Present study aims to evaluate the immunotoxic effects of two biopesticides, Nimbecidine Plus (a neem biopesticide) and mahua oil cake (MOC) on the haemocyte populations of a freshwater crab, Varuna litterata after acute exposure. Four-day static renewal bioassay test was performed where sixteen healthy adult male crabs were exposed to 96-h LC50 values of Nimbecidine Plus (0.006284 ppt) and MOC aqueous extract (7.631 ppt) separately in the laboratory condition. Control groups were maintained throughout the experimental period without any biopesticide exposure. Various haemocyte parameters such as total count (THC), differential count (DHC), haemocyte density, cytomorphological anomalies and reactive oxygen species (ROS) were measured in the biopesticides-exposed and control crabs after 24, 48, 72, and 96 h of exposure. After treatment with Nimbecidine Plus and MOC, several cytomorphological deformities (cytoplasmic and nuclear membrane disintegration, chromatin condensation, pyknosis, karyorrhexis, karyolysis, nuclear vacuolation, altered cell shape, cellular coagulation, cytoplasmic discharge, vacuolation) were observed in hyalinocytes, small granule haemocytes and large granule haemocytes with modulation of their relative percentages at different exposure times. THC, DHC, haemocyte density and ROS levels were significantly altered (p < 0.05) in biopesticides-exposed crabs at different exposure periods. The toxicity of both biopesticides did not persist throughout the entire exposure time. Nimbecidine Plus exhibited nonlinear toxic impacts on different haemocyte parameters at initial, mid and higher exposure periods whereas MOC showed linear toxic effects mostly at initial exposure time. In comparison to MOC, Nimbecidine Plus showed higher immunotoxic effects in V. litterata. Outcome of this experiment might provide useful information to understand the immune responses of V. litterata against biopesticide toxicity.

This study was performed to estimate the corpse age using histological examinations of the fourth and sixth ribs by a morphometric method. One hundred samples of referred bodies of the Legal Medicine Organization of Lorestan province, Iran, were examined. The sampling was performed from the fourth and sixth ribs. The transverse sections of the samples were prepared, in which various variables such as the diameter of the haversian system (DHC), haversian system perimeter (PHS), haversian system area (AHS), and the thickness of the haversian lamellae (TH) were measured using a Motic microscope video system and the Motic Image Plus 2 software. To predict age from sex and the morphometric parameters a stepwise multiple linear regression was used. Accordingly, AHS in rib 4, DHC with lens 10 in rib 4, DHC with lens 10 in rib 6 and TH in rib 6 remained in the model at significance level 0.05 (R square = 0.1654). Although age was associated with some of the studied parameters, the obtained equation was not fit enough to predict the exact age. Further parameters should be studied for prediction of age in corpse.

Stroke is a leading threat to human life. Metabolic dysfunction of glucose may play a key role in stroke pathophysiology. Pharmacological hypothermia (PH) is a potential neuroprotective strategy for stroke, in which the temperature is decreased safely. The present study determined whether neuroprotective PH with chlorpromazine and promethazine (C + P), plus dihydrocapsaicin (DHC) improved glucose metabolism in acute ischemic stroke. A total of 208 adult male Sprague Dawley rats were randomly divided into the following groups: sham, stroke, and stroke with various treatments including C + P, DHC, C + P + DHC, phloretin (glucose transporter (GLUT)-1 inhibitor), cytochalasin B (GLUT-3 inhibitor), TZD (thiazolidinedione, phosphoenolpyruvate carboxykinase (PCK) inhibitor), and apocynin (nicotinamide adenine dinucleotide phosphate oxidase (NOX) inhibitor). Stroke was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by 6 or 24 h of reperfusion. Rectal temperature was monitored before, during, and after PH. Infarct volume and neurological deficits were measured to assess the neuroprotective effects. Reactive oxygen species (ROS), NOX activity, lactate, apoptotic cell death, glucose, and ATP levels were measured. Protein expression of GLUT-1, GLUT-3, phosphofructokinase (PFK), lactate dehydrogenase (LDH), PCK1, PCK2, and NOX subunit gp91 was measured with Western blotting. PH with a combination of C + P and DHC induced faster, longer, and deeper hypothermia, as compared to each alone. PH significantly improved every measured outcome as compared to stroke and monotherapy. PH reduced brain infarction, neurological deficits, protein levels of glycolytic enzymes (GLUT-1, GLUT-3, PFK and LDH), gluconeogenic enzymes (PCK1 and PCK2), NOX activity and its subunit gp91, ROS, apoptotic cell death, glucose, and lactate, while raising ATP levels. In conclusion, stroke impaired glucose metabolism by enhancing hyperglycolysis and gluconeogenesis, which led to ischemic injury, all of which were reversed by PH induced by a combination of C + P and DHC.

