Impact of different cropping systems on properties of soil and water in different micro watersheds

Studies on soils of Navsari Agricultural University (NAU) having different cropping system were carried out in the four micro watersheds that exist in the 400 ha University campus. Soil samples from 0-15 cm depth and water samples from adjacent bore wells were collected and analyzed from different locations of micro watersheds. Soils of watersheds showed that soils texture was clay in nature, having more than 65 % clay, whereas silt was more in watershed ‘A’. Soil organic carbon content (SOC) was 0.32 %, found in the field near University play ground and the highest 0.88 %, in Forestry farm, thus underlining the need of forest species in agricultural farms. SOC levels have reduced significantly due to intensive cultivation in all the watersheds. The result of exchangeable sodium percent (ESP) is supported by the topographic features, as, ESP was more in watershed ‘B’ (5.15) than C (2.95), this showed that infiltration rate was lesser in ‘B’ as compared to ‘C’ due to availability of more sodium (Na). Available N was highest in watershed ‘A’ (246 kg/ha) followed by ‘C’ (225 kg/ha) than ‘B’ (203 kg/ha), the reason was watershed ‘A’ had only horticulture crops whereas B and C had different crops of the region. Electrical conductivity (EC) of ground water collected from wells in watershed ‘C’ was found to be very high both before (3.44 dS/m) and after monsoon (2.95 dS/m), showing that water is highly saline and not fit for surface irrigation and there is need of ground water recharging

Fish oil rich diet in comparison to saturated fat rich diet offered protection against lipopolysaccharide-induced inflammation and insulin resistance in mice

<p>Abstract</p> <p>Background and Objective</p> <p>Systemic chronic inflammation is linked to metabolic syndrome, type-2 diabetes, and heart disease. Lipopolysaccharide (LPS), a Gram negative microbial product, triggers inflammation through toll-like-receptor-4 (TLR-4) signaling. It has been reported that dietary fatty acids also modulate inflammation through TLR-4. We investigated whether fish oil (FO) rich diet in comparison to saturated fat (SF) rich diet would confer protection from pathologies induced by LPS.</p> <p>Methods</p> <p>Twenty C57BL/6 mice were divided into two groups. One group received FO-diet and other received SF-diet <it>ad libitum </it>for 60 days. Diets were isocaloric containing 45% energy from fat. After 60-days of feeding, blood was collected after overnight fast. Mice were allowed to recover for 4-days, fasted for 5-hours, challenged with 100 ng/mL of LPS intraperitonially, and bled after 2-hours. After 7-days of recuperation, mice were challenged with 500 ng/mL of LPS intraperitonially and observed for physical health.</p> <p>Results</p> <p>Food intake was similar in FO- and SF-fed mice. FO-fed mice compared to SF-fed mice had significantly less body weight gain (P = 0.005), epididymal fat weight (P = 0.005), fasting blood glucose (70.8 vs 83.3 ng/dL; P < 0.05), HOMA-IR (5.0 vs 13.6; P < 0.019), and serum cholesterol (167 vs 94 mg/dL; P < 0.05). When challenged with LPS, FO-fed mice had significantly lower serum IL-1β compared to SF-fed mice (2.0 vs 30.0 pg/mL; P < 0.001). After LPS-challenge, SF-fed mice had higher mortality, lost more body weight, and had greater decrease in blood glucose compared to FO-fed mice.</p> <p>Conclusion</p> <p>Overall, FO-diet compared to SF-diet offered protection against deleterious effects of LPS in mice.</p

Gene expression patterns in the hippocampus during the development and aging of Glud1 (Glutamate Dehydrogenase 1) transgenic and wild type mice

BACKGROUND: Extraneuronal levels of the neurotransmitter glutamate in brain rise during aging. This is thought to lead to synaptic dysfunction and neuronal injury or death. To study the effects of glutamate hyperactivity in brain, we created transgenic (Tg) mice in which the gene for glutamate dehydrogenase (Glud1) is over-expressed in neurons and in which such overexpression leads to excess synaptic release of glutamate. In this study, we analyzed whole genome expression in the hippocampus, a region important for learning and memory, of 10 day to 20 month old Glud1 and wild type (wt) mice. RESULTS: During development, maturation and aging, both Tg and wt exhibited decreases in the expression of genes related to neurogenesis, neuronal migration, growth, and process elongation, and increases in genes related to neuro-inflammation, voltage-gated channel activity, and regulation of synaptic transmission. Categories of genes that were differentially expressed in Tg vs. wt during development were: synaptic function, cytoskeleton, protein ubiquitination, and mitochondria; and, those differentially expressed during aging were: synaptic function, vesicle transport, calcium signaling, protein kinase activity, cytoskeleton, neuron projection, mitochondria, and protein ubiquitination. Overall, the effects of Glud1 overexpression on the hippocampus transcriptome were greater in the mature and aged than the young. CONCLUSIONS: Glutamate hyperactivity caused gene expression changes in the hippocampus at all ages. Some of these changes may result in premature brain aging. The identification of these genomic expression differences is important in understanding the effects of glutamate dysregulation on neuronal function during aging or in neurodegenerative diseases

Symptom and Viral Rebound in Untreated SARS-CoV-2 Infection

BackgroundAlthough symptom and viral rebound have been reported after nirmatrelvir-ritonavir treatment, the trajectories of symptoms and viral load during the natural course of COVID-19 have not been well described.ObjectiveTo characterize symptom and viral rebound in untreated outpatients with mild to moderate COVID-19.DesignRetrospective analysis of participants in a randomized, placebo-controlled trial. (ClinicalTrials.gov: NCT04518410).SettingMulticenter trial.Patients563 participants receiving placebo in the ACTIV-2/A5401 (Adaptive Platform Treatment Trial for Outpatients With COVID-19) platform trial.MeasurementsParticipants recorded the severity of 13 symptoms daily between days 0 and 28. Nasal swabs were collected for SARS-CoV-2 RNA testing on days 0 to 14, 21, and 28. Symptom rebound was defined as a 4-point increase in total symptom score after improvement any time after study entry. Viral rebound was defined as an increase of at least 0.5 log10 RNA copies/mL from the immediately preceding time point to a viral load of 3.0 log10 copies/mL or higher. High-level viral rebound was defined as an increase of at least 0.5 log10 RNA copies/mL to a viral load of 5.0 log10 copies/mL or higher.ResultsSymptom rebound was identified in 26% of participants at a median of 11 days after initial symptom onset. Viral rebound was detected in 31% and high-level viral rebound in 13% of participants. Most symptom and viral rebound events were transient, because 89% of symptom rebound and 95% of viral rebound events occurred at only a single time point before improving. The combination of symptom and high-level viral rebound was observed in 3% of participants.LimitationA largely unvaccinated population infected with pre-Omicron variants was evaluated.ConclusionSymptom or viral relapse in the absence of antiviral treatment is common, but the combination of symptom and viral rebound is rare.Primary funding sourceNational Institute of Allergy and Infectious Diseases