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The potential beneﬁt of arterial recanalization has to spasms perineum generic 30 gr rumalaya gel otc be balanced against the risks of adverse effects (particularly major cerebral haemorrhage muscle relaxant antidote buy line rumalaya gel, occurring in 5–10%) and this balance is more favourable the earlier the intervention can be delivered muscle relaxant hiccups cheap rumalaya gel amex. Adult trials suggest a window of up to muscle relaxant benzodiazepine rumalaya gel 30gr overnight delivery four hours from the stroke but even in this group the routine use of throm bolysis remains unestablished. Relative indications for conventional angiography Conventional four-vessel angiography is associated with 71% risk of stroke from the procedure. Radiology Identifying the primary cause of a stroke in childhood guides management, including steps to prevent the occurrence of possible further strokes (Figure 4. Imaging is crucial in distinguishing haemorrhage, arterial ischaemia and venous ischaemia/infarction. Within the arterial ischaemic group, consider ation of lesion location in relation to vascular territories (see b p. The evidence base for secondary prevention measures in paediatric ischaemic stroke is limited; see, for example: M. Recommendations based on these guidelines are indicated later with an asterisk (*). Occurs after even apparently trivial trauma to the head or neck creating an ‘intimal tear’ in the carotid artery. Investigations. Trans-thoracic echocardiogram: discuss need for trans-oesophageal echo with cardiologists. Transient abnormalities in ‘thrombophilia screen’ results are common and may be important in post-infectious and other mechanisms of stroke. Treatment and secondary prevention. All children with radiologically proven ischaemic stroke should be commenced on low-dose aspirin pending further investigation unless the child has sickle cell disease, or radiological evidence of haemorrhage(*). This may be relaxed after 3 yrs to maintain HbS < 50% and stopped after 2 yrs in patients who experienced stroke in the context of a precipitating illness. The term is Japanese for ‘wisp of smoke’ and relates to the angiographic appearances of the many tiny collaterals that open in response to large vessel narrowing. Important causes include sickle cell disease, neuroﬁbromatosis, Down, Noonan, and William syndromes. Primary cerebral vasculitis has protean manifestations and biopsy is often required to establish diagnosis. Treatment and secondary prevention. Treatment of underlying cause: surgical vascular procedures to correct large vessel stenoses if amenable;. surgical bypass and revascularization procedures to ameliorate the effects of Moya–Moya syndrome;. aggressive transfusion programmes in sickle cell disease (see b p. Venous infarction. Radiological appearances of ischaemia in non-arterial distributions. Cerebral aneurysms. Typically occur in the arteries of the Circle of Willis (see Figure 2. Treatment should be delayed and very cautious until vasospasm risk period is passed. Tend to present with focal seizures presumed due to slow leakage of blood products into surrounding area. The male to female ratio is equal except for a male predominance in medulloblastoma and germ cell tumours. Infratentorial tumours. In contrast to adults (where supratentorial tumours predominate), infratentorial tumours at least as common in children. Common presentations Presentation depends on the age of the child and the location of the tumour. Presentations by age. Presentations become increasingly speciﬁc and localizing with age. Presentations by location Supratentorial tumour presentations. Hemispheric gliomas: seizures, focal neurological deﬁcit, personality change. Intramedullary spinal tumour presentations Insidious onset of symptoms (pain, paraesthesia, paresis, sensory level, sphincter disturbance, spinal deformity). Usually spinal tumours are seen in older child, astrocytomas usually occur in upper thoracic cord and ependymomas in the cervical cord. Cerebellar astrocytomas. Usually pilocytic astrocytomas: brightly enhancing, well demarcated partly cystic tumours with minimal surrounding oedema. Adjuvant chemotherapy or radiotherapy is reserved for evidence of disease recurrence or progression. Over expression of p53 and glioblastoma multiforme are associated with poor prognosis. Brainstem gliomas. Tectal tumours are usually slow growing and resection is indicated; however, shunting may be required for hydrocephalus. Further intensiﬁcation of chemotherapeutic regimens with autologous bone marrow or peripheral stem cell reconstitution is being evaluated in children. Mainstay of adjuvant treatment is focal radiotherapy to tumour bed, certainly in over-3s. The role of radiotherapy in under-3s is under evaluation—chemotherapy may have a role if there is residual or disseminated disease, but has failed to reduce the need for radiotherapy in very young children. Less common