Bark-binding is a disease in trees, cured by slitting the bark, or cutting it along the grain of the tree.

Foot binding was the custom of applying tight binding to the feet of young girls to modify the shape of their feet. The practice possibly originated among upper class court dancers during the Five Dynasties and Ten Kingdoms period in 10th century China, then became popular among the elite during the Song dynasty and eventually spread to all social classes by the Qing dynasty. Foot binding became popular as a means of displaying status (women from wealthy families, who did not need their feet to work, could afford to have them bound) and was correspondingly adopted as a symbol of beauty in Chinese culture. Foot binding limited the mobility of women, resulting in them walking in a swaying unsteady gait, although some women with bound feet working outdoor had also been reported. The prevalence and practice of foot binding varied in different parts of the country. Feet altered by binding were called lotus feet.

It has been estimated that by the 19th century, 40–50% of all Chinese women may have had bound feet, and up to almost 100% among upper class Han Chinese women. The Manchu Kangxi Emperor tried to ban foot binding in 1664 but failed. In the later part of the 19th century, Chinese reformers challenged the practice but it was not until the early 20th century that foot binding began to die out as a result of anti-foot-binding campaigns. Foot-binding resulted in lifelong disabilities for most of its subjects, and a few elderly Chinese women still survive today with disabilities related to their bound feet.

Symptoms of mild cinchonism (which may occur from standard therapeutic doses of quinine) include flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity), vertigo, dizziness, dysphoria, nausea, vomiting and diarrhea.

Large doses of quinine may lead to severe (but reversible) symptoms of cinchonism: skin rashes, deafness, somnolence, diminished visual acuity or blindness, anaphylactic shock, and disturbances in heart rhythm or conduction, and death from cardiotoxicity (damage to the heart). Quinine may also trigger a rare form of hypersensitivity reaction in malaria patients, termed blackwater fever, that results in massive hemolysis, hemoglobinemia, hemoglobinuria, and kidney failure. Most symptoms of cinchonism (except in severe cases) are reversible and disappear once quinine is withdrawn. Attempted suicide by intake of a large dose of quinine has caused irreversible tunnel vision and very severe visual impairment.

Patients treated with quinine may also suffer from low blood sugar, especially if it is administered intravenously, and hypotension (low blood pressure).

Quinine, like chloroquine, inactivates enzymes in the lysosomes of cells and has an anti-inflammatory effect, hence its use in the treatment of rheumatoid arthritis. However, inactivation of these enzymes can also cause abnormal accumulation of glycogen and phospholipids in lysosomes, causing toxic myopathy. It is possible this action is the root cause of cinchonism.

Cinchonism or quinism is a pathological condition caused by an overdose of quinine or quinidine, or their natural source, cinchona bark. Quinine and its derivatives are used medically to treat malaria. In much smaller amounts, quinine is an ingredient of tonic drinks, acting as a bittering agent. Cinchonism can occur from therapeutic doses of quinine, either from one or several large doses. Quinidine (Class 1A anti-arrhythmic) can also cause cinchonism symptoms to develop with as little as a single dose.

Defined as those seen in any macrocytic, megaloblastic anemia:

- Anemia: causing fatigue, conjuctival pallor, pale complexion, and in some cases, a mild icterus (yellowing of the eye).

- Glossitis ("shiny tongue"): shiny, glossy tongue.

- Cheilosis (stomatitis): Inflammation of the edges of the lips and the oral mucosa.

- Tabes dorsalis ("subacute combined degeneration of the spinal cord"): This involves the posterior section of the spinal cord and therefore involves proprioception (sense of position), touch, sense of vibration and in severe cases the lateral corticospinal tract, causing spastic paralysis of the limbs.

- Peripheral neuropathy: tingling sensation in the arms and legs.

- Pancytopenia: decreased number of blood cells of all lineages (RBCs, leucocytes, platelets), due to decreased bone marrow production.

- Methylmalonyl CoA-emia: defined as blood having an unusually high concentration of methylmalonyl CoA.

- Peripheral findings such as hypersegmented neutrophils and large RBCs on high field view of the blood smears.

- Laboratory findings indicating increased MCV (Mean Corpuscular Volume), decreased Hgb/Hct (indicating anemia), and decreased value of vitamin B in the blood.

- Proteinuria: protein found in the urine detected by analysis or by dipstick.

