2p13.2 microdeletion syndrome is a rare genetic condition caused by a small missing piece of chromosome 2. People with 2p13.2 microdeletion syndrome often have developmental delay, learning differences, and sometimes speech or motor challenges. Some may have distinctive facial features or growth differences, and seizures or feeding issues can occur in a subset. It is lifelong, recognized in infancy or childhood, and severity can vary. Treatment focuses on supportive therapies, and the outlook can be good with early services and regular follow-up.
Overview
2p13.2 microdeletion syndromeSymptoms
2p13.2 microdeletion syndrome is often noticed in infancy or early childhood. Signs include developmental and speech delay, learning difficulties, low muscle tone, feeding challenges, and distinctive facial features; some have seizures, growth issues, or other birth differences.
Outlook and prognosis
Most people with 2p13.2 microdeletion syndrome grow and learn at their own pace, often needing extra support for speech, learning, and motor skills. Early therapies, school accommodations, and regular checkups can help skills build steadily. Many reach personal milestones and enjoy good quality of life with tailored supports.
Causes and risk factors
Caused by a missing segment of chromosome 2 at 2p13.2, usually a new change before birth. Sometimes inherited from a parent with a chromosome rearrangement. Older parental age may slightly raise risk; environment and lifestyle do not cause it.
Genetic influences
Genetics is central to 2p13.2 microdeletion syndrome, which stems from missing DNA on chromosome 2. The exact size of the deletion and genes involved shape severity and features. Most cases are spontaneous, but parental testing helps clarify recurrence risk.
Diagnosis
Doctors suspect 2p13.2 microdeletion syndrome from developmental patterns and clinical features. The genetic diagnosis of 2p13.2 microdeletion syndrome is confirmed with chromosomal microarray or targeted genetic tests. Imaging or specialist exams may assess associated findings.
Treatment and drugs
Treatment focuses on each person’s needs. Support often includes speech and occupational therapy, learning supports, and care for feeding or growth concerns; some children benefit from seizure management, vision or hearing aids, and heart or kidney monitoring. A coordinated team helps families navigate 2p13.2 microdeletion syndrome.
Symptoms
For many families, 2p13.2 microdeletion syndrome shows up as differences in development, learning, and growth that start in infancy or early childhood. In daily life, tasks like feeding, sitting, or first words may come later and need extra support. Features vary from person to person and can change over time. Early features of 2p13.2 microdeletion syndrome often include low muscle tone and delays in speech or motor skills.
Milestones like rolling, sitting, walking, and first words may arrive later. Early therapies help many children with 2p13.2 microdeletion syndrome build skills over time.
Words may come late and be harder to pronounce. Many with 2p13.2 microdeletion syndrome understand more than they can say and benefit from speech therapy.
Muscles may feel looser than expected, making it harder to hold the head up or sit steadily. Clinicians call this hypotonia, which means lower muscle tone than typical. It can lead to fatigue and slower gross motor progress.
Fine movements like using utensils or buttons can be tricky. Physical and occupational therapy can improve balance, strength, and hand skills.
How people usually first notice 2p13.2 microdeletion syndrome?
Many families first notice 2p13.2 microdeletion syndrome when a baby’s developmental milestones arrive later than expected—things like rolling, sitting, first words, or walking take extra time—and a pediatrician flags low muscle tone or feeding difficulties in infancy. As children grow, doctors may also pick up subtle facial or body differences and learning or speech delays during routine checkups, which can prompt a genetics referral. For many, the first signs of 2p13.2 microdeletion syndrome come together during this evaluation, and chromosomal microarray testing confirms the diagnosis.
Types of 2p13.2 microdeletion syndrome
People living with 2p13.2 microdeletion syndrome can share a core set of features—such as developmental delay, learning differences, and sometimes differences in growth or facial features—but the day-to-day impact varies widely. Not everyone will experience every type. Clinicians often describe them in these categories: developmental/learning, movement and muscle tone, speech and communication, growth and feeding, and health/organ findings. This helps explain the types of 2p13.2 microdeletion syndrome people may notice at different points in life, from early childhood through school years.
Developmental-learning
Many have global developmental delay with later walking and learning that may require tailored school supports. Cognitive abilities range from mild learning differences to more noticeable intellectual disability. Early therapy often improves skills over time.
