How has the COVID-19 pandemic affected patients with primary bladder cancer?

PURPOSE: The COVID-19-induced effects of primary bladder cancer (BC) patients have not yet been clarified. The aim of this study was to investigate the effects of the pandemic on the diagnosis, treatment, and follow-up of primary BC patients. MATERIAL AND METHODS: A retrospective single-center analysis was made of all patients who underwent diagnostic and surgical procedures due to primary BC between November 2018 and July 2021. A total of 275 patients were identified and allocated to one of the groups: Pre-COVIDBC (BC diagnosed before the COVID-19 pandemic) or COVIDBC (during the pandemic). RESULTS: The BC patients diagnosed during the pandemic were mostly at higher stages (T2) (p = 0.04), the risk of non-muscle invasive BC (NMIBC) was higher (p = 0.02), and recurrence and progression scores were increased (p = 0.001) compared to patients diagnosed before the pandemic. The time to surgery from diagnosis (p = 0.001) and symptom duration (p = 0.04) were significantly prolonged during the pandemic and the rate of follow-up significantly decreased (p = 0.03). CONCLUSIONS: The study results highlight the significant increase in muscle invasive BC and the very high risk of NMIBC in patients presenting during the COVID-19 pandemic.

ANTECEDENTES: Los efectos inducidos por la COVID-19 en pacientes con cáncer de vejiga primario no están aclarados actualmente. OBJETIVO: Investigar los efectos de la pandemia en el diagnóstico, el tratamiento y el seguimiento del cáncer de vejiga primario. MÉTODO: Se realizó un análisis retrospectivo unicéntrico de todos los pacientes que se sometieron a procedimientos diagnósticos y quirúrgicos por cáncer primario de vejiga durante noviembre de 2018 y julio de 2021. Se incluyeron 275 pacientes en el estudio. Los pacientes fueron asignados a uno de dos grupos: pre-COVIDBC (antes de la pandemia) o COVIDBC (durante la pandemia). RESULTADOS: Los pacientes con cáncer de vejiga diagnosticados durante la pandemia se encontraban en su mayoría en estadios más altos (T2) (p = 0.04), el grupo de riesgo era más alto en el cáncer de vejiga no invasivo del músculo (p = 0.02), y la recurrencia y las puntuaciones de progresión aumentaron (p = 0.001) en comparación con antes del período pandémico. Además, el tiempo hasta la cirugía desde el diagnóstico (p = 0.001) y la duración de los síntomas (p = 0.04) aumentaron considerablemente durante la pandemia, y la tasa de seguimiento disminuyó significativamente (p = 0.03). CONCLUSIONES: Destaca el aumento significativo del cáncer de vejiga invasivo del músculo y del cáncer de vejiga no invasivo del músculo de muy alto riesgo durante la pandemia.

Effect of Re-TUR time on recurrence and progression in high-risk non-muscle-invasive bladder cancer.

OBJECTIVE: We aimed to investigate the significance of time to re-staging transurethral resection (re-TUR) on recurrence and progression rates in patients with high-risk non-muscle-invasive bladder cancer as a prospective randomized study. METHODS: The patients were randomly separated into three groups according to Re-TUR timing. In Groups 1, 2, and 3, the time interval between initial and re-TUR was 14-28 days, 29-42 days, and 43-56 days, respectively. Cox regression analysis was used to assess the effect of time from initial TUR to re-TUR on oncological outcomes. RESULTS: Twenty patients in Group 1 (14-28 days), 22 patients in Group 2 (29-42 days), and 29 patients in Group 3 (43-56 days) completed the study. Kaplan-Meier plots showed no differences in recurrence-free survival (RFS) and progression-free survival (PFS) rates between the three groups. Cox regression analysis demonstrated that only tumor number was found to be a prognostic factor on RFS rates. CONCLUSION: Our prospective study demonstrated that time laps from initial TUR to re-TUR did not significantly affect on RFS and PFS rates.

