It is not known if these attitudes would have an effect on Nigerian psychiatrists’ prescribing rates for LAIs. Therefore, the study

presented here aimed to determine the prescribing patterns of LAIs by psychiatrists (consultant and trainees) in Nigeria, to elicit factors that are associated with prescribing practices, and to determine the relationship between the Inhibitors,research,lifescience,medical knowledge and attitudes of these professionals towards LAIs. Methods Hypothesis We hypothesized that reported prescribing rates for LAIs would be higher among psychiatrists who believe that LAIs were readily SB216763 accepted by their patients (patient-centred attitudes). This was based on the assumption of patients’ erroneous belief in the superior efficacy of parenteral medications which would influence psychiatrists and senior trainees to commonly Inhibitors,research,lifescience,medical prescribe LAIs. Design A cross-sectional study was conducted of the attitudes and knowledge of senior trainees and consultant psychiatrists working in Nigeria. Setting This study took place in Nigeria. Psychiatric services are provided for its population of approximately 150 million people, mainly through stand alone psychiatric

hospitals, psychiatric departments in teaching hospitals, federal medical centres and some state psychiatric Inhibitors,research,lifescience,medical hospitals. Inhibitors,research,lifescience,medical There are between 150 and 250 practising psychiatrists in the country. Some centres are accredited to offer postgraduate training in psychiatry, with a training duration of between 4 and 6 years. Commonly

available LAIs in Nigeria at the time this study was conducted included fluphenazine decanoate, flupenthixol decanoate, and zuclopenthixol decanoate. Risperidone LAI was introduced in Nigeria some 9–12 months before the study was commenced. Participants A list of hospitals offering psychiatric care in the country was drawn up and grouped into geopolitical zones. Due to logistic constraints Inhibitors,research,lifescience,medical and limited resources, only four of the six geopolitical zones could be selected; north-west, north central, south-west, and south-south. For each selected zone, two hospitals were then selected using a simple random method, with each selected hospital however then sampled as a cluster. Participants at each hospital were consultant psychiatrists as well as trainees. To be included in the study, trainees had to be in the residency program for at least 18 months. All participants who returned a completed questionnaire were deemed to have provided implicit consent. Questionnaire A pre-existing questionnaire on the attitudes and knowledge of clinicians towards depot antipsychotics was used for the study. The first section of the questionnaire enquired about sociodemographic variables.

5 % of rape cases in women, with 38.8 % of combat-related events, and with 21.3 % of women who were faced with criminal assault. Breslau et al4 also report that the highest risks of developing PTSD following civilian traumatic events were associated with rape (49.0 % ±12.2 %), followed by being badly beaten up (31.9 % ± 8.6 %), and other kinds of sexual assault (23.7 % ±10.8 %). Definition and diagnosis Inhibitors,research,lifescience,medical of PTSD The diagnostic criteria for PTSD are listed in both the DSM-IV and the International Classification of Diseases, 10th revision (TCD-10). The criteria are essentially the same, with the exception that no time requirement is stipulated

in the ICD-10. As the authors believe Inhibitors,research,lifescience,medical that the element of time is critical in this disorder, the DSM-IV seems to be a more appropriate diagnostic system, and, indeed, has been applied

much more widely in studies. There are four main diagnostic criteria, or characteristic features, of PTSD. These are: exposure to a traumatic event, reexperiencing, avoidance, and increased arousal. According to the DSM-IV, only extreme traumatic stressors, in contrast with NLG919 mouse general stressful experiences, have been linked etiologically to PTSD. Such traumatic events are defined as situations Inhibitors,research,lifescience,medical in which “the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical

integrity of self or others …” (DSM-IV, Inhibitors,research,lifescience,medical p 427). As per this definition, very severe humiliation, or any other type of disappointment or intense stress, does not fulfill the criteria for a traumatic event. On the other hand, it has been recognized in the DSM-IV that an individual does not need to be exposed to a trauma Inhibitors,research,lifescience,medical that is “outside the range of usual human experience,” as previously defined by DSM-III. Moreover, the DSM-IV has added an important element to the diagnosis: the emotional response, which is characterized as “intense fear, helplessness, or horror”; DSMIV, p 428), and hence, the diagnostic criteria in DSM-IV is more stringent in this regard. The second feature of PTSD is reexperiencing (Criterion B). The PTSD patient is emotionally stuck in the traumatic event, even many years after it medroxyprogesterone has occurred, and constantly reexperiencing it in various ways: flashbacks; stressful recollections; recurrent, distressing dreams; acting or feeling as if the traumatic event were reoccurring or experiencing intense psychological distress or physiological reactivity following exposure to internal or external cues that symbolize or resemble the event. An additional maladaptive mechanism used by patients diagnosed with other anxiety disorders, including patients with PTSD, is avoidance. Avoidance is listed as Criterion C in the DSM-IV’s definition of PTSD.

