Typical composition of sweet and acid whey.
\r\n\tLiterature showed the presence of ACE2 receptors on the membrane of erythrocyte or red blood cell (RBC), indicating that erythrocyte (RBC) can be considered as a peripheral biomarker for SARS-C0V2 infection.
\r\n\r\n\tIncreased levels of glycolysis and fragmentation of RBC membrane proteins were observed in the SARS-C0V2 infected patients, demonstrating that not only RBC’s metabolism and proteome but its membrane lipidome could be influenced by SARS-C0V2 infection changing the homeostasis of the infected erythrocyte. This altered RBC may result in the clot and thrombus formation; the major signs of critically ill Covid-19 patients.
\r\n\r\n\tThis book is going to be a succinct source of knowledge not only for the specialists, researchers, academics and the students in this area but for the general public who are concern about the present situation and are interested in knowing about simple non-invasive measures for identifying viral and bacterial infections through their red blood cells.
",isbn:"978-1-83969-121-8",printIsbn:"978-1-83969-120-1",pdfIsbn:"978-1-83969-122-5",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"fa5f4b6ef59e28b6e7c1a739c57c5d2f",bookSignature:"Prof. Kaneez Fatima Shad",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10494.jpg",keywords:"Spike Protein, Hemoglobin, Proteins for Oxygen Transport, Altered Protein Structures, RBC ACE Receptors, RBC ACE-2 Receptors, Carboxypeptidase, Mas Receptor, Metabolomics, Gas Transport, Glucose-6-Phosphate, Phosphoglycerate",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 15th 2020",dateEndSecondStepPublish:"November 30th 2020",dateEndThirdStepPublish:"January 29th 2021",dateEndFourthStepPublish:"April 19th 2021",dateEndFifthStepPublish:"June 18th 2021",remainingDaysToSecondStep:"2 months",secondStepPassed:!0,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"Dr. Shad is a governing body member and mentor of Women in World Neuroscience (WWN), a division of the International Brain Research Organization (IBRO). 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During this period, she was also engaged in doing research by getting local and international grants (total of over 3.3 million USD) and translating them into products such as a rapid diagnostic test for stroke and other vascular disorders. She published over 60 articles in refereed journals, edited 8 books, and wrote 7 book chapters, presented at 97 international conferences, mentored 34 postgraduate students. 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A small proportion of these patients will be recommended for immediate further investigation, those that demonstrate: loss of sphincter control, progressive lower limb motor weakness, saddle anaesthesia or signs of bilateral nerve root involvement; all symptoms and signs of the surgical emergency Cauda Equina syndrome (CES) [3].
The vertebral column consists of 33 [4] individual vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral and 4 (this can vary between 3 and 5 [5]) coccygeal bony vertebrae [4,5]; protecting the spinal cord (and nerves) that traverse between them [4,6]. The sacral and coccygeal vertebrae are normally fused in adults leaving 24 articulating vertebrae [4,5]. This is demonstrated in figure 1.
Showing the vertebral column.
The vertebrae are bound together via several ligaments and between each vertebrae, resting on the body of each, lie the strong intervertebral discs. Anteriorly and posteriorly are the anterior longitudinal and posterior longitudinal ligaments respectively [4,5,7]. In addition the posterior aspects of the vertebrae are attached to one other by the supraspinous and intraspinous ligaments, posterior facet joints and the ligamentum flavum. [5,7]. Figure 2 illustrates these.
Showing the ligaments of the vertebral column.
The spinal cord is the extension of the medulla oblongata of the brainstem [4,6]. Measuring between 42cm and 45cm (from the foramen magnum to L2) it is the structure responsible for relaying information to the brain, and passing commands down [4,6,8]. It passes through the vertebral canal, which is made by the vertebral foraminae of consecutive vertebrae using the body, pedicles and vertebral arch [4], as well as the iv discs [5]. The canal continues in the fused sacrum through the sacral canal [5]. It has two enlargements due to innervations for upper and lower limbs, cervical and lumbar (upper and lower limbs respectively)[4,6]. Caudal to the lumbar enlargement the cord suddenly narrows to form a cone shaped termination: conus medullaris [6] at L1-L2 (although this may be as high as T12 or as low L3 [4]). Hence the spinal cord only occupies the superior two-thirds of the vertebral canal [4]. This is due to a slower growth rate of the cord compared with the vertebral column [4,6].
The cord itself is a cylindrical structure [6]. It is split into an ‘H’ shaped darker grey matter surrounded by the peripheral white matter [6,8]. The four projections of the grey matter (two dorsal and two ventral horns) are sites of attachment for peripheral nerves [6]. The dorsal horn contains sensory afferent fibres whilst the ventral horn contains efferent motor (skeletal muscle) fibres [6]. A lateral horn is also present at thoracic and upper lumbar levels, containing autonomic neurones [6]. The white matter is organised into a series of longitudinally running ascending and descending neuronal tracts [6]. This is demonstrated in figure 3.
Showing a cross-sectional view of a typical cervical vertebrae with the spinal cord.
The spinal cord connects to the periphery via 31 pairs of spinal nerves: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and a solitary coccygeal nerve[4,6]. Each nerve is formed by the uniting of ventral and dorsal nerve roots close to the cord [4,5]. The mixed spinal nerves pass within the intervertebral foraminae (formed by the joining of subsequent superior and inferior vertebral notches [4]) and immediately divide into dorsal and ventral rami [4,5,6]. The dorsal ramus (thinner and posterior) supplies the true muscles and skin of the back region [4,6]. The ventral (larger and anterior) ramus supplies skin and muscles of front of body and limbs [4,6], giving rise to the myotome and dermatome distribution patterns [6].
Due to the differing lengths of the cord and canal, below the cervical region successive spinal nerve roots follow a progressively longer course to reach their respective intervertebral foraminae, through which they must exit. This is most notable in the Cauda Equina [6]. The Cauda Equina contains the dorsal and ventral nerve roots of lumbar, sacral and coccygeal nerves [4,6]. Each level of the spinal cord is numbered according to the IV foraminae through which the dorsal and ventral roots exit the vertebral canal [4,8].
As with the brain the spinal cord has 3 meningeal coverings. The innermost is the pia mater; a thin, delicate, vascular membrane, covering the cord, nerve roots and cauda equina [4,6]. The arachnoid mater is a loose-fitting layer separated from the pia mater by the subarachnoid space containing cerebrospinal fluid [6]. The outermost covering, the dura mater, is tougher, fibrous sheath, continuous with its cranial counterpart [4,6]. The dura is kept away from the walls of the vertebral canal by adipose tissue and internal vertebral venous plexuses [4,6]. Even though the spinal cord terminates at L1-L2 the arachnoid and dural sheaths continue to S2, even forming meningeal sleeves that cover the nerve roots, which later become continuous with the epineurium sheathing the spinal nerve [4,6]. The filum terminale is a remnant of the embryological spinal cord made out of connective tissue [4,6]. It exits the dural sac at S2 and attaches to the coccyx, securing the cord [4,6].
Most vertebrae are supplied by segmental vessels and spinal arteries, which distribute to the vertebrae, are branches of the (descending order): cervical, posterior intercostal, subcostal, lumbar, iliolumbar and sacral arteries [4]. These spinal arteries enter the IV foraminae and divide into terminal radicular arteries, which supply dorsal and ventral roots and their coverings (and also some of the superficial grey matter), although some radicular arteries continue as medullary segmental arteries that anastamose with spinal arteries [4].
As previously mentioned internal venous plexuses lie within the vertebral canal, and external plexuses lie outside [4]. They receive blood from large tortuous basivertebral veins lying within vertebral and IV veins (both passing through the IV foraminae), which receives veins from the spinal cord and vertebral plexuses [4].
