Currently, lithium, valproate, carbamazepine, chlorpromazine, haloperidol, risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole are indicated for the treatment of acute mania in the majority of European countries and North America, with some minor variations from country to country, and lithium, valproate, lamotrigine, olanzapine, aripiprazole, and quetiapine are indicated for maintenance treatment, Inhibitors,research,lifescience,medical again depending on the country. However, the gap between evidence base and clinical practice is still huge, and the majority of patients have to be treated with combinations of several drugs and psychosocial interventions Inhibitors,research,lifescience,medical in order to achieve

a. reasonable outcome from the clinical as well as functional point, of view. This may be particularly true for patients with rapid-cycling bipolar disorder, who may need complex combinations of therapies and sometimes physical treatments such as electroconvulsive therapy to achieve clinical stability. For these patients, as well as for those with

mixed states, for those with enduring subsyndromal symptoms, and ultimately Inhibitors,research,lifescience,medical for the majority of people with bipolar disorder, more efficacious, tolerable treatments are badly needed.
Bipolar affective disorder, type I (BP-I) is a severe mental illness marked by periodic extremes of mood state (manias), as well as (in most cases) episodes of depression and (in many cases) psychosis. The consequences of BP-I are severe, and involve both direct, and indirect, issues. Rates of suicide in BP-I patients are high,1,2 and =BP-I subjects also suffer from poorer quality of life and lower productivity than unaffected individuals.3 Inhibitors,research,lifescience,medical Annual public health costs Inhibitors,research,lifescience,medical (combined direct, and indirect) of BP have been estimated to be between 24 billion and 45 billion dollars.4,5 BP-I occurs in all populations that have been studied, with lifetime prevalence rates worldwide

of the order of one per every 100 individuals.6 Segregation analyses, why adoption studies, and twin studies have consistently shown that, regardless of the population studied, genetic factors play an important role in determining one’s risk of developing BP-I.7-9 Since little is known about the actual etiology of BP, it would be a major contribution to our understanding of the pathophysiology of BP if the genes responsible for the neurobiologie changes which underlie this disorder could be identified. The difficulty in SP600125 finding genetic loci that, are involved in BP most likely derives from the complex nature of the illness. When multiple transmission models for BP-I (the most, severe form of BP) have been tested, oligogenic epistatic models arc found to be the best fit, rather than models which purport one major locus.

The covariance matrix C results from multivariate statistics representing a central result of the experiments [32,56,57,58,59]. The observed covariance matrix C of metabolite concentrations is linked to the underlying biochemical system and the corresponding genotype by a systematic approach, which is characterized by the following equation [60]: (4) In this equation, J represents the Jacobian matrix and D is the fluctuation/diffusion matrix. The diagonal entries Dii characterize the magnitude of fluctuations of each metabolite, whereas off-diagonal entries

Dij (i≠j) represent Inhibitors,research,lifescience,medical the fluctuation of metabolites caused by the interaction between enzymes i and j. The interconnection between metabolic networks and the Jacobian Matrix as well as the fluctuation matrix is described in detail elsewhere [32,60,61]. In general, the Jacobian matrix characterizes the local dynamics at a steady state condition. In the context Inhibitors,research,lifescience,medical of metabolic networks, the entries of the Jacobian J represent the elasticities of reaction rates to any change of the metabolite concentrations being characterized by the following equation: (5) Here, N is the Inhibitors,research,lifescience,medical stoichiometric matrix, r represents the rates for each reaction and M is the

metabolite concentration. Based on equations (4) and (5), an approach of inverse calculation of a Jacobian from metabolomics covariance data was recently derived [59]. Additionally, the authors developed the differential Jacobian, dJij, defining the relative change of two Jacobians Ja and Jb which are associated with different treatments, i.e., environmental conditions: (6) Inhibitors,research,lifescience,medical Calculation of the differential Jacobian reveals perturbation sites between two different metabolic states hinting at a significant regulatory event, e.g., the change of enzymatic reaction rates due to environmental

perturbations. In principle, using this approach it is possible to conveniently connect a large metabolomics experiment with many samples and thousands of variables directly with the predicted genome-scale metabolic network to calculate biochemical regulation Inhibitors,research,lifescience,medical in the investigated biological system (for more detail see [32]). The approach relies on the assumption that regulation of metabolism buy PS-341 becomes observable in the significant 17-DMAG (Alvespimycin) HCl changes of the local dynamics around a steady state condition, e.g., rates of metabolite synthesis and degradation. Due to the redundancy of pathways and multiple isoforms of numerous enzymes, such calculations and predictions need to be confirmed and validated by further biochemical experiments. Limitations to this approach are currently the low quality knowledge of N and the low number of detected metabolites in measurements compared to the number of predicted metabolites in a metabolome, necessitating the simplification of N in accordance with the data matrix [32,59]. 4.