Why some people become symptomatic when their DLMO becomes delayed or advanced with respect to mid-sleep while others do not Is an Important research question. However, the answer to this may not affect treatment, and would not diminish the clinical importance of the circadian component in SAD: no matter how many necessary-but-not-sufficient causes there may be, correction of just one of these could produce a successful clinical outcome. Implications

for analyses of extant and new data sets It is hoped that the work presented here will Inhibitors,research,lifescience,medical alert researchers to another way of conceptualizing a biological marker, in addition to the current concept of using a biological marker to distinguish between patients and healthy controls, which can often be made by merely taking a good history, that is, identifying patients who are anxious, depressed, obsessivecompulsive, paranoid,

psychotic, substance abusers or poor sleepers, etc. Indeed, a symptom severity biological Inhibitors,research,lifescience,medical marker may be more useful than a chemical test for a DSM diagnosis, particularly if the former informs the type of ROCK activation treatment and provides a way of monitoring treatment in addition to assessing subjective and objective signs and symptoms. Given how relatively inexpensive and noninvasive the salivary DLMO is compared with other markers, neuroimaging for one example, and given how safe and inexpensive low-dose melatonin and Inhibitors,research,lifescience,medical light are compared with most other allopathic treatment modalities, there is ample justification for future investment in circadian research. Our recent study20 establishes the PSH and the circadian component as a necessary but Inhibitors,research,lifescience,medical not sufficient cause of a substantial component of SAD, as well as a biological marker. It is hoped that the

three criteria met by the circadian component for the latter designation will clarify what is important for other biological markers to demonstrate, something like Koch’s postulates. We22 have recently described these; in the same patients: Symptom severity correlates with the biological marker before treatment. Inhibitors,research,lifescience,medical Symptom severity correlates with the biological marker in the course of treatment. Symptom change scores in symptom severity correlate with the change in the biological marker. In our recent study,20 we concluded that (in order of certainty): The prototypical SAD patient is phase and delayed, whereas a less well defined subgroup may be phase advanced; (ii) the circadian component (at least for the prototypical patients) is substantial, and it is consistent with the PSH and a hypothesized therapeutic window for optimal circadian alignment; and (iii) the work presented here will be useful as a template for reanalyzing extant data sets and for implementing new studies of nonseasonal depression, as well as other sleep and psychiatric disorders, in which a circadian component might be present.

The cumulative lifetime risk for colorectal cancer approaches 40% (76). It remains questionable, however, whether the malignancies

occurring in the intestines derive from direct selleck chemical transformation of hamartomatous polyps because dysplasia is exceedingly rare in these polyps. Patients with Peutz-Jeghers syndrome have germline mutations in the LKB1/STK11 gene (77-79). The hamartomatous polyps in Peutz-Jeghers syndrome are most commonly seen in the small intestine, but Inhibitors,research,lifescience,medical can also occur in the colon. They are composed of proliferative epithelium, stroma and smooth muscle arranged in an arborizing pattern (Figure 14). Figure 14 Peutz-Jeghers polyp in the colon. Note the lobular pattern of colonic crypts divided by smooth muscle bundles

