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Difference between Appendix and the Cecum?

Difference between Appendix and the Cecum?



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What's the difference between an appendix and a cecum, and what are their functions?


In herbivores the Cecum is an area that stores plant matter and helps digest it via symbiotic bacteria. Carnivores have smaller Cecums because meat is easier to digest than plant matter. In humans the Cecum is also an anatomical landmark that delineates the change from small intestine (a digesting organ) to the large intestine (mostly a capacity/storage organ).

The Appendix is a small, previously thought "superfluous" fleshy worm-shaped organ at the junction between the small and large intestines. Recent research posits that the appendix is sort of a harbor for a person's gut flora that can re-populate the intestines should the existing bacteria die or get removed (diarrhea being the most common cause). It can also become infected, inflamed, and require surgery to remove (Appendicitis).


Appendix and cecum both are parts of the large intestine.

Appendix is the inferior extension of the cecum of the large intestine. It is a blind pouch-like structure that resembles a worm, hence the name 'vermiform'.

and

Cecum is a small intraperitoneal pouch-like structure located on the right side of the lower abdomen.

Source - Knowyourbody.net


Cecum

Cecum or also known as “caecum,” is a small intraperitoneal pouch-like structure located on the right side of the lower abdomen. It is the starting point of the large intestine and lies between ileum and the ascending colon, into which the ileum (last part of the small intestine) empties digested content from the small intestine, to be further processed and digested in the large intestine.

Cecum helps in absorbing water from the solid waste produced by the small intestine and also lubricates and further processes the waste with the help of various enzymes to be digested in the large intestine and through the end stage of digestion.


Contents

Development Edit

The cecum and appendix are formed by the enlargement of the postarterial segment of the midgut loop. The proximal part of the bud grows rapidly to form the cecum. The lateral wall of the cecum grows much more rapidly than the medial wall, with the result that the point of attachment of the appendix comes to lie on the medial side. [ citation needed ]

Etymology Edit

The term cecum comes from the Latin (intestinum) caecum, literally "blind intestine", here in the sense "blind gut" or "cul de sac". [ citation needed ] It is a direct translation from Ancient Greek τυφλὸν (ἔντερον) - typhlòn (énteron). Thus the inflammation of the cecum is called typhlitis.

In dissections by the Greek philosophers, the connection between the ileum of the small intestines and the cecum was not fully understood. Most of the studies of the digestive tract were done on animals and the results were compared to human structures. [ citation needed ]

The junction between the small intestine and the colon, called the ileocecal valve, is so small in some animals that it was not considered to be a connection between the small and large intestines. During a dissection, the colon could be traced from the rectum, to the sigmoid colon, through the descending, transverse, and ascending sections. The cecum is an end point for the colon with a dead-end portion terminating with the appendix. [5]

The connection between the end of the small intestine (ileum) and the start (as viewed from the perspective of food being processed) of the colon (cecum) is now clearly understood, and is called the ileocolic orifice. The connection between the end of the cecum and the beginning of the ascending colon is called the cecocolic orifice.

A cecal carcinoid tumor is a carcinoid tumor of the cecum. An appendiceal carcinoid tumor (a carcinoid tumor of the appendix) is sometimes found next to a cecal carcinoid. [ citation needed ]

Neutropenic enterocolitis (typhlitis) is the condition of inflammation of the cecum, primarily caused by bacterial infections.

Over 99% of the bacteria in the gut are anaerobes, [6] [7] [8] [9] [10] but in the cecum, aerobic bacteria reach high densities. [11]

A cecum is present in most amniote species, and also in lungfish, but not in any living species of amphibian. In reptiles, it is usually a single median structure, arising from the dorsal side of the large intestine. Birds typically have two paired ceca, as do, unlike other mammals, hyraxes. [12] Parrots do not have ceca. [13]

Most mammalian herbivores have a relatively large cecum, hosting a large number of bacteria, which aid in the enzymatic breakdown of plant materials such as cellulose in many species, it is considerably wider than the colon. In contrast, obligatory carnivores, whose diets contain little or no plant material, have a reduced cecum, which is often partially or wholly replaced by the appendix. [12] Mammalian species which do not develop a cecum include raccoons, bears, and the red panda.

Many fish have a number of small outpocketings, called pyloric ceca, along their intestine despite the name they are not homologous with the cecum of amniotes, and their purpose is to increase the overall area of the digestive epithelium. [12] Some invertebrates, such as squid, [14] may also have structures with the same name, but these have no relationship with those of vertebrates.


