SISTEM INFORMASI BERBASIS WEB PADA TOKO BUKU DI TOKO BATAM

Developments in the field of technology can be used to help work, one of which is by building a web-based information system at a used bookstore in the city of Batam. The sales system in this bookstore is still manual, where buyers have to come to the store to get the desired book. Limitations in terms of product marketing are one of the obstacles in the bookstore. The main problem at this bookstore is the difficulty of buyers when looking for books because of the low stock of books. The data collection method Used on this examine is to apply commentary and interview techniques, where researchers come to the location to make observations to see the existing system in the bookstore and interview the owner to find out the existing problems. The research technique utilized in this study is the System Development Life Cycle (SDLC) method with the waterfall model. By making this online sales system, it can make its easier for sellers to market products, and for buyers to be able to see the available stock of books and choose and buy books without having to come to a bookstor

Drugs that lower the seizure threshold

Drugs with potential to lower the seizure threshold are numerous and diverse. Whether they contribute to clinically overt seizures depends on the dosage in which they are taken, the time-course of their effects and the susceptibility of the patient. Crucially, however, their contribution to seizure risk is potentially modifiable

Delayed Postconditioning Protects against Focal Ischemic Brain Injury in Rats

We and others have reported that rapid ischemic postconditioning, interrupting early reperfusion after stroke, reduces infarction in rats. However, its extremely short therapeutic time windows, from a few seconds to minutes after reperfusion, may hinder its clinical translation. Thus, in this study we explored if delayed postconditioning, which is conducted a few hours after reperfusion, offers protection against stroke.Focal ischemia was generated by 30 min occlusion of bilateral common carotid artery (CCA) combined with permanent occlusion of middle cerebral artery (MCA); delayed postconditioning was performed by repetitive, brief occlusion and release of the bilateral CCAs, or of the ipsilateral CCA alone. As a result, delayed postconditioning performed at 3h and 6h after stroke robustly reduced infarct size, with the strongest protection achieved by delayed postconditioning with 6 cycles of 15 min occlusion/15 min release of the ipsilateral CCA executed from 6h. We found that this delayed postconditioning provided long-term protection for up to two months by reducing infarction and improving outcomes of the behavioral tests; it also attenuated reduction in 2-[(18)F]-fluoro-2-deoxy-D-glucose (FDG)-uptake therefore improving metabolism, and reduced edema and blood brain barrier leakage. Reperfusion in ischemic stroke patients is usually achieved by tissue plasminogen activator (tPA) application, however, t-PA's side effect may worsen ischemic injury. Thus, we tested whether delayed postconditioning counteracts the exacerbating effect of t-PA. The results showed that delayed postconditioning mitigated the worsening effect of t-PA on infarction.Delayed postconditioning reduced ischemic injury after focal ischemia, which opens a new research avenue for stroke therapy and its underlying protective mechanisms

Preconditioning-induced ischemic tolerance: a window into endogenous gearing for cerebroprotection

Ischemic tolerance defines transient resistance to lethal ischemia gained by a prior sublethal noxious stimulus (i.e., preconditioning). This adaptive response is thought to be an evolutionarily conserved defense mechanism, observed in a wide variety of species. Preconditioning confers ischemic tolerance if not in all, in most organ systems, including the heart, kidney, liver, and small intestine. Since the first landmark experimental demonstration of ischemic tolerance in the gerbil brain in early 1990's, basic scientific knowledge on the mechanisms of cerebral ischemic tolerance increased substantially. Various noxious stimuli can precondition the brain, presumably through a common mechanism, genomic reprogramming. Ischemic tolerance occurs in two temporally distinct windows. Early tolerance can be achieved within minutes, but wanes also rapidly, within hours. Delayed tolerance develops in hours and lasts for days. The main mechanism involved in early tolerance is adaptation of membrane receptors, whereas gene activation with subsequent de novo protein synthesis dominates delayed tolerance. Ischemic preconditioning is associated with robust cerebroprotection in animals. In humans, transient ischemic attacks may be the clinical correlate of preconditioning leading to ischemic tolerance. Mimicking the mechanisms of this unique endogenous protection process is therefore a potential strategy for stroke prevention. Perhaps new remedies for stroke are very close, right in our cells

Piracetam attenuates minoxidil-induced antinociception in mice

no abstrac

Reversal of pentylenetetrazole-induced seizure activity in mice by nickel chloride

Objective: The present study was designed to investigate the anticonvulsant potential of nickel which is shown to selectively block t-type calcium channels by using nickel choride on pentylenetetrazole (80 mg/kg) induced seizure activity model in mice. Materials and Methods: Seizures were assessed in terms of onset of Straub′s tail phenomenon and onset of jerky movements of the whole body, convulsions, and death. Sodium valproate served as a standard control in the present study. Results: Nickel chloride (5 mg/kg i.p. and 10 mg/kg i.p.) attenuated pentylenetetrazole-induced seizure activity in mice, as reflected by a significant increase in the onset time of Straub′s tail phenomenon and onset of jerky movements of the whole body, convulsions, and death. High dose of nickel chloride showed more pronounced anticonvulsant action than sodium valproate. Conclusions: The anticonvulsant action of nickel chloride was noticeable in this study. However, further studies are required to elucidate its full anticonvulsant potential

Impact of Hypoglycemia on Brain Metabolism During Diabetes

Diabetes is a metabolic disease afflicting millions of people worldwide. A substantial fraction of world's total healthcare expenditure is spent on treating diabetes. Hypoglycemia is a serious consequence of anti-diabetic drug therapy, because it induces metabolic alterations in the brain. Metabolic alterations are one of the central mechanisms mediating hypoglycemia-related functional changes in the brain. Acute, chronic, and/or recurrent hypoglycemia modulate multiple metabolic pathways, and exposure to hypoglycemia increases consumption of alternate respiratory substrates such as ketone bodies, glycogen, and monocarboxylates in the brain. The aim of this review is to discuss hypoglycemia-induced metabolic alterations in the brain in glucose counterregulation, uptake, utilization and metabolism, cellular respiration, amino acid and lipid metabolism, and the significance of other sources of energy. The present review summarizes information on hypoglycemia-induced metabolic changes in the brain of diabetic and non-diabetic subjects and the manner in which they may affect brain function

Polish Academy of Sciences

Role of phosphoinositide 3-kinase in ischemic postconditioning-induced attenuation of cerebral ischemia-evoked behavioral deficits in mic