Nevertheless, the extracted

component substantially http://www.selleckchem.com/products/PD-0332991.html resembles m-Ins and, moreover, provides highly accurate estimates of m-Ins. So, rather than a limitation, it is an opportunity that ICA provides to extract resonances with singlet peaks, even in the presence of spectrally colocated strong resonances. At the same time, resonances with multiple peaks that tend to be correlated with other (modeled) resonances, are not likely strictly independent to begin with, and therefore are difficult to resolve exactly using ICA, as evident from the slightly lower spectral correlations of such resonances (Table 1). However, even the lowest spectral correlation (other than m-Ins), that of Glc due to Inhibitors,research,lifescience,medical strong overlaps with Tau (r ~0.41), is at ~0.95. The low spectral correlations do not necessarily hurt ICA estimation, especially when the resonances are strong, for an error in their estimation is acutely felt. Our in vivo results demonstrate that ICA can resolve signals of interest from the confounding artifacts and can group covarying resonances Inhibitors,research,lifescience,medical together. Inhibitors,research,lifescience,medical The estimates of identified components resembling Cr, NAA, PCh, and m-Ins signals, while including other covarying resonances (Fig. 7), nonetheless demonstrated strong correlations with the LCModel estimates of the identified metabolites. The weak correlation involving NAAG may be attributable to LCModel’s limitation in resolving

NAAG from NAA; though it makes sense to present NAA + NAAG for real data, we could not present that as our estimates are NAA normalized. An ICA component associated with the s-Ins signal is also consistently extracted by ICA, perhaps due to the lack of overlap with any other signal. Elevated s-Ins in the current Inhibitors,research,lifescience,medical data set may be due to effects of alcohol abuse (Viola et al. 2004) or aging (Kaiser et al. 2005). The ICs that are unidentified include baseline and broadening components and resonances of interest, such as those from Asp, Glu, Gln, and GABA, indiscernible from such confounds. We acknowledge the

difficulty in discerning resonances with multiple peaks, such as those from Glu + Gln, from the in vivo data, which LCModel estimates Inhibitors,research,lifescience,medical with reasonable accuracy. In our future study, we will provide modifications to ICA, by incorporating prior information, in the form of constraints in the ICA algorithm (Lin et al. 2010) to improve the estimations of such metabolites. Appropriate preprocessing steps to effectively Cilengitide reduce noise or baseline artifacts may also improve ICA’s estimation accuracy, as our simulations indicate. Finally, the ICA approach may benefit from the use of all available complex time-domain data, rather than just the real part of the data that we used in this study, with very good performance. These strategies to improve ICA performance will also be explored in the future study. Clearly ICA, which cannot analyze spectra individually, cannot replace the curve-fitting methods, such as LCModel, in individual spectral analysis.

Three of these genes are clearly involved in the process of O-mannosylation (POMT1, POMT2, POMGnT1) (20, 24, 25), while the function of the remaining 3 genes, fukutin, FKRP and LARGE is still not clear (26–29). Of these 6 genes, the most frequently mutated in the Caucasian population is FKRP. While this was the first gene to be associated with an extremely wide range of clinical severity, more recent data suggests that this is also a common theme for mutations in other genes. The FKRP gene Our group originally described mutations in the fukutin-related protein gene (FKRP) in SB431542 research buy patients with a form of CMD (MDC1C) characterized by onset at

birth or in the first few months of life with profound weakness, markedly Inhibitors,research,lifescience,medical elevated Inhibitors,research,lifescience,medical serum CK and inability to achieve independent ambulation or standing (22). Intelligence was preserved and brain imaging normal. These patients had a significant reduction of the glycosylation of ADG both on immunocytochemistry and Western blot analysis (22). Shortly after, our group also identified involvement of the FKRP gene in a much milder variant of limb girdle muscular

dystrophy, LGMD2I, which had already been mapped to chromosome 19q13 where the FKRP gene lies (30). In contrast with MDC1C, the onset of the condition in LGMD2I varied from childhood to late adult life; typical patients Inhibitors,research,lifescience,medical with LGMD2I have a hypertrophic phenotype and a proximal Inhibitors,research,lifescience,medical distribution of weakness, limited or no contractures, markedly elevated serum CK and frequent cardiac complications (30–32). Both intelligence and brain imaging are entirely normal. Surprisingly, this form of LGMD was subsequently found to be the most common LGMD variant in the UK population,

