155 Since there was no benefit at 2 to 3 years, these results for donepezil are consistent with a symptomatic effect that lasts for up to 18 months. A similar 2-year trial of galantamine in MCI failed to show

a benefit on the primary end points, but there was some benefit on a secondary cognitive measure.156 Results of a 3- to 4-year conversion trial of rivastigmine have not as yet been reported, but a similar 4-year trial of the anti-inflammatory drug rofecoxib failed to show any clinical efficacy157 Despite the mixed and generally disappointing results of these initial MCI clinical trials, an important general finding is that Inhibitors,research,lifescience,medical when the patients progressed to Regorafenib dementia over the course of the trial, the specific diagnosis was almost always AD. This result provides some validation for the Inhibitors,research,lifescience,medical operational criteria used to select cases with “amnestic/AD type” MCI. Conclusion The concept of MCI in the elderly has evolved over the past 40 years to the point where study of MCI is at the cutting edge of research on the early pathology, early diagnosis, Inhibitors,research,lifescience,medical and early treatment of AD. The broad syndrome of MCI, defined clinically as a state of mild impairment that is intermediate between the decline associated with brain

aging and the clear deficits that occur in dementia, is clearly heterogeneous with respect to outcome and underlying etiology. However, it is apparent that the major MCI subgroup consists of individuals destined to progress to a diagnosis Inhibitors,research,lifescience,medical of AD. As reviewed above, this conclusion is supported by growing number of cross-sectional and longitudinal studies, as well as by studies examining postmortem neuropathology and in vivo neuroimaging and biomarker

correlates of AD. Furthermore, Inhibitors,research,lifescience,medical since it is feasible clinically to operationalize the identification “amnestic” MCI cases who are likely to have very early AD, such individuals have become an important research group for inclusion in clinical trials designed to examine agents that may slow the progression of AD. Although clearly valuable as a research tool, it may be debated whether physicians in clinical practice should consider a diagnosis of MCI for individual patients. Because MCI is a heterogeneous entity comprising a variety of neuropathological and psychiatric disorders, and because dementia is not an inevitable outcome, the over term may carry too little prognostic and diagnostic weight to legitimize its widespread use on a case-by-case basis. Furthermore, the lack of universally agreed upon criteria and the public’s unfamiliarity with the concept could result in increasing uncertainty, anxiety, and misunderstanding. Rather than invoking MCI, patients might be better served if their physicians simply conveyed an opinion regarding the most likely underlying pathological mechanism.

The question was posed: if the adult brain has pockets of stem cells that

can become neurons, astroglial cells (which play a crucial role in generating and maintaining the health of neurons), and oligodendrocytes (a third type of cell in the brain that insulates the neuronal axons so that they can Bleomycin molecular weight transmit their information efficiently), then why can’t the brain repair itself after Inhibitors,research,lifescience,medical injury or disease? The answer seemed to be that the brain is capable of repairing itself and that it already does, to a limited extent. The current strategy is, therefore, to try to understand how, and perhaps to what end, adult neurogenesis normally occurs, in order to find ways whereby we can enhance it, direct it, and more generally harness the residual elements of neural plasticity that are inherent to neural self-repair as a treatment for brain disorders. Surprisingly, we may not be too far Inhibitors,research,lifescience,medical away from this goal. Let’s first summarize what we know about the process of adult neurogenesis. What is adult neurogenesis/cell genesis? As it turns out, the birth of new brain cells or neurogenesis Inhibitors,research,lifescience,medical is not an all-or-nothing

event. The multipotent stem cell divides periodically in the brain, giving rise to another stem cell (self-renewal) and some progeny that may grow up to be working cells, but the fate is not guaranteed. The progeny must move away from the influence of the mother stem cell into an area that is permissive for maturation. On average, about 50% of these newborn cells never make it and instead die and disappear. Those that do survive may become a neuron or glial cell, depending on where they end up and what type of activity is going on in that brain area at that time. Even so, it takes over a month from the time the new cell is born until it Inhibitors,research,lifescience,medical is functionally integrated in the brain, receiving and sending information. Thus, neurogenesis is a process, not an event, and one that – as I said earlier and will emphasize repeatedly – is highly regulated. The factors that regulate

neurogenesis are being intensely investigated and new factors that modulate different components of Inhibitors,research,lifescience,medical neurogenesis are being discovered on a regular basis. For example, factors known to be important in development of the nervous system, like Sonic hedgehog11 (which was first discovered in fly brain and called hedgehog), mafosfamide have been shown to regulate the proliferation; BMPs (bone morphogenetic proteins) and Notch12 (which were also first discovered in fly brain) appear to be regulators of whether the newborn cells decide to become glia; and molecules associated with the glial cells that surround the stem cells instruct the newborn cells to become neurons. Once the cells are committed to becoming a neuron or glial cell, other growth factors like brain-derived neurotrophic factor (BDNF)13 and insulin-like growth factor (IGF)14play important roles in keeping the cells alive and encouraging the young cells to mature and become functional.

