Testosterone
Androgens
Prostate
Dihydrotestosterone
Seminal Vesicles
Receptors, Androgen
Cyproterone
Testis
Animal Welfare
Gonadotropin-Releasing Hormone
Epididymis
Neoplasms, Hormone-Dependent
Butorphanol
Estradiol
Haptoglobins
Drug Implants
Anesthesia, Local
Ketoprofen
Luteinizing Hormone
Androgen Receptor Antagonists
Xylazine
Gonadal Steroid Hormones
Leuprolide
Testosterone Propionate
5-alpha Reductase Inhibitors
Hydrocortisone
Trematoda
Azasteroids
Sex Characteristics
Prostate-Specific Antigen
Harderian Gland
Finasteride
Random Allocation
Lidocaine
Rats, Inbred Strains
Follicle Stimulating Hormone
Diagnostic Techniques, Radioisotope
Cattle
Feminization
Animal Husbandry
Gonadotropins, Pituitary
Pituitary Hormone-Releasing Hormones
Androgen-Binding Protein
Antineoplastic Agents, Hormonal
Penis
Cyproterone Acetate
Hormones
RNA, Messenger
Rats, Sprague-Dawley
Buserelin
Genitalia, Male
Pituitary Gland
Estrogens
Clusterin
Swine
Nitriles
Androstane-3,17-diol
Diethylstilbestrol
Goserelin
Penile Erection
Anesthetics, Combined
Androstenols
Pituitary Gland, Anterior
Body Weight
Sex Factors
Prostatic Neoplasms, Castration-Resistant
Prostatic Secretory Proteins
Neoplasm Transplantation
Veterinary Medicine
Guaifenesin
Rats, Wistar
Aging
Nuclease Protection Assays
Apoptosis
Acute-Phase Proteins
3-Oxo-5-alpha-Steroid 4-Dehydrogenase
Hypothalamus, Anterior
Cryptorchidism
Anesthetics, Local
Cattle Diseases
Hypothalamus
Immunohistochemistry
Steroids
Mice, Nude
Urogenital System
Sheep
Vas Deferens
Xenograft Model Antitumor Assays
Triptorelin Pamoate
Prolactin
Anti-Inflammatory Agents, Non-Steroidal
Gene Expression Regulation, Neoplastic
Meat
Combined Modality Therapy
Prostatic Hyperplasia
Radioimmunoassay
Hypophysectomy
Disease Progression
Sex Differentiation
Atrophy
Androgen-Insensitivity Syndrome
Neoplasm Metastasis
Epithelium
Sus scrofa
Blotting, Western
Pain
Biomphalaria
Spermatogenesis
Cell Division
Benz(a)Anthracenes
Aromatase
Mice, SCID
Ovary
Androstenedione
Secretory Rate
Cooperative therapeutic effects of androgen ablation and adenovirus-mediated herpes simplex virus thymidine kinase gene and ganciclovir therapy in experimental prostate cancer. (1/1479)
Adenovirus-mediated transduction of the herpes simplex thymidine kinase gene (HSV-tk) in conjunction with ganciclovir (GCV) has been shown to result in significant growth suppression and to enhance survival in a model of mouse prostate cancer. However, this therapeutic activity is not sustained, because in most cases tumors eventually regrow and ultimately cause the death of the host. Androgen ablation, an inducer of apoptosis in prostate cells which is used widely as palliative therapy in patients with prostate cancer, was combined with HSV-tk plus GCV using an androgen-sensitive mouse prostate cancer cell line. The combination of castration and HSV-tk plus GCV led to markedly enhanced tumor growth suppression in both subcutaneous and orthotopic models compared with either treatment alone and resulted in an enhanced survival in which combination-treated animals lived twice as long as controls in the subcutaneous model and over 50% longer than controls in the orthotopic model. Further analysis of apoptotic activity demonstrated high levels of apoptosis only in combined androgen ablation and HSV-tk plus GCV-treated tumors after 14 days of growth in an androgen-depleted environment and 8 days after HSV-tk plus GCV therapy. At this time, the apoptotic index, but not the percent of necrotic tissue, was significantly higher for combination therapy-treated tumors relative to control-treated tumors or either treatment alone. These data indicate that the therapeutic effects of androgen ablation and HSV-tk plus GCV are cooperative and that increased apoptosis may, in part, underlie these activities. (+info)The relationship between adrogen receptors and the hormonally controlled responses of rat ventral prostate. (2/1479)
1. The administration of dihydrotestosterone to rats orchidectomized 7 days previously stimulated the synthesis of nuclear receptor in prostatic cells several hours in advance of DNA synthesis and mitosis. 2. The synthesis of nuclear receptor is tightly coupled to cell proliferation; consequently, in resting cells, there is no further net synthesis of nuclear receptor above the maximum of approx. 8000 molecules/cell. 3. After orchidectomy a rapid decline in the concentration of free androgen in the nuceus and a slower decline in the concentration of nuclear receptor are observed. 4. Owing to the apparent scarcity of receptor-inactivating factors in the nucleus, and the inverse relationship between amounts of nuclear and cytoplasmic receptors, it is concluded that the nuclear receptor is discharged into the cytoplasm after orchidectomy. 5. The formation of the cytoplasmic receptor is an early event preceding the onset of cellular autolysis. 6. Regressing prostate develops the capacity to eliminate cytoplasmic receptor, and this capacity is retained by the regenerating prostate for at least 14 days. 7. The synthesis of nuclear receptor in early G1 phase may control the entry of cells into the cell cycle and the prolonged retention of receptor in the nucleus may prevent the activation of autophagic processes. (+info)Testosterone control of nucleic acid content and proliferation of epithelium and stroma in rat seminal vesicles. (3/1479)
