1.Saccharification of Sugarcane Bagasse by Enzymatic Treatment for bioethanol production
Firoz Md. Ahmed ; Sabita Rezwana Rahman ; Donald James Gomes
Malaysian Journal of Microbiology 2012;8(2):97-103
Aims: The escalating demands for traditional fossil fuels with unsecured deliverance and issues of climate change
compel the researchers to develop alternative fuels like bioethanol. This study examines the prospect of biofuel
production from high carbohydrate containing lignocellulosic material, e.g. sugarcane bagasse through biological means.
Methodology and Results: Cellulolytic enzymes were collected from the culture filtrate of thermotolerant Trichoderma viride grown on variously pre-treated sugarcane bagasse. CMCase and FPase enzyme activities were determined as a measure of suitable substrate pre-treatment and optimum condition for cellulolytic enzyme production. The highest CMCase and FPase activity was found to be 1.217 U/ml and 0.109 U/ml respectively under the production conditions of 200 rpm, pH 4.0 and 50 °C using steamed NaOH treated bagasse as substrate. SEM was carried out to compare and confirm the activity of cellulolytic enzymes on sugarcane bagasse. Saccharification of pre-treated bagasse was carried
out with crude enzymes together using a two-factor experimental design. Under optimized conditions the pre-treated bagasse was saccharified up to 42.7 % in 24 h. The hydrolysate was concentrated by heating to suitable concentration and then used for fermentation by an indigenous isolate of Saccharomyces cerevisiae. With 50 and 80 % brix containing liquor the concentration of alcohol was 0.579 % and 1.15 % respectively.
Conclusion, significance and impact of study: This is the first report in Bangladesh for the production of cellulosic
ethanol using local isolates. Though the rate of alcohol production was very low, a great impetus in this field can
maximize the production thereby meet the demand for fuel in future.
2.Is It Cost Effective to Obtain Fungal and Acid-Fast Bacillus Cultures during Spine Debridement?
Mark J. LAMBRECHTS ; Devin D. St. CLAIR ; Jinpu LI ; James L. COOK ; Bradley S. SPENCE ; Emily V. LEARY ; Theodore J. CHOMA ; Donald K. MOORE ; Christina L. GOLDSTEIN
Asian Spine Journal 2022;16(4):519-525
Methods:
A retrospective review of medical record data from patients undergoing spine irrigation and debridement (I&D) at the University of Missouri over a 10-year period was performed.
Results:
For patients undergoing spine I&D, there was a 4% incidence of fungal infection and 0.49% rate of AFB infection. Steroid use was associated with a higher likelihood (odds ratio, 5.62; 95% confidence interval, 1.33–23.75) of positive fungal or AFB cultures. Although not significant, patients undergoing multiple I&D procedures had higher rates of positive fungal cultures during each subsequent I&D. Over a 10-year period, if fungal cultures are obtained for each patient, it would cost our healthcare system $12,151.58. This is compared to an average cost of $177,297.64 per missed fungal infection requiring subsequent treatment.
Conclusions
Spine fungal infections occur infrequently at a rate of 4%. Physicians should strongly consider obtaining samples for fungal cultures in patients undergoing spine I&D, especially those using steroids and those undergoing multiple I&Ds. Our AFB culture rates mirror the false positive rates seen in previous orthopedic literature. It is unlikely to be cost effective to send for AFB cultures in areas with low endemic rates of AFB.
3.Cortical Thinning in High-Grade Asymptomatic Carotid Stenosis
Randolph S. MARSHALL ; David S. LIEBESKIND ; John Huston III ; Lloyd J. EDWARDS ; George HOWARD ; James F. MESCHIA ; Thomas G. BROTT ; Brajesh K. LAL ; Donald HECK ; Giuseppe LANZINO ; Navdeep SANGHA ; Vikram S. KASHYAP ; Clarissa D. MORALES ; Dejania COTTON-SAMUEL ; Andres M. RIVERA ; Adam M. BRICKMAN ; Ronald M. LAZAR
Journal of Stroke 2023;25(1):92-100
Background:
and Purpose High-grade carotid artery stenosis may alter hemodynamics in the ipsilateral hemisphere, but consequences of this effect are poorly understood. Cortical thinning is associated with cognitive impairment in dementia, head trauma, demyelination, and stroke. We hypothesized that hemodynamic impairment, as represented by a relative time-to-peak (TTP) delay on MRI in the hemisphere ipsilateral to the stenosis, would be associated with relative cortical thinning in that hemisphere.
Methods:
We used baseline MRI data from the NINDS-funded Carotid Revascularization and Medical Management for Asymptomatic Carotid Stenosis–Hemodynamics (CREST-H) study. Dynamic contrast susceptibility MR perfusion-weighted images were post-processed with quantitative perfusion maps using deconvolution of tissue and arterial signals. The protocol derived a hemispheric TTP delay, calculated by subtraction of voxel values in the hemisphere ipsilateral minus those contralateral to the stenosis.
