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91.
92.
Nur Jannah Abdul Hamid Aeslina Abdul Kadir Nurul Nabila Huda Hashar Pawe Pietrusiewicz Marcin Nabiaek Izabela Wnuk Marcek Gucwa Pawe Palutkiewicz Azini Amiza Hashim Noor Amira Sarani Amos Anak Nio Norazian Mohamed Noor Bartomiej Jez 《Materials》2021,14(11)
Wastewater treatment activities in the chemical industry have generated abundant gypsum waste, classified as scheduled waste (SW205) under the Environmental Quality Regulations 2005. The waste needs to be disposed into a secure landfill due to the high heavy metals content which is becoming a threat to the environment. Hence, an alternative disposal method was evaluated by recycling the waste into fired clay brick. The brick samples were incorporated with different percentages of gypsum waste (0% as control, 10, 20, 30, 40 and 50%) and were fired at 1050 °C using 1 °C per minute heating rate. Shrinkage, dry density, initial rate of suction (IRS) and compressive strength tests were conducted to determine the physical and mechanical properties of the brick, while the synthetic precipitation leaching procedure (SPLP) was performed to scrutinize the leachability of heavy metals from the crushed brick samples. The results showed that the properties would decrease through the incorporation of gypsum waste and indicated the best result at 10% of waste utilization with 47.5% of shrinkage, 1.37% of dry density, 22.87% of IRS and 28.3% of compressive strength. In addition, the leachability test highlighted that the concentrations of Fe and Al was significantly reduced up to 100% from 4884 to 3.13 ppm (Fe) and from 16,134 to 0.81 ppm (Al), respectively. The heavy metals content in the bricks were oxidized during the firing process, which signified the successful remediation of heavy metals in the samples. Based on the permissible incorporation of gypsum waste into fired clay brick, this study promised a more green disposing method for gypsum waste, and insight as a potential towards achieving a sustainable end product. 相似文献
93.
Dwornik M Białoszewski D Korabiewska I Wroński Z 《Ortopedia, traumatologia, rehabilitacja》2007,9(2):111-121
Neuro mobilization is a method of conservative treatment of disorders of neural tissue. The rationale for using neuro mobilization in the treatment of musculoskeletal conditions is based on in vivo and in vitro studies which point to a high efficacy of neuro mobilization procedures. Appropriate use of neuro mobilization procedures depends on excellent knowledge of normal and pathological anatomy, differences between individual etiological factors, development of disease and symptom variability. The present paper familiarizes the reader with evidence-based conservative treatment of musculoskeletal conditions by neuro mobilization. 相似文献
94.
Angshuman Maulik Sean M. Davidson Izabela Piotrowska Malcolm Walker Derek M. Yellon 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》2018,32(3):245-253
Purpose
Anthracyclines cause chronic irreversible cardiac failure, but the mechanism remains poorly understood. Emerging data indicate that cardiac damage begins early, suggesting protective modalities delivered in the acute stage may confer prolonged benefit. Ischaemic preconditioning (IPC) activates the pro-survival reperfusion injury salvage kinase (RISK) pathway which involves PI3-kinase and MAPK/ERK1/2.Methods
We investigated whether simulated IPC (sIPC), in the form of a sublethal exposure to a hypoxic buffer simulating ischaemic conditions followed by reoxygenation, protects primary adult rat cardiomyocytes against anthracycline-induced injury. PI3-kinase and MAPK/ERK1/2 were inhibited using LY294002, and PD98059. The role of reactive oxygen species (ROS), mitochondrial membrane potential (Δψm) and mitochondrial permeability transition pore (mPTP) were also investigated in doxorubicin-treated cells. We further examined whether sIPC protected HeLa cancer cells from doxorubicin-induced death.Results
sIPC protected cardiomyocytes against doxorubicin-induced death (35.4?±?1.7% doxorubicin vs 14.7?±?1.5% doxorubicin + sIPC; p?<?0.01). This protection was abrogated by the PI3-kinase inhibitor, LY294002, but not the MAPK/ERK1/2 inhibitor, PD98059. A ROS scavenger failed to rescue cardiomyocytes from doxorubicin toxicity, and no significant influence on Δψm or mPTP opening was identified after subjecting cells to a doxorubicin insult. Importantly, sIPC did not protect HeLa cancer cells from doxorubicin-induced death.Conclusion
sIPC is able to protect cardiomyocytes against anthracycline injury via a pathway involving PI3-kinase. This mechanism appears to be independent of ROS, changes to Δψm, and mPTP. Further investigation of the mechanism of sIPC-induced protection against anthracycline-injury is warranted.95.