central nervous system tumours Craniopharyngioma. This is a benign tumour but is locally aggressive and recurs. Children should have supplemental steroids before surgery and prior to treating hypothyroidism. Endovascular procedures (intra-arterial embolization) may aid subsequent resection. Five-year survival rates are around 25%, with the extent of surgical resection being important for prognosis. Myeloablative chemotherapy or chemoradiotherapy followed by autologous bone marrow transplantation is under investigation for the high risk group. Peripheral nerve tumours Schwannoma, neuroﬁbroma, perineuroma, malignant peripheral nerve sheath tumour. Staging evaluation this is required for posterior fossa medulloblastoma, ependymoma and for pineal lesions. Moya–Moya syndrome), neurocognitive and behaviour problems, secondary tumours (incidence of secondary tumours is around 2%, usually gliomas or meningiomas). Cerebellar mutism (posterior fossa syndrome) this is a complication of posterior fossa surgery, particularly resection of midline posterior fossa tumours, such as medulloblastoma (therefore more common in children than adults). This section, however, deals mainly with inborn errors of metabolism that may be thought of as treatable early epileptic encephalopathies. Although rare, these disorders are potentially treatable, and prompt diagnosis and treatment may have marked impact on outcome. Outcome Life-long treatment; likely learning difﬁculties, particularly language delay; more severe motor disorder and developmental delay if treatment is delayed. Pyridoxine and pyridoxal-responsive seizures There is a group of children with severe symptomatic epilepsy, often infantile spasms, who respond to vitamin B6, but in whom subsequent withdrawal is possible. In such cases withdrawal of pyridoxine to conﬁrm dependency is no longer recommended. Vitamin B12 (cobalamin) this is an essential water-soluble vitamin from meat and dairy products. Most other neurological disorders responsive to cobalamin are inborn errors of metabolism, inherited in an autosomal recessive manner and presenting with: Neurology: developmental delay; peripheral neuropathy. Expect to see improvement in haematological and biochemical indices, mood and well-being within 1 week; in contrast, neurological improvement takes months to years, and indeed in the remethylation defects, progression continues. Acquired B12 deﬁciency and subacute combined degeneration of the cord Acquired B12 deﬁciency occurs in pernicious anaemia, an autoimmune condition resulting in destruction of the gastric parietal cells respon sible for secretion of intrinsic factor. Pre-symptomatic diagnosis of B12 deﬁciency following identiﬁcation of a megaloblastic anaemia is typical, however late diagnosis can result in neurological damage. Many effects of B12 deﬁciency are secondary to folate deﬁciency (as folate regeneration is B12 dependent) and will be ameliorated by folate supplementation. There are, however, some speciﬁcally B12 dependent processes including myeli nation that are not folate-responsive. This has led to debate about the wisdom of introduction of folate fortiﬁcation of ﬂour as a public-health measure to prevent neural tube defects (by ensuring adequate folate levels in women in the early days of pregnancy during neural tube forma tion); as folate supplementation will treat megaloblastic anaemia. The syndrome of late neurological damage due to B12 deﬁciency comprises non-speciﬁc psychiatric features with a characteristic pattern of spinal cord involvement known as subacute combined degeneration of the cord. Folate Folates are water-soluble vitamins, essential from dietary sources (leafy vegetables, nuts, beans).
Even if we cannot obtain and maintain effective protection of exclusivity from our regulatory efforts and intellectual property rights spasms with stretching rumalaya gel 30gr generic, including patent protection spasms near tailbone cheap rumalaya gel uk, data exclusivity or orphan drug exclusivity spasms medication purchase genuine rumalaya gel on-line, for our product candidates muscle relaxant otc meds rumalaya gel 30 gr generic, we believe that our product candidates will be protected by exclusivity that prevents approval of a biosimilar in the United States for a period of twelve years from the time the product to which it claims similarity was first approved. If a biosimilar version of one of our product candidates were approved in the United States, it could have a negative effect on our business. We may not have sufficient patent term protections for our product candidates to effectively protect our business. In the United States, the statutory expiration of a patent is generally 20 years after it is filed. Although various extensions may be available, the life of a patent, and the protection it affords, is limited. Even if patents covering our product candidates are obtained, once the patent life has expired for a product candidate, we may be open to competition. Patent