Ammonia （NH3） is a toxic gas released in different industrial, agricultural and natural processes. It is also a biomarker for some diseases. These require NH3 sensors for health and safety reasons. To boost the sens...Ammonia （NH3） is a toxic gas released in different industrial, agricultural and natural processes. It is also a biomarker for some diseases. These require NH3 sensors for health and safety reasons. To boost the sensitiv- ity of solid-state sensors, the effective sensing area should be increased. Two methods are explored and compared using an evaporating pool of 0.5 mL NH4OH （28% NH3）. In the first method an array of Si nanowires （Si NWA） is obtained via metal-assisted-electrochemical etching to increase the effective surface area. In the second method CVD graphene is suspended on top of the Si nanowires to act as a sensing layer. Both the effective surface area as well as the density of surface traps influences the amplitude of the response. The effective surface area of Si NWAs is 100 × larger than that of suspended graphene for the same top surface area, leading to a larger response in amp- litude by a factor of -7 notwithstanding a higher trap density in suspended graphene. The use of Si NWAs in- creases the response rate for both Si NWAs as well as the suspended graphene due to more effective NH3 diffu- sion processes.展开更多
Sulphur mustard [bis(2 chloro ethyl) sulfide] (SM), a bifunctional alkylating agent has been frequently used as a chemical warfare agent. In the present study, the effects of sodium 2 3 dimercaptopropane sulphonic ...Sulphur mustard [bis(2 chloro ethyl) sulfide] (SM), a bifunctional alkylating agent has been frequently used as a chemical warfare agent. In the present study, the effects of sodium 2 3 dimercaptopropane sulphonic acid (DMPS) on some biochemical and histological parameters in mice, exposed to 1/4LC 50 concentration of SM vapor (10.5 mg/m\+3) were examined over a period of seven days. Exposure of SM resulted in a significant loss of blood, hepatic and pulmonary glutathione (GSH) and an elevation of hepatic and pulmonary oxidized glutathione (GSSG). These biochemical changes were accompanied by a number of histopathological alterations. The most prominent was congestion and degeneration in viscera and obliteration of chromatin material. These biochemical and histopathological changes were less marked in animals pre administered with DMPS followed by DMPS exposure indicating some protective value of the thiol (DMPS) against SM induced oxidative injury in mice.展开更多
Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigaed by exposing mice to 84. 6mg/m3 for 1h duration, using controlled single exposure conditions. A progressive fall in body...Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigaed by exposing mice to 84. 6mg/m3 for 1h duration, using controlled single exposure conditions. A progressive fall in body weight from third day onwards was noticed. Light microscopic examination of the pulmonary tissue of these animals at 6 h post exposure revealed that the tracheobronchial epithelium remained intact, but was infiltrated by inflammatory cells. By 24 h post exposure, the mucosecretory cells were destroyed. The indanunatory reaction was maximum at 48 h. By 7th day post exposure there was swelling and vacuolation of lung parenchymal cells and thrombi formation. In addition SM caused congestion and hemorrhage at alveolar level. SM also caused granulovacuolar degeneration with perinuclear clumping of the cytopasm of hepatocytes and renal parenchymal cells. Renallesions were chazacterized by congestion and hemorrhage. Among visceral tissues, maximum atrophywas observed in spleen. Distribution of lesions increased with post exposure period. The maximum lesions were observed at 7th day post-exposure.展开更多
The effects of atropine, diazepam and pralidoxime were studied for their ability to block the pathological lesions induced by sarin. Rats were exposed to an aerosol of sarin at a concentration of 51.2mg-m for 15 min f...The effects of atropine, diazepam and pralidoxime were studied for their ability to block the pathological lesions induced by sarin. Rats were exposed to an aerosol of sarin at a concentration of 51.2mg-m for 15 min following the pretreatment with one of the following combinations: atropine (10 mg/kg, i.m.) and diazepam (0.5 mg/kg, i.m.); atropine and pralidoxime (25 mg/kg, i.m.); diazepam and pralidoxime; atropine, diazepam and pralidoxime. Lung exposed to sarin aerosols revealed an increased cellular proliferation with progressive diffused interstitial thickening on the 4th day following exposure. On the 16th day, loss of alveolar space and consolidation of large areas of all lobes were observed. Sarin also caused damage to the respiratory bronchioles. All the therapy regime blocked the development of lung lesions in the descending orders: atropine, diazepam and pralidoxime, atropine and diazepam > diazepam and pralidoxime > atropine and pralidoxime. The result suggests that diazepam in combination with atropine and pralidoxime could be an effective drug combination regime for the lung lesions.展开更多