OBJETIVO: Nuestro objetivo fue investigar la importancia del tiempo para volver a estadificar la resección transuretral (re-RTU) en las tasas de recurrencia y progresión en pacientes con cáncer de vejiga no músculo invasivo de alto riesgo como un estudio prospectivo aleatorizado. MÉTODO: Los pacientes se separaron aleatoriamente en 3 grupos de acuerdo con el tiempo de Re-TUR. En el grupo 1, 2 y 3, el intervalo de tiempo entre la RTU inicial y la nueva fue de 14 a 28 días, 29 a 42 días y 43 a 56 días, respectivamente. Cox para evaluar el efecto del tiempo desde la RTU inicial hasta la nueva RTU sobre los resultados oncológicos. RESULTADOS: Veinte pacientes del grupo 1, 22 pacientes del grupo 2, 29 pacientes del grupo 3 completaron el estudio. Los gráficos de Kaplan-Meier no mostraron diferencias en las tasas de SLR y SLP entre los tres grupos. El análisis de regresión de Cox demostró que solo se encontró que el número de tumores era un factor pronóstico en las tasas de RFS. CONCLUSIÓN: Nuestro estudio prospectivo demostró que los lapsos de tiempo desde la RTU inicial hasta la nueva RTU no afectaron significativamente las tasas de SLR y SLP.

Report of a new case with pentasomy X and novel clinical findings.

Pentasomy X is an extremely rare sex chromosome abnormality, a condition that only affects females, in which three more X chromosomes are added to the normally present two chromosomes in females. We investigated the novel clinical findings in a 1-year-old female baby with pentasomy X, and determined the parental origins of the X chromosomes. Our case had thenar atrophy, postnatal growth deficiency, developmental delay, mongoloid slant, microcephaly, ear anomalies, micrognathia and congenital heart disease. A conventional cytogenetic technique was applied for the diagnosis of the polysomy X, and quantitative fluorescent polymerase chain reaction (QF-PCR) using 11 inherited short tandem repeat (STR) alleles specific to the chromosome X for the determination of parental origin of X chromosomes. A cytogenetic evaluation revealed that the karyotype of the infant was 49,XXXXX. Comparison of the infant's features with previously reported cases indicated a clinically recognizable specific pattern of malformations referred to as the pentasomy X syndrome. However, to the best of our know-ledge, this is the first report of thenar atrophy in a patient with 49,XXXXX. The molecular analysis suggested that four X chromosomes of the infant originated from the mother as a result of the non disjunction events in meiosis I and meiosis II. We here state that the clinical manifestations seen in our case were consistent with those described previously in patients with pentasomy X. The degree of early hypotonia constitutes an important early prognostic feature in this syndrome. The pathogenesis of pentasomy X is not clear at present, but it is thought to be caused by successive maternal non disjunctions.

MID TERM RESULTS AFTER OPEN HEART SURGERY IN HEMODIALYSIS PATIENTS AWAITING KIDNEY TRANSPLANT: DOES CARDIOVASCULAR SURGICAL INTERVENTION PRIOR TO TRANSPLANTATION PROLONG SURVIVAL?

The aim of this study was to compare the mid and long term postoperative outcomes between the hemodialysis-dependent patients awaiting kidney transplantat who underwent open heart surgery in our department during the last five years, and those who did not receive a renal transplant, to determine the predictors of mortality, and assess the possible contribution of post heart surgery kidney transplantation to survival. The patients were separated into two groups: those who underwent a transplantation after open heart surgery were included in the Tp+ group, and those who did not in the Tp- group Between June 2008 and December 2012, 127 dialysis dependent patients awaiting kidney transplant and who underwent open heart surgery were separated into two groups. Those who underwent transplantation after open heart surgery were determined as Tp+ (n=33), and those who did not as Tp- (n=94). Both groups were compared with respect to preoperative paramaters including age, sex, diabetes mellitus (DM), hypertension (HT), hyperlipidemia (HL), obesity, smoking, chronic obstructive pulmonary disease (COPD), peripheral vascular disease (PVD), left ventricle ejection fraction (EF), Euroscore; operative parameters including cross clamp time, perfusion time, number of grafts, use of internal mammary artery (IMA); postoperative parameters including revision, blood transfusion, ventilation time, use of inotropic agents, length of stay in the intensive care unit and hospital, and follow up findings. Problems encountered during follow up were recorded. Predictors of mortality were determined and the survival was calculated. Among the preoperative parameters, when compared with the Tp- group, the Tp+ group had significantly lower values in mean age, presence of DM, obesity, PVD, and Euroscore levels, and higher EF values. Assessment of postoperative values showed that blood transfusion requirement and length of hospital stay were significantly lower in the Tp+ group compared to the Tp- group, whereas the length of follow up was significantly higher in the Tp+ group. The use of inotropic agents was significantly higher in the Tp- group. A logistic regression analysis was made to determine the factors affecting mortality. Revision (p=0.013), blood transfusion (p=0.017), ventilation time (p=0.019), and length of stay in the intensive care unit (p=0.009) were found as predictors of mortality. Survival rates at years 1, 2 and 3 were 86.1%, 81%, 77.5% in the Tp- group, and 96.0%, 96.3%, 90.4% in the Tp+ group. Median survival rate was 41.35±2.02 in the Tp- group, and 49.64±1.59 in the Tp+ group which was significantly higher compared to the Tp- group (p=0.048). Chronic renal failure is among the perioperative risk factors for patients undergoing open heart surgery. Transplantation is still an important health issue due to insufficiency of available transplant organs. Patients with chronic renal failure are well known to have higher risks for coronary artery disease. A radical solution of the cardiovascular system problems prior to kidney transplantation seems to have a significant contribution to the post transplant survival.

