The Escherichia coli protein YfeX functions as a porphyrinogen oxidase erectile dysfunction mayo clinic buy zudena 100 mg without prescription, not a heme dechelatase broccoli causes erectile dysfunction order zudena 100 mg without prescription. Congenital erythropoietic porphyria: characterization of murine models of the severe common (C73R/C73R) and later-onset genotypes erectile dysfunction treatment wikipedia discount 100mg zudena amex. Gaucher disease with foamy transformed macrophages and erythrophagocytic activity erectile dysfunction treatment nhs generic zudena 100mg with mastercard. Harderoporphyria due to homozygosity for coproporphyrinogen oxidase missense mutation H327R. Discovery of a gene involved in a third bacterial protoporphyrinogen oxidase activity through comparative genomic analysis and functional complementation. Hepatoerythropoietic porphyria due to a novel mutation in the uroporphyrinogen decarboxylase gene. Low-dose hydroxychloroquine is as effective as phlebotomy in treatment of patients with porphyria cutanea tarda. Molecular expression and characterization of erythroid-specific 5-aminolevulinate synthase gain-of-function mutations causing X-linked protoporphyria. Loss-of-function ferrochelatase and gain-of-function erythroid-specific 5-aminolevulinate synthase mutations causing erythropoietic protoporphyria and x-linked protoporphyria in North American patients reveal novel mutations and a high prevalence of X-linked protoporphyria. Diagnosis of feline acute intermittent porphyria presenting with erythrodontia requires molecular analyses. Recent insights into the biological functions of liver fatty acid binding protein 1. Liver Transplantation for Acute Intermittent Porphyria: Biochemical and Pathologic Studies of the Explanted Liver. Noncanonical coproporphyrin-dependent bacterial heme biosynthesis pathway that does not use protoporphyrin. A method for determining delta aminolevulinic acid synthase activity in homogenized cells and tissues. Pitfalls in Erythrocyte Protoporphyrin Measurement for Diagnosis and Monitoring of Protoporphyrias. Acute Intermittent Porphyria in children: A case report and review of the literature. Experiences and concerns of patients with recurrent attacks of acute hepatic porphyria: A qualitative study. Acute Hepatic Porphyrias: Recommendations for Evaluation and Long Term Management. Identification and characterization of 40 novel hydroxymethylbilane synthase mutations that cause acute intermittent porphyria. Relapse of porphyria cutanea tarda after treatment with phlebotomy or 4-aminoquinoline antimalarial: A Meta analysis. Sex differences in vascular reactivity in mesenteric arteries from a mouse model of acute intermittent porphyria. Murine models of the human porphyrias: Contributions toward understanding disease pathogenesis and the development of new therapies. Managing acute porphyrias: practice considerations in inpatient and outpatient settings. Allogeneic hematopoietic cell transplantation for primary immune deficiency diseases: current status and critical needs. Outcomes of patients with severe combined immunodeficiency treated with hematopoietic stem cell transplantation with and without 130 preconditioning. Improving cellular therapy for primary immune deficiency diseases: recognition, diagnosis, and management. B-cell function in severe combined immunodeficiency after stem cell or gene therapy: a review. Expansion of immunoglobulin-secreting cells and defects in B cell tolerance in Rag-dependent immunodeficiency. Transplantation of hematopoietic stem cells in human severe combined immunodeficiency: longterm outcomes. Long-term outcome and lineage specific chimerism in 194 patients with Wiskott-Aldrich syndrome treated by hematopoietic cell transplantation in the period 1980-2009: an international collaborative study. Autoimmunity in a cohort of 130 pediatric patients with partial DiGeorge syndrome. The case for newborn screening for severe combined immunodeficiency and related disorders. Excellent survival after sibling or unrelated donor stem cell transplantation for chronic granulomatous disease. Laboratory technology for population-based screening for severe combined immunodeficiency in neonates: the winner is T-cell receptor excision circles. Hypomorphic Janus kinase 3 mutations result in a spectrum of immune defects, including partial maternal T-cell engraftment. Controversies in IgG replacement therapy in patients with antibody deficiency diseases. Unresolved issues in hematopoietic stem cell transplantation for severe combined immunodeficiency: need for safer conditioning and reduced late effects. Newborn screening for severe combined immunodeficiency and T-cell lymphopenia in California: results of the first 2 years. The natural history of children with severe combined immunodeficiency: baseline features of the first