Speech-communication
Speech may develop late, and some children rely on gestures or communication aids while speech builds. Understanding language is often stronger than spoken expression. Speech therapy can help clarity and vocabulary grow.
Muscle tone-motor
Low muscle tone and joint flexibility can make sitting, crawling, and walking later than peers. Some have coordination challenges or fine-motor delays affecting tasks like buttons or handwriting. Physical and occupational therapy usually support steady progress.
Growth-feeding
Babies may have trouble feeding, slow weight gain, or reflux in infancy. As they grow, some remain shorter or lighter than peers, while others catch up. Feeding therapy and nutrition support can help improve growth.
Behavior-attention
Some children show attention differences, sensory sensitivities, or autistic features. Routines and behavioral strategies often reduce stress and support learning. For many, certain types stand out more than others.
Health-organ findings
A minority have seizures, heart or kidney differences, or hearing issues that need specialist care. Regular checkups help catch and manage these early. Treatments are based on the specific feature and its severity.
What genetics can tell you about symptoms
Some people with 2p13.2 microdeletion syndrome may have developmental delays, learning difficulties, speech delays, low muscle tone, and distinctive facial features because missing genes in this region can disrupt brain and muscle development. Others may experience seizures or growth differences, depending on which genes are deleted.
Causes and risk factors
2p13.2 microdeletion syndrome happens when a small piece of chromosome 2 at 2p13.2 is missing.
Most cases start as a new change in the egg or sperm and are not inherited.
Some risks are written in our DNA, passed down through families.
In practice, risk factors for 2p13.2 microdeletion syndrome mainly involve a parent with the same deletion or a balanced chromosome rearrangement, so genetic counseling and testing can help estimate recurrence.
Lifestyle and environmental factors do not cause the deletion, but overall health and support can influence how strongly its features show.
Environmental and biological risk factors
Risk factors for 2p13.2 microdeletion syndrome mostly trace back to how chromosomes copy and package during the earliest steps of egg or sperm formation. Doctors often group risks into internal (biological) and external (environmental). For this condition, the best-established risks are biological, and clear environmental triggers are uncommon. When people ask about early risk factors for 2p13.2 microdeletion syndrome, most relate to new chromosome changes at conception rather than exposures during pregnancy.
Most cases happen when a small piece of chromosome 2 is lost as an egg or sperm forms. No clear external trigger is known for 2p13.2 microdeletion syndrome.
Older fathers have more cell divisions in sperm, which can slightly raise the chance of new DNA changes. Any added risk for 2p13.2 microdeletion syndrome appears small, and most pregnancies are unaffected.
Older maternal age is strongly linked to whole-chromosome conditions, but not clearly to small microdeletions. For this syndrome, any maternal-age effect is uncertain and likely small.
Significant radiation to the ovaries or testes from medical treatment or accidents can damage reproductive DNA. No specific link to 2p13.2 microdeletion syndrome is proven at everyday exposure levels.
Genetic risk factors
Genetically, a small deletion in the 2p13.2 region—removing one copy of several genes—drives this condition and helps explain why features can differ from person to person. This section focuses on the genetic causes of 2p13.2 microdeletion syndrome and what they mean for family risk and recurrence. Risk is not destiny—it varies widely between individuals. Most deletions arise as new changes, but some are inherited; a genetics team can clarify your family’s pattern.
De novo deletion: Most cases happen as a new change in the egg or sperm, not passed down from either parent. When de novo, the chance of it happening again in a future pregnancy is generally low but not zero.
Autosomal dominant pattern: If a parent carries the same 2p13.2 microdeletion syndrome change, each child has a 1 in 2 (50%) chance to inherit it. Effects can range from mild to more noticeable, even within the same family.
Parental rearrangement: A parent with a balanced translocation or inversion (a swap or flip of chromosome pieces) involving 2p13.2 can be healthy but have a higher chance of a child with the unbalanced deletion. Testing the parents’ chromosomes helps clarify this risk.
Gonadal mosaicism: Rarely, a parent’s egg or sperm can carry the deletion even when blood testing is normal. This makes recurrence possible despite normal parental results.
Deletion size matters: The number and type of genes lost within 2p13.2 influence which features of 2p13.2 microdeletion syndrome appear and how severe they are. Larger or gene-rich deletions may lead to broader effects.
