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21.
P. L. Deshmukh 《BMJ (Clinical research ed.)》1950,1(4658):905-906
22.
T. R. Deshmukh A. M. Kuthe S. M. Chaware V. Bagaria D. S. Ingole 《Computer methods in biomechanics and biomedical engineering》2013,16(4):363-370
Objective: The objective of this study was to fabricate a successful implant for temporomandibular joint (TMJ) disorder patients who could not be treated through conventional surgeries. Methods: A custom-made implant was fabricated using rapid prototyping (RP) for the TMJ surgery. The stability of the metallic implant was validated using a finite element analysis. Results: The results of finite elements were stable and the design of the TMJ implant was suitable as per the patient's need. The customised implant was made using a fused deposition modelling method of RP and a vertical machining centre. The implant has provided normal jaw function for over 2 years since surgery. Conclusions: The approach utilised will be helpful in providing successful treatment to the deformed mandible and the mandible joints. This method allows to customise and to accurately fabricatie the implant. Advantages of this approach are that the physical model of the implant was tested for stability before the implantation, the surgeon can plan and rehearse the surgery in advance, it is a less invasive and less time-consuming surgical procedure. 相似文献
23.
24.
V KW Wong T Li B YK Law E DL Ma N C Yip F Michelangeli C KM Law M M Zhang K YC Lam P L Chan L Liu 《Cell death & disease》2013,4(7):e720
Autophagy is an important cellular process that controls cells in a normal homeostatic state by recycling nutrients to maintain cellular energy levels for cell survival via the turnover of proteins and damaged organelles. However, persistent activation of autophagy can lead to excessive depletion of cellular organelles and essential proteins, leading to caspase-independent autophagic cell death. As such, inducing cell death through this autophagic mechanism could be an alternative approach to the treatment of cancers. Recently, we have identified a novel autophagic inducer, saikosaponin-d (Ssd), from a medicinal plant that induces autophagy in various types of cancer cells through the formation of autophagosomes as measured by GFP-LC3 puncta formation. By computational virtual docking analysis, biochemical assays and advanced live-cell imaging techniques, Ssd was shown to increase cytosolic calcium level via direct inhibition of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase pump, leading to autophagy induction through the activation of the Ca2+/calmodulin-dependent kinase kinase–AMP-activated protein kinase–mammalian target of rapamycin pathway. In addition, Ssd treatment causes the disruption of calcium homeostasis, which induces endoplasmic reticulum stress as well as the unfolded protein responses pathway. Ssd also proved to be a potent cytotoxic agent in apoptosis-defective or apoptosis-resistant mouse embryonic fibroblast cells, which either lack caspases 3, 7 or 8 or had the Bax-Bak double knockout. These results provide a detailed understanding of the mechanism of action of Ssd, as a novel autophagic inducer, which has the potential of being developed into an anti-cancer agent for targeting apoptosis-resistant cancer cells. 相似文献
25.
Anne-Marie Lundsgaard Jacob B. Holm Kim A. Sjøberg Kirstine N. Bojsen-Møller Lene S. Myrmel Even Fjære Benjamin A.H. Jensen Trine S. Nicolaisen Janne R. Hingst Sine L. Hansen Sophia Doll Philip E. Geyer Atul S. Deshmukh Jens J. Holst Lise Madsen Karsten Kristiansen Jørgen F.P. Wojtaszewski Erik A. Richter Bente Kiens 《Cell metabolism》2019,29(1):50-63.e4
26.
In the mid 1980s, it was observed that photosynthesis could still occur in the absence of the diffusible electron carrier
cytochrome c
2 in the purple non-sulfur facultative phototrophic bacterium Rhodobacter capsulatus. This serendipic finding led to the discovery of a novel class of membrane-anchored electron carrier cytochromes and their
associated electron transfer pathways. Studies of cytochrome c
y of R. capsulatus (and its homologues in other species) have modified the previous dogma of electron transfer between photosynthetic and respiratory
membrane protein complexes with a new paradigm, in which these proteins and their electron carriers can form `hard-wired'
structural super-complexes. Here, we reminisce on the early days of this discovery, its impacts on our understanding of cellular
energy transduction pathways and the physiological roles played by the electron carrier cytochromes c, and discuss the current knowledge and emerging future challenges of this field.