Tissue wet weight, nucleic acid content and epithelial and stromal cell numbers were measured in the seminal vesicles of sexually mature male rats. After castration, tissue weight and RNA decreased rapidly and in aprallel to reach, after 14 days, values only 15-20% of those in control (not castrated) animals. During this period, DNA decreased to a much lesser extent (by about 40%), but this change in DNA correlates well with the observed loss of cells from the epithelium. Testosterone in vivo promoted an immediate resynthesis of RNA, the value characteristic of control animals being reached within 80h. Delays occurred in the hormone-induced regain of tissue weight (30h) and DNA (40h), each of which preceded proliferation of the epithelium (40--50h). The cells of the stroma were unaffected by these changes in the androgenic statls of the animal. It is suggested that these proliferative changes in the epithelium cannot account for the previously reported induction by testosterone of basic secretory proteins in this tissue. (+info)Kinetic analysis of hormone-induced mitoses in epithelial cells of mouse uterus and vagina. (4/1479)
The intracellular localization of 3H-estradiol-17beta and 3H-progesterone to the different types of cells in the mouse uterus was investigated using autoradiographic techniques. The kinetics of cell proliferation in the surface epithelium of the uterus and in the vaginal epithelium (basal layer) are analysed by means of cumulative labeling method and mitosis chase method using 3H-thymidine autoradiographic procedures. The results are as follows, (1) Epithelial cell population of the uterine lumen and basal cell population of the vaginal epithelium in the ovariectomized mouse are divided into a major subpopulation of GO cells and a minor subpopulation of proliferating cells. (2) Proliferative potencies of uterine surface epithelial cells and vaginal basal cells in the ovariectomized mouse are regulated by a steroid-independent mechanisms through which the proportion of the GO cell-compartment and Tc value of the proliferating cell-compartment are determined according to their age; as the castrated mouse grows older, Tc value becomes longer and the proportion of the Go cell-compartment becomes larger. (3) If the dose levels of estrogen administered exceed the threshold value, estrogen-dependent cell proliferation will be provoked by transferring the cells in the GO cell-compartment to the proliferating cell-compartment in all or none fashion, and by reducing the Tc value of proliferating cell to 1/2-1/3 of that in the castrated mouse. (4) It is suggested that proliferating cells in the uterine surface epithelium and in the vaginal epithelium turn the cell cycle at a constant Tc value during estrous cycle, and that the tissue growth during estrous cycle is dependent on the size of the proliferating cell-compartment but not on the Tc value. (5) The results obtained from autoradiography of tritiated steroids in the mouse uterus gave a supporting clue to the kinetic data. (+info)An elevated bax/bcl-2 ratio corresponds with the onset of prostate epithelial cell apoptosis. (5/1479)
The prostate gland in adult male rats is highly dependent on androgenic steroids. Castration initiates the regression of this tissue through a process involving the loss of the vast majority of cells by means of apoptosis. We studied this well characterized in vivo model of apoptosis to evaluate how the expression of two particular gene products, bcl-2 and bax, known to be important for the regulation of apoptosis were affected by castration. An RNase protection assay designed to quantify the levels of bax mRNA showed that this transcript was transiently elevated after castration, reaching a peak in expression at 3 days and declining thereafter. In contrast, bcl-2 mRNA expression was continuously elevated over a period of up to 7 days after castration. The distinct changes in the expression of the mRNAs encoding these two genes were confirmed by an in situ hybridization analysis of regressing rat ventral prostate tissues. The elevation in mRNAs were apparently restricted to the secretory epithelial cells of the gland, the cellular compartment of the tissue most affected by castration. Finally, SDS - PAGE/Western blot analysis of bax and bcl-2 protein expression in the regressing rat prostate gland with bax and bcl-2-specific antibodies showed that the changes in the bax and bcl-2 