Journal of Clinical Research

Aim: To measure the change in depth of periodontal pockets after performing local drug delivery with GREEN TEA GEL and comparing it with chlorhexidine gel (Hexidine Gel).

Materials Method: A total of 20 chronic periodontitis patients participated based on the inclusion and exclusion criteria. Complete Scaling and Root Planing (SRP) was performed for all subjects and LDD was done using green tea gel on one site and with hexidine gel on contralateral site. Following parameters including Gingival Index (GI), Clinical Attachment Loss (CAL), and Probing Pocket Depth (PPD) were recorded at baseline and on the 28th day.

Results: During follow up being done on 28th , tooth sites which received green gel showed significantly lower mean scores (GI=1.72, p=0.006,CAL=1.60,p=0.003 and PPD=3.83 mm,) as compared to baseline (GI=2.00, CAL=1.90, and PPD=4.79).

Conclusion: Green tea gel was found be successful in reducing pocket depths and inflammation, after 4 weeks, in chronic periodontitis patients, when been used as an LDD agent as an adjuvant to SRP

Population of cancer stem cells in solid tumors represents a major factor of resistance to conventional therapy that influences patient survival. We recently identify RASSF1A as a novel regulator of cancer stemness that plays a key role in regulation of mechanical properties provided by ECM in lung cancer. We showed that epigenetic loss of RASSF1A promotes YAP1 nuclear accumulation which, via P4HA2 expression, drives ECM remodeling associated with Cancer Stem Cell (CSC) plasticity during malignant carcinogenesis.

Retinitis Pigmentosa (RP) is an incurable disease for which effective treatments are lacking. Mer tyrosine kinase (MERTK) is a causative gene of RP. Royal College of Surgeons rats with a Mertk mutation showed impaired phagocytosis of the photoreceptor outer segment by the Retinal pigment Epithelium (RPE). Using RPE differentiated from induced Pluripotent Stem Cells (iPSC-RPE) of RP patients carrying MERTK mutations, recent studies have shown deterioration of phagocytosis in the iPSC-RPE. This review focused on the function of phagocytosis of iPSC-RPE cells derived from RP patients carrying MERTK mutations and discussed the possibility of developing treatments for this disease using this in vitro disease model.

Triple-Negative Breast Cancer (TNBC) encompasses heterogeneous subtypes. Apocrine-type TNBC, defined as TNBC immunoreactive for both androgen receptor and forkhead-box protein A1, should be distinguished from basal-like TNBC. In apocrine-type TNBC, neoadjuvant chemotherapy (NAC) tends to be ineffective, but with a favorable prognosis despite chemoresistance. We analyzed 51 cases of TNBC in stages I and II. Thirty-four TNBCs treated with NAC were divided into “good responders” (n=22) showing therapeutic effect G2b or G3 in surgical specimens and “poor responders” (n=12) with therapeutic effect G0, G1a, G1b and G2a. NAC was spared in 17 cases (categorized as the non-NAC group). TNBC other than apocrine-type (n=16) and special types (myoepithelial, medullary, adenoid cystic and spindle cell carcinomas, n=6) was categorized as basal-like subtype (n=29). The prognosis was evaluated in each category. NAC showed significant effects against basal-like TNBC with high Ki-67 labeling (≥ 50%), and tumor-infiltrating lymphocytes predicted high chemosensitivity. NAC was ineffective and avoidable in TNBC of apocrine- and special types showing low (<50%) Ki-67 labeling. Ten (59%) lesions in the non-NAC group belonged to the apocrine-type. When clinical complete remission shown by contrast-enhanced magnetic resonance imaging was reached in the course of NAC against basal-like TNBC, the NAC period was shortened (de-escalated) in 14 (64%) of 22 good responders. Disease-free and overall survival was excellent in all groups. The following two hypothetical proposals should be proven by large-scale clinical trials. Immunohistochemical recognition of apocrine-type TNBC with low Ki-67 labeling is important for avoiding ineffective/unnecessary NAC. By employing appropriate clinical imaging, de-escalation of NAC is achievable in basal-like TNBC with high Ki-67 labeling.

Familial Hypercholesterolaemia (FH) is the most common primitive cause of hypercholesterolaemia, affecting 1: 200-250 individuals and characterized by lifelong elevation of lowdensity lipoprotein cholesterol (LDL-C) levels which significantly accelerate atherosclerosis. Early detection and treatment of hypercholesterolaemia in childhood can reduce the impact on the cumulative life-burden of LDL cholesterol. In the last ten years, many screening strategies involving the whole family have been carried out: selective screening, cascade screening, inverse screening, and universal screening. Blood lipid profile evaluation (total cholesterol, LDL-C, HDL-C and triglycerides) is the first step. It has to be ideally performed between 2 and 10 years of age. Hypercholesterolaemia has to be confirmed with a second sample and followed by the detection of family history for premature (before 55 y in men and 60 y in women) or subsequent cardio-vascular events and/or hypercholesterolaemia in 1st and 2nd degree relatives. The management of hypercholesterolaemia in childhood primarily involves healthy lifestyle and a prudent low-fat diet, emphasizing the benefits of the Mediterranean diet. Statins are the cornerstone of the drug therapy approved in USA and in Europe for use in children. Ezetimibe or bile acid sequestrants may be required to attain LDL-C goal in some patients. Early identification of children with severe hypercholesterolaemia or with FH is important to prevent atherosclerosis at the earliest stage of development, when maximum benefit can still be obtained via lifestyle adaptations and therapy.