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PubMedDate not supplied

Foetal co-relates and mode of delivery in asphyxia neonatorum.

A prospective study was conducted on consequitively born live births for determining the role of certain foetal factors and mode of delivery on asphyxia neonatorum. The difference in the incidence of neonatal asphxia in 1208 singleton births (8.5%) and in the 66 multiple births (9.7%) was statistically significantly (p less than 0.01). Among the singleton live births a significantly increased incidence of asphyxia was recorded in preterms when compared to term and post term babies collectively (p less than 0.001). Small for date babies were at a greater risk for asphxia neonatorum when compared to babies weighing appropriate for gestational age (p less than 0.001). An inverse relationship was observed between birth weight and asphyxia neonatorum. A significant difference was seen in the occurrence of neonatal asphyxia between babies weighing less than 2000 g. and those weighing more than 2000 g. (p less than 0.001). The incidence was significantly influenced by mode of delivery, being highest in vaginal breech delivery followed in decreasing frequency by forceps and normal vaginal delivery. Among vaginal breech delivered neonates those weighing greater than or equal to 2500 g were at the highest risk. Evidence of foetal distress and meconium stained amniotic fluid had a low predictability of asphyxia being 35.0% and 40.0% respectively though both were statistically significant (p less than 0.001).

Asphyxia Neonatorum↗
PubMed1997

Effect of asphyxia on urinary epidermal growth factor levels in newborns.

Urinary epidermal growth factor (EGF) excretion in normal newborn as well as neonates with asphyxia was investigated by using radioimmunoassay, and serum creatinine (Scr) levels determined at the same time. The results showed that in severe asphyxia group the ratio of urinary EGF to urinary creatinine (Cr) (EGF/Cr), an index reflecting EGF excretion, was decreased on the first day (P < 0.05) and reached the lowest level on the third day (P < 0.01). However, EGF/Cr values were decreased only on the third day in neonates with mild asphyxia (P < 0.05). On the seventh day, EGF/Cr values of neonates with asphyxia rose to normal. There were a negative correlation between urinary EGF/Cr and Scr. It is suggested that EGF may play a role in the repair of acute renal injury after asphyxia and the detection of urinary EGF concentration is useful in the judgment of severity of renal injury and in the evaluation of the recovery of renal tubule after injury.

Acute Kidney Injury↗
PubMed1999

Immunohistochemical localization of c-fos in the nuclei of the medulla oblongata in relation to asphyxia.

The immediately early gene product c-fos is known to be induced in neurons under noxious stimuli. Therefore, the immunohistochemistry of c-fos expression in human brains might offer information on the localization of stimulated neurons. In this study, the immunohistochemical localization of c-fos was studied in the neurons of the hypoglossal nucleus (XII), the dorsal motor nucleus of the vagal nerve (X), the nucleus solitarius (Sol), the accessory cuneate nucleus (Cun), the spinal trigeminal nucleus (V) and the inferior olive (Oli) of the human medulla oblongata from forensic autopsy cases. The neurons in the X nucleus showed the highest percentage of positive reactions for c-fos, followed in descending order by the Cun, V, Oli, XII and Sol. The c-fos immunoreactivity in the Cun and X was statistically significantly higher than in the Sol, XII and Oli. Although neurons in the Sol are known to be involved in respiration, there was no statistically significant difference in the c-fos immunoreactivity in the neurons in the Sol between asphyxia and non-asphyxia cases. On the other hand, the percentage of neurons positive for the c-fos immunoreactivity was statistically significantly higher in the Oli of asphyxia cases than of non-asphyxia cases. Our results indicate the difference in the immunoreactivity of c-fos among the nuclei of the human medulla oblongata and that the c-fos immunoreactivity in the Oli might assist the diagnosis of asphyxia.

Adolescent↗
PubMed2000

Immunohistochemical investigation of a pulmonary surfactant in fatal mechanical asphyxia.