due to the high frequency of a C826A mutation, with an estimated heterozygote frequency of ~1:400 (32). Inhibitors,research,lifescience,medical This particular mutation was also found at high frequency in other Caucasian populations, such as in Germany (33) and Scandinavian countries (34), while it was less common in Italians, and even less common in LGMD patients from Brazil (27, 35) and Japan. The expression of glycosylated ADG was only moderately reduced in LGMD2I, in keeping with the less severe muscle involvement compared to children with MDC1C (28). Subsequent studies clarified that Flavopiridol nmr the originally described MDC1C phenotype did not represent the most severe end of the clinical spectrum, as we then identified FKRP mutations in patients with a CMD variant resembling MDC1C but with additional features such as mental retardation and cerebellar dysplasia and cysts on brain MRI (36), followed by the identification of mutations in patients with severe supratentorial cortical dysplasia and structural eye involvement, mimicking classical Muscle-Eye Brain disease (MEB) and Walker Warburg syndrome (WWS) (37). The severity of loss of ADG glycosylation in these patients was more severe than previously found in MDC1C, in keeping with their more severe clinical phenotype.

The relatively fast computing time was a result of reducing the objective function to 10-4 and limiting the data points to three decimal

places in the input dataset. The objective function is the summed squared mean distance selleck chemical Bosutinib measured between the simulated data and input data. Reducing the objective function increased computing time but improves the quality of the parameter fit to input data. We performed an experiment to determine the relationship between the value of the objective function and the time taken to compute PVA for one reaction with two substrates, two products, one enzyme and six kinetic Inhibitors,research,lifescience,medical parameters (Figure 5). The results of this experiment indicate that the computing time for parameter

estimation increases significantly when the objective function is reduced to 10-10 and beyond. The relationship that is observed between the objective function and computing time appears to be linear (PVA was computed on a desktop computer with a quad CPU having 3.00 GHz, 2.99 GHz processor speed Inhibitors,research,lifescience,medical and 4 GB of RAM). Figure 5 Computing times of parameter variability analysis (PVA) against changes in objective function. PVA was performed for a reaction with two substrates, two products, one enzyme and six kinetic parameters. For each PVA run, Inhibitors,research,lifescience,medical the summed squared mean distance … Another variable that can increase computing time in parameter estimation is the number of data points in the experimental dataset. To examine how

the number of data points influences computing time, we performed parameter estimation for a single reaction with two substrates, two products, one enzyme Inhibitors,research,lifescience,medical and six kinetic parameters (Figure 6). The result of this experiment indicates that the Inhibitors,research,lifescience,medical number of data points in the input dataset for parameter estimation increases the computing time in a non-linear manner. This explains why a relatively fast time of 5 hours and 40 minutes was recorded when PVA was performed for such a large model with 2537 kinetic parameters as the number of input data points was only three. Figure 6 Relationship between number of Batimastat input data points and computing time. PVA was performed for a single reaction of two substrates, two products, one enzyme and six kinetic parameters. PVA was repeated six times and for each iteration the number of data points … 3.5. Validation on Model Integrity We tested the predictive capability of our M. tuberculosis model and kinetic parameters by determining whether different conditions could be predicted without re-estimating kinetic parameters. To calibrate the model over a range of glycerol uptakes, we created a virtual time series containing ten repeats of each of the steady-state flux distributions obtained from input conditions with glycerol at 0, 0.5 and 1 mmol/gDW/h, respectively.

There are other stressors whose sequelae may well be due to the uncontrollability of the stressor (eg, social defeat), but since controllability Cyclopamine datasheet cannot be readily manipulated in these paradigms, this cannot

be determined. Indeed, this is why shock is used in our studies. We know of no other aversive event whose controllability can readily be manipulated in such a way Inhibitors,research,lifescience,medical that the subjects with and without control experience identical physical events. Research conducted by numerous laboratories has revealed a constellation of behavioral changes that follow uncontrollable, but not controllable, shocks. Thus, rats exposed to uncontrollable shock later fail to learn to escape shock in a different situation (the so-called “learned helplessness” effect), are inactive in the face of aversive events (so-called

