Family medicine viewed through the public lens: A national cross-sectional study in Lebanon.

Background: Family medicine (FM) is a medical specialty that provides continuing, comprehensive health care for the individual and the family. This study aimed to describe Lebanese citizens' knowledge, attitudes, and practices toward FM as a specialty.

Methods: This is a national cross-sectional phone-based survey targeting the knowledge of the public about FM and its scope of practice.

Gender-Based Violence and Women Reproductive Health in War Affected Area.

Manifestations of gender-based violence although many, and sometimes more pronounced in areas of armed conflict, go unnoticed due to multiple factors. Gender-based violence targeted towards women, affect their overall health negatively, particularly the reproductive well-being. Major conflicts arising in the Middle East over the past 10-15 years, ranging from the Arab uprising to the Syrian civil war, have drawn attention world-wide.

TFG-maintaining stability of overlooked FANCD2 confers early DNA-damage response.

Emerging Fanconi Anemia (FA) signaling in the field of cancer research annotates the extreme importance of its center player, Fanconi Anemia complementation group D2 (FANCD2) in protecting human cells from going awry. However, a previously-unrecognized form of FANCD2, namely FANCD2-V2, is understudied. We report TRK-Fused Gene (TFG) is critical for roles played by FANCD2-V2 in early responses to DNA damage, but not for FANCD2-V1, the long-known form of FANCD2.

A new look at molecular biology of breast cancer.

In the past 25 years, incidence rates of breast cancer have risen about 30% in westernized countries. Mutations in BRCA1 and BRCA2 are the most prominent cause of breast cancer. However, these cancer susceptibility genes (BRCAs) only account for a few percent of women suffering breast tumor.

Fanconi Anemia complementation group C protein in metabolic disorders.

Given importance of 22-Fanconi Anemia (FA) proteins together to act in a signaling pathway in preventing deleterious clinical symptoms, e.g. severe bone marrow failure, congenital defects, an early onset of aging and cancer, studies on each FA protein become increasingly attractive.

Comparative Study of Serum Lipid Profiles in Nepalese Cancer Patients Attending a Tertiary Care Hospital.

Significant efforts have been made to study cancer at the biochemical and cellular level and identify factors associated with progression. The aim of this hospital based randomized comparative study at the Nepalese Army Institute of Health science hospital was to assess factors in 52 people diagnosed with different types of cancer and 56 normal control persons. Fasting blood samples were analyzed for serum total cholesterol (TC), high density lipoprotein (HDL), triglycerides (TG) and low density lipoprotein (LDL).

Multifaceted Fanconi Anemia Signaling.

In 1927 Guido Fanconi described a hereditary condition presenting panmyelopathy accompanied by short stature and hyperpigmentation, now better known as Fanconi anemia (FA). With this discovery the genetic and molecular basis underlying FA has emerged as a field of great interest. FA signaling is crucial in the DNA damage response (DDR) to mediate the repair of damaged DNA.

Fanconi Anemia Signaling and Cancer.

The extremely high cancer incidence associated with patients suffering from a rare human genetic disease, Fanconi anemia (FA), demonstrates the importance of FA genes. Over the course of human tumor development, FA genes perform critical tumor-suppression roles. In doing so, FA provides researchers with a unique genetic model system to study cancer etiology.

FANCD2 and DNA Damage.

Investigators have dedicated considerable effort to understanding the molecular basis underlying Fanconi Anemia (FA), a rare human genetic disease featuring an extremely high incidence of cancer and many congenital defects. Among those studies, FA group D2 protein (FANCD2) has emerged as the focal point of FA signaling and plays crucial roles in multiple aspects of cellular life, especially in the cellular responses to DNA damage. Here, we discuss the recent and relevant studies to provide an updated review on the roles of FANCD2 in the DNA damage response.

Involvement of FANCD2 in Energy Metabolism via ATP5α.

Growing evidence supports a general hypothesis that aging and cancer are diseases related to energy metabolism. However, the involvement of Fanconi Anemia (FA) signaling, a unique genetic model system for studying human aging or cancer, in energy metabolism remains elusive. Here, we report that FA complementation group D2 protein (FANCD2) functionally impacts mitochondrial ATP production through its interaction with ATP5α, whereas this relationship was not observed in the mutant FANCD2 (K561R)-carrying cells.

Evaluation of Osseointegration around Tibial Implants in Rats by Ibandronate-Treated Nanotubular Ti-32Nb-5Zr Alloy.

Materials with differing surfaces have been developed for clinical implant therapy in dentistry and orthopedics. This study was designed to evaluate bone response to titanium alloy containing Ti-32Nb-5Zr with nanostructure, anodic oxidation, heat treatment, and ibandronate coating. Rats were randomly assigned to two groups for implantation of titanium alloy (untreated) as the control group and titanium alloy group coated with ibandronate as the experimental group.

Kaempferol induces chondrogenesis in ATDC5 cells through activation of ERK/BMP-2 signaling pathway.

