#microvillus

[wintcosmetics]

Master pdf editor 3.6.17 mac599 28.10mb

In animal disease models, the ability to mount an immune response is also hindered in GF animals and restored upon conventionalization (i.e., restoration of microbiota from an animal raised under standard laboratory conditions) ( 4, 5). Moreover, GF mice have decreased expression levels of pattern recognition receptors that detect microbes (e.g., Toll and NOD-like), as well as of antimicrobial peptides (e.g., Reg3γ), which strongly highlights how the microbiota impacts the functional role of the immune system ( 2, 3). For example, germ-free (GF) mice have decreased gut lymphoid tissue development, as well as altered microvillus architecture ( 1, 2). Furthermore, several studies have demonstrated the importance of the microbiota in the development and maintenance of health. These body sites serve as the interface that fosters interactions between the microbes and their respective host. At birth, humans become exposed to microorganisms that establish colonization at various body sites, including the skin, mouth, gastrointestinal (GI) tract, and vaginal epithelium. The intestinal microbiota is the collection of microbes, including bacteria, archaea, viruses, helminths, and fungi, that inhabit our gut. The identification of microbial communities that do not negatively impact bone health may provide a foundation for future investigations that seek to identify microbes that are either beneficial or detrimental to bone metabolism. Our results demonstrate that colonization of mice, both outbred and inbred strains, did not have a major impact on bone health. However, we show here that this is not generalizable to all microbial communities and mouse strain backgrounds. With regard to its effect on bone health, a previous study has suggested that gut microbes negatively impact bone density. IMPORTANCE The microbiota has been shown to be an important regulator of health and development. Furthermore, static and dynamic bone parameters and osteoclast precursor and T cell populations, as well as the expression of several inflammatory markers, were mostly unchanged following microbial colonization of GF mice. In spite of the successful colonization of GF mice with gut microbiota of either mouse or human origin, bone mass did not change significantly in any of the groups tested. GF mice displayed a high degree of colonization, as indicated by more than 90% of the operational taxonomic units present in the starting inoculum being successfully colonized in the mice when they were examined at the end of the experiment. To investigate the impact of different microbial communities on bone health in outbred and inbred mouse strains, gavage was performed on GF Swiss Webster and GF C57BL/6 mice to introduce distinct microbiotas that originated from either humans or mice. We therefore investigated the impact of multiple microbial communities in different mice to understand how generalizable the impact of bacterial colonization is on bone health. A previous study on the colonization of germ-free (GF) mice with a microbial community has demonstrated that bacterial colonization dramatically increases bone loss. The identification of novel regulators of bone health is critical for developing more effective therapeutics. Osteoporosis imparts a great burden on the health care system. Annually, an estimated 2 million osteoporotic fractures occur in the United States alone.

[wisdomrays]

TAFAKKUR: Part 58

The Journey of Drugs through the Body: Part 1

We get ill due to various reasons and in order to get better, we sometimes get some rest, sometimes be extra cautious with what we eat and other times use medicine. But how does medicine get absorbed from our intestines and get transported to the sickened area? How does it get removed from the body? What are the events that affect all these?

Some medications are effective directly over the area they are applied to. Some however are transported to distant regions via blood flow and that is where they are most effective. Medication is either taken orally or through injection. When medicine passes into the blood stream from the place of administration, it is considered to be absorbed. A good example is the transportation of medicine into the blood stream of capillary vessels between the muscle cells when injected into muscle tissue. A drug taken orally however is absorbed through the blood vessels in the gastro-intestinal system.

For orally-taken medication to be absorbed, it should be able to dissolve in gastro-intestinal fluids. First, it is broken into smaller units due to the corroding effects of stomach acid and various enzymes are secreted, then chemicals in the drug composition pass into the gastro-intestinal fluid in a molecular form. This event resembles the dissolving of a sugar cube inside a glass of hot tea. First, the sugar cube gets broken into pieces and then dissolves. A mix with a tea spoon makes this event happen a little faster. In a similar fashion gastro-intestinal movements help with the absorption of medicine. Liquid drugs like syrups dissolve in the gastro-intestinal fluid faster since they are already in smaller units; therefore they get absorbed faster.

