In 2200-2500 words describe:
1) biological question under investigation
2) goalsof the researchers
- short term
-long term
3) methods / technologies used
-highlight any novel aspects of the authors methodology
4) Key results of the study
5) Major findings/conclusions -> agree/disagree (this is the important part)
6) critical analysis of the author's claims
7) Conclusions
-summarize your argument
-put the work in perspective for your target audience

Sample Answer

These benevolent reflux scenes are 90% cleared by an optional peristalsis wave and 10% cleared by salivation killing the rest of the substance; and tend not to represent a peril for acid reflux or irritation. In this manner, 80% to 90% of reflux scenes go unnoticed or are asymptomatic. It very well may be considered, at that point, that GERD patients are ordered into two subgroups that have diverse clinical qualities: 1) the erosive esophagitis (EE) bunch that encounters aggravation of the mucosal fixing with interminable hypotensive LES; and 2), the non-erosive reflux sickness (NERD) bunch that has the basic indigestion side effect with obsessive heartburn yet without proof of mucosal harm on endoscopy.

Indigestion is the incitement of chemoreceptors in the mucosa layer by gastric corrosive and bile salts where the pH is under four; and it introduces as the impression of torment or consuming in the thoracic heart district. Geek is evaluated to involve about half to 70% of the GERD populace, and the pathogenic dangers of going from profiles of NERD to EE to BE are thought to be exceptionally low over all classes is still under scrutiny. Basically, when seen as in both of the three classifications, the patient state will stay in that particular class for the rest of their lifetime. The patient profile for both NERD and erosive esophagitis are comparable in that the mean age at finding is around 50, yet a 60/40 split for ladies to men includes the NERD gathering, while 59% of the EE bunch is men. EE patients additionally present with a higher weight record and a higher commonness of hiatal hernia.

It is the point at which the scenes of reflux become progressively visit and extended (longer than five minutes) that the typical esophageal leeway instruments start to lose their viability and lead to esophagitis and BE. Obviously, contrasting solid people with NERD, esophagitis, and BE produces a heightening increment in the quantity of reflux occasions and longer presentation periods to acids not as much as pH 4.0 over the succession. The steadiness of corrosive in the scope of pH 2.0 to 4.0 joined with pepsin instigates harm to the mucosal coating, causing the nearness of widened intercellular spaces that are proof of the main injury. The enlarged spaces between the cells consider the entrance of corrosive more profound into the mucosal covering, which bargains the mucosal protection from corrosive. More profound corrosive entrance additionally initiates or enrolls progressively fringe nociceptors to transmit torment signals. Esophageal harm is surveyed by the Los Angeles

Order of Esophagitis :

• Grade A: One (or more) mucosal break no longer than 5 mm that doesn't stretch out between the highest points of two mucosal folds

• Grade B: (at least one) mucosal break in excess of 5 mm long that doesn't reach out between the highest points of two mucosal folds

• Grade C: (at least one) mucosal break that is nonstop between the highest points of at least two mucosal overlays however which include under 75% of the circuit

• Grade D: (at least one) mucosal break which includes in any event 75% of the esophageal boundary

The best possibilities for reflux happening are 30 to an hour in the wake of eating a dinner, during twisting around, resting, and during rest. Agony may likewise be brought about by mechanical methods like esophageal expansion and peristalsis motility issue. Various creates to the uproar of torment can jumble the genuine idea of GERD, however, and may mean a mix of anatomic and physiologic unsettling influences. Different side effects from GERD may incorporate dysphagia (trouble gulping), laryngitis, pharyngitis, asthma, interminable hack, or dental disintegration. Reflux arriving at all the path back up the throat and into the pharynx may cause aggravation in the pharyngeal tissue or dissolve teeth veneer; and in the event that it escapes into the larynx it can disturb the vocal ropes and trachea.

Failing of the LES assumes a key job in the reflux of stomach liquid in the throat. Ordinarily, the LES's resting pressure is 15 mm Hg to 30 mm Hg more noteworthy than that of the intra-stomach pressure and will satisfactorily hinder the reflux of stomach liquids. The weight at the LES doesn't remain at a consistent rate, however, and will contrast contingent upon the body position, breathing, development, and time of day; where it is low during the day and higher at evening. The LES pressure likewise falls impaired to various outside mixes (Table 2) like drugs, hormones, and nourishment synthetic concoctions.

Table 2. Exacerbates that bother conditions inside the gastric chamber.

