Islamic trauma healing (ITH): A scalable, community-based program for trauma: Cluster randomized control trial design and method.

Background: Somalia has long been in a state of humanitarian crisis; trauma-related mental health needs are extremely high. Access to state-of-the-art mental health care is limited. Islamic Trauma Healing (ITH) is a manualized mosque-based, lay-led group intervention aimed at healing the individual and communal mental wounds of war and refugee trauma. The 6-session intervention combines Islamic principles with empirically-supported exposure and cognitive restructuring principles for posttraumatic stress disorder (PTSD). ITH reduces training time, uses a train the trainers (TTT) model, and relies on local partnerships embedded within the strong communal mosque infrastructure. Methods: We will conduct a hybrid effectiveness-implementation randomized control trial (RCT) in the Somaliland, with implementation in the cities of Hargeisa, Borama, and Burao. In this study, a lay-led, mosque-based intervention, Islamic Trauma Healing (ITH), to promote mental health and reconciliation will be examined in 200 participants, randomizing mosques to either immediate ITH or a delayed (waitlist; WL) ITH conditions. Participants will be assessed by assessors masked to condition at pre, 3 weeks, 6 weeks, and 3-month follow-up. Primary outcome will be assessor-rated posttraumatic stress symptoms (PTSD), with secondary outcomes of depression, somatic symptoms, and well-being. A TTT model will be tested, examining the implementation outcomes. Additional measures include potential mechanisms of change and cost effectiveness. Conclusion: This trial has the potential to provide effectiveness and implementation data for an empirically-based principle trauma healing program for the larger Islamic community who may not seek mental health care or does not have access to such care. Clinical trial registration number: ClinicalTrials.gov NCT05890482. World health organization trial registration data set information: See Supplemental Appendix 1.

The efficacy of metformin as adjuvant to chemotherapy on IGF levels in non-diabetic female patients with progressive and non-progressive metastatic breast cancer.

OBJECTIVE: Some studies have shown that metformin inhibits the proliferation of breast cancer (BC) cells via multiple ways. One of these mechanisms is through the indirect control of the IGF-route mediated via the activation of the AMPK-LKB1 pathway in the liver, which leads to a decrease in blood glucose and insulin levels. The objective of this study was to investigate the effects of metformin as adjuvant to chemotherapy on IGF levels in female patients with progressive and non-progressive metastatic BC. PATIENTS AND METHODS: In this trial, 107 women receiving chemotherapy for metastatic breast cancer (MBC) were divided into two groups: the metformin group received 500 mg of metformin twice daily, whereas the control group did not receive any metformin. All patients received chemotherapy according to the South Egypt Cancer Institute's (SECI) established regimen. The level of IGF-1 was determined in the blood at the initiation of therapy (baseline) and at six months post treatment. RESULTS: No substantial differences were noted regarding IGF-1 levels in both groups at baseline (IGF-1 average level was 40.74 ± 36.16 vs. 32.06 ± 20.00 in the metformin and the placebo group, respectively, p = 0.462). While after six months, the mean IGF-1 level was 37.62 ± 31.35 vs. 39.12 ± 2 5.93 in the metformin and placebo groups, respectively, (p = 0.170). CONCLUSIONS: Metformin as an adjuvant to chemotherapy in MBC patients had no significant effect on reducing IGF-l levels which promotes the inhibition of the proliferation of BC cells in MBC patients.

Effects of intraduodenal administration of HCl and glucose on circulating immunoreactive secretin and insulin concentrations.