Connexin 26 and 30 mutations in paediatric patients with congenital, non-syndromic hearing loss treated with cochlear implantation in Mediterranean Turkey.

OBJECTIVE: Mutations in the genes for connexin 26 (GJB2) and connexin 30 (GJB6) play an important role in autosomal recessive, non-syndromic hearing loss. This study aimed to detect the 35delG and 167delT mutations of the GJB2 gene and the del(GJB6-D13S1830) mutation of the GJB6 gene in paediatric patients diagnosed with congenital, non-syndromic hearing loss and treated with cochlear implantation in Mediterranean Turkey. MATERIALS AND METHOD: We included 94 children diagnosed with congenital, non-syndromic hearing loss and treated with cochlear implantation. Blood samples were collected, DNA extracted and an enzyme-linked immunosorbent assay performed to enable molecular diagnosis of mutations. RESULTS: Of the 94 children analysed, the 35delG mutation was detected in 12 (12.7 per cent): 10 (83.3 per cent) were homozygous and 2 (16.7 per cent) heterozygous mutant. The 167delT and del(GJB6-D13S1830) mutations were not detected. CONCLUSION: The GJB2-35delG mutation is a major cause of congenital, non-syndromic hearing loss in this study population.

Inheritance of a Chromosome 3 and 21 Translocation in the Fetuses, with One also Having Trisomy 21, in Three Pregnancies in One Family.

The majority of chromosome rearrangements are balanced reciprocal and Robertsonian translocations. It is now known that such abnormalities cause no phenotypic effect on the carrier but lead to increased risk of producing unbalanced gametes. Here, we report the inheritance of a translocation between chromosomes 3 and 21 in a family with one of two fetuses with Down Syndrome carrying the same translocation and the other also carrying the same translocation without the additional chromosome 21. Chromosomal analysis from fetal amniotic fluid and peripheral blood lymphocytes from the family were performed at the Çukurova University Hospital at Adana, Turkey. We assessed a family in which the translocation between chromosomes 3 and 21 segregates: one of the three progenies carried the 47,XX,+21,t(3;21)(q21;q22) karyotype and presented with Down Syndrome; another of the three progenies carried the 46,XX,t(3;21) (q21;q22) karyotype and the third had the 46,XY karyotype. Their mother is phenotypically normal. Apparently this rearrangement occurred due to an unbalanced chromosome segregation of the mother [t(3;21)(q21;q22)mat]. This family will enable us to explain the behavior of segregation patterns and the mechanism for each type of translocation from carrier to carrier and their effects on reproduction and numerical aberrations. These findings can be used in clinical genetics and may be used as an effective tool for reproductive guidance and genetic counseling.

Association of the Nramp1 gene polymorphisms and clinical forms in patients with tuberculosis.