“behavioral depression”), become less aggressive and show reduced social dominance, behave anxiously in tests of “anxiety” such as the social interaction test, are neophobic, develop ulcers, respond in exaggerated fashion to drugs of abuse, etc.6 Inhibitors,research,lifescience,medical None of these outcomes follow if the organism is able to Inhibitors,research,lifescience,medical exert control over the stressor. Prior research has focused on the neural mechanism(s) by which uncontrollable stress (inescapable shock, IS) leads to the above behavioral outcomes. Indeed, this can be said of most stress research in animals, since the stres sors that are used (restraint, social defeat, Inhibitors,research,lifescience,medical cold water, etc) have almost always been uncontrollable. There has been very little work directed at understanding the mechanism(s) by which control confers protection from the effects of the stressor. Indeed, most experiments studying the neurobiology of stress do not even contain a group for whom the stressor is controllable – the typical comparison is between a group exposed to an uncontrollable stressor and a home

cage control group. What is known is that uncontrollable stress produces sequelae Inhibitors,research,lifescience,medical that are not produced by physically identical controllable stress. It has been implicitly assumed that this difference occurs because the organism detects/learns/perceives that the uncontrollable stressor is learn more uncontrollable, and that this sets in motion the neural cascade that mediates the behavioral outcomes. The unstated assumption has been that stress per se produces neural consequences that are then magnified by the detection/learning/perception of uncontrollability That is, it has been assumed that uncontrollability is the “active ingredient.” From this point of view, controllable stressors fail to produce outcomes such as exaggerated anxiety simply because they lack the active uncontrollability element. However, it is also possible that instead the presence of control is the “active ingredient.” Here, the detection/learning/perception of control would inhibit neural responses to stressors.

60,79 The segmentation of the frontal cortex by neuroscientists into specific sites associated with inhibition, storage, and conflict, #selleck bio randurls[1|1|,|CHEM1|]# resolution have resulted in changes in the focus of behavioral work away from general explanatory constructs into more focused, operationbased views of age-related changes in cognitive function. Age-related declines in long-term memory have the added complexity of involvement of mediotemporal areas. There is only a weak relationship between mediotemporal volume and cognitive performance41 and relatively little functional evidence Inhibitors,research,lifescience,medical relating hippocampal dysfunction to memory dysfunction in normal older adults – although there

arc few studies of this with age.55 Moreover, the entorhinal cortex appears to be important for understanding Inhibitors,research,lifescience,medical both normal and pathological aging.80 In general, most evidence accounting for age-related declines in long-term memory function have focused on encoding and retrieval operations residing in the frontal cortex, although there is clear evidence that, mediotemporal function is important for long-term memory function in young adults. There is certainly sufficient

evidence to suggest that prefrontal cortex plays a causal role in contributing to age-related changes in behavioral tasks of executive function and Inhibitors,research,lifescience,medical long-term memory. What Inhibitors,research,lifescience,medical is poorly understood is the specific relationship of neural activation patterns to cognitive aging, an issue taken up later in this article. Behavioral researchers may find it productive to focus their work in cognitive aging on specific

executive processes and operations to understand changes in memory and higher order functions, as these operations better reflect neural architecture. Continuous cognitive decline across life span Dopamine receptors decline Inhibitors,research,lifescience,medical continuously across the life span and may play a role in the gradual decline of cognitive ability, along with volumetric declines in frontal cortex. Although there is considerable confusion about, patterns of neural recruitment in old and young, there are some broad generalizations that are reasonably well substantiated about the asymmetry of hemispheric recruitment in young compared with older adults.48 What, remains entirely unexplored is how young adults make GSK-3 the transition from highly focused, latcralized activations in performing a cognitive operation, to the qualitatively dedifferentiated patterns of recruitment observed in older adults. The disconnect between continuous behavioral decline and qualitatively different recruitment patterns with age can only be understood by conducting large life span neuroimaging studies with attention to individual differences in both behavioral and neural domains as well as age.

