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Preeclampsia is a serious complication of pregnancy where the mastery of placenta is crucial. The only effective treatment option of preeclampsia remains premature delivery. Now for the first time, scientists John P. Fisher, Che-Ying Kuo and colleagues have bioprinted a 3-D model of placenta tissue that mimics the organ’s complex structure.

In preeclampsia, special cells called trophoblasts that contribute to the fetal side of the placenta and interlace with the mother’s side of the tissue do not migrate normally. Investigation of this condition remains a major challenge. Current lab models of placenta tissue are two-dimensional which makes the study strenuous. The researchers have succeeded in developing a more accurate 3-D bioprinted model of placenta tissue including trophoblasts, epidermal growth factor and other key components. In the 3-D model the growth factor diffused outward through the printed tissue from the center, and the trophoblasts migrated toward it, mimicking cell movement in real tissue.

In addition to using their 3-D model for studying the development of preeclampsia, the researchers say the demonstration of trophoblast migration toward the growth factor shows the usefulness of factors to augment cell migration. The model, reported in the journal ACS Biomaterials Science & Engineering, could lead to a better understanding of preeclampsia and the development of new treatments

A novel insight about the role of gut flora in the development of gastro-intestinal diseases has been unraveled by the research groups of Prof. Jeroen Raes (expert in metagenomics of the gut flora, VIB/KU Leuven) and prof. Severine Vermeire (expert in gastroenterology, KU Leuven/UZ Leuven). Primary sclerosing cholangitis (PSC) is a liver disease with no effective medical treatment.

Thus far liver transplantation is the only proven long-term treatment of PSC. A vast majority of patients with PSC also have inflammatory bowel disease which hinted a role of intestine in the origin of this PSC. When Prof. Jeroen Raes, using massive DNA sequencing, compared the gut bacteria in patients with PSC and in healthy people he could develop a signature to diagnose PSC based on gut bacteria. The first results of this collaborative research are published in the leading scientific journal Gut.

The results are required to be confirmed before they can be used in clinical practice. The findings may serve as the grassroot factor for the development of microbiota-based therapies, such as fecal microbiota transplantation or targeted pre- and probiotics. Both teams are planning to further investigate the complex interactions between the immune system and the intestinal microbiota in PSC patients.

Folate, a B vitamin found naturally in fruits and vegetables and available in vitamin supplements is usually recommended for women who plan to become pregnant to ensure proper neurodevelopment of their babies. On the contrary, a new research from Johns Hopkins suggests too much folate during pregnancy increases the risk of autism spectrum disorder in their offsprings.

The study further elaborates that a new mother with blood levels of 4 times the adequate amount of folate would double the risk of autism in her child. Very high vitamin B12 levels also triple the risk of autism. The study included 1391 mothers at the time of their children’s birth between 1998 and 2013 and followed for several years. The mother’s blood folate levels were checked once within 1-3 days of delivery. One in 10 of the women had an excess amount of folate and 6% had an excess amount of vitamin B12. Majority of the mothers in the study reported having taken multivitamins -which would include folic acid and vitamin B12-throughout pregnancy.

The study’s lead author Ramkripa Raghavan infers from the study the need to figure out the optimal dose of this important nutrient throughout pregnancy.

An investigation performed at John Hopkins University depicts new data on how low-oxygen conditions stimulate breast cancer stem cell progression. The study lead by Gregg Semenza was published in the Proceedings of the National Academy of Sciences. It’s known that poor oxygen environments affect cancer growth, however its vice-versa in case of advanced tumors.

In aggressive cancer, the tumor cells flourish more in low-oxygen state, resist chemotherapy; and cause metastasis, relapse and eventual death. Working on breast cancer cell lines and mice, Semenza observed that breast cancer stem cells proliferate through the same biochemical mechanism as embryonic stem cells. During embryogenesis, healthy stem cells (immature cells) multiply and develop into mature specific cell types. Chemotherapy wipes out 99% of cancer cells missing about 1% cancer stem cells. These cancer stem cells mimic the same mechanism to preserve cancer progression. It is thus crucial to identify such cells and abandon their stem cell state.

According to recent studies, of the 21% oxygen we breathe, 9% resides in healthy human breast tissue while only 1.4% in breast tumors. Low-oxygen conditions trigger production of a family of proteins–HIFs (hypoxia-inducible factors) which turn on various genes including NANOG that instructs cells to become stem cells. In embryonic stem cells, NANOG protein synthesis may be dropped by methylating NANOG’s mRNA and thereby aborting their stem cell state.

In the present study, exposure of human breast cancer cell lines to low-oxygen state induced production of protein ALKBH5 (which removed methyl groups from NANOG mRNAs) and subsequent cancer stem cell proliferation. Even in zero NANOG levels, low-oxygen state prompted HIFs production which turned on genes for NANOG and ALKBH5. Genetic manipulation of cells to spur ALKBH5 levels without low-oxygen exposure also showed similar results, whereas averting ALKBH5 synthesis lowered NANOG levels and number of cancer stem cells.

Experimentation on live mice also produced similar findings concluding that ALKBH5 protein retains cancer stem cells and their tumor-forming skills.

A recent study published in the Neurology demonstrated that rituximab immunotherapy meaningfully improved modified Rankin Scale (mRS) scores in 76.3% of autoimmune limbic encephalitis (ALE) patients whereas 68.8% of them attained a favorable mRS score (0-2), a median of 22.5 months later. Kon Chu and colleagues chose ALE patients who already underwent first-line immunotherapy after symptom onset of a median of 6.8 months (mRS score of 3).

However, symptoms worsened even in 31.3% patients who responded partially to the treatment with mRS score extending to 4, when rituximab was started 12.1 months after symptom onset. The authors found that ALE patients delivered excellent response with mRS score of 2 at the end of a median rituximab treatment cycle of 5 weeks compared to those who did not receive rituximab treatment after first-line immunotherapy. Thus rituximab can be a good choice to treat ALE patients with poor response to first-line immunotherapy since it works efficiently and is well-tolerated regardless of the patient’s autoantibody status.

According to the authors, patients who responded partially to first-line therapy showed greater favorable effects while those receiving and not receiving rituximab, at 88.0% and 83.3%, respectively. In multivariate analysis, the authors found 9.5-fold uplift in mRS improvement associated with partial response to first-line immunotherapy. They believe that first-line immunomodulators and rituximab share some common mechanisms in alleviating autoimmunity. On the other hand, patients who received rituximab after nonresponsive first-line treatment experienced superior outcomes (60%) than those who did not receive rituximab (22.2%).

These findings propelled the authors to propose that rituximab may be considered as a first-line immunotherapy for ALE.