Introduction

The appendix in humans is a narrow extension from the terminal end of the cecum, with dimensions of about 10 cm by 7–8 mm, and has an internal (luminal) diameter of 1–3 mm. The appendix has been considered, variably, an evolutionary vestige and a synapomorphy uniting all hominoids (apes and humans). The lack of a known function of the appendix has long been associated with the thought that the human appendix is an evolutionary remnant of a cecum that is utilized to ferment plant material. Charles Darwin, for example, noted the apparent lack of a function of the appendix in humans, and concluded that it must be an evolutionary remnant from a primate ancestor that ate leaves ( Darwin, 1871 ). In fact, numerous researchers have argued that the appendix lacks a particular function in humans ( Huntington, 1903 Johnston, 1919 Royster, 1927 ). On the other hand, data from phylogenetic and immunological studies have long suggested that the appendix may have some specific yet unknown function for which it is adapted (e.g. Berry, 1900 Keith, 1912 Neiburger et al., 1976 Gorgollon, 1978 Scott, 1980 Spencer et al., 1985 Zahid, 2004 ).

Because the appendix in humans is associated with substantial amounts of lymphoid tissue, termed gut-associated lymphoid tissue (GALT), it was proposed more than a century ago that the appendix has some sort of immune function ( Berry, 1900 ). Further, studies have consistently shown that, in animals lacking an appendix, the terminal part of the cecum is rich in lymphoid tissue ( Berry, 1900 Malla, 2003 ). This observation is true across a wide range of species, including birds ( Berry, 1900 ) such as Columba livia (pigeon), Bernicla jubata (maned goose), Polioaetus plumheus (plumbeous fish eagle), and Leptoptilos javanicus (lesser adjutant), and carnivores such as Felis domesticus (cat Berry, 1900 Malla, 2003 ) and Canis lupus familiaris (dog Malla, 2003 ). Thus, it is thought that the immune function carried out by the appendix is analogous to the immune function carried out by the terminal portion of the cecum in animals lacking an appendix. However, an apparent function of the human appendix in the immune-mediated maintenance of the commensal bacterial flora of the gut was only recently identified ( Bollinger et al., 2007 ). Such a delay was understandable: It was not until 2003 that it was realized that the immune system apparently supports growth of beneficial (symbiotic) bacteria in the mammalian gut in the form of microbial communities called biofilms ( Bollinger et al., 2003 Everett et al., 2004 Sonnenburg et al., 2004 ). This conclusion was based on several lines of evidence ( Everett et al., 2004 Sonnenburg et al., 2004 ), including the relatively recent observations that immunoglobulin A (IgA) and mucin, two of the most abundantly produced molecules by the immune system, both support growth of microbial biofilms in laboratory experiments and are associated with microbial biofilms in the mammalian gut ( Bollinger et al., 2003 Sonnenburg et al., 2004 ). Finally, it was found that microbial biofilms are more abundant in the human appendix compared with other areas of the human colon ( Bollinger et al., 2007 ). The implications of these new findings were then considered in light of an array of previously known observations, including the following: (a) the architecture of the human gut, including the relative isolation of the appendix from the main flow of the digestive tract and the narrow lumen (internal opening) of the appendix, (b) the association of the appendix with immune tissue, (c) the association of appendicitis with modern medicine and hygiene, (d) the enormous biological impact of diarrhoeal illness in the absence of modern medicine, sewer treatment systems and clean drinking water, (e) the observation that microbial biofilms are constantly in a state of growth and shedding, (f) the importance of biofilms to bacterial colonization in virtually all environments and (g) the vital role of symbiotic gut bacteria in mammalian biology. In light of these and other considerations, it was concluded ( Bollinger et al., 2007 ) that an apparently important function of the human appendix is service as a well-adapted centre or ‘safe-house’ for maintenance of the symbiotic gut bacteria. Thus, in the event that the intestine becomes infected with a pathogenic species and the faecal material is flushed rapidly from the colon as a defence mechanism (diarrhoeal response), the appendix, which contains normal gut bacteria that form biofilms in a constant state of growth and shedding, serves as a source of bacteria to re-inoculate the gut with its normal gut flora, thus facilitating reestablishment of the normal intestinal flora following infection of the gut ( Bollinger et al., 2007 ). Such rapid reconstitution of the gut flora is likely critical for survival in an environment where diarrhoeal illness is, in concert with malnutrition or perhaps lack of water, extremely life-threatening, particularly to the very young. Diarrhoeal disease, for example, has been at times the single greatest cause of disability-adjusted life years lost in the most populated countries in South-East Asia ( WHO, 2001 ). This assessment provides an explanation for the observation that, regardless of the importance of the function of the appendix throughout evolutionary history, the structure is not apparently important in the face of medical care and hygienic practices associated with developed countries.