Arterial supply to the spinal cord is through three main longitudinal spinal arteries: one anterior and two posteriors [4,6]. The anterior spinal artery, formed by the joining of the vertebral arteries (at the level of the medulla), runs in the anteromedian fissure of the cord itself [4,6,9-12]. Sulcul (central) arteries from it enter the cord through the fissure [9], supplying two-thirds of the cross-sectional area of the spinal cord [4,10,11]. Blood flow through the anterior spinal artery is predominantly caudal (away from the head) [9]. The posterior arteries are branches of either the vertebral artery or posterior-inferior cerebellar arteries [4,6,11], with blood flow towards the head (rostral) [9]. They supply the posterior one thirds of the cord and receive collaterals from around 12 unpaired radicular arteries, whilst the anterior cerebral arteries have a less effective collateral circulation with 6-10 unpaired radicular brances [11,12].
The anterior longitudinal artery only supplies the superior cord, with the remainder being supplied by the segmental medullary and radicular arteries previously mentioned (4,6). These run along spinal nerve roots and in the case of segmental medullary arteries are located where the need for blood is greatest: at the cervical and lumbosacral cord enlargements(4,6). Deficiencies in the number of segmental arteries increase susceptibility to ischemia [10].
The great anterior segmental medullary artery of Adamkiewicz (GRA) forms from the inferior intercostal or upper lumbar arteries and enters the vertebral canal via one of their IV foraminae[4,6,9]. It arises around T9-L2 and is larger than other segmental arteries and has significance as it reinforces circulation to the inferior cord including the lumbosacral enlargements [4,11,12)].
Spinal veins follow similar paths as arteries but with 3 anterior and 3 posterior spinal veins[4,6]. They communicate with each other freely and are drained by up to 12 anterior and posterior radicular and medullary veins [4,6]. They also join internal venous plexuses in the extradural space, which communicate with the external plexuses and then the ascending lumbar, azygous and hemiazygous veins [4,6].
There are various types of spinal injury, however most remain out of the scope of this chapter. This chapter focuses particularly on two types: Cauda Equina syndrome and spinal cord ischaemia, also known as spinal stroke and in particular how they may share characteristics. Cord damage and compression can cause similar symptoms in any area of the cord however; CES is a particular syndrome when this happens in the inferior cord.
Cauda Equina syndrome is caused by injury to the lumbosacral nerve roots, contained within the Cauda Equina (figure 4) grossly causing pain, bladder and bowel disturbances as well as focal neurology in the lower limb [4,8]. Essentially any mechanism which can cause compression of the spinal nerve roots, thereby causing shear stresses as well as obstructing blood flow in the vasculature of the nerve roots can cause CES [13]. The most common is cause herniation of the nucleus pulposus, 2% of which cause CES [14,15]. This is especially common in the lumbar spine where the lumbosacral enlargement means the spinal nerves are increasing in size caudally, but the IV foraminae size decrease [4]. The 5th lumbar disc is the most common “slipped disc” causing trauma to the roots of the first sacral nerve [6].
Showing the cauda equina.
Other causes are: spinal cord stenosis, blunt or direct injury through the cauda equina, sacral fractures [16], hematomas, abscesses, lymphomas, solid tumors and other space-occupying lesions [11,14,15]. Rare causes include: ankylosing spondylitis, inferior vena cava thrombosis, sarcoid, and demyelinating lesions [14,15]. CES can occur as a complication of spinal anaesthesia but is rather rare[17]. The cauda equina is supplied by blood from the sacral arteries, which arise from the hypogastric artery [11].
Symptoms can vary depending on the size and location of the lesion. Above the vertebrae L1 (conus medullaris) damage can affect the cord itself or the roots, or both simultaneously however, below this level only the roots can be damaged [11]. Root damage causes lower motor neurone effects and sensory impairment in the affected root only, whilst segmental damage to the cord causes similar effects in the same segmental level but will also cause upper motor neurone effects and a sensory deficit below the level of the lesion [11]. This is due to interruption of the cord fibres. Root damage causes severe sharp, shooting, even burning pain radiating in the specific myotome and dermatome distribution of the root, exacerbated with movement [11]. Segmental damage causes continuous deep, aching pain, which radiates into either one lower limb or one half of the body, and that is not affected by movement [11]. Hence upper cauda equina may cause root or segmental effects with late bladder involvement, whilst a lower cauda equina lesion causes root damage, with early bladder incontinence and saddle anaesthesia (S2-S5) [11].
History and examination can frequently yield key clues to the diagnosis. Spinal imaging is usually required to confirm diagnoses with MRI being the gold standard, CT scanning can illustrate protrusions, X-rays are of little benefit but can show loss of disc space or collapse [11].
Spinal cord infarction is a stroke that occurs within the spinal cord or the arteries that supply it, usually caused by atherosclerosis of the major arteries to the spinal cord [18-20]. It is rare compared to cerebral stroke [10,14,21], accounting for approximately 1-2% of all strokes [22,23]. Spinal stroke can be categorised into two types: local interference with the blood supply (trauma, embolism, aortic surgery, aortic dissection etc.), and generalised hypoxia/hypoperfusion (e.g. cardiac arrest) where often the brain is impacted as well but careful examination can show the spinal cord is also affected [10,14,19]. Spinal cord ischaemia is a serious neurological condition and causes neuronal death, functional neurological loss and paraplegia in up to 33% of patients affected [19]. Thus prompt diagnosis and treatment may significantly alter outcomes. Often there is no relevant past medical history, or signs of inflammation [14], although vascular risk factors are usually present, less than 50% of spinal strokes have a definite cause [24].
The mid-thoracic cord around T4-T8 is known as the ischaemic “watershed region” and because of fewer radicular arteries and narrowing of the anterior spinal artery in this area, was thought to be particularly sensitive to hypoperfusion[11,22]. However in terms of spinal stroke, this traditional view has recently come under scrutiny [12,25] and as seen in post-mortem studies conducted by Duggal et al. 66 patients which had ischaemic myelopathy (secondary to cardiac arrest or severe systemic hypotension) showed 95.5% had involvement of the lumbosacral cord, whilst the thoracic cord was only affected in 7.6% of cases [26)]. Hence the lumbosacral cord which, is mainly supplied by the singular artery of Adamkiewicz, is the most sensitive to hypoperfusion; possibly due to its greater metabolic demands (lumbosacral enlargement) [22,26]. A saddle embolus can cause occlusion of the GRA causing distal cord ischaemia [27]. The cauda equina is mainly supplied by lateral and medial sacral arteries, which arise from the internal iliac artery [27].
Spinal cord infarction presents with sudden onset of severe pain, radiating down the legs (radicular) [24] and progressive sensori-motor deficits in the initial stages. In lumbosacral involvement there may be a rapidly progressive bilateral flaccid paresis initially, with loss of tendon reflexes, possibly an absent plantar response and urinary retention [10,11,14,22,24]. Bowel dysfunction can also develop [19]. The pain may be throbbing or burning in nature and disappear after 2 to 3 days [24]. A sensory level below the infarction is usually present however passive movement may be retained if the posterior circulation is preserved [10,11], with gross rather than fine sensation more affected [14]. As it happens the anterior circulation is more often affected [14], with 88% of infarcts in the central territory of the anterior spinal artery [24]. If the infarction is established it is irreversible and spastic paraplegia, spastic bladder and hyper-reflexia may develop [10,11]. Cervical infarction can cause bilateral paresis in the upper limb [14]. Saddle anaesthesia may also be present[24].
Investigations involve excluding other causes, and later confirmation of the ischaemia with T2 weighted MRI imaging [11,14]. In the initial stages diffusion weighted MRI can detect spinal cord oedema, which is a precursor to infarction [14]. CSF protein can also be raised in some cases [9,11,24]. Treatment is usually symptomatic with a variable outcome [11].