We evaluated the usefulness of pulmonary surfactant protein A (SP-A) as a practical diagnostic marker of fatal mechanical asphyxia in forensic autopsy cases. A total of 27 cases of asphyxia were examined histologically and immunohistochemically and compared with a control group consisting of 16 cases of poisoning (n = 9) and peracute death (n = 7). Both groups showed histological findings of local atelectasis and local emphysema, congestion, intra-alveolar and interstitial edema in most cases and pulmonary hemorrhages in some cases. The mechanical asphyxia group showed a significantly increased intensity of SP-A staining in the intra-alveolar space accompanied by many massive aggregates in approximately 60% of cases, which was not found in the control group. These structures may be interpreted as aggregates of pulmonary surfactant released from the alveolar wall due to enhanced secretion caused by strong forced breathing or over-excitement of the autonomic nervous system by mechanical asphyxia. The results of our investigation suggest the practical usefulness of the immunohistochemical detection of SP-A in distinguishing mechanical asphyxia from other types of hypoxia.

Adolescent↗
PubMed2006

Plasticity of the central nervous system (CNS) following perinatal asphyxia: does nicotinamide provide neuroprotection?

We have investigated the idea that nicotinamide, a non-selective inhibitor of the sentinel enzyme Poly(ADP-ribose) polymerase-I (PARP-1), provides neuroprotection against the long-term neurological changes induced by perinatal asphyxia. Perinatal asphyxia was induced in vivo by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Sibling caesarean-delivered pups were used as controls. The effect of perinatal asphyxia on neurocircuitry development was studied in vitro with organotypic cultures from substantia nigra, neostriatum and neocortex, platted on a coverslip 3 days after birth. After approximately one month in vitro (DIV 25), the cultures were treated for immunocytochemistry to characterise neuronal phenotype with markers against the N-methyl-D-aspartate receptor subunit 1 (NR1), the dopamine pacemaker enzyme tyrosine hydroxylase (TH), and nitric oxide synthase (NOS), the enzyme regulating the bioavailability of NO. Nicotinamide (0.8 mmol/kg, i.p.) or saline was administered to asphyctic and caesarean-delivered pups 24, 48 and 72 h after birth. It was found that nicotinamide treatment prevented the effect of perinatal asphyxia on several neuronal parameters, including TH- and NOS-positive neurite atrophy and NOS-positive neuronal loss; supporting the idea that nicotinamide constitutes a therapeutic alternative for the effects produced by sustained energy-failure conditions, as occurring during perinatal asphyxia.

Animals↗
PubMed2006

Long-term effect of moderate and profound hypothermia on morphology, neurological, cognitive and behavioural functions in a rat model of perinatal asphyxia.

BACKGROUND: Perinatal asphyxia is a frequent cause of neurological handicap with no known therapy. However, hypothermic therapy has recently attracted attention owing to its neuroprotective property in brain of immature organisms. OBJECTIVES: Hypothermia appears to be promising in reversing the immediate effect of perinatal asphyxia, but data on long-term neuroprotection is still lacking. We therefore intended to test the long-term effect of moderate and profound hypothermia on brain morphology and functions using a well established rat model of perinatal asphyxia. METHODS: Rat pups delivered by caesarean section were placed into a water bath, still in patent membranes, at 37 degrees C and variable hypothermic conditions to induce asphyxia and thereafter given to surrogate mothers. Examinations were performed at the age of three months, consisting of a battery of motor, behavioural, cognition and reflex tests including rota-rod, Morris water maze, multiple T-maze, elevated plus maze and open field studies. Morphological alterations were evaluated by Nissl staining of brain areas known to be hypoxia sensitive. Neurotransmission system markers, including tyrosine hydroxylase, vesicular monoamine transporter, vesicular acetylcholine transporter and excitatory amino acid carrier1 were analyzed by immunohistochemistry. RESULTS: Survival increased with hypothermia. The Nissl stain revealed neuronal loss in hippocampus and hypothalamus of normothermic asphyxiated group (20/37) compared to controls (0/37), but no neuroprotective patterns emerged from hypothermia. An overall inconsistent protection of the neural systems was noted by variable periods of hypothermia. Motor function was significantly impaired in 20/37 as compared to 0/37. In the Morris water maze and multiple T-maze, results were comparable between the groups. In the elevated plus maze, time spent in the closed arm was reduced and in the open field, vertical behaviour was altered in the 20/37 group with horizontal motor behaviour being unaffected. Hypothermia reversed all abnormalities seen in 20/37, with short-term moderate and profound hypothermia being superior to long-term hypothermia. CONCLUSION: Hypothermia not only significantly increased survival, but also resulted in unimpaired motor as well as improved cognitive functions. Those findings are in contrast to altered brain morphology. As neuronal loss was present in various brain regions, we conclude that deficits may be compensated in the maturing animal. Intrahypoxic hypothermia was able to protect the rat from the devastating effect of perinatal asphyxia not in morphological, but in functional terms.