Variable penetrance: Not everyone with the deletion shows the same findings, and some may have few signs. This variability is part of the genetic causes of 2p13.2 microdeletion syndrome.
Lifestyle risk factors
Lifestyle habits do not cause 2p13.2 microdeletion syndrome, but they can shape day-to-day functioning, symptom control, and complications. Understanding how lifestyle affects 2p13.2 microdeletion syndrome helps families prioritize routines that support development, comfort, and health. The elements below highlight practical areas where choices can influence outcomes. These reflect lifestyle risk factors for 2p13.2 microdeletion syndrome in terms of symptom worsening or improvement.
Limited movement can worsen hypotonia, balance, and joint stability, increasing fall and contracture risk. Regular, play-based activity and therapy-guided exercises can improve strength and motor skills.
Too few calories or protein can exacerbate growth faltering and fatigue in children with increased developmental energy needs. Overly processed diets may worsen constipation and metabolic health.
Not following recommended textures, pacing, or positioning can raise choking or aspiration risk. Consistent feeding strategies can reduce respiratory infections and support weight gain.
Fragmented or insufficient sleep can intensify irritability, attention difficulties, and learning challenges. For those with seizures, poor sleep may lower seizure threshold.
Risk prevention
For 2p13.2 microdeletion syndrome, there isn’t a way to prevent the chromosome change itself, but you can reduce risks around it and plan ahead. Prevention is about lowering risk, not eliminating it completely. For some families, reproductive options can reduce the chance of passing on the deletion; for children already diagnosed, early checks and supportive care can prevent avoidable complications and help development.
A genetics professional can review your family history, explain how 2p13.2 microdeletion syndrome happens, and discuss recurrence risk. They can outline testing options before or during pregnancy.
Testing parents’ DNA can show whether the deletion is new or inherited. This helps estimate the chance of 2p13.2 microdeletion syndrome in future pregnancies.
Chorionic villus sampling or amniocentesis can check the fetus’s chromosomes if you choose testing. Results can guide planning and perinatal care for 2p13.2 microdeletion syndrome.
With IVF, embryos can be tested before transfer if the familial deletion is known. This can lower the chance of a future child having 2p13.2 microdeletion syndrome.
Transmission
2p13.2 microdeletion syndrome is a genetic condition, not an infection—you can’t catch it or pass it through everyday contact. It occurs when a small piece of chromosome 2 is missing.
Genetic transmission of 2p13.2 microdeletion syndrome can happen in an autosomal dominant way: a parent with the microdeletion has a 50% chance of passing it to each child. Still, many cases are de novo (a new change in the egg or sperm), so there may be no family history. If neither parent carries the deletion, the chance of it happening again is low, though not zero; a genetics professional can discuss recurrence risk and testing options.
When to test your genes
Consider genetic testing if you or your child have multiple unexplained features—such as developmental delay, learning differences, congenital anomalies, or growth concerns—or if a close relative has a known 2p13.2 deletion. Testing also helps with family planning and care customization. A genetic counselor can guide timing, test type, and next steps.
Diagnosis
For many families, the path to answers starts with noticing developmental delays, speech challenges, or learning differences and seeking an evaluation. In 2p13.2 microdeletion syndrome, doctors look for a pattern of features and then confirm it with specific genetic tests. Getting a diagnosis is often a turning point toward answers and support. In most cases, the genetic diagnosis of 2p13.2 microdeletion syndrome is confirmed by tests that can detect small missing pieces of a chromosome.
Providers review growth, development, and a detailed physical exam for patterns seen in this syndrome. Findings like developmental delay, low muscle tone, and certain facial traits can raise suspicion. This step guides which genetic tests to order.
This is the first-line genetic test to detect small missing segments. It can identify a deletion at 2p13.2 and estimate which genes are involved. Results help confirm the diagnosis of 2p13.2 microdeletion syndrome.
These focused tests can confirm a known deletion or test relatives for the same change. They are useful when microarray results need clarification or when a quicker, targeted answer is helpful. Your provider may suggest one of these to look closer.
Sequencing with copy-number analysis can detect the 2p13.2 deletion or refine its boundaries. It may also reveal additional genetic findings that influence care. This is often considered if microarray is inconclusive.
