Bradykinin receptors of cerebral microvessels stimulate phosphoinositide turnover.

We examined by ligand binding methods whether bradykinin (BK) receptors exist in rat and pig cerebral microvessels, and in the cerebral cortex from which the microvessels were isolated. We found a high-affinity and saturable BK receptor site in both rat and pig cerebral microvessels, but not in their cerebral cortex. The maximal density of binding and the dissociation constant were 8.0 +/- 4.1 and 6.8 +/- 1.5 fmol/mg of protein and 47 +/- 24 and 150 +/- 8 pM (mean +/- SD) in cerebral microvessels of the pig and rat, respectively. The high-affinity specific binding of BK was effectively displaced by des-Arg0[Hyp3-Thi5-8,D-Phe7]BK, a specific B2 receptor antagonist, but not by des-Arg9[Leu8]BK, a specific B1 antagonist. We also demonstrated that BK increases phosphatidylinositol hydrolysis in cerebral microvessels of the rat and pig. This effect was also blocked by the B2, but not by the B1, antagonist. Increased phosphatidylinositol hydrolysis was manifested by a rapid transient increase in inositol trisphosphate and the later slow accumulation of inositol bisphosphate and inositol monophosphate. Preincubation of microvessels with phorbol ester, stable GTP analogs, pertussis toxin, or in Ca(2+)-free buffer did not influence BK activation of phosphatidylinositol hydrolysis. These results demonstrate the existence of BK receptors of the B2 subtype in brain microvessels, which may play an important role in modulation of the brain microcirculation, probably via increased phosphoinositide turnover.     

Evaluating mechanism and severity of injuries among trauma patients admitted to Sina Hospital, the National Trauma Registry of Iran

Purpose: Injuries are one of the leading causes of death and lead to a high social and financial burden. Injury patterns can vary significantly among different age groups and body regions. This study aimed to evaluate the relationship between mechanism of injury, patient comorbidities and severity of injuries. Methods: The study included trauma patients from July 2016 to June 2018, who were admitted to Sina Hospital, Tehran, Iran. The inclusion criteria were all injured patients who had at least one of the following: hospital length of stay more than 24 h, death in hospital, and transfer from the intensive care unit of another hospital. Data collection was performed using the National Trauma Registry of Iran minimum dataset. Results: The most common injury mechanism was road traffic injuries (49.0%), followed by falls (25.5%). The mean age of those who fell was significantly higher in comparison with other mechanisms (p < 0.001). Severe extremity injuries occurred more often in the fall group than in the vehicle collision group (69.0% vs. 43.5%, p < 0.001). Moreover, cases of severe multiple trauma were higher amongst vehicle collisions than injuries caused by falls (27.8% vs. 12.9%, p = 0.003). Conclusion: Comparing falls with motor vehicle collisions, patients who fell were older and sustained more extremity injuries. Patients injured by motor vehicle collision were more likely to have sustained multiple trauma than those presenting with falls. Recognition of the relationship between mechanisms and consequences of injuries may lead to more effective interventions.     

N-nitro- -arginine methylester is protective against ethanol-induced gastric damage in cholestatic rats

In this study the effect of nitric oxide (NO) synthesis inhibition on ethanol-induced gastric damage was evaluated in bile duct-ligated, sham-operated and unoperated rats. The animals were injected intraperitoneally with saline, -arginine (200 mg/kg) or N^G-nitro- -arginine methylester ( -NAME) in doses of 5, 15 and 30 mg/kg, 30 min before ethanol administration. The animals were killed 1 h after ethanol administration and their stomachs were removed for measurement of gastric mucosal damage. The results showed that -NAME significantly enhanced the development of gastric mucosal lesions in sham-operated and unoperated rats, while in bile duct-ligated animals, -NAME decreased and -arginine enhanced the potentiation of ethanol-induced gastric mucosal damage. The plasma level of nitrite and nitrate was also measured and was significantly higher in bile duct-ligated rats than in control groups. The results suggest that inhibition of NO synthase with -NAME has different effects on ethanol-induced gastric damage in cholestatic groups and in normal rats and that these effects can be explained by overproduction of NO in bile duct-ligated animals.     

A Three-Dimensional Developmental Measurement of the Temporomandibular Joint

This article presents an anthropologic study of the growth and developmental changes that occur within the bony components of the temporomandibular joint. The material used was provided by the Department of Physical Anthropology of the Smithsonian Institution Museum of Natural History, Washington, D.C.