As we can see, the symptoms and even aetiology of spinal stroke and CES may well overlap. Although history and examination can indicate other causes of CES, spinal stroke is moreover a diagnosis of exclusion, confirmed only by MRI[**] (fig 5,6) of the cord [11]. In the literature, there are not many cases to report relationship between the abdominal aortic aneurysm, spinal stroke and cauda equina syndrome.
P. Jauslin et al[32] in 1991 describe a case report of cauda equina syndrome associated with an Aorto-caval Fistula. In this particular case history and clinical examination demonstrated symptoms of: pain, tachycardia, peri-umbilical tenderness and a systolo-diastolic murmur. The patient was apyrexial and normotensive with femoral pulses present but cyanosis in both legs. Neurologically, there was perineal anaesthesia ("anesthesie en selle") with markedly reduced anal sphincter tone, paresis and anaesthesia of the left leg in the L1 territory. Lumbar percussion was painless and deep sensitivity was intact.
Verneuil A et Al[33] in 1997 reported a case of persistent cauda equina syndrome following bilateral aortoiliac dissection as a complication of cardiac angiography. In this case report they describe the symptoms as follows: numbness in the gluteal region and the soles of the feet with urinary retention and faecal incontinence. In this case report, the MRI scan of the lumbar region was completely normal in the absence of anal tone in rectal manometry. Electromographic study (EMG) was consistent with cauda equine at level S1 & S2.
Normal MRI scan
Abdominal Aortic Aneurysm , [**] Copyright for the Author of this Chapter who is the same the Author of the Case Report
Patel NM et Al[34] published in 2002 a case report describing aortic dissection presenting as an acute cauda equina syndrome. In this case, the patient had acute, but transient, neck pain following a short coughing episode. The patient was able to walk to the restroom, but began to have severe low-back pain and lower extremity numbness and weakness that rapidly progressed to frank lower extremity paralysis. While en-route to the hospital, the patient became incontinent of both bowel and bladder. Upon admission to the emergency department, the patient complained of low-back pain, bilateral hip and thigh pain, and the inability to move or feel the lower extremities. The diagnosis of dissecting aortic aneurysm was made on the basis of a CT scan.
An unusual cause of spinal cord infarction, first documented in 2009 by EL-Osta et al. is from emboli thrown off an abdominal aortic aneurysm (AAA), with symptoms mimicking CES [28].
An aneurysm is a focal increase in diameter of the aorta of at least 50% in relation to the normal expected diameter [29]. Though by definition it can occur anywhere in the abdominal cavity the vast majority are infra-renal [30]. Thrombus frequently collects in the walls of an aneurysm and fragments can easily be thrown-off in the direction of a spinal artery, thus causing spinal cord ischaemia.
In this particular case the patient had sudden onset of lower back whilst heavy lifting. The pain radiated to his groins and there was a progressive bilateral weakness worse on one side. On examination profound neurological deficit was seen in both legs, with arreflexia, altered sensation and reduced bladder sensation and anal tone.
Although MRI showed lumbar disc protrusions there was no cord compression, hence spinal arteriography was performed. The final diagnosis was through a combination of clinical, diagnostic and radiological tests. CT had shown a 6.6 by 5.8cm infra-renal aneurysm[28].
As a result of reviewing the literature, it seems that patients who are admitted with query cauda equina syndrome and with unusual symptoms, should be investigated for other causes. It seems that the patient had more than simply weakness in the leg, paraesthesia and decreased anal tones. Some patients will present with abdominal discomfort and neck discomfort. Past medical history may be unremarkable with no trauma, but sudden onset cauda equina symptoms. In those particular cases, the responsible surgeon has to be extra cautious especially in orthopaedics.
In all four cases that have been reported in the literature, none of the patients recovered fully and in one case the patient deteriorated and died immediately. However, one patient did recover partially and the authors could not explain this. This implies that either way patients will have some gross disability and this may be as a result of delayed treatment.
Though spinal stroke is uncommon the high level of incidence and prevalence of AAAs may mean such cases may become more common, and hence should be an important thought in the surgeons mind when assessing CES. The key difference between atherosclerosis and thrombi in the spinal arteries will be the speed of onset of symptoms. With sudden CES-like symptoms affecting the patient with a significant spinal artery thrombus.
Initially after thorough history and examination (including abdominal examination for a pulsatile mass [31]) all other causes of CES must be ruled out, hence urgent CT/MRI of the spinal cord is appropriate.
On the other hand, when acute aortic dissection is suspected, an emergent diagnostic workup should be initiated with ultrasound techniques involving either a transthoracic or transesophageal approach or computerized tomography. Magnetic resonance imaging is also a diagnostic resource but may be difficult to obtain rapidly. Other vascular phenomena, such as aneurysms of the abdominal aorta or pelvic arteries, can also cause neurological symptoms, further pointing to the need for close attention to the vascular tree during orthopaedic examination[35].
Prompt diagnosis of such disorders may help in hastening treatment, which is particularly important in the context of neurological ischaemia, which can be irreversible. Thus this may help to improve outcomes for such patients in the future.
Figures
Gray H (1918). Lateral view of the vertebral column in: Anatomy of the Human Body. 20th U.S. edition. Philadelphia: Lea & Febiger. From www.wikipedia.com.
Gray H (1918). Median sagittal section of two lumbar vertebræ and their ligaments. Anatomy of the Human Body. 20th U.S. edition. Philadelphia: Lea & Febiger. From www.wikipedia.com.
Debivort user (2007). Annotated diagram of cervical vertebrae. From www.wikipedia.com.
Gray H (1918). Cauda equine in:Anatomy of the Human Body. 20th U.S. edition. Philadelphia: Lea & Febiger. From www.wikipedia.com.
El-Osta B, Ghoz A, Singh VK, Saed E, Abdunabi M (2009). Spontaneous spinal cord infarction secondary to embolism from an aortic aneurysm mimicking as cauda equina due to disc prolapse: a case report. Cases J 2: 7460.
A number of by-products like whey, buttermilk, skim milk, and ghee residue (GR) and derived by-products like caseins, caseinates, lactose, whey proteins (WP), etc. are produced by the dairy industry. Attempts have been made globally to utilize these by-products because of their high nutritive value. Dairy plants in India are still confronted with the problem of by-product utilization because of lack of adequate technology and high cost of new technologies. However the Indian dairy industry is making advancement in this direction. Whey is the major by-product of the dairy industry. It is a useful resource of nutrients containing about 50% of the solids of milk [1]. Whey production is steadily growing, and its high organic content is an important environmental and health issue. Therefore, suitable management of this by-product is required. Like milk, whey may have different origins (e.g., goat, sheep, and buffalo), but the most relevant in terms of production volume and economical value is that obtained from cow milk processing. Skim milk is a by-product obtained from cream manufacture. It is rich in SNF content and has high nutritional value and has been utilized in the manufacture of a number of dairy products or in powder form. Buttermilk, a by-product of butter manufacture, has been used as such or in dried form. Ghee residue from ghee manufacture has also found applications in many food products.
\nWhey, a by-product of cheese manufacturing, contains approximately 7% dry matter of which 13% is proteins. It generally represents a volume fraction of 90% in milk and is being classified into sweet and acid whey. The sweet whey originates from cheese manufacturing or from industrial casein production where the casein is coagulated by rennet, at pH of 6.0–6.5, while the acid whey (pH < 5.0), resulting from processes in which casein is coagulated by fermentation or addition of organic or mineral acids, as in the processing of fresh, acid-coagulated cheeses (e.g., cottage cheese or quark) or strained yogurt (e.g., Greek-style yogurt). The main components for both types of wheys are given in Table 1. Water constitutes approximately 93% of the whey, while the total solid fraction contains lactose (70–72%), minerals (12–15%), and whey proteins (8–10%). The main difference between both wheys is the mineral content, the acidity, and the composition of the whey protein fraction. Acid whey has higher calcium content as, at this low pH, the colloidal calcium contained in the casein micelles in normal milk solubilized and partitioned into the whey [2]. Composition of whey protein fraction is different as sweet whey contains glycomacropeptide, a fragment of the κ-casein molecule produced by rennet clotting, constituting 20% of the whey protein fraction of sweet, rennet-based wheys [2]. Acid whey has a large potential to be used as the main component of beverages because of its nutritional composition. The utilization of liquid acid whey offers an interesting approach as there is no need for using complex technology other than pasteurization.