Greater depression severity at baseline generally predicts a poorer response to pharmacotherapy35 and/or psychotherapy.36 Duration of the index episode and the number of prior episodes are the strongest baseline predictors of the subsequent well interval.35,37-41 The presence of Axis I comorbidity, both at the syndromal and the subsyndromal level, impedes the achievement of full remission. Panic or anxiety symptoms or disorder are particularly pernicious in

this respect.42-45 Axis II comorbidity has also been found by numerous investigators to be associated with incomplete remission of depression.35,46-48 Inhibitors,research,lifescience,medical To some extent, the association of both of these forms of comorbidity (Axis I and Axis II) with incomplete remission may represent an artifactual inflation of depression rating scale scores via the presence of symptoms associated with the Axis I or Axis II condition. However, there also are well-articulated descriptions of how, for example, anxiety disorders or subsyndromal anxiety conditions and Axis II conditions might interfere with obtaining the full Inhibitors,research,lifescience,medical benefit from a treatment Inhibitors,research,lifescience,medical such as CT or IPT49 More recently, Katon and colleagues50,51 have focused on the extent to which

medical comorbidities, such as diabetes (Axis III conditions), may interfere with remission of depression. Again, some of this may be artifact caused by inflation of depression scores or by somatic symptoms associated with a comorbid medical condition. On the other hand, there are specific hypothesized routes through which medical comorbidity might interfere with either pharmacotherapy or psychotherapy. Somatic preoccupation may preclude the individual’s ability to focus on the specific work involved in the psychotherapy, whereas the medical condition or the pharmacological treatment Inhibitors,research,lifescience,medical of the medical condition may interfere with the metabolism of antidepressant pharmacotherapy. Finally, failure to adhere to the requirements of either a pharmacotherapeutic or a psychotherapeutic regimen can

certainly interfere with the achievement of full remission of symptoms. Psychotherapy and pharmacotherapy combinations Inhibitors,research,lifescience,medical and sequences also have a clear Thiamine-diphosphate kinase role in the prevention of recurrence, another key goal of treatment of unipolar disorders. Since we now recognize that the majority of unipolar depressions are recurrent, perhaps the most challenging part of depression treatment is that which find more focuses on the prevention of relapse and recurrence. As we describe below, it is here that pharmacotherapy-psychotherapy combinations and sequences have shown themselves to be particularly valuable approaches to treatment. Combination acute treatment: achieving remission and return of function As noted above, efforts to achieve full remission and return of function have encompassed the evaluation of combination therapy in comparison with either pharmacotherapy or psychotherapy monotherapy as well as treatment sequences.

The single positive correlation was found between the anterior thalamic radiation, which connects the anterior and dorsomedial thalamic nuclei with the prefrontal cortex, and

BOLD activity throughout the amygdala, prefrontal cortex, and parahippocampal gyrus. Involvement of the amygdala is particularly interesting because it receives direct input from the olfactory bulb, which presumably would be a primary sensory substrate for the alcohol taste cue. Frank and Claus (2006) put forward a model of striato-orbitofrontal interaction in which the orbitofrontal cortex receives input from the amygdala about reinforcement value of outcomes associated with sensory cues. The orbitofrontal cortex, which in turn projects Inhibitors,research,lifescience,medical to the basal ganglia, encodes and maintains in working memory information about reward to enable adaptive, differential Inhibitors,research,lifescience,medical responding (Frank and Claus 2006). The positive correlation invites speculation that repeated experiences with alcohol selectively strengthens the influence of subcortical outputs to prefrontal cortex and limbic structures through enhanced white matter connectivity, possibly increasing the relative influence of subcortical