Based on a Class I normal occlusion, the authors selected a total of 100 skulls with mandibles from the Aleutian Islands collection. These skulls, which were from 2-to 20-year-old subjects, were divided into four age groups. The approximate age of each skull was determined by charts based on eruption sequence, the number of permanent teeth present, and suture closure.

Anatomic landmarks and anthropologic techniques were used to make direct linear measurements on the bony components of the 200 temporomandibular joints. Three-dimensional measurements were made on the condyles, fossae, and articular eminences of each skull.

Several variables were chosen for statistical analysis: (1) The size of the individual components of the TMJ within each age group. (2) The changes with age in the anteroposterior, medial-lateral, and vertical dimensions of the individual TMJ components. (3) Asymmetries in size between the right and the left TMJ components. (4) The interrelationship of the individual TMJ components as seen in their growth changes.

The results obtained from the various measurements used in this study were compared to the findings of a number of earlier studies.     

Review of policies,data, and interventions to improve maternal nutrition in Afghanistan

Malnutrition contributes to direct and indirect causes of maternal mortality, which is particularly high in Afghanistan. Women's nutritional status before, during, and after pregnancy affects their own well‐being and mortality risk and their children's health outcomes. Though maternal nutrition interventions have documented positive impact on select child health outcomes, there are limited data regarding the effects of maternal nutrition interventions on maternal health outcomes globally. This scoping review maps policies, data, and interventions aiming to address poor maternal nutrition outcomes in Afghanistan. We used broad search categories and approaches including database and website searches, hand searches of reference lists from relevant articles, policy and programme document requests, and key informant interviews. Inclusion and exclusion criteria were developed by type of source document, such as studies with measures related to maternal nutrition, relevant policies and strategies, and programmatic research or evaluation by a third party with explicit interventions targeting maternal nutrition. We abstracted documents systematically, summarized content, and synthesized data. We included 20 policies and strategies, 29 data reports, and nine intervention evaluations. The availability of maternal nutrition intervention data and the inclusion of nutrition indicators, such as minimum dietary diversity, have increased substantially since 2013, yet few nutrition evaluations and population surveys include maternal outcomes as primary or even secondary outcomes. There is little evidence on the effectiveness of interventions that target maternal nutrition in Afghanistan. Policies and strategies more recently have shifted towards multisectoral efforts and specifically target nutrition needs of adolescent girls and women of reproductive age. This scoping review presents evidence from more than 10 years of efforts to improve the maternal nutrition status of Afghan women. We recommend a combination of investments in measuring maternal nutrition indicators and improving maternal nutrition knowledge and behaviours.     

Orbitofrontal cortex neurons as a common target for classic and glutamatergic antipsychotic drugs

Until recently, all known antipsychotic drugs were thought to block the dopamine D2 receptor. New evidence that agonists of the metabotropic glutamate 2/3 (mGlu2/3) receptors ameliorate psychotic and affective symptoms of schizophrenia suggests that compounds with different molecular targets may act on a common cellular target to treat schizophrenia. We hypothesized that normalizing the activity of neurons in the orbitofrontal cortex (OFC), a region that is increasingly implicated in the pathophysiology of schizophrenia, presents such a target. We disrupted OFC activity in behaving rats with a use-dependent NMDA antagonist to model the NMDA hypofunction state that may occur in schizophrenia. This systemic treatment increased the activity of most pyramidal cells while inhibiting the activity of putative inhibitory GABA interneurons and increasing behavioral stereotypy. A similar pattern of OFC firing disruption was observed after amphetamine, which models a dopamine hyperactivity state in schizophrenia and which produces a pattern of firing disruption different from those of NMDA antagonists in other prefrontal cortex regions. Antipsychotic drugs haloperidol and clozapine, which target monoamine receptors, as well as an mGlu2/3 agonist and an mGlu5 receptor modulator proposed to have antipsychotic efficacy, reversed the impact of NMDA hypofunction on OFC cells and on behavior. A similar pattern of normalization of OFC activity was observed when treatments were given after amphetamine. Thus, proven or putative antipsychotic drugs with different mechanisms of action similarly reduced the impact of NMDA hypofunction and dopamine hyperfunction on OFC neurons, suggesting that these neurons are a candidate target for the therapeutic effects of antipsychotic medications.