fifty patients of the primary immune deficiency treatment consortium prospective study 6901. Expanding the spectrum of recombination-activating gene 1 deficiency: a family with early-onset autoimmunity. Effect of weight and maturation on busulfan clearance in infants and small children undergoing hematopoietic cell transplantation. Etoposide selectively ablates activated T cells to control the immunoregulatory disorder hemophagocytic lymphohistiocytosis. A systematic analysis of recombination activity and genotype phenotype correlation in human recombination-activating gene 1 deficiency. Recommendations for live viral and bacterial vaccines in immunodeficient patients and their close contacts. Comparison of outcomes of hematopoietic stem cell transplantation without chemotherapy conditioning by using matched sibling and unrelated donors for treatment of severe combined immunodeficiency. Stem cell transplantation for primary immunodeficiency diseases: the North American experience. History and current status of newborn screening for severe combined immunodeficiency. Population pharmacokinetics of busulfan in pediatric and young adult patients undergoing hematopoietic cell transplant: a model-based dosing algorithm for personalized therapy and implementation into routine clinical use. Molecular mechanisms of functional natural killer deficiency in patients with partial DiGeorge syndrome. Radiation-sensitive severe combined immunodeficiency: the arguments for and against conditioning before hematopoietic cell transplantation-what to do? Lentiviral hematopoietic stem cell gene therapy for X-linked severe combined immunodeficiency. Human mesenchymal stromal cell-secreted lactate induces M2-macrophage differentiation by metabolic reprogramming. The Second Pediatric Blood and Marrow Transplant Consortium International Consensus Conference on Late Effects after Pediatric Hematopoietic Cell Transplantation: Defining the Unique Late Effects of Children Undergoing Hematopoietic Cell Transplantation for Immune Deficiencies, Inherited Marrow Failure Disorders, and Hemoglobinopathies. Treatment of infants identified as having severe combined immunodeficiency by means of newborn screening. Reticular dysgenesis: international survey on clinical presentation, transplantation, and outcome. Long-term outcomes of 176 patients with X linked hyper-IgM syndrome treated with or without hematopoietic cell transplantation. Lentivirus Mediated Correction of Artemis-Deficient Severe Combined Immunodeficiency. Transplacental maternal engraftment and posttransplantation graft-versus-host disease in children with severe combined immunodeficiency. Outcome of domino hematopoietic stem cell transplantation in human subjects: An international case series. Consensus approach for the management of severe combined immune deficiency caused by adenosine deaminase deficiency.
Wiedemann Oldigs Oppermann syndrome
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While overall these rates are similar to erectile dysfunction vegan generic zudena 100mg free shipping those of previous years erectile dysfunction email newsletter discount zudena generic, the proportion of abnormalities in women aged under 20 fell to erectile dysfunction treatment urologist cheap zudena 100mg on line 10 erectile dysfunction za purchase zudena 100 mg without prescription. The age distribution of negative cytology results, as well as low-grade and high-grade cytology results, is shown in Figure 3. An indication of quality is the proportion of Pap tests that are unsatisfactory—those from which the pathologist was unable to determine a clear result. This may be due to too few or too many cells, or to the presence of blood or other factors obscuring the cells, or to poor staining or preservation. While low, the proportion of unsatisfactory cytology tests has increased slightly, from 2. The performance measures for unsatisfactory cytology and abnormalities detected by cytology are detailed in Table 3. The number of Pap tests with no endocervical component increased from 350,670 to 508,758. This increase is also reflected in the steady increase in the proportion of cytology tests with no endocervical component, from 17. As sampling of the transformation zone is required for endocervical cells to be present in a cervical cytology sample, a transformation zone high up in the endocervical canal is likely to be more difficult to sample than a transformation zone on the ectocervix. Cervical cytology is only a prediction, as a screening test is not intended to be diagnostic, but aims to identify people who are more likely to have a cervical abnormality or cervical cancer and therefore require further investigation from diagnostic tests. With this in mind, where cytology was followed by histology (either to confirm the presence or absence of disease as predicted by the