Stages of 2p13.2 microdeletion syndrome
2p13.2 microdeletion syndrome does not have defined progression stages. It doesn’t follow a predictable step‑by‑step decline; instead, features are present from early development and can vary widely, changing gradually with growth, supports, and individual differences. Your medical team will review development, learning, and day‑to‑day skills, including any early symptoms of 2p13.2 microdeletion syndrome that showed up in infancy or early childhood. Different tests may be suggested to help confirm the diagnosis, often using genetic testing that looks for tiny missing pieces of chromosome 2, and ongoing care may include regular checks of hearing, vision, growth, and any specific medical needs.
Outlook and prognosis
Looking ahead can feel daunting, but most children with 2p13.2 microdeletion syndrome make steady gains when therapies start early and are tailored to their needs. Many families first notice early symptoms of 2p13.2 microdeletion syndrome such as slower speech or motor milestones, low muscle tone, or learning differences; with time and support, many kids walk, communicate, and participate in school and play in ways that fit their abilities. In medical terms, the long-term outlook is often shaped by both genetics and lifestyle. Severe medical complications are uncommon in many reported cases, and life expectancy appears near typical when major organ problems or uncontrolled seizures are not present.
Everyone’s journey looks a little different. Some children need ongoing speech, occupational, and physical therapy through school years, while others require additional supports like special education plans or assistive communication. If seizures, feeding challenges, or heart or kidney findings are part of the picture, the prognosis depends on how well those issues respond to treatment, and on regular monitoring to catch changes early. Doctors call this the prognosis—a medical word for likely outcomes.
People living with 2p13.2 microdeletion syndrome often see progress continue into adolescence and adulthood, though learning and coordination differences may persist. Published data on mortality are limited because the condition is rare; in available reports, deaths are uncommon and usually linked to severe, unrelated medical complications rather than the microdeletion itself. Support from friends and family can make day-to-day goals—like joining a classroom activity, using a new word, or managing a routine—more attainable. Talk with your doctor about what your personal outlook might look like, including which checkups to prioritize and what warning signs should prompt a call.
Long-term effects
2p13.2 microdeletion syndrome can lead to ongoing developmental and health differences that show up from childhood into adulthood. Long-term effects vary widely, and no two people have the same combination or severity. Many families search online for early symptoms of 2p13.2 microdeletion syndrome; over the years, those early signs often settle into stable patterns that doctors can describe and track. Outlook depends on which features are present, rather than the diagnosis alone.
Ongoing developmental delay and intellectual disability can range from mild to more pronounced. School-age years often clarify strengths and areas needing support.
Speech may be slow to develop and can remain limited or atypical over time. Some people rely more on gestures or devices to communicate.
Low muscle tone and coordination challenges can persist. Fine motor tasks like buttons or handwriting may remain effortful into adulthood.
Some have smaller head size or shorter stature compared with peers. Feeding difficulties in infancy may transition into selective eating or lean body build.
How is it to live with 2p13.2 microdeletion syndrome?
Living with 2p13.2 microdeletion syndrome often means navigating developmental delays, learning differences, and sometimes medical needs like low muscle tone or feeding challenges in infancy, with supports that change over time. Daily life may involve early intervention, speech and occupational therapy, structured learning plans at school, and periodic specialist visits to track growth, hearing, vision, or seizures if present. Families and caregivers usually become strong coordinators—sharing information with teachers and clinicians—and many find routines, visual supports, and community services reduce stress for everyone at home. With the right therapies and educational accommodations, many children gain new skills steadily, and families often build a practical toolkit that helps them participate in school, friendships, and daily activities more comfortably.
Treatment and drugs
Treatment for 2p13.2 microdeletion syndrome focuses on managing symptoms and supporting development, since there’s no single medicine that corrects the chromosome change itself. Care usually involves a team: early intervention therapies for speech and motor skills, special education supports, physical and occupational therapy, and behavioral therapies as needed; seizures, if present, are typically managed with standard anti-seizure medicines. Doctors sometimes recommend a combination of lifestyle changes and drugs, for example using sleep routines and, when appropriate, medication to address sleep or attention challenges. Regular hearing and vision checks, feeding support, and monitoring growth help catch issues early, and many benefit from a personalized care plan that adjusts as needs change. It’s common to try more than one medication before finding the best fit, so keep track of how you feel, and share this with your care team.
