Sustainable Synthesis of Non‐Isocyanate Polyurethanes Based on Renewable 2,3‐Butanediol

In this work, three different cyclic carbonates are obtained from renewable diols and transformed into carbamates by reacting them with renewable 11-amino undecanoic acid methyl ester to synthesize non-isocyanate poly(ester urethane)s in a sustainable manner. A procedure using 2,3-butanediol (2,3-BDO) as a renewable starting material to synthesize a cyclic carbonate with dimethyl carbonate (DMC) is introduced, catalyzed by 1,5,7-triazabicylco[4.4.0]dec-5-ene (TBD). Three purification strategies, i.e., column chromatography, extraction, and distillation, are compared regarding their E-Factors. Propylene glycol (PG) and ethylene glycol (EG) are used as alternative starting materials to broaden the substrate scope and compare material properties, their cyclic carbonates likewise react to carbamates with 11-amino undecanoic acid methyl ester. All carbamates are then polymerized in a bulk polycondensation reaction, yielding non-isocyanate polyurethanes (NIPUs), specifically poly (ester urethane)s, with molecular weights (M$_n$) up to 10 kDa. Complete characterization is reported using differential scanning calorimetric (DSC), size exclusion chromatographic measurements (SEC), $^1$H-NMR as well as IR spectroscopy. The rheological properties of the poly(ester urethane)s are investigated in the framework of small amplitude oscillatory shear (SAOS) and uniaxial elongation

Does α-Amino-β-methylaminopropionic Acid (BMAA) Play a Role in Neurodegeneration?

The association of α-amino-β-methylaminopropionic acid (BMAA) with elevated incidence of amyotrophic lateral sclerosis/Parkinson’s disease complex (ALS/PDC) was first identified on the island of Guam. BMAA has been shown to be produced across the cyanobacterial order and its detection has been reported in a variety of aquatic and terrestrial environments worldwide, suggesting that it is ubiquitous. Various in vivo studies on rats, mice, chicks and monkeys have shown that it can cause neurodegenerative symptoms such as ataxia and convulsions. Zebrafish research has also shown disruption to neural development after BMAA exposure. In vitro studies on mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca2+ influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. The current review pertaining to the neurotoxicity of BMAA clearly demonstrates its ability to adversely affect neural tissues, and implicates it as a potentially significant compound in the aetiology of neurodegenerative disease. When considering the potential adverse health effects upon exposure to this compound, further research to better understand the modes of toxicity of BMAA and the environmental exposure limits is essential

Determining the Frequency of Patients\' Attendance for Preventive Treatment after Periodontal Surgery

Introduction: Supportive periodontal treatment prevents the progress and recurrence of periodontal disease in patients previously diagnosed and treated for periodontitis, decreases tooth loss and increases the possibility for treating other diseases or conditions resulting from oral pathologies. Therefore, the present study aimed to determine the frequency of patients' returns for gingival check-up after periodontal surgery at a private periodontist office in Yazd. Methods: 365 files of the patients who had received periodontal surgery between 1996 and 2005 were randomly selected. The frequency of the patients' return to the office for periodontal check-up and their demographic features were recorded in a checklist. The study data was analyzed via SPSS software (ver,16) using descriptive statistics. Results: The patients' files belonged to 205 females (57.6%) and 151 males (42.4%). The patients’ age ranged between 14-67 years with an average of 37.8 + 9.48 years. 281 patients (93.70%) had never returned for gingival check-up after the periodontal surgery. 42 patients (11.79%) had only returned once and 22 patients (6.7%) had returned twice after the periodontal surgery. Only 1.68% of patients had returned more than three times. No significant relationship was observed between the patients' return after periodontal surgery and their age, sex, education level and occupation. Conclusion: Despite the importance of supportive treatment after the periodontal surgery, more than 90% of the patients never returned for the supporting treatment. Therefore, periodontitis needs to be emphasized for the patients to regularly return for periodontal check-up after periodontal surgery to maintain the results, and prevent the disease recurrence

The Association Between Gelsolin-like Actin-capping Protein (CapG) Overexpression and Bladder Cancer Prognosis