term extensions under the Hatch-Waxman Act in the United States and under supplementary protection certificates in Europe may be available to extend the patent or data exclusivity terms of our product candidates. We will likely seek patent term extensions, and we cannot provide any assurances that any such patent term extensions will be obtained and, if so, for how long. As a result, we may not be able to maintain exclusivity for our product candidates for an extended period after regulatory approval, if any, which would negatively impact our business, financial condition, results of operations and prospects. If we do not have sufficient patent terms or regulatory exclusivity to protect our product candidates, our business and results of operations will be adversely affected. As is the case with other biotechnology companies, our success is heavily dependent on patents. Obtaining and enforcing patents in the biotechnology industry involves both technological and legal complexity, and is therefore costly, time-consuming and inherently uncertain. In addition, the United States has recently enacted and is currently implementing wide-ranging patent reform legislation. Supreme Court rulings have narrowed the scope of patent protection available in specified circumstances and 42 weakened the rights of patent owners in specified situations. In addition to increasing uncertainty with regard to our ability to obtain patents in the future, this combination of events has created uncertainty with respect to the value of patents, once obtained. If we are unable to maintain effective proprietary rights for our product candidates or any future product candidates, we may not be able to compete effectively in our proposed markets. In addition to the protection afforded by patents, we rely on trade secret protection and confidentiality agreements to protect proprietary know-how that is not patentable or that we elect not to patent. In addition, other elements of our products, and many elements of our product candidate discovery and development processes involve proprietary know-how, information or technology that is not covered by patents. We seek to protect our proprietary technology and processes, in part, by entering into confidentiality agreements with our employees, consultants, collaborators, advisors, independent contractors or other third parties. We also seek to preserve the integrity and confidentiality of our data and trade secrets, including by maintaining physical and electronic security of our premises and our information technology systems. While we have confidence in these individuals, organizations and systems, agreements or security measures may be breached, and we may not have adequate remedies for any breach. In addition, competitors may otherwise gain access to our trade secrets or independently develop substantially equivalent information and techniques. Furthermore, the laws of some foreign countries do not protect proprietary rights to the same extent or in the same manner as the laws of the United States. As a result, we may encounter significant problems in protecting and defending our intellectual property both in the United States and abroad. If we are unable to prevent unauthorized material disclosure of our intellectual property to third parties, or misappropriation of our intellectual property by third parties, we may not be able to establish or maintain a competitive advantage in our market, which could materially adversely affect our business, operating results, and financial condition. Although we expect all of our employees and consultants to assign their inventions to us, and all of our employees, consultants, collaborators, advisors, independent contractors and any third parties who have access to our proprietary know-how, information, or technology to enter into confidentiality agreements, we cannot provide any assurances that all such agreements have been duly executed or that our trade secrets and other confidential proprietary information will not be disclosed or that competitors will not otherwise gain access to our trade secrets or independently develop substantially equivalent information and techniques. Misappropriation or unauthorized disclosure of our trade secrets could impair our competitive position and may have a material adverse effect on our business, financial condition or results of operations. Additionally, if the steps taken to maintain our trade secrets are deemed inadequate, we may have insufficient recourse against third parties for misappropriating the trade secret. Third-party claims of intellectual property infringement may prevent or delay our development and commercialization efforts. Our commercial success depends in part on our ability to develop, manufacture, market and sell our product candidates and use our proprietary technology without infringing the patent rights of third parties. In addition, or alternatively, we may consider whether to seek to negotiate a