protein levels were similar and consistent to that found for the mRNAs. In summary, the expression of both bax and bcl-2 gene products are uniquely modulated during castration-induced regression of the rat ventral prostate gland. The changes we observed identify a transient but marked increase in the bax/bcl-2 expression ratio of the tissue that peaks on the second and third days after castration, coinciding with the peak periods of prostate cell apoptosis. These data support previous studies done on in vitro systems wherein it was shown that the bax/bcl-2 ratio determines the apoptotic potential of a cell. (+info)Occurrence of permanent changes in vaginal and uterine epithelia in mice treated neonatally with progestin, estrogen and aromatizable or non-aromatizable androgens. (6/1479)
Female mice of the C57 Black/Tw strain were injected daily with 100 microng testosterone, 50 microng testosterone propionate (TP), 100 microng 5 alpha-dihydrotestosterone (DHT) or 50 microng 5 alpha-dihydrotestosterone propionate (DHTP), for 10 days from the day of birth. Two other groups of female mice were given neonatal injections with 20 microng estradiol-17 beta and 100 microng progesterone for 10 days, respectively. All mice were ovariectomized at 60 days of age and killed at 90 days. In 100% of neonatally estrogenized or androgenized, ovariectomized mice, the cranial part of the vagina was lined with stratified epithelium with either cornification or parakeratosis or mucification. Stratification only or stratification with superficial squamous metaplasia or cornification took place in the uterine epithelia of 18% of the TP-treated, 75% of the DHT-treated and 50% of the DHTP-treated, ovariectomized mice. In contrast, neonatally estrogenized, ovariectomized mice did not show the estrogen-independent, persistent uterine changes. Neonatal progesterone treatment failed to induce the permanent changes in the vaginal and uterine epithelia. (+info)Development of the vaginal epithelium showing estrogen-independent proliferation and cornification in neonatally androgenized mice. (7/1479)
Female mice of the C57 Black/Tw strain given 5 daily injections with 100 microng testosterone (T) or 5 alpha-dihydrotestosterone (DHT) from the day of birth showed estrogen-independent persistent proliferation and cornification of the vaginal epithelium in adulthood. The vaginal epithelium of the mice was essentially similar to that of the controls in histological structure during or shortly after neonatal injections of the androgens. In T- and DHT-mice aged over 20 days, however, a marked proliferation with or without superficial cornification took place in the epithelium lining the proximal and middle parts of the vagina (Mullerian vagina), while neither proliferation nor cornification occurred in the epithelium of the distal vagina (urogenital sinus vagina). On the second day of postnatal life in mice given a single injection with T on the day of birth, the mitotic activity in the epithelium of the middle vagina was heightened, but it dropped to the control level on the third day and remained low until 20 days. By contrast, the mitotic rates in the epithelium of the rest of the vagina in T-mice and of all parts of the vagina in DHT-mice were approximately the same as in the controls until 20 or 30 days. The mitotic rates in the epithelium of the Mullerian vagina were markedly elevated in T-mice at 20 days of age and DHT-mice at 30 days, and thereafter remained almost unchanged until 60 days of age. These results were different from the findings in mice given neonatal injections with the dose of estradiol-17 beta (E) capable of estrogen-independent vaginal cornification (Iguchi et al., 1976). The present finding seem to indicate that the mechanism involved in the induction of estrogen-independent vaginal changes by neonatal administration of androgen (T, DHT) is different from that following neonatal treatment with estrogen (E), although androgen and estrogen act directly on the vaginal epithelium of neonates. (+info)Ultrastructural characteristics of the vaginal epithelium of neonatally estrogenized mice in response to subsequent estrogen treatment. (8/1479)