cytology sample, or for other clinical reasons, such as to investigate symptoms even in the absence of predicted disease), correlation between the cytology prediction and the histology finding allowed the accuracy of cytological predictions to be assessed. A complete assessment of cytology would have required all cytology results (including negative) to be followed up by histology, but this is neither feasible nor desirable (as it would be unethical to require all women who had a Pap test to also undergo a biopsy). Rather, this assessment is restricted to cytology and histology results available on cervical screening registers, and is intended to provide measures that could be monitored annually to detect early indications of changes to the predictive ability of cervical cytology. Correlation between squamous cytology results and any squamous histology that was performed within 6 months is shown in Figure 3. These data do not include cytology tests not followed by histology, for which it is not possible to know the true disease state, or for cytology tests followed by histology more than 6 months after the cytology test. A cytology prediction of ‘possible high-grade’ was usually found to be high-grade, and a cytology prediction of ‘high-grade’ was almost always found to be high-grade; ‘squamous cell carcinoma’ cytology was usually found to be squamous cell carcinoma. Negative and low-grade abnormalities were not usually followed up with histology, so these results should not be considered indicative of all negative and low-grade cytology. Cervical screening in Australia 2018 15 Possible and definite high-grade squamous abnormalities were usually followed up by colposcopy, and often by histology, so these results can be considered indicative. This is despite abnormalities preceding adenocarcinoma being less well understood than the abnormalities preceding squamous cell carcinoma, and the adequate sampling and subsequent interpretation of endocervical cells being more difficult. These factors all affect the correlation between endocervical cytology and endocervical histology. Detection of high-grade abnormalities in this context is by histology, not by cytology. This is because cytology is not diagnostic, and may under-call or over-call true disease (as visible in the cytology–histology correlation data in Section 3. In 2016, a high-grade abnormality was detected by histology in 14,731 women aged 20–69, which equates to 7. This means that, for every 1,000 women screened, just over 7 had a high-grade abnormality discovered, providing an opportunity for treatment before possible progression to cervical cancer. It is not clear why there was an increase in high-grade abnormality detection for those years. Contributing factors may include the increased use of immunohistochemistry, which can assist in the confirmation of high-grade abnormalities. In contrast with the overall trend of increasing detection over time, there was a steady decline in high-grade abnormality detection in younger women. Visible in the under-20 age group several years ago, this is now clearly contributing to results for the 20–24 age group, and has started contributing to results for the 25–29 age group and, more recently, the 30–34 age group. In addition, this continued decrease in rates for the younger age groups appears to be affecting the overall high-grade abnormality detection rate, despite the other factors that have driven it up, as the latest age-standardised rates of 7. Data for the age groups 25–29 and 30–34 are deceptive—despite showing clear decreases in more recently years (Table A. As expected, coverage decreases with increasing number of doses; in 2016 vaccine coverage for 1 dose was 86. In addition, by moving to the nonavalent vaccine, and decreasing the number of recommended doses, the rate of compliance with the vaccination schedule is expected to increase. The latest national data available are for new cases in 2014; in this latest year 898 new cases of cervical cancer were diagnosed in Australia. Cervical cancer over time There was a modest decrease in the age-standardised incidence of cervical cancer for women aged 20–69 between 1982 and 1990, from 19. Incidence remained steady for this age group at around 9 new cases per 100,000 women until 2010 to 2014, for which incidence was around 10 new cases per 100,000 women (Figure 4. Cervical screening in Australia 2018 27 Number of new cases per 100,000 women 35 1982–1991 1992–2001 30 2002–2011 25 20 15 10 5 0 Age group (years) Note: Rates age-standardised to the Australian population as at 30 June 2001. Histology codes for cancers are collected in the Australian Cancer Database, which allows the analysis of trends in cervical cancer incidence for different histological types. The histological types presented are based on the histological groupings for cervical