47,49 Noradrenergic and specific serotonergic antidepressant mafosfamide The noradrenergic and specific serotonergic antidepressant (NaSSA) mirtazapine was shown to promote sleep in HCs. It shortened sleep onset and deep sleep was increased. RL was increased; nighttime wakening was reduced.50 In MDD patients, sleep efficiency and total sleep time were increased. REMS was not affected.51 Other antidepressants Tianeptine was not shown to suppress REMS in a significant way in HCs52,53 or patients with comorbid depression and alcoholism.54 Moreover, a study in young HCs found no effect on EEG sleep parameters at therapeutic dosages (37.5 mg/day).

The demographic data will be analyzed and processed to render approximate geolocation. A high-performance query interface will be enabled to co-query records based

on geography, clinical, and genomic attributes. Interactive data maps and heat maps will be created. The data set will be mined for the derivation of knowledge, and, utilizing The Terra Fly Inhibitors,research,lifescience,medical Geospatial Analytics System (http://terrafly.com), correlates of eco-system components with DM and obesity will be determined. For example, studies have indicated that residents of neighborhoods without sidewalks tend to be overweight.115 The absence of sidewalks seems to be a factor in Inhibitors,research,lifescience,medical discouraging people from walking, thus reducing the potential benefits of this simple exercise to prevent and treat DM. The presence of sidewalks is automatically derivable from analysis of aerial and satellite images and property boundaries represented by polygons; it allows correlation of findings from imagery analysis and the obesity demographics statistics.

PERSONALIZED MEDICINE AND DM TREATMENT TARGETS Recent guidelines recommend moving away from uniform glycemic control goals for people with DM,4,8 with the result that the majority of DM patients may not be candidates for the most aggressive HbA1c goals.116 Personalization of glycemic control target is based on clinical parameters, Inhibitors,research,lifescience,medical including age, duration of Inhibitors,research,lifescience,medical DM, and presence of DM complications or co-morbidities, and eco-system components. If microvascular or macrovascular risk could be more precisely assessed than currently, more or less aggressive treatment targets could be used, not just for glucose, but also for blood pressure and lipid lowering treatments. CONCLUSIONS Inhibitors,research,lifescience,medical Patients, SB525334 datasheet physicians, health care organizations, and policy planners are grappling with the worldwide rise in incidence of DM. Diabetes mellitus and its related complications cause substantial morbidity and mortality and are consuming an increasing proportion

of health care budgets. There is wide individual and ethnic variation in susceptibility to DM as well as environmental factors, until making a “one size fits all” approach to DM management inefficient. The vision of DM care in the era of personalized medicine is that patients and physicians, using decision support systems embedded in the electronic medical record at the point of care, will have access to the results of individualized genomic, proteomic, and metabolic information, as well as the most current evidence-based guidelines and literature updates.12 This will provide them with up-to-date, accurate, and actionable information on risk for DM and its diverse manifestations, allowing them jointly to prioritize and optimize diagnostic, treatment, and monitoring plans.

This suggests that the change in response bias was indeed adaptive. The present results showed that “yes” decisions were significantly faster than “no” decisions. Given that there is a known trade-off between speed and accuracy in forced-choice, perceptual decisions (Binder et al. 1999; Huettel et al. 2004; Wenzlaff et al. 2011), and that participants were biased Inhibitors,research,lifescience,medical toward “yes” choices in the motivated conditions, it was important to establish whether there was a general change in decision-making strategy between motivational conditions beyond the motivation-mediated change in bias. Although faster, “yes” decisions

resulted in significantly more correct responses than “no” decisions. This is contrary to the established trade-off between speed and accuracy where slower decisions are more accurate than fast decisions (Binder et al. 1999; Huettel et al. 2004; Wenzlaff et al. 2011). The absence of an interaction between decision type and motivation indicates Inhibitors,research,lifescience,medical that “yes” responses were faster than “no” responses in all conditions. This then excludes a possible confound of a more general strategy shift on change in response bias and its corresponding changes in brain activity. It is possible that the faster, “yes” responses reflect immediate identification of the animal target, while the slower “no” responses are driven

Inhibitors,research,lifescience,medical by the continuing search for a target that is not present. The combined behavioral results suggest Inhibitors,research,lifescience,medical that motivation induced a change in response bias that was adaptive and that the change in bias was not confounded by another more general change in strategy. The IFG met the two criteria proposed a priori—its activity correlated with the change in bias between motivational conditions, and the relationship held true regardless of the valence of motivation that drove the shift in response bias This region

has previously been implicated in the choice between alternatives (Zhang et al. 2004; Moss et al. 2005). For example, Zhang Inhibitors,research,lifescience,medical and colleagues (Zhang et al. 2004) found increased activation in the left IFG when participants viewed a cue that indicated that they must choose between two sets of letters compared to when they viewed a cue indicating they did not have to make a choice. It has also been suggested that the left IFG is Adenosine involved in switching between rules that guide choice selection (Crone et al. 2006; Philipp et al. 2013). During a task where participants were cued as to which choice rule to use when selleck products observing a subsequent target, Crone and colleagues (Crone et al. 2006) found that there was greater left IFG activation during trials that required participants to switch to a different choice rule. This study’s finding that left IFG activation correlated with the change in response bias for both positive and negative motivation is in accordance with the region’s previously observed role in choice selection and rule switching.