Endochondral bone formation occurs when mesenchymal cells condense to differentiate into chondrocytes, the primary cell types of cartilage. The aim of the present study was to identify novel factors regulating chondrogenesis. We investigated whether kaempferol induces chondrogenic differentiation in clonal mouse chondrogenic ATDC5 cells.

Hispidulin attenuates bone resorption and osteoclastogenesis via the RANKL-induced NF-κB and NFATc1 pathways.

Hispidulin, a flavonoid that is known to have anti-inflammatory and anti-oxidant effects, attenuates osteoclastogenesis and bone resorption. To investigate the molecular mechanism of its inhibitory effect on osteoclastogenesis, we employed the receptor activator of the nuclear factor κB (NF-κB) ligand (RANKL)-induced murine monocyte/macrophage RAW 264.7 cells and bone marrow-derived macrophages (BMMs) for osteoclastic differentiation in vitro.

Anti-angiogenic and anti-tumor activity of Bavachinin by targeting hypoxia-inducible factor-1α.

Hypoxia-inducible factor-1 (HIF-1) consists of two subunits, the HIF-1β, which is constitutively expressed, and HIF-1α, which is oxygen-responsive. HIF-1α is over-expressed in response to hypoxia, increasing transcriptional activity linked to tumor progression, angiogenesis, metastasis, and invasion. This study aimed to demonstrate that the natural compound, Bavachinin, has potent anti-angiogenic activity in vitro and in vivo.

Isopsoralen Induces Differentiation of Prechondrogenic ATDC5 Cells via Activation of MAP Kinases and BMP-2 Signaling Pathways.

Endochondral bone formation is the process by which mesenchymal cells condense to become chondrocytes, which ultimately form new bone. The process of chondrogenic differentiation and hypertrophy is critical for bone formation and as such is regulated by many factors. In this study, we aimed to indentify novel factors that regulate chondrogenesis.

An activator of PHD2, KRH102140, decreases angiogenesis via inhibition of HIF-1α.

Hypoxia-inducible transcription factors (HIFs) play a pivotal role in the response of cells to hypoxia. HIFs are dimers of an oxygen-sensitive α-subunit (HIF-1α or HIF-2α), and a constitutively expressed β-subunit. In normoxia, HIF-1α is destabilized by post-translational hydroxylation of Pro-564 and Pro-402 by a family of oxygen-sensitive dioxygenases.

Stimulation of chondrogenesis in ATDC5 chondroprogenitor cells and hypertrophy in mouse by Genkwadaphnin.

The growth in height of the bone plate is a result of endochondral proliferation in epiphyseal growth plates and the conversion of chondrocytes into new bone. The control of chondrogenic differentiation and hypertrophy is critical for these processes. The present study was aimed to demonstrate the chondromodulating activity of Genkwadaphnin.

Inhibition of osteoclastogenic differentiation by Ikarisoside A in RAW 264.7 cells via JNK and NF-kappaB signaling pathways.

Osteoclasts are specialized bone-resorbing cells derived from multipotent myeloid progenitor cells. They play a crucial homeostatic role in skeletal modeling and remodeling and destroy bone in many pathologic conditions. Receptor activator of NF-kappaB ligand (RANKL) is essential to osteoclastogenesis.

Hexane-Soluble Fraction of the Common Fig, Ficus carica, Inhibits Osteoclast Differentiation in Murine Bone Marrow-Derived Macrophages and RAW 264.7 Cells.

Osteoclasts, derived from multipotent myeloid progenitor cells, play homeostatic roles in skeletal modeling and remodeling, but may also destroy bone in pathological conditions such as osteoporosis and rheumatoid arthritis. Osteoclast development depends critically on a differentiation factor, the receptor activator of NF-kappaB ligand (RANKL). In this study, we found that the hexane soluble fraction of the common fig Ficus carica (HF6-FC) is a potent inhibitor of osteoclastogenesis in RANKL-stimulated RAW264.

Fluticasone-associated cutaneous allergic granulomatous vasculitis: an underrecognized but important cause of drug-induced cutaneous Churg-Strauss syndrome.

Allergic granulomatous vasculitis, or Churg-Strauss syndrome, is a small vessel, multisystem vasculitis that can affect multiple organs. It is usually idiopathic, but recent case reports have implicated leukotriene receptor antagonists (LTRA) and inhaled corticosteroids in the development of this rare syndrome. We report a case that acutely developed skin-limited Churg Strauss-like cutaneous allergic granulomatous vasculitis after initiating therapy with inhaled fluticasone and salmeterol for poorly controlled asthma symptoms.

Impact of long term socio-political conflict on health: a traumatic Nepalese experience.

Twelve years of traumatic experience of thousands of poor Nepalese is still lingering aftermath of the ceasefire between the government and the Maoist rebels and it has devastated all sectors of health care in the country. Almost twenty thousand peoples have lost their lives during this period as a direct result of or consequence of insurgency. About a quarter million people are internally displaced; many homeless and many more skilled people have fled the country.