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.

This is a rare disease with prevalence about 1 in 200,000 to 1 in 600,000. Studies showed that mutations in "CUBN" or "AMN" clustered particularly in the Scandinavian countries and the Eastern Mediterranean regions. Founder effect, higher clinical awareness to IGS, and

frequent consanguineous marriages all play a role in the higher prevalence of IGS among these populations

Since the essential pathology is due to the inability to absorb vitamin B from the bowels, the solution is therefore injection of IV vitamin B. Timing is essential, as some of the side effects of vitamin B deficiency are reversible (such as RBC indices, peripheral RBC smear findings such as hypersegmented neutrophils, or even high levels of methylmalonyl CoA), but some side effects are irreversible as they are of a neurological source (such as tabes dorsalis, and peripheral neuropathy). High suspicion should be exercised when a neonate, or a pediatric patient presents with anemia, proteinuria, sufficient vitamin B dietary intake, and no signs of pernicious anemia.

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.

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.

Possible ethnic differences in physiological pathways for ingested vitamin D, such as the Inuit, may confound across the board recommendations for vitamin D levels. Inuit compensate for lower production of vitamin D by converting more of this vitamin to its most active form.

A Toronto study of young Canadians of diverse ancestry applied a standard of serum 25(OH)D levels that was significantly higher than official recommendations. These levels were described to be 75 nmol/L as "optimal", between 75 nmol/L and 50 nmol/L as "insufficient" and < 50 nmol/L as "deficient". 22% of individuals of European ancestry had 25(OH)D levels less than the 40 nmol/L cutoff, comparable to the values observed in previous studies (40nmol/L is 15 ng/mL). 78% of individuals of East Asian ancestry and 77% of individuals of South Asian ancestry had 25(OH)D concentrations lower than 40 nmol/L. The East Asians in the Toronto sample had low 25(OH)D levels when compared to whites. In a Chinese population at particular risk for esophageal cancer and with the high serum 25(OH)D concentrations have a significantly increased risk of the precursor lesion.

Studies on the South Asians population uniformly point to low 25(OH)D levels, despite abundant sunshine. Rural men around Delhi average 44nmol/L. Healthy Indians seem have low 25(OH)D levels which are not very different from healthy South Asians living in Canada. South Indian patients with ischemic heart disease have serum 25-hydroxyvitamin D levels which are above 222.5 nmol/l and considered extremely high. Measuring melanin content to assess skin pigmentation showed an inverse relationship with serum 25(OH)D. The uniform occurrence of very low serum 25(OH)D in Indians living in India and Chinese in China does not support the hypothesis that the low levels seen in the more pigmented are due to lack of synthesis from the sun at higher latitudes.

A study of French Canadians found that a significant minority did not maximize ingested serum 25(OH)D for genetic reasons; vitamin D-binding protein polymorphisms explained as much of the variation in circulating 25(OH)D as did total ingestion of vitamin D.

Evidence suggests that dietary vitamin D may be carried by lipoprotein particles into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages. This raises questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk as it may be causing vascular calcification. Calcifediol is implicated in the etiology of atherosclerosis, especially in non-Caucasians.

The levels of the active form of vitamin D, calcitriol, are inversely correlated with coronary calcification. Moreover, the active vitamin D analog, alfacalcidol, seems to protect patients from developing vascular calcification. Serum vitamin D has been found to correlate with calcified atherosclerotic plaque in African Americans as they have higher active serum vitamin D levels compared to Euro-Americans. Higher levels of calcidiol positively correlate with aorta and carotid calcified atherosclerotic plaque in African Americans but not with coronary plaque, whereas individuals of European descent have an opposite, negative association. There are racial differences in the association of coronary calcified plaque in that there is less calcified atherosclerotic plaque in the coronary arteries of African-Americans than in whites.

A case control study on a population in southern India found that more than 50% of patients with ischaemic heart disease had serum levels of vitamin D higher than 222.5 nmol/L, but the study did not evaluate causation.

Among descent groups with heavy sun exposure during their evolution, taking supplemental vitamin D to attain the 25(OH)D level associated with optimal health in studies done with mainly European populations may have deleterious outcomes. Despite abundant sunshine in India, vitamin D status in Indians are low and suggests a public health need to fortify Indian foods with vitamin D. However, the levels found in India are consistent with many other studies of tropical populations which have found that even an extreme amount of sun exposure, does not raise 25(OH)D levels to the levels typically found in Europeans.

Recommendations stemming for a single standard for optimal serum 25(OH)D concentrations ignores the differing genetically mediated determinates of serum 25(OH)D and may result in ethnic minorities in Western countries having the results of studies done with subjects not representative of ethnic diversity applied to them. Vitamin D levels vary for genetically mediated reasons as well as environmental ones.