This revised version was published online in August 2006 with corrections to the Cover Date. 相似文献
27.
Ro60 peptides induce antibodies to similar epitopes shared among lupus-related autoantigens 总被引:1,自引:0,他引:1
Deshmukh US Lewis JE Gaskin F Dhakephalkar PK Kannapell CC Waters ST Fu SM 《Journal of immunology (Baltimore, Md. : 1950)》2000,164(12):6655-6661
The coexistence of autoantibodies to ribonucleoproteins (RNP) in sera of patients with systemic lupus erythematosus has been attributed to intermolecular determinant spreading among physically associated proteins. Recently, we showed that murine Ab responses to rRo60 or Ro60 peptides were diversified unexpectedly to small nuclear RNP. In this investigation, the mechanisms for this autoantibody diversification were examined. Intramolecular determinant spreading was demonstrated in mice immunized with human or mouse Ro60316-335. Immune sera depleted of anti-peptide Ab immunoprecipitated Ro60-associated mY1 and mY3 RNA and remained reactive to a determinant on Ro60128-285. Absorption with the immunogen depleted the immune sera completely of anti-Golgi complex Ab (inducible only with human Ro60316-335) and anti-La Ab, and reduced substantially Ab to SmD and 70-kDa U1RNP. Mouse rRo60 completely inhibited the immune sera reactivity to La, SmD, and 70-kDa U1RNP. However, La, SmD, and 70-kDa U1RNP preferentially inhibited the antiserum reactivities to these Ags, respectively. Affinity-purified anti-La Ab were reactive with Ro60, La, SmD, and 70-kDa U1RNP. These results provide evidence that a population of the induced autoantibodies recognized determinants shared by these autoantigens. Lack of sequence homology between Ro60316-335 and La, SmD, or 70-kDa U1RNP suggests that these determinants are conformational. Interestingly, similar cross-reactive autoantibodies were found in NZB/NZW F1 sera. Thus, a single molecular mimic may generate Ab to multiple RNP Ags. Furthermore, cross-reactive determinants shared between antigenic systems that are not associated physically (Ro/La RNP and small nuclear RNP) may be important in the generation of autoantibody diversity in systemic lupus erythematosus. 相似文献
28.
During development, neurons are acutely dependent on target-derived trophic factors for survival. This dependence on trophic support decreases dramatically with maturation in several neuronal populations, including sympathetic neurons. Analyses of nerve growth factor deprivation in immature and mature sympathetic neurons indicate that maturation aborts the cell death pathway at a point that is mechanistically indistinguishable from Bax deletion. However, neither the mRNA nor protein level of BAX changes with neuronal maturation. Therefore, BAX must be regulated posttranslationally in mature neurons.Nerve growth factor deprivation in immature sympathetic neurons induces two parallel processes: (a) a protein synthesis-dependent, caspase-independent translocation of BAX from the cytosol to mitochondria, followed by mitochondrial membrane integration and loss of cytochrome c; and (b) the development of competence-to-die, which requires neither macromolecular synthesis nor BAX expression. Activation of both signaling pathways is required for caspase activation and apoptosis in immature sympathetic neurons. In contrast, nerve growth factor withdrawal in mature sympathetic neurons did not induce the translocation of either BAX or cytochrome c. Moreover, mature neurons did not develop competence-to-die with cytoplasmic accumulation of cytochrome c. Therefore, inhibition of both BAX-dependent cytochrome c release and the development of competence-to-die contributed to the loss of trophic factor dependence associated with neuronal maturation. 相似文献
29.
A M Mujumdar J N Dhuley V K Deshmukh P H Raman S L Thorat S R Naik 《Indian journal of experimental biology》1990,28(5):486-487
Piperine (1-peperoyl piperidine), a major alkaloid isolated from Piper nigrum Linn, potentiated pentobarbitone sleeping time in dose dependant manner, with peak effect at 30 min. Blood and brain pentobarbitone levels were higher in piperine treated animals. Piperine treatment in rats, treated chronically with phenobarbitone, significantly potentiated pentobarbitone sleeping time, as compared to the controls. There was no alteration in barbital sodium sleeping time. It is possible that, piperine inhibits liver microsomal enzyme system and thereby potentiates the pentobarbitone sleeping time. 相似文献