Effect of alcohol on liver health

Effect of Alcohol on Liver Health Alcohol has a significant impact on liver health. The liver has a fairly important role in the body, which regulates the metabolism of sugar, detoxifies the body, and helps relieve infection.

Also Read: Why Alcohol Reduces Chances of Pregnancy

If there is damage, the liver or liver can regenerate itself. Even so, an unhealthy lifestyle such as consuming alcoholic beverages interferes with this regeneration ability. If not treated immediately, the liver will suffer serious damage. One of the liver diseases caused by alcohol consumption is alcoholic fatty liver.

When it enters the body, alcohol travels to the bloodstream to the liver so as not to cause serious harm to other organs in the body. When digesting this alcohol, some of the liver cells are damaged and die. If you constantly consume alcohol, the liver can no longer do its job, in this case, it is digesting fat. As a result, fat will accumulate and there will be fatty liver.

The study, uploaded in the US National Library of Medicine, National Institutes of Health, states that the maximum limit of alcohol consumption associated with fatty liver disease in men is more than 80 grams and 40 grams for women per day.

If this habit is not stopped, the stage of fatty liver disease will increase to alcoholic hepatitis and cirrhosis as the most acute stage of alcohol-induced liver dysfunction.

Symptoms that arise in the body affected by fatty liver include swelling in the legs and abdomen, drastic weight loss, yellowing of the eyes and skin, chills fever, and vomiting of blood. In the chronic stage, the person experiences a coma and leads to death. This is why you are not allowed to consume excessive amounts of alcohol.

Recommendations on breast cancer population screening

 Recommendations on population screening

Population mammography screening recommendations (for women with average risk)  differ between countries and agencies, reflecting persistent non-consensus on the  magnitude of benefit (mortality reduction) and harms (in particular, the extent of  overdiagnosis), and how these outcomes balance out overall and in specific age groups.  

This is exemplified in selected recommendations:

• The US Preventive Services Task Force recommends screening every 2 years for women aged 50–74 years, and emphasizes individualized decisions for those aged 40–49 years that take account of the woman’s values

• Canadian guidelines support shared decisions, do not recommend screening for women aged 40–49 years and recommend screening every 2–3 years for women aged 50–69 years

• The American Cancer Society recommends annual screening for women aged 40–54 years, and a transition to 2-yearly screening for those aged ≥55 years (with the opportunity to continue annual screening)

• The International Agency for Research on Cancer reports that there is sufficient evidence that screening confers benefit in women aged 50–74 years (but limited evidence in the 40–49 years age group) and that there is sufficient evidence that mammography detects breast cancers that would never have been diagnosed or would never have caused harm if women had not been screened (overdiagnosis)

• European recommendations specify mammography through organized screening  programmes every 2–3 years in women aged 45–74 years (and suggest against annual screening)

Women at average risk do not have a pre-existing breast cancer or a previous diagnosis of a high-risk breast lesion (such as atypical ductal hyperplasia), and do not harbour arisk-enhancing genetic mutation (such as BRCA1 or BRCA2 mutations or other familial breast cancer syndromes).

Trple-negative breast cancer molecular classification

Triple-negative breast cancer molecular classification, Gene expression assays have identified six different triple-negative breast cancer (TNBC) molecular subtypes (Lehman’s classification).

These are

• basal-like 1 (BL1), 
• basal-like 2 (BL2), 
• mesenchymal-like (M),
• mesenchymal/stem-like (MSL),
• immunomodulatory (IM),
• and luminal androgen receptor (LAR).

BL1 has a high TP53 mutation rate (92%), alterations in genes involved in DNA repair mechanisms (such as BRCA1, BRCA2, TP53 and RB1) and a cell-cycle gene signature.

BL2 has cell-cycle gene signatures, overexpression of growth factor signalling genes and overexpression of myoepithelial differentiation genes.

M and MSL subtypes are enriched for genes encoding regulators of cell motility, invasion and mesenchymal differentiation, but the MSL subtype is uniquely enriched for the genes that encode regulators of epithelial–mesenchymal transition and stemness.