Adult mice which had received 10 daily injections of 20 microng estradiol beginning with the day of birth were in a "persistent-estrous" state, showing ovary-independent proliferation and cornification of the vaginal epithelium. Ultrastructural changes of the vaginal epithelium in neonatally estrogenized mice was examined after a single postpuberal injection of 10 microng estradiol and compared with those seen in normal mice to estrogen. In ovariectomized normal mice, the basal cells were round. The nucleus was polygonal and contained peripheral condensed chromatin. After estradiol treatment, the basal cells became columnar. The nucleus was round to oval, containing dispersed chromatin. In neonatally estrogenized ovariectomized mice, the basal layer of vaginal epithelium consisted of round cells with polygonal nuclei, much as in normal ovariectomized mice. The nucleus occupied a large area of the cytoplasm and contained prominent nucleoli. Intercellular spaces were moderately distended. Late estradiol treatment resulted in distended intercellular spaces and in the appearance of the other cell type along with round cells in the basal layers: the columnar cells containing an oval nucleus with dispersed chromatin, resembled the basal cells in normal ovariectomized mice receiving postpuberal estrogen injection. The intercellular spaces between the columnar cells were narrow compared with those between round cells. However, the nuclei of round cells still had prominent nucleoli and peripheral condensed chromatin regardless of subsequent estrogen treatment. This fact suggests that these nuclei do not respond to estrogen. These results clearly show that the vaginal epithelium of neonatally estrogenized mice with ovary-independent persistent cornification consists of a mixed population of cells. (+info)Examples of hormone-dependent neoplasms include:
1. Breast cancer: Many breast cancers are estrogen receptor-positive (ER+), meaning that they grow in response to estrogen. These cancers can be treated with selective estrogen receptor modulators (SERMs) or aromatase inhibitors, which block the effects of estrogen on cancer growth.
2. Prostate cancer: Some prostate cancers are androgen-dependent, meaning that they grow in response to androgens such as testosterone. These cancers can be treated with androgen deprivation therapy (ADT), which reduces the levels of androgens in the body to slow or stop cancer growth.
3. Uterine cancer: Some uterine cancers are estrogen-dependent, meaning that they grow in response to estrogen. These cancers can be treated with hormone therapy to reduce estrogen levels.
Hormone-dependent neoplasms are often characterized by the presence of hormone receptors on the surface of the cancer cells. These receptors can bind to specific hormones and trigger signals that promote cancer growth and progression. Targeting these hormone receptors with hormone therapy can be an effective way to slow or stop the growth of these cancers.
In the medical field, the term is often used to describe various conditions that affect gender development or sexual differentiation in individuals with variations in sex chromosomes, hormones, or genitalia. Feminization can occur in individuals assigned male at birth but who exhibit female physical characteristics, such as those with congenital adrenal hyperplasia (CAH) or other intersex traits.
The term is also used to describe the effects of estrogen on the male body, particularly during puberty. For example, boys taking estrogen medication for hormone therapy may experience feminization of their physical features, such as breast tissue growth and a softer voice.
It's important to note that the term feminization is sometimes used in medical contexts to describe a process or outcome that is perceived as negative or undesirable, particularly when it comes to gender identity or expression. However, it's essential to recognize that all individuals, regardless of their gender identity or expression, deserve respect and support in their healthcare needs.
In summary, feminization within the medical field refers to a process or condition whereby male characteristics are acquired by an individual or group, often as a result of hormonal or genetic factors. The term is used to describe various conditions affecting gender development or sexual differentiation and the effects of estrogen on the male body. However, it's important to recognize that the term can be perceived as negative, and healthcare providers should approach patients with respect and sensitivity regardless of their gender identity or expression.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
Synonyms: Castration-resistant prostatic neoplasm, Hormone-refractory prostate cancer, Androgen-independent prostate cancer
Example sentence: "The patient's prostate cancer had progressed to castration-resistant prostatic neoplasms, and he was experiencing severe bone pain despite undergoing multiple treatments."
There are several different types of weight gain, including:
1. Clinical obesity: This is defined as a BMI of 30 or higher, and is typically associated with a range of serious health problems, such as heart disease, type 2 diabetes, and certain types of cancer.
2. Central obesity: This refers to excess fat around the waistline, which can increase the risk of health problems such as heart disease and type 2 diabetes.
3. Muscle gain: This occurs when an individual gains weight due to an increase in muscle mass, rather than fat. This type of weight gain is generally considered healthy and can improve overall fitness and athletic performance.