Results:
Among 110 consecutive patients enrolled in CREST-H to date, 45 (41%) had TTP delay of at least 0.5 seconds and 9 (8.3%) subjects had TTP delay of at least 2.0 seconds, the maximum delay measured. For every 0.25-second increase in TTP delay above 0.5 seconds, there was a 0.006-mm (6 micron) increase in cortical thickness asymmetry. Across the range of hemodynamic impairment, TTP delay independently predicted relative cortical thinning on the side of stenosis, adjusting for age, sex, hypertension, hemisphere, smoking history, low-density lipoprotein cholesterol, and preexisting infarction (P=0.032).
Conclusions
Our findings suggest that hemodynamic impairment from high-grade asymptomatic carotid stenosis may structurally alter the cortex supplied by the stenotic carotid artery.
4.Absence of Glia Maturation Factor Protects from Axonal Injury and Motor Behavioral Impairments after Traumatic Brain Injury
Govindhasamy Pushpavathi SELVAKUMAR ; Mohammad Ejaz AHMED ; Shankar S. IYER ; Ramasamy THANGAVEL ; Duraisamy KEMPURAJ ; Sudhanshu P. RAIKWAR ; Kieran BAZLEY ; Kristopher WU ; Asher KHAN ; Klaudia KUKULKA ; Bret BUSSINGER ; Smita ZAHEER ; Casey BURTON ; Donald JAMES ; Asgar ZAHEER
Experimental Neurobiology 2020;29(3):230-248
Traumatic brain injury (TBI) causes disability and death, accelerating the progression towards Alzheimer’s disease and Parkinson’s disease (PD). TBI causes serious motor and cognitive impairments, as seen in PD that arise during the period of the initial insult. However, this has been understudied relative to TBI induced neuroinflammation, motor and cognitive decline that progress towards PD. Neuronal ubiquitin-C-terminal hydrolase- L1 (UCHL1) is a thiol protease that breaks down ubiquitinated proteins and its level represents the severity of TBI. Previously, we demonstrated the molecular action of glia maturation factor (GMF); a proinflammatory protein in mediating neuroinflammation and neuronal loss. Here, we show that the weight drop method induced TBI neuropathology using behavioral tests, western blotting, and immunofluorescence techniques on sections from wild type (WT) and GMF-deficient (GMF-KO) mice. Results reveal a significant improvement in substantia nigral tyrosine hydroxylase and dopamine transporter expression with motor behavioral performance in GMF-KO mice following TBI. In addition, a significant reduction in neuroinflammation was manifested, as shown by activation of nuclear factor-kB, reduced levels of inducible nitric oxide synthase, and cyclooxygenase- 2 expressions. Likewise, neurotrophins including brain-derived neurotrophic factor and glial-derived neurotrophic factor were significantly improved in GMF-KO mice than WT 72 h post-TBI. Consistently, we found that TBI enhances GFAP and UCHL-1 expression and reduces the number of dopaminergic TH-positive neurons in WT compared to GMF-KO mice 72 h post-TBI. Interestingly, we observed a reduction of THpositive tanycytes in the median eminence of WT than GMF-KO mice. Overall, we found that absence of GMF significantly reversed these neuropathological events and improved behavioral outcome. This study provides evidence that PD-associated pathology progression can be initiated upon induction of TBI.