(original magnification ×100) Juvenile polyposis syndrome This is also Inhibitors,research,lifescience,medical an autosomal dominant inherited cancer syndrome diagnosed if, (I) 5 juvenile polyps in the colorectum; (II) juvenile polyps throughout the gastrointestinal tract; or (III) any number of juvenile polyps and a family history of juvenile polyposis Inhibitors,research,lifescience,medical (80). Similar to Peutz-Jeghers syndrome, the cumulative lifetime risk to develop colorectal cancer in patients with juvenile polyposis syndrome also approaches 40% (80,81). In contrast to Peutz-Jeghers syndrome, however, colorectal cancers in patients with juvenile polyposis syndrome are believed to develop directly from neoplastic transformation within a juvenile polyp because dysplasia is a frequent finding in these polyps. Approximately 50-60% of the patients Inhibitors,research,lifescience,medical have germline mutations in the SMAD4 or BMPR1A genes (82). Histologically, juvenile polyps feature cystically dilated crypts with edematous and inflamed stroma (Figure 15). The surface of the polyp may be eroded, with granulation tissue and epithelial regenerative Inhibitors,research,lifescience,medical changes. Figure 15 Juvenile polyp showing dilated crypts and inflamed stroma (original magnification ×40) It should be pointed out that syndromic juvenile polyps cannot be distinguished

from sporadic counterparts, and can be confused with inflammatory polyps on histologic ground. Despite the name, juvenile polyps can occur in adults or even elderly. Patients with sporadic juvenile polyps do not have an increased risk for malignancy (83). MUTYH-associated polyposis Edoxaban MUTYH-associated polyposis (MAP) is an autosomal recessive polyposis syndrome that carries an increased risk for colorectal cancers (84,85). It is caused by biallelic germline mutations in the MUTYH gene (also known as MYH gene) that encodes a base excision repair (BER) enzyme responsible for preventing mutations following oxidative DNA damage. The most common mutations are missense variants Y165C and G382D, accounting for >70% of all mutant alleles (86,87). MAP patients usually have >10 synchronous colorectal adenomas and can have several hundreds or even up to 1,000 polyps. Most patients have <100 polyps at the time of diagnosis, however (88).

It usually affects postmenopausal women between ages 58–75.2 Clinical features of this syndrome mimic those of an acute coronary syndrome, namely chest pain, dyspnea, ST-T changes with or without a prolonged

QT interval, and mild elevations of cardiac enzymes.2-4 On angiography patients will have normal-appearing coronary arteries. Left ventriculogram will show wall motion abnormalities, which is the Inhibitors,research,lifescience,medical basis in defining the different variants. 2 Case Report We report a case of a 64-year-old Hispanic female with a significant past medical history of hypertension, hyperlipidemia, depression, and gastroesophageal reflux disease who presented to the emergency room with intermittent substernal chest pain that began about an hour after having an argument with her son. Troponin was 7.69 and creatine kinase-MB was 39.7 on admission. Electrocardiography (EKG) showed ST-segment elevations in leads Inhibitors,research,lifescience,medical II, III, aVF, V5, and V6 that were consistent with acute ischemia (Figure 1). Her

coronary angiogram revealed normal coronary arteries. Left ventriculogram showed hypokinesis of the midventricular section with a hyperdynamic base and apex (Figures ​(Figures22 and ​and3).3). Cardiac magnetic resonance imaging showed mild hypokinesis of the midinferior and lateral walls and a left ventricular ejection fraction of 70%. The following Inhibitors,research,lifescience,medical day, the patient also had a prolonged QTc of 478 ms, which is commonly seen in patients with nonapical TC.5 The patient was treated with an aspirin, statin, beta blocker, and angiotensin converting enzyme inhibitor. The next day, the patient had sinus bradycardia that was probably secondary to the beta blocker. By day two the patient improved clinically and the acute ischemic changes on EKG had resolved (Figure 4). Figure 1 EKG on initial Inhibitors,research,lifescience,medical presentation. ST-segment elevations in leads II, III, aVF, V5, and V6. QTc is prolonged (478 ms). Figure 2 Left ventriculogram during systole. Figure 3 Left ventriculogram during diastole. Figure 4 EKG on day 2 of admission. ST-segment elevations resolved. QTc Inhibitors,research,lifescience,medical interval is 443 ms. Discussion

Typical and Atypical Takotsubo Cardiomyopathy Typical or classic TC is much more common than the atypical Resminostat variants. It is characterized by transient apical hypokinesis and basal hyperkinesis.3, 4 Several variants of TC have been described. In reverse or inverted TC, the apex is hyperdynamic and the base is akinetic.6 The midventricular type is characterized by akinesis with or without ballooning of the midventricular segment and a hyperdynamic base and apex.7-11 Akinesis of other LV and RV segments have also been described.3, 12 Patients may also have repeated episodes of TC manifesting in the classic and atypical forms.11, 13, 14 Pathophysiology Although the pathophysiology of TC is still not well established, a few theories have been proposed. selleck chemical Emotional or physical stress is considered to be a trigger.

