This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Osteochondritis dissecans, or OCD, is a bone disease that wears away joints and the cartilage that covers them. It occurs most often in children and adolescents. While OCD has been documented and studied for nearly 150 years, researchers still don’t know what causes it. Reporting in The American Journal of Sports Medicine, one group offers up new findings that point to at least one factor that surgeons should look out for. The team looked at radiographs of 61 knees of patients undergoing surgery for OCD. Those patients were just over 23 years old on average, and 77% of them were men. The researchers reviewed the radiographs for mechanical alignment, as previous studies have speculated that deformities due to malalignment contribute to OCD. What they found was that patients with OCD did in fact show signs of off-axis effects. Specifically, they observed that the location of OCD lesions correlated with the deviation of the mechanical axis of the leg..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

In this presentation, we will discuss how bacteria are causing disease. Furthermore, we will introduce the student to the term pathogenesis, and in continuation of this present the four main steps, that causes pathogenesis.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Osteoarthritis is the most common form of joint disease, affecting hundreds of millions of people worldwide. One promising therapeutic target is TGF-β signaling. Studies have shown that blocking this signaling pathway can slow the progression of osteoarthritis. The problem is that TGF-β signaling is also critical for repairing the cartilage cells that are degraded in osteoarthritis. To help separate the bad from the good, researchers recently examined the genetic blueprints that control TGF-β signaling. They discovered a key player in circPhf21a, a type of rare genetic material known as circular RNA. Initially believed to be misshapen RNA, circular RNA is being revealed as an important mediator of disease. In the current study, the team found that overexpression of circPhf21a led to the growth of fewer-than-normal cartilage cells in mice. And in mice with osteoarthritis, levels of circPhf21a were found to be significantly increased..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Colorectal cancer is the most common cancer worldwide and among the top 3 causes of cancer-related death in men and women. Despite advances in diagnosing and treating colorectal cancer prognosis remains poor because of persistent mechanisms of tumor proliferation. A new study has zeroed in on one protein that could be behind some of these mechanisms of colorectal cancer spread. JARID1B is a demethylase enzyme encoded by the gene KDM5B and has been implicated in the development of several cancers, including breast, prostate, and liver cancer. Researchers found that JARID1B was significantly upregulated in colorectal cancer tissue versus adjacent normal tissue. In patients with colorectal cancer, high JARID1B expression was associated with poor overall survival. Experiments revealed that JARID1B promoted the spread of colorectal tumor cells through the Wnt/β-catenin signaling pathway. Specifically, by inhibiting the protein CDX2..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Malignant gliomas are the most common and the deadliest type of tumor affecting the central nervous system. Even after surgery, chemotherapy, and radiotherapy, gliomas can still have a poor prognosis. But growing evidence is pointing to one promising target for fighting glioma. Exosomes are tiny sacs of cellular matter implicated in numerous cell processes. including signaling and communication and glioma progression. miRNAs are among the most important glioma-related payloads shuttled between cells by exosomes. In addition to increasing the risk of developing glioma. miRNAs can confer chemotherapy drug resistance from one cell to another or they can even help inhibit glioma tumor growth. Researchers are discovering that exosomal proteins may play similar roles. Understanding how exosomes operate and how they might be manipulated. could help researchers and clinicians deliver more powerful anti-cancer therapies to patients with glioma..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Gastric cancer is one of the highest mortality cancer types, and the leading cause of gastric cancer is persistent Helicobacter pylori infection. H. pylori secretes the enzyme HtrA, which cleaves adhesion proteins like E-cadherin and allows H. pylori to cross the epithelium. Recently, researchers used proteomics to find novel targets of HtrA associated with H. pylori. They confirmed E-cadherin as a target and identified human desmoglein-2 (hDsg2), neuropilin-1, ephrin-B2, and semaphorin-4D as potential targets. hDsg2 is a component of the desmosome junctions, which play important roles in epithelial cell-to-cell adhesion. Given the importance of cell-to-cell adhesion to epithelial health, the researchers focused on hDsg2. In vitro tests confirmed that HtrA secreted by H. pylori, and not other host cell proteases, cleaved hDsg2. This study is the first to demonstrate that HtrA secreted by H. pylori directly breaks down hDsg2 and suggests that HtrA is a ‘master key’ that allows H..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Welcome to the Teachers' Corner of Small Things Considered. In this section, we include the posts we deem most adequate for teaching purposes. We have reorganized them into subject areas geared for a typical microbiology course. To date, this material has been used for various forms of intellectual enrichment, e.g., suggested readings, class presentations, a source of topics for term papers. You can also find here our Talmudic Questions, which we characterize as those whose answers cannot be found in Google. We are told that some of these questions have been used in exams ranging from tests for undergraduate courses to qualifying/prelims for graduate students.