4. Fat gain: This occurs when an individual gains weight due to an increase in body fat, rather than muscle or bone density. Fat gain can increase the risk of health problems such as heart disease and type 2 diabetes.
Weight gain can be measured using a variety of methods, including:
1. Body mass index (BMI): This is a widely used measure of weight gain that compares an individual's weight to their height. A BMI of 18.5-24.9 is considered normal, while a BMI of 25-29.9 is considered overweight, and a BMI of 30 or higher is considered obese.
2. Waist circumference: This measures the distance around an individual's waistline and can be used to assess central obesity.
3. Skinfold measurements: These involve measuring the thickness of fat at specific points on the body, such as the abdomen or thighs.
4. Dual-energy X-ray absorptiometry (DXA): This is a non-invasive test that uses X-rays to measure bone density and body composition.
5. Bioelectrical impedance analysis (BIA): This is a non-invasive test that uses electrical impulses to measure body fat percentage and other physiological parameters.
Causes of weight gain:
1. Poor diet: Consuming high amounts of processed foods, sugar, and saturated fats can lead to weight gain.
2. Lack of physical activity: Engaging in regular exercise can help burn calories and maintain a healthy weight.
3. Genetics: An individual's genetic makeup can affect their metabolism and body composition, making them more prone to weight gain.
4. Hormonal imbalances: Imbalances in hormones such as insulin, thyroid, and cortisol can contribute to weight gain.
5. Medications: Certain medications, such as steroids and antidepressants, can cause weight gain as a side effect.
6. Sleep deprivation: Lack of sleep can disrupt hormones that regulate appetite and metabolism, leading to weight gain.
7. Stress: Chronic stress can lead to emotional eating and weight gain.
8. Age: Metabolism slows down with age, making it more difficult to maintain a healthy weight.
9. Medical conditions: Certain medical conditions such as hypothyroidism, Cushing's syndrome, and polycystic ovary syndrome (PCOS) can also contribute to weight gain.
Treatment options for obesity:
1. Lifestyle modifications: A combination of diet, exercise, and stress management techniques can help individuals achieve and maintain a healthy weight.
2. Medications: Prescription medications such as orlistat, phentermine-topiramate, and liraglutide can aid in weight loss.
3. Bariatric surgery: Surgical procedures such as gastric bypass surgery and sleeve gastrectomy can be effective for severe obesity.
4. Behavioral therapy: Cognitive-behavioral therapy (CBT) and other forms of counseling can help individuals develop healthy eating habits and improve their physical activity levels.
5. Meal replacement plans: Meal replacement plans such as Medifast can provide individuals with a structured diet that is high in protein, fiber, and vitamins, and low in calories and sugar.
6. Weight loss supplements: Supplements such as green tea extract, garcinia cambogia, and forskolin can help boost weight loss efforts.
7. Portion control: Using smaller plates and measuring cups can help individuals regulate their portion sizes and maintain a healthy weight.
8. Mindful eating: Paying attention to hunger and fullness cues, eating slowly, and savoring food can help individuals develop healthy eating habits.
9. Physical activity: Engaging in regular physical activity such as walking, running, swimming, or cycling can help individuals burn calories and maintain a healthy weight.
It's important to note that there is no one-size-fits-all approach to treating obesity, and the most effective treatment plan will depend on the individual's specific needs and circumstances. Consulting with a healthcare professional such as a registered dietitian or a physician can help individuals develop a personalized treatment plan that is safe and effective.
Cryptorchidism can be classified into two types:
1. Abdomenal cryptorchidism: In this type, the testis is located in the abdominal cavity above the inguinal ring and is not covered by any skin or membrane.
2. Inguinoscrotal cryptorchidism: In this type, the testis is located in the inguinal canal and may be covered by a thin layer of skin or membrane.
Cryptorchidism is usually diagnosed at birth or during childhood, and it can occur as an isolated condition or as part of other congenital anomalies. Treatment options for cryptorchidism include:
1. Watchful waiting: In mild cases, doctors may choose to monitor the child's development and delay any treatment until they are older.
2. Surgical repair: In more severe cases or those that cause discomfort or other complications, surgery may be recommended to move the testes into the scrotum.
3. Hormone therapy: In some cases, hormone therapy may be used to stimulate the descent of the testes.
4. Assisted reproductive technology (ART): In cases where fertility is a concern, ART such as in vitro fertilization (IVF) may be recommended.