The animals behaved normally in a wide range of behavioral tests except when exposed to aversive situations caused by either natural or CI994 datasheet conditioned fear stimuli. Under such conditions, enhanced anxiety responses and a bias for threat cues were observed.22 The bias of the animals for threat

cues was especially significant since this behavior Inhibitors,research,lifescience,medical corresponds to the cognitive deficit contributing to the inability of anxious individuals to distinguish an ambiguous from a threatening situation.23 Thus, a GABAA receptor deficit is considered as a predisposition for anxiety disorders in humans. It appears that anxiety symptoms are a sensitive manifestation of an impaired GABAergic neurotransmission.21,22,24 Epilepsy Modification of activity at GABAergic synapses powerfully influences Inhibitors,research,lifescience,medical epileptic phenomena. This is a consequence of the role of GABAergic synapses in recurrent inhibitory systems in cortical and other structures, and their effect in limiting the excessive discharge of principal neurons in time and space. Genetic evidence provided the most direct link of epilepsy to GABAA receptor dysfunction. A K289M mutation located in the extracellular loop Inhibitors,research,lifescience,medical of the γ2-subunit

between the transmembrane domain 2 and 3, was linked to familial generalized epilepsy with febrile seizures.25 At recombinant GABAA receptors, the K289M mutation reduced the GABA-activated current. Another mutation in the γ2-subunit Inhibitors,research,lifescience,medical of GABAA receptor was linked to childhood absence epilepsy and febrile seizures with a conserved arginine residue being mutated to glutamine (R43Q).26 However, since childhood absence epilepsy is not inherited in a simple mendelian manner,

the point mutation is not Inhibitors,research,lifescience,medical considered to be sufficient by itself to cause this phenotype. Another example of an altered GABAergic function is that of generalized seizures in infancy related to a pyridoxine deficiency. Since pyridoxal phosphate is a cofactor of glutamic acid decarboxylase, the seizures are related to a deficient synthesis of GABA and can be treated by moderate or high doses of pyridoxine. Furthermore, multiple others forms of epilepsy occur in the neurodevelopmental disorder, known as Angelman syndrome, which also shows mental retardation and facial dysmorphism. Genetic studies commonly reveal a major deletion on maternal chromosome 15q11-1327 with two genes being the major contributors to the syndrome – one is UBE3A, encoding a ubiquitin ligase, the other is GABRB3 encoding the β2 subunit of GABAA receptor. Absence epilepsy in man, with a 2- to 3-Hz spike-and wave discharge in the cortex, is dependent on a thalamocortical loop, which involves several sets of GABAergic synapses in cortex and thalamus. The “waves” correspond to hyperpolarizing activity resulting from synchronous firing of GABAergic neurons.28 The effects of GABA-related drugs are however complex.

The seeded connectivity analysis showed similar results to the PPI analysis in DLPFC-HF coupling. Overall

then, functional connectivity analysis offers some insight into correlation between different brain regions, but is limited in that it does not account for directionality, influence, or causality between putatively interacting regions; it makes no assumptions about the nature of underlying pathways, their structure, nor anatomical connectivity. So while correlative methods provide a way to characterize neural functional networks by temporal coherence of Inter-regional activation patterns, it yields neither an understanding of driving neural origins nor of the directionality of the observed network. Inhibitors,research,lifescience,medical The next wave of imaging genetics: effective connectivity modeling In contrast to functional connectivity approaches, effective connectivity analyses promise extended insight, referring explicitly to the influence that one learn more neuronal system exerts over another, and may be used to better explain Inhibitors,research,lifescience,medical integration within a distributed neural system. Models employed in analyzing imaging data to uncover effective connectivity are based on regression models, or structural equation models, and these models may be linear or nonlinear.