9 HISTORICAL DEFICIENCIES IN TEACHING COMMUNICATION SKILLS When I attended medical school over half a century ago there were no courses whatsoever on physician–patient communication. It is almost amusing to recall the only formal discussion that I remember from my student days. One of the senior attending physicians in the department of obstetrics and gynecology told us on rounds one morning that if the patient requests information about her disease the most useful

word to use is “condition”. “Just tell her”, he said, “that she has a ‘uterine condition’, without Inhibitors,research,lifescience,medical any further elaboration. That will satisfy 95% of the patients, and you will not have to supply any further details about her

diagnosis.” That was the sum of the teaching of Inhibitors,research,lifescience,medical communication skills that was provided to me and my Ruxolitinib manufacturer fellow students during 4 years of medical school! Nor were these defects remedied in any significant way during my residency training at outstanding academic institutions. But the lack of attention to communication skills has come to haunt the medical profession. Perhaps the research published Inhibitors,research,lifescience,medical in the late 1960s by Barbara Korsch and her colleagues,10–11 highlighting the gaps in doctor–patient communication, provided the scientific impetus for further research and then remediation of the situation. Recent articles continue to report serious shortcomings in communication skills.12 Even with outstanding formal teaching unless there is reinforcement during the clinical

years and good role models the gains of the teaching may deteriorate significantly under the stresses Inhibitors,research,lifescience,medical of work and the “hidden curriculum”. “PATHOPHYSIOLOGY” OF DEFICIENCIES IN PHYSICIAN–PATIENT COMMUNICATION One should examine first the “pathophysiology” of the problem in physician–patient Inhibitors,research,lifescience,medical communication in order to prescribe appropriate solutions. PRIORITIES OF TECHNOLOGY The advent of technological and sophisticated methods of diagnosis and treatment of disease has relegated the communicative interaction with the patient to a lower priority. A leading daily newspaper pointed out the following: “The CT and MRI scans, the 17-DMAG (Alvespimycin) HCl lasers and the laparoscopics, the chemo cocktails and DNA codes – all the advances that make modern medicine so effective (and expensive) have isolated physicians from the patient as a person. In the process, the ancient therapeutic art of listening is being ignored, much to the dismay of many physicians who recognize the limits of technology.”13 Going back to the invention of Laennec, who introduced the stethoscope to replace the direct placement of the physician’s ear on the patient’s chest, we have progressively decreased the direct contact of the physician with the patient.

0 g/dL (maximum of 3 L removed) and infused with a combination of albumin and crystalloid to restore isovolemia. Prospective randomized controlled studies demonstrate that it is safe and that ANH protected against allogeneic transfusions (22,28). As compared with standard volume management, Jarnagin et al. demonstrated that ANH resulted in fewer intraoperative transfusions (1.6% versus Inhibitors,research,lifescience,medical 10.4%, P=0.04). While interesting in concept, ANH is not routinely used in many centers at this time. We have not adopted

this strategy yet in our own practice. Blood loss-limiting surgical techniques Surgeons can take measures during hepatic parenchymal transection to further limit hemorrhage. These include temporary hepatic inflow occlusion (Pringle maneuver) and total vascular exclusion (TVE). These techniques are designed to isolate hepatic circulation (inflow and/or outflow) from the systemic circulation and minimize blood loss during dissection and Inhibitors,research,lifescience,medical transection of the hepatic parenchyma (Figure 1). A central Inhibitors,research,lifescience,medical tenet to the success of vascular exclusion is based on the BIBW2992 cell line premise that the liver (and

patient) is more tolerant to warm ischemia with reperfusion than to bleeding and the consequences of bleeding (e.g. transfusions.). Figure 1 Demonstration of potential sites of vascular occlusion. Pringle maneuver Originally performed for hepatic trauma, the Pringle maneuver is a straightforward way to minimizing blood loss during hepatectomy (47). A noncrushing clamp or a rumel tourniquet is placed around the structures in the porta hepatis to occlude