- Reversal of all symptoms except neurological symptoms, by IV injection of vitamin B.

- Schilling test indicating no radioactive vitamin B in the urine. (This test has dropped out of favor and should not be tried in patients with any form of renal failure).

Imerslund–Gräsbeck syndrome, is a rare autosomal recessive, familial form of vitamin B deficiency caused by malfunction of the ""Cubam"" receptor located in the terminal ileum. This receptor is composed of two proteins, amnionless (AMN), and cubilin. A defect in either of these protein components can cause this syndrome. This is a rare disease, with a prevalence about 1 in 200,000, and is usually seen in patients of European ancestry.

Vitamin B is an important vitamin needed for bone marrow functioning, the deficit of which causes decreased marrow output and anemia. Vitamin B has two forms, one of which, along with folate, is important in DNA synthesis. Vitamin B is sensitive to acid deformation in the stomach, so a molecule called haptocorrin (R-factor), protects it in the stomach. In the small bowel, a molecule named intrinsic factor (IF), allows vitamin B to be absorbed in the ileum. IGS is caused by a mutation in the receptors located in the terminal portion of ileum. This is a very rare, and unlikely cause of vitamin B deficiency but is a cause nonetheless.

In farming, aviculture and animal husbandry, the term egg binding refers to a medical condition in birds or other egg-laying animals, where the female is unable to pass an egg that has formed.

The egg may be stuck near the cloaca, or further inside. Egg binding is a reasonably common, and potentially serious, condition that can lead to infection or damage to internal tissue. The bound egg may be gently massaged out; failing this it may become necessary to break the egg "in situ" and remove it in parts. If broken, the oviduct should be cleaned of shell fragments and egg residue to avoid damage or infection.

Velvet Blight is a disease that affects the stems, branches, leaves, fruits or trunks of plants and trees. This disease is primarily caused by three fungal species from the genus "Septobasidium": "S. bogoriense", "S. pilosum" and "S. theae".

It is known to affect mainly tea plants ("Thea" genus).

The most studied of these species is "S. bogoriense", most notably due to the work of Ernst Albert Gäumann. "S. bogoriense" is named after the Herbarium Bogoriense (Bogor, West Java, Indonesia) which is the place where it was first identified on the bark of an unspecified tree and named by E. Nyman on June 3, 1898. This species was also listed in Otto Warburg's Monsunia in 1900.

Goldberg–Shprintzen is a condition associated with mutations in "KIAA1279" gene which encodes KIF-binding protein (KBP), a protein that may interact with microtubules and actin filament. KBP may play a key role in cytoskeleton formation and neurite growth.

Hirschsprung's disease may be part of the presentation. Individuals with the syndrome exhibit ocular (ptosis, hyperopia, or megalocornea), cardiac, urogenital (vesicoureteral reflux, multicystic renal dysplasia), and skeletal (oligodontia, scoliosis, high-arched palate) developmental abnormalities.

Dutch elm disease (DED) is caused by a member of the sac fungi (Ascomycota) affecting elm trees, and is spread by elm bark beetles. Although believed to be originally native to Asia, the disease was accidentally introduced into America and Europe, where it has devastated native populations of elms that did not have resistance to the disease. It has also reached New Zealand. The name "Dutch elm disease" refers to its identification in 1921 and later in the Netherlands by Dutch phytopathologists Bea Schwarz and Christine Buisman who both worked with Professor Johanna Westerdijk. The disease affects species in the genera "Ulmus" and "Zelkova", therefore it is not specific to the Dutch elm hybrid.

The specific problems produced differ according to the particular abnormal synthesis involved. Common manifestations include ataxia; seizures; retinopathy; liver fibrosis; coagulopathies; failure to thrive; dysmorphic features ("e.g.," inverted nipples and subcutaneous fat pads; and strabismus. If an MRI is obtained, cerebellar atrophy and hypoplasia is a common finding.

Ocular abnormalities of CDG-Ia include: myopia, infantile esotropia, delayed visual maturation, low vision, optic disc pallor, and reduced rod function on electroretinography.

Three subtypes of CDG I (a,b,d) can cause congenital hyperinsulinism with hyperinsulinemic hypoglycemia in infancy.

Bleeding canker of horse chestnut is a common canker of horse chestnut trees ("Aesculus hippocastanum", also known as conker trees) that is known to be caused by infection with several different pathogens.