One reason for this difference is a lack of clear understanding of sexual dysfunction caused by depression itself. Mitchell and Popkin showed that difficulty with arousal, ejaculation and change in sexual interest after antidepressant use have been reported by patients, although no related cases of priapism have been noted [Mitchell and Popkin, 1983]. The sexual experience can broadly be divided into three stages: stage 1, interest and desire (libido); stage 2, physiologic arousal; and stage 3, orgasm. Neurotransmitters and

hormones are believed to influence Inhibitors,research,lifescience,medical SSRI-associated sexual dysfunction. Dopamine, serotonin [5-hydroxytryptamine (5HT)], testosterone and oestrogen all have an influence on sexual interest and desire (libido). Sapitinib Nitric oxide, acetylcholine and 5HT are important modulators of physiological sexual arousal. Finally, norepinephrine and 5HT play important roles in orgasm. Recent evidence suggests that additional neurotransmitters such as glutamate may

also be involved Inhibitors,research,lifescience,medical in sexual physiology [Perlis et al. 2009]. Among the antidepressants, SSRIs cause delayed ejaculation and interfere with orgasm [Arjmand and Sadeghi, 2005]. Precise statistics are not available but difficulty Inhibitors,research,lifescience,medical with orgasm has been reported in 15–50% of men and women in most studies. Sexual dysfunction with use of MAOI and TCA drugs were first reported in the 1960s. With the introduction of new antidepressants in Inhibitors,research,lifescience,medical the 1980s and 1990s, these reports have increased in number. Patients on SSRIs have reported more problems than those taking TCA medications and other antidepressants. SSRIs may have a negative effect on one or all stages of sexual functioning, difficulty

with ejaculation or delayed orgasm, but delayed ejaculation or orgasm are the most commonly reported side effects [Baonm, 2006]. One of the obstacles that make it difficult to evaluate the prevalence of sexual dysfunction in relation to antidepressants is that patients who have Inhibitors,research,lifescience,medical psychiatric disorders are more likely to have sexual dysfunction due to the effect of their illness on their behaviour and relationships [Corretti et al. 2006]. In one study, the prevalence of sexual dysfunction CI994 in vitro in relation to antidepressant use (SSRIs and others) in England and France was estimated at 39% and 27%, respectively [Williams et al. 2006]. Some other research has shown that up to 60% of patients who use SSRIs have sexual problems [Zajecka et al. 1997]. Since many patients discontinue SSRIs due to their impact on sexual function, developing strategies to predict who may be at highest risk of adverse changes in their wellbeing is an important step in improving the quality of life and treatment of patients who require antidepressant therapy.

Dextran (Dex), polysialic acid (PSA), hyaluronic acid (HA), chitosan (CH), and heparin are the most used natural polysaccharides. Synthetic polymers

include polyvinyl pyrrolidone (PVP), polyvinyl alcohol (PVA), polyacrylamide (Pam), poly(ethylene glycol) (PEG), and PEG-based copolymers such as poloxamers, poloxamines, and polysorbates. 2.2.1. PEG Poly(ethylene glycol) (PEG) is the polymer of choice to produce stealth nanocarriers. This neutral, flexible, and hydrophilic material Inhibitors,research,lifescience,medical can in fact properly produce surface barrier layers that reduce the adhesion of opsonins present in the blood serum on the nanoparticles making them “DAPT secretase DAPT Inhibitor invisible” to phagocytic cells. The protein repulsion operated by PEG was also visualized by freeze-fracture transmission

electron microscopy (TEM) [29]. A few physical protocols have been adopted to coat nanoparticle with PEG [22], even though these procedures entail the risk of polymer desorption in the blood with Inhibitors,research,lifescience,medical consequent loss of the beneficial contribution of the polymer [30]. In order to overcome this problem, covalent PEG conjugation protocols have been developed [31, 32]. Biodegradable nanoparticles with PEG covalently bound to the surface have been produced using PEG derivatives of poly(lactic Inhibitors,research,lifescience,medical acid), poly(lactic acid-co-glycolic acid) [33], or poly(alkylcyanoacrylates) [34]. The nanoparticles are prepared by emulsion, precipitation, or dispersion protocols in aqueous media. These procedures allow for the PEG orientation toward Inhibitors,research,lifescience,medical the water phase, while the biodegradable hydrophobic polymer fraction is physically entangled in the inner nanoparticle matrix [22]. Alternatively, PEG chains may be covalently conjugated to preformed nanoparticles through surface functional groups [35, 36]. 2.2.2. Poloxamine and Poloxamer Poloxamines (Tetronics) Inhibitors,research,lifescience,medical and poloxamers (Pluronics) are amphiphilic block copolymers consisting of hydrophilic blocks of ethylene