It's important to note that cryptorchidism can increase the risk of complications such as testicular cancer, infertility, and twisting or inflammation of the testes (torsion). Regular check-ups with a healthcare provider are essential for monitoring and managing this condition.
Cattle diseases refer to any health issues that affect cattle, including bacterial, viral, and parasitic infections, as well as genetic disorders and environmental factors. These diseases can have a significant impact on the health and productivity of cattle, as well as the livelihoods of farmers and ranchers who rely on them for their livelihood.
Types of Cattle Diseases
There are many different types of cattle diseases, including:
1. Bacterial diseases, such as brucellosis, anthrax, and botulism.
2. Viral diseases, such as bovine viral diarrhea (BVD) and bluetongue.
3. Parasitic diseases, such as heartwater and gapeworm.
4. Genetic disorders, such as polledness and cleft palate.
5. Environmental factors, such as heat stress and nutritional deficiencies.
Symptoms of Cattle Diseases
The symptoms of cattle diseases can vary depending on the specific disease, but may include:
1. Fever and respiratory problems
2. Diarrhea and vomiting
3. Weight loss and depression
4. Swelling and pain in joints or limbs
5. Discharge from the eyes or nose
6. Coughing or difficulty breathing
7. Lameness or reluctance to move
8. Changes in behavior, such as aggression or lethargy
Diagnosis and Treatment of Cattle Diseases
Diagnosing cattle diseases can be challenging, as the symptoms may be similar for different conditions. However, veterinarians use a combination of physical examination, laboratory tests, and medical history to make a diagnosis. Treatment options vary depending on the specific disease and may include antibiotics, vaccines, anti-inflammatory drugs, and supportive care such as fluids and nutritional supplements.
Prevention of Cattle Diseases
Preventing cattle diseases is essential for maintaining the health and productivity of your herd. Some preventative measures include:
1. Proper nutrition and hydration
2. Regular vaccinations and parasite control
3. Sanitary living conditions and frequent cleaning
4. Monitoring for signs of illness and seeking prompt veterinary care if symptoms arise
5. Implementing biosecurity measures such as isolating sick animals and quarantining new animals before introduction to the herd.
It is important to work closely with a veterinarian to develop a comprehensive health plan for your cattle herd, as they can provide guidance on vaccination schedules, parasite control methods, and disease prevention strategies tailored to your specific needs.
Conclusion
Cattle diseases can have a significant impact on the productivity and profitability of your herd, as well as the overall health of your animals. It is essential to be aware of the common cattle diseases, their symptoms, diagnosis, treatment, and prevention methods to ensure the health and well-being of your herd.
By working closely with a veterinarian and implementing preventative measures such as proper nutrition and sanitary living conditions, you can help protect your cattle from disease and maintain a productive and profitable herd. Remember, prevention is key when it comes to managing cattle diseases.
Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:
1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)
The symptoms of adenocarcinoma depend on the location of the cancer and can include:
1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
7. Fatigue
8. Coughing up blood (in the case of lung adenocarcinoma)
The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.
Treatment options for adenocarcinoma depend on the location of the cancer and can include:
1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.
The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.
Treatment options include medications such as alpha-blockers and 5-alpha-reductase inhibitors, minimally invasive therapies such as transurethral microwave therapy or laser therapy, and surgical intervention such as a transurethral resection of the prostate (TURP) or robotic-assisted laparoscopic surgery.
There are also lifestyle changes that can help manage Prostatic Hyperplasia, including limiting fluid intake before bedtime, avoiding caffeine and alcohol, and following a healthy diet. It is important to consult with a healthcare professional for proper diagnosis and treatment of this condition.
In simpler terms, Prostatic Hyperplasia is an enlargement of the prostate gland which can cause urinary problems and discomfort. Treatment options include medication, minimally invasive therapies, and surgery, and lifestyle changes can also help manage the condition.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
There are several types of atrophy that can occur in different parts of the body. For example:
1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.
Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.
In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.
People with AIS typically have female physical characteristics, such as a lack of facial and body hair, a narrow pelvis, and underdeveloped genitalia. They may also experience infertility and heightened risk of certain medical conditions, such as gonadal dysgenesis and cardiovascular disease.
AIS is diagnosed through a combination of clinical evaluation, hormone level testing, and genetic analysis. Treatment options for the condition include hormone replacement therapy to promote masculinization and address any associated medical issues, as well as psychological support and counseling to address any gender identity or expression concerns.