\nComponent | \nSweet whey (g/L) | \nAcid whey (g/L) | \n
---|---|---|
Total solids | \n63.0–70.0 | \n63.0–70.0 | \n
Lactose | \n46.0–52.0 | \n44.0–46.0 | \n
Protein | \n6.0–10.0 | \n6.0–8.0 | \n
Calcium | \n0.4–0.6 | \n1.2–1.6 | \n
Phosphate | \n1.0–3.0 | \n2.0–4.5 | \n
Lactate | \n2 | \n6.4 | \n
Chloride | \n1.1 | \n1.1 | \n
Up until very recently, whey resulting from the curd during manufacture of cheese was regarded as a polluting effluent from the dairy industry. Nowadays, the potential of a vast range of whey proteins and their peptides with great potential health benefits is well known. Recently, whey gained interest as a food ingredient, coming into use as a technological agent particularly through whey proteins, achieving a unique blend between nutritional and functional properties with applications both in food and health. Whey components are being separated by isolation and fractionation on selective porous membranes. Extensive investigations focused on the exploitation of techno functional, biological, and nutritional properties of the whey [3]. By far, membrane technology enabled the breakthrough of whey processing into several derivatives favoring their incorporation as ingredients into different foods. These whey proteins are separated and purified from the liquid whey in an efficient membrane filtration process and subsequent spray drying to obtain either whey protein concentrate (WPC) (65–80% protein in dry matter) or whey protein isolate (WPI) (90% protein in dry matter). Ultrafiltration (UF) techniques have been used for cheese milk to retain whey proteins to increase the yield of the end product. Moreover, whey proteins have been added into cheese to boost its nutritional profile. Different pre-treatments of cheese milk have been developed to incorporate native or denatured WP in the cheese matrix. These options opened new avenues for progress in cheese-making.
\nAlthough these whey proteins are used as additives in the agro-food industry, such as the athletic drinks, still, 40% of whey remains unprocessed, which makes it an interesting resource in view of its excellent oxygen barrier properties [4, 5]. Whey protein films have excellent oxygen, aroma, and oil barrier properties. They have excellent mechanical properties that provide durability when used as coatings on food products, films separating layers of heterogeneous foods, or films formed into pouches for food ingredients. These films do not significantly compromise the desirable primary barrier and mechanical properties as packaging films and hence add value for ultimate commercial applications [6, 7]. Whey-based formulations are processed for packaging applications and edible coatings through extrusion as well as compression molding. Incorporation of plasticizing agents is necessary to overcome the intrinsic brittleness. Whey protein isolate films are fully transparent. Whey coatings with a barrier layer and an active layer have been developed. The barrier layer contains whey protein isolates supplemented with plasticizers, and the active layer contains antimicrobials or antioxidants to extend the shelf life of the packaged food. Whey-based films may improve the sensory attributes of the coated goods while providing some health benefits to the consumers. These proteins have been used as a coating on paper as well as on plastics, polypropylene (PP), polyvinylchloride (PVC), and low-density polyethylene (LDPE), which demonstrated excellent visual properties, such as excellent gloss and high transparency, as well as good mechanical properties.
\nThe incorporation of whey proteins into the cheese matrix has been made possible with a number of new technologies. Whey protein addition enhances the nutritional and functional properties as well as the economic effectiveness of cheese production. Addition of whey proteins increases the yield but may result in a slightly poor flavor and texture [8]. Whey protein concentrate and whey protein powder addition has been reported in a variety of cheeses that include cream cheese, cheese spreads, Cheddar cheese, Gouda cheese, processed cheese, Domiati cheese, etc. Addition of WPC was found to increase the yields in all cheeses with softer texture in camembert and Iranian white cheese. The influence of whey protein incorporation in processed cheese on its functional and sensory properties has been extensively studied. It has been found that whey proteins can be used to replace caseins up to 2% in processed cheese [9]. Whey protein concentrates are used as fat replacers in processed cheese, and they reduce the hardness of the cheese [10]. Addition of whey proteins/carboxymethyl cellulose complex recovered from whey, corresponding to 25–75% of cheese milk weight in Domiati cheese, increased cheese yield, reduced loss of weight during pickling, and enhanced the body of cheese. Flavor intensity was not affected by the addition of whey proteins [11]. Replacement of rennet casein in part with WPC in mozzarella cheese analogue resulted in greater firmness and meltability, lower cohesiveness and fat leakage, and moderate chewiness [12].
\nMembrane separation techniques have been largely explored by dairy industries for their effective and economic implementation. These techniques work on the basis of size and shape of molecules as well as on charge and affinity for the membrane. Among these techniques UF was the first to be exploited for cheese enrichment with WP [1, 13]. Whey proteins, which remain entrapped in the curd matrix, contribute to the enhanced yield of cheese. Rennet-curd cheeses, such as mozzarella, cottage, and Cheddar, can be manufactured by this technique [14]. The implementation of spray drying has reduced the thermal degradation of whey components, as well as the cost associated with its concentration. Membrane filtration technique employs semipermeable surfaces (membranes) with specific pore sizes, where the permeate flows through, while the retentate is blocked based on size/molecular weight. Throughout the combination of successive filtrations steps, it is possible to produce protein fractions with different compositions and degrees of purity. This technology leads to a selective concentration of proteins, which after drying is called whey protein concentrate containing about 35–80% of protein. Further purification, often conjugating other techniques as ion-exchange chromatography, allows the achievement of higher degrees of purity with residual or no lactose content and higher desalination, resulting in whey protein isolate containing at least 90% of protein. With the application of more advanced techniques, such as chromatography, partial hydrolyses, and selective precipitation combined with centrifugation and dialysis, it is yet possible to obtain pure whey protein fractions. WPI and WPC can be widely used for food applications because of higher protein and amino acid contents; low calorie, fat, and sodium contents; absence of pathogens and toxic compounds; biocompatibility and generally recognized as safe status; ready availability; and inexpensive products.
\nGhee is an important constituent of Indian meal prepared using different methods. It is clarified milk fat with incomparable organoleptic properties, which make it an important ingredient in a wide variety of food applications [15]. About 30–35% of the milk produced in India (112 million tons in 2009–2010) is converted into ghee [16]. A blackish brown residue mainly the SNF part of cream was coagulated out during ghee preparation as a by-product when cream is heated is known as ghee residue. It is obtained as moist brownish sediment after molten ghee has been strained out [17]. The amount of ghee residue was found to depend upon the method of preparation of ghee. This was due to the variation of nonfatty serum constituents of the different raw materials used for the preparation of ghee. Ghee yield was higher from creamery butter method in comparison to direct cream method, whereas ghee residue content was higher in direct cream method in comparison to creamery butter method. The average yield of ghee residue was maximum (12%) in direct creamery (DC) method followed by almost the same yield in creamery butter (CB) and desi butter (DB) methods, that is, 3.7%. Ripening of cream prior to clarification reduces the yield of ghee residue [18, 19]. It is one of the largest by-products of the dairy industry and consists mainly of milk proteins and small quantity of lactose and minerals. The ghee residue has been used in food industries for making sweets, bakery products, and as a flavor enhancer [20]. An appreciable amount of GR is produced in the country which is a nutritionally rich source of proteins and nitrogenous compounds. Ghee residue has been utilized for preparing burfi by mixing it with skim milk powder (SMP), khoa, chocolate, and sugar [21]. It can be utilized for preparing coconut burfi, candies, toffees, pinni, etc. after mixing with other ingredients. The nutritious by-product should be utilized as a food supplement in a variety of foods, food spreads, soups, etc. [22]. The utilization of this by-product in the preparation of some type of candies, toffees, edible pastes, etc. was suggested about two decades ago but was not adopted commercially by the industry due to lack of awareness about its nutritive value. In general, the residue contains appreciable amounts of nutrients of milk. Ghee residue has been used in the preparation of candy, chocolate, burfi-type sweet, and bakery products.
