Numbers posted by the National Center for Health Statistics show that more than 34 percent of Americans are obese, compared to 32.7 percent who are overweight. It said just under 6 percent are "extremely" obese.
More than one-third of adults, or over 72 million people, were obese in 2005-2006, the NCHS said in its report
In May, the CDC reported that 32 percent of U.S. children fit the definition of being overweight, 16 percent were obese and 11 percent were extremely obese.
These data demonstrate a high cooperation rate with in-home salivary specimen collection from older adults and good validity of sex hormone measurements
Generation X more obese than baby boomers. There was no difference in physical activity levels. This points only to environment i.e. diet, environmental toxins...
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The opposite effect strikes again: elevated free androgen index is associated with CV risk in perimenopause women across 5 ethnic groups. Low SHBG was associated with increased CVD.
Is our effect on the environment and the environments, in turn, effect on us politics or science? It is science that is manipulated by politicians for political gain/power. In this study of male small/large mouth bass in NE America are found to have significant female characteristics i.e. eggs where testes should exist...where none should exist. The numbers were as high as 85% in the small mouth base compared to 27% for the large mouth bass. Is there any wonder we have a low T epidemic in men? The most likely cause are endocrine disruptors. It is a concern that the authors did not look for endocrine disruptors in the water at the time of this study of the fish.
Usually and mostly we know about three types of pollutions; air pollution, water pollution, and noise pollution. These changes to the planet have already caused much of the disastrous conditions for the future. So, in this article, we will discuss Environmental Issues in Pakistan.
New prospective study of 1023 patients finds that high-insulogenic diet, also know as a traditional American diet, high glycemic, high sugar diet... is associated with an increased risk of cancer recurrence and mortality compared to low insulogenic diet. The authors concluded that this would be beneficial for after surgical resection in people with stage III colon cancer. My question, is why wait on the development of cancer: use a low-insulogenic diet to prevent the cancer all together or when diagnosed implement immediately. Why wait? Treat early! Prevent!
the mortality rate of EOC has not been significantly changed for several decades
Sequencing revealed that almost all tumors (96%) had mutations in TP53, which serves as a major driver of this cancer
Low-prevalence but statistically significant mutations in nine other genes including NF1, BRCA1, BRCA2, RB1, and CDK12 were also identified, but the majority of genes were mutated at low frequency, making it difficult to distinguish between driver and passenger mutations
KPNB1 inhibition via any of three KPNB1 siRNAs or importazole treatment induced apoptosis in human EOC cell lines (Fig. 3 A–F and Fig. S4), and was accompanied by an increase in the expression levels of the proapoptotic proteins BAX and cleaved caspase-3
Stable overexpression of KPNB1 in SKOV3 and OVCAR3 (Fig. S6) significantly accelerated cell proliferation/survival (Fig. 5 A–C), confirming that KPNB1 functions as an oncogene in EOC
KPNB1 overexpression significantly decreased caspase-3/7 activity (Fig. 5D), in addition to the expression levels of cleaved caspase-3 and BAX proteins (Fig. 5E). KPNB1 overexpression also decreased p21 and p27 protein levels (Fig. 5E), as opposed to their increase by KPNB1 inhibition
KPNB1 functions as an antiapoptotic and proproliferative oncogene in EOC.
Patients with higher expression levels of KPNB1 showed earlier recurrence and worse prognosis than those with lower expression levels of KPNB1
KPNB1 acts as an oncogene in human EOC and represents a promising therapeutic target.
ivermectin treatment suppressed cell proliferation/viability in a dose-dependent manner (Fig. 7A), indicating that it exerts an antitumor effect on EOC
ivermectin also induced apoptosis
ivermectin increased the expression levels of BAX, and cleaved PARP, as well as p21 and p27
KPNB1 inhibition is responsible for the antitumor effect of ivermectin
we found that ivermectin synergistically reduced cell proliferation/viability in combination with paclitaxel in human EOC cells
Single treatment of ivermectin or paclitaxel reduced tumor growth in nude mice, but, notably, combination treatment of ivermectin and paclitaxel almost completely suppressed tumor growth
ERBB2, is amplified and overexpressed in many cancers, including breast (31), ovary (31), colon (32), bladder (33), non-small-cell lung (34), and gastric cancer (35), and is a poor prognostic factor in certain cancer types
KPNB1 was the second-highest-ranked gene identified in our screen
Increased KPNB1 protein levels have been reported in several cancers, including cervical cancer (42), hepatocellular carcinoma (43), and glioma (44), suggesting KPNB1’s oncogenic potential in these tumor types
our findings suggest that KPNB1 might serve as a master regulator of cell cycle by regulating several cell cycle-related proteins, including p21, p27, and APC/C family members
higher and/or more-frequent doses of ivermectin than currently approved for humans are well tolerated in humans
none of the mice in this study treated with the effective dosage of ivermectin for in vivo anticancer therapy showed severe adverse event
we found that the combination of ivermectin and paclitaxel produces a stronger antitumor effect on EOC cell lines than either drug alone
Ivermectin found to be pro-apoptotic for the epithelial ovarian cancer oncogene, KPNB1 in in Vivo study. This effective anti-parasitic drug inhibits the KPNB1 oncogene.
use of PET in clinical research, clinical trials, and drug discovery
use of PET/CT in assessing response to therapy
In some cases, such as Hodgkins lymphoma, quantitative PET/CT imaging may not actually be needed, as success can be defined by the complete absence of tracer uptake in the PET image following a course of standardized therapy
The utilization of PET/CT to assess response to therapy is increasing in the US related, in part, to the creation and subsequent favorable results of the National Oncologic PET Registry (NOPR)
Changes in size as a result of therapy may take many months to develop and any opportunity to make early decisions about therapy success or failure is often unduly delayed or lost altogether
measures of changes in metabolic activity via FDG PET/CT can provide an alternate approach to assess response to therapy -- often very early in the course of treatment
Current recommendations are that tumor SUVs should be reported
The true tracer uptake in a patient is composed of two components: the first being the amount of tracer uptake (e.g. FDG) associated with the disease status (the signal of interest), which can be modified by the biophysiological status of the patient. One of the more important patient parameters is the blood glucose level, which has been shown to inversely-linearly affect SUVs
A prospective study by Crippa et al.30 in eight patients showed that as blood glucose levels were increased from 92.4 ±10.2 to 158 ± 13.8 mg/100 ml by glucose loading, the average SUV of 20 liver metastases decreased from 9.4 ± 5.7 to 4.3 ± 8.3
chemotherapy can result in impaired renal function, significantly reducing the clearance of plasma FDG through the kidney and thus increasing tumor SUV relative to an initial PET scan
The second component of the true tracer uptake is biological variability
The biological variability has been estimated in several test-retest studies7,32–35 at approximately 10% for scans repeated within a few days