Cyclin-dependent kinase 5（Cdk5） is a member of the serine-threonine kinase family of cyclin-dependent kinases. Cdk5 is critical to normal mammalian nervous system development and plays important regulatory roles in ...Cyclin-dependent kinase 5（Cdk5） is a member of the serine-threonine kinase family of cyclin-dependent kinases. Cdk5 is critical to normal mammalian nervous system development and plays important regulatory roles in multiple cellular functions. Recent evidence indicates that Cdk5 is inappropriately activated in several neurodegenerative conditions, including Parkinson＇s disease（PD）. PD is a chronic neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, and consequent extrapyramidal motor dysfunction. During neurotoxicity, p35 is cleaved to form p25. Binding of p25 with Cdk5 leads deregulation of Cdk5 resulting in number of neurodegenerative pathologies. To date, strategies to specifically inhibit Cdk5 hyperactivity have not been successful without affecting normal Cdk5 activity. Here we show that inhibition of p25/Cdk5 hyperactivation through TFP5/TP5, truncated 24-aa peptide derived from the Cdk5 activator p35 rescues nigrostriatal dopaminergic neurodegeneration induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine（MPTP/MPP＋） in a mouse model of PD. TP5 peptide treatment also blocked dopamine depletion in the striatum and improved gait dysfunction after MPTP administration. The neuroprotective effect of TFP5/TP5 peptide is also associated with marked reduction in neuroinflammation and apoptosis. Here we show inhibition of Cdk5/p25-hyperactivation by TFP5/TP5 peptide, which identifies Cdk5/p25 as a potential therapeutic target to reduce neurodegeneration in PD.展开更多
The Indus River flows through Ladakh, one of the driest and coldest places on earth, in a tectonically active domain. Fluvial, glaciofluvial, lacustrine and debris dominated sequences represent the Late Quaternary sed...The Indus River flows through Ladakh, one of the driest and coldest places on earth, in a tectonically active domain. Fluvial, glaciofluvial, lacustrine and debris dominated sequences represent the Late Quaternary sedimentary record along the river course. Karakoram Fault, a major crustal scaled feature reported to be active during the Quaternary, is associated with the Indus River drainage. Linkages between a major, active fault and deposits formed during the activity period of the fault are explored using heavy mineral deduced provenance and Optically Stimulated Luminescence(OSL) chronology.Five deposits in a ~200 km long stretch of the Indus River have been examined for a ~80 ka period to decipher the climate linked aggradation history. Damming of the Indus River at ~79 ka and existence of the Spituk Lake for >30 ka is demonstrated. Using geology of the provenance in relation to the mineralogical attributes of the Quaternary deposits, the major drainage reorganization when the connection of the Tangtse Valley to the Indus was blocked, is inferred at ~73 ka. It is supported by the geologicalgeomorphological evidence. The study demonstrates the application of provenance linked mineralogy in terrestrial aggradation in a tectonically active region.展开更多
基金financial support of EPSRC via the EEE department
文摘Ammonia （NH3） is a toxic gas released in different industrial, agricultural and natural processes. It is also a biomarker for some diseases. These require NH3 sensors for health and safety reasons. To boost the sensitiv- ity of solid-state sensors, the effective sensing area should be increased. Two methods are explored and compared using an evaporating pool of 0.5 mL NH4OH （28% NH3）. In the first method an array of Si nanowires （Si NWA） is obtained via metal-assisted-electrochemical etching to increase the effective surface area. In the second method CVD graphene is suspended on top of the Si nanowires to act as a sensing layer. Both the effective surface area as well as the density of surface traps influences the amplitude of the response. The effective surface area of Si NWAs is 100 × larger than that of suspended graphene for the same top surface area, leading to a larger response in amp- litude by a factor of -7 notwithstanding a higher trap density in suspended graphene. The use of Si NWAs in- creases the response rate for both Si NWAs as well as the suspended graphene due to more effective NH3 diffu- sion processes.
文摘Sulphur mustard [bis(2 chloro ethyl) sulfide] (SM), a bifunctional alkylating agent has been frequently used as a chemical warfare agent. In the present study, the effects of sodium 2 3 dimercaptopropane sulphonic acid (DMPS) on some biochemical and histological parameters in mice, exposed to 1/4LC 50 concentration of SM vapor (10.5 mg/m\+3) were examined over a period of seven days. Exposure of SM resulted in a significant loss of blood, hepatic and pulmonary glutathione (GSH) and an elevation of hepatic and pulmonary oxidized glutathione (GSSG). These biochemical changes were accompanied by a number of histopathological alterations. The most prominent was congestion and degeneration in viscera and obliteration of chromatin material. These biochemical and histopathological changes were less marked in animals pre administered with DMPS followed by DMPS exposure indicating some protective value of the thiol (DMPS) against SM induced oxidative injury in mice.