\nThe phospholipids of milk occur in a complex form with proteins in the fat globule membrane. When butter is heated to 120°C and above, the phospholipids are liberated from the phospholipid-protein complex and transferred to the oil phase. When the ghee-making process is kept much below 120°C, phospholipids, which remain in a complex form with proteins, will not enter ghee and, therefore, will be retained by GR. GR is a rich source of phospholipids from which phospholipids can be recovered and added to ghee. Pruthi et al. [23] described a heat-processing method for the extraction and fortification of ghee with GR phospholipids. The fortification of ghee with phospholipids at 0.1% level showed that the oxidative stability of ghee can be increased by increasing its phospholipid content either through heat treatment of GR with ghee or by the addition of solvent-extracted phospholipids from GR.
\nButtermilk is a by-product of butter-making. It contains components derived both from fragments of milk fat globule membrane (MFGM), mainly consisting of proteins and neutral as well as polar lipids and all water-soluble components of cream [24]. Fortification with buttermilk is done to increase the yield provided cheese quality is unchanged. Buttermilk has high phospholipid content that has a significant function as emulsifiers in food systems and makes this dairy ingredient interesting for use as a functional ingredient [25] in an array of food products like chocolate, cheese seasonings, margarine, bread, ice cream mixes, or yogurt [26, 27, 28]. The buttermilk concentrate (BMC) rich in phospholipids has been utilized in processed cheese spread to improve its organoleptic, rheological, and functional properties [29]. The use of BMC in processed cheese spreads makes this dairy product useful as a functional food. This perspective could also bring economical income by enhancing the product yield or using low-value by-products from the dairy industry, such as buttermilk. Sweet buttermilk, condensed by heat and vacuum, supplemented at levels of 4 or 6% in regard to cheese milk improved the yield of pizza cheese with the contribution of denatured WP [30]. Kumari et al. [31] verified the effect of buttermilk as an ingredient in buffalo milk-derived chhana, an Indian-style soft cottage cheese analogue. Substitution of milk with variable proportions of sweet buttermilk (from 0 to 50%) was technologically tested in cream cheese [32]. The authors revealed that the progressive increase of buttermilk percentage was followed by increase in moisture and yield. Buttermilk has been added to reduced-fat cheese up to 40% and was found to improve the sensory scores in comparison to the control [33].
\nSkim milk powder for cheese-making requires adequate reconstitution and recombination techniques compared to whole milk powders, and at places where modern equipment and processing facilities for the reconstitution and recombination are not available, the use of whole milk powders could be advantageous. Addition of skim milk powder has been reported in Karish cheese, Domiati cheese, and processed cheese. Skim milk along with milk protein and stabilizers were used to produce high-quality and acceptable Karish cheese with increased yield. Domiati cheese production was attempted earlier by an Egypt-based company, but the cheese obtained was inferior to that made from fresh milk. The recombined Domiati cheese had a firm texture and developed weak flavor even after the normal maturation period. Later attempts were made to improve the quality of recombined Domiati cheese, and direct addition of skim milk powder to buffalo or cow milk up to 35% total solids and coagulating the concentrated milk covered with brine resulted in acceptable taste and flavor after a month of storage. The FDA recommends the use of nonfat dry milk in processed cheese foods and processed cheese spreads. However, processed cheese made using cheese base produced from reconstituted skim milk powder results in markedly firmer cheese than the control. Skim milk powder has been reported for fortification of nontraditional white soft cheese in Egypt.
\nUtilization of whey proteins in cheese through either the adoption of techniques favoring WP retention in the cheese network or the direct addition of dairy-based ingredients or their combination is a challenging area in dairy sector. Some techniques have been implemented and emerged in industrial processes. In addition, ultrafiltration process can be used to restrain and recover whey proteins from drained whey that can later be added to the cheese milk. Utilizing whey protein into cheese preparation puts whey to good use. Whey protein-based edible films are a viable alternative packaging process for food and improvement of shelf life. Ghee residue is a good source of proteins, and about 100,000 tonnes of proteins can be recovered annually from GR only, and this can help in combating severe problem of protein-energy malnutrition. Potential uses of either crude or purified caseins include the production of plastics, adhesives, gels, composites, and films.
\nIntechOpen implements a robust policy to minimize and deal with instances of fraud or misconduct. As part of our general commitment to transparency and openness, and in order to maintain high scientific standards, we have a well-defined editorial policy regarding Retractions and Corrections.
",metaTitle:"Retraction and Correction Policy",metaDescription:"Retraction and Correction Policy",metaKeywords:null,canonicalURL:"/page/retraction-and-correction-policy",contentRaw:'[{"type":"htmlEditorComponent","content":"IntechOpen’s Retraction and Correction Policy has been developed in accordance with the Committee on Publication Ethics (COPE) publication guidelines relating to scientific misconduct and research ethics:
\\n\\n1. RETRACTIONS
\\n\\nA Retraction of a Chapter will be issued by the Academic Editor, either following an Author’s request to do so or when there is a 3rd party report of scientific misconduct. Upon receipt of a report by a 3rd party, the Academic Editor will investigate any allegations of scientific misconduct, working in cooperation with the Author(s) and their institution(s).
\\n\\nA formal Retraction will be issued when there is clear and conclusive evidence of any of the following:
\\n\\nPublishing of a Retraction Notice will adhere to the following guidelines:
\\n\\n1.2. REMOVALS AND CANCELLATIONS
\\n\\n2. STATEMENTS OF CONCERN
\\n\\nA Statement of Concern detailing alleged misconduct will be issued by the Academic Editor or publisher following a 3rd party report of scientific misconduct when:
\\n\\nIntechOpen believes that the number of occasions on which a Statement of Concern is issued will be very few in number. In all cases when such a decision has been taken by the Academic Editor the decision will be reviewed by another editor to whom the author can make representations.
\\n\\n3. CORRECTIONS
\\n\\nA Correction will be issued by the Academic Editor when:
\\n\\n3.1. ERRATUM
\\n\\nAn Erratum will be issued by the Academic Editor when it is determined that a mistake in a Chapter originates from the production process handled by the publisher.
\\n\\nA published Erratum will adhere to the Retraction Notice publishing guidelines outlined above.
\\n\\n3.2. CORRIGENDUM
\\n\\nA Corrigendum will be issued by the Academic Editor when it is determined that a mistake in a Chapter is a result of an Author’s miscalculation or oversight. A published Corrigendum will adhere to the Retraction Notice publishing guidelines outlined above.
\\n\\n4. FINAL REMARKS
\\n\\nIntechOpen wishes to emphasize that the final decision on whether a Retraction, Statement of Concern, or a Correction will be issued rests with the Academic Editor. The publisher is obliged to act upon any reports of scientific misconduct in its publications and to make a reasonable effort to facilitate any subsequent investigation of such claims.
\\n\\nIn the case of Retraction or removal of the Work, the publisher will be under no obligation to refund the APC.
\\n\\nThe general principles set out above apply to Retractions and Corrections issued in all IntechOpen publications.
\\n\\nAny suggestions or comments on this Policy are welcome and may be sent to permissions@intechopen.com.
