A study conducted by Scaramelli et al. (2009) revealed that 39 out of 100 patients reported premonitory signs, including behavioral U0126 ic50 and cognitive changes, prior to seizure onset. Humans may report confusion prior to a seizure but such a qualitative sign cannot be obtained in animal models other than by careful behavioral evaluations (e.g. disorientation, ataxia). To support interpretation, video recording concomitant to EEG monitoring allows for observation of premonitory signs

of seizure (e.g. salivation, emesis, ataxia, tremors) ( Podell, 2010) that are not otherwise captured by EEG recording alone. In addition, the margin between plasma exposure at onset of premonitory clinical signs, and at seizure onset, can be measured and serves to evaluate the risk associated with the drug candidate. Observation of such premonitory signs in clinical trials will often halt dosing.

The onset of click here adverse effects is unpredictable and restraining an animal for an extended period of time (i.e. several hours) is not feasible or ethical. In fact, restraint has been shown to lower seizure threshold during seizure susceptibility studies ( Swinyard, Radhakrishnan, & Goodman, 1962). Continuous video-EEG monitoring by telemetry can be an alternative to monitor freely moving animals, therefore decreasing the potential for stress-related artifacts or changes in seizure threshold. The current study aimed to present representative EEG results obtained by telemetry combined with video in conscious Beagle dogs, cynomolgus monkeys and Sprague–Dawley rats after determination of the pentylenetetrazol (PTZ)-induced seizure threshold. Our hypothesis was that the Beagle dog would be more sensitive to PTZ both on the seizurogenic dose and premonitory clinical signs determination. Moreover, quantitative EEG spectral changes (qEEG) considered

Mephenoxalone as an advanced analysis strategy was undertaken in rats and monkeys to illustrate methodologies to screen for drug-induced stimulatory or neuro-depressive effects. Doses of non-seizurogenic drugs used for qualification of qEEG were selected to induce slight to moderate effects based on historical data (unpublished). These results are discussed in the context of seizure liability study design and interpretation. During the study, care and use of animals were conducted in accordance with principles outlined in the current Guide to the Care and Use of Experimental Animals published by the Modulators Canadian Council on Animal Care and the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (National Research Council, 2011). CiToxLAB North America’s facility is AAALAC accredited. All procedures were conducted as per Standard Operating Procedures (SOPs) and with approval and overview of the institutional animal care and use committee.

Tonic LC firing is increased in WKY rats as compared to non-depressive-like Wistar and Sprague Dawley rats (Bruzos-Cidon et al., 2014) and although NPY levels in the LC have not been assessed, plasma levels of NPY are three time lower in WKY rats as compared to Sprague Dawley rats (Myers et al., 1993). Furthermore, it has been established that NPY and NPY receptor mRNA is downregulated in the hippocampus and hypothalamus of rats and tree shrews following social defeat stress, although this study Venetoclax molecular weight did not address differences in coping

responses (Zambello et al., 2010). Since NPY has been established as an “anti-stress” neuropeptide studies have begun evaluating individual differences in NPY levels within susceptible and resilient populations of rats from the same strain. Decreased NPY levels were reported in the amygdala, hippocampus and periaqueductal gray of rats that were Libraries vulnerable to a predator-scent stress paradigm compared with

the resilient phenotype (Cohen et al., 2012). In addition, NPY mRNA in the amygdala was negatively correlated with anxious behavior in rats characterized as exhibiting high or low levels of anxiety (Primeaux et al., 2006). Future studies in rodents capable of evaluating the impact of coping strategy on NPY levels follow social stress will be an important advancement in understanding http://www.selleckchem.com/erk.html the role of NPY in stress resilience. Notably, preclinical data linking NPY to resilience are relevant to findings in humans; deficiencies within the central NPY system have been demonstrated in patients with major depression (Widerlov et al., 1988). Individuals Casein kinase 1 with combat-related PTSD also have significantly lower levels of NPY in

their cerebrospinal fluid (Rasmusson et al., 2000 and Sah et al., 2014) and NPY levels recover during remission (Yehuda et al., 2006). Similarly, elevated levels of NPY were reported in highly resilient special operations soldiers (Morgan et al., 2000). The single prolonged stress model in rodents produces many behavioral and biochemical features of PTSD (Liberzon et al., 1997) and in a recent study, intranasal NPY effectively blocked or reversed many of the stress-related consequences (Serova et al., 2014 and Serova et al., 2013). Several lines of evidence from studies in animals and humans point towards NPY in the psychobiology of resilience to stress-induced psychiatric disorders, while deficits of NPY in the brain are related to psychiatric disorders. Studies designed to evaluate NPY levels in rodents demonstrating differing coping strategies will be an important advancement in elucidating the neural basis of stress resiliency. d. Others A recent study suggests a role for Acetylcholinergic mechanisms in mediating resilience (Mineur et al., 2013).