Animals↗
PubMed1975

Clinical characteristics of pregnancies complicated by intrapartum fetal asphyxia.

The clinical characteristics of 124 pregnancies complicated by intrapartum fetal asphyxia have been reviewed. The evidence of fetal asphyxia tends to appear earlier in patients with maternal medical and obstetric complications than in those with labor complications. Evidence of clinical fetal distress was present in 36 per cent and was not related to the severity of the asphyxia. Low Apgar scores occurred in 40 per cent of infants with moderate asphyxia and in 80 per cent of infants with severe asphyxia at delivery. In the newborn infants, clinical evidence of cerebral abnormality was observed in 3 per cent, and evidence of the respiratory distress syndrome was seen in 3 per cent of the study group.

Acidosis↗
PubMed1978

Intrapartum fetal asphyxia: a preliminary report in regard to long-term morbidity.

This is a preliminary report of a prospective follow-up study of 42 infants who had episodes of intrapartum fetal asphyxia at delivery identified by an acid-base assessment and a control group of 69 babies who had no evidence of intrapartum fetal asphyxia. The newborn infants were mature at delivery. There were no major neurologic disabilities in the asphyxia group. The pattern of physical growth and the mental and physical development indices of the babies of the asphyxia group were similar to those of the control group babies at 12 months of age. Results have not as yet indicated that the mature fetus with at least a terminal episode of asphyxia will exhibit evidence of handicap due to central nervous system injury.

Asphyxia Neonatorum↗
PubMed1990

The association of intrapartum asphyxia in the mature fetus with newborn behavior.

A matched cohort study of mature newborns with biochemically determined intrapartum fetal asphyxia and mature newborns with normal blood gas and acid-base assessments at delivery were studied to demonstrate the effect of fetal asphyxia on newborn behavior as expressed by the Brazelton newborn behavioral assessment scale. The newborn behavioral assessment scale was administered 3 days after delivery and again 2 weeks after delivery. The Lester newborn behavioral assessment scale summary scores for the group with asphyxia were of the same order as those in the control group. This was also true of the group of newborns with asphyxia with the more severe metabolic acidosis and those with low Apgar scores. These findings support the contention that many newborns who have undergone an intrapartum asphyxial insult will not have evidence of central nervous system injury and that the threshold of central nervous system injury is at the severe end of the spectrum of asphyxia as expressed by a metabolic acidosis.

Age Factors↗
PubMed1984

Asphyxia, cardiac arrest and resuscitation in rats. II. Long term behavioral changes.

This study in 53 rats was conducted to investigate a mild insult, sensitive parameter model in contrast to a severe insult, severe damage model of brain resuscitation. Up to now, the latter approach, which causes neuropathologic changes and neurological abnormalities, has not provided unequivocal data on pharmacological measures to ameliorate post-anoxic brain damage, because of logistical difficulties and many extracranial complicating factors. As tracheotomy and oral intubation in rats proved impractical in studies on recovery from asphyxia, transtracheal jet ventilation was tested in 14 rats as a measure for effective prolonged and reversible control of airway and ventilation. Subsequently, in 37 other rats we studied, during the first post-insult week, the effects of anesthesia, with or without 6 min asphyxia, on behavior, i.e. unrestrained spontaneous locomotor activity and two sessions of one-trial passive avoidance. Transtracheal jet ventilation proved a reliable method for reversible and prolonged controlled ventilation in rats. Spontaneous locomotor activity was affected for at least 48 h after anesthesia and differently so after asphyxia. Passive avoidance was affected only after asphyxia. The recovery of behavior was delayed for days, whereas the recovery of neurologic deficits was only delayed for several post-asphyxia hours. The asphyxiated rats showed hyper-excitability for at least 2 weeks. The existence of abnormal behavior during recovery from mild anoxic-ischemic insults to the brain provides parameters for evaluation of therapies of the post-resuscitation disease in a model without the difficulties encountered in models with severe insults, which made post-insult intensive care necessary. The mild insult, sensitive parameter model is promising and further work in this direction is indicated.