Non-drug treatment
Living with 2p13.2 microdeletion syndrome often involves delays in movement, speech, and learning that affect daily routines at home and school. Non-drug treatments often lay the foundation for progress by building skills, supporting communication, and easing day-to-day care. Plans are tailored to each child or adult and change over time as needs evolve. Recognizing early symptoms of 2p13.2 microdeletion syndrome can help families start therapies sooner.
Coordinated services in infancy and preschool help build movement, language, and social skills. Therapists coach families so practice continues during meals, play, and bath time. Family members often play a role in supporting new routines.
Exercises and play-based activities improve strength, balance, and coordination. This can help with head control, sitting, crawling, and walking in people with 2p13.2 microdeletion syndrome.
Fine-motor and self-care skills are taught step by step, from grasping utensils to getting dressed. Sensory strategies can reduce overwhelm in noisy or bright settings.
Sessions focus on understanding words, using language, and clear speech sounds. Therapists also teach social communication, like taking turns and starting interactions.
Your genes may have an impact on how drugs work for you
Genes can affect how your body absorbs, breaks down, and responds to medicines used for 2p13.2 microdeletion syndrome, changing dose needs and side‑effect risk. Pharmacogenetic testing may help clinicians choose safer options, but treatment still centers on careful monitoring and adjustment.
Pharmacological treatments
There isn’t a one-size-fits-all medicine for 2p13.2 microdeletion syndrome, so treatment focuses on easing the specific symptoms someone has. Drugs that target symptoms directly are called symptomatic treatments. Choices often reflect early symptoms of 2p13.2 microdeletion syndrome, like seizures, reflux, or sleep problems, and they may change as needs change. Medicines are usually paired with therapies, nutrition support, and educational or behavioral plans.
Levetiracetam, valproate, or lamotrigine are commonly used to reduce seizure frequency. Doctors watch for side effects like sleepiness or mood changes and adjust doses over time. For many with 2p13.2 microdeletion syndrome, steady seizure control can open the door to better learning and therapy progress.
Diazepam gel or intranasal midazolam can stop a prolonged seizure. Care teams often provide a written plan for when and how to use rescue medicine. Families may be trained to give the dose safely at home or school.
Baclofen or diazepam may ease spasticity when tight muscles limit movement or comfort. These medicines are started low and adjusted slowly to balance benefit and drowsiness. In 2p13.2 microdeletion syndrome, reducing stiffness can make therapy and daily care easier.
Omeprazole or lansoprazole can lessen acid reflux and protect the esophagus. This may improve feeding comfort, weight gain, and sleep. Doctors may also suggest feeding and positioning changes alongside medication.
Genetic influences
In 2p13.2 microdeletion syndrome, a small stretch of DNA is missing from chromosome 2 at a location called 2p13.2. Losing that segment can remove several nearby genes at once, and the exact size of the missing piece helps shape which features appear and how severe they are—this also explains why early symptoms of 2p13.2 microdeletion syndrome can differ from child to child. DNA testing can sometimes identify these changes. Most cases happen as a new change around the time of conception, so neither parent carries the deletion. Less often, a parent has the same microdeletion or a chromosome change that can pass on the missing piece; if a parent carries the microdeletion, each pregnancy has about a 50% chance of inheriting it, while the chance is low when it arose as a new change. Even in the same family, the effects can vary widely because different genes and individual biology can act like a dimmer switch on how the deletion shows up.
Is 2p13.2 microdeletion syndrome genetic?
Genetics is central to 2p13.2 microdeletion syndrome, which stems from missing DNA on chromosome 2. The exact size of the deletion and genes involved shape severity and features. Most cases are spontaneous, but parental testing helps clarify recurrence risk.
Pharmacogenetics—how genetics influence drug effects
For many living with 2p13.2 microdeletion syndrome, medicines help manage day‑to‑day needs like seizures, attention or mood symptoms, sleep difficulties, and reflux, so getting dosing and drug choice right matters. The deletion doesn’t directly determine how most medicines are broken down, but the condition can increase sensitivity to sedating or brain‑acting drugs because of low muscle tone, breathing or feeding challenges, and developmental differences. Genetic testing can sometimes identify how your body processes certain drugs and guide safer starting doses or alternative choices. This can be especially helpful when choosing or dosing anti‑seizure medicines, some antidepressants, or pain medicines, where well‑studied links between genes and specific medicines support dose adjustments and can reduce trial‑and‑error in medication response in 2p13.2 microdeletion syndrome. For a few medicines, doctors may also screen for certain immune‑system markers tied to rare but serious skin reactions, depending on ancestry and local practice. No test replaces careful monitoring, so clinicians usually start with low doses, check for drug–drug interactions, watch for side effects, and then tailor treatment over time for the individual with 2p13.2 microdeletion syndrome.
