Feasibility Study of Malachite Green Dye Removal from Aqueous Solution Using Groundnut Cake Activated Carbon

The preparation of activated carbon by the activation of groundnut cake from orthophosphoric acid and its ability to remove the Malachite Green (MG) dye from the aqueous solution in batch process were presented in this study. The effect of adsorbent dose, initial pH of the dye solution, temperature and initial dye concentration on the removal of MG were explored. The activated carbon was characterised by the Field emission scanning electron microscopy (FESEM) and Fourier transform infra-red (FTIR) spectroscopy. Result shows that the adsorption was more effective in the acidic medium and increase with contact time and initial dye concentration but decreases with temperature. The adsorption capacity of the prepared groundnut cake activated carbon was 6.45 mg/g. The kinetic study of adsorption was better described by Pseudo-2nd order kinetic model and Freundlich isotherm describes the MG adsorption equilibrium data better than Langmuir isotherm. Thermodynamic parameters such as change in Gibbs free energy, enthalpy and entropy also determined

Post COVID nocardiosis-an opportunistic enemy

Nocardia is an opportunistic infection seen mostly in immunocompromised individuals. It has become an important pathogen especially in these post covid times in which multiple individuals had to go through high dose corticosteroid therapy as part of their severe COVID-19 treatment. We present a 62 years old male with diabetes mellitus and hypertension who had previously been hospitalized for a month for COVID-19 and received high dose corticosteroids for the same. He presented again one month later with symptoms of fever and breathlessness and was worked up extensively for infections in which all his investigations came negative. For suspicion of opportunistic pathogen his HRCT thorax was done which showed consolidation and cavitation in lung along with other infective changes. In view of HRCT thorax findings bronchoscopy was done and bronchoalveolar lavage was sent for examination which grew Nocardia beijingensis on culture. Cotrimoxazole was started for the patient and 3 days after the initiation of therapy he became afebrile and was weaned off of oxygen support gradually over next one month

Cell death in denervated skeletal muscle is distinct from classical apoptosis

Denervation of skeletal muscle is followed by the progressive loss of tissue mass and impairment of its functional properties. The purpose of the present study was to investigate the occurrence of cell death and its mechanism in rat skeletal muscle undergoing post-denervation atrophy. We studied the expression of specific markers of apoptosis and necrosis in experimentally denervated tibialis anterior, extensor digitorum longus and soleus muscles of adult rats. Fluorescent staining of nuclear DNA with propidium iodide revealed the presence of nuclei with hypercondensed chromatin and fragmented nuclei typical of apoptotic cells in the muscle tissue 2, 4 and to a lesser extent 7 months after denervation. This finding was supported by electron microscopy of the denervated muscle. We found clear morphological manifestations of muscle cell death, with ultrastructural characteristics very similar if not identical to those considered as nuclear and cytoplasmic markers of apoptosis. With increasing time of denervation, progressive destabilization of the differentiated phenotype of muscle cells was observed. It included disalignment and spatial disorganization of myofibrils as well as their resorption and formation of myofibril-free zones. These changes initially appeared in subsarcolemmal areas around myonuclei, and by 4 months following nerve transection they were spread throughout the sarcoplasm. Despite an increased number of residual bodies and secondary lysosomes in denervated muscle, we did not find any evidence of involvement of autophagocytosis in the resorption of the contractile system. Dead muscle fibers were usually surrounded by a folded intact basal lamina; they had an intact sarcolemma and highly condensed chromatin and sarcoplasm. Folds of the basal lamina around the dead cells resulted from significant shrinkage of cell volume. Macrophages were occasionally found in close proximity to dead myocytes. We detected no manifestations of inflammation in the denervated tissue. Single myocytes expressing traits of the necrotic phenotype were very rare. A search for another marker of apoptosis, nuclear DNA fragmentation, using terminal deoxyribonucleotidyl transferase mediated dUTP nick end labeling (the TUNEL method) in situ, revealed the presence of multiple DNA fragments in cell nuclei in only a very small number of cell nuclei in 2 and 4 month denervated muscle and to less extent in 7 month denervated muscle. Virtually no TUNEL reactivity was found in normal muscle. Double labeling of tissue denervated for 2 and 4 months for genome fragmentation with the TUNEL method and for total nuclear DNA with propidium iodide demonstrated co-localization of the TUNEL-positive fragmented DNA in some of the nuclei containing condensed chromatin and in fragmented nuclei. However, the numbers of nuclei of abnormal morphology containing condensed and/or irregular patterns of chromatin distribution, as revealed by DNA staining and electron microscopy, exceeded by 33–38 times the numbers of nuclei positive for the TUNEL reaction. Thus, we found a discrepancy between the frequences of expression of morphological markers of apoptosis and DNA fragmentation in denervated muscle. This provides evidence that fragmentation of the genomic DNA is not an obligatory event during atrophy and death of muscle cells, or, alternatively, it may occur only for a short period of time during this process. Unlike classical apoptosis described in mammalian thymocytes and lymphoid cells, non-inflammatory death of muscle fibers in denervated muscle occurs a long time after the removal of myotrophic influence of the nerve and is preceded by the progressive imbalance of the state of terminal differentiation. Our results indicate that apoptosis appears to be represented by a number of distinct isotypes in animals belonging to different taxonomic groups and in different cell lineages of the same organism. Anat Rec 258:305–318, 2000. © 2000 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34287/1/10_ftp.pd

