Electrochemical Performance of Chemically Activated Carbons from Sawdust as Supercapacitor Electrodes.

Activated carbons (ACs) have been the most widespread carbon materials used in supercapacitors (SCs) due to their easy processing methods, good electrical conductivity, and abundant porosity. For the manufacture of electrodes, the obtained activated carbon based on sawdust (karagash and pine) was mixed with conductive carbon and polyvinylidene fluoride as a binder, in ratios of 75% activated carbon, 10% conductive carbon black, and 15% polyvinylidene fluoride (PVDF) in an N-methyl pyrrolidinone solution, to form a slurry and applied to a titanium foil. The total mass of each electrode was limited to vary from 2.0 to 4.0 mg. After that, the electrodes fitted with the separator and electrolyte solution were symmetrically assembled into sandwich-type cell construction. The carbon's electrochemical properties were evaluated using cyclic voltammetry (CV) and galvanostatic charge-discharge (CGD) studies in a two-electrode cell in 6M KOH. The CV and CGD measurements were realized at different scan rates (5-160 mV s-1) and current densities (0.1-2.0 A g-1) in the potential window of 1 V. ACs from KOH activation showed a high specific capacitance of 202 F g-1 for karagash sawdust and 161 F g-1 for pine sawdust at low mass loading of 1.15 mg cm-2 and scan rate of 5 mV s-1 in cyclic voltammetry test and 193 and 159 F g-1 at a gravimetric current density of 0.1 A g-1 in the galvanostatic charge-discharge test. The specific discharge capacitance is 177 and 131 F g-1 at a current density of 2 A g-1. Even at a relatively high scan rate of 160 mV s-1, a decent specific capacitance of 147 F g-1 and 114 F g-1 was obtained, leading to high energy densities of 26.0 and 22.1 W h kg-1 based on averaged electrode mass. Surface properties and the porous structure of the ACs were studied by scanning electron microscopy, energy-dispersive X-ray analysis, Raman spectroscopy, and the Brunauer-Emmett-Teller method.

Biomass-Derived Porous Carbon Materials for Li-Ion Battery.

Biomass-based carbon nanofibers (CNF) were synthesized using lignin extracted from sawdust and polyacrylonitrile (PAN) (30:70) with the help of the electrospinning method and subsequent stabilization at 220 °C and carbonization at 800, 900, and 1000 °C. The synthesized CNFs were studied by scanning electron microscopy, energy-dispersive X-ray analysis, Raman spectroscopy, and the Brunauer-Emmett-Teller method. The temperature effect shows that CNF carbonized at 800 °C has excellent stability at different current densities and high capacitance. CNF 800 in the first test cycle at a current density of 100 mA/g shows an initial capacity of 798 mAh/g and an initial coulomb efficiency of 69.5%. The CNF 900 and 1000 show an initial capacity of 668 mAh/g and 594 mAh/g, and an initial Coulomb efficiency of 52% and 51%. With a long cycle (for 500 cycles), all three samples at a current density of 500 mA/g show stable cycling in different capacities (CNF 800 in the region of 300-400 mAh/g, CNF 900 and 1000 in the region of 100-200 mAh/g).

Gastric Cancer in Aktobe Region of Western Kazakhstan from 2009 to 2018: Incidence Rates, Trends, and Five-Year Survival.

OBJECTIVE: to assess the current state of gastric cancer (GC) incidence and its five-year survival across Aktobe region of western Kazakhstan from 2009 to 2018 by presenting key indicators and analyzing the most significant features. METHODS: Rough incidence rates (per 100,000) and average annual percent changes (aAPCs) were estimated for each age group at diagnosis with respect to gender, ethnicity, residence, the disease stages, tumor subsite, and histology type using linear regression analysis, including the prognostic index for 2019-2020. Overall five-year survival rates were estimated by the Kaplan-Meier method. RESULTS: Overall GC incidence increased from 19.2 to 29.3, and averaged 25.8 (R2 0.65) with aAPC of 3.2%, with a potential to further rise (30.4 by 2020, p<0.001). Non-cardia location (17.8, p<0.001, aAPC 6.4%) and intestinal type of the tumor (17.0, p<0.001, aAPC 7.35%) were predominant. The observed overall five-year survival rate was 28.4% (95% CI 24.5;32.3) with a median survival time of 8.0 months (95% CI 6.6;9.4). Groups aged 40-49 and ≥70 had the lowest rates (24.4% and 22.1%, respectively, log-rank p 0.008), but the youngest individuals (18-39 years) showed the shortest median survival time, 5.0 months after diagnosis at the survival rate of 29.4%. Resectional surgery contributed significantly to the median survival time, 23.0 months vs. 6.0 in non-operated patients (log-rank p<0.001). CONCLUSION: GC in Aktobe region was featured by growing incidence and unsatisfactory five-year survival rates. Indigenous males of 60-69 years old with intestinal histology type, as well as the youngest patients irrespective of their gender, ethnicity, and other characteristics were recognized as high risk groups. Besides, relatively high aAPC 5.1% in the youngest revealed their further expected vulnerability. Further research is suggested to focus on risk factors, including gene expression profiling, to find out an accessible preventive strategy.
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Familial aggregation of parkinsonism in progressive supranuclear palsy.