BACKGROUND: Recent studies have reported that Nramp1 polymorphisms might have an important role in the development of tuberculosis in various populations. In this study, we aimed to determine Nramp1 polymorphisms in our patients with tuberculosis population. METHODS: We enrolled 127 patients with active tuberculosis and 116 healthy adults with similar age and gender. Peripheral blood samples were taken for determining the Nramp1 polymorphisms. By using Polymerase Chain Reaction (PCR) - Restriction Fragment Length Polymorphisms (RFLP) technique, we evaluated the polymorphisms of Nramp1 at the regions of D543N and INT4. RESULTS: We found that the Nramp1 polymorphisms at the region of D543N (OR: 0.44, 95%CI: 0.09-2.06 for GA allele) were not a risk factor for tuberculosis. Furthermore, we could not able to detect Nramp1 polymorphism at the regions of INT4 (OR: 0.97, 95%CI: 0.55-1.72 for GC allele and OR: 0.90, 95%CI: 0.21-3.77 for CC allele). CONCLUSION: The findings of the present study do not support the hypothesis that Nramp1 at the regions of D543 and INT4 might play a role in influencing the growth of bacilli and progression of cavitary tuberculosis rather than susceptibility to M. tuberculosis infection. Future studies are needed to elucidate the role of Nramp1 variants in the pathogenesis of tuberculosis (Tab. 3, Ref. 29).

Rapid detection of fetal aneuploidies by quantitative fluorescent-polymerase chain reaction for prenatal diagnosis in the Turkish population.

Prenatal diagnosis is testing for diseases or conditions in a fetus or embryo before it is born. It employs a variety of techniques to determine the health and condition of an unborn fetus. The main goal of this process is to perform prenatal diagnosis at the earliest possible stage of gestation. In this regard, quantitative fluorescent-polymerase chain reaction (QF-PCR), a novel technique that is fast and reliable, was employed to detect aneuploidies (13, 18, 21, X and Y) without the need of the time-consuming culturing process. The QF-PCR method can detect five different chromosome aneuploidies with 98.6% accuracy. In this study, 1874 amniotic fluid samples of pregnant subjects, who were referred to the Department of Medical Biology and Genetics, Adana, Turkey (molecular biology section), were analyzed with the QF-PCR technique by employing 27 short tandem repeat (STR) markers to detect chromosomes 13, 18, 21, X and Y aneuploidies. We detected 31 subjects (1.7%) with aneuploidies or euploidies out of the 1874 subjects. The average age of the pregnant subjects was 32 (range: 14-49). Abnormal karyotypes detected were as follows: 47,XX,+21 (19.4%, 6/31), 47,XY,+21 (48.4%, 15/31), 48,XXX,+21 (3.2%, 1/31), 69,XXX (3.2%, 1/31), 47,XY,+13 (3.2%, 1/31), 47,XXY (9.6%, 3/31), 47,XXX (9.6%, 3/31) and 45,X (3.2%, 1/31). Moreover, some STR markers were found to be more specific to the Turkish population. In conclusion, QF-PCR can be regarded as an alternative method of conventional cytogenetic analysis as it is a rapid and reliable method; however, in most cases it is required to be supported or validated with conventional cytogenetic karyotyping and some STR markers employed for QF-PCR can be more informative for a given population.

Association of serum sex steroid levels and bone mineral density with CYP17 and CYP19 gene polymorphisms in postmenopausal women in Turkey.

Many clinical conditions, including osteoporosis, are associated with serum levels of sex steroids. Enzymes that regulate rate-limiting steps of steroidogenic pathways, such as CYP17 and CYP19, are also regarded as significant factors that may cause the development of these conditions. We investigated the association of two common polymorphisms, in the promoter region (T→C substitution) of CYP17 and exon 3 (G→A) of CYP19, with bone mineral density (BMD) in the lumbar spine and femoral neck and serum androgen/estradiol, in a case-control study of 172 postmenopausal women aged 62.3 ± 9.6 years (mean ± SD). The CYP17 TC genotype was significantly overrepresented in patients compared to controls, and TC genotype neck T-score and lumbar T-score values were significantly higher in patients compared to controls. CYP17 TC and TT genotype testosterone and DHEA-SO(4) levels were lower in patients compared to controls. All three genotypes of CYP19 had almost the same distribution among patients. The CYP19 AG genotype, however, was most frequent among controls. CYP19 lumbar BMD levels were close to each other among the different genotypes; however, AA and AG genotypes were significantly lower in patients. Testosterone and DHEA-SO(4) levels in the CYP19 GG genotype were higher compared to those of the other genotypes in patients but not in controls. CYP19 GA individuals had lower E(2) levels and lower BMD in controls and patients. Femoral neck BMD and lumbar T-score were also diminished with GA transition. In conclusion, CYP17 and CYP19 gene polymorphisms were found to be associated with osteoporosis in postmenopausal women in Turkey.