The technological

progress of medicine is medicalizing the death more and more, and the gap between the “good” and the actual death has been widening during the last decades[3,4]. Medicine did not deal with dying and death until the birth – some 50 years ago – of the hospice movement, which has the paramount merit of having focused the need of caring for dying persons in order to provide them the best quality of life achievable in their conditions. Actually, the aim of the hospice movement, explicitly or implicitly expressed by its Inhibitors,research,lifescience,medical leading persons, is letting terminal patients die better [5,6]. The praxis of palliative medicine, the discipline originated from hospice movement, grounded on scientific approach and rational methods, mainly consists in comprehensive treatments of pain and physical symptoms, in caring for the patient’s and their family’s needs, and in helping them to face anguish and solitude [7]. Palliative interventions are Inhibitors,research,lifescience,medical quite effective on physical suffering. Nevertheless, being free from physical symptoms, even if an important aspect of palliative care practice, is not always enough: psychological, social, emotional and spiritual suffering ought to be also controlled Inhibitors,research,lifescience,medical [8]. The non-physical suffering, however, is a much more individual and private matter, and refers to the individual’s biography, psychology,

beliefs, expectations and cultural mind-set [9,10]. Treating mental and spiritual anguish

with the same approach of body problems does not seem that effective and correct, and for some persons, a good death is sometimes missed [11-13]. It seems that an explicit model of best palliative care practice, accepted by all – at least in western Countries – actually does Inhibitors,research,lifescience,medical not exist, but the palliative care literature converges Inhibitors,research,lifescience,medical towards some specific aspects that contribute to define a death as a good one: symptom control, careful consideration for the social and relational context, preparation to die, and existential wellbeing [14,15]. Thus, care must be centred on the patient’s wishes and choices [16-18]: palliative care is, in fact, based on autonomy. A model of best practice in palliative care should be flexible and discussable, and, specially, manifold. It is hardly maintainable that a unique model can be used in a world all of moral and cultural strangers [19-21] given that what makes death “good” is different for everyone. In reality, inside hospice check details movement and palliative care, there are no official statements which state and describe that model. It is, however, probable that the practice of palliative care is actually grounded on a implicit model. Recently, the category of “good death” as an outcome of palliative medicine has been broadly discussed [7,22-31]. Furthermore the hospice movement has a strong stand against euthanasia and assisted suicide [32-34].

8°C), and dyspnea. On admission,

the patient was conscious and reported chills, coughs, and rhinorrhea of two days’ duration. She had developed rash on her face six days after starting epilepsy treatment, with the condition progressing rapidly to her trunk, limbs, neck, and chest over the next four days. The facial rash subsequently evolved into pustules. On examination, there were multiple erosions over the mouth and vulva, and the conjunctiva was inflamed. Nikolsky’s sign Inhibitors,research,lifescience,medical was positive. The total extent of the erythematous rash was 55% of the BSA. Histological investigation of the injured skin revealed an aspect for drug eruption (extensive epidermal necrosis, focal subepidermal necrotic inhibitors blisters, melanin incontinence, and moderate perivascular lymphocytic infiltrate in the absence of eosinophils, neutrophils, and viral inclusions). Immunofluorescence

Inhibitors,research,lifescience,medical markers showed negative staining. The diagnosis of SJS-TEN caused by antiepileptic drugs was established. On the other hand, laboratory testing Inhibitors,research,lifescience,medical revealed anemia, eosinophilia, increased inflammatory markers, and white blood cell count of 10×109 /µL. Chest X-ray demonstrated multifocal patch consolidations with ground-glass opacity in both lungs. No bacterial pathogen was isolated in the respiratory tract, urine, and blood. Viral serology (HIV and hepatitis B and C) was negative. Real Time Polymerase Chain Reaction (RT-PCR) (R-gène® Kits) of bronchoalveolar lavage (BAL) revealed that the cause of the respiratory symptom was cytomegalovirus (CMV); the finding was thereafter confirmed Inhibitors,research,lifescience,medical by cell culture on MRC-5 cells. Prior serology data showed that our patient had already sustained a primary CMV infection at 6 years old, which was in favour of the current reactivation. As was expected, RT-PCR in blood showed fulminant viremia

with 459 copies/ml (threshold: Inhibitors,research,lifescience,medical 350). The antiepileptic drugs were withdrawn and anticoagulant therapy, parenteral analgesia, eye drops, and mouth antiseptic therapy were initiated. Intravenous Ganciclovir (10 mg/kg/day) was started. Oxygen therapy was initiated with parenteral nutrition and adequate hydration. Serial BAL assays were negative six days after the commencement of antiviral therapy, and the skin lesions began to heal without the need to introduce corticosteroids. The patient’s condition MycoClean Mycoplasma Removal Kit improved, and she was transferred to the general ward with a prescription of Ganciclovir for a further two weeks. Discussion TEN and SJS are severe adverse cutaneous drug reactions.4,5 Treatment with corticosteroids is recommended but not necessarily effective.5-7 Several drugs are at “high” risk of inducing TEN-SJS.1 Mycoplasma pneumoniae and herpesvirus infections are well-documented causes. In some rare cases, however, the etiology remains unknown.