\\n\\nPolicy last updated: 2017-09-11
\\n"}]'},components:[{type:"htmlEditorComponent",content:'IntechOpen’s Retraction and Correction Policy has been developed in accordance with the Committee on Publication Ethics (COPE) publication guidelines relating to scientific misconduct and research ethics:
\n\n1. RETRACTIONS
\n\nA Retraction of a Chapter will be issued by the Academic Editor, either following an Author’s request to do so or when there is a 3rd party report of scientific misconduct. Upon receipt of a report by a 3rd party, the Academic Editor will investigate any allegations of scientific misconduct, working in cooperation with the Author(s) and their institution(s).
\n\nA formal Retraction will be issued when there is clear and conclusive evidence of any of the following:
\n\nPublishing of a Retraction Notice will adhere to the following guidelines:
\n\n1.2. REMOVALS AND CANCELLATIONS
\n\n2. STATEMENTS OF CONCERN
\n\nA Statement of Concern detailing alleged misconduct will be issued by the Academic Editor or publisher following a 3rd party report of scientific misconduct when:
\n\nIntechOpen believes that the number of occasions on which a Statement of Concern is issued will be very few in number. In all cases when such a decision has been taken by the Academic Editor the decision will be reviewed by another editor to whom the author can make representations.
\n\n3. CORRECTIONS
\n\nA Correction will be issued by the Academic Editor when:
\n\n3.1. ERRATUM
\n\nAn Erratum will be issued by the Academic Editor when it is determined that a mistake in a Chapter originates from the production process handled by the publisher.
\n\nA published Erratum will adhere to the Retraction Notice publishing guidelines outlined above.
\n\n3.2. CORRIGENDUM
\n\nA Corrigendum will be issued by the Academic Editor when it is determined that a mistake in a Chapter is a result of an Author’s miscalculation or oversight. A published Corrigendum will adhere to the Retraction Notice publishing guidelines outlined above.
\n\n4. FINAL REMARKS
\n\nIntechOpen wishes to emphasize that the final decision on whether a Retraction, Statement of Concern, or a Correction will be issued rests with the Academic Editor. The publisher is obliged to act upon any reports of scientific misconduct in its publications and to make a reasonable effort to facilitate any subsequent investigation of such claims.
\n\nIn the case of Retraction or removal of the Work, the publisher will be under no obligation to refund the APC.
\n\nThe general principles set out above apply to Retractions and Corrections issued in all IntechOpen publications.
\n\nAny suggestions or comments on this Policy are welcome and may be sent to permissions@intechopen.com.
\n\nPolicy last updated: 2017-09-11
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She performed research in perioperative autotransfusion and obtained the degree of PhD in 1993 publishing Peri-operative autotransfusion by means of a blood cell separator.\nBlood transfusion had her special interest being the president of the Haemovigilance Chamber TRIP and performing several tasks in local and national blood bank and anticoagulant-blood transfusion guidelines committees. Currently, she is working as an associate professor and up till recently was the dean at the Albert Schweitzer Hospital Dordrecht. She performed (inter)national tasks as vice-president of the Concilium Anaesthesia and related committees. \nShe performed research in several fields, with over 100 publications in (inter)national journals and numerous papers on scientific conferences. \nShe received several awards and is a member of Honour of the Dutch Society of Anaesthesia.",institutionString:null,institution:{name:"Albert Schweitzer Hospital",country:{name:"Gabon"}}},{id:"83089",title:"Prof.",name:"Aaron",middleName:null,surname:"Ojule",slug:"aaron-ojule",fullName:"Aaron Ojule",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Port Harcourt",country:{name:"Nigeria"}}},{id:"295748",title:"Mr.",name:"Abayomi",middleName:null,surname:"Modupe",slug:"abayomi-modupe",fullName:"Abayomi Modupe",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/no_image.jpg",biography:null,institutionString:null,institution:{name:"Landmark University",country:{name:"Nigeria"}}},{id:"94191",title:"Prof.",name:"Abbas",middleName:null,surname:"Moustafa",slug:"abbas-moustafa",fullName:"Abbas Moustafa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94191/images/96_n.jpg",biography:"Prof. Moustafa got his doctoral degree in earthquake engineering and structural safety from Indian Institute of Science in 2002. He is currently an associate professor at Department of Civil Engineering, Minia University, Egypt and the chairman of Department of Civil Engineering, High Institute of Engineering and Technology, Giza, Egypt. He is also a consultant engineer and head of structural group at Hamza Associates, Giza, Egypt. Dr. Moustafa was a senior research associate at Vanderbilt University and a JSPS fellow at Kyoto and Nagasaki Universities. He has more than 40 research papers published in international journals and conferences. He acts as an editorial board member and a reviewer for several regional and international journals. His research interest includes earthquake engineering, seismic design, nonlinear dynamics, random vibration, structural reliability, structural health monitoring and uncertainty modeling.",institutionString:null,institution:{name:"Minia University",country:{name:"Egypt"}}},{id:"84562",title:"Dr.",name:"Abbyssinia",middleName:null,surname:"Mushunje",slug:"abbyssinia-mushunje",fullName:"Abbyssinia Mushunje",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Fort Hare",country:{name:"South Africa"}}},{id:"202206",title:"Associate Prof.",name:"Abd Elmoniem",middleName:"Ahmed",surname:"Elzain",slug:"abd-elmoniem-elzain",fullName:"Abd Elmoniem Elzain",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Kassala University",country:{name:"Sudan"}}},{id:"98127",title:"Dr.",name:"Abdallah",middleName:null,surname:"Handoura",slug:"abdallah-handoura",fullName:"Abdallah Handoura",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"École Supérieure des Télécommunications",country:{name:"Morocco"}}},{id:"91404",title:"Prof.",name:"Abdecharif",middleName:null,surname:"Boumaza",slug:"abdecharif-boumaza",fullName:"Abdecharif Boumaza",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Abbès Laghrour University of Khenchela",country:{name:"Algeria"}}},{id:"105795",title:"Prof.",name:"Abdel Ghani",middleName:null,surname:"Aissaoui",slug:"abdel-ghani-aissaoui",fullName:"Abdel Ghani Aissaoui",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/105795/images/system/105795.jpeg",biography:"Abdel Ghani AISSAOUI is a Full Professor of electrical engineering at University of Bechar (ALGERIA). He was born in 1969 in Naama, Algeria. He received his BS degree in 1993, the MS degree in 1997, the PhD degree in 2007 from the Electrical Engineering Institute of Djilali Liabes University of Sidi Bel Abbes (ALGERIA). He is an active member of IRECOM (Interaction Réseaux Electriques - COnvertisseurs Machines) Laboratory and IEEE senior member. He is an editor member for many international journals (IJET, RSE, MER, IJECE, etc.), he serves as a reviewer in international journals (IJAC, ECPS, COMPEL, etc.). He serves as member in technical committee (TPC) and reviewer in international conferences (CHUSER 2011, SHUSER 2012, PECON 2012, SAI 2013, SCSE2013, SDM2014, SEB2014, PEMC2014, PEAM2014, SEB (2014, 2015), ICRERA (2015, 2016, 2017, 2018,-2019), etc.). His current research interest includes power electronics, control of electrical machines, artificial intelligence and Renewable energies.",institutionString:"University of Béchar",institution:{name:"University of Béchar",country:{name:"Algeria"}}},{id:"99749",title:"Dr.",name:"Abdel Hafid",middleName:null,surname:"Essadki",slug:"abdel-hafid-essadki",fullName:"Abdel Hafid Essadki",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"École Nationale Supérieure de Technologie",country:{name:"Algeria"}}},{id:"101208",title:"Prof.",name:"Abdel Karim",middleName:"Mohamad",surname:"El Hemaly",slug:"abdel-karim-el-hemaly",fullName:"Abdel Karim El Hemaly",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/101208/images/733_n.jpg",biography:"OBGYN.net Editorial Advisor Urogynecology.