license of rights to technology covered by one or more of such patents and patent applications. If any patents or patent applications cover our product candidates or technologies, we may not be free to manufacture or market our product candidates as planned, absent such a license, which may not be available to us on commercially reasonable terms, or at all. It is also possible that we have failed to identify relevant third-party patents or applications. For example, applications filed before November 29, 2000 and applications filed after that date that will not be filed outside the United States remain confidential until patents issue. Moreover, it is difficult for industry participants, including us, to identify all third-party patent rights that may be relevant to our product candidates and technologies because patent searching is imperfect due to differences in terminology among patents, incomplete databases and the difficulty in assessing the meaning of patent claims. We may fail to identify relevant patents or patent applications or may identify pending patent applications of potential interest but incorrectly predict the likelihood that such patents may issue with claims of relevance to our technology. In addition, we may be unaware of one or more issued patents that would be infringed by the manufacture, sale or use of a current or future product candidate, or we may incorrectly conclude that a third-party patent is invalid, unenforceable or not infringed by our activities. Additionally, pending patent applications that have been published can, subject to specified limitations, be later amended in a manner that could cover our technologies, our product candidates or the use of our product candidates. As the biotechnology and pharmaceutical industries expand and more patents are issued, the risk increases that our product candidates may be subject to claims of infringement of the patent rights of third parties. Parties making claims against us may obtain injunctive or other equitable relief, which could effectively block our ability to further develop and commercialize one or more of our product candidates. In the event of a successful claim of infringement against us, we may have to pay substantial damages, including treble damages and attorneys’ fees for willful infringement, pay royalties, redesign our infringing products or obtain one or more licenses from third parties, which may be impossible or require substantial time and monetary expenditure. We depend, in part, on our licensors to file, prosecute, maintain, defend and enforce patents and patent applications that are material to our business. While we normally seek and gain the right to fully prosecute the patent applications relating to our product candidates, there may be times when the patent applications enabling our product candidates are controlled by our licensors. If any of our existing or future licensors fail to appropriately and broadly prosecute and maintain patent protection for patents covering any of our product candidates, our ability to develop and commercialize those product candidates may be adversely affected and we may not be able to prevent competitors from making, using, importing, and selling competing products. In addition, even where we now have the right to control patent prosecution of patents and patent applications we have licensed from third parties, we may still be adversely affected or prejudiced by actions or inactions of our licensors in effect from actions prior to us assuming control over patent prosecution. If we fail to comply with obligations in the agreements under which we license intellectual property and other rights from third parties or otherwise experience disruptions to our business relationships with our licensors, we could lose license rights that are important to our business. We are a party to certain intellectual property license agreements that are important to our business and expect to enter into additional license agreements in the future. Our existing agreements impose, and we expect that future license agreements will impose, certain obligations, including the payment of milestones and royalties based on revenues from sales of our products utilizing the technologies licensed from our licensors, and such obligations could adversely affect the overall profitability for us of any products that we may seek to commercialize. In addition, we will need to outsource and rely on third parties for many aspects of the clinical development, sales and marketing of our product candidates covered under our license agreements. Delay or failure by these third parties could adversely affect the continuation of our license agreements with our third-party licensors. If we fail to comply with our obligations under these agreements, or we are subject to a bankruptcy, these agreements may be subject to termination by the licensor which could have a material adverse effect on our business. We may be involved in lawsuits to protect