Effects of pH on algal abundance: a model of Bay Harbor, Michigan

General Ecology - spring term.Cement production, while an important process, creates toxic cement kiln dust as a byproduct. When mixed with water, this cement kiln dust creates a toxic leachate that has a high pH and has detrimental effects on wildlife and human health. Bay Harbor, Michigan has been highly contaminated with this leachate, and this study models Bay Harbor by manipulating pH in a controlled environment and examining the effect on algal abundance. We hypothesized that raising pH will reduce algal abundance, measured as chlorophyll levels. We took water samples from Little Traverse Bay and had one control treatment and two alkalinity treatments in which we raised the pH to 8.9 and 9.9 from the initial level of 7.9. We found a statistically significant difference in the algal abundance of the controls versus each of the two experimental groups. We therefore suggest that the abundance of algae in Bay Harbor is being negatively affected by cement kiln dust leachate.http://deepblue.lib.umich.edu/bitstream/2027.42/57443/1/Bergstrom_McKeel_Patel_2007.pd

On the origin of trisomy 21 Down syndrome

Background: Down syndrome, characterized by an extra chromosome 21 is the most common genetic cause for congenital malformations and learning disability. It is well known that the extra chromosome 21 most often originates from the mother, the incidence increases with maternal age, there may be aberrant maternal chromosome 21 recombination and there is a higher recurrence in young women. In spite of intensive efforts to understand the underlying reason(s) for these characteristics, the origin still remains unknown. We hypothesize that maternal trisomy 21 ovarian mosaicism might provide the major causative factor. Results: We used fluorescence in situ hybridization (FISH) with two chromosome 21-specific probes to determine the copy number of chromosome 21 in ovarian cells from eight female foetuses at gestational age 14–22 weeks. All eight phenotypically normal female foetuses were found to be mosaics, containing ovarian cells with an extra chromosome 21. Trisomy 21 occurred with about the same frequency in cells that had entered meiosis as in pre-meiotic and ovarian mesenchymal stroma cells. Conclusion: We suggest that most normal female foetuses are trisomy 21 ovarian mosaics and the maternal age effect is caused by differential selection of these cells during foetal and postnatal development until ovulation. The exceptional occurrence of high-grade ovarian mosaicism may explain why some women have a child with Down syndrome already at young age as well as the associated increased incidence at subsequent conceptions. We also propose that our findings may explain the aberrant maternal recombination patterns previously found by family linkage analysis

Measurement of Myofilament-Localised Calcium Dynamics in Adult Cardiomyocytes and the Effect of Hypertrophic Cardiomyopathy Mutations

Rationale: Subcellular Ca2+ indicators have yet to be developed for the myofilament where disease mutation, or small molecules may alter contractility through myofilament Ca2+ sensitivity. Here we develop and characterise genetically encoded Ca2+ indicators restricted to the myofilament to directly visualise Ca2 changes in the sarcomere. Objective: To produce and validate myofilament restricted Ca2+ imaging probes in an adenoviral transduction adult cardiomyocyte model using drugs that alter myofilament function (MYK-461, omecamtiv mecarbil and levosimendan) or following co-transduction of two established hypertrophic cardiomyopathy (HCM) disease causing mutants (cTnT R92Q and cTnI R145G) that alter myofilament Ca2+ handling. Methods and Results: When expressed in adult ventricular cardiomyocytes RGECO-TnT/TnI sensors localise correctly to the sarcomere without contractile impairment. Both sensors report cyclical changes in fluorescence in paced cardiomyocytes with reduced Ca2+ on and increased Ca2+ off rates compared with unconjugated RGECO. RGECO-TnT/TnI revealed changes to localised Ca2+ handling conferred by MYK-461 and levosimendan, including an increase in Ca2+ binding rates with both levosimendan and MYK-461 not detected by an unrestricted protein sensor. Co-adenoviral transduction of RGECO-TnT/TnI with HCM causing thin filament mutants showed that the mutations increase myofilament [Ca2+] in systole, lengthen time to peak systolic [Ca2+], and delay [Ca2+] release. This contrasts with the effect of the same mutations on cytoplasmic Ca2+, when measured using unrestricted RGECO where changes to peak systolic Ca2+ are inconsistent between the two mutations. These data contrast with previous findings using chemical dyes that show no alteration of [Ca2+] transient amplitude or time to peak Ca2+. Conclusions: RGECO-TnT/TnI are functionally equivalent. They visualise Ca2+ within the myofilament and reveal unrecognised aspects of small molecule and disease associated mutations in living cells

Identification and Description of Emotions by Current Large Language Models - Dataset