Nourishments Peppermint, chocolate, caffeine, liquor, tobacco, citrus products of the soil, hot food sources, crude onions, tomatoes

Hormones and Neurotransmitters Secretin, cholecystokinin, glucagon, progesterone, vasoactive intestinal polypeptide, gastric inhibitory polypeptide, serotonin, dopamine

Prescriptions Nitrates, morphine, barbiturates, diazepam, calcium channel blockers, atropine, tricyclic antidepressants, ganglion blockers

A second line of control becomes possibly the most important factor with the left and right crural muscles of the stomach, which interface with the LES by means of the phrenoesophageal tendon. These stomach muscles regularly help in forestalling reflux during times of truly difficult work, pregnancy, and some other reasons for expanded stomach pressure. Transient LES relaxations (TLESRs) are relaxations of the LES directed by the vagus nerve and for the most part brought about by the development of gastric gases or stomach distension, as in, they are disconnected to gulping or peristalsis. These relaxations of the LES can last anyplace between 10 to 35 seconds and lessen the weight of the LES to levels lined up with the gastric weight. During TLESRs, the crural muscles of the stomach are repressed, discharging pressure on the sphincter opening. TLESRs are increasingly visit in GERD by adding to practically 90% of reflux scenes, and hiatal hernias worsen the issue much further by prompting expanded sphincter openings. Hiatal hernias are the point at which a segment of the stomach pushes upwards past the stomach. 90% of hiatal hernias are Type 1, where the LES moves upwards and pushes through the stomach. Rarer structures include the crushing of the fundus bit of stomach past the stomach and results in a pocket favorable for waiting stomach corrosive. Type 1 causes a decrease of LES weight and length, restricting corrosive leeway and expanding mucosa introduction to corrosive mixes. Weight and debilitating of the encompassing muscles are the primary driver for hiatal hernias, with expanding age adding to the debilitating of muscle structures. More seasoned individuals ordinarily have a higher weight file, too. The phrenoesophageal tendons may likewise lose flexibility with age and add to the development of the hernias. When hiatal hernias surpass two centimeters, at that point the rate of esophagitis and BE is higher.

Components that can add to the advancement of GERD include a few methods of brokenness. Peristaltic brokenness frustrates corrosive freedom from the distal throat and comes in the types of disappointment for peristaltic compression or low-adequacy withdrawal waves. Brokenness in the purging of the stomach can happen through gastroparesis, neuromuscular infections, pyloric brokenness, duodenal motility issue, and even duodenogastric reflux (DGR). DGR is the reflux of bile from the duodenum over into the stomach. Some bile reflux is ordinary, because of nearness, yet reflux may happen in bigger amounts and blend in with the substance of the stomach. Upon gastric reflux, the gastric corrosive and bile blend goes up into the throat. DGR is found to assume a job in irritation and damage of the throat. In those with esophagitis, DGR is substantially more typical and means bile corrosive alongside gastric corrosive are aggravating damage to the mucosal covering (Fig. 9). With patients displaying the Los Angeles esophagitis rating framework from A-D in expanding mucosal breaks, DGR has been in found in 67, 68, 80, and 100% of patients in those classes, individually. This discovering builds up an unmistakable connection between the transaction of DGR, bile corrosive, and esophagitis paving the way to metaplastic change. Different factors are Zollinger-Ellison disorder (where corrosive is discharged in better than average sums), ulcers or strictures that discourage the gastric outlet, and connective tissue issue like scleroderma.

Figure 9. Contrasting corrosive bile profiles among various GERD subgroups shows that having corrosive and bile together prompts more serious hazard for convoluted BE, or the precancerous state of dysplasia.

Stomach Acids and Bile

As has been referenced already, stomach acids and bile acids assume a focal job in the advancement of metaplastic BE tissue. Under ordinary conditions, stomach acids are crucial to the breakdown of nourishments and the correct working of the stomach related framework. Our sensory system is exceptionally delicate to improvements including nourishment, where the sight, smell, contact, and taste of nourishment trigger the corrosive administrative pathways in the stomach: acetylcholine, gastrin, and histamine. The gastric organs of the stomach lining manage the corrosive pathways and produce various substances like bodily fluid, gastrin, pepsinogen, histamine, and inherent factor. Bodily fluid emitting cells are found externally in the organs and are intended to shield the stomach lining from its own one of a kind corrosive through a bicarbonate cradle. The cells found further in the organs are parietal cells, which emit hydrochloric corrosive (HCL) in view of surface receptor initiation. Those receptors are touchy for histamine, acetylcholine, and gastrin; and will cause a surge of HCL that can bring down the pH of the gastric liquid to 1 or less. Upon an upgrade, gastrin is discharged from G cells in the antrum of the stomach. The gastrin goes through the circulatory system to gastrin receptors on parietal cells in the gastric body and fundus; and starts the concoction initiation of proton siphons situated on the contrary side of the cells. Parietal cells will likewise initiate the HCL pathway through receptors for histamin