Dynamic causal modeling (DCM) is a type of effective connectivity analysis that yields directional, pathway information and allows for a quantification of the influence of a given neural region Inhibitors,research,lifescience,medical over another.57,58 DCM analysis, introduced in 2003 for fMRI data, is a Bayesian framework for inferring hidden neuronal states from Inhibitors,research,lifescience,medical measurements of brain activity; it is a hypothesisdriven approach, requiring an a priori definition of a set of interconnected neural areas that mediate a given function of interest.59 DCMs are generative models of brain responses, which provide estimates of neurobiologically interpretable quantities including strength of synaptic connections

among neuronal populations and their Inhibitors,research,lifescience,medical context-dependent modulation.60 Causality in DCM is based on control theory, ie, causal interactions among hidden state variables that are expressed by differential equations that describe how the present state of one neuronal population causes dynamics in another via synaptic connection, and how these interactions change under the influence of external perturbations (eg, experimental manipulations) or brain activity. DCM tests hypotheses about neuronal mechanisms, allowing one to specify a generative model of measured Adenylyl cyclase brain data, which is a probabilistic mapping from experimentally controlled manipulations to observed data, via neuronal dynamics. DCM has begun to be applied to imaging genetics. Using a DCM approach, distributed circuits that putatively underlie working memory — prefrontal-parietal and prefrontal-striatal circuits — were identified in healthy, normal subjects, and COMT, DRD2, and AKT1 functional variants were associated with the circuits.

43±4.23 years). None of the patients in the case group had a normal size thymus, nor was the size close to normal. Discussion In our study, the thymus was seen in all patients in the control group. In the only previous study in this regard, the thymus was seen in 92% of the patients in control group and in the remaining patients the thymus was Inhibitors,research,lifescience,medical not visible for unknown reasons.8 In our case group the thymus was visible in 53.8% of the patients by axial HASTE image. This finding suggested that more than half of the children had either a persistent

or regenerated thymus after open cardiac surgery which could be attributed to the type of patient selection. We have selected patients with a higher age (over 5 years) or those who had underwent surgery only once by a single surgeon using a similar method. As the thymus consists of a wide variety Inhibitors,research,lifescience,medical of shapes and sizes, prediction of the shape and size of

any remaining thymic tissues can be difficult. These three factors of a higher age over 5 years, only one surgery, and similar surgical method can enhance the visualization of the remaining portion of the thymus after mid-sternatomy, however in the superior mediastinum this leads to increased thymic identification in Inhibitors,research,lifescience,medical comparison with a report by MacDonald and Mackenzic who have reported 29% thymus identification.8 A unique Inhibitors,research,lifescience,medical feature of our study was that we chose only patients with TOF rather than different types of ongenital heart disease

(CHD). Patients were operated on by a single surgeon using a similar method. All images were obtained Inhibitors,research,lifescience,medical by the same device with a standard protocol and by a single technician. Images were examined under the supervision of a radiology resident and the undesirable images were repeated until an acceptable image was obtained. Less than half of the children in our study, regardless of their age at sternotomy, did not have an http://www.selleckchem.com/products/dynasore.html identifiable thymus according to MRI after surgery. In our study the control group consisted of individuals with no history of chest surgery or known illness which referred to the MRI center for other reasons. In Edoxaban most patients in the case group the thymus was clearly smaller. The signal was heterogeneous in 3 patients and the shape of the thymus was irregular in 5 patients. These were normal changes after surgery, thus the remainder of the thymus could be of any shape and dimension and located in any part of the mediastinum. An important question which arises is why the thymus is seen in some patients after median sternotomy. The best explanation can be the use of different techniques during surgery.

Mutations in CNTNAP2 are associated with autism in a small number of individuals, particularly with language disabilities.107,116 Cntnap2 knockout mice were generated to understand the actions of this protein on brain development and autism-relevant behaviors.40 Seizures were detected in 9 out of 10 null mutants. Social behaviors were impaired on the 3-chambered task, during reciprocal interactions, Inhibitors,research,lifescience,medical and in home cage nesting. Repetitive self-grooming was elevated. Resistance to change was seen in the Morris water maze, in which the initial learning was normal but the Cntnap2 knockouts failed the reversal test when the escape platform location was changed. Less PR-619 ic50 spontaneous

alternation in a T-maze was seen in the null mutants, concomitant with moderate hyperactivity Reduced number of GABAergic interneurons and impaired migration of cortical projection neurons in this line of Cntnap2 mice underlie their seizures and some of their behavioral abnormalities. The Geschwind team proceeded to test risperidone, the antipsychotic Inhibitors,research,lifescience,medical approved by the US Food and Drug Administration for the treatment of irritability Inhibitors,research,lifescience,medical in autism. At 0.2 mg/kg IP daily for 7 days, a dose and regimen which did not affect locomotion in the wildtype controls, risperidone reduced the hyperactivity and