Interactions with other conditions
Families often notice that feeding challenges, low muscle tone, or speech delay can bump into other health issues over time. Doctors call it a “comorbidity” when two conditions occur together. For example, low muscle tone can make reflux or constipation more likely, and untreated reflux may worsen sleep and daytime behavior. If seizures are present, antiseizure medicines can interact with treatments for attention or mood, so healthcare teams adjust doses carefully. Recurrent ear infections or hearing loss can intensify language delays, while vision problems can add to motor and learning hurdles. Early symptoms of 2p13.2 microdeletion syndrome often overlap with autism spectrum features or ADHD, and this overlap can shape therapy choices and school supports. Interactions can look very different from person to person, so coordinated, team-based care helps align therapies and reduce medication conflicts in 2p13.2 microdeletion syndrome.
How genes can cause diseases
Humans have more than 20,000 genes, each carrying out one or a few specific functions in the body. One gene instructs the body to digest lactose from milk, another tells the body how to build strong bones and another prevents the body's cells from beginning to multiply uncontrollably and developing into cancer. As all of these genes combined are the building instructions for our body, a defect in one of these genes can have severe health consequences.
Through decades of genetic research, we know the genetic code of any healthy/functional human gene. We have also identified that in certain positions on a gene, some individuals may have a different genetic letter from the one you have. We call these hotspots "Genetic Variations" or "Variants" in short. In many cases, studies have been able to show that having the genetic letter "G" in the position makes you healthy, but having the letter "A" in the same position disrupts the gene function and causes a disease. Genopedia allows you to view these variants in genes and summarizes all that we know from scientific research, which genetic letters (Genotype) have good or bad consequences on your health or on your traits.
History
Families and communities once noticed patterns of children who were slower to sit or speak, had smaller head size, and sometimes distinctive facial features, long before a unifying diagnosis was possible. In schools and clinics, many were given broad labels like “developmental delay” without knowing the underlying cause. Medical files often sat separate, each describing a few features, but not yet linking them together.
From early theories to modern research, the story of 2p13.2 microdeletion syndrome has unfolded with improvements in genetic testing. In the 1990s and early 2000s, clinicians could see missing pieces of chromosomes only when they were large. Small, hard‑to‑spot losses on chromosome 2—especially around position p13.2—were simply invisible. As technologies like chromosomal microarray and later genome sequencing became standard in clinics, those tiny gaps could be detected, and a pattern emerged.
Initially understood only through symptoms, later cases began to cluster when the same small stretch at 2p13.2 was missing. Reports collected children and adults with shared features such as motor and speech delays, low muscle tone, growth differences, and sometimes seizures. Some had learning differences but were otherwise healthy; others had medical needs that required ongoing support. This variability made it clear that 2p13.2 microdeletion syndrome can look different from person to person, depending on the exact size of the missing segment and which nearby genes are involved.
In recent decades, knowledge has built on a long tradition of observation. Once a handful of families were identified, clinicians could compare early symptoms of 2p13.2 microdeletion syndrome across ages and populations. Follow‑up into adolescence and adulthood helped refine expectations about learning, mobility, and health monitoring. These historical steps also shifted care—from searching broadly for a cause to offering targeted evaluations, early therapies, and family counseling once the microdeletion was found.
Advances in genetics also clarified inheritance. While many 2p13.2 microdeletions happen as a new change in the child, some are inherited from a parent who may have milder features. Documenting both scenarios helped families understand recurrence risks and the value of testing parents and siblings when appropriate.
Understanding has changed over time, but the direction has been steady: more precise detection, clearer natural history, and earlier support. Today, 2p13.2 microdeletion syndrome is recognized not because of one single sign, but because genetic tools can pinpoint the missing segment and link it to a growing body of shared experience. This history explains why someone diagnosed years ago might have received a broad label, while a child tested today can receive a specific name and a care plan that meets their needs sooner.