It is important to note that AIS is a rare condition, and its prevalence is estimated to be around 1 in 10,000 to 1 in 20,000 male births. However, the condition is often misdiagnosed or undiagnosed, and some individuals may not receive an accurate diagnosis until later in life.
Overall, Androgen Insensitivity Syndrome is a complex and rare genetic disorder that can have significant implications for the physical and psychological well-being of affected individuals. It is important to provide appropriate medical care and support to those with AIS to help them live healthy and fulfilling lives.
Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.
Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.
There are several different types of pain, including:
1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.
The medical field uses a range of methods to assess and manage pain, including:
1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.
It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.
Castration
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The question: What's chemical castration?
Metastatic Prostate Cancer1
- Despite initially responding to castration, most metastatic prostate cancer patients eventually experience progression. (bvsalud.org)
Chemical castration5
- The bill would give offenders a choice: agree to something called "chemical castration" as a condition of release, or stay in jail. (krqe.com)
- According to Cleveland Clinic, "chemical castration" refers to the use of chemicals or drugs to stop sex hormone production. (krqe.com)
- They call it chemical castration, that's basically Depo-Provera [a hormonal contraceptive] injections. (krqe.com)
- Research over the last 50 years suggests that drugs like medroxyprogesterone acetate, which can be used for chemical castration, are associated with a decline in male libido. (krqe.com)
- This type of treatment is sometimes called "chemical castration. (medlineplus.gov)
Enzalutamide6
- The purpose of this study is to assess the safety and efficacy of nivolumab in combination with rucaparib, docetaxel, or enzalutamide in participants with castration-resistant prostate cancer that has spread. (clinicaltrials.gov)
- For a study, researchers investigated the safety, pharmacokinetic impact, and efficacy of the glucocorticoid receptor (GR) antagonist mifepristone combined with enzalutamide in a castration-resistant prostate cancer (CRPC) phase I/II trial. (physiciansweekly.com)
- In this context, a post-hoc analysis of the phase 3 PREVAIL study was performed with the aim to compare enzalutamide with placebo in terms of OS, adjusting for potential confounding from switching to antineoplastic therapies that are not part of standard metastatic castration-resistant prostate cancer (mCRPC) treatment pathways in some jurisdictions. (whiterose.ac.uk)
- The US Food and Drug Administration (FDA) has approved the oral PARP inhibitor talazoparib (Talzenna, Pfizer) plus enzalutamide (Xtandi) to treat homologous recombination repair (HRR) gene-mutated metastatic castration-resistant prostate cancer . (medscape.com)
- Patients with metastatic castration-resistant prostate cancer harboring HRR genetic alterations have even worse outcomes, and thus the FDA's approval of the talazoparib and enzalutamide combination "represents a treatment option deserving of excitement and attention. (medscape.com)
- 2. Ríos González E, Martínez-Piñeiro L. Enzalutamide in castration resistant prostate cancer. (who.int)
Docetaxel2
- Randomization was stratified according to PTEN-loss by immunohistochemical assay, receipt of prior docetaxel in the castration-sensitive disease space, progression by PSA alone, presence of visceral metastases, and geographic region. (urotoday.com)
- Salvage therapy for castration-refractory prostate cancer resistant to docetaxel]. (bvsalud.org)
Abiraterone Acetate2
- BACKGROUND: Abiraterone acetate plus prednisone significantly improved radiographic progression-free survival compared with placebo plus prednisone in men with chemotherapy-naive castration-resistant prostate cancer at the interim analyses of the COU-AA-302 trial. (lu.se)
- These results further support the favourable safety profile of abiraterone acetate in patients with chemotherapy-naive metastatic castration-resistant prostate cancer. (lu.se)
Patients7
- This study investigates how well radium-223 works in treating patients with castration-resistant prostate cancer than has spread to the bones (bone metastases). (clinicaltrials.gov)
- UroToday.com) There has been a rapid change in the past few years for patients with advanced prostate cancer, including metastatic castration-resistant prostate cancer (mCRPC). (urotoday.com)
- Eligible patients had asymptomatic or mildly symptomatic metastatic castration-resistant prostate without previous treatment in this disease space. (urotoday.com)
- Une fois le taux de castration atteint à la fin du premier mois, ce taux de testostérone est ensuite maintenu aussi longtemps que les patients. (bridgeinnovationinstitute.com)