pathways over subsequent reward-seeking behavior. Again, given that the anterior thalamic radiation is a bidirectional tract, the direction and order of effects remain unknown. Although white matter damage has Inhibitors,research,lifescience,medical been established as a hallmark injury of AUD, causal mechanisms are still under investigation. In animal Inhibitors,research,lifescience,medical models of alcohol dependence, the presence of alcohol in the brain triggers stimulation of proinflammatory

cascades leading to cell death or dysfunction and inhibition of neurogenesis in adult neural stem cells in the olfactory bulb and hippocampus (Crews and Nixon 2009). Pinpointing mechanisms of alcohol-induced brain damage in vivo in humans presents a challenge, but our findings support the notion that Inhibitors,research,lifescience,medical long-term heavy Selleck VE-822 drinking contributes to decreased white matter integrity. Alcohol-related white matter damage is likely to be one constituent of the AUD cycle in which heavy drinking contributes to impaired cognition and emotion regulation, leading to further problematic drinking (Crews 1999). A potential clinical implication is that those with long-standing AUD, and therefore greater damage all to white matter substrates, may have more difficulty applying cognitive or emotional-regulation strategies in the context of AUD intervention. A strength of this study is its use of multimodal imaging methods to explore functional correlates of white matter integrity in problem drinking. Further strengths are the size of the sample and the variability in participants’ drinking histories. A major limitation is the inherent inability of cross-sectional design to establish causal relations between white matter profiles and cue reactivity. Whether greater cue reactivity preceded or followed heavy drinking remains a topic for further investigation.

The minimum concentration of menthol to evoke cold sensation (CS) at the menthol application site was determined as the cold sensation detection threshold (CDT). The conventional clinical grading system was used to assess the severity of neurotoxicity in relation to CDT. Patients also completed self-report ratings of their sensitivity to cold sensation, and the results of these objective and subjective findings were compared. Materials and Methods Subjects and treatment regimen A total of 76 subjects were enrolled Inhibitors,research,lifescience,medical in this study: 40 healthy subjects (24 women, 16 men; median age, 54 years; range, 22–85) and 36 patients (22 women, 14 men;

median age, 57 years; range, 33–80) with advanced-stage colorectal cancer who received standard oxaliplatin in combination

with infusional 5-fluorouracil/leucovorin (FOLFOX) as a first-line treatment. In the FOLFOX regimens, oxaliplatin (modified FOLFOX 6, 85 mg/m2) was given intravenously over 2 h on day 1 in conjunction with leucovorin (200 mg/m2) Inhibitors,research,lifescience,medical and followed by a 5-fluorouracil (5-FU) bolus injection Inhibitors,research,lifescience,medical (400 mg/m2), repeated every 2 weeks. A continuous 24-h infusion of 5-FU (600 mg/m2) was given over days 1 and 2. On day 2, leucovorin (200 mg/m2; over 2 h) and 5-FU bolus (400 mg/m2) were given intravenously. The subjects did not consume any spicy food 1 day prior to testing. They were also asked to refrain from eating, drinking, chewing gum, brushing their teeth, and using mouthwash for 2 h before testing, and we verified

that the participants had observed these restrictions at the beginning Inhibitors,research,lifescience,medical of each session. The present study was conducted in accordance with the Declaration of Helsinki for the care for human studies adopted by the Ethics Committee of Higashi-Asahikawa Hospital. All patients provided written informed consent. Assessment of menthol in experiments 1 and 2 A solution of 5% L-menthol (from dry crystals; MERCK, Tokyo, Japan) was Inhibitors,research,lifescience,medical prepared in warm distilled water (41°C) at the time of application, and this solution was further diluted in warm distilled water to yield menthol solutions of 0.005%, 0.01%, 0.05%, 0.1%, 0.5%, and 1% (0.32 mM, 0.64 mM, 3.2 mM, 6.4 mM, 32 mM, and 64 mM, respectively). These solutions were topically applied with a cotton swab to the dorsal anterior tongue in two experiments (Fig. 1a). In experiment 1, the six different menthol solutions were administered to healthy subjects and patients with colon cancer prior to oxaliplatin exposure, and their subjective ratings of cold sensitivity were recorded. In experiment through 2, patients were selleck inhibitor examined for alterations in the menthol-induced cold sensations before and 5–6 h after the patients receiving individual oxaliplatin infusions. The menthol concentrations used in this study were based on a previous human study (Albin et al. 2008). The vehicle control (warmed distilled water) was applied in the same manner. Figure 1 Effects of menthol on cold sensation and the detection threshold in healthy human subjects.

