A Novel in vitro Human Macrophage Model to Study the Persistence of Mycobacterium tuberculosis Using Vitamin D(3) and Retinoic Acid Activated THP-1 Macrophages.

Mycobacterium tuberculosis (Mtb) replicates within the human macrophages and we investigated the activating effects of retinoic acid (RA) and vitamin D(3) (VD) on macrophages in relation to the viability of intracellular Mtb. A combination of these vitamins (RAVD) enhanced the levels of DC-SIGN and mannose receptors on THP-1 macrophages that increased mycobacterial uptake but inhibited the subsequent intracellular growth of Mtb by inducing reactive oxygen species and autophagy. RAVD also enhanced antigen presenting and chemotactic receptors on THPs suggesting an activated phenotype for RAVD activated THPs.

Integration of international medical graduates in u.s. Psychiatry: the role of acculturation and social support.

Objective: the authors investigated whether social support and acculturation could predict the mental health of international medical graduates pursuing psychiatric residencies in the United States.

Methods: a 55-item online survey was assembled by combining three validated instruments for mental health, social support, and acculturation. A link to the survey was e-mailed to training directors of all psychiatric residency and fellowship programs.

Assessment of free dye in solutions of dual-labeled antibody conjugates for in vivo molecular imaging.

Purpose: Recent preclinical and clinical studies show that dyes that excite and fluoresce in the near-infrared range may be used for tracking and detecting disease targets in vivo. A method for quantifying free dye molecules in antibody conjugate preparations is required for agent batch release and for translation into the clinic.

Procedures: Herein, we developed and validated a SDS-PAGE method to determine the percentage of free IRDye 800 CW in (DTPA)(n)-trastuzumab-(IRDye 800)(m) conjugate sample preparations in which high-performance liquid chromatography (HPLC) assessment of free dye was not possible.

Pneumocystis-associated organizing pneumonia as a manifestation of immune reconstitution inflammatory syndrome in an HIV-infected individual with a normal CD4+ T-cell count following antiretroviral therapy.

We describe a rare case of Pneumocystic jirovecii-associated organizing pneumonia (PJP) in an HIV-infected individual on highly active antiretroviral therapy (HAART) with a CD4(+) T-cell count of 835 x 10(3) cells/mL and a low viral load. PJP was confirmed using transbronchial biopsies and bronchoalveolar lavage. The presentation in this patient suggests immune reconstitution inflammatory syndrome (IRIS) after institution of antiretroviral therapy (ART).

Cardiovascular therapeutic uses of targeted ultrasound contrast agents.

The therapeutic use of ultrasound contrast agents (UCAs) is an emerging methodology with high potential for enhanced directed therapeutic gene, bioactive gas, drug, and stem cell delivery. Ultrasound-targeted microbubble destruction has already demonstrated feasibility for plasmid DNA delivery. Similarly, therapeutic ultrasound for thrombolysis treatment has been taken into the clinical setting, and the addition of UCAs for therapeutic delivery or enhanced effect through cavitation is a natural progression to this investigation.

Barriers and facilitators of cervical cancer screening among Hispanic women.

Hispanic women are less likely than non-Hispanic white women to utilize Pap test screening. Additionally, Hispanic women have higher rates of cervical cancer than non-Hispanic white women. To better understand the barriers and facilitators for Pap test screening, we conducted 13 focus groups with 84 Hispanic women aged 18-61 years.

Idiopathic talipes equinovarus (ITEV) (clubfeet) in Texas.

Idiopathic talipes equinovarus (ITEV) is the most common form of clubfoot with a birth prevalence of 1 per 1,000 births. Serial casting and surgical correction impose a substantial financial burden on families and the health care system. While the etiology of ITEV is considered to be complex, the causes remain elusive.

Requirement for SAPK-JNK signaling in the induction of apoptosis by ribosomal stress in REH lymphoid leukemia cells.