A new radioimmunoassay for secretin was used to investigate (a) serum secretin responses to intraduodenally infused HCl and glucose, (b) the metabolic half-life and the volume of distribution of exogenous secretin and (c) the effect of endogenously released secretin on insulin secretion in 25 anesthetized dogs. Portal and femoral venous blood samples were taken simultaneously before, during, and after intraduodenal infusion of HCl (21 meq/30 min) and glucose (131 ml/30 min). Control experiments were performed with intraduodenal infusion of saline. Mean portal venous immunoreactive secretin concentration of six dogs rose from 313 muU/ml before to 1,060 muU/ml 10 min after initiation of the intestinal acidification (P < 0.005). Femoral venous immunoreactive secretin concentration rose from 220 muU/ml before to 567 muU/ml 15 min after intestinal acidification (P < 0.01). Secretin concentrations remained elevated during the remainder of the infusion. In the same six dogs mean portal venous immunoreactive insulin concentration rose from 38 muU/ml before to 62 muU/ml at the end of the infusion (P < 0.05). Peripheral immunoreactive insulin, glucose, and free fatty acid concentrations, however, did not change significantly. Pancreatic exocrine function was studied in four dogs. The rise in secretin concentration was followed promptly by a highly significant increase in exocrine pancreatic flow rate and bicarbonate secretion, indicating biological activity of the circulating immunoreactive secretin. The effect of intraduodenal infusion of glucose on immunoreactive secretin concentration was studied in 12 dogs. Glucose in concentrations ranging from 2.5% to 10% had no detectable influence on portal or peripheral secretin concentration. Infusion of 50% glucose caused a slight decline in secretin concentration. The metabolic clearance rate, half-life of disappearance, and volume of distribution of exogenous secretin was studied in three dogs by the constant infusion technic. The metabolic clearance rate was 730+/-34 ml/min, volume of distribution was 17.4+/-0.8% of body weight, and the half-life of disappearance was 2.8+/-0.1 min. It could be calculated that 1.38 U/kg-h(-1) of endogenous secretin was released into the peripheral circulation during the steady state period of the HCl infusion experiments. The data indicated that immunoreactive secretin was released rapidly after intestinal acidification, continued to be secreted throughout the duration of HCl infusion, and was promptly distributed in the extracellular compartment. Furthermore, they suggested that endogenously released secretin could stimulate insulin secretion. The HCl-mediated insulinogenic effect of immunoreactive secretin, however, was too weak to influence peripheral immunoreactive insulin, glucose, and free fatty acid concentrations. The failure of intraduodenal glucose to stimulate secretin release suggests that secretin is not the insulin-stimulatory factor released from the gastrointestinal tract in response to glucose.

Cecropins as a marker of Spodoptera frugiperda immunosuppression during entomopathogenic bacterial challenge.

An antimicrobial peptide (AMP) of the cecropin family was isolated by HPLC from plasma of the insect pest, Spodoptera frugiperda. Its molecular mass is 3910.9 Da as determined by mass spectrometry. Thanks to the EST database Spodobase, we were able to describe 13 cDNAs encoding six different cecropins which belong to the sub-families CecA, CecB, CecC and CecD. The purified peptide identified as CecB1 was chemically synthesized (syCecB1). It was shown to be active against Gram-positive and Gram-negative bacteria as well as fungi. Two closely related entomopathogenic bacteria, Xenorhabdus nematophila F1 and Xenorhabdus mauleonii VC01(T) showed different susceptibility to syCecB1. Indeed, X. nematophila was sensitive to syCecB1 whereas X. mauleonii had a minimal inhibitory concentration (MIC) eight times higher. Interestingly, injection of live X. nematophila into insects did not induce the expression of AMPs in hemolymph. This effect was not observed when this bacterium was heat-killed before injection. On the opposite, both live and heat-killed X. mauleonii induced the expression of AMPs in the hemolymph of S. frugiperda. The same phenomenon was observed for another immune-related protein lacking antimicrobial activity. Altogether, our data suggest that Xenorhabdus strains have developed different strategies to supplant the humoral defense mechanisms of S. frugiperda, either by increasing their resistance to AMPs or by preventing their expression during such host-pathogen interaction.

A scanning and transmission electron microscope study of the luminal coating on Dacron prostheses in the canine thoracic aorta.

The sequence of events occurring in a woven Dacron bypass in the canine thoracic aorta was followed from the first exposure to flowing blood for a period of 27 months. After 10 and 40 minutes exposure to flowing blood the surface was covered with masses of leukocytes, platelets, red cells, and some fibrin. By 24 and 48 hours most of the leukocytes had disappeared leaving the two end areas of the bypass covered with a thick film composed of red cells entrapped in a fibrin net. In the central portion of the bypass the Dacron fibers were covered by a rough film of particulate material and widely spaced clumps of platelets and occasional leukocytes connected by a few fibrin strands. AT 6 AND 7 DAYS THE SURFACE COVERING CONSISTED PRIMARILY OF RED CELLS AND FIBRIN. Between 2 and 8 weeks this was replaced by a matrix that was composed mostly of cells resembling fibroblasts or transition forms between these and smooth muscle cells. Some typical smooth muscle cells were observed in grafts 4 months or older. A sheet of flat cells had grown a few millimeters below the anastomoses at 7, 12, and 14 months. By 27 months the entire length of the graft had a patchy covering of endothelium. Only occasional isolated platelets were stuck to the exposed collagen. Thickening of the intraprosthetic lining was associated with infiltration of the cell-fiber matrix by masses of red cells. Thus it appears that under proper conditions of flow, thrombogenic surfaces such as Dacron and collagen are "conditioned" to become nonthrombogenic by the limited deposition of blood elements.