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Background: Semmelweis reflex is a human behavioral tendency to stick to preexisting beliefs and to reject fresh ideas that contradict them (despite adequate evidence). We aim to familiarize the readers with the term that not only has a significant historical background but also grave clinical implications.

Methods: A keyword search for "Semmelweis reflex," "Belief perseverance," "handwashing," and "Idea rejection" was conducted using PubMed Central, MEDLINE, and Google SCHOLAR. Literature published in paper-based journals and books was also searched. All manuscripts pertaining to these keywords were thoroughly analyzed for this review.

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Conclusions: The age-old prejudice that is Semmelweis reflex is explored in this review. With careful and thorough study design, scientific rigor, and critical self-analysis of the manuscript, one can avoid being victimized by this reflex. The dual edged nature of this reflex lays unveiled when its importance is highlighted in the prematurely accepted medical failures. Understanding that any new idea goes through the grill of being critically analyzed and perceived encourages the scientist to hold on to the original thought as it may rather be practice changing.

The gastrocolic reflex is a physiological reflex that controls the motility of the lower gastrointestinal tract following a meal. As a result of the gastrocolic reflex, the colon has increased motility in response to the stretch of the stomach with the ingestion of food. The gastrocolic reflex allows room for the consumption of more food via control over peristalsis and movement of ingested food distally toward the rectum. Myoelectric recordings demonstrate the reflex in the large intestine that shows a spike in electrical activity within minutes of food consumption. The gastrocolic reflex initiates and controls migrating motor complexes throughout the colon. These motor complexes act cyclically during the digestion process and can be broken up into four phases.

Alteration in the gastrocolic reflex has been a suspected etiology in patients with irritable bowel syndrome (IBS). Patients with IBS have demonstrated a stronger colonic response to the gastrocolic reflex. These patients may experience a strong urge to defecate following ingestion of a meal and may experience symptoms like abdominal distension, flatulence, pain, and tenesmus.[3][4] Furthermore, alternations in the gut microbiome can cause a downstream effect that alters the enteroendocrine cells' ability to sense and carry out paracrine functions, thus indirectly affecting the motility of the colon.

Profound gastrocolic reflex has been implicated in the idiopathic variant of dumping syndrome (DS). Although abdominal pain is present in both DS and IBS, systemic signs including palpitations, hypotension, dizziness, diaphoresis often accompany DS. Another key difference in the presentation of DS is that they often present with protein-calorie malnutrition due to increased excess nutritional loss in diarrhea.[5]

Both IBS and DS are caused by profound gastrocolic reflex, whereas poor gastrocolic reflex results in constipation. Neuronal dysfunction may lead to impaired gastrocolic reflex and poor gut motility. Diabetic patients with neuropathy often have gastroparesis resulting in delayed gastric emptying and also impaired gastrocolic reflex leading to constipation.[6]

The gastrocolic reflex is multisystemic in origin. The reflex involves the autonomic nervous system, the enteric nervous system, and cells of the GI tract that regulate endocrine functions. Signals from the central nervous system communicate with the enteric nervous system and vice versa controlling peristalsis. The enteric nervous system proves to be paramount and is demonstrated by the morbid effects of enteric nervous system neuropathies; this is in contrast with the importance of vagal and sympathetic inputs, which have shown not to carry as much of an effect if these connections become interrupted.[14]

When food gets introduced into the stomach, a coordinated response via stretch receptors, neuropeptides, and the enteric nervous system activate the gastrocolic reflex, which in turn increases the motility in the colon to make room for more food. Migrating motor complexes induce food bolus movement through slow waves and faster segments of increased electrical activity, know as spike waves; this is very similar to how the stomach and small intestine move food. The large bowel also employs stronger, more frequent contractions known as mass movements in response to signals from mechanical stretch receptors in the stomach and the products of digestion in the small intestine. The enteric nervous system controls these mass movements and is most active in the transverse and left colon, which helps move food toward the rectum for defecation, which is the reason behind the urge to defecate following ingestion of a meal.[17][2]