Phage phAE 129, a second generation of TM4 derived Mycobacteria phage, was constructed in the Laboratory of Tuberculosis Research Centre, Chennai, India and used in this study. PD98059 ic50 High titer phage stocks were prepared as serial dilution of phage was made in MP butter. To the required dilution equal volume of Mycobacterium smegmtis Mc 2 155 suspection in G7H9 (Turbidity: 0.8 O.D.) was added and incubated at 37 °C for 30 min 200 ml of the cell and phage mixture

was mixed with 3.0 ml of top agar and overlaid on 7H9 base agar plate. The plates were incubated after setting and incubated at 37 °C overnight. The positive culture plates show a lackey pattern of phage formation. It was flooded with 5 ml of MP butter and kept in rotator incubator for 1 h. After 1 h, the buffer was aspirated and filtered through 0.45 μ membrane and stored at 4 °C. LJ slants were incubated in an atmosphere of 5–10% CO2 on LJ medium. They were checked visually every 7 days and considered positive upon appearance of colonies. Time to detection was based on the earliest date of detection at colonies. Culture was checked for Mycobacterial growth on post

incubation days 1, 3, 5, 7, 11, 15, 19, 27, 41 and 55. On each designated day 500 ml/ml of each culture was infected with 100 ml of phage at a tire 1–3 × 1010 pfu/ml, with 50 ml of 1 nm CaCl2 and was incubate for 6 h at 37 °C. Six hours after the phage infection 100 μl aliquots were transferred to disposable cuvettes for quantitative luciferase assay. Upon auto injection of 100 μl of 0.33 mM luciferin solution (Sigma St.Louis, MO) into each inhibitors cuvette, luminescence production was quantified and expressed in Relative OSI-906 molecular weight Light Units (RLU). The value from a blank read was automatically subtracted from each reading. Samples with ≥0.5 RLU (Relative Light Units) were considered positive and those with <0.1 RLU were considered negative. Samples with <0.5 and ≥0.1 RLU were considered equivocal and were rechecked at 6 h post phage infection. All positive were confirmed with a duplicate

read. Samples with a negative 3-times read 3 and 6 h reads were considered negative Thalidomide for that day. The TTD was based on the earlier date of LRP assay positive. Samples with negative reads on day 55 were reported as negative cultures. PhAE 129 strain used: clinical isolates of M-16 TRC; M. smegmatis MC2-1555 TRC sputum samples – TRC. Luminometer – model 2010 A, Analytical Luminescence Lab, Ann./Ambet, Michigon, USA. Sputum was mixed with double volume of 1% chitin in 5% H2SO4 shaken for 15 min diluted with 20 ml of double distilled water. It was centrifuged at 3000 rpm for 15 min. The deposit was washed with sterile 20 ml of double distilled water again centrifuged. The supernatant was discarded. The final deposit used for inoculation and for LRP assays. The method aimed to modify and alternative processing of sputum for speedy identification of M. tuberculosis.

The perceived quality of both interventions and the child’s co-operation with them was good or excellent for almost all participants, with no important differences between the interventions. Satisfaction scores were also high for both interventions, although notably satisfaction with the exercise intervention was

significantly higher, especially among the children younger than check details 12 years. The higher satisfaction scores corroborate our and others’ experience that people with cystic fibrosis get frustrated with conventional airway clearance techniques and prefer exercise or a combination of both interventions (Moorcroft et al 1998, Bilton et al 1992, Baldwin et al 1994). The fact that satisfaction is Modulators greater after one treatment is promising for exercise, given that there are many ways it can be modified to keep it novel, enjoyable, and challenging while maintaining a suitable exercise selleck screening library load (Kuys et al 2011). Two more caveats are worth noting here. Some other exercise modalities may not have the same airway clearance effects and any exercise modality may not be effective without the incorporation of the short bouts of expiratory manoeuvres. Therefore extrapolation of these results should be done with caution until further assessment of the airway clearance effects of other exercise