or enforce our patents or the patents of our licensors, which could be expensive, time consuming, and unsuccessful. To cease such infringement or unauthorized use, we or one of our licensing partners may be required to file patent infringement claims against a third party to enforce one of our patents which can be expensive, time-consuming and unpredictable. In addition, in an infringement proceeding or a declaratory judgment action against us, a court may decide that one or more of our patents is not valid or is unenforceable, or may refuse to stop the other party from using the technology at issue on the grounds that our patents do not cover the technology in question. An adverse result in any litigation or defense proceeding could put one or more of our patents at risk of being invalidated, held unenforceable or interpreted narrowly and could put our patent applications at risk of not issuing. If we or one of our licensing partners were to initiate legal proceedings against a third party to enforce a patent covering one of our product candidates, the defendant could counterclaim that the patent covering our product candidate is invalid and/or unenforceable. In patent litigation in the United States, defendant counterclaims alleging invalidity and/or unenforceability are commonplace, and there are numerous grounds upon which a third party can assert invalidity or unenforceability of a patent. Grounds for a validity challenge could be an alleged failure to meet any of several statutory requirements, including lack of novelty, obviousness, written description, clarity or non-enablement. Third parties may also raise similar claims before administrative bodies in the United States or other jurisdictions, 44 even outside the context of litigation. Such mechanisms include re-examination, inter partes review, post-grant review and equivalent proceedings in foreign jurisdictions, such as opposition or derivation proceedings.
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Adverse selection A term used in the insurance industry to back spasms 20 weeks pregnant buy rumalaya gel 30gr cheap describe the situation in which individuals with private knowledge of having an increased risk for illness muscle relaxant no drowsiness order rumalaya gel line, disability spasms between ribs rumalaya gel 30 gr mastercard, or death buy disproportionately more coverage than those at a lower risk spasms near heart order 30gr rumalaya gel visa. As a result, insurance premiums, which are based on averaging risk across the population, are inadequate to cover future claims. Allelic heterogeneity In a population, there may be a number of different mutant alleles at a single locus. In an individual, the same or similar phenotypes may be caused by different mutant alleles rather than by identical alleles at the locus. The most extreme example is monoallelic expression, which can be random, as in X-inactivation, or determined by parent of origin of the allele (genomic imprinting). Allogenic In transplantation, denotes individuals (or tissues) that are of the same species but have different antigens (alternative spelling: allogeneic). Alternate segregation Pattern of chromosome segregation in a cell with a balanced reciprocal translocation following synapsis of a quadrivalent in which balanced gametes are formed that have either a normal chromosome complement or contain the two reciprocal balanced translocation chromosomes. Amniocentesis A procedure used in prenatal diagnosis to obtain amniotic fluid, which contains cells of fetal origin that can be cultured for analysis. Amniotic fluid is withdrawn from the amniotic sac by syringe after insertion of a hollow needle into the amnion through the abdominal wall and uterine wall. Analytic validity In reference to a clinical laboratory test, the ability of that test to perform correctly, that is, measure what it is designed to measure. Anaphase Stage in mitosis when chromosomes separate at the centromere and sister chromatids become independent daughter chromosomes, which move to opposite poles of the dividing cell. Ancestry informative markers Loci with alleles that show large differences in frequency among populations originating in different parts of the world. Aneuploidy Any chromosome number that is not an exact multiple of the haploid number. The common forms of aneuploidy in humans are trisomy (the presence of an extra chromosome) and monosomy (the absence of a single chromosome). Anomalies Birth defects resulting from malformations, deformations, or disruptions. Anticipation the progressively earlier onset and increased severity of certain diseases in successive generations of a family. Anticipation is caused by expansion of the number of repeats that constitute a dynamic mutation within the gene responsible for the disease. Apoenzyme the protein component of an enzyme that also requires a cofactor to become active. Apoptosis Programmed cell death characterized by a stereotypic pattern of