Bacterial biofilms and high concentrations of GALT are in fact associated with the terminal portion of the cecum in rats ( Palestrant et al., 2004 ) and in mice ( Swidsinski et al., 2005 ), and with the human appendix ( Bollinger et al., 2007 ) more so than with other portions of the large bowel of these animals. Microbial biofilms have also been found in the ceca of nonhuman primates ( Palestrant et al., 2004 ) and the koala (Phascolarctos cinereus McKenzie, 1978 ). However, it should be noted that the distribution of bacterial biofilms and immune tissue in the gut of many species, including some species possessing an appendix, has not yet been described, and more work in this area is warranted.

The evidence that the appendix may be well suited to serve an important role in humans challenges the belief that this anatomical structure lacks a function, and brings to the forefront the question as to when in mammalian evolutionary history the structure and its current function evolved. In light of the apparent function of the appendix, and of the possible adaptive advantage the appendicular morphology provides for the maintenance of the gut flora, the comparative anatomy and evolution of appendicular morphology are examined and discussed.


Content: Small Intestine Vs Large Intestine

Comparison Chart

PropertiesSmall intestineLarge intestine
DefinitionIt is the intestinal part which extends from the stomach to the large intestineIt is the terminal intestinal part which extends from the appendix to the anus
Length9 meters in length1.5 meters in length
Width3.5 - 4.5 cm in diameter4-6 cm in diameter
ComponentsDuodenum, jejunum and ileumColon, cecum, rectum and anal canal
MovementExhibits small movementThere is no movement as the large intestine is fixed
VilliPresent in the internal surfaceAbsent
Peyers PatchesPresent in the internal surface as aggregation of lymphoid tissueAbsent
HaustraAbsentPresent
Epiploic appendagesAbsentPresent
Circular foldsPalicae circulares presentAbsent
Muscle bandsConsist of circular layer of longitudinal muscleConsist of longitudinal muscles in three bands known as Tineae coli
Wall surfaceSmoothSacculated
AbsorptionInvolved in absorption of nutrients from the digested foodInvolved in absorption of water and electrolytes from the undigested portion of food
FunctionHelps in digestion of the undigested or partially digested food by secreting intestinal fluidsIt expels out the waste material through the anus

Definition of Small Intestine

The small intestine extends from a lower part of the stomach to a large intestine part. It is a very long and narrow tube with a smooth wall surface. It appears as a coiled tube in the abdominal region and comprises three components from the proximal end to the distal end. Duodenum, jejunum and ileum are the three sections of the small intestine. It performs several functions in the abdominal region like digestion of food, absorption of nutrients etc.

Definition of Large Intestine

The large intestine extends from the appendix to the anus. It appears as a wider and short tube with a sacculated wall surface. The large intestine frames the coiled tube (small intestine) in the abdominal region and comprises four components. Cecum, colon, rectum and anal canal are the four sections of the large intestine. It conducts several functions in the abdominal region like the movement of food, adsorption of electrolytes and water etc.

Parts of Small Intestine

It comprises of three components like:

  1. Duodenum: It is the first part of the small intestine, which is the shortest region (measures 25.4 cm). Duodenum begins from the pyloric sphincter. It bends posteriorly behind the peritoneum. Then duodenum appears as a C-shape around the pancreas. Duodenum then again bends or returns to the peritoneal cavity and joins with the jejunum cavity. The ampulla is the region that opens into the duodenum.
  2. Jejunum: It is the second portion of the small intestine that measures 0.9 m length. The jejunum is the part of the small intestine that begins from the duodenum’s distal end to the terminal part of the ileum. It is present in the posterior abdominal wall.
  3. Ileum: It is the longest part of the small intestine that measures 1.8 m length. The ileum appears thick and develops mucosal folds. It joins the cecum of the large intestine to the ileocecal valve. The ileum is located at the posterior abdominal wall.