5.Male Oxidative Stress Infertility (MOSI): Proposed Terminology and Clinical Practice Guidelines for Management of Idiopathic Male Infertility
Ashok AGARWAL ; Neel PAREKH ; Manesh Kumar PANNER SELVAM ; Ralf HENKEL ; Rupin SHAH ; Sheryl T HOMA ; Ranjith RAMASAMY ; Edmund KO ; Kelton TREMELLEN ; Sandro ESTEVES ; Ahmad MAJZOUB ; Juan G ALVAREZ ; David K GARDNER ; Channa N JAYASENA ; Jonathan W RAMSAY ; Chak Lam CHO ; Ramadan SALEH ; Denny SAKKAS ; James M HOTALING ; Scott D LUNDY ; Sarah VIJ ; Joel MARMAR ; Jaime GOSALVEZ ; Edmund SABANEGH ; Hyun Jun PARK ; Armand ZINI ; Parviz KAVOUSSI ; Sava MICIC ; Ryan SMITH ; Gian Maria BUSETTO ; Mustafa Emre BAKIRCIOĞLU ; Gerhard HAIDL ; Giancarlo BALERCIA ; Nicolás Garrido PUCHALT ; Moncef BEN-KHALIFA ; Nicholas TADROS ; Jackson KIRKMAN-BROWNE ; Sergey MOSKOVTSEV ; Xuefeng HUANG ; Edson BORGES ; Daniel FRANKEN ; Natan BAR-CHAMA ; Yoshiharu MORIMOTO ; Kazuhisa TOMITA ; Vasan Satya SRINI ; Willem OMBELET ; Elisabetta BALDI ; Monica MURATORI ; Yasushi YUMURA ; Sandro LA VIGNERA ; Raghavender KOSGI ; Marlon P MARTINEZ ; Donald P EVENSON ; Daniel Suslik ZYLBERSZTEJN ; Matheus ROQUE ; Marcello COCUZZA ; Marcelo VIEIRA ; Assaf BEN-MEIR ; Raoul ORVIETO ; Eliahu LEVITAS ; Amir WISER ; Mohamed ARAFA ; Vineet MALHOTRA ; Sijo Joseph PAREKATTIL ; Haitham ELBARDISI ; Luiz CARVALHO ; Rima DADA ; Christophe SIFER ; Pankaj TALWAR ; Ahmet GUDELOGLU ; Ahmed M A MAHMOUD ; Khaled TERRAS ; Chadi YAZBECK ; Bojanic NEBOJSA ; Damayanthi DURAIRAJANAYAGAM ; Ajina MOUNIR ; Linda G KAHN ; Saradha BASKARAN ; Rishma Dhillon PAI ; Donatella PAOLI ; Kristian LEISEGANG ; Mohamed Reza MOEIN ; Sonia MALIK ; Onder YAMAN ; Luna SAMANTA ; Fouad BAYANE ; Sunil K JINDAL ; Muammer KENDIRCI ; Baris ALTAY ; Dragoljub PEROVIC ; Avi HARLEV
The World Journal of Men's Health 2019;37(3):296-312
Despite advances in the field of male reproductive health, idiopathic male infertility, in which a man has altered semen characteristics without an identifiable cause and there is no female factor infertility, remains a challenging condition to diagnose and manage. Increasing evidence suggests that oxidative stress (OS) plays an independent role in the etiology of male infertility, with 30% to 80% of infertile men having elevated seminal reactive oxygen species levels. OS can negatively affect fertility via a number of pathways, including interference with capacitation and possible damage to sperm membrane and DNA, which may impair the sperm's potential to fertilize an egg and develop into a healthy embryo. Adequate evaluation of male reproductive potential should therefore include an assessment of sperm OS. We propose the term Male Oxidative Stress Infertility, or MOSI, as a novel descriptor for infertile men with abnormal semen characteristics and OS, including many patients who were previously classified as having idiopathic male infertility. Oxidation-reduction potential (ORP) can be a useful clinical biomarker for the classification of MOSI, as it takes into account the levels of both oxidants and reductants (antioxidants). Current treatment protocols for OS, including the use of antioxidants, are not evidence-based and have the potential for complications and increased healthcare-related expenditures. Utilizing an easy, reproducible, and cost-effective test to measure ORP may provide a more targeted, reliable approach for administering antioxidant therapy while minimizing the risk of antioxidant overdose. With the increasing awareness and understanding of MOSI as a distinct male infertility diagnosis, future research endeavors can facilitate the development of evidence-based treatments that target its underlying cause.
Antioxidants
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Classification
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Clinical Protocols
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Diagnosis
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DNA
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Embryonic Structures
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Female
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Fertility
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Health Expenditures
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Humans
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Infertility
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Infertility, Male
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Male
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Membranes
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Ovum
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Oxidants
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Oxidation-Reduction
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Oxidative Stress
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Reactive Oxygen Species
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Reducing Agents
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Reproductive Health
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Semen
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Spermatozoa
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Subject Headings
6.Exogenous phosphatidic acid reduces acetaminophen-induced liver injury in mice by activating hepatic interleukin-6 signaling through inter-organ crosstalk.
Melissa M CLEMENS ; Stefanie KENNON-MCGILL ; Joel H VAZQUEZ ; Owen W STEPHENS ; Erich A PETERSON ; Donald J JOHANN ; Felicia D ALLARD ; Eric U YEE ; Sandra S MCCULLOUGH ; Laura P JAMES ; Brian N FINCK ; Mitchell R MCGILL
Acta Pharmaceutica Sinica B 2021;11(12):3836-3846
We previously demonstrated that endogenous phosphatidic acid (PA) promotes liver regeneration after acetaminophen (APAP) hepatotoxicity. Here, we hypothesized that exogenous PA is also beneficial. To test that, we treated mice with a toxic APAP dose at 0 h, followed by PA or vehicle (Veh) post-treatment. We then collected blood and liver at 6, 24, and 52 h. Post-treatment with PA 2 h after APAP protected against liver injury at 6 h, and the combination of PA and