oxide (EO) and hydrophobic blocks of propylene oxide (PO) monomer units. Cilengitide Poloxamers are a-b-a type triblock copolymers (PEO-PPO-PEO) while poloxamines are tetrablock copolymers of PEO-PPO connected through ethylenediamine bridges [(PEO-PPO)2–N–CH2–CH2–N–(PPO-PEO)2] [37–39]. These polymers can be physically adsorbed on the nanocarrier surface through the hydrophobic PPO fraction [22]. Following intravenous injection to mice and rats, poloxamer- or poloxamine-coated sub-200nm poly(phosphazene) [40], PLGA nanoparticles [41], and liposomes [42, 43] did not show prolonged circulation time as compared to the uncoated counterparts. This unexpected behaviour was ascribed to the desorption of the polymers from the nanocarrier surface [30] as well as to the polymer capacity to adsorb opsonins [44].

The patient convalesced and began ambulating with use of a walker. He regained some element of sphincter control. At the 1-year follow-up office visit, he was ambulating well with the assistance of a walker. Discussion The cause of FAS has been attributed to infection, thrombophlebitis, and spinal AVM or AVF (Matsuo et al. 2008). Scattered reports Inhibitors,research,lifescience,medical of venous infarction of the spinal cord have been associated with decompression sickness, gliosarcoma, orchiectomy, pulmonary emboli, furunculosis,

leukemia, polycythemia, and thrombosis of leg veins (Srigley et al. 1981; Clarke and Cumming 1987; Niino et al. 1999). In classic FAS, venous drainage of the AVF is to the coronal venous plexus lying posterolaterally over the Inhibitors,research,lifescience,medical cord’s surface (Renowden and Molyneux 1993). Elevation of venous pressure occurs; the absence of valves promotes transmission of high pressure to the radial intramedullary vein and cord parenchyma, causing myelopathy. From a pathophysiologic perspective, VCM represents irreversibly progressive disease due to damage of the spinal cord molecular weight calculator parenchyma caused by venous congestion. Unlike

cases of hemorrhagic or embolic spinal venous infarction, which typically present with symptoms of sudden onset Inhibitors,research,lifescience,medical of low back pain and progress rapidly, VCM carries more insidious onset and protracted course. Although patients uniformly present with paraparesis or sensory disturbance, the pattern of distribution and progression of VCM can be heterogeneous,

often precluding prompt diagnosis. Inhibitors,research,lifescience,medical Imaging characteristics compound the diagnostic evasiveness of VCM. Typified by an intramedullary lesion with high signal intensity on T2-weighted imaging, flow voids of tortuous vessels can be seen on the dorsal surface of the spinal cord. The increased T2 signal reflects increased water content of necrotic tissue and the proliferated vessels Inhibitors,research,lifescience,medical in VCM. MR imaging can also show mass effect with cord swelling, iso- or hypointense T1 signal changes and parenchymal enhancement with contrast, making it difficult to distinguish VCM from spinal infarction, transverse myelitis, multiple sclerosis (Scolding 2001), Dacomitinib or intramedullary tumor (Rodriguez et al. 2005). Not uncommonly, MR findings of VCM with spinal cord enlargement/enhancement are so suggestive of tumor that they prompt biopsy (Rodriguez et al. 2005), as in this case (biopsy obtained at an outside hospital was negative). It is not inconceivable that a vascular malformation undergoes spontaneous thrombosis (Renowden and Molyneux 1993). Although myelography can demonstrate dilated tortuous coronal venous plexus as serpentine filling defects, in reported cases of spontaneous thrombosis, the cause of abnormal veins visualized by myelography cannot be demonstrated by angiography (Wrobel et al. 1988; Renowden and Molyneux 1993).

White-matter anomalies in the anatomical connections relevant to language and/or myelination of these connections could be involved. The ability to have specific MRI predictors of who will develop schizophrenia among those at high risk appears hopeful for the near future. Having the ability to predict, the development, of illness will then lead to studies to determine whether early pharmacological treatment, will prevent, the cortical progressive brain cortical change and, in doing so, have a significant effect, on clinical outcome. Notes This work was supported

by R21 MH071720-01 from Inhibitors,research,lifescience,medical the National Institute of Mental Health. The co-authors wish to thank the following investigators from the Center for Advanced Brain Imaging at the Nathan S. Kline Institute for assistance in developing and implementing the new MRI protocol as well as image analysis for preliminary pilot data shown here: Babak Ardekani, Inhibitors,research,lifescience,medical Craig Branch, Matthew Hoptman, and Raj Sangoi.
Interest in the subjective well-being (SW) of psychiatric Axitinib patients has significantly increased over recent years. While, for a long time, symptom reduction alone was the most essential outcome parameter, more detailed success criteria are now being implemented, approximately 50 years after the introduction of neuroleptic treatment.