repetitive selfgrooming in Cntnapl null mutant mice.40 Social behaviors were unaffected by the treatment with risperidone, which is an atypical antipsychotic. Single gene mutations, chromosomal deletions, Inhibitors,research,lifescience,medical and duplications cause a variety of neurodevelopmental disorders, including Fragile X, Rett, Angelman, PraderWilli, Smith-Lemli-Opitz, Timothy, Williams, and PhelanMcDermid syndromes, and tuberous sclerosis.97,108 A surprisingly large number of these de novo mutations code for signaling proteins that mediate the biochemical events downstream to postsynaptic neurotransmitter receptors. Interactome

network analyses revealed convergences in genes that mediate transcriptional and splicing Inhibitors,research,lifescience,medical mechanisms that may be dysregulated in autism spectrum disorders.117 Mutant mouse models of many of these syndromes have been generated.43,44,114,118-122 While clinically distinct disorders caused by known single gene mutations suggest straightforward targets, as compared with complex disorders such as cases of autism in which the genetic substrates are unknown, increasing knowledge about the actions of downstream below signaling proteins could identify pharmacological interventions which target key mechanistic sites in convergent biochemical cascades. Mice with homologous mutations are being employed as translational tools to evaluate convergent downstream target mechanisms, and to screen compounds that yield useful interventions at those sites. Tuberous sclerosis Tuberous sclerosis, caused by a mutation in the Tsc1 or Tsc2 gene, is characterized by benign tubers in the cerebral cortex, seizures, a high incidence of intellectual impairment, and frequent comorbidity with autism.

Like fibrin, platelets play an integral role

in thrombus formation and offer a target for thrombus-specific contrast agents. Antibodies capable of binding the activated glycoprotein αIIbβ3 platelet binding site (gpIIb/IIIa) have demonstrated thrombus uptake.19 Using a murine model of carotid thrombosis, Klink et al. demonstrated that a gpIIb/IIIa-based agent (P975) bound to gadolinium chelates manifested persistent enhancement 2 hours following administration, suggesting its utility for delayed thrombus imaging as compared Inhibitors,research,lifescience,medical to conventional gadolinium (which typically manifests myocardial/cardiac washout within 30 minutes). Non-gadolinium-based contrast agents also have been used to target platelets. In a study of in-vivo murine and ex-vivo human carotid specimens, von zur Muhlen et al. reported that a contrast agent consisting of micro particles of iron oxide in conjunction with gpIIb/IIIa antibodies yielded improved mural thrombus Inhibitors,research,lifescience,medical detection as compared to control (P <.01).20 To date, clinical performance of targeted contrast agents for thrombus have not yet been reported in large-scale cohorts. Conclusions As the prevalence

Inhibitors,research,lifescience,medical of heart failure and coronary artery disease continues to increase, the clinical importance of accurate diagnostic imaging for thrombus is heightened. Although echo is widely available, it can be diagnostically limited given its reliance on the anatomic appearance of thrombus, even when image quality is Selleck LDK378 judged to be optimal. DE-CMR provides tissue characterization of thrombus Inhibitors,research,lifescience,medical and has been shown to improve LV thrombus detection compared to echo-based anatomic imaging. CMR also identifies structural risk Inhibitors,research,lifescience,medical factors for LV thrombus, including infarct size/distribution and contractile dysfunction. Novel CMR

techniques, including use of targeted contrast agents, may further refine thrombus characterization. Future studies are anticipated to broaden the utility of CMR in the evaluation of cardiac thrombi. Funding Statement Funding/Support: Dr. Weinsaft has a sponsored research agreement with Lantheus Medical Imaging. Footnotes Conflict of Interest Disclosure: The authors have completed and submitted the Methodist DeBakey Cardiovascular Journal Conflict of Interest Statement and none were reported. Contributor Edoxaban Information Parag Goyal, Weill Cornell Medical College, New York, New York. Jonathan W. Weinsaft, Weill Cornell Medical College, New York, New York.

Case Report A 29-year-old female with a history of Wegener’s granulomatosis presented with new-onset chest pain and shortness of breath. The chest pain was described as a sharp, pressure type of pain located over her entire chest, radiating to her back, and becoming worse when both lying down and breathing deeply.