Buyandelger B Ng KE Miocic S Piotrowska I Gunkel S Ku CH Knöll R 《Pflügers Archiv : European journal of physiology》2011,462(1):135-142
Muscle LIM protein (MLP, also known as cysteine rich protein 3 (CSRP3, CRP3)) is a muscle-specific-expressed LIM-only protein.
It consists of 194 amino-acids and has been described initially as a factor involved in myogenesis (Arber et al. Cell 79:221–231,
1994). MLP soon became an important model for experimental cardiology when it was first demonstrated that MLP deficiency leads
to myocardial hypertrophy followed by a dilated cardiomyopathy and heart failure phenotype (Arber et al. Cell 88:393–403,
1997). At this time, this was the first genetically altered animal model to develop this devastating disease. Interestingly, MLP
was also found to be down-regulated in humans with heart failure (Zolk et al. Circulation 101:2674–2677, 2000) and MLP mutations are able to cause hypertrophic and dilated forms of cardiomyopathy in humans (Bos et al. Mol Genet Metab
88:78–85, 2006; Geier et al. Circulation 107:1390–1395, 2003; Hershberger et al. Clin Transl Sci 1:21–26, 2008; Kn?ll et al. Cell 111:943–955, 2002; Kn?ll et al. Circ Res 106:695–704, 2010; Mohapatra et al. Mol Genet Metab 80:207–215, 2003). Although considerable efforts have been undertaken to unravel the underlying molecular mechanisms—how MLP mutations, either
in model organisms or in the human setting cause these diseases are still unclear. In contrast, only precise knowledge of
the underlying molecular mechanisms will allow the development of novel and innovative therapeutic strategies to combat this
otherwise lethal condition. The focus of this review will be on the function of MLP in cardiac mechanosensation and we shall
point to possible future directions in MLP research. 相似文献
96.
Pawel Mierzejewski Agnieszka Korkosz Artur Rogowski Izabela Korkosz Wojciech Kostowski Anna Scinska 《Progress in neuro-psychopharmacology & biological psychiatry》2009
A large body of evidence indicates that reactivation of aversive memories leads to protein synthesis-dependent memory reconsolidation which can be disrupted by cycloheximide (CHX) and other protein synthesis inhibitors. The aim of the present study was to investigate whether CHX would alter maintenance of well-trained instrumental responding for 0.1% saccharin. Male Wistar rats were trained to lever press for saccharin. When lever pressing stabilized, experimental self-administration sessions with CHX (3 mg/kg, s.c.) started. The animals received four experimental sessions, with each session separated by 5 days. The protein synthesis inhibitor was injected immediately after the experimental sessions 1–3. Repeated post-session injections of CHX did not alter saccharin self-administration. A two-bottle choice test conducted after the last experimental session revealed that CHX had not induced any conditioned taste aversion to 0.1% saccharin. The present results suggest that well-consolidated long-term memory of an appetitive instrumental task does not depend on de novo protein synthesis. 相似文献
97.