Persistent PFO occurs in around 20-25% of the adult population.1) PFO has been known to be the cause of transient ischemic attacks (TIA) or stroke. Meta-analyses and observational check details studies indicate that the prevalence of PFO is approximately 3-fold higher in patients with cryptogenic stroke and migraine compared to controls. Conversely, observational evidences indicate a 2-3-fold increased prevalence of migraine and cerebrovascular events in PFO carriers.2) Transcatheter device closure Inhibitors,research,lifescience,medical has been the treatment of choice for these defects. The persistent left superior vena cava (LSVC) is the most common abnormality

of systemic venous return. It has been observed in 0.5% of the general population and in up to 10% of patients with congenital heart disease.3),4) This anomaly is due to an abnormal development of the sinus venosus in the early stages of fetal life. In 92% of cases, drainage occurs in the right atrium; in the remainder of cases, drainage occurs in the left atrium (LA), either directly or through Inhibitors,research,lifescience,medical an unroofed Inhibitors,research,lifescience,medical coronary sinus.5) Combined defect of abnormal drainage of LSVC to left superior pulmonary vein (LSPV) in PFO patients is uncommon, and we report simultaneous device closure

of LSVC with Amplatzer® Vascular Plug II (St. Jude Medical, St. Paul, MN, USA). Case A 37-year-old female patient with chief Inhibitors,research,lifescience,medical complaint of left arm weakness (duration less than 1 minute) and left-sided lip twitching was diagnosed with PFO under evaluation at Myongji Hospital. Laboratory

test results showed normal value of erythrocyte sedimentation rate, C-reactive protein, no abnormality of coagulopathy, and no suspicious sign of vasculitis. While continuation of warfarin treatment Inhibitors,research,lifescience,medical and medication in regards of rhematoid arthritis diagnosed in 2007, she was referred to Pediatrics Cardiology for PFO closure. Brain magnetic resonance imaging showed signs of stroke and transcatheter closure of PFO was scheduled. Contrast echocardiography performed via the left upper extremity prior to the procedure showed sequential filling of the bubble in the LA followed by left ventricle and then through the PFO to the right all atrium (Fig. 1). For further evaluation, heart computed tomography (CT) was performed and an abnormal connection of LSVC to LSPV which drained into LA was diagnosed (Fig. 2). Fig. 1 Agitation saline injection test. On contrast echo conducted on Rt. arm, the enhancement was seen at not only Rt. side of heart, but also Lt. side. Sequential filling of the bubble in the left atrium followed by left ventricle and then through the patent … Fig. 2 Abnormal Drainage of LSVC to LUPV are shown on three dimensional computed tomography. LSVC: left superior vena cava, LUPV: left upper pulmonary vein, RSVC: right superior vena cava.

When the protocol was written, a hospital chart Bcl-2 inhibitor review to estimate possible participants for the study was conducted. The initial chart review suggested that approximately 20% of the clinical patient population were possible participants. In this chart review, we were unable to estimate patients’ attitude towards study drugs. When inclusion was initiated, the main barrier to inclusion was either patients’ or clinicians’ concern for metabolic Inhibitors,research,lifescience,medical side effects of olanzapine [Citrome et al. 2011]. Many of the screened patients had been offered treatment with olanzapine previously, but had refused due to concerns about side effects. Sertindole had been withdrawn due to concerns

about increased cardiac mortality and had been reintroduced shortly before initiation of the current study [Peuskens et al. 2008]. Despite the early concern of cardiac mortality, most patients and clinicians were positive towards potential treatment Inhibitors,research,lifescience,medical with sertindole. Gallhofer and colleagues compared sertindole with haloperidol in a 12-week study with

reaction time Inhibitors,research,lifescience,medical decomposition and Wisconsin Card Sorting Test (WCST) as outcome measures. Participants treated with sertindole did significantly better in all subtests of the reaction time decomposition test than participants treated with haloperidol. A similar pattern was seen in the WCST, except for the non perseverative errors, for which sertindole and haloperidol Inhibitors,research,lifescience,medical did not differ at study end point in this study of 34 participants [Gallhofer et al. 2007]. Nielsen and colleagues compared adjunctive treatment with sertindole or placebo with an original treatment with clozapine and did not show any difference in cognitive outcomes between the groups [Nielsen et al. 2012]. More than 25 randomized trials on patients diagnosed with schizophrenia have been conducted comparing olanzapine with other antipsychotic drugs with most studies being against atypical antipsychotic drugs only. Some studies investigated the effects Inhibitors,research,lifescience,medical of olanzapine compared with typical antipsychotic drugs only, and other studies had