Drugs mostly get absorbed through the small intestine. The most important task of this organ is to enable the absorption of nutrients. It is approximately 10 meters long and 4 centimeters wide. The inner lining of the small intestine has finger-like projections called villus and even smaller projections that are located on these villi are called microvillus. One of the reasons, maybe the most important reason, why the our intestines are created in this way is that as a result, the inner surface area of intestines increases multifold. Such that the inner surface area of a human beings small intestine can increase up to 200 m2 and this greatly facilitates the absorption. These projections are made of intestinal cells.

The molecules carrying the medication reach the capillary vessels by passing through these cells and then join the blood stream by crossing through capillary vessel cells. Furthermore, intestinal cell membranes host a special protein that filters unwanted substances for the cell and returns them back to intestinal lumen. Thus these unwanted substances are excreted out of the body along with other unabsorbed matter. In the same way, some drugs are held by this protein and released back into the lumen thus decreasing absorption rate for drugs experiencing this reaction.

Liver: The organ responsible for eliminating the harmful effects of medication

As soon as medication joins the bloodstream after absorption, it is first transported to the liver. This is because pulmonary veins that collect blood from the intestines are connected primarily to the liver. One of the many functions of the liver is the elimination of harmful substances entering the body. For this reason, absorbed substances are directly sent to the liver. The liver is employed with the task of chemical conversion with these substances that are transported to it. One of the wisdoms behind liver metabolism is to reduce the effects of these harmful substances via these events and to convert them into an excretal material. In the same way, drugs are metabolized in the liver, lose their efficacy and prepare for excretion.

Many drugs interfere with each other’s metabolism. If one drug’s metabolism is inhibited, blood concentration of such chemicals increase and adverse effects of drugs become more frequent. Irresponsible drug use must be avoided for this reason. Drug interactions may lead to major damage in addition to the drug’s individual adverse effects. Moreover different nutrients also affect drug metabolism. For instance, grapefruit inhibits metabolism of certain medicines, as a result blood concentration of these medicines increase and adverse effects can be observed. On the other hand, some nutrients like broccoli, cabbage, and charcoal roasted meat speed up the metabolism of certain medicines. In this case, the blood concentration of the affected drug drops and may lead to reduced benefits from intended use. Because of this reason, patients on long-term medicine treatment should not consume these types of food.

The rest of the drug molecules that escape these metabolisms is directed towards blood vessels feeding other organs. Some drug metabolisms in the liver present individual differences as metabolic levels change from person to person. Thus, a drug with the same dosage develops desired blood concentrations for some people, fails to meet this level for others or can even cause high blood concentrations enough to generate adverse effects in other individuals. That is why a medicine that has benefited a patient should never be used by somebody else without consulting a doctor.

[ksstradio]

Social Security Accelerates Decisions For People With Severe Disabilities

Social Security Accelerates Decisions For People With Severe Disabilities

Monday, August 15, 2022 – Mark Hinkle, Press Officer, press.office@ssa.gov Agency Expands Compassionate Allowances List By 12 Conditions Kilolo Kijakazi, Acting Commissioner of Social Security, today announced 12 new Compassionate Allowances conditions: Angioimmunoblastic T-cell Lymphoma, Blastic Plasmacytoid Dendritic Cell Neoplasm, Gerstmann-Straussler-Scheinker Disease, Microvillus Inclusion…

[abdulnadeem5150]

Microvillus inclusion disease is a very rare genetic intestinal condition that usually manifests as within hours or days of birth.Read more..

[campplay]

What are villi

There is connective tissue in the outermost part of the small intestine, smooth muscle tissue in the middle, and cylindrical epithelial tissue in the innermost. This epithelial tissue folds into the intestinal cavity. Those convoluted structures are called villi. MICROVILLUS The cytoplasmic (transparent semi-fluid liquid that fills the inside of the cell) and smaller extensions made by the…

[chromoscience]

Intermediate Filaments

Related Posts

A structural role of microfilaments. The surface area of this nutrient-absorbing intestinal cell is increased by its many microvilli (singular, microvillus), cellular extensions reinforced by bundles of microfilaments. These actin filaments are anchored to a network of intermediate filaments (TEM). Source: Urry, Lisa A.. Campbell Biology (p. 116). Pearson…