BACKGROUND: Progressive supranuclear palsy (PSP) is a progressive neurodegenerative disorder characterized by aggregates of the microtubule-associated protein tau (MAPT). A nonsignificant trend for positive family history has been observed in two case-control studies and several pedigrees with familial clustering of parkinsonism have been described. Occasionally, mutations in MAPT are found in patients with a clinical phenotype similar to PSP. In this case-control study, we compared the occurrence of dementia and parkinsonism among first-degree relatives of patients with PSP with an age- and sex-matched control group. METHODS: Family history of dementia and parkinsonism was collected from all first-degree relatives of patients with PSP who fulfilled the international National Institute of Neurological Disorders and Stroke criteria for PSP. Age- and sex-matched controls were selected from the Rotterdam Study. Genetic testing and pathologic examination was performed in a subset of familial PSP cases. RESULTS: Fifty-seven (33%) of the 172 patients with PSP had at least one first-degree relative who had dementia or parkinsonism compared to 131 (25%) of the control subjects (odds ratio [OR] 1.5, 95% confidence interval [CI] 1.01-2.13). In patients with PSP, more first-degree relatives with parkinsonism were observed compared to controls, with an OR 3.9 (95% CI 1.99-7.61). Twelve patients with PSP (7%) fulfilled the criteria for an autosomal dominant mode of transmission. The intrafamilial phenotype within these pedigrees varied among PSP, dementia, tremor, and parkinsonism. Genetic studies revealed one patient with a P301L mutation in MAPT. Pathologic examination of five familial cases confirmed the clinical diagnosis of PSP, with predominant four repeat tau pathology in affected brain areas. CONCLUSION: This study demonstrates familial aggregation of parkinsonism in progressive supranuclear palsy.

Distinct genetic forms of frontotemporal dementia.

BACKGROUND: Frontotemporal dementia (FTD) is the second most common type of presenile dementia and can be distinguished into various clinical variants. The identification of MAPT and GRN defects and the discovery of the TDP-43 protein in FTD have led to the classification of pathologic and genetic subtypes. In addition to these genetic subtypes, there exist familial forms of FTD with unknown genetic defects. METHODS: We investigated the frequency, demographic, and clinical data of patients with FTD with a positive family history in our prospective cohort of 364 patients. Genetic analysis of genes associated with FTD was performed on all patients with a positive family history. Immunohistochemical studies were carried out with a panel of antibodies (tau, ubiquitin, TDP-43) in brains collected at autopsy. RESULTS: In the total cohort of 364 patients, 27% had a positive family history suggestive for an autosomal mode of inheritance, including MAPT (11%) and GRN (6%) mutations. We identified a new Gln300X GRN mutation in a patient with a sporadic FTD. The mean age at onset in GRN patients (61.8 +/- 9.9 years) was higher than MAPT patients (52.4 +/- 5.9 years). In the remaining 10% of patients with suggestive autosomal dominant inheritance, the genetic defect has yet to be identified. Neuropathologically, this group can be distinguished into familial FTLD+MND and familial FTLD-U with hippocampal sclerosis. CONCLUSION: Future genetic studies need to identify genetic defects in at least two distinct familial forms of frontotemporal dementia (FTD) with unknown genetic defects: frontotemporal lobe degeneration with ubiquitin-positive inclusions with hippocampal sclerosis and frontotemporal lobe degeneration with motor neuron disease.

Screening for the fragile X syndrome among mentally retarded males by hair root analysis.

A noninvasive antibody test was used to identify male fragile X patients in special education schools, on the basis of the lack of FMRP in hair roots. We studied 300 males with mental retardation of unknown cause attending special schools. Patients were divided into two groups, based on the scores according to a fragile X check list (Group 1 /= 10 points). Group 2 consists of 51 males and only 5 males in this group showed no FMRP expression in hair roots within the abnormal range (91%). Fragile X diagnosis in these cases was confirmed by DNA analysis. None of the males scoring more than 10 on the check list was diagnosed positive for the fragile X syndrome using DNA analysis. With our antibody test on hair roots we did not detect a fragile X patient in Group 1. The FMRP antibody test on hair roots is suitable in a screening program for the fragile X syndrome among mentally retarded males attending special education schools.

Clinical and genetic correlate in childhood onset Friedreich ataxia.

We analyzed the clinical and genetic aspects of 28 FRDA patients from 20 families. 19 families were consanguineous. The onset was between 4 and 13 1/2 years of age (mean 15.4 +/- 6.2). Three patients presented with cardiomyopathy, one with weakness, and the rest with ataxia. There were two patients with preserved lower-limb deep tendon reflexes. Sensory nerve action potentials were reduced in 14/14 patients. Cardiac echograms were abnormal in 17/19 cases, and this was between 6 and 16 years of age (mean 10.1 +/- 3.5). Four families were multiplex. Clinical intra-familial variability was observed. Increased GAA repeats of the X25 gene were found in 27/28 patients studied, all in a homozygous state. 88.9% of patients had a smaller allele larger than 500 repeats, and 66.7% had more than 700 repeats. The patient who did not have increased GAA repeats in both alleles had peculiar findings. Significant correlation of expansion was obtained for the early onset, and cardiomyopathy as the onset.