Parts of Large Intestine

It includes four components like:

  1. Cecum: It is the first region of the large intestine that seems sac-like. The cecum is inferior to the ileocecal valve. It measures a length of 6 cm. A vermiform appendix comprises of lymphoid tissues, and it opens into the cecum.
  2. Colon: It moves upwards on the right side of the abdomen called ascending colon. Then the colon slightly bent and termed as transverse colon where it forms right colic or hepatic flexure. Colon then moves towards the abdomen’s left side and bends sharply to form left colic or splenic flexure. Then, it travels downward and termed as the descending colon. Finally, colon inferiorly enters to the pelvis and forms a sigmoid colon that extends medially.
  3. Rectum: Sigmoid colon opens into the rectum and reaches anteriorly to the sacrum and coccyx. Rectum possesses rectal valves that hold three lateral bends of the transverse folds. Its primary function is the separation of faeces and gas to prevent simultaneous release.
  4. Anal canal: It is the last part of the large intestine. The anal canal is located in the perineum region and outside the abdominal pelvic cavity. It measures 3.8-5 cm in length. Anal canal comprises of two sphincters:
    • Internal anal sphincters : It is composed of smooth muscle, i.e. it is under the control of involuntary muscle activity.
    • External anal sphincters : It is composed of skeletal muscle, which is under voluntary control.

Interaction with microbial flora

The intestinal biofilm

The most luminal lining of the large intestinal wall contains the biofilm, a layer of commensal gut bacteria within a matrix of mucus that is believed to aid immune exclusion of pathogens by preventing them from crossing the intestinal barrier. The layer of thick, firm mucin that lays directly upon the intestinal epithelial cells is insoluble, thus preventing (pathogenic) bacteria from being in contact with the epithelium 38. On top of this firm layer and directly adjacent to the lumen is a layer of looser mucin and commensal gut bacteria, together forming the biofilm 39, 40. In addition to the direct barrier function of the firm inner mucus layer, immune exclusion of potential pathogens could also be an indirect effect of the inclusion of microbiota in the biofilm, as bacteria within a biofilm are less likely to cross the epithelial barrier compared to single, planktonic bacteria 4, 25.

Apart from mechanical barrier formation, biofilms shed bacteria actively from their surface. Shedding of planktonic bacteria could be seen as the mechanism behind immune exclusion of pathogens throughout the whole large intestine. Conversely, the shedding of parts of the biofilm itself is rather believed to facilitate (re)colonization of beneficial bacteria 41, 42 (Fig. ​ (Fig.3). 3 ). This could be a function carried out exclusively by the appendix, as it is believed to be the only place within the large intestine that has not been cleared from its normal biofilm after diarrhoeal illness. During diarrhoea, turnover of enterocytes and thus shedding of the biofilm is accelerated 43, thereby leaving the intestinal wall derived of its protective barrier.

The process of biofilm formation, shedding and recolonization. Bacteria adhere to the surface. Biofilm formation and expansion by embedding bacteria within the mucin layer. Parts of the biofilm shed, which allows bacteria to relocate and recolonize (adapted from reference 42).

In contrast to the suggested induction of biofilm shedding by pathogens during acute diarrhoeal illness, diarrhoea‐inducing infectious agents actually enhance mucin gene expression 44, 45. This enhancement, mediated particularly by cytokines such as tumour necrosis factor (TNF)‐α 44, may indicate a stronger binding instead of an easier shedding. This could be seen as a reaction to the disruption of the mucus layers following bacterial invasion, but the definite function has not been determined. However, during an infection the intestinal wall shows an increase in goblet cells and mucus secretion compared to the healthy situation, which may explain the enhanced mucin gene expression. As this is associated with a better clearance of the pathogen 39, whether by speeding up the mucus turnover or creating a thicker layer, it could be seen as a defence mechanism against the infection.

Special role for the appendiceal biofilm

The protected location in the most proximal part of the colon and its relatively little contact with faeces because of this location, and its narrow (worm‐like) lumen, have given rise to the assumption that the appendiceal lumen is spared from the diarrhoeal clearance. Thus, the biofilm in the appendix is thought to act as a ‘safe house’ for commensal bacteria and to facilitate their reinoculation of the gut after a gastrointestinal infection 2, 3, 4. Secretory IgA (sIgA) and mucin assist in biofilm formation by increasing adhesive growth of the agglutinated gut flora 4, 25, 26, as sIgA stimulates the agglutination of bacteria and mucin binds these bacteria to the mucus layer. In the appendix, there is an overall high density of mucin and sIgA produced by B cells in the mucosa. Thus, the outer loose mucus layer of the appendix has a promicrobiotic environment, once again supporting its function as a ‘safe house’ 4.