\nAbdel Karim M. A. El-Hemaly, MRCOG, FRCS � Egypt.\n \nAbdel Karim M. A. El-Hemaly\nProfessor OB/GYN & Urogynecology\nFaculty of medicine, Al-Azhar University \nPersonal Information: \nMarried with two children\nWife: Professor Laila A. Moussa MD.\nSons: Mohamad A. M. El-Hemaly Jr. MD. Died March 25-2007\nMostafa A. M. El-Hemaly, Computer Scientist working at Microsoft Seatle, USA. \nQualifications: \n1.\tM.B.-Bch Cairo Univ. June 1963. \n2.\tDiploma Ob./Gyn. Cairo Univ. April 1966. \n3.\tDiploma Surgery Cairo Univ. Oct. 1966. \n4.\tMRCOG London Feb. 1975. \n5.\tF.R.C.S. Glasgow June 1976. \n6.\tPopulation Study Johns Hopkins 1981. \n7.\tGyn. Oncology Johns Hopkins 1983. \n8.\tAdvanced Laparoscopic Surgery, with Prof. Paulson, Alexandria, Virginia USA 1993. \nSocieties & Associations: \n1.\t Member of the Royal College of Ob./Gyn. London. \n2.\tFellow of the Royal College of Surgeons Glasgow UK. \n3.\tMember of the advisory board on urogyn. FIGO. \n4.\tMember of the New York Academy of Sciences. \n5.\tMember of the American Association for the Advancement of Science. \n6.\tFeatured in �Who is Who in the World� from the 16th edition to the 20th edition. \n7.\tFeatured in �Who is Who in Science and Engineering� in the 7th edition. \n8.\tMember of the Egyptian Fertility & Sterility Society. \n9.\tMember of the Egyptian Society of Ob./Gyn. \n10.\tMember of the Egyptian Society of Urogyn. \n\nScientific Publications & Communications:\n1- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Asim Kurjak, Ahmad G. Serour, Laila A. S. Mousa, Amr M. Zaied, Khalid Z. El Sheikha. \nImaging the Internal Urethral Sphincter and the Vagina in Normal Women and Women Suffering from Stress Urinary Incontinence and Vaginal Prolapse. Gynaecologia Et Perinatologia, Vol18, No 4; 169-286 October-December 2009.\n2- Abdel Karim M. El Hemaly*, Laila A. S. Mousa Ibrahim M. Kandil, Fatma S. El Sokkary, Ahmad G. Serour, Hossam Hussein.\nFecal Incontinence, A Novel Concept: The Role of the internal Anal sphincter (IAS) in defecation and fecal incontinence. Gynaecologia Et Perinatologia, Vol19, No 2; 79-85 April -June 2010.\n3- Abdel Karim M. El Hemaly*, Laila A. S. Mousa Ibrahim M. Kandil, Fatma S. El Sokkary, Ahmad G. Serour, Hossam Hussein.\nSurgical Treatment of Stress Urinary Incontinence, Fecal Incontinence and Vaginal Prolapse By A Novel Operation \n"Urethro-Ano-Vaginoplasty"\n Gynaecologia Et Perinatologia, Vol19, No 3; 129-188 July-September 2010.\n4- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Laila A. S. Mousa and Mohamad A.K.M.El Hemaly.\nUrethro-vaginoplasty, an innovated operation for the treatment of: Stress Urinary Incontinence (SUI), Detursor Overactivity (DO), Mixed Urinary Incontinence and Anterior Vaginal Wall Descent. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/ urethro-vaginoplasty_01\n\n5- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamed M. Radwan.\n Urethro-raphy a new technique for surgical management of Stress Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/\nnew-tech-urethro\n\n6- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamad A. Rizk, Nabil Abdel Maksoud H., Mohamad M. Radwan, Khalid Z. El Shieka, Mohamad A. K. M. El Hemaly, and Ahmad T. El Saban.\nUrethro-raphy The New Operation for the treatment of stress urinary incontinence, SUI, detrusor instability, DI, and mixed-type of urinary incontinence; short and long term results. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=urogyn/articles/\nurethroraphy-09280\n\n7-Abdel Karim M. El Hemaly, Ibrahim M Kandil, and Bahaa E. El Mohamady. Menopause, and Voiding troubles. \nhttp://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly03/el-hemaly03-ss\n\n8-El Hemaly AKMA, Mousa L.A. Micturition and Urinary\tContinence. Int J Gynecol Obstet 1996; 42: 291-2. \n\n9-Abdel Karim M. El Hemaly.\n Urinary incontinence in gynecology, a review article.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/abs-urinary_incotinence_gyn_ehemaly \n\n10-El Hemaly AKMA. Nocturnal Enuresis: Pathogenesis and Treatment. \nInt Urogynecol J Pelvic Floor Dysfunct 1998;9: 129-31.\n \n11-El Hemaly AKMA, Mousa L.A.E. Stress Urinary Incontinence, a New Concept. Eur J Obstet Gynecol Reprod Biol 1996; 68: 129-35. \n\n12- El Hemaly AKMA, Kandil I. M. Stress Urinary Incontinence SUI facts and fiction. Is SUI a puzzle?! http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly/el-hemaly-ss\n\n13-Abdel Karim El Hemaly, Nabil Abdel Maksoud, Laila A. Mousa, Ibrahim M. Kandil, Asem Anwar, M.A.K El Hemaly and Bahaa E. El Mohamady. \nEvidence based Facts on the Pathogenesis and Management of SUI. http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly02/el-hemaly02-ss\n\n14- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Mohamad A. Rizk and Mohamad A.K.M.El Hemaly.\n Urethro-plasty, a Novel Operation based on a New Concept, for the Treatment of Stress Urinary Incontinence, S.U.I., Detrusor Instability, D.I., and Mixed-type of Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/urethro-plasty_01\n\n15-Ibrahim M. Kandil, Abdel Karim M. El Hemaly, Mohamad M. Radwan: Ultrasonic Assessment of the Internal Urethral Sphincter in Stress Urinary Incontinence. The Internet Journal of Gynecology and Obstetrics. 2003. Volume 2 Number 1. \n\n\n16-Abdel Karim M. El Hemaly. Nocturnal Enureses: A Novel Concept on its pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecolgy/?page=articles/nocturnal_enuresis\n\n17- Abdel Karim M. El Hemaly. Nocturnal Enureses: An Update on the pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecology/?page=/ENHLIDH/PUBD/FEATURES/\nPresentations/ Nocturnal_Enuresis/nocturnal_enuresis\n\n18-Maternal Mortality in Egypt, a cry for help and attention. The Second International Conference of the African Society of Organization & Gestosis, 1998, 3rd Annual International Conference of Ob/Gyn Department � Sohag Faculty of Medicine University. Feb. 11-13. Luxor, Egypt. \n19-Postmenopausal Osteprosis. The 2nd annual conference of Health Insurance Organization on Family Planning and its role in primary health care. Zagaziz, Egypt, February 26-27, 1997, Center of Complementary Services for Maternity and childhood care. \n20-Laparoscopic Assisted vaginal hysterectomy. 