The Claudin-low subtype from the intrinsic classification is mostly composed of the M and MSL subtypes312. MSL also shares numerous genes involved in the regulation of immune response with the IM subtype.

Finally, LAR is characterized by a higher mutational burden with overexpression of genes coding for mammary luminal differentiation, overexpression of the regulators of the androgen receptor (AR) signalling pathway and increased mutations in PI3KCA (55%), AKT1 (13%) and CDH1 (13%) genes.

This classification has been refined into four groups: 

1. BL1 (immunoactivated),
2. BL2 (immunosuppressed),
3. M (including most of the MSL),
4. and LAR, with implications for response to neoadjuvant chemotherapy.

Combining RNA and DNA profiling analyses, a similar classification of TNBC has been reported (Burstein’s classification), divided into four distinct subtypes.

These subtypes are: 

• LAR,
• mesenchymal (MES),
• basal-like immunosuppressed (BLIS),
• and basal-like immune-activated (BLIA).

Each subtype has specific therapeutic targets (for example, the LAR subtype can be targeted via the AR and the cell surface protein mucin) and different prognosis (for example, the BLIA subtype is associated with better prognosis than BLIS). Despite these multiple efforts, there is no established diagnostic assay yet for the classification of TNBC in routine practice.

Breast cancer diagnostic work-ip

Women experiencing breast symptoms or breast changes, such as a lump, localized pain, nipple symptoms or skin changes, require appropriate diagnostic evaluation, as do women who are recalled for further testing because of positive screening mammography.

Diagnosing breast cancer is based on a triple test comprising clinical examination, imaging (usually mammography and/or ultrasonography) and needle biopsy. Assessment entails performing the appropriate elements of the triple test, factoring in the patients’ characteristics and presentation, and should be performed before beginning treatment.

Appropriate assessment helps to accurately discriminate between those who have breast cancer and those who have benign conditions (such as fibroadenoma) or normal breast changes and can be reassured or safely managed with follow-up, obviating the need for surgical intervention.

Ultrasonography is almost universally used to assess localized symptoms, as an initial imaging modality in young women, to identify and characterize screen- detected abnormalities and, preferentially, for imaging- guided percutaneous biopsy. Breast ultrasonography may also be used to characterize and biopsy axillary lymph nodes in women suspected of having breast cancer.

Imaging evaluation also includes MRI for specific clinical indications, such as in women for whom conventional imaging tests have been equivocal, inconclusive or discordant, for evaluating women with breast implants and for evaluating women with axillary nodal metastases but no detectable (occult) breast tumour.

Preoperative MRI is also selectively used for staging newly diagnosed disease, but this is a debated practice given the limited evidence on whether it enhances a patient’s clinical outcomes. However, MRI is advised for preoperative assessment of newly diagnosed invasive lobular cancers.

Target of acquired immunity in trichomoniasis vaginalis

Targets of Acquired Immunity in trichomoniasis vaginalis. The presence of parasite-specific immunoglobulin G and immunoglobulin A responses also indicates priming of helper Trichomoniasis cells, although the relevant antigens are largely unknown, as are the exact effects of antibodies on the parasites. One obvious target of protective antibody could be the ahesin molecules used by the parasite to facilitate close contact to host cells, a process previously shown to lead to efficient host cell destruction.

The molecular basis of adhesion of Trichomoniasis vaginalis has been investigated, and four antigenic surface molecules have also been implicated in the adhesion of Trichomoniasis vaginalis to vaginal epithelial cells; their expression is being upregulated during attachment to host cells.

Antibodies to these molecules protected target cells from parasite-mediated cytotoxicity, suggesting that antiadhesion immune responses could be important in in vivo protection against the pathogenic effects of Trichomoniasis vaginalis. However, our current understanding of immunity to Trichomoniasis vaginalis remains unsatisfactory, and it is not clear whether acquired immune responses are required for protection and, if so, what role is played by acquired immunity in containing or eliminating infections.

