Evidence That Up-Regulation of MicroRNA-29 Contributes to Postnatal Body Growth Deceleration.

Body growth is rapid in infancy but subsequently slows and eventually ceases due to a progressive decline in cell proliferation that occurs simultaneously in multiple organs. We previously showed that this decline in proliferation is driven in part by postnatal down-regulation of a large set of growth-promoting genes in multiple organs. We hypothesized that this growth-limiting genetic program is orchestrated by microRNAs (miRNAs).

Evolutionary conservation and modulation of a juvenile growth-regulating genetic program.

Body size varies enormously among mammalian species. In small mammals, body growth is typically suppressed rapidly, within weeks, whereas in large mammals, growth is suppressed slowly, over years, allowing for a greater adult size. We recently reported evidence that body growth suppression in rodents is caused in part by a juvenile genetic program that occurs in multiple tissues simultaneously and involves the downregulation of a large set of growth-promoting genes.

Type 1 diabetes mellitus in a patient with homozygous sickle cell anemia.

In children with sickle cell disease, reports of type 1 diabetes mellitus (T1D) are extremely rare. Several studies failed to show the co-existence of the two conditions. In the few cases reported, the diagnosis has been made solely based on the clinical presentation.

Diabetic ketoacidosis with cerebral hemorrhage and alpha coma in an adolescent female.

Background: Diabetic ketoacidosis (DKA) is one of the most common and harmful complications of type 1 diabetes in children. The neurologic morbidities, including seizure activity, motor/sensory deficit, and coma, can be seen secondary to cerebral edema, hemorrhage, or ischemia. Alpha-frequency is a normal 8-13 Hz physiologic electroencephalogram rhythm that is seen most prominently in the occipital region of awake people and is augmented by eye closure.

A set of imprinted genes required for normal body growth also promotes growth of rhabdomyosarcoma cells.

Introduction: In many normal tissues, proliferation rates decline postnatally, causing somatic growth to slow. Previous evidence suggests that this decline is due, in part, to decline in the expression of growth-promoting imprinted genes including Mest, Plagl1, Peg3, Dlk1, and Igf2. Embryonal cancers are composed of cells that maintain embryonic characteristics and proliferate rapidly in childhood.

The galactocele of male infants: an intriguing entity. Study and reflection about a case, with review of the literature.

In this report, the authors investigate and discuss a galactocele that developed in the breast of a 5-month-old male. Based on the histological and immunohistochemical findings, they suggest that the rare and intriguing process that is exclusively observed in males in the absence of any detectable hormonal stimulation at time of investigation could represent a developmental anomaly possibly promoted by an obstructive phenomenon involving a defect of hollowing of some primary epidermal buds, the precursors of the mammary ducts.

Short stature in partially corrected X-linked severe combined immunodeficiency--suboptimal response to growth hormone.

Background: X-linked severe combined immunodeficiency (XSCID) results from defects in the common cytokine receptor gamma chain (gamma c) required for signaling by receptors for interleukin (IL)-2, -4, -7, -9, -15, and -21. Following haploidentical bone marrow transplant without myelo-conditioning for XSCID, most patients achieve partial reconstitution often limited to T lymphocytes. Many partially corrected patients manifest extreme short stature (<5th percentile).

Stimulatory effects of insulin-like growth factor-I on growth plate chondrogenesis are mediated by nuclear factor-kappaB p65.

Insulin-like growth factor-I (IGF-I) is an important regulator of endochondral ossification. However, little is known about the signaling pathways activated by IGF-I in growth plate chondrocytes. We have previously shown that NF-kappaB-p65 facilitates growth plate chondrogenesis.

Hypocalcemia in a patient with osteosarcoma and 22q11.2 deletion syndrome.

Hypocalcemia is a rare complication of osteosarcoma, having been described in only 4 reports. We present the case of a 16-year-old male with metastatic osteosarcoma of the right humerus who was found to have severe asymptomatic hypocalcemia. Cytogenetic analysis of peripheral blood revealed a microdeletion in band 22q11.

Nuclear factor-kappaB p65 facilitates longitudinal bone growth by inducing growth plate chondrocyte proliferation and differentiation and by preventing apoptosis.

NF-kappaB is a group of transcription factors involved in cell proliferation, differentiation, and apoptosis. Mice deficient in the NF-kappaB subunits p50 and p52 have retarded growth, suggesting that NF-kappaB is involved in bone growth. Yet, it is not clear whether the reduced bone growth of these mice depends on the lack of NF-kappaB activity in growth plate chondrocytes.