an extension of the period of nephrogenesis by at least 24 hours

an increased number of nephron progenitor cells in each nephrogenic niche

faster branching morphogenesis in the developing kidneys

Adverse conditions during late pregnancy can impair fetal growth and/or promote disproportionate fetal growth.  These adaptations may promote survival of the fetus, but lead to disease in later life. 

Adverse conditions during prenatal and postnatal development can impair the development of many organs and result in adult diseases. Outcomes in males and females tend to be similar with the brain, heart and kidneys particularly susceptible. 

Adverse conditions prior to conception, during gestation and the early postnatal period can impair organ and tissue growth and/or promote disproportionate growth.  These adaptations may promote survival, but can lead to disease in later life. Some organs are more susceptible to these effects than others, and sex differences in outcomes are common.

Low birth weight is associated with impaired development of many organs. Accelerated weight gain after birth can resolve some of these developmental disorders, but not all. As a result, diseases in adulthood can arise, with the brain, heart and kidneys particularly vulnerable. 

Prevalence rates of impaired glucose tolerance

Standardised mortality rates for coronary heart disease

Prevalence rates of hypertension

Standardised mortality rates for end stage kidney disease

It is likely that the overall mean is greater than 1.5 million nephrons

This is due to more advanced imaging technology in Japanese studies

Studies with larger sample sizes show more similar means

Genetic variation makes it difficult to estimate the overall mean

Distal convoluted tubules, collecting ducts, major calyces, minor calyces

Glomeruli, proximal convoluted tubules, distal convoluted tubules

Collecting ducts, major calyces, minor calyces

Proximal convoluted tubules, distal convoluted tubules, collecting ducts

The disease causes multi-tissue damages

The disease can occur in both male and female populations

IL4 acts to target activation induced cytidine deaminase (AID) to the S regions adjacent to IgG1 and IgE.  

IL4 activates activation induced cytidine deaminase (AID), making double strand breaks in S-region DNA more likely and thus more switching.

IL4 promotes activation induced cytidine deaminase (AID) activity in general, with the isotype chosen by TLR ligands binding to the B cell.

IL4 increases B cell proliferation and CSR isotype selection is closely related to cell division number

intrinsically long-lived and only require an anchor-point for persistence

depend on surrounding cells for their survival

typically reflect the initial stages of the response in terms of isotype and affinity

resident in the organ in which they are formed

because they have immune complexes, patients with rheumatoid arthritis will ultimately develop lupus if left untreated

broad immunosuppression is more effective a treatment strategy than blocking a single pro-inflammatory cytokine

an environmental trigger such as smoking might cause the different autoimmune diseases in individuals because of their particular genetic variations

because both diseases are caused by autoantibodies, the therapeutic approach to treating both diseases would be similar

acts with the transcription factor BLIMP1 to initiate plasma cell differentiation

is required in B cells for initiation of germinal centres

inhibits V gene somatic mutation in germinal centre B cells

protects germinal centre B cells that don’t improve their affinity from BLIMP1-inducd apoptosis