hepatic Inhibitors,research,lifescience,medical venous and arterial inflow during parenchymal transection. This can be performed in an intermittent or continuous manner with similar outcomes. It is recommended that the occlusion time be limited to an hour or less, as the ischemic insult will ultimately result in further hepatic parenchymal loss. After hepatic pedicle clamping with the Pringle, there is a 10% decrease in the cardiac index with a 40% increase in SVR and a 40% increase in mean arterial pressure (48-51). Inhibitors,research,lifescience,medical As compared with the previously mentioned occlusion techniques, the Pringle maneuver is relatively well-tolerated, but the anesthesiology staff should be continuously informed when it is applied because of the possibility of cardiac dysfunction and of air embolism, particularly if the hepatectomy is being done under low CVP. The potential sequela below of air emboli, in the patient with a low CVP who may have an open hepatic vein, can be minimized by placing the patient in 15 degree Trendelenberg (24,25,52). The Pringle maneuver can be applied in a continuous or intermittent fashion. Many retrospective studies and prospective clinical trials have been performed examining the role and type of the Pringle maneuver, and its relationship to blood loss and reperfusion injury. Belghiti et al.

2010). The underlying mechanisms for OL differentiation

are rather complex. Many cytokines, including members of IGF family, CNTF/LIF (leukemia inhibitory factor) family of cytokines, certain chemokines and neurotrophins, have been shown to enhance OL differentiation (Mayer et al. 1994; Heinrich et al. 1999; Hsieh et al. 2004; Xiao et al. 2009). Those extracellular ligands activate intracellular signaling pathways leading to transcriptional regulation of myelin proteins such as MBP, PLP, and CNPase (Wegner 2008; Emery 2010b). Although the current work did not explore much of the mechanisms underlying MCDM-enhanced OL differentiation, we speculate that IGF-1 may play such a role, as IGF-1 levels were more than sixfold higher in Inhibitors,research,lifescience,medical MCDM than in ACDM. Many studies have Inhibitors,research,lifescience,medical reported that Akt and Erk pathways are involved in OL differentiation (Pang et al. 2007; Guardiola-Diaz et al. 2012). However, in the current study neither pAkt nor pErk was detected in OLs upon MCDM exposure. Interestingly, CREB was weakly activated in OLs, suggesting a possible involvement of this signaling pathway in MCDM-enhanced OL differentiation. In Inhibitors,research,lifescience,medical fact, accumulating evidence suggests that CREB is a potential downstream pathway involved in OL differentiation (Paez et al. 2004; Shiga et al. 2005; Bhat et al. 2007). Whether activation of CREB pathway principally underlies MCDM-enhanced OL differentiation needs

to be addressed in future studies. Myelination is a relatively late developmental event of mammalian nervous system, which is fine VX-770 cost turned by a comprehensive transcription network (Bradl and Lassmann 2010). Neuron-derived factors, including neurotrophins and axonal surface molecules are known to play critical roles in initiating myelination (Xiao et al. 2009). As for glial cells, astrocytes have been Inhibitors,research,lifescience,medical implicated to affect myelination, presumably through secreted factors. However, most of the Inhibitors,research,lifescience,medical data regarding the role of astrocytes in myelination are observed from studies of multiple sclerosis, in which astrocytes

are often activated. Nevertheless, a few studies directly investigated the effect of astrocytes on myelination in cell cultures. For example, Ishibashi et al. (2006) reported that astrocytes could promote myelination in response to neuronal activity by releasing of LIF. Watkins et al. (2008) showed that the presence of astroctyes in myelinating cultures could increase the speed of myelin wrapping around axons, but was not others required for the initiation of myelination. The lack of myelin promoting effect of ACDM in the current study is not clear, but may be due to several factors. First, astrocytes were presented in the cocultures (Pang et al. 2012), and astrocyte-derived factors may contribute to the baseline level of myelination. Therefore, ACDM may no longer show additional effect. Second, the phenotypes of astrocytes seem to be important in determining whether astrocytes affect myelination positively or negatively (Nash et al.