both typical and atypical drugs as comparator drugs. No uniform patterns of change in cognitive function in specific domains were found in patients treated with olanzapine. Due to a low inclusion rate, the number of participants proposed by power calculation was not reached (N = L-NAME HCl 100). Our study did not show any of the comparator drugs being superior on cognitive outcomes or PANSS. The low inclusion rate increased the risk of type II error, but a simple sign test did not shown any of the comparator drugs trending towards being superior on the majority of tests. Our study did not evaluate previous educational level or job training, which could have influenced the participants’ ability to perform the cognitive tests.

Overall, most studies demonstrate a slow progression of cognitive symptoms in ALS relative to motor decline and show that these cognitive deficits are present early in the course of the disease. Overlapping between ALS and FTD Although ALS #CDK inhibitor randurls[1|1|,|CHEM1|]# and FTD are two different entities, it is now clear that these disorders are neurodegenerative conditions with overlapping clinical and neuropathological features. The overlap is further confirmed by the presence of the ubiquitinated Tar DNA binding protein (TDP-43) inclusions both in FTD patients without Inhibitors,research,lifescience,medical tau pathology, as well as in sporadic and familial case of ALS (Neumann et al. 2006; Kwong et al. 2007). Moreover, as will

be described in the next section, ALS patients show an impairment of cerebral regions beyond the motor system, including Inhibitors,research,lifescience,medical cortical areas typically involved in FTD and a proportion of ALS patients displays cognitive and behavioral changes that in some instance

reach criteria for FTD Strong and Rosenfeld 2003; (Irwin et al. 2007). Strong et al. (2006) found a pattern of mental change that was indistinguishable from that of FTD in a group of patients with dementia and ALS. In a large study involving 279 ALS patients, 50% manifest cognitive impairment and 15% met criteria for FTD (Ringholz et al. 2005). Murphy et al. (2007) found a spectrum Inhibitors,research,lifescience,medical of frontal lobe dysfunction in half of the patients, with five Inhibitors,research,lifescience,medical of them (22%) meeting neary criteria for FTD. These studies support the hypothesis of a clinical continuum between ALS and FTD, according to which FTD is an integral component of ALS and can be expected in any ALS patients. The timescale of onset and the pattern of the cognitive symptoms in FTD/ALS are not clear, but reports Inhibitors,research,lifescience,medical have suggested that FTD reflects one end of the disease continuum. However, this argument is difficult

to support when considering that some studies have found no meaningful progression of cognitive deficits over time. If cognitive deficit exists, these could affect an assessment in these patients; in general, there is always cognition CYTH4 needed as prerequisite to test cognition. More, BCI could also have problems when deficits exists. To overcome this circularity could be more effective to use a P300 BCI system. The good thing about P300 BCI is that the response itself does not need major load of cognition to perform a P300 ERP (P300 is used in unconscious patients as well and an oddball paradigm should nevertheless work). So if the production of the signal does not need any cognitive load than testing with cognition with BCI is just the same as testing cognition with paper and pencil which is a standardized procedure. The use of BCI in ALS patients with cognitive impairment has already been studied (Iversen et al. 2008a; Perego et al. 2011).

Our results also confirm the previous finding that verbal material that is self-generated is more

accurately remembered than material that is passively read whether it is in health or disease states (Slamecka and Graf 1978; Schefft et al. 2008b). However, in the specific case of paired associates, this self-generation effect differed depending on the linguistic relationship between the word pair. Generated words were significantly Inhibitors,research,lifescience,medical better remembered than read words in the synonym and opposite relationships, and somewhat in the category and association relationships while no recognition difference existed between read and generated words in the rhyme condition. Together, this provides support for Inhibitors,research,lifescience,medical our hypothesis that the choice of linguistic relationship has implications for memory. As discussed above, several theories were proposed to explain the memory improvement associated

with self-generation. This pattern can be attributed to the active participation that the individual is taking in achieving a task (Schefft et al. 2008b). The active learning process leads to improved Inhibitors,research,lifescience,medical mood state and self-esteem, and greater generalization of new knowledge (Schefft and Biederman 1990; Basso et al. 1994; Walsh et al. 1995). McDaniel et al. (1988) posited that self-generation improves memory because there is a heightened particularity in the items that need to be remembered. Another theory hypothesized that memory of 17-AAG chemical structure information is enhanced when people feel self-empowered by generating that information on their own (Olofsson and Nilsson 1992;