Noninvasive test for fragile X syndrome, using hair root analysis.

Identification of the FMR1 gene and the repeat-amplification mechanism causing fragile X syndrome led to development of reliable DNA-based diagnostic methods, including Southern blot hybridization and PCR. Both methods are performed on DNA isolated from peripheral blood cells and measure the repeat size in FMR1. Using an immunocytochemical technique on blood smears, we recently developed a novel test for identification of patients with fragile X syndrome. This method, also called "antibody test," uses monoclonal antibodies against the FMR1 gene product (FMRP) and is based on absence of FMRP in patients' cells. Here we describe a new diagnostic test to identify male patients with fragile X syndrome, on the basis of lack of FMRP in their hair roots. Expression of FMRP in hair roots was studied by use of an FMRP-specific antibody test, and the percentage of FMRP-expressing hair roots in controls and in male fragile X patients was determined. Control individuals showed clear expression of FMRP in nearly every hair root, whereas male fragile X patients lacked expression of FMRP in almost all their hair roots. Mentally retarded female patients with a full mutation showed FMRP expression in only some of their hair roots (<55%), and no overlap with normal female controls was observed. The advantages of this test are (1) plucking of hair follicles does no appreciable harm to the mentally retarded patient, (2) hairs can be sent in a simple envelope to a diagnostic center, and (3) the result of the test is available within 5 h of plucking. In addition, this test enabled us to identify two fragile X patients who did not show the full mutation by analysis of DNA isolated from blood cells.

Different targets for the fragile X-related proteins revealed by their distinct nuclear localizations.

Fragile X syndrome is caused by the absence of the fragile X mental retardation protein (FMRP). FMRP and its structural homologues FXR1P and FXR2P form a family of RNA-binding proteins (FXR proteins). The three proteins associate with polyribosomes as cytoplasmic mRNP particles. Here we show that small amounts of FMRP, FXR1P and FXR2P shuttle between cytoplasm and nucleus. Mutant FMRP of a severely affected fragile X patient (FMRPI304N) does not associate with polyribosomes and shuttles more frequently than normal FMRP, indicating that the association with polyribosomes regulates the shuttling process. Using leptomycin B we demonstrate that transport of the FXR proteins out of the nucleus is mediated by the export receptor exportin1. Finally, inactivation of the nuclear export signal in two FXR proteins shows that FMRP shuttles between cytoplasm and nucleoplasm, while FXR2P shuttles between cytoplasm and nucleolus. Therefore, molecular dissection of the shuttling routes used by the FXR proteins suggests that they transport different RNAs.

Association of the 677C-->T mutation on the methylenetetrahydrofolate reductase gene in Turkish patients with neural tube defects.

We report the analysis of the 677C-->T mutation on the 5, 10-methylenetetrahydrofolate reductase gene in Turkish controls and cases of neural tube defects. Mutation analysis of 91 patients with neural tube defects, 72 mothers, 63 fathers, and 93 healthy controls has been made by polymerase chain reaction and allele specific restriction digestion with Hinf I. We did not find a significant difference in the 677C-->T allele and genotype distribution among the patients with neural tube defects, their parents, and the control group. This result suggests that another mutation in the folate-related enzyme genes could be responsible for neural tube defects in Turkey. None of the mothers of patients with neural tube defects was advised to use folic acid as recommended to prevent neural tube defects. An immediate attempt to establish an education program for healthcare providers and women of childbearing age is crucial in Turkey. Furthermore, fortification of foods with folate would be a better approach.

Angiotensin converting enzyme gene polymorphism and the risk and extent of ischemic heart disease among Turkish patients.

OBJECTIVE: To evaluate the effects of the angiotensin converting enzyme gene polymorphism on the presence and extent of coronary artery disease and myocardial infarction among Turkish patients. METHODS: In total 393 consecutive patients undergoing coronary angiography were evaluated for cardiac risk factors including the lipoprotein profile, lipoprotein (a), apoprotein B, and apoprotein A1 levels. The angiotensin converting enzyme genotype was determined by polymerase chain reaction. The extent of coronary atherosclerosis was determined from the angiograms using the Gensini and Leaman scores. RESULTS: The angiotensin converting enzyme genotype was found not to be associated either with coronary artery disease (odds ratio 0.81, P > 0.05) or with myocardial infarction (odds ratio 1.16, P > 0.05). Exclusion of high-risk individuals failed to reveal any association for these subgroups. Furthermore, there was no association between aneurysm formation and the genotype (P > 0.05). The lipid parameters were also not affected by the genotype (P > 0.05). However, the extent of coronary atherosclerosis determined by the Gensini score was related significantly to the genotype by multivariate analysis (P = 0.007). CONCLUSION: The DD genotype is not associated with coronary artery disease and myocardial infarction among these angiographically assessed Turkish patients, even when low-risk subgroups are analysed. Nonetheless, the extent of coronary atherosclerosis in patients with coronary artery disease is affected by their genotype.