Infections by the gram-negative fluorescent bacterium "Pseudomonas syringae" pathovar "aesculi" are a new phenomenon, and have caused most of the bleeding cankers on horse chestnut that are now frequently seen in Britain.

Mutations in several genes have been associated with the traditional clinical syndromes, termed muscular dystrophy-dystroglycanopathies (MDDG). A new nomenclature based on clinical severity and genetic cause was recently proposed by OMIM. The severity classifications are A (severe), B (intermediate), and C (mild). The subtypes are numbered one to six according to the genetic cause, in the following order: (1) POMT1, (2) POMT2, (3) POMGNT1, (4) FKTN, (5) FKRP, and (6) LARGE.

Most common severe types include:

The most common problem with bound feet was infection. Despite the amount of care taken in regularly trimming the toenails, they would often in-grow, becoming infected and causing injuries to the toes. Sometimes for this reason the girl's toenails would be peeled back and removed altogether. The tightness of the binding meant that the circulation in the feet was faulty, and the circulation to the toes was almost cut off, so any injuries to the toes were unlikely to heal and were likely to gradually worsen and lead to infected toes and rotting flesh. The necrosis of the flesh would also initially give off a foul odour, and later the smell may come from various microorganisms that colonized the folds.

If the infection in the feet and toes entered the bones, it could cause them to soften, which could result in toes dropping off; although, this was seen as a benefit because the feet could then be bound even more tightly. Girls whose toes were more fleshy would sometimes have shards of glass or pieces of broken tiles inserted within the binding next to her feet and between her toes to cause injury and introduce infection deliberately. Disease inevitably followed infection, meaning that death from septic shock could result from foot-binding, and a surviving girl was more at risk for medical problems as she grew older. It is thought that as many as 10% of girls may have died from gangrene and other infections due to footbinding.

At the beginning of the binding, many of the foot bones would remain broken, often for years. However, as the girl grew older, the bones would begin to heal. Even after the foot bones had healed, they were prone to re-breaking repeatedly, especially when the girl was in her teenage years and her feet were still soft. Bones in the girls' feet would often be deliberately broken again in order to improve the size or the shape of the feet. This was especially the case with the toes, as small toes were especially desirable. Older women were more likely to break hips and other bones in falls, since they could not balance securely on their feet, and were less able to rise to their feet from a sitting position. Other issues that might arise from foot binding included paralysis and muscular atrophy.

Globozoospermia (also known as round-headed sperm syndrome) is a rare and severe form of monomorphic teratozoospermia. This means that the spermatozoa show the same abnormality, and over 85% of spermatozoa in sperm have this abnormality. Globozoospermia is responsible for less than 0.1% of male infertility. It characterised by round-headed spermatozoa without acrosome, an abnormal nuclear membrane and midpiece defects. Affected males therefore suffer from either reduced fertility or infertility. Studies suggest that globozoospermia can be either total (100% round-headed spermatozoa without acrosomes) or partial (20-60% round acrosomeless spermatozoa with normal sperm also identified in the sperm count,) however it is unclear whether these two forms are variations on the same syndrome, or actually different syndromes.

Studies have suggested mutations or deletions in three genes are responsible for this condition: SPATA16, PICK1 and DPY19L2. ICSI (intracytoplasmic sperm injection) has previously been used to assist reproduction in globozoospermic patients, however it has not been particularly effective in all patients, due to low fertilisation rates.

Puppy pregnancy syndrome is a psychosomatic illness in humans brought on by mass hysteria.

The syndrome is thought to be localized to villages in several states of India, including West Bengal, Assam, Bihar, Jharkhand, Orissa, and Chhattisgarh, and has been reported by tens of thousands of individuals. It is far more prevalent in areas with little access to education.

People suffering from this condition believe that shortly after being bitten by a dog, puppies are conceived within their abdomen. This is said to be especially likely if the dog is sexually excited at the time of the attack. Victims are said to bark like dogs, and have reported being able to see the puppies inside them when looking at water, or hear them growling in their abdomen. It is believed that the victims will eventually die – especially men, who will give birth to their puppies through the penis.

Witch doctors offer oral cures, which they claim will dissolve the puppies, allowing them to pass through the digestive system and be excreted "without the knowledge of the patient".