Inhibitors,research,lifescience,medical Considering the extensive use of typical neuroleptics over the last decades, surprisingly little evaluation of patients’ subjective complaints while being medicated has been performed.1-6 In terms of Inhibitors,research,lifescience,medical tolerability, investigators focused on motor symptoms when looking at drug-induced complaints and reasons for noncompliance. With Inhibitors,research,lifescience,medical the development of atypical

antipsychotics, treatment goals became more ambitious, the patient’s perspective was considered more, and complaints such as affective blunting and cognitive slowing, as well as volition and loss of spontaneity, received greater interest.7-12 These emotional restrictions have been described as “neuroleptic dysphoria,” “pharmacogenetic depression,” “akinetic depression,” “neuroleptic depression,” and “neuroleptic-induced anhedonia.” 13 The increased Dacomitinib interest in subjective well-being was not only due to a conceptual shift in therapeutic outcome criteria: Studies on subjective well-being disproved the former belief that schizophrenic patients are not able to reliably assess their SW. The majority of schizophrenic patients, if not acutely psychotic or suffering from severe cognitive impairment, are able to complete selfrating scales in a consistent and reliable manner.14-17 The impact of antipsychotic drugs on SW, together with the quality of the doctor-patient relationship, is one of the two agreed major determinants for medication compliance.

If the range of CCT was wider in group 1, this result might not have been obtained. In addition, the inclusion of glaucoma selleck chem patients may confound the association between IOP measurements and CCT because in these participants, IOP may be altered as a result of the disease process. With respect to the results of the multiple regression

analysis, CRF was related to the measured IOP; this is consistent with the results of a study by Hager et al.20 The present study has some limitations, which must be addressed. There was no independent reference method to assess true IOP to allow us to conclude which method of IOP Inhibitors,research,lifescience,medical evaluation was more representative of the true IOP status. To answer this issue, experimental studies involving concomitant manometric and tonometric Inhibitors,research,lifescience,medical readings are necessary. Our study also suffers from a limited number of patients. However, this seems to be the first study of its kind, and the rarity of aphakic glaucoma with a thick cornea should be taken into account. Conclusion We believe that, in patients with aphakic glaucoma and a thick cornea, the TXL IOP measurements are

closer to the GAT measurements compared to the ORA. Additionally, relying on the result of the ORA, which is proposed to be independent of corneal biomechanical Inhibitors,research,lifescience,medical characteristics, may be misleading in this group of patients. Corneal biomechanical properties seem to be changed in this subgroup of patients, which can be determined by CRF. The results of our preliminary study need to be supported with larger studies detecting the biomechanical Inhibitors,research,lifescience,medical properties of the cornea and agreement between various tonometers in this group of patients. We still are in need of a tonometer to measure IOP independent of the corneal factor, because IOP measurement errors Inhibitors,research,lifescience,medical induced by corneal properties can

lead to substantial misclassification and possible mismanagement of patients. Acknowledgment This study was a thesis for a medical degree and was supported financially by Shiraz University of Medical Sciences. Conflict of Interest: None declared.
Dear Editor, Methamphetamine is a potent neurotoxin which can cause dopaminergic degeneration.1 In emergency department settings of hospitals, common Brefeldin_A presenting symptoms relating to Methamphetamine intoxication include chest pain, hypertension, shortness of breath, and tachycardia.2 In Iran, Methamphetamine intoxication has recently emerged as a crucial health problem in clinical and therapeutic settings. For example, in a study on 2,325 admitted amphetamine and opioid-intoxicated patients in Aliasghar Hospital in Isfahan, 542 (23.3%) patients reported using amphetamines, while the remaining patients reported co-administration of opioids and amphetamines.3 In a study on the prevalence and complications of drug-induced seizures in Baharloo Hospital in Tehran, the capital city of Iran, 143 patients were examined.