cancer set out in Chapter 4 of Cancer incidence in five continents vol. Thus, cervical cancer has been disaggregated into the broad histological types of carcinoma (cancers of epithelial origin), sarcoma (cancers originating in connective tissue such as bone, muscle and fat), and other specified and unspecified malignant neoplasms (unusual cancers and cancers too poorly differentiated to be classified). Further, adenosquamous carcinoma has been listed as a separate group under ‘Carcinoma’, rather than included in ‘Other specified carcinoma’ as specified in Curado and others (2007). The latter change is to allow the carcinoma histological groupings to be consistent with the cervical cancer types collected by the cervical cytology registries and reported under the ‘Histology’ performance indicator. Trends in age-standardised incidence for women aged 20–69 for squamous cell carcinoma, adenocarcinoma, adenosquamous carcinoma and other carcinomas are shown in Figure 4. As a result, squamous cell carcinomas now comprise 67% of cervical cancers, much reduced from their historical proportion of 95% (Blomfield & Saville 2008). In contrast, adenocarcinomas have not been reduced by cervical screening to the same degree. In 2009–2013, cervical cancer incidence increased with increasing remoteness and increasing socioeconomic disadvantage. Incidence of cervical cancer in 2009–2013 was similar for Major cities and Inner regional areas, being 9. In 2009–2013, cervical cancer incidence was highest for women living in the lowest socioeconomic areas at 12. In 2010–2014, 5-year survival from cervical cancer decreased with age; women aged 25–29 had the highest survival at 92. Conditional survival for cervical cancer for women aged 20–69 is illustrated in Figure 4. It is related to incidence and survival; if incidence and survival are both high, prevalence will be high, whereas if incidence and survival are both low, prevalence will be low. At the end of 2013, there were 2,924 women aged 20–69 alive who had been diagnosed with cervical cancer in the previous 5 years and 5,060 who had been diagnosed in the previous 10 years (Table 4. The latest national data available at the time of publication were for deaths in 2015. Note that actual mortality data for 2016–2018 may differ from estimated data for these years, due to current and ongoing program or practice changes. Deaths from 1982–2011 were derived by year of death, and are based on the final version of cause of death data. Deaths from 2011–2014 were derived by year of death; deaths in 2015 were derived by year of registration of death. It is also the fifth most common cancer in Indigenous women (behind breast, lung, colorectal and uterus). This chapter therefore aims to bring together the cervical screening participation, incidence and mortality data, and supplements these with additional analyses on incidence, survival and mortality data, as well as incorporating relevant data and findings from other published sources. At the time of reporting, participation in cervical screening cannot be measured nationally for Indigenous women because Indigenous status is not included on all pathology forms in all states and territories, the only source of information for cervical screening registers. However, we can draw on some published data, and a growing body of evidence indicates that Indigenous women are under-screened. A decade ago, Coory and others (2002) and Binns & Condon (2006) estimated participation in cervical screening in communities with high proportions of Indigenous women in Queensland and the Northern Territory, respectively. As this data set matures, it will become increasingly useful for understanding the extent of participation by Indigenous women attending these services.
In another kind of study (cohort study) a large number of people are assigned to erectile dysfunction ed treatment effective zudena 100mg groups on the basis of chemical exposure or nutritional status herbal erectile dysfunction pills nz purchase zudena, and pregnancy outcome is monitored erectile dysfunction doctors in orange county order zudena cheap online. The National Collaborative Perinatal Project erectile dysfunction doctor visit order zudena australia, launched in the 1950s, enrolled more than 4 50,000 pregnant women and followed them until their children were 8 years old. In this kind of study, many factors may contribute to pregnancy outcome and must be controlled for. Case-control studies are most commonly used to study the relationship between environmental factors and birth defects in people. In this kind of study, a group of children with a particular classification of defect is compared with a control group of children without the defect, but otherwise similar, to see if some difference in previous environmental exposures can be identified. This study design is often