regimens is available. As well as being a satisfying alternative to traditional airway clearance techniques, the exercise regimen we examined appears to be a safe alternative. Adverse events were few, mild and transient. Our results indicate that the participants had relatively low quantities of sputum to expectorate compared to adult studies, which report higher sputum production, eg, 10 to 20 g over periods of 50 to 150 min (Bilton et al 1992, Baldwin et al 1994, Salh et al 1989). The Vasopressin Receptor smaller amount of sputum

in our participants is likely to be due to their mild lung disease. Given our efforts to ensure expectoration, we do not think that the small amount of sputum indicates that sputum was swallowed. However, this is a theoretical source of bias that must be considered. The vigour of the exercise intervention may have entailed a higher risk of accidental or unnoticed swallowing of secretions than the control intervention. However, if such bias did occur, this would only further support our conclusion that the exercise intervention was a suitable substitute for the control intervention in this study. The conclusions of our study are limited because each intervention was only applied once for 20 min, and in a hospital environment, where treatment co-operation and quality may surpass that achieved at home. Also, although eligibility was not restricted to a specific FEV1 range, most of the children had excellent lung function so the results may not apply to more severely affected children.

In contrast, recombinant protein vaccines require multiple doses to achieve consistently high antibody titers: five doses of P. yoelii MSP119 in Freund’s adjuvant are required for high and protective antibody titres [24] and three doses of RTS,S are

required to achieve optimal titres in humans [47]. Although www.selleckchem.com/products/fg-4592.html some mice receiving P–P in this study achieved high antibody titers, there was considerable variation within this regime. Once responses were primed by adenovirus, protein appeared to be the optimal platform for boosting antibody responses with antibody titers after A–P exceeding those following A–M. Three-component regimes could also achieve simultaneous antibody and antigen-specific CD8+ T cell responses which equalled both antibody induction by adenovirus–protein and CD8+ T cell induction by A–M—hitherto

the best regimes available. This pattern remained unchanged at time points up to 138 days after the final vaccination. Virus like particles (VLPs) are a fourth clinically relevant vaccine platform, noted for their ability to induce strong antibody responses. Adenovirus–MVA–VLP combinations may have potential to improve further upon the antibody results achieved here, while maintaining or enhancing viral-vector induced CD4+ and CD8+ T cell responses. In the absence of a vaccine which protects humans against blood-stage P. falciparum, INK 128 supplier it is not yet fully understood which attributes of an antibody

response are protective. In animal challenge models the induction of high antibody concentrations seems to be the Resminostat inhibitors principal predictor of MSP1 and AMA1 vaccine-mediated protection [48] and [49]. Most published work in the field simply uses ELISA titer as a quantitative readout of antibody induction. There are a further four quantitative properties of the vaccine-induced antibody response which we believe to be of interest: isotype balance; antibody avidity; rate of decline of ELISA titer; and recall response to re-exposure to antigen. The current results demonstrate significant differences between the viral vectored PfMSP1-based vaccines and the protein-adjuvant PfMSP119 vaccine in some of these attributes. These may be due to differences between viral vector and recombinant protein delivery platforms or differences in the processing and inherent antigenicity of the differently sized antigens. There are conflicting data regarding the importance of Fc-dependent functions of Th1-type cytophilic antibody subclasses (human IgG1 and IgG3; murine IgG2a and IgG2b) in protection against blood-stage malaria, and the impact of Th1 cytokines and IgG isotype on protective efficacy [50], [51], [52] and [53].

A representative example from one donor is shown in Fig. 2A. Individual tetanus (T) and diphtheria (D) peptides showed limited Selleck NVP-BKM120 induction of CD4 + CD45RAlowCD62L+ cells expressing IFN-γ compared to a non-stimulated (NS) control (0.04% and 0.08% vs. 0.01% respectively). The chimeric peptide with no cleavage site (TD) and the peptide with the kvsvr cathepsin cleavage site (TkD) showed slightly more cells expressing IFN-γ (0.32%). However the peptide with the pmglp cathespsin cleavage site (TpD) induced a superior response (1.28%), 4-fold higher than the chimeric peptide with

no cleavage site. We went on to analyze PBMC from 20 donors (Fig. 2B) and found that we could not detect a specific response in most cases using either individual T (2/20 donors) or D (7/20 donors)

