The Monteggia fracture is a fracture of the proximal third of the ulna with dislocation of the proximal head of the radius. It is named after Giovanni Battista Monteggia. Causes
Mechanisms include:

Fall outstretched hand with the forearm in excessive pronation (hyper-pronation injury). The ulna fractures in the proximal one-third of the shaft due to extreme dislocation. Depending on the impact and forces applied in each direction, degree of energy absorption determines pattern, involvement of the radial head and whether or not open soft tissue occurs. Direct blow on back of upper forearm would be a very uncommon cause. In this context, isolated ulnar shaft fractures are most commonly seen in defence against blunt trauma (e.g. nightstick injury). Such an isolated ulnar shaft fracture is not a Monteggia fracture. It is called a nightstick fracture. Diagnosis
Classification
There are four types (depending upon displacement of the radial head):

I - Extension type (60%) - ulna shaft angulates anteriorly (extends) and radial head dislocates anteriorly. II - Flexion type (15%) - ulna shaft angulates posteriorly (flexes) and radial head dislocates posteriorly. III - Lateral type (20%) - ulna shaft angulates laterally (bent to outside) and radial head dislocates to the side. IV - Combined type (5%) - ulna shaft and radial shaft are both fractured and radial head is dislocated, typically anteriorly.These are known as the Bado types.
Disease-associated variants of either subunit of KATP, KCNJ11 and ABCC8, can result in a channel that is "stuck open", rendering the β cell unable to secrete insulin in response to high blood glucose. Children born with disease-associated KATP variants often have intrauterine growth restriction and resulting low birthweight. Similarly, the second most common cause of permanent neonatal diabetes is alterations to the gene that encodes insulin. Mutations associated with neonatal diabetes tend to cause misfolding of the insulin protein; misfolded insulin accumulates in the endoplasmic reticulum (ER), leading to ER stress and β-cell death.Most transient neonatal diabetes is caused by the over-expression of a cluster of genes on chromosome 6, a region called 6q24. Over-expression of 6q24 is often caused by anomylous epigenetic regulation of the locus. The copy of 6q24 inherited from ones father normally has much higher gene expression than the copy inherited from ones mother. Therefore, inheriting two copies of the gene region from ones father (either through uniparental disomy, or receiving two copies from ones father in addition to the copy from ones mother) commonly results in over-expression of the locus. Alternatively, inheriting a maternal copy of 6q24 with defective DNA methylation can result in similar over-expression of the locus.Variants in several other genes can cause neonatal diabetes, though these cases are much rarer. Genetic changes that disable the transcription factors CNOT1, GATA4, GATA6, PDX1, PTF1A, or RFX6 – all involved in the development of the pancreas – result in a shrunken or missing pancreas.