Recent results from the same study group indicate, as above, that gray matter loss in the ACC seems on the contrary to be an acquired feature.65 Studies are needed to identify the timing and/or etiology of other hallmark neurobiological features of PTSD. Risk and resilience for developing PTSD Individuals exposed to an event that either threatens serious injury/death, or

is perceived as such, respond in different ways. Most will experience minimal (seconds) to brief (hours) to short-term (days/weeks) abnormalities while a smaller number will suffer from significant psychopathology over longer-term (months) and chronic (lifetime) Inhibitors,research,lifescience,medical time frames. In short, not all individuals who face potentially catastrophic trauma go on to Palbociclib ic50 develop PTSD. Why some individuals will develop PTSD following trauma, whereas others do not, is of paramount Inhibitors,research,lifescience,medical importance. Because the majority of trauma survivors do not go on to develop PTSD, it is crucial going forward to understand vulnerability and resiliency factors.

In this section, the role of genetic factors, gender differences, and early developmental stress experiences in moderating risk for developing PTSD in response to psychological trauma are discussed as is the increased risk for developing PTSD in the context of co-occurring physical traumas Inhibitors,research,lifescience,medical (including Inhibitors,research,lifescience,medical TBI). Genetic risk factors for PTSD Studies on the genetics of PTSD have been hampered by a variety of factors, such as genetic heterogeneity (similar phenotypes develop from different genotypes) and incomplete phenotypic penetrance (a person with genetic risk for PTSD, who is not exposed to trauma, will not develop PTSD). Despite these confounds, there is accumulating evidence that risk for PTSD is heavily influenced by genetic factors. Evidence from family and twin studies

Inhibitors,research,lifescience,medical has long suggested a heritable contribution to the development of PTSD. In addition, there is evidence for heritable contributions to some of the neurobiological endophenotypes of PTSD as discussed above, such as decreased hippocampal volume72 or exaggerated amygdala reactivity.58 Although it is beyond the scope of this review to comprehensively discuss the genetics Idoxuridine of PTSD, it should be noted that there is an emerging literature on genetic variations in those neurobiological systems that drive responses to trauma and, consequently, risk versus resilience to develop PTSD.73 One study has linked a polymorphism in the DA transporter gene to PTSD risk. In this study, PTSD patients were found to have an excess of the SLC6A39 repeat allele. This finding suggests that genetically determined features of DA transmission may contribute to the development of PTSD among trauma survivors.

The scores for

the cells stained were as follows: 0; no staining in the majority of cells, 1; staining in 25-50% of cells, 3; staining in 50-75% of cells, 4; staining in more than 75% of cells. The grades were summed up, and the averages were taken as the readings. This procedure followed previous studies with some modifications.21 The statistical software used for data analysis was the Statistical Package for Social Sciences (SPSS) version 12. The 11β-HSD1 evaluations by the two independent viewers were tested by Pearson Correlation prior to the normality test. The data were Inhibitors,research,lifescience,medical tested for normality using Kolmogrov-Smirnov test. Since the groups were found to be normally distributed, the data were analyzed using ANOVA test followed by the Tukey pos-hoc test for pairwise comparison s A P values of < 0.05 was taken as statistically significant. Data are presented as mean±SEM. Results The adrenalectomized rat treated with intramuscular injection of dexamethasone Inhibitors,research,lifescience,medical (G3) had significantly lower 11β-HSD1 dehydrogenase activity in femoral bone compared to the sham-operated (G2) and baseline (G1) group. Supplementing the dexamethasone-treated adrenalectomized rats with GCA (G4) and Piper sarmentosum

water extract (G5) extract significantly increased the 11β-HSD1 dehydrogenase activity compared to Inhibitors,research,lifescience,medical the control group. There were no significant difference in the 11β-HSD1 dehydrogenase activity of rats treated with GCA and Piper sarmentosum extract, and control or sham-operated group (figure 1). Figure 1 The activity Inhibitors,research,lifescience,medical of 11β-HSD1 dehydrogenase activity in femoral bones of G1; control group, G2; sham-operated group, G3; adrenalectomized