A colon transit study may be employed to test for the functionality of the gastrocolic reflex. The gold standard for measuring colon transit time utilizes a radiopaque indicator that is easy to do and relatively low cost. The only downside to this test is that it subjects the patient undergoing radiation exposure. Another test utilized is radionuclide scintigraphy. This is done using a labeled radioisotope and viewed through a specialized camera. The patient swallows a labeled radioisotope, and it gets followed throughout transit through the GI tract; this approach exposes a lesser degree of radiation. Both of these transit studies are usually for research purposes and less often used in clinical practice. Colonic manometry and bead expulsion are more frequently used to assess the contractility and motility of the colon. Colonic manometry is a more common modality in children with colonic dysmotility, encopresis, and abdominal pain. They record various colonic motor contractions and guide the further courses of treatment, including the need for surgical interventions.[18] Lastly, a test that uses wireless motility capsules has been considered.[19]

The gastrocolic reflex has correlations with the pathogenesis of irritable bowel syndrome. The act of food consumption can provoke an overreaction of the gastrocolic response due to heightened visceral sensitivity seen in IBS patients, resulting in abdominal pain, constipation, diarrhea, bloating, and tenesmus. It is also a known fact that ondansetron decreases the tonic response to stretch, giving evidence toward its use in providing relief for patients with IBS. Commonly prescribed medications to treat overreactive gastrocolic response include antispasmodics, tricyclic antidepressants, and SSRIs. Antibiotics and probiotics have also been utilized to restore normal colonic flora, which in turn helps regulate the response of integral components of the reflex.

The gastrocolic reflex is most active during morning time and immediately after meals. Using this physiological reflex to our advantage helps treat constipation. For both children and geriatric patients with constipation, using the toilet immediately after having breakfast and establishing a daily routine helps to improve constipation. The use of stimulant laxatives like sennosides or bisacodyl will augment the gastrocolic reflex and helps in improved colonic contractions and defecation.

How's your day! Photographers. I heard that Canon will stop making Single-Reflex cameras but Non-Reflex cameras. What do you think? Do you feel like non-reflex cameras will replace single reflex cameras? How long?

For me, I just got my Canon 5D Mark IV. I really love the kinda heavy camera (I work out a lot so it's not an issue for me, it's too light weight tbh lol). I also love the sound the single-reflex cameras make.

The single lens reflex was a solution to these problems but it presented its own issues and added to the cost and complexity of the camera. I'm sure the clever folks at Nikon, Canon et al are thinking that now that we CAN dispense with the mirror box, why wouldn't we? It creates so many obstacles to camera design that dispensing with it frees up the designers to innovate in many ways, not least new compact designs of lens.

Currently variety of career development tools is available, some of them are formal and structured, other are based on informal and self-directed approach. But how to ensure that these tools, usually designed for the use in certain research environments, can be transferred to other contexts? And how to make them more reflexive to the increasing variability of career patterns and opportunities which arise with the creation of brand new jobs in the near future?

First described in 1908, the oculocardicac reflex (OCR; also known as the Aschner reflex or trigeminovagal reflex) is a reduction of the heart rate resulting from direct pressure placed on the extraocular muscles (EOM), globe, or conjunctiva.[1] The reflex is defined by a decrease in heart rate by greater than 20% following the exertion of the aforementioned eye pressure.[2] The reflex is mediated by the connection between the ophthalmic branch of the trigeminal nerve and the vagus nerve. Most commonly, the reflex induces bradycardia, though it has also been reported to cause arrhythmias and, in extreme cases, cardiac arrest. The reflex has most often been encountered during ophthalmologic procedures such as strabismus surgery, though it has also been seen in cases of facial trauma, regional anesthetic nerve blocks, and mechanical stimulation.[3] Historically, the oculocardiac reflex was used as a diagnostic tool to evaluate syncope, as well as to terminate supraventricular tachycardias, but this is no longer done given the limited clinical application and the associated risks.[4]

The OCR arc is comprised of an afferent limb (carried by the trigeminal nerve (CN V)) and an efferent limb (carried by the vagus nerve (CN X)). The reflex begins with the activation of stretch receptors in periorbital and ocular tissues. The long and short ciliary nerves carry the impulses to the ciliary ganglion, where the ophthalmic division of CN V carries the impulses to the Gasserian ganglion, and subsequently to the trigeminal nucleus. The afferent nerves synapse with the visceral motor nucleus of the vagus nerve in the reticular formation of the brain stem, where the impulses are then carried to the myocardium to activate the vagal motor response at the sinoatrial (SA) node, resulting in bradycardia.[5] 2351a5e196