[iyakuhonyaku]

digestive system 消化器系 しょうかきけい

calorie カロリー

ingestion 摂取 せっしゅ or 経口摂取 けいこうせっしゅ

propulsion 推進 すいしん

mechanical breakdown 機械的消化 きかいてきしょうか

chemical digestion 化学的消化 かがくてきしょうか

absorption 吸収 きゅうしゅう

defecation 排便 はいべん

enzyme 酵素 こうそ

macromolecule 巨大分子 きょだいぶんし

lipid 脂質 ししつ

carbohydrate 炭水化物 たんすいかぶつ

protein タンパク質 たんぱくしつ

nucleic acid 核酸 かくさん

caloric value カロリー価 か or カロリー値 ち

polymer ポリマー or 高分子 こうぶんし

monomer モノマー or 単量体 たんりょうたい

fatty acid 脂肪酸 しぼうさん

sugar 糖 とう

amino acid アミノ酸 あみのさん

nucleotide ヌクレオチド

nutrient 栄養分 えいようぶん or 栄養素 えいようそ

alimentary canal or gastrointestinal tract 消化管 しょうかかん

mouth 口 くち

pharynx 咽頭 いんとう

oesophagus 食道 しょくどう

stomach 胃 い

small intestine 小腸 しょうちょう

large intestine 大腸 だいちょう

anus 肛門 こうもん

mucus 粘液 ねんえき

mucosal layer 粘膜層 ねんまくそう

epithelium 上皮 じょうひ

lamina propria 粘膜固有層 ねんまくこゆうそう or 固有層 こゆうそう

muscularis mucosae 粘膜筋板 ねんまくきんばん

submucosal layer 粘膜下層 ねんまくかそう

muscularis externa layer 外筋層 がいきんそう

teeth 歯 は or 歯牙 しが, しげ

tongue 舌 した

gallbladder 胆嚢 たんのう

salivary gland 唾液腺 だえきせん

liver 肝臓 かんぞう

pancreas 膵臓 すいぞう

swallowing 嚥下 えんげ

peristalsis 蠕動 ぜんどう

gastric acid 胃酸 いさん

microvillus 微絨毛 びじゅうもう

villus 絨毛 じゅうもう

coprophagia 食糞 しょくふん

[skywalkerapologist]

The fourth grader from Kalamazoo suffers from an extremely rare illness called Microvillus Inclusion Disease....The disease is life-threatening, which is why Bo qualified for a “wish” from Make-a-Wish.

...He unleashed two questions to Hamill that every "Star Wars" fan would like answered.

“Does Luke die in [The Last Jedi]?,” Bo asked.

Hamill smiled, then answered by saying, “Well, you know, we have to promise to keep secrets; we’ll get in big trouble with the bosses.”

Bo then followed up by asking Hamill, “Who’s Rey’s father?”

Hamill said, “I don’t know; again, you’ll have to wait.

Video of their chat at the link

[infolisstar-blog]

Pathophysiology of gestational diabetes

The precise mechanisms underlying gestational diabetes remain unknown. The hallmark of GDM is increased insulin resistance. Pregnancy hormones and other factors are thought to interfere with the action of insulin as it binds to the insulin receptor. The interference probably occurs at the level of the cell signaling pathway beyond the insulin receptor.

Since insulin promotes the entry of glucose into most cells, insulin resistance prevents glucose from entering the cells properly. As a result, glucose remains in the bloodstream, where glucose levels rise. More insulin is needed to overcome this resistance; about 1.5 to 2.5 times more insulin is produced than in a normal pregnancy.

Insulin resistance is a normal phenomenon emerging in the second trimester of pregnancy, which in cases of GDM progresses thereafter to levels seen in a non-pregnant person with type 2 diabetes. It is thought to secure glucose supply to the growing fetus. Women with GDM have an insulin resistance that they cannot compensate for with increased production in the β-cells of the pancreas.

Placental hormones, and to a lesser extent increased fat deposits during pregnancy, seem to mediate insulin resistance during pregnancy. Cortisol and progesterone are the main culprits, but human placental lactogen, prolactin and estradiol contribute, too.

Multivariate stepwise regression analysis reveals that, in combination with other placental hormones, leptin, tumor necrosis factor alpha, and resistin are involved in the decrease in insulin sensitivity occurring during pregnancy, with tumor necrosis factor alpha named as the strongest independent predictor of insulin sensitivity in pregnancy.