Analysis of peripheral blood T-cell subsets, natural killer cells and serum levels of cytokines in children with Down syndrome.

The objective of this study was to evaluate the relationship between humoral and cell-mediated immune response parameters and impairment of immune functions in children with Down syndrome (DS). The patient group was consisted of cytogenetically documented 32 children with DS. Lymphocyte subsets and natural killer cells were counted by flow-cytometry system. Levels of interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, IL-10 and tumour necrosis factor-alpha (TNF-alpha) were detected by enzyme-linked immunosorbent assay method. Serum IgG, IgM, IgA levels were measured by turbidimetric methods. The percentage of CD8+ lymphocytes and CD56+ cells of patients with DS were significantly higher, whereas CD20+ lymphocytes were lower than that of controls (P < 0.05). The percentage of CD2 and CD4 levels and CD4/CD8 ratio of patients with DS and normal controls were similar (P > 0.05). Levels of IL-4 and IL-10 were significantly increased, but IL-6 and TNF-alpha levels were decreased in children with DS (P < 0.05). Levels of other studied cytokines between patients with DS and controls were not statistically different (P > 0.05, for all). Serum IgG, IgM and IgA levels were found to be similar between the groups (P > 0.05). It has been known that IL-4 and IL-10 are anti-inflammatory molecules which inhibit the synthesis of proinflammatory cytokines such as IL-6 and TNF-alpha. In this study, levels of IL-4 and IL-10 were significantly increased, but IL-6 and TNF-alpha levels were decreased in children with DS. These results may suggest that continuing anti-inflammatory state in DS and this process may explain the cause of recurrent infection of the disease. On the other hand, in contrast to the low percentage of CD20+ cells, high percentage of CD8+ and CD56+ cells were found. Our findings may demonstrate that the cell-mediated and humoral immune system parameters in children with DS were altered according to healthy children.

The clinical effects of isochromosome Xq in Klinefelter syndrome: report of a case and review of literature.

We describe a male with a variant Klinefelter syndrome (KS), and trisomy Xq resulting from an isochromosome Xq [47,Xi(Xq)Y]. He had many characteristics of classical KS: bilateral atrophic testes and microcalcifications, normal masculinization, azoospermia, hypergonadotropic hypogonadism, elevated FSH and LH, normal intelligence and normal androgenization, but his stature was not increased. Ultrasonographic evaluation also revealed parenchymal alterations secondary to previous epididymo-orchitis. After initial evaluation the patient underwent incisional biopsy of testes which showed tubular hyalinisation, Leydig cell hyperplasia and Certoli cell syndrome. The i(Xq) was found in all cells analyzed. These findings indicate that extra copies of the long arm of X have phenotypic expression, even though activated only in early development. In conclusion, review of literature on 20 adult patients supports the view that the presence of an isochromosome Xq in KS has a favorable prognosis in terms of normal mental development and normal stature.

Inheritance of a translocation between chromosomes 12 and 16 in a family with recurrent miscarriages and a newborn with Down syndrome carrying the same translocation.

Reciprocal translocation carriers have reduced fertility, increased risk of spontaneous abortion or unbalanced karyotype in their offspring. Here, we report the inheritance of a translocation between chromosomes 12 and 16 in a family with recurrent miscarriages and a newborn with Down syndrome carrying the same translocation. Chromosomal analysis from fetal amniotic fluid and peripheral blood lymphocytes from the family were performed at the Cukurova university hospital in Turkey. We assessed a family in which the translocation between chromosomes 12 and 16 segregates; one of the eight progenies with the karyotype 47,XY,+21,t(12;16)(q24;q24) was heterozygote for the translocation and presented with Down syndrome. His mother is phenotypically normal, one brother and one sister were also carrying the same translocation. Apparently, this rearrangement occurred due to the unbalanced chromosome segregation of the mother [t(12;16)(q24;q24)mat]. This case will enable us to explain the behavior of segregation patterns and the mechanism for each type oftranslocation from carrier to carrier and their effects on reproduction and numerical aberrations. The t(12;16) is also associated with fetal wastage and may play a role in the etiology of the family's miscarriages. These findings can be used in clinical genetics and may be used as an effective tool for reproductive guidance and genetic counseling.