mitochondrial breakdown and chromatin degradation. Ascertainment the method of selection of individuals for inclusion in a genetic study. Ascertainment bias A difference in the likelihood that affected relatives of affected individuals will be identified, compared with similarly affected relatives of controls. In genetic epidemiology, describes the situation in which a particular allele is found either significantly more or significantly less frequently in a group of affected individuals than would be expected from the frequency of the allele in the general population from which the affected individuals were drawn; not to be confused with linkage. In dysmorphology, a group of abnormalities of unknown etiology and pathogenesis that is seen together more often than would be expected by chance. Assortative mating Selection of a mate with preference for a particular genotype; that is, nonrandom mating. Usually positive (preference for a mate of the same genotype), less frequently negative (preference for a mate of a different genotype). Assortment the random distribution of different combinations of the parental chromosomes to the gametes. Autologous Refers to grafts in the same animal from one part to another or to malignant cells and the cells of the individual in which they have arisen. Autosome Any nuclear chromosome other than the sex chromosomes; 22 pairs in the human karyotype. A disease caused by mutation in an autosomal gene or gene pair shows autosomal inheritance. Balanced polymorphism A polymorphism maintained in the population by heterozygote advantage, allowing an allele, even one that is deleterious in the homozygous state, to persist at a relatively high frequency in the population. Barr body the sex chromatin as seen in female somatic cells, representing an inactive X chromosome. Bayesian analysis A mathematical method widely used in genetic counseling to calculate recurrence risks. The method combines information from several sources (genetics, pedigree information, and test results) to determine the probability that a specific individual might develop or transmit a certain disorder. Beneficence the ethical principle of behaving in a way that promotes the well-being of others. Binomial expansion When there are two alternative classes, one with probability p and the other with probability 1 − p = q, the frequencies of the possible combinations of p n and q in a series of n trials is (p + q). Biochemical genetics the study of the genetic basis for phenotype at the level of proteins, biochemical pathways, and metabolism. Bioinformatics Computational analysis and storage of biological and experimental data, widely applied to genomic and proteomic studies. Bivalent A pair of homologous chromosomes in association, as seen at metaphase of the first meiotic division. Blastocyst A stage in early embryogenesis in which the initial ball of cells derived from the fertilized egg (the morula) secrete fluid and form a fluid-filled internal cavity within which is a separate group of cells, the inner cell mass. Blood group the phenotype produced by genetically determined antigens on a red blood cell. The term is used for heterozygotes for autosomal recessive alleles, for females heterozygous for X-linked alleles, or, less commonly, for an individual heterozygous for an autosomal dominant allele but not expressing it. Case-control study An epidemiological method in which patients with a disease (the cases) are compared with suitably chosen individuals without the disease (the controls) with respect to the relative frequency of various putative risk factors. Cell cycle the stages between two successive mitotic divisions, described in the text. Centimorgan (cM) the unit of distance between genes along chromosomes, named for Thomas Hunt Morgan. Two loci are 1 cM apart if recombination is detected between them in 1% of meioses. Centromere the primary constriction on the chromosome, a region at which the sister chromatids are held together and at which the kinetochore is formed. Centrosomes A pair of centers that organize the growth of the microtubules of the mitotic spindle; visible at the poles of the dividing cell in late prophase. Checkpoint Positions in the cell cycle, usually at the junction between the G and S or the1 G and M stages, at which the cell determines whether to proceed to the next stage of2 the cycle. Chemical individuality A term coined by Archibald Garrod to describe the naturally occurring differences in the genetic and biochemical makeup of each individual. Chemical library An annotated collection of hundreds to tens of thousands of small molecules, increasingly used in drug discovery. High-throughput screening against a drug target may identify a compound that interacts with the target, for example to restore activity to a mutant protein. Chimera An individual composed of cells derived from two genetically different zygotes. In humans, blood group chimeras result from exchange of hematopoietic stem cells by dizygotic