Neurotrophic Factors Improve Motoneuron Survival and Function of Muscle Reinnervated by Embryonic Neurons

Motoneuron death can occur over several spinal levels following muscle denervation due to disease or trauma. We tested whether co-transplantation of embryonic neurons with one or more neurotrophic factors into peripheral nerve improved axon regeneration, muscle fiber area, reinnervation and function to a greater degree than cell transplantation alone. Sciatic nerves of adult Fischer rats were cut to denervate muscles; 1 week later, embryonic day 14–15 ventral spinal cord cells were transplanted into the tibial nerve stump as the only source of neurons for muscle reinnervation. Factors that promote motoneuron survival (i.e. cardiotrophin-1; fibroblast growth factor-2; glial cell line-derived neurotrophic factor [GDNF]; insulin like growth factor-1 [IGF-1]; leukemia inhibitory factor; and hepatocyte growth factor [HGF]) were added to the transplant individually or in combinations. Inclusion of a single factor with the cells resulted in comparable myelinated axon counts, muscle fiber areas, and evoked electromyographic activity (EMG) to cells alone 10 weeks after transplantation. Only cell transplantation with GDNF, HGF and IGF-1 significantly increased motoneuron survival, myelinated axon counts, muscle reinnervation and evoked EMG compared to cells alone. Thus, immediate application of a specific combination of factors to dissociated embryonic neurons improves survival of motoneurons and the long-term function of reinnervated muscle

Improved approximate prediction methods for compressible boundary layer flows

SIGLEGBUnited Kingdo

Properties of medial gastrocnemius motor units and muscle fibers reinnervated by embryonic ventral spinal cord cells

Severe muscle atrophy occurs after complete denervation. Here, Embryonic Day 14–15 ventral spinal cord cells were transplanted into the distal tibial nerve stump of adult female Fischer rats to provide a source of neurons for muscle reinnervation. Our aim was to characterize the properties of the reinnervated motor units and muscle fibers. Some reinnervated motor units contracted spontaneously. Electrical stimulation of the transplants at increasing intensity produced an average (± SE) of 7 ± 1 electromyographic and force steps. Each signal increment represented the excitation of another motor unit. These reinnervated units exerted an average force of 12.0 ± 1.5 mN, strength similar to that of control fatigue-resistant units. Repeated transplant stimulation depleted 17% of the muscle fibers of glycogen, an indication of some functional reinnervation. Reinnervated (glycogen-depleted), denervated (no cells transplanted), and control fibers were of histochemical type I, IIA, or IIB. Fibers of the same type were grouped after reinnervation. The proportion of fiber types also changed. Reinnervated fibers were primarily type IIA, whereas most fibers in denervated and control muscles were type IIB. Reinnervated fibers of each type had significantly larger cross-sectional areas than the corresponding fiber types in denervated muscles. These data suggest that neurons with different properties can reside in the unusual environment of the adult rat peripheral nerve, make functional connections with muscle, specify muscle fiber type, and reduce the amount that each type atrophies

Long-term delivery of FGF-6 changes the fiber type and fatigability of muscle reinnervated from embryonic neurons transplanted into adult rat peripheral nerve

Motoneuron death leads to muscle denervation and atrophy. Transplantation of embryonic neurons into peripheral nerves results in reinnervation and provides a strategy to rescue muscles from atrophy independent of neuron replacement in a damaged or diseased spinal cord. But the count of regenerating axons always exceeds the number of motor units in this model, so target-derived trophic factor levels may limit reinnervation. Our aim was to examine whether long-term infusion of fibroblast growth factor-6 (FGF-6) into denervated medial gastrocnemius muscles improved the function of muscles reinnervated from neurons transplanted into nerve of adult Fischer rats. Factor delivery (10 microg, 4 weeks) began after sciatic nerve transection. After a week of nerve degeneration, 1 million embryonic day 14-15 ventral spinal cord cells were transplanted into the distal tibial stump as a neuron source. Ten weeks later, neurons that expressed motoneuron markers survived in the nerves. More myelinated axons were in nerves to saline-treated muscles than in FGF-6-treated muscles. However, each group showed comparable reductions in muscle fiber atrophy because of reinnervation. Mean reinnervated fiber area was 43%-51% of non-denervated fibers. Denervated fiber area averaged 11%. FGF-6-treated muscles were more fatigable than other reinnervated muscles but had stronger motor units and fewer type I fibers than did saline-treated muscles. FGF-6 thus influenced function by changing the type of fiber reinnervated by transplanted neurons. Deficits in FGF-6 may also contribute to the increase in type I fibers in muscles reinnervated from peripheral axons, suggesting that the effects of FGF-6 on fiber type are independent of the neuron source used for reinnervation