The present studies examined performance of SAPK cascades and apoptotic commitment following ribosomal trauma in REH lymphoid leukemia cells. Ribostatic insults included disruption of ribosomal activity by mechanistically dissimilar agents such as blasticidin-S (BCS) (which binds 28S-rRNA to block peptidyl bond formation), kasugamycin (KSM) (which binds 18S-rRNA to prevent translational initiation), and cycloheximide (CHX) (which blocks A-site to P-site translocation of peptidyl-tRNA). Exposure of REH cells to BCS elicited DNA degradation and apoptotic cytolysis.

Homologous and heterologous regulation of somatostatin receptor 2.

We previously demonstrated that phosphorylation of somatostatin receptor 2A (sst2A) is rapidly increased in transfected cells both by agonist and by the protein kinase C (PKC) activator phorbol myristate acetate (PMA). Here, we investigate whether PKC-mediated receptor phosphorylation is involved in the homologous or heterologous regulation of endogenous sst2 receptors in AR42J pancreatic acinar cells upon stimulation by agonist or by cholecystokinin (CCK) or bombesin (BBS). Somatostatin, PMA, CCK, and BBS all increased sst2A receptor phosphorylation 5- to 10-fold within minutes.

Calf compartment syndrome and lumbar plexopathy following topical bovine thrombin-induced coagulopathy.

We describe a patient with acquired thrombin inhibitor who developed tibial and peroneal neuropathies followed by lumbar plexopathy as a result of large calf and psoas muscle hematomas. Thrombin time, Prothombin time, and partial thromboplastin time were prolonged after repeated exposures to topical bovine thrombin in two orthopedic procedures Specific coagulation tests revealed that the coagulopathy was the result of an inhibitor to bovine thrombin that cross-reacted with human thrombin. We emphasize the risk of spontaneous hematomas that can compromise peripheral nerves as a result of an acquired coagulopathy following bovine thrombin exposure.

Protein kinase C activation stimulates the phosphorylation and internalization of the sst2A somatostatin receptor.

The sst2A receptor is expressed in the endocrine, gastrointestinal, and neuronal systems as well as in many hormone-sensitive tumors. This receptor is rapidly internalized and phosphorylated in growth hormone-R2 pituitary cells following somatostatin binding (Hipkin, R. W.

Triphenylethylene antiestrogens induce uterine vascular endothelial growth factor expression via their partial estrogen agonist activity.

Estradiol induces vascular endothelial growth factor (VEGF) expression in the rat uterus and this may contribute to the hyperemia and increased vascularity produced by estrogens in this target tissue. Triphenylethylene antiestrogens such as tamoxifen have mixed agonist/antagonist activity and their specific effects are tissue and gene specific. These drugs exhibit primarily antiestrogenic actions in mammary tissue and are thus used for the treatment of breast cancer.

Progestin regulation of vascular endothelial growth factor in human breast cancer cells.

Vascular endothelial growth factor (VEGF) is a potent angiogenic factor associated with the degree of vascularity, progression, and metastasis of breast cancer, and cases of this disease with increased vascular density have a poor prognosis. We show that in T47-D human breast cancer cells, progesterone induces a dose-dependent increase of 3-4-fold in media VEGF levels, with a maximum response occurring at a concentration of 10 nM. This effect is blocked by the antiprogestin RU 486.

Medial temporal lobe structures and autism: a review of clinical and experimental findings.

Although substantive understanding of brain dysfunction in autism remains meager, clinical evidence as well as animal brain research on the effects of early damage to selective brain system have now yielded enough knowledge that some provisional hypotheses concerning the etiology of autism can be generated. Basically, the underlying premise of this review is that a major dysfunction of the autistic brain resides in neural mechanisms of the structures in the medial temporal lobe, and, perhaps, more specifically the amygdaloid complex. This review begins with a summary of clinical evidence of the involvement of the medial temporal lobe structures in autism.