Walsh et al. 1995). In addition, generating a word with deleted letters presents an interruption of automatic reading Inhibitors,research,lifescience,medical processes, requiring an additional amount of conscious processing (McDaniel et al. 1989) leading to better recall. Furthermore, it has also been suggested that increased memory Inhibitors,research,lifescience,medical by way of self-generation is attributed to the depth of processing of the semantic information, rather than structural or phonological information (Craik and Tulving 1975; Craik 2002; Lespinet-Najib et al. 2004). The different effects found on recognition memory for each linguistic relationship support Olopatadine the notion that deeper semantic processing enhances memory performance (Craik and Tulving 1975; Craik 2002; Lespinet-Najib et al. 2004); and semantic and phonological relationships among words are processed by separate memory mechanisms (Martin et al. 1999), or at least require different cognitive resources (Menenti et al. 2012). Rhyming word pairs employs phonetic knowledge to self-generate a missing word according to how the words sound, while generating other types of related word pairs, such as categories, synonyms, opposites, and associations, employs semantic knowledge of what the word actually means (Craik and Tulving 1975; Martin et al. 1999; Kircher et al. 2011).

Patients’ files were retrospectively reviewed and data were recorded. Characteristics of patients, who were not operated due to any reason and treated with CRT alone or CT following CRT, were assessed. Patients with stage II and III rectal cancer, according to American Joint Committee on Cancer’s (AJCC) Cancer Staging 6th edition 2002 TNM staging system (21) were included in the study. Accordingly, T3-4N0/N+ was considered locally advanced and, T3-4N0 was considered of stage II, as N+ was stage III. Preoperative evaluations were performed by thoracic,

lower, and upper abdominal computerized tomography (CT), lower abdominal (pelvic) Inhibitors,research,lifescience,medical magnetic resonance imaging (MRI), and endorectal ultrasound (US) studies in all patients. Absence of distant metastasis was

confirmed by thoracic, upper, and lower abdominal CT and/or positron emission tomography-computerized tomography (PET-CT). The patients receiving CRT were administered RT in 1.8 Gy/fraction/day dosage for Inhibitors,research,lifescience,medical 25 fractions, a total of 45 Gy and in addition they were given 5-fluorourasil (5-FU) 225 mg/m2/day as continuous infusion. The dosage of oxaliplatin was 50 mg/m2/day in cases who received oxaliptalin in addition to RT and 5-FU Inhibitors,research,lifescience,medical in CRT protocol. Capecitabine was administered with a dosage of 1,000 mg/m2 every day in cases who received capecitabine instead of 5-FU in CRT protocol. Following CRT, capecitabine Inhibitors,research,lifescience,medical was administered as monotherapy with a dosage of 2,500 mg/m2/d for 14 days followed by a 7 day rest. Following CRT, CT was administered in a modified FOLFOX6

regimen was given once in 14 days, including folinic acid 400 mg/m2 + 5-FU 400 mg/m2 bolus + 5-FU 2,400 mg/m2 46 hours of infusion + oxaliplatin 85 mg/m2. Time from diagnosis to progression was defined as progression free survival (PFS) and time from diagnosis to death was defined as overall survival (OS). The statistical analyses of the data were performed by Statistical Package for Social Sciences for Windows (SPSS) Version 15.0 Inhibitors,research,lifescience,medical click here software; and Kaplan-Meier Method was used for PFS and OS analyses. Results The retrospective click here analyses of 263 patients with rectal cancer were performed. 86 patients (32.6%) with stage II and 177 patients (67.4%) with stage III rectal cancer had a median age of 59 [18-85] years. The patient characteristics are presented in Table 1. Table 1 General characteristics of all patients with locally advanced stage rectal cancer Among those, 14 patients (5.3%) were determined who could not undergo surgery due to any reason, but received CRT or CT following CRT. 4 of them were women (28.6%) and 10 were men (71.4%) and the median age was 72 [42-87] years. All of these 14 patients had CRT, and additional CT was received by 2 (14.3%) patients.