An inverse correlation with the changes in insulin sensitivity from the time before conception through late gestation accounts for about half of the variance in the decrease in insulin sensitivity during gestation: in other words, low levels or alteration of TNF alpha factors corresponds with a greater chance of, or predisposition to, insulin resistance or sensitivity. GABBE,STEVEN G; sixth Edition page 890.

It is unclear why some women are unable to balance insulin needs and develop GDM; however, a number of explanations have been given, similar to those in type 2 diabetes: autoimmunity, single gene mutations, obesity, along with other mechanisms.

Though the clinical presentation of gestational diabetes is well characterized, the biochemical mechanism behind the disease is not well known. One proposed biochemical mechanism involves insulin-producing β-cell adaptation controlled by the HGF/c-MET signaling pathway. β-cell adaption refers to the change that pancreatic islet cells undergo during pregnancy in response to maternal hormones in order to compensate for the increased physiological needs of mother and baby.

These changes in the β-cells cause increased insulin secretion as a result of increased β-cell proliferation. HGF/c-MET has also been implicated in β-cell regeneration, which suggests that HGF/c-MET may help increase β-cell mass in order to compensate for insulin needs during pregnancy. Recent studies support that loss of HGF/c-MET signaling results in aberrant β-cell adaptation.

c-MET is a receptor tyrosine kinase (RTK) that is activated by its ligand, hepatocyte growth factor (HGF), and is involved in the activation of several cellular processes. When HGF binds c-MET, the receptor homodimerizes and self-phosphorylates to form an SH2 recognition domain. The downstream pathways activated include common signaling molecules such as RAS and MAPK, which affect cell motility, cell motility, and cell cycle progression.

Studies have shown that HGF is an important signaling molecule in stress related situations where more insulin is needed. Pregnancy causes increased insulin resistance and so a higher insulin demand. The β-cells must compensate for this by either increasing insulin production or proliferating.

If neither of the processes occur, then markers for gestational diabetes are observed. It has been observed that pregnancy increases HGF levels, showing a correlation that suggests a connection between the signaling pathway and increased insulin needs. In fact, when no signaling is present, gestational diabetes is more likely to occur.

The exact mechanism of HGF/c-MET regulated β-cell adaptation is not yet known but there are several hypotheses about how the signaling molecules contribute to insulin levels during pregnancy. c-MET may interact with FoxM1, a molecule important in the cell cycle, as FOXM1 levels decrease when c-MET is not present. Additionally, c-MET may interact with p27 as the protein levels increase with c-MET is not present.

Another hypothesis says that c-MET may control β-cell apoptosis because a lack of c-MET causes increases cell death but the signaling mechanisms have not been elucidated. Although the mechanism of HGF/c-MET control of gestational diabetes is not yet well understood, there is a strong correlation between the signaling pathway and the inability to produce an adequate amount of insulin during pregnancy and thus it may be the target for future diabetic therapies.

Because glucose travels across the placenta (through diffusion facilitated by GLUT1 carrier), which is located in the syncytiotrophoblast on both the microvillus and basal membranes, these membranes may be the rate-limiting step in placental glucose transport.

There is a two- to three-fold increase in the expression of syncytiotrophoblast glucose transporters with advancing gestation. Finally, the role of GLUT3/GLUT4 transport remains speculative. If the untreated gestational diabetes fetus is exposed to consistently higher glucose levels, this leads to increased fetal levels of insulin (insulin itself cannot cross the placenta).

The growth-stimulating effects of insulin can lead to excessive growth and a large body (macrosomia). After birth, the high glucose environment disappears, leaving these newborns with ongoing high insulin production and susceptibility to low blood glucose levels (hypoglycemia)

[digitaltariq]

Hospital bills cross Dh2 million for Dubai expat's baby with rare condition - News

Hospital bills cross Dh2 million for Dubai expat’s baby with rare condition – News

[ad_1]

The baby cannot eat or drink milk and is surviving on intravenous feeding because of a rare intestinal disorder.

Ten-month-old Mohammed Subhan has been lying on a hospital bed in Dubai since his birth. He cannot eat or drink milk and is surviving on intravenous feeding because of a rare intestinal disorder called Microvillus Inclusion Disease (MVID).