rats given intramuscular dexamethasone (120 µg/kg/day), G4; adrenalectomized rats given intramuscular … The adrenalectomized group treated with intramuscular injection of dexamethasone (G3) had a significantly higher 11β-HSD1 dehydrogenase 11β-HSD1 expression than the sham-operated Inhibitors,research,lifescience,medical group (G2). Supplementing the Dexamethasone-treated adrenalectomized rats with Piper sarmentosum extract (G5) caused a significant reduction in 11β-HSD1 dehydrogenase expression compared to the G3 group. Despite that, the 11β-HSD1 dehydrogenase expression in the control group (G1) and the dexamethasone-treated group check details supplemented with GCA (G4) was significantly higher than those in the sham-operated (G2) or the Piper sarmentosum extract supplemented no (G5) group (figures 2, ​,33). Figure 2 The 11β-HSD1 dehydrogenase expression in femoral bones of G1; control group, G2; sham-operated group, G3; adrenalectomized rats given intramuscular dexamethasone (120 µg/kg/day), G4; adrenalectomized rats given intramuscular dexamethasone … Figure 3 Photomicrographs (x200) of slides from femoral bones of G1; control group, G2; sham-operated group, G3; adrenalectomized rats given intramuscular dexamethasone (120 µg/kg/day), G4; adrenalectomized rats given intramuscular dexamethasone (120 µg/kg/day) …

Gastrointestinal side effects, such as nausea and diarrhea, are common, but. often transient side effects. Cardiac conduction abnormalities may occur, due to vagotonic effects on the sinoatrial and atrioventricular nodes. Cholinesterase inhibitors are likely to exaggerate succinylcholine-type muscle relaxation during anesthesia due to anticholinesterase properties. Three studies have

used memantine, a moderate-affinity NMDA antagonist, to treat motor symptoms in PD, including an early study of Inhibitors,research,lifescience,medical intravenous administration.80-82 These results suggest there are some beneficial effects with respect to PD motor symptoms; however, there were side effects, including behavioral changes. Further Inhibitors,research,lifescience,medical work is needed to determine safety and efficacy of this agent for treatment of both cognitive and motor symptoms in PD. Neuroprotective agents, which are being studied for prevention of dementia in various neurodegenerative illnesses, are being tested for use in PD.83, 84 DBS and behavioral changes There is increasing recognition that deep brain

stimulation (DBS) and other surgical interventions for motor symptoms of PD may have additional effects on behavior. The basic premise of DBS is that ncuropathological change in PD leads to abnormal neural transmission from several structures, including the subthalamic Inhibitors,research,lifescience,medical nucleus and globus pallidus internus. DBS interrupts this aberrant selleck chemicals llc activity, and ameliorates motor symptoms of Inhibitors,research,lifescience,medical PD. Given that frontalsubcortical circuits are known to affect behavior,85 in addition to their modulation of movement, it. is important that patients are evaluated for behavioral symptoms prior to surgery, and that, potential postoperative changes in psychiatric or cognitive status are addressed quickly. Possible negative Inhibitors,research,lifescience,medical effects of DBS on a patient’s emotional state and cognition should be considered along with other potential surgical complications of DBS. Depression and depressed mood, the most commonly seen psychiatric symptoms in PD, have received the most. study in DBS patients. Other behavioral changes, including euphoric mood and frank mania, hallucinations, anxiety, and sleep disorders

have also received some limited study.86 The efficacy of DBS is being evaluated in refractory cases of obsessive – compulsive disorder, an approach that, may help illuminate the neurobiology underlying both disorders, since similar frontostriatal circuitry Rolziracetam may be involved. Rates of depressed mood associated with DBS vary widely, from less than 10% to over 30% of patients experiencing these symptoms.87-91 The role of past, psychiatric history as a predictor of psychiatric outcome after DBS is not definitive at this time, but. there is some indication from existing reports that, patients with a prior history of mood symptoms may be more likely to develop depressed mood following DBS.87, 88, 91 Suicidal ideation and suicide have also been reported.

1 Unlike other head and neck malignancies, the incidence has not decreased in association with the decreasing prevalence of one of the major risk factors, cigarette

smoking. This discrepancy has been attributed to the increasing proportion of oropharyngeal cancers which are related to human papillomavirus (HPV) infection. These HPV-related tumors occur in younger patients, are more likely to occur in never-smokers and never-drinkers, and have better survival rates than HPV-negative tumors.2,3 Management of oropharyngeal cancers generally involves a combination of surgery, radiation, Inhibitors,research,lifescience,medical and chemotherapy. Historically, locally advanced cancers of the tonsils and tongue base have been difficult to visualize from a transoral viewpoint and required extensive Inhibitors,research,lifescience,medical tissue dissections from an open approach or were treated predominantly with chemotherapy or radiation. The introduction of transoral robotic surgery (TORS) has allowed an increase in the ability to manage oropharyngeal cancer via primary minimally invasive surgery.4 In the context of a rising number of HPV-related cancers, TORS is an increasingly GSK1120212 mouse important tool in the approach to management of oropharyngeal cancer. In this article, we review the role of transoral robotic surgery