limited by inability to estimate accurately exposures that occurred months or years previously. Sources of Uncertainty: Additional Challenges to Studying Environmental Causes of Birth Defects Identifying, quantifying, and timing exposures: Identifying, quantifying, and timing chemical exposures during fetal development are major challenges to investigating the role of environmental factors in causing birth defects. A large body of scientific research shows that not only the magnitude of exposure but also its timing is an extremely important determinant of risk because of the specific sequencing of developmental events. If the timing of potentially harmful exposures is not known, a link between birth defects and environmental factors may be missed. For example, children exposed to the drug thalidomide during the third to sixth week of gestation often suffered severe limb deformities, while children exposed later had either no or different health effects. Early exposures to thalidomide, approximately 20-24 days after conception, increased the risk of autism (Rodier, 2000). Classifying birth defects: Regardless of study design, it is often difficult to know how best to group birth defects for analysis. For example, in an attempt to increase the statistical power of a study to identify causal environmental factors by increasing the number of cases, researchers may “lump together” defects that should not be considered in the same category from the standpoint of developmental biology. Yet, because individual defects are relatively rare, statistical power is lost when the number of cases is small. Multifactorial causes of birth defects: Scientific evidence indicates that not all people are equally susceptible to birth defects. Genetic and nutritional factors may combine with other environmental factors to increase the risk. This combination of factors makes it extremely difficult to conduct epidemiologic studies in populations of people when the entire collection of risk factors is not well understood or identified. Though extremely important, modest increases in risk are difficult to demonstrate with a high degree of certainty and often remain unidentified. As a result, some reports of chemical agents that are known to cause birth defects are often limited to those that cause a large increase in risk. For example, some people 5 argue that environmental agents should only be considered relevant and causally related to birth defects if they produce an increased risk of at least 6-fold (Shepard, 1995). In numerous studies, many chemicals, or classes of chemicals, are implicated as significant contributors to the risk of birth defects, though the risk is frequently less than 6 times higher than in unexposed groups. Some Examples of Environmental Exposures That Cause or Are Associated with Birth Defects in Humans this section is based on published reports showing potential links between environmental agents and classes of birth defects in people. This is an important limitation inasmuch as studies of the developmental impacts of chemical exposures are much more numerous in laboratory animals than in humans. It is important to recognize that, for some environmental agents, the evidence for a causal role in birth defects is strong whereas for others, the evidence is less consistent or weaker. For example, an increased risk of oral clefts associated with maternal smoking, is much better established than other environmental risks for clefts. In some cases, studies that are not cited do not find the same associations, and additional investigations may or may not confirm the positive study’s findings. A series of reports investigating the same agent or class of agents may have inconsistent or conflicting conclusions. For many, the best we can conclude is that available data “implicate” particular agents but further investigations are necessary to confirm the findings. This is the state of the science at the current time, highlighting the need for more systematic and focused attention, while at the same time asking when the weight of evidence is sufficient to act to protect health. Some heart defects such as holes in the heart wall may be mild and resolve without surgical intervention. Others like hypoplastic left heart syndrome are incompatible with life unless the baby can survive long enough to receive a heart transplant. Environmental Exposures Associated with Heart Defects Exposure References Maternal medications (Cedergren 2002) (Ericson 2001) (Hernandez-Diaz 2000) (Hook 1994) Hormones, antinauseants, (Loffredo 1993) (Ferencz 1991) (Rubin seizure medications, anti-inflammatory 1991) (Zierler 1985) (Hendrickx 1985) drugs, tranquilzers, antibiotics, codeine, (Rothman 1979) (Heinonen 1977) (Nora ibuprofen 1975) Maternal illness (Cedergren 2002) (Vohra 2001) (Loffredo 1993) (Rosenberg 1987) (Freij 