Subhan’s medical expenses are…

[katalk-mfasia]

낙태약구입 미프진아시아  ka talk-mfasia

안녕하세요 미프진 아시아 복용관리팀 입니다 (♣톡:mfasia ♣)

정자의 핵과 난자의 핵을 합쳐서 형성한 것.

반수체 정자의 핵과 반수체 난자의 핵이 합쳐져 융합하는 수정 과정의 결과 형성된다. 접합자(zygote)라고도 한다. 수정란에 대하여 수정 전의 난을 미수정란(unfertilized egg)이라 한다. 다세포 생물에서의 수정(fertilization)이란 반수체의 정자핵과 반수체의

난자핵이 융합하는 것이나 보다 넓은 의미로 정자의 난자로의 접근, 정자와 난자의 접촉, 정자와 난자의 원형질막의 융합, 정자의 난자로의 침입, 이어서 정자와 난자의 세포막이 융합하여 2개의 생식세포가 하나의 세포가 되는 핵융합이라는 마지막 단계에 이르기까지 모든 사건을 포함한다. 이후 수정란은 체세포 분열(mitosis)를 하며 여러 단계의 발생과정을 거치게 된다.

극피동물에서 정자가 난자에 접근하여 젤리막에 침입하면 효소가 들어있는 첨체에서 첨체반응(acrosomal reaction)이 일어나 젤리막과 난황층을 통과하는 길을 소화하는 효소를 방출하고, 긴 첨체돌기(acrosomal process)가 돌출하여 난의 표면에 붙으면 수정에 성공하게 된다. 수정에 성공하면 난의 표면의 정자를 향해 융기 되어 수정돌기(fertilization cone)을 형성하며, 미세융모(microvillus)가 정자의 머리부��을 감싸 난자 속으로 잡아당긴다. 정자의 원형질막은 난자의 원형질막과 융합되고 막이 벗겨진 정자의 머리 부분이 난자의 세포질 속으로 들어간 후 핵을 방출하며, 정자와 난자의 핵 사이에 미세 소관이 형성되어 두 핵을 서로 잡아당김으로써 수정이 완결된다. 인간 역시, 극피동물과 유사한 방식으로 한 개의 정자가 난자의 표면에 접촉하면 막끼리 융합되고, 난이 활성화되며, 정자가 난자의 세포질 속으로 들어간다. 인간에 있어 수정의 표시는 두 번째 감수분열의 결과인 제2극체의 출현이며, 수정이 일어나지 않으면 감수분열이 완결되지 않는다.

수정란의 경우, 무성생식에 의한 방법보다 환경에 대한 내성을 가질 수 있다는 장점을 갖기도 한다. 민물플랑크톤의 일종인 윤충은 무성생식과 유성생식을 모두 사용할 수 있는데, 유성생식에 의하여 형성된 수정란은 두꺼운 껍질을 갖고 있어 얼거나 건조하여 생존에 어려운 환경을 견뎌낼 수 있다.

https://asiamifegyne.com/ 구글에서 미프진아시아 검색해주세요 24시간 상담가능합니다 실시간 상담 :https://open.kakao.com/o/sBkhi2Vb

#낙태약 #정품낙태약 #낙태비용 #낙태약후기 #낙태약복용 #낙태약구매 #낙태약구입 #낙태약가격 #낙태유도제 #낙태가능시기 #낙태알약 #먹는낙태약 #낙태방법 #낙태수술

[mrlongkgraves]

Parent-to-parent: Tips for Home Parenteral Nutrition families

Four-year-old Thomas Onorato is a young zoologist at heart. Often seen with binoculars in hand, the adventurous preschooler is particularly drawn to bird watching. He enjoys talking about his feathery friends and studying their beauty and habitat.

Thomas’ love of animals runs so deep that he says he wants to be a veterinarian when he grows up. “Thomas is obsessed with animals. It’s his love,” says his mother, Melissa.

Beyond his quest to care for animals, Thomas has two other important missions — to manage the rare condition, microvillus inclusion disease (MVID) and receive the lifesaving parenteral nutrition (PN) support he needs to grow and thrive.

Microvillus inclusion disease is a genetic condition of the intestines that causes severe diarrhea and the inability to absorb nutrients. The inability to absorb nutrients is why Thomas receives long-term, home-based PN support.