peptides. More donors responded to the chimeric TD peptide (15/20) but all 20 donors showed a recall response to the TpD chimeric peptide. The percentage of CD4 + CD45RAlowCD62L+ cells expressing IFN-γ normalized to a non-stimulated control for each of the peptides is shown in Fig. 2B. In addition to providing the highest percentage of responders, the TpD peptide induced the highest levels of IFN-γ among all peptides tested. Interestingly TkD had diminished activity compared to TpD, suggesting that the kvsvr cleavage site may be detrimental. We next evaluated the type of memory cells stimulated by TpD. Central memory cells, thought to be the most effective at generating a recall response, are CD4 + CD45RAlowCD45RO + CD27 + CCR7+ [27] and express multiple cytokines including

IFN-γ and TNF-α [4], whereas effector memory cells are CD4 + CD45RAlowCD45RO+/−CD27-CCR7-. PR-171 order Multicolor flow cytometry analysis suggested that the cells responding to TpD express a phenotype of central memory T cells (Fig. 2C). We next addressed if the memory cells favored a Th1 or Th2 phenotype upon activation. Memory T cells can be divided based on differential chemokine receptor expression into subsets that will produce either the Th1 inhibitors cytokine IFN-γ, or Th2 cytokine IL-4, on activation [28] and [29]. We analyzed four separate donors and found that individual T and D peptides, as well as chimeric peptides induced expression of IFN-γ in more memory T cells than IL-4, suggesting a bias toward a Th1 subset (Fig. 2D). Based on these characteristics TpD was selected as the Carnitine dehydrogenase memory T helper stimulating peptide for a nanoparticle based vaccine. PLGA/PLA nanoparticles have been useful vehicles for vaccine development. We designed a nanoparticle vaccine carrying nicotine as the B cell antigen (Fig. 3). The components of the nanoparticle include: PLA-PEG-Nicotine, which is a block copolymer with nicotine covalently bound to the free end of PLA-PEG; the adjuvant R848 linked to PLGA, and the memory T cell helper antigen TpD (Fig. 3). To assess the contribution of TpD, nanoparticles were also generated that lacked TpD. As an initial test for efficacy, we immunized mice with nanoparticles containing or lacking TpD (Fig. 4).

Deletion of synaptotagmin-1 (Syt1) in forebrain neurons blocks fast synchronous release induced by isolated action potentials but retains an asynchronous,

slower, and facilitating form of release induced by bursts of action potentials (Geppert et al., 1994, Yoshihara and Littleton, 2002, Maximov and Südhof, 2005 and Xu et al., 2012). Although in most synapses asynchronous release becomes manifest only when Syt1 is deleted, in some synapses asynchronous release normally predominates. This is observed in GABAergic synapses formed by CCK-containing Nutlin-3 manufacturer dentate gyrus interneurons (Hefft and Jonas, 2005 and Daw et al., 2009) and inferior olive interneurons (Best and Regehr, 2009). The mammalian genome encodes 16 synaptotagmins, eight of which bind Ca2+ (reviewed in Gustavsson and Han, 2009). Of these eight synaptotagmins, Syt1, Syt2, and Syt9 are localized to synaptic and neuroendocrine vesicles and function as Ca2+ sensors for fast synaptic and neuroendocrine

exocytosis (Perin et al., 1990, Brose et al., 1992, Littleton et al., 1993, Geppert et al., 1994, Sørensen et al., 2003, Pang et al., 2006, Sun et al., 2007 and Xu et al., 2007). Syt10, in contrast, is localized to IGF-1-containing vesicles in olfactory bulb neurons and acts as Ca2+ sensor for IGF-1 secretion in these neurons (Cao et al., 2011 and Cao et al., 2013). Among the remaining four Ca2+-binding synaptotagmins, Syt7 is particularly interesting because it is highly expressed in neurons and enriched Thiamine-diphosphate kinase in synapses (Sugita et al., 2001 and Virmani check details et al., 2003). Surprisingly, Syt7 is dispensable for neurotransmitter release in cultured neurons (Maximov et al., 2008), although it contributes to asynchronous release in zebrafish neuromuscular junctions (Wen et al., 2010). At synapses, Syt7 was not detected in synaptic vesicles but in the synaptic plasma membrane, whereas Syt1 was found in synaptic