1988) Diabetes, rubella, thyroid disease, 6 toxoplasmosis, Coxsackie virus B Maternal alcohol (Tikkanen 1992, 1988) Maternal occupations/exposures (Loffredo 1997) (Ferencz 1996) (Tikkanen 1992) (Tikkanen 1990) Nursing, dye, lacquer, paint Paternal occupations/exposures (Steinberger 2002) (Loffedo 1993) (Correa Villasenor 1993) (Olshan 1991) Jewelry making, welding, paint stripping, lead soldering, janitors, forestry and logging, painting, plywood mill work, marijuana use, alcohol, smoking Solvents. A cleft lip means that the two sides of the upper lip did not grow together properly. The opening in the lip or palate may be on one side only (unilateral) or on both sides (bilateral). Oral clefts affect approximately one in every 700-1000 newborns with incidence variations in different racial groups. Families with a history of oral clefts in a parent, another child, or close relative, are more likely to have a baby with an oral cleft. This had led researchers to believe that environmental factors can interact with specific genes to interfere with the patterns of normal palate closure and lip development. Babies with encephalocele have a hole in the skull allowing brain tissue to protrude and babies with spina bifida have an opening in the spine that may allow part of the spinal cord to protrude. The defect occurs 5-8 weeks after conception and is thought to be caused by a disruption in the blood flow to the developing abdominal wall. Studies have linked certain medications and environmental chemicals that are known to alter blood flow to increases in gastroschisis. Environmental Exposures Associated with Gastroschisis: Exposure References Maternal medications/exposures (Kozer 2002) (Martainez-Frajas 1997) (Torfs 1996, 1994) (Werler 1992) Aspirin, decongestants, marijuana, cocaine, ibuprofen, acetaminophen, oral (Drongowski 1991) contraceptives Maternal occupations/exposures (Barlow 1982) (Torfs 1996) Printing, exposure to colorants Paternal occupations/exposures (Stoll 2001) Solvents (Torfs 1996, 1994) Living near hazardous waste sites (Dolk 1998) Maternal Smoking (Haddow 1993) (Goldbaum 1989) Maternal radiation (Torfs 1994) Hypospadias Hypospadias is an abnormality of the penis in which the urinary tract opening is not at the tip. It is a relatively common condition that occurs in about 1 per 300-500 live births. Over the last 25 years, however, the incidence and severity of hypospadias has reportedly doubled in the United States and Europe. Recent 10 studies indicate that exposures that affect hormone balance during pregnancy may be associated with increases in hypospadias. The data in this table are limited to major structural defects and do not include premature birth, retarded growth, or other developmental toxicity. Babies can be small either because of premature birth or because of retarded growth in the uterus. Strong predictors of prematurity include multiple gestation, prior preterm birth, and African-American ethnicity (Vintzileos, 2002). Other Kinds of Developmental Abnormalities Associated with Environmental Exposures Testing for developmental toxicity is an emerging science. Test methods are still undergoing development in laboratory animals and relatively few environmental chemicals have been examined for their ability to alter development in people. As a result, the functional impacts of fetal exposure to the large majority of environmental chemicals on the immune, reproductive, nervous, and endocrine systems are unknown. Considerable information does exist for a few environmental contaminants, showing that the fetus is commonly more sensitive to exposures than an adult. Exposures during developmental windows of susceptibility can have long-term and even life-long impacts, many of which are not detectable at birth. The growing human brain, for example, is uniquely vulnerable to exposures to lead, mercury, manganese, polychlorinated biphenyls, alcohol, toluene, various other drugs of abuse, and pesticides (see table). Animal studies confirm the unique susceptibility of the developing brain to these and other commonly encountered chemicals. Similarly, the immature immune system is vulnerable to long-term disruption after exposure to some industrial and environmental chemicals. The field of developmental immunotoxicology is in its infancy, and there is little consensus surrounding the meaning of various changes in immune system parameters after fetal exposures. Based on available information, however, it is clear that developmental immunotoxicants can alter susceptibility to infection and other diseases, including allergies. For example: Maternal use of the synthetic estrogen, diethylstilbestrol, during pregnancy increases the risk of their daughters later developing vaginal, cervical, and breast cancer as well as other abnormalities of the reproductive and immune systems. Their sons are also at increased risk of reproductive tract abnormalities that are not apparent at birth (Herbst, 1970; Giusti, 1995). Similar changes in humans would be expected to increase the risk of prostate and testicular cancer later in life. Although more research will be necessary to clarify our understanding of details, the weight of current scientific evidence demonstrates the unique vulnerability of embryonic and fetal development to environmental exposures.