Furthermore, the presence of commensal bacteria in neonatal intestines of mice causes an immune reaction by stimulating B cells in germinal centres to produce antibodies, thereby assuring a normal development of the immune system 46. In humans, timing of the development of lymphoid follicles is consistent with the presence of bacteria in gut mucosa, both of which occur after the first 4 weeks postnatally 1.

The intestines of germ𠄏ree animals show a decrease in IELs, IgA levels and lamina propria lymphocytes 47, an impaired maturation of lymphocyte aggregates into isolated lymphoid follicles or Peyer's patches 48, 49 and smaller germinal centres 49 caused possibly by the absence of proliferating B cells 50. As the immune function within the intestine is otherwise impaired, it is therefore suggested that interaction with the commensal flora helps the GALT in developing an adequate immune response to pathogens 1, 25, 48, 49. Considering the high density of bacteria in the appendix and its assumed function as a ‘safe house’, it could indicate that the appendiceal biofilm has a crucial immunological role in aiding the development of a normal (intestinal) immune system.


Prognosis

The prognosis is somewhat poorer for cancers of the cecum than for other colon cancers, most likely related to the greater difficulty in diagnosing the disease in the early stages.

Diagnosis can be more difficult for cancers of the cecum because symptoms differ from colon cancers further along in the colon, and because it's harder to visualize this area on screening tests. Compared with left-sided colon cancers, right-sided colon cancers, such as those of the cecum, have somewhat poorer survival rates.

Despite this prognosis, right-sided colon cancers are less likely to spread (metastasize) to the liver and lungs than left-sided colon cancers.


The cecum is also responsible for breaking down the cellulose fibers from digesting plant matter. Animals, both herbivores and omnivores, take in cellulose when eating plants. Bacteria and enzymes in the cecum of these animals cause fermentation that breaks down cellulose fibers, which then allows the rest of the large intestine to digest the nutrients from cellulose.

The cecum functions differently in various animal species. Though most vertebrates’ digestive systems include a cecum, carnivores such as tigers and wolves have either a very small cecum, or it is nonexistent. Since these animals do not consume plant matter, the cecum is unnecessary. The cecum of herbivores is much larger than the cecum of omnivores. These animals consume more cellulose and water, making a larger cecum necessary for effective digestion.


The Riddle of the Appendix

I recently spent a few days recovering from having my appendix removed. As I padded around my house in my pajamas, I pondered that dear departed bit of my gut.

I only became aware of my appendix when it flared with infection. Soon I was lying in an ambulance, with a paramedic poking at my abdomen. "Oh yeah," he said, and went back to filling out paperwork.

The nurses and doctors at the hospital agreed, and a CT scan confirmed the diagnosis. Not long after, I was unconscious, and a surgeon was cutting open my side to get my appendix out before it ruptured. My life might be hanging in the balance, but the procedure had the routine efficiency of a teeth cleaning.

That's what comes with practice. When I got back home, I began doing some research and found that each year, more than 250,000 Americans had appendectomies. The more I thought about that figure, the more absurd it seemed. Why should an organ fail in so many healthy people? What makes it more puzzling is that no one ever needs an appendix transplant. Appendix-free, I can expect a normal life.

I called Dr. Rebecca Fisher, a physical anthropologist at Midwestern University in Glendale, Ariz., who has given serious thought to the paradox of the appendix. "There are a lot of questions about this little thing that everybody takes for granted," Dr. Fisher said.

The fact that I was alive without my appendix, she said, did not necessarily mean it had no function. The appendix buds off from a bulge at the front of the large intestine, called the cecum. It forms a narrow, finger-size pouch.

The appendix does not seem to be involved in digesting food, but it may help the gut to fight disease. The appendix is packed with immune-cell-producing tissues.

That fact has led some scientists to suggest that during childhood it teaches the gut's immune system how to tell the difference between dangerous pathogens that should be attacked and harmless food that should be ignored.