10th International Annual Congress Modern Trends in Reproductive Techniques 23-24 March 1995. Alexandria, Egypt. \n21-Immunological Studies in Pre-eclamptic Toxaemia. Proceedings of 10th Annual Ain Shams Medical Congress. Cairo, Egypt, March 6-10, 1987. \n22-Socio-demographic factorse affecting acceptability of the long-acting contraceptive injections in a rural Egyptian community. Journal of Biosocial Science 29:305, 1987. \n23-Plasma fibronectin levels hypertension during pregnancy. The Journal of the Egypt. Soc. of Ob./Gyn. 13:1, 17-21, Jan. 1987. \n24-Effect of smoking on pregnancy. Journal of Egypt. Soc. of Ob./Gyn. 12:3, 111-121, Sept 1986. \n25-Socio-demographic aspects of nausea and vomiting in early pregnancy. Journal of the Egypt. Soc. of Ob./Gyn. 12:3, 35-42, Sept. 1986. \n26-Effect of intrapartum oxygen inhalation on maternofetal blood gases and pH. Journal of the Egypt. Soc. of Ob./Gyn. 12:3, 57-64, Sept. 1986. \n27-The effect of severe pre-eclampsia on serum transaminases. The Egypt. J. Med. Sci. 7(2): 479-485, 1986. \n28-A study of placental immunoreceptors in pre-eclampsia. The Egypt. J. Med. Sci. 7(2): 211-216, 1986. \n29-Serum human placental lactogen (hpl) in normal, toxaemic and diabetic pregnant women, during pregnancy and its relation to the outcome of pregnancy. Journal of the Egypt. Soc. of Ob./Gyn. 12:2, 11-23, May 1986. \n30-Pregnancy specific B1 Glycoprotein and free estriol in the serum of normal, toxaemic and diabetic pregnant women during pregnancy and after delivery. Journal of the Egypt. Soc. of Ob./Gyn. 12:1, 63-70, Jan. 1986. Also was accepted and presented at Xith World Congress of Gynecology and Obstetrics, Berlin (West), September 15-20, 1985. \n31-Pregnancy and labor in women over the age of forty years. Accepted and presented at Al-Azhar International Medical Conference, Cairo 28-31 Dec. 1985. \n32-Effect of Copper T intra-uterine device on cervico-vaginal flora. Int. J. Gynaecol. Obstet. 23:2, 153-156, April 1985. \n33-Factors affecting the occurrence of post-Caesarean section febrile morbidity. Population Sciences, 6, 139-149, 1985. \n34-Pre-eclamptic toxaemia and its relation to H.L.A. system. Population Sciences, 6, 131-139, 1985. \n35-The menstrual pattern and occurrence of pregnancy one year after discontinuation of Depo-medroxy progesterone acetate as a postpartum contraceptive. Population Sciences, 6, 105-111, 1985. \n36-The menstrual pattern and side effects of Depo-medroxy progesterone acetate as postpartum contraceptive. Population Sciences, 6, 97-105, 1985. \n37-Actinomyces in the vaginas of women with and without intrauterine contraceptive devices. Population Sciences, 6, 77-85, 1985. \n38-Comparative efficacy of ibuprofen and etamsylate in the treatment of I.U.D. menorrhagia. Population Sciences, 6, 63-77, 1985. \n39-Changes in cervical mucus copper and zinc in women using I.U.D.�s. Population Sciences, 6, 35-41, 1985. \n40-Histochemical study of the endometrium of infertile women. Egypt. J. Histol. 8(1) 63-66, 1985. \n41-Genital flora in pre- and post-menopausal women. Egypt. J. Med. Sci. 4(2), 165-172, 1983. \n42-Evaluation of the vaginal rugae and thickness in 8 different groups. Journal of the Egypt. Soc. of Ob./Gyn. 9:2, 101-114, May 1983. \n43-The effect of menopausal status and conjugated oestrogen therapy on serum cholesterol, triglycerides and electrophoretic lipoprotein patterns. Al-Azhar Medical Journal, 12:2, 113-119, April 1983. \n44-Laparoscopic ventrosuspension: A New Technique. Int. J. Gynaecol. Obstet., 20, 129-31, 1982. \n45-The laparoscope: A useful diagnostic tool in general surgery. Al-Azhar Medical Journal, 11:4, 397-401, Oct. 1982. \n46-The value of the laparoscope in the diagnosis of polycystic ovary. Al-Azhar Medical Journal, 11:2, 153-159, April 1982. \n47-An anaesthetic approach to the management of eclampsia. Ain Shams Medical Journal, accepted for publication 1981. \n48-Laparoscopy on patients with previous lower abdominal surgery. Fertility management edited by E. Osman and M. Wahba 1981. \n49-Heart diseases with pregnancy. Population Sciences, 11, 121-130, 1981. \n50-A study of the biosocial factors affecting perinatal mortality in an Egyptian maternity hospital. Population Sciences, 6, 71-90, 1981. \n51-Pregnancy Wastage. Journal of the Egypt. Soc. of Ob./Gyn. 11:3, 57-67, Sept. 1980. \n52-Analysis of maternal deaths in Egyptian maternity hospitals. Population Sciences, 1, 59-65, 1979. \nArticles published on OBGYN.net: \n1- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Laila A. S. Mousa and Mohamad A.K.M.El Hemaly.\nUrethro-vaginoplasty, an innovated operation for the treatment of: Stress Urinary Incontinence (SUI), Detursor Overactivity (DO), Mixed Urinary Incontinence and Anterior Vaginal Wall Descent. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/ urethro-vaginoplasty_01\n\n2- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamed M. Radwan.\n Urethro-raphy a new technique for surgical management of Stress Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/\nnew-tech-urethro\n\n3- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamad A. Rizk, Nabil Abdel Maksoud H., Mohamad M. Radwan, Khalid Z. El Shieka, Mohamad A. K. M. El Hemaly, and Ahmad T. El Saban.\nUrethro-raphy The New Operation for the treatment of stress urinary incontinence, SUI, detrusor instability, DI, and mixed-type of urinary incontinence; short and long term results. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=urogyn/articles/\nurethroraphy-09280\n\n4-Abdel Karim M. El Hemaly, Ibrahim M Kandil, and Bahaa E. El Mohamady. Menopause, and Voiding troubles. \nhttp://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly03/el-hemaly03-ss\n\n5-El Hemaly AKMA, Mousa L.A. Micturition and Urinary\tContinence. Int J Gynecol Obstet 1996; 42: 291-2. \n\n6-Abdel Karim M. El Hemaly.\n Urinary incontinence in gynecology, a review article.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/abs-urinary_incotinence_gyn_ehemaly \n\n7-El Hemaly AKMA. Nocturnal Enuresis: Pathogenesis and Treatment. \nInt Urogynecol J Pelvic Floor Dysfunct 1998;9: 129-31.\n \n8-El Hemaly AKMA, Mousa L.A.E. Stress Urinary Incontinence, a New Concept. Eur J Obstet Gynecol Reprod Biol 1996; 68: 129-35. \n\n9- El Hemaly AKMA, Kandil I. M. Stress Urinary Incontinence SUI facts and fiction. Is SUI a puzzle?! http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly/el-hemaly-ss\n\n10-Abdel Karim El Hemaly, Nabil Abdel Maksoud, Laila A. Mousa, Ibrahim M. Kandil, Asem Anwar, M.A.K El Hemaly and Bahaa E. El Mohamady. \nEvidence based Facts on the Pathogenesis and Management of SUI. http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly02/el-hemaly02-ss\n\n11- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Mohamad A. Rizk and Mohamad A.K.M.El Hemaly.\n Urethro-plasty, a Novel Operation based on a New Concept, for the Treatment of Stress Urinary Incontinence, S.U.I., Detrusor Instability, D.I., and Mixed-type of Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/urethro-plasty_01\n\n12-Ibrahim M. Kandil, Abdel Karim M. El Hemaly, Mohamad M. Radwan: Ultrasonic Assessment of the Internal Urethral Sphincter in Stress Urinary Incontinence. The Internet Journal of Gynecology and Obstetrics. 2003. Volume 2 Number 1. \n\n13-Abdel Karim M. El Hemaly. Nocturnal Enureses: A Novel Concept on its pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecolgy/?page=articles/nocturnal_enuresis\n\n14- Abdel Karim M. El Hemaly. 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