Animals↗
PubMed1995

Nicotine treatment counteracts perinatal asphyxia-induced changes in the mesostriatal/limbic dopamine systems and in motor behaviour in the four-week-old male rat.

In the present study, the effects of nicotine treatment on the changes induced by perinatal asphyxia in exploratory and D-amphetamine-induced behaviour, and in the number of brain tyrosine hydroxylase-immunoreactive nerve cell bodies were investigated in four-week-old male rats. Asphyxia was induced in pups by placing the fetuses, still in their uterus horns removed by hysterectomy from full-term pregnant rats, in a 37 degrees C water bath for 15-16 min or 19-20 min. Surviving male pups were treated with nicotine via suckling from surrogate mothers implanted subcutaneously with Alzet minipumps containing nicotine (0.2 mumol/kg per h) for four weeks. The minipumps implanted in the mothers of sham-treated animals contained saline only. After treatment, exploratory behaviour and D-amphetamine-induced behaviour was analysed in a computerized "activity" box. After the behavioural experiments, the rats were taken for tyrosine hydroxylase immunohistochemistry, and the total number of tyrosine hydroxylase immunoreactive cell bodies were counted in the A9 and A10 regions of the substantia nigra and the ventral tegmental area, respectively. Nicotine serum levels were measured using gas chromatography in selected asphyctic and control pups at different periods after delivery. During the exploratory phase, in saline-nurtured rats, 15-16 min of asphyxia slightly increased (approximately 25%) locomotion, motility and rearing. In contrast, 19-20 min of asphyxia reduced the locomotion and rearing by approximately 50%, as compared to controls. An increase in amphetamine-induced behaviours was observed after 15-16 min, but not after 19-20 min of asphyxia, as compared to controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

The renal response to acute asphyxia in spontaneously breathing newborn lambs.

The effects of acute asphyxia on neonatal renal function were examined in spontaneously breathing newborn lambs. 25 min of asphyxia were induced by addition of a respiratory dead space to reduce PaO2 to 41 +/- 3 mm Hg, pH to 7.03 +/- 0.05 and increase PaCO2 to 68 +/- 5 mm Hg (mean +/- S.E.M.). Glomerular filtration rates did not change significantly during or after asphyxia. Immediately following asphyxia significant (P less than 0.05) increases over the baseline were found in urinary flow rates, fractional sodium excretion, absolute sodium excretion and osmolar clearances. These changes were in part secondary to significant (P less than 0.05) increases in plasma glucose concentrations associated with increases (P less than 0.05) in circulating arterial catecholamine concentrations. The percentage of tubular reabsorption of glucose decreased significantly (P less than 0.05) and urinary glucose excretion increased significantly. Renal blood flow was unchanged. Therefore, asphyxia induced significant hyperglycemia which contributed to the concomitant natriuresis and osmotic diuresis in these newborn lambs.

Acute Disease↗
PubMed1984

Dynamic aspects of guinea pig inner hair cell receptor potentials with transient asphyxia.

DC and AC receptor potentials of cochlear inner hair cells in response to tone bursts of various frequencies and intensities were continuously measured during and following periods of transient asphyxia. The effects of asphyxia were most pronounced for low sound pressure level (SPL) acoustic stimuli near the characteristic frequency (CF) of the inner hair cell, leading to vulnerability of the 'tip' of the cell's frequency tuning curve (FTC). The resulting changes in the shape of the FTC are, first, a reduction in tip criterion sensitivity of 10-20 dB without significant loss in sharpness of tuning. Later, when the full effect of 30-45 s asphyxia occurs, tip sensitivity loss between 30 and 65 dB is accompanied by greatly broadened tuning and a shift downward in frequency of the CF by greater than 1/4 octave. The CF shift is due to a progressive loss of high frequency sensitivity. The linear segment of the input-output (intensity) function, plotted as log DC receptor potential versus SPL (at the original CF), becomes longer during the early phase asphyxia, and the slope of the segment declines by 50%. At high SPLs, for all frequencies, the time course of the receptor potential change was similar in shape to that exhibited by the endocochlear potential (EP). In particular, for high sound levels, the recovery of response matches the EP while for low level tip frequency sounds recovery is protracted. No difference between the decline of the AC and DC receptor potentials at CF was observed. Inner hair cell resting membrane potential (Em) hyperpolarized during asphyxia by 2-6 mV, correlating with the change in EP according to a ratio of 1/10 (Em/EP).