Cytogenetic study of recurrent miscarriages and their parents.

There are substantial evidences that genetic alterations are contributing factors to the risk for recurrent miscarriages. This study was conducted to determine the frequency and contribution of chromosomal abnormalities in miscarriages and in couples with recurrent miscarriages. We studied a total of 41 miscarriages and their parents with a history of 2-11 recurrent miscarriages. Chromosomal analysis from chorionic villus sampling (CVS) and fetal tissues were performed according to standard cytogenetic methods using G-banding technique. Major chromosomal aberrations and polymorphic variants were found in 51 and 4.8%, respectively. The chromosomal abnormalities were structural (34.4%) and numerical (65.1%) of which 26.1, 21.7, 8.7 and 8.7% were fetal sex aneuploid, triploid, mosaics and trisomic, respectively. Unbalanced and balanced rearrangements were found in 17.2% and 8.6% of all abnormalities, respectively. Major chromosomal abnormalities in couples were seen in 4.9%. The chromosomal abnormalities associated with pregnancy losses and recurrent miscarriages are mostly numerical ones. The incidence of balanced translocations found here is 4.9% which is near to the mode (about 3-6%) observed in the previous studies. Those frequencies are greater than in the general population (0.3%). This indicates that balanced translocations, seen in parents, have some importance in causing miscarriage. The major parental chromosomal aberrations are significantly associated with fetal wastage. Mosaicism should be taken into account for cytogenetic analyses of pregnancy losses. Thus, cytogenetic analyses should be recommended in couples with recurrent miscarriages, when clinical data fail to clarify the cause.

Chromosomal fragile sites in schizophrenic patients.

Schizophrenia is a common and complex mental disorder. Cytogenetic and molecular studies have shown that genetic factors play an important role in the etiology of schizophrenia. As a preliminary step in the search for chromosomal location of a susceptible gene predisposing to schizophrenia, cytogenetic screening patients might be useful. Therefore, this report is aimed at studying the relationship between chromosomal fragile sites (FS: gaps, breaks, triradial figures, and several rearrangements) and the etiology of schizophrenia. Because of this, we were compared the frequencies of folate-sensitive FS from schizophrenic patients and normal individuals in short-term whole blood cultures. The rate of FS expression in the patients was considerably higher than in the controls. We determined 15 common FS (cFS) (1q21, 1q32, 2q21, 2q31, 3p14, 4q31, 5q31, 6q21, 6q26, 7q22, 7q32, 10q22, 13q32, Xp22 and Xq22), 6 rare FS (rFS) (6p21, 8q22, 11q23, 12q24, 16q22, and Xq26) and 2 previously unknown FS (3p25 and 5q22). Among these expressed FS, there was a significantly higher frequency of 12 FS at 2q31, 3p25, 3p14, 5q31, 6q21, 7q22, 7q32, 10q22, 11q23, 12q24, Xq22 and Xq26 in patient group than in controls by chi2 test (P = between 0.0001 to 0.036). Sites 3p14, 5q31 and 7q22 were also the most frequently observed cFS. Males exhibited twice as many FS as females, but no age effects were observed. The potential relationship between increased FS frequency and the occurrence of schizophrenia in these patients is discussed.

Cerebellar hypoplasia and quadrupedal locomotion in humans as a recessive trait mapping to chromosome 17p.

BACKGROUND: Congenital hereditary non-progressive hypoplasia of the cerebellum is a rare condition, frequently associated with other neuropathology such as lissencephaly. Clinically, the condition is associated with variable degrees of mental retardation, microcephaly, seizures, and movement disorders due to ataxia. In severe cases, patients are unable to ambulate independently, but nevertheless do use bipedal locomotion. METHODS AND RESULTS: Here we present a family with seven affected members, five of whom never learned to walk on two legs but have fully adapted to quadrupedal palmigrade locomotion. These subjects show signs of cerebellar ataxia and are mentally retarded. MRI analysis demonstrated hypoplasia of the cerebellum and the cerebellar vermis as well as a small nucleus dentatus and a thin corpus callosum but no other malformations. We show, by a genome-wide linkage scan, that quadrupedal locomotion is a recessive trait linked to chromosome 17p. CONCLUSIONS: Our findings have implications for understanding the neural mechanism mediating bipedalism, and, perhaps, the evolution of this unique hominid trait.