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Oncogenic PIM kinases and the tumor suppressor LKB1 regulate cell growth and metabolism in different directions. LKB1 suppresses tumorigenesis largely by phosphorylating and activating the energy sensing kinase AMPK. Anti-oncogenic PIM inhibitors also increase AMPK phosphorylation. However, the exact mechanism by which PIM inhibition affects AMPK remains unclear. A recent study explored the potential PIM-LKB1 interaction related to AMPK phosphorylation in prostate (PC3) and breast (MCF7) cancer cells. Inhibition of activity (by DHPCC9 or AZD1208) or expression (by triple knockout, TKO) of all three PIM kinases increases AMPK phosphorylation. These effects are LKB1-dependent, suggesting that PIM kinases regulate AMPK via LKB1. Additional assays confirmed that PIM kinases phosphorylate LKB1 to inactivate it, identifying LKB1 as a novel PIM substrate. In a chick embryo xenograft model, LKB1 knockout increased tumorigenic growth of prostate cancer cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The human protein Tid-1 sits at the nexus of many key cellular processes and signaling pathways. These processes include cellular proliferation, growth, survival, aging, apoptosis, and even movement. Tid-1 is a member of the heat shock protein 40 family and helps other proteins fold correctly after translation or refold after a damaging stress event. Dysregulated Tid-1 behavior is involved in numerous human diseases including cancers, cardiomyopathies, and neurodegenerative disorders. Given its wide influence within the cell, Tid-1 could be a key biomarker or even therapeutic target for these diseases, but to leverage Tid-1 effectively, researchers need to understand its functionality in detail. To this end, a team of scientists consolidated the current research on human Tid-1. They found that Tid-1’s protein-protein interactions corresponded to its roles in various diseases and provide insight into how Tid-1 affects pathogenic developments..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The transcription factor CREB plays an important role in the development of pulmonary hypertension (PH). However, both increased and decreased CREB expression have been proposed to mediate the proliferation of pulmonary artery smooth muscle cells (PASMCs). Additionally, the regulatory signaling of CREB activation in PASMCs proliferation has not been well characterized in PH. Researchers recently used various in vitro techniques to clarify CREB’s role. CRE-containing genes were upregulated in PH PASMCs, and total and phosphorylated CREB protein levels were elevated in PASMCs from rats with monocrotaline (MCT)-induced PH. Prolonged upregulation of serum-induced CREB phosphorylation was also observed in hypoxia-pretreated PASMCs. These results may have been due to activation of multiple protein kinases and downregulation of numerous phosphatases targeting CREB..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"While best known for its role in the brain, serotonin does more in our body than influence mood. There is even growing evidence that it is involved in tumor development. However, little is known about its role in colorectal cancer. In a recent study, researchers found that serotonin promotes colon cancer cell growth in cell culture and animal models. Further tests revealed that serotonin is moved into colorectal cancer cells via its transporter SERT and that once the serotonin is inside the cancer cells, the enzyme TG2 links serotonin to the protein RhoA, activating it. Through down-stream signaling mediators, activated RhoA increases expression of the known cancer-promoting protein YAP. Blocking SERT from transporting serotonin with citalopram reversed the serotonin-induced YAP expression and cell proliferation increases and blocked serotonin’s effects on tumor formation in mice..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cholangiocarcinoma (CCA) is an aggressive form of cancer that forms in the biliary tract. CCA has high mortality and high rates of recurrence. While early diagnosis is critical, the molecular mechanisms by which CCA forms are poorly understood. A new study reports key interactions between three proteins during CCA development: TLR3, a mediator of both innate and adaptive immune responses and a promising target for anti-cancer therapy; IAP proteins that regulate apoptosis and orchestrate cancer cell death; and RIPK1, a multifunctional protein that regulates inflammation and cell death through apoptosis and necroptosis.TLR3 expression was found to be significantly higher in primary CCA tissue than in adjacent normal tissue. Meanwhile, Smac mimetic, an IAPs antagonist, sensitized CCA cell lines to TLR3 ligand, Poly(I:C)-induced apoptosis. This mode of cell death was switched to necroptosis in CCA cells expressing RIPK1, RIPK3, and MLKL..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Mutations in the gene tp53 are often detected in the early stages of colitis-associated colorectal cancer (CAC). The development of CAC is facilitated by gut microbiota disruption (dysbiosis) and chronic intestinal inflammation, but whether tp53 mutations are linked to this dysbiosis and inflammation remains unclear. To learn more, a recent study examined zebrafish larvae with a tp53 mutation. The mutant fish exhibited intestinal inflammation that was due to gut microbiota disruption. confirming the link between tp53 and these pathological changes. Overall, gut microbiome diversity was decreased, while pathogenic Aeromonas bacteria were abnormally abundant, aggressively colonizing the gut. Further investigation revealed that the gut dysbiosis in the mutants induced inflammation by disrupting sialic acid metabolism. Supporting this finding, inhibition of the sialic acid-releasing enzyme sialidase alleviated the pathologies in mutant zebrafish larvae..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.