Animals↗
PubMed2005

Perinatal asphyxia pathophysiology in pig and human: a review.

In utero fetuses are evidently exposed to several factors that cause an interruption of the oxygen flow through the umbilical cord causing asphyxia leading to hypoxia and metabolic acidosis. These conditions are important causes of intra-partum and neonatal mortality. The main objective of this review is to provide current information regarding the pathophysiology of asphyxia in piglets around parturition; the physiological mechanisms invoked by affected piglets to compensate perinatal hypoxemia are discussed. This review also addresses some similarities and differences of asphyxia between piglets and other mammals, including human neonates. Metabolic acidosis and hypoxia are sequela to asphyxia and can cause profound health effects in postnatal performance because of an abnormal suckling, a reduced absorption of colostrum and inadequate passive transfer of neonatal immunity. Acidosis also cause hypothermia, increased mortality and reduced survival in neonates. One of the first deleterious effects of intrauterine hypoxia is the expulsion of meconium into the amniotic sac leading to meconium staining of the skin, and in severe cases, meconium aspiration into the lungs. Even though there have been technological changes and improvements in husbandry, piglet mortality due to asphyxia remains a major problem. One potential alternative to reduce neonatal mortality in pigs is the monitoring of fetal stress during birth and the implemention of strategies such as the Apgar score, that is often used in human pediatrics. It is also important to consider the physiological, behavioral and biochemical changes that take place during parturition which subsequently impact the vitality, maturity and development of neonatal pigs. Understanding the pathophysiology of fetal hypoxia should help practitioners and farmers implement more effective delivery techniques aimed at reducing neonatal mortality and improving postnatal performance.

Acidosis↗
PubMed2004

Brain-stem auditory impairment during the neonatal period in term infants after asphyxia: dynamic changes in brain-stem auditory evoked response to clicks of different rates.

OBJECTIVE: To explore dynamic changes in brain-stem auditory electrophysiology during the neonatal period in term infants after perinatal asphyxia. METHODS: Sixty-eight term newborn infants who suffered asphyxia were studied on days 1, 3, 5, 7, 14 and 30 after birth. Brain-stem auditory evoked response (BAER) was recorded with clicks, delivered at 21, 51 and 91 s(-1) and > or =40 dB above BAER threshold of each subject. RESULTS: During the neonatal period wave I latency in the infants after asphyxia increased slightly while later BAER components changed more significantly. On the first day after birth wave III and V latencies and I-V and III-V intervals increased significantly at all rates of clicks (ANOVA P<0.01-0.001). On day 3, the latencies and intervals increased further. III-V/I-III interval ratio increased at 51 and 91 s(-1), suggesting a relatively more significant increase in III-V interval than in I-III interval at higher rates. Thereafter, wave III and V latencies and all intervals decreased progressively, although these BAER variables were still significantly longer than in normal controls on days 5 and 7 (P<0.05-0.001) On day 30, all latencies and intervals approached near normal values, with a slight increase in wave V latency and I-V and III-V intervals at 51 and 91 s(-1). CONCLUSIONS: Perinatal asphyxia has a major effect on central auditory function, resulting in acute impairment. The impairment progresses during the first 3 days and then tends towards recovery. By 1 month the impaired auditory function has largely returned to normal. Significant increase in click rates can moderately improve the detection of auditory impairment. SIGNIFICANCE: After perinatal asphyxia early detection of hypoxic-ischaemic damage to the central auditory system and initialisation of neuroprotective and therapeutic measures during the first hours after birth are critical to prevent or reduce deterioration of central impairment.

Acoustic Stimulation↗
PubMed2006

Continued reduction in the incidence of birth trauma and birth asphyxia related to instrumental deliveries after the study period: was this the Hawthorne effect?