vesicles (Sugita et al., 2001, Han et al., 2004, Takamori et al., 2006 and Maximov et al., 2007). In neuroendocrine cells, however, Syt7 was colocalized with Syt1 on secretory granules and was shown to mediate Ca2+ triggering of exocytosis similar to Syt1 (Sugita et al., 2001, Shin et al., 2002, Fukuda et al., 2004, Tsuboi and Fukuda, 2007, Schonn et al., 2008, Gustavsson et al., 2008, Gustavsson et al., 2009, Li et al., 2009 and Segovia et al., 2010), albeit with a slower time course (Schonn et al., 2008). Thus, Syt7 is an evolutionarily conserved synaptotagmin highly expressed in brain that functions in neuroendocrine exocytosis but whose neural function is unclear. Despite its importance, the identity of the Ca2+ sensor mediating asynchronous release that becomes manifest in Syt1-deficient synapses has remained enigmatic. One study implicated Doc2A as a Ca2+ sensor for asynchronous release (Yao et al., 2011), but other studies failed to detect any role for Doc2 proteins in asynchronous release (Groffen et al., 2010 and Pang et al., 2011a).

, 2000). Alternatively, such differences in ERK1/2 phosphorylation may result from the submaximal defeat protocol used. We also observed induction of total levels of Ras in NAc of mice treated chronically with cocaine followed by repeated social defeat (Figure 6C). In contrast, total levels of other proteins in this cascade, including BDNF, TrkB, Raf, MEK1/2, ERK1/2, and CREB, were not altered. Also unaltered was Protein Tyrosine Kinase inhibitor Ras-GRF1, a guanine nucleotide exchange factor that activates Ras (Figure 6C, inset). These results suggest that induction of Ras expression per se may be responsible for activating downstream components of this signaling pathway

necessary for the cocaine enhancement of depressive-like behaviors (Figure 6C). Overexpression of G9a, which blocks cocaine-induced vulnerability to stress, significantly reduced cocaine- and stress-mediated increases in SCH 900776 order Ras expression in NAc, without affecting total

protein levels of any of the other members of this pathway examined (Figure 6C and Figures S5A–S5H). NAc-specific overexpression of G9a did, however, significantly reduce the phosphorylation state of all downstream-signaling molecules, including phospho-Raf, phospho-MEK1/2, phospho-ERK1/2, and phospho-CREB, indicating that transcriptional repression of Ras activity by G9a suppresses the activity of this entire signaling cascade. It is important to note that G9a overexpression had no effect on total levels or phosphorylation state of any of the proteins examined in this pathway under control conditions (i.e., HSV-G9a in cocaine- and stress-naive mice), suggesting that G9a acts in a stimulus-dependent manner to block BDNF-TrkB signaling. To further investigate the possibility that Cell press cocaine’s induction of Ras contributes to increased stress vulnerability, we examined expression of H-Ras1, the Ras transcript most predominately expressed in adult brain, in NAc of animals receiving either saline, acute, or repeated cocaine, either immediately after cocaine exposure (1 hr)

or 24 hr after the final drug dose. Although H-Ras1 mRNA expression was unaffected by a single dose of cocaine, it was significantly induced by repeated cocaine at 1 hr, an effect that persisted for 24 hr ( Figure 6D). A substantial literature indicates functional differences between NAc and dorsal striatum in the development of stress- and drug-induced behaviors ( Saka et al., 2004, Di Ciano et al., 2008 and Dias-Ferreira et al., 2009). We thus investigated Ras, ERK, and CREB in dorsal striatum in response to repeated cocaine or stress ( Figures S6A–S6G). Phospho-CREB was decreased in dorsal striatum by acute cocaine, and increased by repeated cocaine, similar to our observations in NAc ( Figure S6D). Cocaine had no effect on Ras or ERK in dorsal striatum. Ras protein levels were increased in dorsal striatum after chronic social stress, but only in unsusceptible mice ( Figure S6E). In contrast, Ras induction in NAc was observed exclusively in susceptible animals.