Contractors are required to erectile dysfunction kit purchase zudena 100 mg without a prescription provide follow-up erectile dysfunction treatment chandigarh cheap zudena online american express, tracking and individualized patient navigation of clients with abnormal results laptop causes erectile dysfunction buy generic zudena line. Identify and take action to erectile dysfunction causes heart generic 100mg zudena amex overcome client barriers such as transportation, scheduling, language and lack of understanding about follow-up procedures; iii. Make a good faith effort to ensure clients receive or are referred to treatment resources for breast or cervical cancer; and iv. Program Component 4 Quality Management Contractors must ensure the quality of services by monitoring internal and subcontractor performance and identifying opportunities for improvement. Contractors must ensure that providers follow evidence-based clinical guidelines consistent with national recognized standards of care. Program Component 6 Recruitment Contractors must establish and promote evidence-based outreach and inreach methods, including development of a plan to recruit priority populations and provide public education. Program Components 8 Partnerships Contractors must establish and maintain partnerships with coalitions, community-based organizations, and other health and human services agencies that further the goal of providing breast and cervical cancer services in the proposed target service area. An Applicant may submit their certification at the time it submits its Application. Applicants are strongly encouraged to propose to use funds to provide both breast and cervical cancer services, however, Applicants may propose to provide either breast or cervical cancer services. If the Applicant proposes to provide only one service, the Applicant must provide an explanation that documents how providing both services would create duplication of services or how it is not viable for Applicant to provide both services. Applicants must document in their Work Plan how eligible women and priority populations will receive services from them. Applicants must provide estimates of the number of women to be provided breast and cervical cancer screening and diagnostic services in the Project period (September 1, 2017 to August 31, 2018) (see Form L). Failure to meet these measures may result in reduction and/or termination of funding. P a g e | 12 Health and Human Services Commission Breast and Cervical Cancer Services Open Enrollment Number: 529 17 0134 C. Contractor locations should have access to a broadband connection with a minimum of: i. Quality Monitoring Contractor will be monitored for quality and compliance with programmatic and clinical policies and standards as set forth in the resulting contract. The final required matching contribution will be determined based on the final award amount. Subcontractors providing services under the resulting contract shall meet the same requirements and level of experience as required of the Applicant. No subcontract under the contract shall relieve the Contractor of the responsibility for ensuring the requested services are provided. Applicants planning to subcontract all or a portion of the work to be performed shall identify the proposed subcontractors in their Application. All Contractors must comply with applicable cost principles, audit requirements, and administrative requirements. All Contractors are required to maintain a financial management system that meets federal and state standards for expending and accounting for funds received under an award. This requires establishing within the chart of accounts and general ledger, a separate set of accounts for each program attachment. All financial reports should be prepared with information that comes directly from the organization’s accounting system. There should be a reconciliation of the information that is reported to amounts recorded in the accounting system. All services and deliverables under the resulting contract shall be provided at an acceptable quality level and in a manner consistent with acceptable industry standard, custom, and practice. Contractors must provide services as required under the resulting contract that meet the following performance measures and quality indicators for this Project. A minimum of twenty percent (20%) of clients newly enrolled for cervical cancer