“Thomas will unfortunately be in and out of the hospital for the rest of his life because there is no cure for microvillus inclusion disease,” says Melissa, who travels from Long Island, New York to Boston Children’s for Thomas’ care. “PN is one of the major reasons our precious son is alive today.”

Thomas currently receives Omegaven, a fish oil-based experimental drug developed by Boston Children’s Dr. Mark Puder, and medical support from the HPN team, including Dr. Bram Raphael, director of the Home Parenteral Nutrition Program. Thomas gets the nutrients he needs to grow, in the comfort of his own home.

Since his arrival at Boston Children’s, Melissa says her son has seen major improvement — his growth is age appropriate, his energy level is high and “he’s the best he has ever been.”

“We feel very blessed that Thomas has come as far as he has,” says Melissa. “The level of care he receives at Boston Children’s is hands-down the best.”

Melissa shares some of her family’s learnings and offers the following parent-to-parent tips to manage parenteral nutrition care at home.

1. Create emergency/back up HPN supply kits

Emergency supply kits include extra alcohol, gloves, antibacterial gel, saline, heparin, swab caps, central line dressing such as Tegaderm, injection caps, a plastic clamp and even tubing in various sizes. Store emergency supplies in a medium-size Ziploc bag so everything is visible. Keep an emergency kit in your car, diaper bag and child’s backpack. Also leave larger emergency kits at close family and friend’s houses that you frequent. Sometimes supplies have been defective (or dropped accidentally on the floor) when away from home. Boston’s HPN team has always stressed the importance of preparation and the critical importance of keeping supplies sterile and clean. This is especially important when you’re away from home and hooking up HPN.

2. The power of 2: Have two people present for sterile dressing changes

Sometimes there are emergencies and only one adult is present, but Boston’s HPN team encourages having two people present as standard practice. There have been several times when I forgot a supply after putting on my sterile gloves or a supply drops on the floor. Having an extra pair of hands is incredibly helpful. It is also nice to have someone entertain your child and make sure they keep their arms up away from the site until the dressing change is complete.

3. Make HPN functional for active toddlers

Thomas is now four years old and is more conscious that he is connected to tubing and a backpack containing HPN. But sometimes he forgets. I recommend using Vygon’s lectrospiral tubing. It resembles a telephone cord and allows further range of motion. Also, another precaution is to place a piece of medical tape near the end of the tubing where it connects to his broviac. If your child sprints while being hooked up there will be initial tension on the tubing not on the broviac.

4. Manage your HPN schedule

Don’t be afraid to ask family and friends to accommodate your HPN schedule in order to maximize quality time. Thomas has many cousins and it’s such a great feeling to watch him interact with them. He wants to be active and run around with them. If we can, we usually ask family and friends to spend time with us when he is off his infusion so we don’t have to hover over him while he wears his HPN backpack. More importantly, Thomas loves the freedom!

5. Remind others to include HPN kids at mealtime

I’ve noticed that teachers, family members and friends are always curious about mealtimes in our home and want to know how to include Thomas during birthday and holiday celebrations that focus on special meals. Mealtime is a social event across cultures. We include Thomas at the table and take advantage of that time to talk and laugh. Also, Thomas loves to cook! He might not be interested in the end result (eating a delicious meal), but he enjoys the process.

6. Educate others about HPN  

It is very important to us to educate others in order to raise awareness. We enjoy sharing our story and educating others about our HPN lifestyle. I find that children will ask questions immediately if they see Thomas’ tubing, HPN backpack or his central line. Once they understand it’s how he gets his nutrition it’s no longer the elephant in the room. I even notice that children show compassion and increased tolerance in his presence, which is a beautiful thing to see in young people.

7. Stay connected

Having a child with a medical condition can be very isolating, especially if your child has a rare disease. Our family is very fortunate to be a part of a private Facebook page for families affected by microvillus inclusion disease and Boston Children’s HPN Group. To have a platform, to discuss a spectrum of topics from medical challenges to personal victories is a very powerful tool and resource.

Learn more about Home Parenteral Nutrition and Boston Children’s HPN Facebook community.