But when people get their appendix removed, other immune-cell-producing tissues in the cecum and elsewhere can compensate for the loss.

Even if the appendix serves a function, it is hard to understand why it has such a peculiar shape. "There's no real good explanation for why youɽ have a blind end," Dr. Fisher said. "The immune cells can still enter the cecum, but why make it harder? We really don't know."

The shape of the appendix is also the reason it is so dangerous. Its narrow channel can become sealed, either by a minor overgrowth of its own cells, or by a bit of half-digested food. Once the appendix is inflamed, the swelling cuts off blood vessels, making it vulnerable to bacteria.

You sometimes hear people who say they reject evolution claim that our bodies show clear signs of being "intelligently designed." I wonder how many of them have had appendicitis.

To solve the paradox of the human appendix, Dr. Fisher wants to know how it evolved. "If only the appendix fossilized," she said ruefully. Instead, she compared our guts to those of other species.

Chimpanzees and other apes are our closest living relatives, and they all have an appendix that looks a lot like ours. So it's reasonable to infer that our common ancestor 30 million years ago also had one.

But when Dr. Fisher researched the guts of other primates, the picture got blurrier. "In some cases it's absent, but in other cases it's spot-on looking like a human appendix," she said.

Some primate species fall somewhere in between these two extremes, with just a narrowed tip forming on the cecum. Dr. Fisher suspects that the appendix evolved several times in primates, but she cannot say what conditions favored its evolution. "Since the data is so poor, I think any trend would just be a lucky happenstance," she said.

Still, I wondered how such a dangerous and disposable organ could survive over evolutionary time. "We consider it maladaptive because we want to live to a very old age," Dr. Fisher said. "But from a strictly Darwinian view, it might not be."

Imagine a trait that helps an animal survive to adulthood, but that also has side effects that can cause trouble later in life. If, on balance, animals produce more offspring with the trait than without it, natural selection will favor it.

Perhaps the appendix lifted the odds that our ancestors could resist childhood diseases and live to childbearing years. Even if it also caused deaths by appendicitis, the appendix might have been a net plus. (It's also possible that appendicitis wasn't such a big problem in the past. Some scientists have argued that modern Western life has made appendicitis more common, either as a result of a change in hygiene or in the foods we eat.)

Dr. Fisher's "net-plus" hypothesis is one of several possible explanations. But they all remain speculation, she said, until scientists learn a lot more about the appendix. "It seems basic, but it's also very hard," she said.

As fascinating as the evolution of the appendix may be, my conversation with Dr. Fisher got me thinking about another part of the human body: the brain.

I was grateful that we have not only inherited a danger-prone appendix, but a brain that can invent surgery. Now I may live long enough to see the mystery of the appendix solved.


The pattern of neural crest advance in the cecum and colon ☆

Neural crest cells leave the hindbrain, enter the gut mesenchyme at the pharynx, and migrate as strands of cells to the terminal bowel to form the enteric nervous system. We generated embryos containing fluorescent enteric neural crest-derived cells (ENCCs) by mating Wnt1-Cre mice with Rosa-floxed-YFP mice and investigated ENCC behavior in the intact gut of mouse embryos using time-lapse fluorescent microscopy. With respect to the entire gut, we have found that ENCCs in the cecum and proximal colon behave uniquely. ENCCs migrating caudally through either the ileum, or caudal colon, are gradually advancing populations of strands displaying largely unpredictable local trajectories. However, in the cecum, advancing ENCCs pause for approximately 12 h, and then display an invariable pattern of migration to distinct regions of the cecum and proximal colon. In addition, while most ENCCs migrating through other regions of the gut remain interconnected as strands ENCCs initially migrating through the cecum and proximal colon fragment from the main population and advance as isolated single cells. These cells aggregate into groups isolated from the main network, and eventually extend strands themselves to reestablish a network in the mid-colon. As the advancing network of ENCCs reaches the terminal bowel, strands of sacral crest cells extend, and intersect with vagal crest to bridge the small space between. We found a relationship between ENCC number, interaction, and migratory behavior by utilizing endogenously isolated strands and by making cuts along the ENCC wavefront. Depending on the number of cells, the ENCCs aggregated, proliferated, and extended strands to advance the wavefront. Our results show that interactions between ENCCs are important for regulating behaviors necessary for their advancement.


Watch the video: 10- Cecum u0026 Appendix part 1 Dr Basma Anatomy GIT (August 2022).