Interestingly, LI contains two distinct populations of either highpass or lowpass cells, with relatively few bandpass cells, which may help explain the similarity in the high and low cutoffs observed for this area (Figure 5D). All areas except AM have significantly different

low cutoff values than V1. This effect was toward lower values in all areas except areas LI and PM, which had a higher mean low cutoff than V1 (Figure 5D, one-way ANOVA, F(6,1205) = 9.91, p < 0.0005; post-hoc comparisons p < 0.05, HSD). Visual areas could also be distinguished in terms of SF high cutoffs ( Figure 5D). All extrastriate areas had significantly lower mean high cutoff than V1, with the exception of PM, which had a slightly higher

mean cutoff than V1, but this effect was not found buy ON-01910 to be significant. Comparing across extrastriate areas showed that high cutoff SFs were similar for all higher visual areas, except LM, which had a significantly higher mean high cutoff than area AL ( Figure 5D, one-way ANOVA, F(6,1445) = 27.55, p < 0.0005; post-hoc comparisons p < 0.05, HSD). Tuning bandwidth for SF was sharper in all extrastriate areas compared to V1, except area LI (Figure S5, one-way ANOVA F(6,903) = 15.23, p < 0.0005; post-hoc comparisons p < 0.05, HSD). Area LM had significantly broader SF tuning than extrastriate areas AL, RL, and AM ( Figure S5, p < 0.05, buy INCB024360 HSD). Area AM had the sharpest spatial frequency tuning bandwidth. These results demonstrate that extrastriate visual areas are more Resminostat selective for SF than V1. We calculated the orientation selectivity index (OSI) at the optimal SF for each neuron (Experimental Procedures). A clear separation could be seen between the cumulative distributions of area V1 compared to all other areas, with the distributions of all extrastriate areas shifted toward higher OSI values (Figure 6A). Population distributions in areas PM,

AL, RL, and especially AM stand out as particularly well tuned for orientation relative to the other areas (Figure 6A). All extrastriate areas except area LI had significantly higher mean OSI values than V1 (Figure 6B, one-way ANOVA F(6,1783) = 41.74, p < 0.0005; post-hoc comparisons p < 0.05, HSD). A subset of areas stood out above the rest: AL, RL, and especially area AM had higher mean OSI values than all other areas, except area PM, which was only significantly lower than area AM ( Figure 6B, p < 0.05, HSD). AM showed the highest OSI of any of the areas, with significantly higher tuning than all areas except AL ( Figure 6B, p < 0.05, HSD). These results were also reflected in the proportion of cells that were highly orientation selective (OSI > 0.5, Figure 6C). All extrastriate areas had a larger proportion of highly orientation selective cells than V1, with AL, RL, AM, and PM having the largest proportions of highly selective cells.

While this is understandable, increasingly

male faculty also serve as important role models for work-life balance. I would strongly suggest to women students that as they evaluate potential graduate advisors, male or female, they examine to what extent prospective mentors have a good track record of having trained successful women scientists. As you gauge the mentoring environment of a prospective lab, make sure to ask whether the students are generally happy. If not, this is selleck kinase inhibitor a warning sign. I strongly believe that when a talented student is in the right lab, with a good mentor, that going to lab every day should feel almost like being in summer camp. Someone once told me with great sincerity that he felt that you had not done a real PhD until you hated your advisor and he or she hated

you. This is a tragic way of thinking! I have heard of many cases HDAC inhibitor in which a student has been told that they are not working long enough hours in a lab and that the advisor expects the student to work 60+ hours per week. In 20 years, I have never said or implied such a thing to any student. I feel that the advisor’s job is to provide a fun and exciting environment, to set a good example, and the rest must come from the heart of a student. Henry Ford once said, “Hire good people, and then get the hell out of their way.” What great advice! If all is well, doing science will feel like play, and students will freely choose to work long hours because it is fun and exciting (that does not mean

there will be frustrating times when your experiments are not working, of course). Moreover, if trained well, there should be no problem being successful in science while leading a happy and balanced life (okay, I am not a great example of and this—but most of my previous students have accomplished a balanced life in their own labs despite my poor example. And I am living the life I love, just as I hope for my students.) Here are some signs that a prospective advisor is thinking more about his own career and less about your career: he (or she) never mentions his students’ names when he presents their work in a talk or only mentions them in a long list in small print at the end of the talk, he does not practice the students’ talks with them, he puts two students in the lab on the same project so that they must compete with each other, he tells you what experiments you must do, he insists on writing the research papers rather than allowing the student to write it and then editing it with the student, he allows the students’ papers to sit on his desk (sometimes for years, sometimes never even submitting them), and he refuses to allow students to take their projects or reagents with them (or fails to make sure they have lots of good starting points for projects in their own labs). Although most faculty do not behave this way, I have seen these things happen to many students over the years.