(TORS) in the management of oropharyngeal cancers, and specifically Inhibitors,research,lifescience,medical how this minimally invasive technique will affect the management of HPV-related tumors. HISTORICAL PERSPECTIVES While robotic technology has been routinely used for industrial purposes for over 60 years, it was not until relatively

recently that it was introduced to the field of surgery. The first reported employment of Inhibitors,research,lifescience,medical a surgical robot was in 1985 when the PUMA 560 robot was used by a group of neurosurgeons in California to improve the accuracy of CT-guided stereotactic biopsies.5 Urologists were not far behind, and within 6 years the same PUMA 560 was used Inhibitors,research,lifescience,medical to perform the first minimally invasive robotic procedure during a transurethral resection of the prostate.6 From there, robot-assisted procedures continued to develop and became popular in a number of other specialties including gynecologic, cardiothoracic, orthopedic, and general surgery. In spite of its growing popularity, application of this new technology by otolaryngologists was initially quite limited. The early instruments were designed for use in spacious cavities, such as the abdomen or pelvis, with widely spaced Methisazone access ports. They were bulky and not well-designed for the anatomic constraints of the head and neck. However, as robot technology continued to adapt for use in surgery and newer instruments were developed, head and neck surgeons began developing transoral robotic surgery (TORS).7 In 2005, McLeod and Melder performed the first transoral robotic-assisted procedure when they used the da Vinci surgical robot (Intuitive Surgical, Inc., Sunnyvale, CA, USA) to excise a vallecular cyst.8 During that same time, O’Malley et al.

Studies have documented in subjects with high HDL an inflammatory index to classify it as pro inflammatory i.e dysfunctional and this assay allows the identification of individuals at high risk.6 Concentration of HDL in plasma is an individual risk predictor. However, the association of atherosclerotic coronary artery disease with dysfunctional Inhibitors,research,lifescience,medical HDL has been proven in many studies. The measurement of HDL alone might be a true predictive of coronary artery diseases. The association of HDL concentration and the disease seem to depend on whether or not HDL

is proinflammatory. Further large scale research is required to establish such an association.
Background: Influenza virus is a major infectious pathogen of the respiratory system causing a high degree of morbidity and mortality annually. The worldwide vaccines are decided and produced annually by World Health Organization and licensed companies based on the samples collected from all over the world. The aim of this study was to Selleck Pictilisib determine Inhibitors,research,lifescience,medical phylogenecity and heterogenecity of the circulating influenza isolates during 2008-2009 outbreaks in Tehran, compare them with the vaccine strains that

were recommended by WHO for the same period. Methods: Nasopharyngeal swabs (n=142) were collected from patients with influenza and influenza-like illness. Typing and subtyping of the isolates were performed using multiplex RT-PCR Inhibitors,research,lifescience,medical and phylogenetic analysis was carried out for hemagglutinin genes of the isolates. Results: Fifty out of 142 samples were positive for influenza A virus, and no influenza B virus was detected. Phylogenetic analyses revealed that the A/H1N1 isolates were related closely to A/Brisbane/59/2007, Inhibitors,research,lifescience,medical and the A/H3N2 isolates were close to A/Brisbane/10/2007 vaccine strains. Conclusion: The findings of the present study demonstrate that Inhibitors,research,lifescience,medical the A/H1N1 was the predominant subtype of human influenza virus among the patients studied in Tehran during 2008-2009 winter seasons. In addition, some amino acid variation was found in Tehran/2008/H1N1 isolates from the 2008-2009 vaccine strain, but the H3N2

isolates showed higher genetic resemblance to the vaccine strain. Key Words: Influenza A Virus, hemagglutinin, influenza vaccine, sequence analysis Introduction Influenza viruses are negative-stranded, segmented RNA viruses belonging to the family of Orthomyxoviridae. There are three types of A, B, and C Linifanib (ABT-869) of the virus according to antigenic differences in two of their internal proteins, nucleoprotein (NP) and matrix protein (M).1 Every year, influenza A and B viral infections cause high levels of morbidity and mortality worldwide.2 Influenza A viruses are further subdivided into subtypes based on the surface antigens, hemagglutinin (HA) and neuraminidase (NA).3 To date, 16 HA and 10 NA subtypes have been found in avian species, but only three HA (H1-H3) and two NA (N1and N2) subtypes have been identified in human.