screening should be women who have not had a Pap test in the last 5 years. A minimum of seventy-five percent (75%) of all program-reimbursed mammograms should be provided to program eligible women who are 50 years of age and older and not enrolled in Medicare-Part B. Cervical Cancer Diagnostic Indicators P a g e | 14 Health and Human Services Commission Breast and Cervical Cancer Services Open Enrollment Number: 529 17 0134 i. A minimum of ninety percent (90%) of abnormal cervical screening results must have a complete follow-up with no more than 10% lost to follow up, refused, and/or pending. The intervals between initial screening and diagnosis of abnormal cervical cancer screenings should be ninety (90) days or less for a minimum of seventy-five percent (75%) of the women with abnormal results. The interval between diagnosis and initiation of treatment for invasive cervical cancer should be sixty (60) days or less for a minimum of 80% of the women diagnosed. A minimum of ninety percent (90%) of abnormal breast screening results must have a complete follow-up with no more than ten percent (10%) lost to follow up, refused, and/or pending. The interval between initial screening and diagnosis of abnormal breast cancer screening result should be sixty (60) days or less for a minimum of seventy-five percent (75%) of women with abnormal results. A minimum of ninety percent (90%) of breast cancer diagnoses must have started treatment. The interval between diagnosis and initiation of treatment for breast cancer should be sixty (60) days or less for a minimum of eighty percent (80%) of women needing treatment. A minimum of eighty-five percent (85%) of proposed unduplicated clients must be served. P a g e | 15 Health and Human Services Commission Breast and Cervical Cancer Services Open Enrollment Number: 529 17 0134 3. Costs of developing applications, preparing for or participating in oral presentations and site visits, or any other similar expenses incurred by an Applicant are entirely the responsibility of the Applicant, and will not be reimbursed in any manner by the State of Texas. Application Submission Instructions Applicant must submit the required documents in one of the following forms: (i) mail one (1) electronic copy of all required documents as scanned versions (. All portable media devices and their content must be compatible with Microsoft Office 2013. Organization of Electronic Submission of Application Applicant should organize its scanned and signed Application packets in the below order and format. Each electronic copy of the Application packet should include the following respective listed documents and the documents should be in the following order. All Applications must be submitted by hand delivery, by courier, by email, by fax, or by mail. P a g e | 18 Health and Human Services Commission Breast and Cervical Cancer Services Open Enrollment Number: 529 17 0134 4. If the Application passes the initial screening, the Applicant will be contacted for further instructions or actions. P a g e | 19 Health and Human Services Commission Breast and Cervical Cancer Services Open Enrollment Number: 529 17 0134 4. P a g e | 20 Health and Human Services Commission Breast and Cervical Cancer Services Open Enrollment Number: 529 17 0134 5. Federal agency responsible for protecting the health and safety of all Americans, both foreign and domestic, by providing funding for Centers for Disease essential health services and conducting critical scientific research. In accordance with Performance Measure requirements, any day of Day the week including weekends. The set minimum amount of income that a family needs for food, clothing, transportation, shelter and other necessities. In the United States, this level is determined by the Department of Health Federal Poverty and Human Services. The number of people residing together for which legal responsibility Household exists. Activities that are conducted with the purpose of informing and In-reach educating existing clients within an organization about services they are not receiving, but may be eligible to receive. The Breast and Cervical Cancer Prevention and Treatment Act of 2000 authorizes the state to provide medical assistance through Medicaid for breast and cervical cancer treatment for eligible women. An individualized approach of identifying and assessing barriers to care where establishing, brokering, and sustaining a system of Patient Navigation available clinical and essential support services ensures clients receive timely and appropriate services. P a g e | 22 Health and Human Services Commission Breast and Cervical Cancer Services Open Enrollment Number: 529 17 0134 6. Email: I, the undersigned, am the authorized representative of the applicant filing this contract renewal application.
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