BACKGROUND: The incidence of birth trauma and birth asphyxia related to instrumental deliveries in our obstetric unit was high (2.8%) in 1998-1999. A study was performed in 2000 to identify the risk factors. Unexpectedly, the incidence (0.6%) was reduced significantly during the study period. We attributed this phenomenon to the famous Hawthorne effect (tendency to improve performance because of awareness of being studied). OBJECTIVES: The objectives were to study whether there is a continued reduction in the incidence of birth trauma and birth asphyxia related to instrumental deliveries in the post-study period (2001-2003) and to investigate the presence of underlying confounding factors apart from the Hawthorne effect. METHOD: To compare the hospital obstetric statistics among the pre-study period (1998-1999), the study period (2000) and the post-study period (2001-2003), in particular the incidence of birth trauma and birth asphyxia related to instrumental deliveries, the instrumental delivery rate, the overall Caesarean section rate, the Caesarean section rate for no progress of labour, the incidence of failed instrumental delivery, the incidence of attempted instrumental delivery in the operating theatre, and incidence of direct second-stage Caesarean sections. RESULTS: The incidence of birth trauma and birth asphyxia related to instrumental deliveries (0.6%) during the study period (2000) was significantly lower than that (2.8%) during the pre-study period (1998-1999; RR 0.27, 95% CI 0.11-0.70). This phenomenon continued into the post-study period (2001-2003) when the incidence of 1.0% was similarly lower than that in the pre-study period (RR 0.35, 95% CI 0.20-0.64). The instrumental delivery rate decreased further in the post-study period (13.5%) compared with those in the study (16.6%) and pre-study (19.5%) periods (RR 0.81, 95% CI 0.75-0.89 and RR 0.69, 95% CI 0.65-0.74, respectively). There was a marked increase in the direct second-stage Caesarean section rate in the post-study period (7.1%) compared to those in the study (0.4%) and pre-study (0.7%) periods (RR 15.9, 95% CI 5.05-49.73 and RR 9.77, 95% CI 5.28-18.08, respectively). CONCLUSION: A change in obstetric practice was identified that may explain the continued reduction in the incidence of birth trauma and birth asphyxia related to instrumental deliveries in the post-study period.

Asphyxia Neonatorum↗
PubMed1989

Temporal relationships of neuropathologic conditions caused by perinatal asphyxia.

The neuropathologic conditions in 120 perinatal deaths attributed to fetal or newborn asphyxia were examined. Central nervous system necrosis was present in 16 of these deaths. The approximate time of asphyxial insult was established by determining the duration of the process, based on the findings of neuronal necrosis, macrophage response, or an astrocyte response, in conjunction with clinical data. The time of the asphyxial insult for the 16 perinatal deaths was as follows: antepartum fetal asphyxia, two cases; antepartum-intrapartum fetal asphyxia, five cases; intrapartum fetal asphyxia, four cases; and neonatal asphyxia, five cases. These observations indicate that an asphyxial insult may occur in the antepartum period, in the prodromal period of preterm labor, in the intrapartum period, and in the neonatal period. Five to ten percent of the asphyxial insults in each reproductive time period were initially sublethal, allowing necrosis of the brain of the fetus or newborn to develop.

Asphyxia Neonatorum↗
PubMed1994

Failure of acute perinatal asphyxia or meconium aspiration to produce persistent pulmonary hypertension in a neonatal baboon model.

OBJECTIVE: Our purpose was to determine whether perinatal asphyxia or meconium aspiration, or both, can produce the physiologic and histologic pulmonary vascular changes associated with the meconium aspiration syndrome. STUDY DESIGN: Twenty neonatal baboons were studied in four groups: 1, control; 2, meconium aspiration; 3, asphyxia (intermittent cord compression); and 4, asphyxia with meconium aspiration. Animals were ventilated for 24 hours under ketamine, diazepam, and pancuronium. Data were analyzed by means of mixed model analysis of measures. RESULTS: Meconium significantly impaired oxygenation (p < 0.001), whereas concurrent asphyxia moderated this effect (p < 0.034). Meconium also increased the need for ventilatory support (p < 0.002). No animal had persistent pulmonary hypertension; neither systemic nor pulmonary systolic pressures differed statistically between the groups. No animal showed evidence of abnormal pulmonary arteriolar muscularization. CONCLUSION: Sublethal perinatal asphyxia or meconium aspiration were insufficient to produce either the physiologic or histologic changes of severe meconium aspiration syndrome. It is unlikely that intrapartum fetal distress alone can produce this syndrome in human neonates.

Acute Disease↗