Anxiety disorders may be mediated in part by disruptions in serotonin (5-hydroxytryptamine, 5-HT) system function. Behavioral measures of approach-avoidance conflict suggest that serotonin neurons within the median raphe nucleus (MRN) promote an anxiogenic state, and some evidence indicates this may be mediated by serotonergic signaling within the dorsal hippocampus. Here, we test this hypothesis using an optogenetic approach to examine the contribution of MRN 5-HT neurons and 5-HT innervation of the dorsal hippocampus (dHC) to anxiety-like behaviours in female mice. Mice expressing the excitatory opsin ChR2 were generated by crossing the ePet-cre serotonergic cre-driver line with the conditional Ai32 ChR2 reporter line, resulting in selective expression of ChR2 in 5-HT neurons. Electrophysiological recordings confirmed that this approach enabled reliable optogenetic stimulation of MRN 5-HT neurons, and this stimulation produced downstream 5-HT release in the dHC as measured by in vivo microdialysis. Optogenetic stimulation of the MRN elicited behavioral responses indicative of an anxiogenic effect in three behavioural tests: novelty-suppressed feeding, marble burying and exploration on the elevated-plus maze. These effects were shown to be behaviourally-specific. Stimulation of 5-HT terminals in the dHC recapitulated the anxiety-like behaviour in the novelty-suppressed feeding and marble burying tests. These results show that activation of 5-HT efferents from the MRN rapidly induces expression of anxiety-like behaviour, in part via projections to the dHC. These findings reveal an important neural circuit implicated in the expression of anxiety in female mice.

Many studies have implicated hippocampal dysregulation in the pathophysiology of alcohol use disorder (AUD). However, over the past twenty years, a growing body of evidence has revealed distinct functional roles of the dorsal (dHC) and ventral (vHC) hippocampal subregions, with the dHC being primarily involved in spatial learning and memory and the vHC regulating anxiety- and depressive-like behaviors. Notably, to our knowledge, no rodent studies have examined the effects of chronic ethanol exposure on synaptic transmission along the dorsal/ventral axis. To that end, we examined the effects of the chronic intermittent ethanol vapor exposure (CIE) model of AUD on dHC and vHC synaptic excitability. Adult male Long-Evans rats were exposed to CIE or AIR for 10 days (12 h/day; targeting blood ethanol levels of 175-225 mg%) and recordings were made 24 h into withdrawal. As expected, this protocol increased anxiety-like behaviors on the elevated plus-maze and successive alleys test. Extracellular recordings revealed marked CIE-associated increases in synaptic excitation in the CA1 region that were exclusively restricted to the ventral domain of the hippocampus. Western blot analysis of synaptoneurosomal fractions revealed that the expression of two proteins that regulate synaptic strength, GluA2 and SK2, were dysregulated in the vHC, but not the dHC, following CIE. Together, these findings suggest that the ventral CA1 region may be particularly sensitive to the maladaptive effects of chronic ethanol exposure and provide new insight into some of the neural substrates that may contribute to the negative affective state that develops during withdrawal.

The position of the mitotic spindle is tightly controlled in animal cells as it determines the plane and orientation of cell division. Contacts between cytoplasmic dynein and astral microtubules (MTs) at the cell cortex generate pulling forces that position the spindle. An evolutionarily conserved Gα-GPR-1/2Pins/LGN-LIN-5Mud/NuMA cortical complex interacts with dynein and is required for pulling force generation, but the dynamics of this process remain unclear. In this study, by fluorescently labeling endogenous proteins in Caenorhabditis elegans embryos, we show that dynein exists in two distinct cortical populations. One population directly depends on LIN-5, whereas the other is concentrated at MT plus ends and depends on end-binding (EB) proteins. Knockout mutants lacking all EBs are viable and fertile and display normal pulling forces and spindle positioning. However, EB protein-dependent dynein plus end tracking was found to contribute to force generation in embryos with a partially perturbed dynein function, indicating the existence of two mechanisms that together create a highly robust force-generating system.