Although there is some evidence that protection may be achieved by immunization of laboratory animals, strong protective immunity does not seem to follow natural infection in humans. A recent study of patients infected with Trichomoniasis vaginalis and HIV indicated no evidence of increased levels or longevity of parasite infection in these patients compared to those in patients infected with Trichomoniasis vaginalis but not HIV.

These observations may indicate that innate immunity involving chemotaxis and subsequent influx of neutrophils is much more important than acquired immunity in controlling infections with Trichomoniasis vaginalis, since neutrophils are often the most numerous leukocytes present in response to infection .

The Right Way to Provide Supplements for Children

 The Right Way to Provide Supplements for Children

A health expert named dr. Belilovsky said that dependence on vitamins or supplements can have a negative impact on children's health, because they are unable to replace the role of carbohydrates, protein, or fat as the main source of nutrition for the body.

Therefore, parents need to know how to provide tips and how to provide supplements for children, so that they do not cause negative side effects for their bodies. Check out the complete tips below.

Be careful when choosing supplements for children

Although vitamins and supplements are good for body immunity, parents must also be careful in choosing them. Do not provide supplements that can be consumed by all ages for children. We recommend that you give supplements that are specifically for children according to their age.

Give Supplements to Children According to Their Needs

The impact of children's supplements on the body will appear when children take supplements that they don't need. Therefore, give children vitamins according to their needs, such as vitamin C to increase endurance, or vitamin A when the child has vision problems.

Give Supplements at Low Doses to Children

Apart from being in accordance with the needs, parents should provide supplements for children with low doses. This is because fat-soluble vitamins will accumulate in the body's tissues if given in excessive amounts.

Careful in Viewing Supplement Composition

Make sure to provide supplements for children with the right composition and dosage. Also pay attention to storage methods and usage warnings on the packaging label to prevent negative impacts on children.

Genetic predisposition in breast cancer

 

Genetic predisposition; Approximately 10% of breast cancers are inherited and associated with a family history, although this varies frequently by ethnicity and across countries in the context of early-onset, bilateral and/or TNBC. Individuals with a first-degree relative who had breast cancer have an elevated relative risk (RR) of 3 of early-onset breast cancer (before 35 years of age).

However, a family history of breast cancer is associated with an ‘erratic’ individual risk of breast cancer composed of different variables, including the size of the family and environmental factors. To determine the family’s risk, models such as the family history score have been developed.

Mutations in two high-penetrance tumour suppressor genes, BRCA1 and BRCA2, whose proteins are involved in DNA repair through homologous repair, show an autosomal-dominant inheritance pattern (loss of function>missense). BRCA1 and BRCA2 mutations are associated with an average cumulative risk of developing breast cancer by the age of 80 years of 72% and 69%, respectively; the relative risk of breast cancer in men harbouring BRCA2 mutations is 6%.

More than 2,000 BRCA gene alterations have been described (mutations and large rearrangements), but only few have been found repeatedly in unrelated families, for example, founder mutations in Ashkenazi Jewish families (BRCA1 185delAG or BRCA2 6174delT) or Icelandic families (BRCA2 999del5).

The prevalence of BRCA1 and BRCA2 mutations varies between ethnic groups, being lower in the Asian group (0.5%) and higher in the Ashkenazi group (10.2%) in a US nationwide study. Germline BRCA testing will now be performed as a companion diagnostic in patients with metastatic breast cancer given the availability of poly(ADPribose) polymerase (PARP) inhibitors, which prolong progression-free survival (PFS) and improve quality of life, as a targeted therapy for BRCA mutation carriers in HER2-negative metastatic breast cancer.

Several syndromes related to germline mutations of genes involved in DNA repair and maintaining genomic integrity have been shown to be linked to, to a lesser degree, the inherited breast cancer risk. Next-generation sequencing has enabled panels of genes to be screened — beyond BRCA1 and BRCA2 — to determine the inherited breast cancer risk, and include ATM, CHEK2, PALB2, PTEN, STK11 and TP53.