The assertion that artificial intelligence (AI) cannot grasp the complexities of human emotions has been a long-standing debate. However, recent advancements in large language models (LLMs) challenge this notion by demonstrating an increased capacity for understanding and generating human-like text. In this study, we evaluated the empathy levels and the identification and description of emotions by three current language models: Bard, GPT 3.5, and GPT 4. We used the Toronto Alexithymia Scale (TAS-20) and the 60-question Empathy Quotient (EQ-60) questions to prompt these models and score the responses. The models' performance was contrasted with human benchmarks of neurotypical controls and clinical populations. We found that the less sophisticated models (Bard and GPT 3.5) performed inferiorly on TAS-20, aligning close to alexithymia, a condition with significant difficulties in recognizing, expressing, and describing one's or others' experienced emotions. However, GPT 4 achieved performance close to the human level. These results demonstrated that LLMs are comparable in their ability to identify and describe emotions and may be able to surpass humans in their capacity for emotional intelligence. Our novel insights provide alignment research benchmarks and a methodology for aligning AI with human values, leading toward an empathetic AI that mitigates risk.</p

On the paternal origin of trisomy 21 Down syndrome

Background: Down syndrome (DS), characterized by an extra free chromosome 21 is the most common genetic cause for congenital malformations and learning disability. It is well known that the extra chromosome 21 originates from the mother in more than 90% of cases, the incidence increases with maternal age and there is a high recurrence in young women. In a previous report we have presented data to indicate that maternal trisomy 21 (T21) ovarian mosaicism might provide the major causative factor underlying these patterns of DS inheritance. One important outstanding question concerns the reason why the extra chromosome 21 in DS rarely originates from the father, i.e. in less than 10% of T21 DS cases. We here report data indicating that one reason for this parental sex difference is a very much lower degree of fetal testicular in comparison to ovarian T21 mosaicism. Results: We used fluorescence in situ hybridisation (FISH) with two chromosome 21-specific probes to determine the copy number of chromosome 21 in fetal testicular cell nuclei from four male fetuses, following termination of pregnancy for a non-medical/social reason at gestational age 14-19 weeks. The cells studied were selected on the basis of their morphology alone, pending immunological specification of the relevant cell types. We could not detect any indication of testicular T21 mosaicism in any of these four male fetuses, when analysing at least 2000 cells per case (range 2038-3971, total 11.842). This result is highly statistically significant (p < 0.001) in comparison to the average of 0.54% ovarian T21 mosaicism (range 0.20-0.88%) that we identified in eight female fetuses analysing a total of 12.634 cells, as documented in a previous report in this journal. Conclusion: Based on these observations we suggest that there is a significant sex difference in degrees of fetal germ line T21 mosaicism. Thus, it would appear that most female fetuses are T21 ovarian mosaics, while in sharp contrast most male fetuses may be either very low grade T21 testicular mosaics or they may be non-mosaics. We further propose that this sex difference in germ line T21 mosaicism may explain the much less frequent paternal origin of T21 DS than maternal. The mechanisms underlying the DS cases, where the extra chromosome 21 does originate from the father, remains unknown and further studies in this respect are required

On the origin of the maternal age effect in trisomy 21 Down syndrome : the Oocyte Mosaicism Selection model

We have recently documented that trisomy 21 mosaicism is common in human foetal ovaries. On the basis of this observation we propose that the maternal age effect in Down syndrome (DS) is caused by the differential behaviour of trisomy 21 in relation to disomy 21 oocytes during development from foetal life until ovulation in adulthood. in particular, we suggest that trisomy 21 oocytes, lagging behind those that are disomic, may escape the timed pruning of the seven million in foetal life to the 300-400 finally selected for ovulation. The net effect of this preferential elimination will be an accumulation of trisomy 21 oocytes in the ovarian reserve of older women. We here highlight the implications of this Oocyte Mosaicism Selection (OMS) model with respect to the prevalent view that the maternal age effect is complex, dependent on many different biological and environmental factors. We examine conclusions drawn from recent large-scale studies in families, tracing DNA markers along the length of chromosome 21q between parents and DS children, in comparison to the OMS model. We conclude that these family linkage data are equally compatible with the maternal age effect originating from the accumulation of trisomy 21 oocytes with advancing maternal age. One relatively straightforward way to get to grips with what is actually going on in this regard would be to compare incidence of trisomy 21 oocytes (and their pairing configurations) in foetal ovaries with that in oocytes at the meiosis I stage from adult women. Reproduction (2010) 139 1-

Postoperative urinary retention in men is common after carotid endarterectomy and is associated with advanced age and prior urinary tract infection.