twins in utero; dispermic chimeras, which are very rare, result from fusion of two zygotes into one individual. Fetal tissue for analysis is withdrawn from the villous area of the chorion either transcervically or transabdominally under ultrasonographic guidance. Chromosome One of the threadlike structures in the cell nucleus; consists of chromatin. Chromosome disorder A clinical condition caused by an abnormal chromosome constitution in which there is duplication, loss, or rearrangement of chromosomal material. Chromosome instability syndrome Hereditary condition that predisposes to a high frequency of chromosome breakage and rearrangements. Chromosome mutation Mutation that leaves a chromosome intact but changes the number of chromosomes in a cell. Chromosome segregation the separation of chromosomes or chromatids in cell division so that each daughter cell gets an equal number of chromosomes. Chromosome shattering Phenomenon seen in some cancer cells in which novel and complex chromosome rearrangements occur because the chromosomes break into numerous pieces and rejoin. Chromosome spread the chromosomes of a dividing cell as seen under the microscope in metaphase or prometaphase.
Food phobias or a post-traumatic feeding disorder may result from a painful episode muscle relaxant renal failure rumalaya gel 30gr. After two years of age gastric spasms order rumalaya gel 30gr line, pica is a behavioural condition more frequent in children with insufficient stimulation muscle relaxant triazolam buy discount rumalaya gel 30 gr on line, psychological disorders and mental retardation spasms left side abdomen order rumalaya gel 30 gr visa. Unhealthy food choice: Food preferences are established through exposure and accessibility to foods, modelling and advertisements. Vegan families children and/or vegan adolescents have preferences towards nonmeat food. Like vegan diets most “alternative” diets are not harmful, but specific nutrient deficiencies should be addressed (eg. Menus and Variety Variety may be the spice of life, but children don’t always agree. It is important to provide menus with variety to ensure that the children are receiving all kinds of vitamins and minerals. On the other hand, they can’t learn to eat new foods unless they have the opportunity. Parents should try to introduce the new food as much as possible and keep on trying. They’d be surprised how children will suddenly try something after refusing it in the past (some kids need to be exposed to a new food at least 10 times before they’ll try it). Promoting healthy lifestyles in young children is limited and tends focus on school-based İnterventions. Feeding in Adolescence Adolescence is a special period that involves transition from childhood to adulthood. Therefore, nutritional needs are increased because of the increased growth rate and changes in body composition associated with puberty. However, adolescents often fail to meet dietary recommendations for esantial nutrient intakes. Many of them receive a higher proportion of energy from fat and/or added sugar and have a lower intake of a vitamin A, folic acid, fiber, iron, calcium, vitamin D, and zinc than is recommended (5). The low intake of iron and calcium among adolescent girls are specially important. Vitamin D deficiency is also common, and it is associated with decreased bone density and fracture risk. It may determine not only the choice of child feeding but also associated behaviours, and exposure to feeding environments outside and inside the home. Though, family meals having higher diet quality (higher intakes of fruits, dark-green and orange vegetables, and lower intakes of soft drinks), there is a decline in family meal frequency during adolescence. As they become more independent, adolescents increasingly make their own decisions about what to eat. Fast foods are popular choices, as, they are inexpensive, and available at places where many adolescents socialize with their peers. Fast foods are low in micronutrients and high in energy, sodium, cholesterol, and total and saturated fat. This pattern tends to impair nutrition, as, high fat/energy-dense snacks usually compensate for the nutritional value of the meals that are skipped. Breakfast and lunch are the meals most often missed, but social, school, and work activities can cause evening meals to be missed as well (6). Total nutrient intakes are lower among adolescents who skip breakfast and this can affect school performance and the overall quality of the diet. Eating habits display some general trends over time, reflecting sociocultural trends in food availability. It has been shown that total energy intake among adolescents increased through 2004, then after decreased through 2010(7). As the authors mentioned, intakes of full-fat milk, meats, ready-to-eat cereals, burgers, fried potatoes, fruit juice, and vegetables decreased, whereas nonfat milk, poultry, sweet snacks and candies, and tortilla and corn based dishes increased through 