Domysławska I Ciołkiewicz M Kowal-Bielecka O Lewszuk A Klimiuk PA Sierakowski S 《Polskie Archiwum Medycyny Wewn?trznej》2007,117(8):370-373
Systemic sclerosis (SSc) is characterized by immunological disturbances, vascular damage and overproduction of extracellular matrix by stimulated fibroblasts. It has been postulated that immunological reactions involved in the pathogenesis of SSc may promote the development of malignancies. Coexistence of this disease with neoplasmatic processes is relatively frequent. In our report we describe a case a 54-year-old woman with scleroderma-like syndrome, which has preceded the occurrence of idiopathic myelofibrosis by many years. Owing to multiple repeated diagnostic tests we managed to diagnose this disease at the early stage, which enabled effective therapy with remission of blood dyscrasia as well as inhibition of skin lesions and lung fibrosis. 相似文献
98.
Intraneuronal Aβ immunoreactivity is not a predictor of brain amyloidosis-β or neurofibrillary degeneration 总被引:3,自引:3,他引:0
Wegiel J Kuchna I Nowicki K Frackowiak J Mazur-Kolecka B Imaki H Wegiel J Mehta PD Silverman WP Reisberg B Deleon M Wisniewski T Pirttilla T Frey H Lehtimäki T Kivimäki T Visser FE Kamphorst W Potempska A Bolton D Currie JR Miller DL 《Acta neuropathologica》2007,113(4):389-402
Amyloid β (Aβ) immunoreactivity in neurons was examined in brains of 32 control subjects, 31 people with Down syndrome, and
36 patients with sporadic Alzheimer’s disease to determine if intraneuronal Aβ immunoreactivity is an early manifestation
of Alzheimer-type pathology leading to fibrillar plaque formation and/or neurofibrillary degeneration. The appearance of Aβ
immunoreactivity in neurons in infants and stable neuron-type specific Aβ immunoreactivity in a majority of brain structures
during late childhood, adulthood, and normal aging does not support this hypothesis. The absence or detection of only traces
of reaction with antibodies against 4–13 aa and 8–17 aa of Aβ in neurons indicated that intraneuronal Aβ was mainly a product
of α- and γ-secretases (Aβ17–40/42). The presence of N-terminally truncated Aβ17–40 and Aβ17–42 in the control brains was confirmed by Western blotting and the identity of Aβ17–40 was confirmed by mass spectrometry. The prevalence of products of α- and γ -secretases in neurons and β- and γ-secretases
in plaques argues against major contribution of Aβ-immunopositive material detected in neuronal soma to amyloid deposit in
plaques. The strongest intraneuronal Aβ17–42 immunoreactivity was observed in structures with low susceptibility to fibrillar Aβ deposition, neurofibrillary degeneration,
and neuronal loss compared to areas more vulnerable to Alzheimer-type pathology. These observations indicate that the intraneuronal
Aβ immunoreactivity detected in this study is not a predictor of brain amyloidosis or neurofibrillary degeneration. The constant
level of Aβ immunoreactivity in structures free from neuronal pathology during essentially the entire life span suggests that
intraneuronal amino-terminally truncated Aβ represents a product of normal neuronal metabolism.
This study was supported in part by funds from the New York State Office of Mental Retardation and Developmental Disabilities
and grants from the National Institutes of Health (The National Institute of Child Health and Human Development R01 HD43960
and PO1 HD35897; and the National Institute of Aging P30 AG08051, AG03051, and PO1 AG11531). 相似文献
99.
Anna Scinska Lukasz Swiecicki Izabela Korkosz Pawel Mierzejewski Marcin Kolaczkowski 《Neuroscience letters》2009
It is assumed that depressive symptomatology can alter taste preferences in humans. The aim of the present study was to search for correlations between immobility in the tail suspension test (TST) and consumption of saccharin (0.0025–0.1%, w/w) and quinine (0.0024–0.04%) solutions. Male C57BL/6J mice were divided into high immobility and low immobility groups based on their immobility scores in the TST. The groups consumed similar amounts of saccharin solutions in the two-bottle choice test. There were significant differences between the groups in quinine intake and preference. Intake of, and preference for, 0.0024% quinine was significantly higher in the high immobility than in low immobility subjects. In line with some animal and human studies, our results suggest that behavioral despair in the TST can correlate with taste responses to bitter stimuli. 相似文献
100.