OBJECTIVE: This study was undertaken to analyze the occurrence of postoperative urinary retention (POUR) after carotid endarterectomy (CEA) and determine whether there are any associated modifiable risk factors. CEA was chosen to minimize the confounding effects of known risk factors for POUR, including immobilization, regional and severe pain, and neuroaxial anesthesia. METHODS: This was a retrospective record review of 186 male patients undergoing CEA between 2007 and 2011. Demographic, comorbidities, and operative characteristics were compared. Continuous variables are reported as median and interquartile range (IQR) and categoric variables as frequencies and proportions. Pearson χ(2) or Mann-Whitney U tests compared categoric and continuous variables, respectively. Logistic regression was used to examine univariate and multivariate odds of POUR. Multivariate analysis controlled for known predictors of urinary retention. Association with other complications was examined with the Pearson correlation coefficient. RESULTS: POUR occurred in 34 patients (18.3%). Median age and history of urinary tract infection (UTI) were significantly associated with POUR: median age was 73.0 years (IQR, 67-80 years) for those with POUR vs 69.5 years (IQR, 63-76 years) for those without (P = .047); 17.6% of patients with a history of UTI developed POUR vs 5.9% without (P = .023). These findings persisted on multivariate analysis controlling for known predictors of POUR (body mass index, history of diabetes, benign prostate hyperplasia, and prior prostate surgery): median age (odds ratio, 1.05; 95% confidence interval, 1-1.1) and history of UTI (odds ratio, 4.16; 95% confidence interval, 1.23-14.05; P = .022). The occurrence of POUR was significantly correlated with postoperative UTI: 18.8% with POUR vs 0.7% without (Pearson r = 0.369; P \u3c .001). CONCLUSIONS: POUR requiring bladder catheterization after CEA predisposes patients to postoperative UTI and is more common in older patients and those with a history of UTI. CEA patients lack inherent risk factors for POUR and would be a useful population for prospective studies involving POUR

Postoperative urinary retention in men is common after carotid endarterectomy and is associated with advanced age and prior urinary tract infection

OBJECTIVE: This study was undertaken to analyze the occurrence of postoperative urinary retention (POUR) after carotid endarterectomy (CEA) and determine whether there are any associated modifiable risk factors. CEA was chosen to minimize the confounding effects of known risk factors for POUR, including immobilization, regional and severe pain, and neuroaxial anesthesia. METHODS: This was a retrospective record review of 186 male patients undergoing CEA between 2007 and 2011. Demographic, comorbidities, and operative characteristics were compared. Continuous variables are reported as median and interquartile range (IQR) and categoric variables as frequencies and proportions. Pearson χ(2) or Mann-Whitney U tests compared categoric and continuous variables, respectively. Logistic regression was used to examine univariate and multivariate odds of POUR. Multivariate analysis controlled for known predictors of urinary retention. Association with other complications was examined with the Pearson correlation coefficient. RESULTS: POUR occurred in 34 patients (18.3%). Median age and history of urinary tract infection (UTI) were significantly associated with POUR: median age was 73.0 years (IQR, 67-80 years) for those with POUR vs 69.5 years (IQR, 63-76 years) for those without (P = .047); 17.6% of patients with a history of UTI developed POUR vs 5.9% without (P = .023). These findings persisted on multivariate analysis controlling for known predictors of POUR (body mass index, history of diabetes, benign prostate hyperplasia, and prior prostate surgery): median age (odds ratio, 1.05; 95% confidence interval, 1-1.1) and history of UTI (odds ratio, 4.16; 95% confidence interval, 1.23-14.05; P = .022). The occurrence of POUR was significantly correlated with postoperative UTI: 18.8% with POUR vs 0.7% without (Pearson r = 0.369; P \u3c .001). CONCLUSIONS: POUR requiring bladder catheterization after CEA predisposes patients to postoperative UTI and is more common in older patients and those with a history of UTI. CEA patients lack inherent risk factors for POUR and would be a useful population for prospective studies involving POUR

Increased Expression of Phosphorylated FADD in Anaplastic Large Cell and Other T-Cell Lymphomas

FAS-associated protein with death domain (FADD) is a major adaptor protein involved in extrinsic apoptosis, embryogenesis, and lymphocyte homeostasis. Although abnormalities of the FADD/death receptor apoptotic pathways have been established in tumorigenesis, fewer studies have analyzed the expression and role of phosphorylated FADD (pFADD). Our identification of FADD as a lymphoma-associated autoantigen in T-cell lymphoma patients raises the possibility that pFADD, with its correlation with cell cycle, may possess role(s) in human T-cell lymphoma development. This immunohistochemical study investigated pFADD protein expression in a range of normal tissues and lymphomas, particularly T-cell lymphomas that require improved therapies. Whereas pFADD was expressed only in scattered normal T cells, it was detected at high levels in T-cell lymphomas (eg, 84% anaplastic large cell lymphoma and 65% peripheral T cell lymphomas, not otherwise specified). The increased expression of pFADD supports further study of its clinical relevance and role in lymphomagenesis, highlighting phosphorylation of FADD as a potential therapeutic target