The post Parent-to-parent: Tips for Home Parenteral Nutrition families appeared first on Thriving Blog.

from Thriving Blog http://ift.tt/2zDMb4I

[thetruthseekerway]

A System Organised in Its Every Detail

New Post has been published on http://www.truth-seeker.info/refuting-darwinism/system-organised-every-detail/

A System Organised in Its Every Detail

By Harun Yahya

The system in the stomach could in no way have been formed step by step

Breathing, eating, walking, etc., are very natural human functions. But most people do not think how these basic actions take place. For example, when you eat a fruit, you do not think how it will be made useful to your body. The only thing on your mind is eating a healthy meal; at the same time, your body is involved in extremely detailed processes unimaginable to you in order to make this meal a health-giving thing.

The digestive system where these detailed processes take place starts to function as soon as a piece of food is taken into the mouth. Being involved in the system right at the outset, the saliva wets the food and helps it to be ground by the teeth and slide down the oesophagus.

The oesophagus helps the food be transported to the stomach where a perfect balance is at work. Here, the food is digested by the hydrochloric acid present in the stomach. This acid is so strong that it has the capacity to dissolve not only the food but also the stomach walls. Of course, such a flaw is not permitted in this perfect system. A secretion called mucus which is secreted during digestion covers all the walls of the stomach and provides a perfect protection against the destructive effect of the hydrochloric acid. Thus the stomach is prevented from destroying itself.

The rest of the digestive system is likewise planned. The useful food pieces broken down by the digestive system are absorbed by the small intestine walls and enter the blood stream. The inner surface of the small intestine is covered with tiny tendrils called ‘villus’. On top of the cells over the villus are microscopic extensions called the microvillus. These extensions function as pumps to absorb the nutrition. This way the nutrition absorbed by these pumps is delivered all around the body by the circulatory system.

The point that deserves attention here is that evolution can by no means explain the system briefly summarised earlier. Evolution maintains that today’s complex organisms have evolved from primitive beings by the gradual accumulation of small structural changes. However, as stated clearly, the system in the stomach could in no way have been formed step by step. The absence of even one factor would bring about the death of the organism.

When food is received into the stomach, the gastric juices acquire the ability to break down food as a result of a series of chemical changes. Now, imagine a living being in the so-called evolutionary process in whose body such a planned chemical transformation is not possible. This living being, unable to acquire this ability, would not be able to digest the food it ate and would starve to death with an undigested mass of food in its stomach.

In addition, during the secretion of this dissolving acid, the stomach walls simultaneously have to produce the secretion called mucus. Otherwise, the acid in the stomach would destroy the stomach. Therefore, in order for life to continue, the stomach must secrete both fluids (acid and mucus) at the same time. This shows that not a step-by-step coincidental evolution but Creation with all its systems must, in effect, have been at work.

What all this shows is that the human body resembles a huge factory made up of many small machines that work together in perfect harmony. Just as all factories have a designer, an engineer and a planner, the human body has an Exalted Creator. This Creator is Allah, the All-Wise.

A Note by the Editor:

Allah the Almighty says in the Ever-Glorious Qur’an what means,

“He [Allah] hath created the heavens without supports that ye can see, and hath cast into the earth firm hills, so that it quake not with you; and He hath dispersed therein all kinds of beasts. And We send down water from the sky and We cause (plants) of every goodly kind to grow therein. This is the Creation of Allah. Now show me that which those (ye worship) beside Him have created. Nay, but the wrong doers are in error manifest!” (Luqman 31: 10-11)

And,

“We shall show them Our portents on the horizons and within themselves until it will be manifest unto them that it is the Truth. Doth not thy Lord suffice, since He is Witness over all things? How! Are they still in doubt about the meeting with their Lord? Lo! Is not He surrounding all things?” (Fussilat 41: 53-54)

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Harun Yahya was born in Ankara in 1956. He studied arts at Istanbul’s Mimar Sinan University and philosophy at Istanbul University. Since the 1980s, the author has published many books on political, faith-related and scientific issues. Harun Yahya is well known as an author who has written very important works disclosing the imposture of evolutionists, the invalidity of their claims and the dark liaisons between Darwinism and bloody ideologies. Some of the books of the author have been translated into English, German, French, Spanish, Italian, Portuguese, Albanian, Arabic, Polish, Russian, Bosnian, Indonesian, Turkish, Tatar, Urdu and Malay and published in the countries concerned. Harun Yahya’s books appeal to all people, Muslims and non-Muslims alike, regardless of their age, race and nationality, as they center around one goal: to open the readers mind by presenting the signs of Gods eternal existence to them.