Doctors in India have tried to educate the public about the dangers of believing in this condition. Most sufferers are referred to psychiatric services, but in rare instances patients fail to take anti-rabies medication in time, thinking that they have puppy pregnancy syndrome and thus the witch doctor's medicine will cure them. This is further compounded by witch doctors stating that their medicine will fail if sufferers seek conventional treatment.

Some psychiatrists believe that the syndrome meets the criteria for a culture-bound disorder.

The clinical picture is heterogeneous and includes motor delay, seizures, moderate to severe mental retardation, absent speech, growth delay, muscular hypotonia and autistic features.

D-Bifunctional protein deficiency (officially called 17β-hydroxysteroid dehydrogenase IV deficiency) is an autosomal recessive peroxisomal fatty acid oxidation disorder. Peroxisomal disorders are usually caused by a combination of peroxisomal assembly defects or by deficiencies of specific peroxisomal enzymes. The peroxisome is an organelle in the cell similar to the lysosome that functions to detoxify the cell. Peroxisomes contain many different enzymes, such as catalase, and their main function is to neutralize free radicals and detoxify drugs, such as alcohol. For this reason peroxisomes are ubiquitous in the liver and kidney. D-BP deficiency is the most severe peroxisomal disorder, often resembling Zellweger syndrome.

Characteristics of the disorder include neonatal hypotonia and seizures, occurring mostly within the first month of life, as well as visual and hearing impairment. Other symptoms include severe craniofacial disfiguration, psychomotor delay, and neuronal migration defects. Most onsets of the disorder begin in the gestational weeks of development and most affected individuals die within the first two years of life.

The causative agents of DED are ascomycete microfungi. Three species are now recognized:

- "Ophiostoma ulmi", which afflicted Europe from 1910, reaching North America on imported timber in 1928.

- "Ophiostoma himal-ulmi", a species endemic to the western Himalaya.

- "Ophiostoma novo-ulmi", an extremely virulent species from Japan which was first described in Europe and North America in the 1940s and has devastated elms in both continents since the late 1960s.

DED is spread in North America by three species of bark beetles (Family: Curculionidae, Subfamily: Scolytinae):

- The native elm bark beetle, "Hylurgopinus rufipes".

- The European elm bark beetle, "Scolytus multistriatus".

- The banded elm bark beetle, "Scolytus schevyrewi".

In Europe, while "S. multistriatus" still acts as a vector for infection, it is much less effective than the large elm bark beetle, "S. scolytus". "H. rufipes" can be a vector for the disease, but is inefficient compared to the other vectors. "S. schevyrewi" was found in 2003 in Colorado and Utah.

Other reported DED vectors include "Scolytus sulcifrons", "S. pygmaeus", "S. laevis", "Pteleobius vittatus" and "Р. kraatzi". Other elm bark beetle species are also likely vectors.

MBL deficiency refers to Mannan-binding lectin pathway components such as MBL2.

It is thought that 5-10% of the population have an MBL deficiency of some degree There are varying degrees of MBL deficiency; some people in a given population will not even know they have the deficiency, while others may have such low levels that they experience infections with great frequency. Babies and young children are most at risk.

Laminated root rot also known as yellow ring rot is caused by the fungal pathogen "Phellinus weirii". Laminated root rot is one of the most damaging root disease amongst conifers in northwestern America and true firs, Douglas-fir, Mountain hemlock, and Western hemlock are highly susceptible to infection with "P. weirii". A few species of plants such as Western white pine and Lodgepole pine are tolerant to the pathogen while Ponderosa pine is resistant to it. Only hardwoods are known to be immune to the pathogen.

Aminoacylase 1 deficiency is a rare inborn error of metabolism. To date only 21 cases have been described.

Aside from the effect on fertility globozoospermia is symptomless. People with globozoospermia have normal physical and mental development, normal clinical features and normal hormonal profile.

Laron's syndrome, or Laron-type dwarfism, is an autosomal recessive disorder characterized by an insensitivity to growth hormone (GH), usually caused by a mutant growth hormone receptor. It causes short stature and an increased sensitivity to insulin which means that they are less likely to develop diabetes mellitus type 2 and possibly cancer as well. It can be treated with injections of recombinant IGF-1.

X-linked lymphoproliferative disease (also known as "Duncan's disease" or "Purtilo syndrome") is a lymphoproliferative disorder.