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.

The term can also be seen in herpetoculture, as this condition can occur in female reptiles. It is inadvisable to attempt to break a reptile egg to remove it from an egg-bound female. This procedure may be done by a veterinarian, who will insert a needle into the egg, and withdraw the contents with a syringe, allowing the egg to collapse and be removed. Non-surgical interventions include administering oxytocin to improve contractions and allow the egg(s) to pass normally. In many cases, egg-bound reptiles must undergo surgery to have stuck eggs removed.

Egg binding in reptiles is quickly fatal if left untreated; therefore, gravid females who become very lethargic and cease feeding need immediate medical treatment in order to treat the potentially life-threatening condition. An episode of the Animal Planet reality show "E-Vet Interns" featured the treatment of an egg-bound turtle named Napoleon. Exotics specialist Dr. Kevin Fitzgerald of Alameda East Veterinary Hospital is shown treating her with oxytocin and then eventually having to resort to surgery with footage of the large number of eggs that were removed. Dr. Fitzgerald was shown explaining to the new interns how dangerous this condition can be for a pet turtle and the need for early veterinary intervention.

Egg binding can occur if an egg is malformed and/or too large, the animal is weakened by illness, improper husbandry, stress, or if hormonal balances are wrong (producing weak contractions). Factors that can contribute to the risk of egg binding include calcium deficiency, breeding animals that are too young or too small, not providing suitable laying areas (leading to deliberate retention of eggs), and overfeeding of species in which clutch size is dependent on food intake (such as Veiled Chameleons).

In the context of behavioral ecology, egg binding can be an important factor in limiting clutch size. Lizards that lay fewer, but larger eggs are at higher risk for egg binding, and so there is selection pressure towards a minimum clutch size. For example, in common side-blotched lizards, females that lay fewer than the average 4–5 eggs per clutch have significantly increased risk of egg binding.

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.

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.

People with Laron syndrome have strikingly low rates of cancer and diabetes, although they appear to be at increased risk of accidental death due to their stature.

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.

The observation has been made many times that globozoospermia arises in siblings which points towards an underlying genetic cause. Recent progress has been made into determining what genes could be implicated in this pathology, with the previously mentioned genes being found to play a role. There are more genes which have been shown to be mutated in globozoospermia in mice, but these are yet to be connected to the human disease process. Examples of these include Gopc, Hrb and Csnka2. There are thousands of genes which guide the process of spermatogenesis, and knowing how they’re involved in globozoospermia is an important current area of research.

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.

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.

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.

No treatment is available for most of these disorders. Mannose supplementation relieves the symptoms in PMI-CDG (CDG-Ib) for the most part, even though the hepatic fibrosis may persist. Fucose supplementation has had a partial effect on some SLC35C1-CDG (CDG-IIc or LAD-II) patients.

This disease is mainly found in tropical climates in Southern Asia, however some scattering exists:

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.

A congenital disorder of glycosylation (previously called carbohydrate-deficient glycoprotein syndrome) is one of several rare inborn errors of metabolism in which glycosylation of a variety of tissue proteins and/or lipids is deficient or defective. Congenital disorders of glycosylation are sometimes known as CDG syndromes. They often cause serious, sometimes fatal, malfunction of several different organ systems (especially the nervous system, muscles, and intestines) in affected infants. The most common subtype is CDG-Ia (also referred to as PMM2-CDG) where the genetic defect leads to the loss of phosphomannomutase 2, the enzyme responsible for the conversion of mannose-6-phosphate into mannose-1-phosphate.

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.

In the past few years, the bacterial pathogen "Pseudomonas syringae pv. aesculi" has emerged as a new and virulent agent for this disease in Western Europe. Specific to horse chestnut trees, this pathogen infects the bark (cambium) around the trunk and main branches. As it spreads, it cuts off the water supply to the crown; and when it completely encircles the trunk, the tree will die.

This particular infective agent emerged in the past few years, and has now spread rapidly to infect many trees in Western Europe.

Initially the outbreak was attributed to "Phytophthora", until DNA tests suggested that a pathovar of "Pseudomonas syringae" was responsible; and this hypothesis was confirmed in 2007 with tests satisfying Koch's postulates.

The disease has risen markedly in the UK since 2003, and now approximately one half of all horse chestnuts in Great Britain are affected and showing symptoms to some degree.

The disease is spreading at an alarming rate in the Netherlands,

where one third of all horse chestnuts are affected to a greater or lesser extent.

A similar upsurge is reported in Belgium and France.