2010 (7). Spending more than 120 minutes watching television is associated with significantly higher intakes of total fat and lower intake of minerals and vitamins. More than 90 percent of the advertised foods during television programs designed for children, were high in fat, sodium, or added sugars, or low in overall nutrients (8). Nutritional Requirements (5) Energy and nutrient requirements for children vary depending upon age, sex, and activity level. Protein: It should constitute 5 to 20 percent of total energy intake for children 1-2 years of age and 10 30 percent of total energy intake for children 4 18 years of age. Milk ≥24 months: these children should consume fat-free (skim) or low-fat cow milk, calcium and vitamin D-fortified soy milk, or equivalent cow milk or fortified soy milk products (eg, yogurt, cheese). However, switching from whole milk to fat-free or low-fat milk should not, in and of itself, be expected to prevent obesity or lower body mass index if total daily energy intake exceeds metabolic needs. Fat: Dietary fat is an important source of energy, supports the transport of fat-soluble vitamins, and provides the essential fatty acids. Total fat intake should be between 30 – 35% of energy intake for children two to three years of age; 25 – 35% for children 4-18 years of age. Essential fatty acid intake, primarily as linoleic and linolenic acid, should be 3% of total daily energy intake. Adequate carbohydrate intake contributes to sufficient intake of dietary fiber, iron, thiamine, niacin, riboflavin, and folic acid. Added sugars should be avoided in children <2 years and limited to <5% of total energy intake in children ≥2 years (approximately 25 g, 100 kilocalories, or 6 teaspoons). No more than one half of the recommended daily servings of fruit should be provided in the form of 100 percent fruit juice (rather than "fruit drinks"). Diet shoul contain high-fiber whole grain foods at least once every day, where sugary and salty foods have a lot of “empty” calories they sould be served occasionally. Soda and fruit drinks are full of sugar and “empty calories” (few nutrients, many calories). Serving low fat milk with meals and snacks provides calcium but doesn’t add many calories. The following table gives guidelines for how much your preschooler should be eating each day. Grain Group at least 6 servings each day 1 slice of bread 4-6 crackers ½ cup cooked rice, pasta, or cereal ½ bun, muffin, or bagel Fruit and Vegetable Group at least 5 servings each day ½ cup cooked, canned, or chopped raw ½ 1 small fruit/vegetable ½ cup juice Milk Group at least 3 servings each day ¾ cup milk or yogurt ¾ ounce of cheese Meat Group 2 servings each day 1-3 tablespoons lean meat, chicken, fish 4-5 tablespoons dry beans and peas 1 egg Fat Group 3-4 servings each day 1 teaspoon margarine, butter, oils An important first step is to identify the feeding problem in order to clarify the treatment methods and objectives. Behavioral treatment strategies are the mainstay for the management of feeding disorders and are designed to reinforce positive behaviors and minimize maladaptive behaviors. Sadi Konuk Eğitim ve Araştırma Hastanesi Çocuk Sağlığı ve Hastalıkları Kliniği, Çocuk Metabolizma Hastalıkları Malabsorption is a clinical and laboratory finding that results from the loss of nutrients by feces due to insufficient absorption of nutrients from the gastrointestinal tract. Diarrhea, weight loss, growth retardation, indigestion, unpleasant smelly-light color defecation, anemia, edema, rickets, tendency to bleed are the main clinical findings. The main treatment approach in malabsorption is the treatment of the underlying disease, concomitant treatment for diarrhea and replacement of nutrient deficiencies. Case: A 28-day-old girl presented with vomiting, diarrhea and weight loss for 15 days. He was the first child of consanguineous parents with an unremarkable family history. He was in the dehydrated case, the turgor was reduced but other system examinations were normal. Aslı İnci Gazi University Scool of Medicine, Ankara Nutritional therapy is an important part of the medical care in a patient with chronic renal disease. Nutritional management should be individualised in every patient for his nutritional assesment, his developmental status, comorbid disorders, drugs and individulised outcomes. The primary aim of the diet therapy in a patient with chronic renal disease is to maintain the disease in a steady state,to control uremic symptoms, to prevent hypertensive attacks, metabolic abnormalities and to decrease the morbidity and mortality in the period of adulthood. Therapy is based on adequate low protein diet to provide development and to prevent uremic symptoms and malnutrition. The adequate protein and caloric intake is the most important part of the therapy. The evaluation of the nutritional factors should include food consumption, antropoemetric measurements and also biochemical tests such as sodium, calcium and potasium.