- All patients maintained castration status. (bvsalud.org)
- Despite treatment advancement in metastatic castration-resistant prostate cancer, the disease can progress quickly, and many patients may only receive one line of therapy," lead investigator Neeraj Agarwal, MD, of the Huntsman Cancer Institute, University of Utah, said in a statement . (medscape.com)
- Patients with metastatic castration-resistant prostate cancer (mCRPC), who have not received previous a.2. (who.int)
Hormone1
- Some endocrine facts, such as the sequelae coined the term "hormone" for this internal of castration, are deeply rooted in the past. (who.int)
Infection2
Surgery1
- Surgery to remove the testicles (castration) stops the production of most androgens in the body. (medlineplus.gov)
Rubber1
- Rubber rings were used for band castration in the 1-week and 2-month calves and a Callicrate bander was used in 4-month calves. (beefresearch.ca)
Techniques4
- Ranch owners and employees were advised to use standardized, age-specific techniques for lamb castration (e.g. (cdc.gov)
- Melches S, Mellema SC, Doherr MG, Wechsler B, Steiner A. Castration of lambs: a welfare comparison of different castration techniques in lambs over 10 weeks of age. (cdc.gov)
- Canada's Code of Practice for the Care and Handling of Beef Cattle requires that castration be performed by an experienced person who uses proper, clean, well-maintained equipment and accepted techniques. (beefresearch.ca)
- Strictly speaking, the effect of castrating at different ages couldn't be compared statistically, because the calves were castrated in different months, and because handling and castration techniques varied slightly between the age groups. (beefresearch.ca)
Production1
- Chez l'homme, le testicule est en partie responsable de la production de cette vitamine. (bridgeinnovationinstitute.com)
Actual1
- I read several accounts where people went for actual castration because they could not stop themselves from being attracted to young boys - usually that's the case - and so, I presented it as: This is compassionate. (krqe.com)
Weeks1
- Standing and lying behavior was significantly altered in the six to nine weeks following castration in calves banded at 4-months of age compared to control or surgically castrated calves. (beefresearch.ca)
Similar1
- Regarding children with or without disabilities, 2) State University of Campinas to despise equity is a gesture similar to castration. (bvsalud.org)
Care1
- The lawyer for a Wakefield man charged with sexually abusing multiple children at his wife's unlicensed day care center says his client is willing to undergo "physical castration" in exchange for a reduced sentence, but prosecutors aren't interested in a deal. (wbur.org)
Trial1
- Horst B. last lived in Markt Schwaben and admitted to the castration offenses as the trial got underway on Thursday. (dw.com)
Metastatic castration-resistant prostate5
- The treatment of patients with metastatic castration-resistant prostate cancer (mCRPC) has seen stepwise improvement since 2002, when it was shown that zoledronic acid could reduce skeletal-related event incidence. (medscape.com)
- Non-metastatic castration-resistant prostate cancer (nmCRPC) is only seen in about 4% to 7% of patients with prostate cancer. (medscape.com)
- Characterization of the prostate cancer transcriptome and genome has identified chromosomal rearrangements and copy number gains and losses, including ETS gene family fusions, PTEN loss and androgen receptor (AR) amplification, which drive prostate cancer development and progression to lethal, metastatic castration-resistant prostate cancer (CRPC). (nih.gov)
- non-metastatic castration-resistant prostate cancer (nmCRPC). (nih.gov)
- These metastatic castration-resistant prostate cancers (mCRPC) have a spectrum of molecular aberrations. (nih.gov)
Prostate4
- In spite of early responses to treatment with androgen deprivation therapy , most patients eventually progress to castration-resistant prostate cancer (CRPC). (medscape.com)
- Until recently, patients with castration-resistant prostate cancer (CRPC) had limited therapeutic options once they became refractory to docetaxel chemotherapy, and no treatments improved survival. (nih.gov)
- The mutational landscape of lethal castration-resistant prostate cancer. (nih.gov)
- Even after castration, dogs may still serve as a source of infection because the bacteria can persist in the prostate and lymphoid tissues ( 13 , 14 ). (cdc.gov)
MCRPC1
- The presence of SPOP mutation (SPOP-mutant [SPOP-mut]) may therefore impact therapeutic outcomes with AR-directed therapies and docetaxel in metastatic castration-resistant (mCRPC). (nih.gov)
Body1
- Surgery to remove the testicles (castration) stops the production of most androgens in the body. (medlineplus.gov)
Study1
- Stemming from Freud's clinical report on a child's animal phobia, a careful study is done on the process of building a chain of signifiers which points to the equation castration-anxiety-repression. (bvsalud.org)