PURPOSE: Muscle-invasive bladder cancer (MIBC) is associated with disease progression and metastasis leading to poor prognosis. Current chemotherapy approaches have not adequately increased patient survival. Therefore, in this study, tissue proteome of patients with MIBC was performed to introduce possible protein candidates for bladder cancer prognosis as well as targeted therapy. MATERIALS AND METHODS: The tumoral and normal adjacent bladder tissues were obtained from patients diagnosed with bladder cancer. Two-dimensional gel electrophoresis (2-DE) and liquid chromatography-mass spectrometry (LC-MS/MS) were used to analyze tissue proteome. CAPG protein was further examined using Real-time PCR and western blot analysis. RESULTS: The 2-DE analysis and LC-MS/MS identified Gelsolin-like Actin-capping (CAPG) protein as differentially expressed protein in tumor tissues of bladder cancer compared with normal adjacent tissues. Western blot analysis showed the CAPG overexpression in tumor tissues compared with normal adjacent tissues in a stage-dependent manner. Correspondingly, Real- time PCR showed a higher mRNA expression in tumoral bladder tissues than normal adjacent ones. CAPG mRNA overexpression had significantly a positive relation with tumor size (p = 0.019), the TNM staging (p = 0.001), and tumor differentiation (grade) (p = 0.006). Patients with lower levels of CAPG had higher recurrence-free survival in comparison with patients with higher level of CAPG (p = .027). CONCLUSION: CAPG overexpression was correlated with size, stage, grade, and shorter time to recurrence of tumor. Therefore, CAPG overexpression could be related to poor prognosis of bladder cancer. These results suggest that CAPG may be considered as a prognostic factor and also for targeted therapy in bladder cancer

Decrease in glial glutamate transporter variants and excitatory amino acid receptor down-regulation in a murine model of ALS-PDC

Glutamate transporter proteins appear crucial to controlling levels of glutamate in the central nervous system (CNS). Abnormal and/or decreased levels of various transporters have been observed in amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD) and in other neurological disorders. We have assessed glutamate transporter (GLT-1/EAAT2) levels in mice fed washed cycad flour containing a suspected neurotoxin that induces features resembling the Guamanian disorder, ALS-PDC. Down-regulation of glutamate transporter subtypes was detected by immunohistology using antibodies specific for two glial glutamate transporter splice variants (GLT-1α and GLT-1B). Immunohistology showed a "patchy" loss of antibody label with the patches centered on blood vessels. Computer densitometry showed significantly decreased GLT-1α levels in the spinal cord and primary somatosensory cortex of cycad-fed mice. GLT-1B levels were significantly decreased in the spinal cord, in the motor, somatosensory, and piriform cortices, and in the striatum. Western blots showed a 40% decrease in frontal motor cortex and lumbar spinal cord of cycad-fed mice that appeared to be phosphorylation-dependent. Receptor-binding assays showed decreased NMDA and AMPA receptor levels and increased GABA receptor levels in cycad-fed mice cortex. These receptor data are consistent with an increased level of extracellular glutamate. The generalized decrease in GLT-1, decreased excitatory amino acid receptor levels, and increased GABA receptor levels may reflect an early glutamate-mediated excitotoxicity following cycad exposure. Deciphering the series of events leading to neurodegeneration in cycad-fed animals may provide clues leading to therapeutic approaches to halt the early stages of disease progression

A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam

As root symbionts of cycad trees, cyanobacteria of the genus Nostoc produce β-methylamino-l-alanine (BMAA), a neurotoxic nonprotein amino acid. The biomagnification of BMAA through the Guam ecosystem fits a classic triangle of increasing concentrations of toxic compounds up the food chain. However, because BMAA is polar and nonlipophilic, a mechanism for its biomagnification through increasing trophic levels has been unclear. We report that BMAA occurs not only as a free amino acid in the Guam ecosystem but also can be released from a bound form by acid hydrolysis. After first removing free amino acids from tissue samples of various trophic levels (cyanobacteria, root symbioses, cycad seeds, cycad flour, flying foxes eaten by the Chamorro people, and brain tissues of Chamorros who died from amyotrophic lateral sclerosis/Parkinsonism dementia complex), we then hydrolyzed the remaining fraction and found BMAA concentrations increased 10- to 240-fold. This bound form of BMAA may function as an endogenous neurotoxic reservoir, accumulating and being transported between trophic levels and subsequently being released during digestion and protein metabolism. Within brain tissues, the endogenous neurotoxic reservoir can slowly release free BMAA, thereby causing incipient and recurrent neurological damage over years or even decades, which may explain the observed long latency period for neurological disease onset among the Chamorro people. The presence of BMAA in brain tissues from Canadian patients who died of Alzheimer's disease suggests that exposure to cyanobacterial neurotoxins occurs outside of Guam