文摘Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigaed by exposing mice to 84. 6mg/m3 for 1h duration, using controlled single exposure conditions. A progressive fall in body weight from third day onwards was noticed. Light microscopic examination of the pulmonary tissue of these animals at 6 h post exposure revealed that the tracheobronchial epithelium remained intact, but was infiltrated by inflammatory cells. By 24 h post exposure, the mucosecretory cells were destroyed. The indanunatory reaction was maximum at 48 h. By 7th day post exposure there was swelling and vacuolation of lung parenchymal cells and thrombi formation. In addition SM caused congestion and hemorrhage at alveolar level. SM also caused granulovacuolar degeneration with perinuclear clumping of the cytopasm of hepatocytes and renal parenchymal cells. Renallesions were chazacterized by congestion and hemorrhage. Among visceral tissues, maximum atrophywas observed in spleen. Distribution of lesions increased with post exposure period. The maximum lesions were observed at 7th day post-exposure.
文摘The effects of atropine, diazepam and pralidoxime were studied for their ability to block the pathological lesions induced by sarin. Rats were exposed to an aerosol of sarin at a concentration of 51.2mg-m for 15 min following the pretreatment with one of the following combinations: atropine (10 mg/kg, i.m.) and diazepam (0.5 mg/kg, i.m.); atropine and pralidoxime (25 mg/kg, i.m.); diazepam and pralidoxime; atropine, diazepam and pralidoxime. Lung exposed to sarin aerosols revealed an increased cellular proliferation with progressive diffused interstitial thickening on the 4th day following exposure. On the 16th day, loss of alveolar space and consolidation of large areas of all lobes were observed. Sarin also caused damage to the respiratory bronchioles. All the therapy regime blocked the development of lung lesions in the descending orders: atropine, diazepam and pralidoxime, atropine and diazepam > diazepam and pralidoxime > atropine and pralidoxime. The result suggests that diazepam in combination with atropine and pralidoxime could be an effective drug combination regime for the lung lesions.
文摘Cyclin-dependent kinase 5（Cdk5） is a member of the serine-threonine kinase family of cyclin-dependent kinases. Cdk5 is critical to normal mammalian nervous system development and plays important regulatory roles in multiple cellular functions. Recent evidence indicates that Cdk5 is inappropriately activated in several neurodegenerative conditions, including Parkinson＇s disease（PD）. PD is a chronic neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, and consequent extrapyramidal motor dysfunction. During neurotoxicity, p35 is cleaved to form p25. Binding of p25 with Cdk5 leads deregulation of Cdk5 resulting in number of neurodegenerative pathologies. To date, strategies to specifically inhibit Cdk5 hyperactivity have not been successful without affecting normal Cdk5 activity. Here we show that inhibition of p25/Cdk5 hyperactivation through TFP5/TP5, truncated 24-aa peptide derived from the Cdk5 activator p35 rescues nigrostriatal dopaminergic neurodegeneration induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine（MPTP/MPP＋） in a mouse model of PD. TP5 peptide treatment also blocked dopamine depletion in the striatum and improved gait dysfunction after MPTP administration. The neuroprotective effect of TFP5/TP5 peptide is also associated with marked reduction in neuroinflammation and apoptosis. Here we show inhibition of Cdk5/p25-hyperactivation by TFP5/TP5 peptide, which identifies Cdk5/p25 as a potential therapeutic target to reduce neurodegeneration in PD.
基金Council of Scientific & Industrial Research (CSIR) (Sr. No1121020574 and Ref. No: 19-12/2010(i)EU-IV) funded a fellowship to RL Ministry of Earth Sciences (MoES) has supported the project(MoES/PAMC/H&C/51/2013-PC-II)
文摘The Indus River flows through Ladakh, one of the driest and coldest places on earth, in a tectonically active domain. Fluvial, glaciofluvial, lacustrine and debris dominated sequences represent the Late Quaternary sedimentary record along the river course. Karakoram Fault, a major crustal scaled feature reported to be active during the Quaternary, is associated with the Indus River drainage. Linkages between a major, active fault and deposits formed during the activity period of the fault are explored using heavy mineral deduced provenance and Optically Stimulated Luminescence(OSL) chronology.Five deposits in a ~200 km long stretch of the Indus River have been examined for a ~80 ka period to decipher the climate linked aggradation history. Damming of the Indus River at ~79 ka and existence of the Spituk Lake for >30 ka is demonstrated. Using geology of the provenance in relation to the mineralogical attributes of the Quaternary deposits, the major drainage reorganization when the connection of the Tangtse Valley to the Indus was blocked, is inferred at ~73 ka. It is supported by the geologicalgeomorphological evidence. The study demonstrates the application of provenance linked mineralogy in terrestrial aggradation in a tectonically active region.
